Autopsy

Question 1

Lungs normal

Answer 1

The lungs are normally lobulated and situated at a normal anatomical position exhibiting a normal (regular) shape and size with 700 g weight.

The pleural surfaces are smooth and glistening.

The consistency of the lobes is spongy having an evenly air-filled parenchyma.

The color of the lungs is gray in the upper and reddish in the lower located regions, the alveolar structures are grossly preserved.

On cut section there is no significant fluid escaping from the pulmonary parenchyma.

The trachea and the bronchi are in normal anatomical positions with regular caliber, and their inner layers are covered by intact mucosal surfaces; their lumen is empty all along the bronchial system.

The branches of the pulmonary arteries are patent with smooth intima, and without the presence of thrombotic/embolic occlusion. The hilar and mediastinal lymph nodes show black pigmentation.

Question 2

Answer 2

diffuse alveolar damage, exudative stage (numerous causes)

Hyaline membrane, edema, inflammatory cell infiltration

Diffuse alveolar damage (DAD) is a pathological term used to describe the lung injury pattern typically seen in acute respiratory distress syndrome (ARDS). It involves widespread damage to the alveoli, the tiny air sacs in the lungs responsible for gas exchange, leading to inflammation, fluid leakage, and impaired oxygenation.

ARDS stands for Acute Respiratory Distress Syndrome. It’s a severe lung condition characterized by rapid onset of widespread inflammation in the lungs, leading to difficulty breathing and low oxygen levels in the blood.

Causes can include pneumonia, sepsis, aspiration of stomach contents, trauma, inhalation of toxins, and other severe injuries or infections that trigger an inflammatory response in the lungs.

The pathomechanism of diffuse alveolar damage (DAD) involves several key steps:

1. Initial Injury: This can be caused by various factors such as infection, trauma, toxins, or aspiration. The injury damages the alveolar epithelium and capillary endothelium.
2. Inflammatory Response: The damaged cells release inflammatory mediators, such as cytokines and chemokines, leading to the recruitment and activation of immune cells, primarily neutrophils and macrophages.
3. Increased Permeability: The inflammatory response disrupts the integrity of the alveolar-capillary barrier, leading to increased permeability. This allows fluid, protein, and inflammatory cells to leak into the alveolar space.
4. Edema Formation: The increased permeability results in the accumulation of fluid in the alveoli, leading to pulmonary edema. This impairs gas exchange and reduces lung compliance.
5. Fibrin Deposition: Fibrin, a protein involved in blood clotting, accumulates in the alveolar space due to increased permeability and activation of coagulation pathways. This contributes to the formation of hyaline membranes, a characteristic feature of DAD.
6. Tissue Repair and Fibrosis: In severe cases, the ongoing inflammation and repair processes can lead to fibrosis of the lung tissue, impairing lung function and potentially leading to long-term complications.

Overall, diffuse alveolar damage is a complex process involving inflammation, increased permeability, edema formation, and tissue repair, ultimately leading to impaired gas exchange and respiratory failure.

Question 3

Answer 3

Slightly elevated, granular, firm gray-red to yellow, poorly demarcated areas
(up to 4 cm) patchily distributed around airways; may be multilobar; often
basilar:
• bronchopneumonia

areas of lighter tan consolidation. The hilum is seen at the lower right with radiating pulmonary arteries and bronchi.Many bronchopneumonias follow an earlier viral pneumonia, particularly in older persons in the winter months when influenza is more common.

Bronchopneumonia is a type of pneumonia characterized by inflammation and infection of the bronchioles (small airways) and surrounding lung tissue.

It typically results from the spread of bacteria, viruses, or other pathogens from the upper respiratory tract into the lungs.

Bronchopneumonia often presents with patchy areas of consolidation and inflammation in the lungs, rather than the more homogeneous involvement seen in other types of pneumonia.

The pathomechanism of bronchopneumonia involves a series of events:

1. Inhalation or Aspiration of Pathogens: The process often begins with the inhalation or aspiration of infectious agents such as bacteria, viruses, or fungi into the respiratory tract.
2. Colonization and Infection of Airways: The pathogens colonize and infect the bronchioles (small airways) and adjacent lung tissue. This can occur due to impaired mucociliary clearance, compromised immune function, or pre-existing lung conditions.
3. Inflammatory Response: The presence of pathogens triggers an inflammatory response in the affected airways and lung tissue. Immune cells, particularly neutrophils and macrophages, are recruited to the site of infection to combat the invading pathogens.
4. Exudate Formation: In response to inflammation, the airways may produce excessive mucus and inflammatory exudate, leading to obstruction of the air passages and impaired gas exchange.
5. Consolidation and Infiltrates: As the infection progresses, areas of consolidation and inflammatory infiltrates develop in the affected lung tissue. This can be observed as patchy or lobar patterns on imaging studies such as chest X-rays or CT scans.
6. Clinical Manifestations: Patients with bronchopneumonia typically present with symptoms such as cough, fever, chest pain, shortness of breath, and production of purulent sputum. The severity of symptoms can vary depending on the extent and severity of the infection.
7. Complications: In severe cases, bronchopneumonia can lead to complications such as respiratory failure, sepsis, and lung abscess formation.

Overall, bronchopneumonia is characterized by inflammation and infection of the bronchioles and surrounding lung tissue, resulting in respiratory symptoms and potential complications. Treatment usually involves antibiotics targeted at the causative pathogens, along with supportive care to alleviate symptoms and promote recovery.

Question 4

Answer 4

Consolidation in large areas of lobe or even in entire lobe = lobar pneumonia

most lobar pneumonias are due to Streptococcus pneumoniae (pneumococcus)

Stages of lobar pneumonia:
• Stage of congestion:
• lungs heavy and boggy
• Red hepatization:
• lungs red, firm, airless
• Gray hepatization:
• lungs gray-brown, dry, firm
• Resolution:
• patchy return to normal-appearing lung parenchyma
• Organization:
• areas of firm, gray-tan lung

The pathomechanism of lobar pneumonia involves a series of events triggered by the inhalation or aspiration of infectious agents, typically bacteria, into the lungs. Here’s how it typically unfolds:

1. Initial Exposure to Pathogens:
   
   • Lobar pneumonia usually begins with the inhalation or aspiration of bacteria, such as Streptococcus pneumoniae, into the lower respiratory tract. This can occur during breathing or when pathogens from the upper respiratory tract are aspirated into the lungs.
2. Adherence and Colonization:
   
   • The inhaled pathogens adhere to the mucosal surfaces of the airways and alveoli in the affected lobe(s) of the lung, allowing them to colonize and multiply.
3. Inflammatory Response:
   
   • The presence of bacteria triggers an inflammatory response in the lung tissue. This involves the release of pro-inflammatory cytokines, recruitment of immune cells (such as neutrophils and macrophages), and activation of the complement system.
4. Alveolar Exudate Formation:
   
   • Inflammatory mediators induce increased vascular permeability and leakage of fluid and proteins into the alveolar spaces. This leads to the formation of an exudate rich in inflammatory cells, fibrin, and cellular debris.
5. Consolidation and Hepatization:
   
   • The exudate fills the alveoli and airways, causing consolidation of lung tissue within the affected lobe(s). The affected lung becomes firm and solid, resembling the texture of the liver, a process known as “hepatization.”
6. Impaired Gas Exchange:
   
   • The consolidation of lung tissue impairs gas exchange within the affected lobe(s), leading to ventilation-perfusion mismatch and hypoxemia (low blood oxygen levels).
7. Clinical Manifestations:
   
   • Patients with lobar pneumonia typically present with symptoms such as fever, productive cough (with rusty or purulent sputum), chest pain, dyspnea (shortness of breath), and systemic symptoms such as fatigue and malaise.
8. Resolution or Complications:
   
   • With appropriate treatment (such as antibiotics and supportive care), lobar pneumonia can resolve, with resolution of inflammation and restoration of normal lung function. However, untreated or severe cases can lead to complications such as abscess formation, pleural effusion, or sepsis.

Overall, lobar pneumonia is characterized by the focal consolidation of lung tissue within one or more lobes, resulting from an inflammatory response to bacterial infection in the lower respiratory tract. Early recognition and prompt treatment are crucial in preventing complications

Question 5

Answer 5

1- to 1.5-cm gray-white, subpleural caseous lesion typically in superior
portion of lower lobe with associated gray-white caseous lesion in hilar lymph
nodes:

• primary pulmonary tuberculosis

• Small foci of caseous necrosis typically in apex of one or both lungs with
similar lesions in regional lymph nodes:

• early secondary (reactivation) tuberculosis

• Cavities lined by yellow-gray caseous material:
• progressive secondary tuberculosis (cavitary fibrocaseous tuberculosis)
• Fibrocalcific scars, cavities in lung apices:
• healed secondary tuberculosis

The pathomechanism of tuberculosis (TB) involves a complex interplay between the infecting organism, Mycobacterium tuberculosis, and the host immune response. Here’s an overview:

1. Infection and Primary Lesion Formation:
   
   • TB infection typically begins when M. tuberculosis bacilli are inhaled and reach the alveoli of the lungs.
   • Alveolar macrophages phagocytose the bacilli, but M. tuberculosis can survive and replicate within these cells.
   • Infected macrophages may transport the bacilli to regional lymph nodes, where an adaptive immune response is initiated.
2. Granuloma Formation:
   
   • In most cases, the immune response successfully contains the infection within granulomas, which are organized structures composed of immune cells, primarily macrophages, surrounded by lymphocytes.
   • Within the granuloma, infected macrophages undergo a process called “caseous necrosis,” leading to the formation of a central necrotic core.
3. Latent TB vs. Active Disease:
   
   • In latent TB infection, the immune response controls the infection, and the individual remains asymptomatic. However, viable bacilli persist within the granulomas.
   • In some cases, especially when the immune system is compromised, latent TB can progress to active disease, leading to symptomatic illness and transmission of the bacteria.
4. Immune Response and Tissue Damage:
   
   • The immune response to M. tuberculosis involves both cellular and humoral components. T cells play a crucial role in controlling the infection, but excessive inflammation can lead to tissue damage.
   • Cytokines released during the immune response contribute to the recruitment and activation of immune cells, formation of granulomas, and tissue destruction in severe cases.
5. Dissemination and Extrapulmonary TB:
   
   • In some cases, particularly in immunocompromised individuals or those with weakened immune responses, M. tuberculosis can disseminate beyond the lungs to other organs, causing extrapulmonary TB.
   • Extrapulmonary TB can affect sites such as the lymph nodes, bones, joints, meninges, and kidneys, leading to a wide range of clinical manifestations.

Overall, tuberculosis is characterized by a dynamic interplay between the host immune response and the pathogen, leading to the formation of granulomas, tissue damage, and potentially disseminated infection. Factors influencing the outcome include the virulence of the infecting strain, the immune status of the host, and environmental factors.

Question 6

Patchy, or confluent, unilateral or bilateral consolidation and congestion

Lungs

Answer 6

acute interstitial pneumonias due to viruses,
• Mycoplasma pneumoniae,
• Chlamydia species,
• Coxiella species

Question 7

Patchy, firm parenchyma

Answer 7

interstitial lung diseases of various causes

interstitial lung disease (ILD) refers to a group of lung conditions where there’s inflammation and scarring of the tissue around the air sacs in the lungs. This scarring makes it harder for the lungs to work properly, causing symptoms like shortness of breath, coughing, and fatigue. There are many different causes of ILD, including things like autoimmune diseases, exposure to certain substances, and infections. Treatment depends on the specific cause and can include medications, oxygen therapy, and sometimes lung transplantation.

The pathomechanism of interstitial lung diseases (ILDs) involves a complex interplay of factors that lead to inflammation and fibrosis (scarring) of the lung tissue. While the specific mechanisms can vary depending on the underlying cause of ILD, there are common pathways involved:

1. Inflammatory Response:
   
   • In response to various triggers such as infections, environmental exposures, autoimmune diseases, or unknown factors, the immune system mounts an inflammatory response in the lungs.
   • Immune cells, including macrophages, lymphocytes, and neutrophils, are recruited to the lung tissue, leading to inflammation.
2. Fibroblast Activation and Fibrosis:
   
   • Chronic or persistent inflammation triggers the activation of fibroblasts, specialized cells responsible for producing collagen and other extracellular matrix components.
   • Activated fibroblasts proliferate and deposit excessive collagen, leading to the formation of scar tissue within the interstitium (the tissue between the air sacs and blood vessels in the lungs).
3. Alveolar Epithelial Injury:
   
   • In some ILDs, injury to the alveolar epithelial cells, which line the air sacs in the lungs, plays a central role in disease pathogenesis.
   • Alveolar epithelial injury can result from direct damage by toxins or pathogens, as well as indirect injury due to inflammation or autoimmune processes.
4. Dysregulated Repair Processes:
   
   • In ILDs, the normal repair processes that occur in response to tissue injury become dysregulated, leading to excessive scarring and fibrosis.
   • Abnormal signaling pathways, including those involving growth factors, cytokines, and chemokines, contribute to the dysregulated repair process.
5. Oxidative Stress and Oxidative Damage:
   
   • Oxidative stress, caused by an imbalance between reactive oxygen species (ROS) and antioxidant defenses, plays a role in the pathogenesis of ILDs.
   • ROS can directly damage lung tissue and contribute to inflammation and fibrosis.
6. Genetic and Environmental Factors:
   
   • Genetic predisposition may influence an individual’s susceptibility to developing ILDs in response to environmental exposures or other triggers.
   • Environmental factors such as occupational exposures (e.g., dust, asbestos), pollutants, smoking, and infections can contribute to the development or exacerbation of ILDs.
7. Vascular Abnormalities:
   
   • Some ILDs are associated with abnormalities in the lung vasculature, including pulmonary hypertension and abnormal blood vessel remodeling, which further contribute to disease progression.

Overall, the pathomechanism of ILDs involves a complex interplay of inflammatory, fibrotic, and repair processes, influenced by genetic, environmental, and immune factors. The specific mechanisms can vary widely depending on the underlying cause of the ILD.

Question 8

Answer 8

Black scars, 2-10cm in diameter:
• may be complicated coal workers’ pneumoconiosis (progressive
massive fibrosis)

The pathomechanism of coal workers’ pneumoconiosis (CWP), also known as black lung disease, involves a series of events triggered by the inhalation of coal mine dust over a prolonged period. Here’s how it typically unfolds:

1. Inhalation of Coal Mine Dust:
   
   • Coal mine workers inhale coal dust particles during their work in coal mines, especially in environments with poor ventilation systems.
2. Deposition and Retention in Lungs:
   
   • Once inhaled, the coal dust particles deposit and accumulate in the lungs, particularly in the smaller airways and alveoli (air sacs).
3. Inflammatory Response:
   
   • The presence of coal dust particles triggers an inflammatory response in the lungs. Macrophages, the immune cells in the lungs, attempt to engulf and remove the dust particles.
4. Fibrotic Response:
   
   • Prolonged exposure to coal dust leads to chronic inflammation and tissue damage. This stimulates the production of fibrous tissue (fibrosis) in the lungs as a part of the healing process.
5. Nodular Lesions and Fibrosis:
   
   • Over time, the accumulation of coal dust and fibrous tissue leads to the formation of nodules and fibrotic lesions within the lung tissue. These nodules may coalesce, resulting in larger areas of fibrosis.
6. Functional Impairment:
   
   • The fibrotic changes in the lungs reduce their elasticity and compliance, making it harder for the affected individual to breathe. This leads to symptoms such as coughing, shortness of breath, and decreased exercise tolerance.
7. Progression to Complications:
   
   • In severe cases of CWP, the fibrotic changes may progress to more advanced forms of pneumoconiosis, such as progressive massive fibrosis (PMF), where large areas of the lung become severely scarred and non-functional.

Overall, coal workers’ pneumoconiosis is characterized by the chronic deposition of coal mine dust in the lungs, leading to inflammation, fibrosis, and ultimately impaired lung function. Prevention through improved workplace safety measures, including dust control and personal protective equipment, is crucial in reducing the risk of developing CWP among coal mine workers.

Question 9

Hard scars with central softening and cavitation, fibrotic lesions in hilar lymph
nodes and pleura

Answer 9

silicosis

The pathomechanism of silicosis involves a series of events triggered by the inhalation of crystalline silica dust, typically in occupational settings such as mining, quarrying, sandblasting, or construction work. Here’s how it typically unfolds:

1. Inhalation and Deposition of Silica Dust:
   
   • Workers inhale crystalline silica dust generated during activities involving cutting, drilling, or crushing silica-containing materials such as rocks, sand, or minerals.
   • Fine silica particles (respirable dust) reach the small airways and alveoli of the lungs, where they deposit and accumulate.
2. Phagocytosis by Macrophages:
   
   • Alveolar macrophages, the immune cells in the lungs, attempt to engulf and remove the inhaled silica particles.
   • However, silica particles are not effectively cleared from the lungs and persist within the macrophages.
3. Inflammatory Response:
   
   • Silica particles trigger an inflammatory response in the lungs, characterized by the release of pro-inflammatory cytokines and chemokines.
   • This leads to the recruitment and activation of additional immune cells, such as neutrophils and lymphocytes, to the site of injury.
4. Fibrogenic Response:
   
   • Prolonged or chronic exposure to silica dust stimulates the activation of fibroblasts, specialized cells responsible for producing collagen and other extracellular matrix components.
   • Activated fibroblasts proliferate and deposit excessive collagen, leading to the formation of scar tissue (fibrosis) within the lung interstitium.
5. Nodular and Progressive Massive Fibrosis:
   
   • Over time, the accumulation of scar tissue may lead to the formation of small nodules (silicotic nodules) and larger, confluent areas of fibrosis known as progressive massive fibrosis (PMF).
   • PMF can result in significant impairment of lung function and respiratory symptoms.
6. Impaired Gas Exchange and Symptoms:
   
   • The fibrotic changes in the lungs reduce lung compliance and impair gas exchange, leading to symptoms such as cough, dyspnea (shortness of breath), and chest pain.
   • These symptoms may worsen over time as the disease progresses and lung function deteriorates.
7. Increased Risk of Complications:
   
   • Silicosis increases the risk of developing complications such as tuberculosis (due to impaired immune function), chronic bronchitis, emphysema, and respiratory failure.

Overall, silicosis is characterized by chronic inflammation and progressive fibrosis of the lungs resulting from the inhalation and retention of crystalline silica dust. Prevention through dust control measures and proper workplace safety practices is essential to reduce the risk of developing silicosis among workers exposed to silica dust.

Question 10

Solid firm areas alternating with normal lung, subpleural cysts; worse in lower lobes

Answer 10

usual interstitial pneumonia

Interstitial pneumonia, also known as interstitial lung disease (ILD), refers to a group of disorders characterized by inflammation and fibrosis of the lung interstitium, which is the tissue surrounding the air sacs (alveoli) in the lungs. The pathomechanism of interstitial pneumonia involves several key steps:

1. Inhalation or Aspiration of Irritants:
   
   • Interstitial pneumonia can result from the inhalation or aspiration of various irritants, including infectious agents (such as bacteria, viruses, or fungi), environmental pollutants (such as dust, asbestos fibers, or chemicals), or certain medications.
2. Activation of Immune Response:
   
   • The presence of irritants triggers an immune response in the lungs, involving the recruitment and activation of immune cells, such as macrophages, neutrophils, and lymphocytes, to the site of injury.
3. Inflammatory Cascade:
   
   • The inflammatory response leads to the release of pro-inflammatory cytokines, chemokines, and other mediators that promote further recruitment and activation of immune cells, as well as the proliferation of fibroblasts.
4. Fibroblast Activation and Fibrosis:
   
   • Prolonged or excessive inflammation leads to the activation of fibroblasts, which are responsible for producing collagen and other extracellular matrix components.
   • Activated fibroblasts proliferate and deposit excessive collagen, leading to the formation of scar tissue within the interstitium of the lungs.
5. Alveolar Epithelial Injury:
   
   • In some cases of interstitial pneumonia, injury to the alveolar epithelial cells, which line the air sacs in the lungs, plays a central role in disease pathogenesis.
   • Alveolar epithelial injury can result from direct damage by irritants or pathogens, as well as indirect injury due to inflammation or autoimmune processes.
6. Dysregulated Repair Processes:
   
   • The normal repair processes that occur in response to tissue injury become dysregulated in interstitial pneumonia, leading to excessive scarring and fibrosis.
   • Abnormal signaling pathways, including those involving growth factors, cytokines, and chemokines, contribute to the dysregulated repair process.
7. Oxidative Stress and Oxidative Damage:
   
   • Oxidative stress, caused by an imbalance between reactive oxygen species (ROS) and antioxidant defenses, plays a role in the pathogenesis of interstitial pneumonia.
   • ROS can directly damage lung tissue and contribute to inflammation and fibrosis.

Overall, the pathomechanism of interstitial pneumonia involves a complex interplay of inflammatory, fibrotic, and repair processes, influenced by genetic, environmental, and immune factors. The specific mechanisms can vary widely depending on the underlying cause of the interstitial pneumonia.

Question 11

Answer 11

Cysts of varying sizes surrounded by firm, gray-tan parenchyma resembling
honeycombs:
• honeycomb lung due to end-stage interstitial fibrosis

Honeycomb lung refers to a pattern of lung damage characterized by the presence of cystic airspaces surrounded by fibrotic tissue. It is commonly seen in advanced stages of interstitial lung diseases (ILDs), particularly idiopathic pulmonary fibrosis (IPF). Here’s the pathomechanism of honeycomb lung:

1. Chronic Inflammation and Injury:
   
   • The initial trigger for honeycomb lung formation is often chronic inflammation and injury to the lung tissue. This inflammation may be due to various factors, including environmental exposures, autoimmune diseases, or unknown causes in the case of idiopathic pulmonary fibrosis.
2. Activation of Fibroblasts:
   
   • Chronic inflammation leads to the activation of fibroblasts, specialized cells responsible for producing collagen and other extracellular matrix components.
   • Activated fibroblasts proliferate and deposit excessive collagen, leading to the formation of scar tissue (fibrosis) within the lung interstitium.
3. Remodeling of Lung Architecture:
   
   • As fibrosis progresses, the normal architecture of the lung tissue is disrupted. The deposition of collagen and other fibrotic tissue causes distortion and stiffening of the lung parenchyma.
4. Alveolar Destruction and Airspace Enlargement:
   
   • In advanced stages of fibrosis, repeated cycles of injury and repair lead to the destruction of alveoli (air sacs) and small airways in the affected areas of the lung.
   • As adjacent alveoli coalesce and fuse together, larger cystic airspaces are formed, giving rise to the characteristic honeycomb appearance on imaging studies.
5. Loss of Lung Function:
   
   • The presence of honeycomb lung signifies significant loss of functional lung tissue, as the cystic airspaces are non-functional and do not participate in gas exchange.
   • This loss of lung function contributes to respiratory symptoms such as dyspnea (shortness of breath), cough, and reduced exercise tolerance.
6. Progression to Respiratory Failure:
   
   • In severe cases of honeycomb lung associated with ILDs like IPF, the progressive fibrotic changes eventually lead to respiratory failure and death.

Overall, honeycomb lung formation in ILDs such as IPF is a consequence of chronic inflammation, fibrosis, and remodeling of the lung architecture. It represents an advanced stage of disease characterized by irreversible loss of lung function and poor prognosis. Early diagnosis and appropriate management are crucial to slowing disease progression and improving outcomes in patients with ILDs.

Question 12

Answer 12

Heavy, red-brown consolidation and blood in airways:
• pulmonary hemorrhage syndromes

Pulmonary hemorrhage refers to bleeding within the lungs, which can occur due to various underlying causes. The pathomechanism of pulmonary hemorrhage depends on the specific etiology but generally involves disruption of the normal blood vessels within the lungs. Here’s an overview:

1. Vascular Injury or Damage:
   
   • Pulmonary hemorrhage can result from direct injury or damage to the blood vessels within the lungs. This injury may be caused by trauma, inflammation, infection, or autoimmune processes.
2. Inflammatory and Infectious Causes:
   
   • Inflammatory conditions such as vasculitis (e.g., Wegener’s granulomatosis) or infections (e.g., pneumonia) can cause inflammation of the blood vessel walls (vasculitis), leading to weakening and rupture of the vessels.
3. Autoimmune Disorders:
   
   • Autoimmune diseases such as Goodpasture syndrome or systemic lupus erythematosus (SLE) can lead to the production of autoantibodies directed against components of the lung tissue, including the basement membrane of the alveolar capillaries. This immune-mediated damage can result in pulmonary hemorrhage.
4. Pulmonary Embolism:
   
   • Pulmonary embolism, which occurs when a blood clot (embolus) travels to the lungs from elsewhere in the body, can cause disruption of the pulmonary vasculature and subsequent bleeding.
5. Capillary Damage:
   
   • Damage to the delicate capillaries within the alveolar walls can occur due to factors such as increased pressure within the pulmonary circulation (e.g., pulmonary hypertension) or toxic exposures (e.g., to certain medications or environmental toxins).
6. Infections:
   
   • Infections such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in COVID-19 can cause damage to the pulmonary vasculature and endothelial cells, leading to microvascular injury and hemorrhage.
7. Underlying Medical Conditions:
   
   • Certain underlying medical conditions, such as coagulopathies (disorders of blood clotting) or liver disease, can predispose individuals to bleeding disorders and increase the risk of pulmonary hemorrhage.
8. Secondary Effects:
   
   • Pulmonary hemorrhage can lead to complications such as respiratory distress, hypoxemia (low blood oxygen levels), and respiratory failure. In severe cases, massive pulmonary hemorrhage can be life-threatening.

Overall, the pathomechanism of pulmonary hemorrhage involves disruption of the pulmonary vasculature and blood vessels within the lungs, leading to bleeding into the lung tissue. Identifying and treating the underlying cause of pulmonary hemorrhage is essential for managing this condition effectively.

Question 13

Dilation of air spaces

Answer 13

Emphysema is a chronic lung condition characterized by the gradual destruction of the air sacs (alveoli) in the lungs, leading to airspace enlargement and loss of lung elasticity.

This results in difficulty exhaling air from the lungs, leading to symptoms such as shortness of breath, wheezing, and coughing. Emphysema is commonly associated with long-term exposure to irritants, especially cigarette smoke. It is a type of chronic obstructive pulmonary disease (COPD) and is often accompanied by chronic bronchitis, another form of COPD. Emphysema is a progressive condition that can significantly impair lung function and quality of life if left untreated. Treatment typically involves lifestyle modifications, medications to manage symptoms, and pulmonary rehabilitation.

emphysema
• Centriacinar emphysema:
- upper lobe involvement worse than lower lobe involvement

• Panacinar emphysema:
- lower lobe involvement worse than upper lobe involvement

• Paraseptal (distal acinar) emphysema:
- subpleural, along lobular septa

• Air space enlargements 1cm or greater in diameter:
- bullae

Question 14

Answer 14

Air space enlargements 1cm or greater in diameter:
- bullae

The pathomechanism of emphysema involves a series of events that lead to the destruction of the alveoli (air sacs) in the lungs and the enlargement of the air spaces. Here’s how it typically unfolds:

1. Inhalation of Irritants:
   
   • Emphysema is often associated with long-term exposure to irritants, particularly cigarette smoke. Other irritants such as air pollution, industrial chemicals, and genetic factors may also play a role.
2. Inflammatory Response:
   
   • Inhalation of irritants triggers an inflammatory response in the lungs. This inflammatory response involves the recruitment and activation of immune cells, such as neutrophils and macrophages, to the lung tissue.
3. Release of Proteases:
   
   • Chronic inflammation leads to the release of proteolytic enzymes, particularly elastase, from activated immune cells. Elastase is capable of breaking down elastin, a key structural protein that provides elasticity to the lung tissue.
4. Destruction of Alveolar Walls:
   
   • Excessive activity of elastase and other proteases leads to the destruction of the alveolar walls, particularly the walls between adjacent alveoli. This results in the formation of larger air spaces and loss of alveolar surface area for gas exchange.
5. Reduced Elastic Recoil:
   
   • The destruction of elastin fibers in the lung tissue reduces the elastic recoil of the lungs. Elastic recoil is essential for maintaining the patency of the airways and facilitating expiration of air from the lungs.
6. Air Trapping and Hyperinflation:
   
   • With reduced elastic recoil, the small airways in the lungs may collapse during expiration, trapping air within the alveoli. This leads to hyperinflation of the lungs, with increased residual volume and functional residual capacity.
7. Impaired Gas Exchange:
   
   • The destruction of alveolar walls and enlargement of air spaces impair gas exchange in the lungs. This results in decreased surface area available for oxygen and carbon dioxide exchange, leading to hypoxemia (low blood oxygen levels) and hypercapnia (high blood carbon dioxide levels).
8. Respiratory Symptoms:
   
   • The structural changes in the lungs lead to respiratory symptoms such as shortness of breath, coughing, wheezing, and decreased exercise tolerance.

Overall, the pathomechanism of emphysema involves a cascade of events triggered by chronic inflammation and protease-mediated destruction of alveolar tissue, leading to the enlargement of air spaces, loss of lung elasticity, and impaired gas exchange.

Question 15

Mucus secretions filling normal-sized airways

Answer 15

chronic bronchitis
asthma

• Chronic bronchitis

The pathomechanism of chronic bronchitis involves chronic inflammation and irritation of the airways, particularly the larger bronchi (bronchial tubes), leading to excessive mucus production and persistent coughing. Here’s how it typically unfolds:

1. Inhalation of Irritants:
   
   • Chronic bronchitis is often associated with long-term exposure to irritants, particularly cigarette smoke. Other irritants such as air pollution, industrial chemicals, and respiratory infections may also contribute.
2. Inflammatory Response:
   
   • Inhalation of irritants triggers an inflammatory response in the airway epithelium, the lining of the bronchial tubes. This inflammatory response involves the recruitment and activation of immune cells, such as neutrophils and macrophages, to the airway mucosa.
3. Mucus Hypersecretion:
   
   • Chronic inflammation leads to increased production of mucus by the goblet cells and submucosal glands in the bronchial epithelium. This excess mucus production is a characteristic feature of chronic bronchitis.
4. Mucociliary Clearance Dysfunction:
   
   • The cilia, tiny hair-like structures on the surface of the bronchial epithelial cells, normally help to sweep mucus and trapped particles out of the airways. In chronic bronchitis, chronic inflammation can impair ciliary function, leading to reduced mucociliary clearance.
5. Mucus Plugging and Airway Obstruction:
   
   • Excessive mucus production and impaired mucociliary clearance result in the accumulation of mucus in the airways. This can lead to mucus plugging and partial obstruction of the bronchial tubes.
6. Chronic Cough:
   
   • The presence of mucus and airway inflammation irritates the nerve endings in the airway epithelium, triggering a persistent cough. This cough is typically productive, with the production of thick, tenacious sputum.
7. Airway Remodeling:
   
   • Prolonged exposure to inflammation and irritation can lead to structural changes in the airway walls, including thickening of the bronchial epithelium, submucosal fibrosis, and hypertrophy of the bronchial smooth muscle. These changes contribute to airway narrowing and obstruction.
8. Respiratory Symptoms:
   
   • The chronic inflammation and airway obstruction characteristic of chronic bronchitis lead to respiratory symptoms such as coughing, wheezing, shortness of breath, and increased susceptibility to respiratory infections.

Overall, the pathomechanism of chronic bronchitis involves a cascade of events triggered by chronic airway inflammation and mucus hypersecretion, leading to airway obstruction and respiratory symptoms. Reduction of exposure to irritants, smoking cessation, and appropriate medical management are essential for controlling symptoms and slowing disease progression in patients with chronic bronchitis.

+ Asthma

The pathomechanism of asthma involves a complex interplay of genetic, environmental, and immunological factors that lead to chronic inflammation and hyperreactivity of the airways. Here’s how it typically unfolds:

1. Genetic Predisposition:
   
   • Asthma often runs in families, suggesting a genetic predisposition. Various genes related to immune regulation, airway inflammation, and bronchial hyperreactivity have been implicated in asthma susceptibility.
2. Environmental Triggers:
   
   • Exposure to certain environmental triggers can initiate or exacerbate asthma symptoms. Common triggers include allergens (such as pollen, dust mites, animal dander), respiratory infections (such as viral infections), air pollution, tobacco smoke, cold air, and exercise.
3. Airway Inflammation:
   
   • Upon exposure to triggers, the immune system in the airways mounts an inflammatory response characterized by the activation of various immune cells, including mast cells, eosinophils, T lymphocytes, and dendritic cells.
   • Mast cells play a central role in asthma by releasing inflammatory mediators such as histamine, leukotrienes, and cytokines, which contribute to bronchoconstriction, mucus production, and airway inflammation.
4. Bronchial Hyperreactivity:
   
   • In individuals with asthma, the airways become hyperresponsive or hyperreactive to various stimuli, leading to exaggerated bronchoconstriction and airway narrowing in response to triggers that would not affect non-asthmatic individuals.
   • Smooth muscle contraction, mucus secretion, and airway edema contribute to airway narrowing and obstruction, resulting in symptoms such as coughing, wheezing, chest tightness, and shortness of breath.
5. Chronic Inflammation and Remodeling:
   
   • Prolonged exposure to inflammation leads to structural changes in the airway walls, including thickening of the basement membrane, subepithelial fibrosis, hypertrophy and hyperplasia of airway smooth muscle, and goblet cell hyperplasia (increased mucus production).
   • These structural changes contribute to airway remodeling, which is associated with irreversible airflow limitation and poor asthma control in severe cases.
6. Immune Dysregulation:
   
   • Asthma is considered an immune-mediated disorder involving dysregulation of both innate and adaptive immune responses. Imbalance between Th1 and Th2 responses, aberrant activation of eosinophils and other inflammatory cells, and impaired regulatory T cell function are implicated in asthma pathogenesis.
7. Triggers and Exacerbations:
   
   • Asthma symptoms can be triggered or exacerbated by various factors, including allergens, respiratory infections, exercise, stress, irritants, and changes in weather or air quality.
   • Asthma exacerbations, characterized by sudden worsening of symptoms and decreased lung function, may require emergency medical treatment.

Overall, the pathomechanism of asthma involves a complex interplay of genetic susceptibility, environmental triggers, airway inflammation, hyperreactivity, and structural changes in the airways. Understanding these underlying mechanisms is essential for developing effective strategies for asthma management and prevention of exacerbations.

Question 16

Mucus plugs, alternating overdistention and small areas of atelectasis

Answer 16

acute asthma
status asthmaticus

Question 17

Dilated airways that reach pleural surface and are often filled with pus

Answer 17

bronchiectasis

Bronchiectasis is a chronic lung condition characterized by abnormal and irreversible widening and thickening of the bronchial tubes (bronchi) due to recurrent inflammation and infection. This leads to the accumulation of mucus and impaired clearance of secretions from the airways, which can result in persistent coughing, sputum production, and recurrent respiratory infections. Bronchiectasis can be caused by various factors, including respiratory infections (such as pneumonia or tuberculosis), underlying lung diseases (such as cystic fibrosis or primary ciliary dyskinesia), airway obstruction, or immune deficiencies. Treatment typically focuses on managing symptoms, preventing infections, and improving mucus clearance through medications, airway clearance techniques,

The pathomechanism of bronchiectasis involves a cascade of events that lead to abnormal dilation and thickening of the bronchial tubes (bronchi), impairing their function and causing recurrent respiratory symptoms. Here’s how it typically unfolds:

1. Initial Airway Injury:
   
   • Bronchiectasis often begins with injury or damage to the bronchial walls, which can be caused by various factors such as respiratory infections (e.g., pneumonia, tuberculosis), aspiration of foreign material, airway obstruction (e.g., due to tumors or inhaled objects), or congenital conditions (e.g., cystic fibrosis, primary ciliary dyskinesia).
2. Impaired Mucus Clearance:
   
   • Damage to the bronchial walls impairs the normal clearance of mucus from the airways. Mucus is produced by the epithelial cells lining the bronchi and serves to trap and remove inhaled particles, pathogens, and debris from the respiratory tract.
   • In bronchiectasis, impaired mucus clearance allows mucus to accumulate and become thickened, leading to the formation of mucus plugs and providing a favorable environment for bacterial growth and colonization.
3. Chronic Inflammation and Infection:
   
   • The presence of retained mucus and debris in the dilated bronchi triggers a chronic inflammatory response in the airway walls. This inflammation attracts immune cells, such as neutrophils and macrophages, to the site of injury.
   • Chronic inflammation contributes to further damage to the bronchial walls and promotes tissue remodeling, leading to structural changes such as dilation, thickening, and scarring of the bronchi.
4. Persistent Respiratory Symptoms:
   
   • The structural changes in the bronchi result in the characteristic symptoms of bronchiectasis, including chronic cough, excessive sputum production, recurrent respiratory infections (such as bronchitis or pneumonia), wheezing, and shortness of breath.
   • These symptoms may worsen over time and can significantly impact the quality of life of affected individuals.
5. Vicious Cycle of Infection and Inflammation:
   
   • Recurrent respiratory infections and inflammation perpetuate a vicious cycle in bronchiectasis, further damaging the bronchial walls and exacerbating mucus accumulation and airway obstruction.
   • Over time, the progressive dilation and scarring of the bronchi lead to irreversible structural changes and functional impairment of the airways.

Overall, the pathomechanism of bronchiectasis involves a combination of airway injury, impaired mucus clearance, chronic inflammation, and recurrent respiratory infections, leading to structural changes in the bronchi and persistent respiratory symptoms. Management strategies focus on controlling symptoms, preventing exacerbations, and addressing underlying causes when possible.

and sometimes surgery in severe cases.

Question 18

Diffuse bronchiectasis

Answer 18

• more likely cystic fibrosis
• ciliary dyskinesia,
• immunodeficiency states

The pathomechanism of cystic fibrosis (CF) involves genetic mutations that lead to dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR) protein, resulting in abnormal ion transport across cell membranes. Here’s how it typically unfolds:

1. Genetic Mutation:
   
   • Cystic fibrosis is caused by mutations in the CFTR gene, which encodes the CFTR protein. These mutations result in defective or dysfunctional CFTR protein, affecting its ability to regulate chloride and bicarbonate ion transport across cell membranes.
2. Impaired Ion Transport:
   
   • Normally, the CFTR protein functions as an ion channel in epithelial cells lining the respiratory tract, digestive system, sweat glands, and other organs. It regulates the flow of chloride ions (Cl-) and bicarbonate ions (HCO3-) across cell membranes, maintaining proper hydration and pH balance of mucosal surfaces.
   • In CF, defective CFTR protein leads to impaired chloride secretion and excessive absorption of sodium ions (Na+) and water, causing dehydration of the mucosal surfaces.
3. Mucus Dehydration and Thickening:
   
   • The dehydration of mucus in the airways, pancreas, and other organs results in the production of thick, sticky mucus. This abnormal mucus is difficult to clear from the airways and ducts, leading to obstruction and accumulation.
4. Airway Obstruction and Inflammation:
   
   • Thickened mucus obstructs the airways, impairing mucociliary clearance and trapping bacteria, viruses, and other pathogens. This leads to chronic airway inflammation and recurrent respiratory infections, characteristic features of CF.
   • Persistent inflammation and infection contribute to airway damage, bronchiectasis (dilation of the bronchi), and progressive lung function decline.
5. Pancreatic Insufficiency:
   
   • In the pancreas, thickened mucus blocks the ducts that deliver digestive enzymes to the small intestine. This results in pancreatic insufficiency, leading to malabsorption of nutrients, steatorrhea (fatty stools), and poor growth and weight gain.
6. Sweat Electrolyte Imbalance:
   
   • The dysfunctional CFTR protein also affects sweat gland function, leading to increased salt (sodium chloride) concentration in sweat. This characteristic electrolyte imbalance is used as a diagnostic marker for CF through sweat chloride testing.
7. Multiorgan Involvement:
   
   • CF affects multiple organs and systems, including the respiratory, digestive, and reproductive systems, as well as the sweat glands. Complications may include chronic lung disease, pancreatic insufficiency, liver disease, infertility, and nutritional deficiencies.

Overall, the pathomechanism of cystic fibrosis involves dysfunction of the CFTR protein, leading to abnormal ion transport, dehydration of mucus, airway obstruction, inflammation, and multiorgan involvement. Current treatments aim to alleviate symptoms, prevent complications, and improve quality of life for individuals with CF. Emerging therapies targeting the underlying genetic defect hold promise for future disease management.

Question 19

Localized bronchiectasis

Answer 19

more likely postinfection (tuberculosis, suppurative pneumonias,
measles, adenovirus)

Question 20

Answer 20

Gray, yellow, white masses, predominantly central (90% in segmental or
larger bronchi), with or without cavitation:
• squamous cell carcinoma

The pathomechanism of squamous cell carcinoma (SCC) involves a series of steps that lead to the development and progression of cancerous growths originating from squamous epithelial cells. Here’s how it typically unfolds:

1. Initiation:
   
   • Squamous cell carcinoma often begins with genetic mutations or alterations in squamous epithelial cells, which can be triggered by various factors such as exposure to carcinogens (e.g., tobacco smoke, ultraviolet radiation), chronic inflammation, or viral infections (e.g., human papillomavirus HPV).
2. Dysregulated Cell Growth:
   
   • Genetic mutations lead to dysregulation of cellular signaling pathways involved in cell growth, proliferation, and differentiation. This results in uncontrolled growth and accumulation of abnormal squamous cells within the epithelial layer.
3. Formation of Dysplastic Lesions:
   
   • As the abnormal squamous cells proliferate, they may form precancerous lesions known as squamous intraepithelial lesions (SILs) or dysplasia. These lesions are characterized by cellular atypia, disorganized growth patterns, and loss of normal tissue architecture.
4. Invasion and Metastasis:
   
   • Over time, dysplastic lesions may progress to invasive squamous cell carcinoma, characterized by infiltration of malignant squamous cells into surrounding tissues and structures.
   • Invasive SCC has the potential to metastasize, spreading to regional lymph nodes and distant organs via lymphatic and hematogenous routes.
5. Angiogenesis:
   
   • In order to support their rapid growth and proliferation, invasive SCC cells induce the formation of new blood vessels through a process called angiogenesis. This provides the tumor with a blood supply, facilitating nutrient and oxygen delivery.
6. Immune Evasion:
   
   • SCC cells may develop mechanisms to evade detection and destruction by the immune system, allowing them to survive and proliferate unchecked within the host tissue.
7. Local Tissue Destruction and Symptoms:
   
   • As the tumor grows and invades surrounding tissues, it may cause local tissue destruction, inflammation, ulceration, and symptoms such as pain, bleeding, and functional impairment depending on its location.
8. Clinical Presentation:
   
   • The clinical presentation of SCC varies depending on its location. Common sites of SCC include the skin, oral cavity, larynx, esophagus, cervix, and anus. Symptoms may include skin lesions, changes in voice or swallowing, persistent ulcers or growths, and abnormal bleeding or discharge.

Overall, the pathomechanism of squamous cell carcinoma involves a complex interplay of genetic, environmental, and immunological factors that lead to the malignant transformation of squamous epithelial cells and the development of invasive cancer. Early detection, prompt treatment, and targeted therapies are crucial for managing SCC and improving patient outcomes.

Question 21

Answer 21

Gray or white peripheral masses, rarely with cavitation, though areas of
necrosis may be present:
• adenocarcinoma

The pathomechanism of adenocarcinoma involves the development and progression of cancerous growths originating from glandular epithelial cells. Here’s how it typically unfolds:

1. Initiation:
   
   • Adenocarcinoma often begins with genetic mutations or alterations in glandular epithelial cells. These mutations may be caused by various factors such as exposure to carcinogens (e.g., tobacco smoke, asbestos), hormonal imbalances, chronic inflammation, or genetic predisposition.
2. Dysregulated Cell Growth:
   
   • Genetic mutations lead to dysregulation of cellular signaling pathways involved in cell growth, proliferation, and differentiation. This results in uncontrolled growth and accumulation of abnormal glandular cells within the epithelial layer.
3. Formation of Dysplastic Lesions:
   
   • As the abnormal glandular cells proliferate, they may form precancerous lesions known as adenomatous polyps or adenomas. These lesions are characterized by cellular atypia, disorganized growth patterns, and loss of normal tissue architecture.
4. Invasion and Metastasis:
   
   • Over time, dysplastic lesions may progress to invasive adenocarcinoma, characterized by infiltration of malignant glandular cells into surrounding tissues and structures.
   • Invasive adenocarcinoma has the potential to metastasize, spreading to regional lymph nodes and distant organs via lymphatic and hematogenous routes.
5. Angiogenesis:
   
   • In order to support their rapid growth and proliferation, invasive adenocarcinoma cells induce the formation of new blood vessels through a process called angiogenesis. This provides the tumor with a blood supply, facilitating nutrient and oxygen delivery.
6. Immune Evasion:
   
   • Adenocarcinoma cells may develop mechanisms to evade detection and destruction by the immune system, allowing them to survive and proliferate unchecked within the host tissue.
7. Clinical Presentation:
   
   • The clinical presentation of adenocarcinoma varies depending on its location. Common sites of adenocarcinoma include the lungs, colon and rectum, prostate, breast, pancreas, stomach, and ovaries. Symptoms may include cough, changes in bowel habits, rectal bleeding, urinary symptoms, breast lumps, abdominal pain, and abnormal vaginal bleeding.

Overall, the pathomechanism of adenocarcinoma involves a complex interplay of genetic, environmental, and immunological factors that lead to the malignant transformation of glandular epithelial cells and the development of invasive cancer. Early detection, prompt treatment, and targeted therapies are crucial for managing adenocarcinoma and improving patient outcomes.

Question 22

Answer 22

Single nodules or multiple diffuse or coalescing nodules with gelatinous or
solid, gray-white regions resembling pneumonia:
• bronchioloalveolar carcinoma

adenocarcinoma-in-situ

Bronchoalveolar carcinoma (BAC), also known as adenocarcinoma in situ, is a subtype of lung adenocarcinoma that originates from the alveolar epithelium in the lungs. The pathomechanism of bronchoalveolar carcinoma involves several steps:

1. Initiation:
   
   • Bronchoalveolar carcinoma often begins with genetic mutations in the alveolar epithelial cells lining the air sacs (alveoli) of the lungs. These mutations may be caused by exposure to carcinogens such as tobacco smoke, environmental pollutants, or occupational hazards.
2. Dysregulated Cell Growth:
   
   • Genetic mutations lead to dysregulation of cellular signaling pathways involved in cell growth, proliferation, and differentiation. This results in uncontrolled growth and accumulation of abnormal alveolar epithelial cells within the alveolar spaces.
3. Formation of Dysplastic Lesions:
   
   • As the abnormal alveolar epithelial cells proliferate, they may form precancerous lesions known as atypical adenomatous hyperplasia (AAH) or adenocarcinoma in situ (AIS). These lesions are characterized by cellular atypia and increased cell proliferation, but they have not yet invaded through the basement membrane into surrounding tissue.
4. Invasion and Metastasis (Invasive BAC):
   
   • In some cases, dysplastic lesions may progress to invasive bronchoalveolar carcinoma, characterized by infiltration of malignant cells through the basement membrane and into adjacent lung tissue.
   • Invasive BAC has the potential to metastasize, spreading to regional lymph nodes and distant organs via lymphatic and hematogenous routes.
5. Angiogenesis:
   
   • In order to support their growth and proliferation, invasive bronchoalveolar carcinoma cells induce the formation of new blood vessels through a process called angiogenesis. This provides the tumor with a blood supply, facilitating nutrient and oxygen delivery.
6. Immune Evasion:
   
   • BAC cells may develop mechanisms to evade detection and destruction by the immune system, allowing them to survive and proliferate unchecked within the lung tissue.
7. Clinical Presentation:
   
   • The clinical presentation of bronchoalveolar carcinoma may vary depending on its stage and location within the lungs. Common symptoms may include cough, shortness of breath, chest pain, hemoptysis (coughing up blood), and weight loss.

Overall, the pathomechanism of bronchoalveolar carcinoma involves a complex interplay of genetic mutations, dysregulated cell growth, and tumor progression within the alveolar epithelium of the lungs. Early detection, prompt treatment, and targeted therapies are crucial for managing bronchoalveolar carcinoma and improving patient outcomes.

adenocarcinoma-in-situ

Question 23

Soft, gray or tan, frequently necrotic masses, 50% central, 50% peripheral

Answer 23

large cell carcinoma

Question 24

Answer 24

Gray to white, somewhat fleshy masses, generally arising centrally:
• neuroendocrine carcinoma, small cell type

The pathomechanism of small cell neuroendocrine carcinoma (SNEC) involves the development and progression of highly aggressive tumors originating from neuroendocrine cells in various organs, most commonly the lungs. Here’s how it typically unfolds:

1. Initiation:
   
   • Small cell neuroendocrine carcinoma often begins with genetic mutations or alterations in neuroendocrine cells, which are specialized cells that produce hormones and neurotransmitters. These mutations may be triggered by exposure to carcinogens such as tobacco smoke, although the exact causes are not fully understood.
2. Dysregulated Cell Growth:
   
   • Genetic mutations lead to dysregulation of cellular signaling pathways involved in cell growth, proliferation, and differentiation. This results in uncontrolled growth and accumulation of abnormal neuroendocrine cells within the affected tissue.
3. Rapid Tumor Growth:
   
   • Small cell neuroendocrine carcinoma is characterized by rapid tumor growth and high proliferation rates. The tumor cells have a high nuclear-cytoplasmic ratio and scant cytoplasm, giving them a small, “oat cell” appearance under the microscope.
4. Invasion and Metastasis:
   
   • Small cell neuroendocrine carcinoma is highly invasive and has a propensity for early metastasis. The tumor cells infiltrate surrounding tissues and can spread to regional lymph nodes and distant organs via lymphatic and hematogenous routes.
5. Neuroendocrine Differentiation:
   
   • Small cell neuroendocrine carcinoma cells retain features of neuroendocrine differentiation, including the production of neuroendocrine markers such as chromogranin A, synaptophysin, and neuron-specific enolase (NSE).
6. Paraneoplastic Syndromes:
   
   • Small cell neuroendocrine carcinoma is associated with the production of various paraneoplastic syndromes, which are systemic effects of the tumor unrelated to local mass effects or metastasis. These syndromes may include ectopic hormone production (e.g., ACTH, ADH, PTHrP), Lambert-Eaton myasthenic syndrome (LEMS), and paraneoplastic encephalomyelitis.
7. Clinical Presentation:
   
   • The clinical presentation of small cell neuroendocrine carcinoma depends on the site of origin and the extent of metastatic spread. In pulmonary SNEC, common symptoms may include cough, dyspnea, chest pain, hemoptysis, and constitutional symptoms such as weight loss and fatigue.

Overall, the pathomechanism of small cell neuroendocrine carcinoma involves a complex interplay of genetic mutations, dysregulated cell growth, neuroendocrine differentiation, and aggressive tumor behavior. Early detection, prompt treatment, and targeted therapies are crucial for managing SNEC and improving patient outcomes, although the prognosis is often poor due to the aggressive nature of the disease.

In the respiratory system, neuroendocrine cells are primarily found in the epithelial lining of the airways and serve various functions related to airway homeostasis, sensory perception, and local immune regulation. Here are the main types of neuroendocrine cells found in the respiratory system:

1. Pulmonary Neuroendocrine Cells (PNECs):
   
   • Pulmonary neuroendocrine cells are specialized epithelial cells located within the respiratory epithelium, particularly in the bronchi and bronchioles.
   • They produce and secrete bioactive substances such as neuropeptides, neurotransmitters, and hormones, including serotonin, calcitonin gene-related peptide (CGRP), substance P, and bombesin.
   • PNECs function as chemosensors, detecting changes in the local microenvironment such as hypoxia, hypercapnia, and airway irritants. They play a role in regulating airway tone, bronchomotor activity, mucus secretion, and local immune responses.
   • PNECs are implicated in the pathophysiology of respiratory diseases such as asthma, chronic obstructive pulmonary disease (COPD), and lung cancer, where their dysregulation may contribute to airway inflammation, hyperreactivity, and remodeling.
2. Kulchitsky Cells (Enterochromaffin Cells):
   
   • Kulchitsky cells are a type of neuroendocrine cell found in the respiratory epithelium, particularly in the bronchial mucosa and submucosal glands.
   • Similar to PNECs, Kulchitsky cells produce and release bioactive substances such as serotonin, histamine, and neuropeptides.
   • They play a role in regulating airway smooth muscle tone, mucus secretion, local immune responses, and sensory perception within the respiratory tract.
   • Dysregulation of Kulchitsky cells has been implicated in the pathogenesis of airway diseases such as asthma, allergic rhinitis, and chronic cough.
3. Neuroepithelial Bodies (NEBs):
   
   • Neuroepithelial bodies are specialized clusters of neuroendocrine cells found in the bronchial and bronchiolar epithelium, particularly at branching points of the airway tree.
   • NEBs contain a mixture of neuroendocrine cells, including PNECs, Kulchitsky cells, and other epithelial cells.
   • They serve as sensory organs, detecting mechanical and chemical stimuli in the airway lumen and transmitting signals to the central nervous system via afferent nerve fibers.
   • NEBs are involved in regulating breathing, cough reflex, mucociliary clearance, and local immune responses in the respiratory tract.

Overall, neuroendocrine cells of the respiratory system play important roles in maintaining airway homeostasis, sensory perception, and local immune regulation. Dysregulation of these cells may contribute to the pathogenesis of respiratory diseases and represent potential targets for therapeutic intervention.

Question 25

Answer 25

Polypoid masses projecting into bronchial lumen:
• neuroendocrine carcinoma, carcinoid type

Neuroendocrine tumors (NETs), including carcinoid tumors, arise from neuroendocrine cells dispersed throughout the body. Carcinoid tumors, a type of NET, most commonly originate in the gastrointestinal tract (especially the small intestine and appendix) and the lungs. Here’s a general outline of the pathomechanism of carcinoid tumors:

1. Initiation:
   
   • Carcinoid tumors often develop sporadically, although some cases may be associated with genetic syndromes such as multiple endocrine neoplasia type 1 (MEN1) or neurofibromatosis type 1 (NF1). The exact cause of sporadic carcinoid tumors is unclear, but factors such as exposure to certain chemicals or chronic inflammation may contribute to their development.
2. Cellular Transformation:
   
   • Neuroendocrine cells undergo neoplastic transformation due to genetic mutations or alterations. These mutations may affect genes involved in cell cycle regulation, tumor suppression, or differentiation pathways.
3. Tumor Growth and Differentiation:
   
   • Carcinoid tumors consist of well-differentiated neuroendocrine cells that retain some degree of resemblance to their normal counterparts. These cells proliferate and form nodules or masses within the affected organ.
4. Hormone Secretion:
   
   • Carcinoid tumors often produce and secrete various bioactive substances, including serotonin, histamine, bradykinin, prostaglandins, and tachykinins. These substances can cause characteristic symptoms such as flushing, diarrhea, wheezing, and cardiac valvular lesions (in cases of metastatic disease).
5. Metastasis:
   
   • Carcinoid tumors have the potential to metastasize to regional lymph nodes, liver, and other distant sites. Metastatic spread may occur via lymphatic or hematogenous routes.
6. Clinical Manifestations:
   
   • The clinical presentation of carcinoid tumors varies depending on their location, size, and hormone production. Carcinoid syndrome, characterized by flushing, diarrhea, bronchospasm, and right-sided heart valve lesions (carcinoid heart disease), may occur in patients with advanced disease and hepatic metastases.
7. Treatment and Prognosis:
   
   • Treatment options for carcinoid tumors depend on factors such as tumor location, extent of disease, and presence of symptoms. Surgical resection is often the mainstay of treatment for localized tumors, while systemic therapies (e.g., somatostatin analogs, chemotherapy, targeted therapies) may be used for advanced or metastatic disease.
   • The prognosis of carcinoid tumors varies widely depending on tumor grade, stage, and responsiveness to treatment. Well-differentiated, localized tumors generally have a favorable prognosis, whereas poorly differentiated or metastatic tumors may have a worse outcome.

Overall, the pathomechanism of carcinoid tumors involves neoplastic transformation of neuroendocrine cells, leading to the development of well-differentiated tumors with variable hormone production and clinical manifestations. Early detection, accurate diagnosis, and appropriate management are essential for optimizing outcomes in patients with carcinoid tumors.

Question 26

Heart normal + pericardium alternation

Answer 26

The heart is in normal anatomical position.

The shape of the heart is regular, the size is
normal (usual), with 350 g weight.

The layers of the pericardium are smooth, shiny and
glistening.

The subepicardial adipose tissue at the apex of the right ventricle is approx. 2
mm thick) and has a sharp border to the myocardium.

The volumes of the heart chambers
are regular.

The left ventricular wall is 15 mm, the right ventricular is 5 mm in thickness.

The auricles are free of thrombus.

The valves of the chambers are intact without grossly
visible deformation, smooth and delicate.

The endocardial layers including the valves are
smooth, intact (i.e., no thrombotic precipitates or thickenings are recognized).

The foramen ovale is membranously closed. The coronary arteries are in a normal anatomical
position, their orifices are free of thrombus.

Their lumen is empty and the caliber is not
narrowed by plaques.

The endothelial surface of the coronary arteries is smooth and intact.

The myocardium is moderately firm in consistency and has a dark red color.

The gross architecture of the myocardium is preserved throughout the chambers showing
fibrillary structure.

Question 27

Hypertrophy and normal or reduced cavity diameter

Answer 27

(concentric hypertrophy

pressure overload (e.g., hypertension, aortic stenosis)

Aortic stenosis is a condition characterized by narrowing of the aortic valve opening, restricting blood flow from the left ventricle of the heart into the aorta and the rest of the body. Here’s a simplified explanation of its pathomechanism:

1. Valve Calcification:
   
   • Aortic stenosis often develops due to calcification and thickening of the aortic valve leaflets over time. This process is similar to atherosclerosis, where calcium deposits and fibrous tissue build up on the valve leaflets, causing them to become stiff and less flexible.
2. Obstruction of Blood Flow:
   
   • As the valve leaflets become calcified and stiff, they fail to open fully during systole (contraction of the heart). This obstruction impedes the flow of blood from the left ventricle into the aorta, leading to increased pressure within the left ventricle and decreased cardiac output.
3. Left Ventricular Hypertrophy:
   
   • To compensate for the increased resistance to blood flow, the left ventricle of the heart undergoes hypertrophy (thickening of the muscle wall). This hypertrophy helps maintain cardiac output initially but can eventually lead to impaired ventricular function and heart failure if left untreated.
4. Symptoms and Complications:
   
   • Patients with aortic stenosis may initially be asymptomatic. However, as the stenosis progresses and the heart’s ability to compensate diminishes, symptoms such as chest pain (angina), shortness of breath (dyspnea), fainting (syncope), and heart failure may develop.
   • Severe aortic stenosis can also increase the risk of complications such as arrhythmias, infective endocarditis, and sudden cardiac death.
5. Progression of Stenosis:
   
   • Aortic stenosis typically progresses slowly over time, but the rate of progression can vary among individuals. Once symptoms develop, the prognosis worsens, and surgical intervention (aortic valve replacement) may be necessary to relieve the obstruction and improve outcomes.

Overall, the pathomechanism of aortic stenosis involves calcification and thickening of the aortic valve leaflets, leading to obstruction of blood flow from the left ventricle into the aorta. This obstruction results in increased pressure load on the heart and can lead to symptoms, complications, and impaired cardiac function if left untreated.

pressure overload (e.g., hypertension, aortic stenosis)

Question 28

Hypertrophy with dilation

Answer 28

Eccentric hypertrophy

volume overload or pressure and volume overload (e.g., mitral or aortic
valve insufficiency—walls of dilated hearts may be of normal thickness
while still being markedly hypertrophied)
• valvular disease
• cardiomyopathies

Cardiomyopathies are a group of diseases that affect the heart muscle, leading to structural and functional abnormalities. These conditions can affect the heart’s ability to pump blood efficiently and may result in symptoms such as heart failure, arrhythmias, and sudden cardiac death. Cardiomyopathies are classified into several types based on their underlying causes, including:

1. Dilated Cardiomyopathy (DCM): Characterized by enlargement (dilation) of the heart chambers, thinning of the heart muscle walls, and reduced contractile function. DCM can be inherited (genetic) or acquired, with causes ranging from viral infections and alcohol abuse to autoimmune disorders.
2. Hypertrophic Cardiomyopathy (HCM): Characterized by abnormal thickening (hypertrophy) of the heart muscle, particularly the left ventricle, without an obvious cause such as high blood pressure. HCM is often inherited and can lead to symptoms such as chest pain, shortness of breath, and fainting.
3. Restrictive Cardiomyopathy (RCM): Characterized by stiffness and rigidity of the heart muscle, which impairs its ability to fill properly during the relaxation phase of the cardiac cycle. RCM can be caused by infiltrative diseases (e.g., amyloidosis), storage diseases (e.g., hemochromatosis), or idiopathic factors.
4. Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC): Characterized by progressive replacement of the right ventricular muscle with fibrous and fatty tissue, leading to arrhythmias and risk of sudden cardiac death. ARVC is often inherited and may present with palpitations, syncope, or sudden cardiac arrest.
5. Unclassified Cardiomyopathies: Some cardiomyopathies do not fit neatly into the above categories and may have unique features or causes. These include noncompaction cardiomyopathy, takotsubo cardiomyopathy (stress-induced cardiomyopathy), and peripartum cardiomyopathy (develops late in pregnancy or shortly after childbirth).

Management of cardiomyopathies involves a multidisciplinary approach, including medications, lifestyle modifications, implantable devices (e.g., pacemakers, defibrillators), and, in some cases, heart transplantation. Early diagnosis and appropriate treatment are essential for improving outcomes and reducing complications associated with these conditions.

Question 29

Answer 29

Hypertrophy, dilation, mural thrombi in ventricles or atrial appendages,
normal valves

dilated (primary or secondary) cardiomyopathy

The pathomechanism of dilated cardiomyopathy (DCM) involves a complex interplay of genetic, environmental, and acquired factors that lead to structural and functional abnormalities in the heart muscle. Here’s a simplified explanation:

1. Genetic Factors:
   
   • Inherited genetic mutations are believed to play a significant role in the development of DCM. These mutations affect proteins involved in maintaining the structure, function, and integrity of cardiac muscle cells (cardiomyocytes), including sarcomeric proteins, cytoskeletal proteins, and proteins involved in calcium handling and cellular signaling pathways.
2. Environmental and Acquired Factors:
   
   • Environmental factors such as viral infections (e.g., coxsackievirus), exposure to toxins (e.g., alcohol, certain chemotherapeutic agents), and autoimmune diseases may trigger or exacerbate the development of DCM in individuals with genetic predisposition.
   • Chronic conditions such as hypertension, diabetes, thyroid disorders, and chronic kidney disease can also contribute to the progression of DCM by increasing the workload on the heart and promoting adverse remodeling of the myocardium.
3. Myocardial Remodeling:
   
   • In response to genetic and environmental stressors, the heart undergoes a process of maladaptive remodeling characterized by structural changes in the myocardium. This includes myocyte hypertrophy (enlargement), myocyte apoptosis (cell death), interstitial fibrosis (accumulation of collagen fibers between cells), and chamber dilation (enlargement).
   • Progressive remodeling of the myocardium leads to thinning of the ventricular walls, dilation of the cardiac chambers (particularly the left ventricle), and impaired contractile function. As a result, the heart’s ability to pump blood efficiently is compromised, leading to symptoms of heart failure.
4. Neurohormonal Activation:
   
   • As DCM progresses, there is activation of neurohormonal pathways including the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system. These pathways are activated in an attempt to maintain cardiac output and systemic perfusion but can exacerbate myocardial injury and remodeling over time.
5. Clinical Manifestations:
   
   • Patients with DCM may present with symptoms such as fatigue, dyspnea (shortness of breath), orthopnea (difficulty breathing while lying flat), paroxysmal nocturnal dyspnea (sudden onset of breathlessness at night), edema (swelling), and exercise intolerance. Severe cases can lead to arrhythmias, thromboembolic events, and sudden cardiac death.

Overall, the pathomechanism of dilated cardiomyopathy involves a complex interplay of genetic predisposition,. environmental factors, myocardial remodeling, and neurohormonal activation, ultimately leading to progressive dysfunction of the heart muscle and the development of heart failure symptoms. Early detection, risk factor modification, and targeted therapies are essential for managing DCM and improving outcomes.

Question 30

Left ventricle usually more involved than right ventricle;
• often disproportionate thickening of interventricular septum compared
with left ventricular free wall (3 : 2 ratio);
• ventricular cavity becomes slitlike rather than round

Answer 30

hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is primarily a genetic disorder characterized by abnormal thickening (hypertrophy) of the heart muscle, particularly the left ventricle, without an obvious cause such as high blood pressure. Here’s an overview of its pathomechanism:

1. Genetic Mutations:
   
   • HCM is predominantly caused by mutations in genes that encode proteins of the cardiac sarcomere, the contractile unit of the heart muscle. Mutations affecting sarcomeric proteins such as beta-myosin heavy chain (MYH7), cardiac myosin-binding protein C (MYBPC3), and cardiac troponin T (TNNT2) are commonly implicated.
   • These genetic mutations lead to abnormalities in sarcomere structure and function, disrupting the normal contractile properties of cardiomyocytes and contributing to myocardial hypertrophy.
2. Myocardial Hypertrophy:
   
   • Mutations in sarcomeric proteins result in increased contractility and impaired relaxation of cardiomyocytes, leading to compensatory hypertrophy of the myocardium. This hypertrophy is often asymmetric and involves thickening of the interventricular septum (septal hypertrophy) and/or the left ventricular free wall.
   • Asymmetric hypertrophy can cause dynamic obstruction of the left ventricular outflow tract (LVOT), leading to left ventricular outflow tract obstruction (LVOTO) and symptoms such as dyspnea, chest pain, and syncope, especially during exercise.
3. Microvascular Dysfunction:
   
   • HCM is associated with microvascular dysfunction, characterized by abnormalities in the small blood vessels within the myocardium. Microvascular dysfunction impairs myocardial perfusion and oxygen delivery, contributing to myocardial ischemia, fibrosis, and arrhythmias.
4. Arrhythmias and Sudden Cardiac Death:
   
   • HCM is a common cause of sudden cardiac death, particularly in young athletes. Arrhythmias such as ventricular tachycardia, atrial fibrillation, and ventricular fibrillation can occur due to abnormal electrical conduction within the hypertrophied myocardium, fibrosis, and myocardial ischemia.
   • Ventricular arrhythmias may precipitate sudden cardiac death, emphasizing the importance of risk stratification and preventive strategies such as implantable cardioverter-defibrillator (ICD) placement in high-risk individuals.
5. Clinical Manifestations:
   
   • Patients with HCM may present with a wide range of symptoms, including dyspnea, chest pain, palpitations, syncope, and fatigue. Some individuals may be asymptomatic and diagnosed incidentally during routine screening or family screening due to a known genetic predisposition.

Overall, the pathomechanism of hypertrophic cardiomyopathy involves genetic mutations in sarcomeric proteins, resulting in abnormal myocardial hypertrophy, microvascular dysfunction, arrhythmias, and an increased risk of sudden cardiac death. Management focuses on symptom relief, risk stratification for sudden cardiac death, and appropriate therapies tailored to individual patient needs.

Question 31

Firm myocardium, variably hypertrophied or normal ventricles, biatrial
dilation, variably dilated ventricles

Answer 31

restrictive cardiomyopathies (idiopathic, radiation fibrosis,
amyloidosis, sarcoidosis, metastatic tumor, inborn metabolic errors)

Restrictive cardiomyopathy (RCM) is a rare type of cardiomyopathy characterized by impaired ventricular filling during diastole, resulting in reduced cardiac output and symptoms of heart failure. Here’s an overview of its pathomechanism:

1. Abnormal Myocardial Compliance:
   
   • The primary pathomechanism of RCM involves increased stiffness and reduced compliance of the myocardium, particularly the ventricles. This impaired relaxation and filling of the ventricles during diastole lead to decreased ventricular end-diastolic volumes and reduced stroke volume, impairing cardiac output.
2. Underlying Causes:
   
   • RCM can be caused by various underlying conditions that lead to myocardial fibrosis, infiltration, or deposition of abnormal substances within the myocardium. These conditions include:
     
     • Infiltrative diseases: Conditions such as amyloidosis, sarcoidosis, hemochromatosis, and glycogen storage diseases can cause infiltration of the myocardium with abnormal substances, leading to increased stiffness and reduced compliance.
     • Storage diseases: Disorders such as Fabry disease and Gaucher disease involve the accumulation of abnormal substances within cardiac cells, leading to myocardial fibrosis and stiffening.
     • Endomyocardial diseases: Conditions such as endomyocardial fibrosis and eosinophilic myocarditis can lead to fibrosis and scarring of the endocardium and myocardium, impairing ventricular filling.
     • Radiation-induced heart disease: Previous thoracic radiation therapy for cancer treatment can cause fibrosis and stiffness of the myocardium, leading to RCM.
3. Hemodynamic Consequences:
   
   • The reduced ventricular compliance and impaired diastolic filling in RCM result in elevated filling pressures within the ventricles and atria. This can lead to congestion and increased filling pressures in the pulmonary circulation (left-sided RCM) or systemic circulation (right-sided RCM), causing symptoms such as dyspnea, fatigue, peripheral edema, and ascites.
4. Compensatory Mechanisms:
   
   • In response to the decreased ventricular compliance and reduced stroke volume, compensatory mechanisms such as increased heart rate and activation of neurohormonal pathways (e.g., renin-angiotensin-aldosterone system) may be activated to maintain cardiac output and systemic perfusion. However, these compensatory mechanisms may eventually become maladaptive and contribute to disease progression.
5. Clinical Manifestations:
   
   • Patients with RCM typically present with symptoms of heart failure, including dyspnea, fatigue, orthopnea, paroxysmal nocturnal dyspnea, and peripheral edema. Diagnosis is confirmed based on echocardiographic findings of restrictive ventricular filling patterns, along with evidence of underlying etiologies on imaging or laboratory testing.

Overall, the pathomechanism of restrictive cardiomyopathy involves increased stiffness and reduced compliance of the myocardium, leading to impaired ventricular filling during diastole and symptoms of heart failure. Treatment focuses on managing symptoms, addressing underlying causes, and optimizing cardiac function and hemodynamics.

Question 32

• Waxy, rubbery myocardium and tan, waxy endocardial deposits

Answer 32

Amyloidosis is a condition characterized by the deposition of abnormal proteins called amyloids in various tissues and organs throughout the body. In cardiac amyloidosis, these amyloid deposits can affect the myocardium (heart muscle) and endocardium (inner lining of the heart). Here’s how amyloidosis leads to the characteristic features of waxy, rubbery myocardium and tan, waxy endocardial deposits:

1. Myocardial Infiltration:
   
   • In cardiac amyloidosis, abnormal proteins, primarily amyloid fibrils composed of misfolded proteins such as immunoglobulin light chains (AL amyloidosis) or transthyretin (ATTR amyloidosis), accumulate within the myocardium.
   • The deposition of amyloid fibrils in the myocardium disrupts the normal architecture of the cardiac muscle fibers and interstitium, leading to myocardial infiltration and stiffening.
2. Waxy, Rubbery Myocardium:
   
   • The accumulation of amyloid fibrils within the myocardium results in the characteristic appearance of a waxy, rubbery texture of the heart muscle. This alteration in myocardial consistency is due to the replacement of normal myocardial tissue with amyloid deposits, which have a firm and gel-like consistency.
3. Endocardial Deposits:
   
   • In addition to infiltrating the myocardium, amyloid deposits can also affect the endocardium, the inner lining of the heart chambers and valves. Amyloid infiltration of the endocardium may result in the formation of tan-colored, waxy deposits on the endocardial surfaces.
   • These endocardial deposits can be visualized during cardiac surgery or autopsy as thickened, waxy plaques adherent to the endocardium, particularly in areas of turbulent blood flow such as the atria and ventricular outflow tracts.
4. Consequences for Cardiac Function:
   
   • The infiltration of amyloid deposits into the myocardium and endocardium can lead to a variety of cardiac manifestations, including diastolic dysfunction, restrictive cardiomyopathy, arrhythmias, and heart failure. The stiffening of the myocardium and impairment of ventricular relaxation result in reduced ventricular compliance and impaired filling during diastole, leading to elevated filling pressures and symptoms of heart failure.

Overall, the characteristic features of waxy, rubbery myocardium and tan, waxy endocardial deposits seen in cardiac amyloidosis are the result of the accumulation of abnormal amyloid fibrils within the heart tissue, disrupting normal cardiac structure and function. These changes contribute to the clinical manifestations and complications associated with cardiac amyloidosis, highlighting the importance of early detection and management of this condition.

Question 33

Granulomata causing visible scars

Answer 33

endothelial lesions
• sarcoidosis

Sarcoidosis is a multisystem inflammatory disorder characterized by the formation of granulomas, which are collections of immune cells, particularly macrophages and lymphocytes. Granulomas can form in various organs, including the lungs, lymph nodes, skin, eyes, and heart. When granulomas form in the heart, they can lead to the development of visible scars. Here’s how sarcoidosis causes granulomas and visible scars in the heart:

1. Immune Response:
   
   • Sarcoidosis is thought to result from an abnormal immune response triggered by exposure to environmental or unknown antigens in genetically susceptible individuals. This immune response leads to the formation of granulomas as the body attempts to contain and eliminate the perceived threat.
2. Granuloma Formation:
   
   • In sarcoidosis, activated immune cells, particularly macrophages, aggregate and form granulomas within affected tissues. Granulomas are characterized by a central core of activated macrophages surrounded by lymphocytes and fibrous tissue.
   • In the heart, granulomas can form in the myocardium, endocardium, pericardium, or within the conduction system. These granulomas may be focal or diffuse and can disrupt normal cardiac structure and function.
3. Tissue Damage and Scarring:
   
   • Granulomas in the heart can lead to tissue damage and scarring (fibrosis) through several mechanisms:
     
     • Direct compression and infiltration of cardiac muscle fibers by granulomatous inflammation can disrupt myocardial architecture and impair cardiac function.
     • Chronic inflammation and fibrosis surrounding granulomas can lead to the formation of visible scars within the myocardium or on the endocardial surface of the heart.
     • Fibrosis and scarring can also affect the conduction system of the heart, leading to arrhythmias and conduction abnormalities.
4. Clinical Manifestations:
   
   • Sarcoidosis affecting the heart, known as cardiac sarcoidosis, can present with a variety of cardiac symptoms, including palpitations, chest pain, dyspnea, syncope, and heart failure. Cardiac involvement in sarcoidosis may be asymptomatic or may manifest as sudden cardiac death due to arrhythmias or conduction disturbances.
   • Diagnosis of cardiac sarcoidosis often requires a multimodal approach, including clinical evaluation, electrocardiography (ECG), echocardiography, cardiac magnetic resonance imaging (MRI), positron emission tomography (PET) scanning, endomyocardial biopsy, and evaluation for extracardiac involvement.

Overall, sarcoidosis can cause the formation of granulomas in the heart, leading to tissue damage, fibrosis, and visible scars. Cardiac involvement in sarcoidosis can have significant clinical implications, requiring careful monitoring and management to prevent complications and preserve cardiac function.

Question 34

Answer 34

Left ventricular dilation and hypertrophy, gray-white myocardial scars, left
ventricular aneurysms, patchy endocardial fibrous thickening, coronary artery
atherosclerosis:
• chronic ischemic heart disease (ischemic cardiomyopathy)

Question 35

Marked thinning, yellow discoloration, slight or focal dilation of right ventricle

Answer 35

right ventricular cardiomyopathy (arrhythmogenic right ventricular
dysplasia

Arrhythmogenic right ventricular cardiomyopathy (ARVC), also known as arrhythmogenic right ventricular dysplasia (ARVD), is a rare inherited disorder that primarily affects the right ventricle of the heart. It is characterized by progressive replacement of the myocardium (heart muscle) with fibrous and fatty tissue, leading to arrhythmias, impaired cardiac function, and an increased risk of sudden cardiac death. Here are some of the key causes and consequences of ARVC:

1. Genetic Mutations:
   
   • ARVC is often caused by mutations in genes that encode proteins involved in cardiac cell structure and function, particularly desmosomal proteins such as desmoplakin, plakoglobin, and desmoglein. These mutations disrupt the normal integrity and function of cardiac cell junctions, leading to cell death, fibrofatty replacement, and arrhythmogenicity.
   • ARVC is typically inherited in an autosomal dominant pattern, meaning that individuals with a mutation in one copy of the affected gene have a 50% chance of passing the mutation on to each of their children.
2. Myocardial Fibrofatty Replacement:
   
   • The hallmark pathological feature of ARVC is the replacement of myocardial tissue with fibrous and fatty deposits, particularly in the right ventricle. This process can lead to structural abnormalities such as ventricular enlargement, wall thinning, and aneurysms, as well as impaired contractility and electrical instability.
   • Fibrofatty replacement of the myocardium creates a substrate for reentrant arrhythmias, which can manifest as ventricular tachycardia, ventricular fibrillation, or sudden cardiac arrest.
3. Arrhythmias and Conduction Abnormalities:
   
   • ARVC is associated with a high prevalence of ventricular arrhythmias and conduction abnormalities, which are major contributors to the risk of sudden cardiac death. Ventricular arrhythmias may arise from focal triggers within the diseased myocardium or from reentrant circuits involving areas of fibrofatty replacement.
   • Conduction abnormalities such as right bundle branch block, intraventricular conduction delays, and atrioventricular block can occur due to fibrosis and fatty infiltration of the conduction system.
4. Clinical Manifestations:
   
   • Patients with ARVC may present with a variety of symptoms, including palpitations, syncope, presyncope, chest pain, and exertional dyspnea. Symptoms often occur during adolescence or early adulthood but can manifest at any age.
   • Sudden cardiac death may be the initial presentation in some cases, particularly in young athletes with undiagnosed ARVC who experience ventricular arrhythmias during physical exertion.
5. Diagnosis and Management:
   
   • Diagnosis of ARVC requires a combination of clinical evaluation, imaging studies (e.g., echocardiography, cardiac MRI), electrocardiography (ECG), and genetic testing. Endomyocardial biopsy may be performed in select cases to confirm the presence of fibrofatty replacement.
   • Management of ARVC involves risk stratification for arrhythmias, lifestyle modification (e.g., restriction from competitive sports), pharmacological therapy (e.g., beta-blockers, antiarrhythmic drugs), implantable cardioverter-defibrillator (ICD) placement for secondary prevention of sudden cardiac death, and consideration of catheter ablation or heart transplantation in select cases.

Overall, ARVC is a complex disorder with genetic and structural abnormalities in the right ventricle, leading to ventricular arrhythmias, impaired cardiac function, and an increased risk of sudden cardiac death. Early diagnosis, risk stratification, and appropriate management are essential for improving outcomes in individuals with ARVC.

Question 36

Causes of right ventricular hypertrophy

Answer 36

Right ventricular hypertrophy (RVH) refers to the thickening or enlargement of the muscular wall of the right ventricle of the heart. There are several possible causes of RVH, which can be broadly categorized into primary or secondary causes:

1. Primary Causes:
   
   • Congenital Heart Diseases: Certain congenital heart defects, such as pulmonary stenosis, pulmonary atresia, tetralogy of Fallot, and Ebstein’s anomaly, can lead to increased pressure load on the right ventricle, resulting in RVH.
   • Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC): This inherited condition is characterized by fibrofatty replacement of the right ventricular myocardium, leading to RVH, ventricular arrhythmias, and an increased risk of sudden cardiac death.
   • Genetic Syndromes: Rare genetic syndromes such as arrhythmogenic right ventricular dysplasia (ARVD), which is a subtype of ARVC, and Carney complex may predispose individuals to RVH.
2. Secondary Causes:
   
   • Pulmonary Hypertension: Increased pressure in the pulmonary circulation, often due to conditions such as chronic obstructive pulmonary disease (COPD), pulmonary embolism, pulmonary fibrosis, or left-sided heart failure, can lead to increased right ventricular afterload and subsequent RVH.
   • Chronic Lung Diseases: Chronic lung conditions such as COPD, emphysema, and pulmonary fibrosis can cause chronic hypoxemia and pulmonary hypertension, leading to RVH as a compensatory response.
   • Left-Sided Heart Diseases: Certain left-sided heart diseases, such as mitral stenosis or left ventricular failure, can cause pulmonary hypertension and subsequent RVH due to increased right ventricular afterload.
   • Sleep-Disordered Breathing: Conditions such as obstructive sleep apnea can lead to chronic hypoxemia and pulmonary hypertension, contributing to RVH.
   • Hypoxia: Chronic exposure to high altitudes or conditions causing chronic hypoxemia can lead to RVH as a compensatory response to maintain adequate oxygen delivery.
   • Athletic Training: Intense athletic training, particularly endurance sports such as long-distance running or cycling, can lead to RVH due to increased cardiac output and volume overload.
   • Systemic Hypertension: Uncontrolled systemic hypertension can lead to increased afterload on the right ventricle, contributing to RVH.

Overall, the causes of right ventricular hypertrophy can vary widely and may involve primary cardiac conditions, pulmonary conditions, genetic factors, or systemic diseases. Treatment depends on identifying and addressing the underlying cause, and may include medications, lifestyle modifications, and, in some cases, surgical intervention.

Question 37

myocarditis

Answer 37

Variable hypertrophy, flabby myocardium, subtle mottling with pale foci or
minute hemorrhages, sometimes mural thrombi
Myocarditis is inflammation of the heart muscle (myocardium) usually caused by viral, bacterial, or other infectious agents, although it can also result from non-infectious causes. Here are some common causes of myocarditis:

1. Viral Infections:
   
   • Enteroviruses: Coxsackievirus B, in particular, is a common cause of viral myocarditis, especially during outbreaks.
   • Adenoviruses
   • Influenza virus
   • Herpesviruses: Including herpes simplex virus (HSV) and cytomegalovirus (CMV)
   • Human immunodeficiency virus (HIV)
2. Bacterial Infections:
   
   • Borrelia burgdorferi: Lyme disease, transmitted by tick bites, can lead to Lyme myocarditis.
   • Chlamydia pneumoniae
   • Corynebacterium diphtheriae: Diphtheria, a bacterial infection, can cause myocarditis as a complication.
3. Parasitic Infections:
   
   • Trypanosoma cruzi: Chagas disease, caused by the parasite T. cruzi and transmitted by triatomine bugs, is a common cause of myocarditis in endemic regions.
4. Non-Infectious Causes:
   
   • Autoimmune Disorders: Conditions such as systemic lupus erythematosus (SLE), rheumatoid arthritis, and sarcoidosis can lead to autoimmune-mediated myocarditis.
   • Drug-Induced: Certain medications, including chemotherapeutic agents (e.g., doxorubicin), immune checkpoint inhibitors, and some antibiotics, can cause myocarditis as an adverse drug reaction.
   • Toxins: Exposure to toxins such as alcohol, heavy metals (e.g., lead), and certain drugs of abuse (e.g., cocaine) can lead to myocarditis.
   • Allergic Reactions: Severe allergic reactions, such as those to bee stings or certain medications, can trigger myocarditis.
   • Radiation Therapy: Radiation therapy to the chest area, often used in the treatment of cancer, can cause inflammation and damage to the heart tissue, leading to myocarditis.
5. Unknown Causes:
   
   • In some cases, the cause of myocarditis may not be identified, and it is classified as idiopathic myocarditis.

Myocarditis can vary widely in severity, ranging from mild cases with minimal symptoms to severe cases with acute heart failure, arrhythmias, and even sudden cardiac death. Treatment depends on the underlying cause and severity of the condition, and may include supportive care, anti-inflammatory medications, immunosuppressive therapy, and treatment of complications such as heart failure or arrhythmias.

Question 38

Atrioventricular valves with thickened, distorted leaflets and short, thickened
chordae tendineae

Answer 38

semilunar valves with thick, distorted and fused cusps
• rheumatic valvular heart disease (chronic)

When the semilunar valves (aortic and pulmonary valves) are affected by rheumatic valvular heart disease, leading to thickened, distorted, and fused cusps, several consequences can arise:

1. Valvular Stenosis:
   
   • Thickening, distortion, and fusion of the cusps can lead to narrowing (stenosis) of the valve orifice. This restricts the flow of blood through the affected valve, resulting in increased pressure load on the heart chambers upstream of the valve (left ventricle for the aortic valve, right ventricle for the pulmonary valve).
   • Aortic valve stenosis can lead to left ventricular hypertrophy (LVH) and eventually heart failure. Pulmonary valve stenosis can lead to right ventricular hypertrophy (RVH) and impaired right ventricular function.
2. Valvular Regurgitation:
   
   • The thickened, distorted, and fused cusps may not close properly, resulting in incomplete closure of the valve leaflets and regurgitation (backflow) of blood through the valve during ventricular relaxation.
   • Aortic regurgitation can lead to increased diastolic volume and pressure overload in the left ventricle, potentially resulting in left ventricular dilation and heart failure. Pulmonary regurgitation can lead to volume overload of the right ventricle.
3. Hemodynamic Consequences:
   
   • Both stenosis and regurgitation of the semilunar valves can lead to hemodynamic disturbances, including increased pressure or volume load on the affected ventricle, altered cardiac output, and impaired systemic or pulmonary circulation.
   • The degree of valvular dysfunction and the resulting hemodynamic consequences depend on the severity of the valve lesions and the presence of other coexisting cardiac conditions.
4. Clinical Manifestations:
   
   • Patients with rheumatic valvular heart disease involving the semilunar valves may present with symptoms such as chest pain, dyspnea (shortness of breath), fatigue, palpitations, syncope, and signs of heart failure.
   • Severe cases may present with acute decompensation, hemodynamic instability, or symptoms of end-organ dysfunction.
5. Complications:
   
   • Chronic rheumatic valvular heart disease involving the semilunar valves can lead to complications such as infective endocarditis, atrial fibrillation, thromboembolic events (e.g., stroke), and progressive deterioration of cardiac function.
   • Without appropriate management, severe valve dysfunction can lead to irreversible damage to the heart and increased risk of mortality.

Overall, the consequences of thick, distorted, and fused cusps in the semilunar valves due to chronic rheumatic valvular heart disease can significantly impact cardiac function and overall patient health. Early detection, appropriate medical therapy, and timely intervention (such as valve repair or replacement) are crucial for improving outcomes and preventing complications in affected individuals.

Rheumatic valvular heart disease is a condition characterized by damage to the heart valves due to rheumatic fever, an inflammatory disease caused by untreated or inadequately treated streptococcal infections, particularly group A streptococcus. Here are key points about rheumatic valvular heart disease:

1. Pathophysiology:
   
   • Rheumatic fever develops as an immune response to certain strains of group A streptococcus bacteria, primarily affecting children aged 5 to 15 years. The immune response can lead to inflammation and damage in various tissues, including the heart.
   • Rheumatic valvular heart disease typically affects the mitral valve, followed by the aortic valve. The tricuspid and pulmonary valves are less commonly involved.
   • The inflammatory process in rheumatic fever can lead to scarring, thickening, and distortion of the valve leaflets, resulting in valvular dysfunction.
2. Clinical Presentation:
   
   • Patients with rheumatic valvular heart disease may present with symptoms related to valvular stenosis (narrowing) or regurgitation (leakage) depending on the affected valve(s).
   • Common symptoms include dyspnea (shortness of breath), orthopnea (difficulty breathing while lying flat), paroxysmal nocturnal dyspnea (sudden onset of breathlessness at night), palpitations, fatigue, chest pain, and signs of heart failure such as peripheral edema and jugular venous distension.
3. Diagnosis:
   
   • Diagnosis of rheumatic valvular heart disease is based on clinical evaluation, including history and physical examination, as well as echocardiography to assess valve structure and function.
   • Echocardiography can reveal abnormalities such as valve thickening, restricted leaflet motion (stenosis), or abnormal valve closure (regurgitation).
4. Management:
   
   • Treatment of rheumatic valvular heart disease aims to relieve symptoms, prevent complications, and manage underlying streptococcal infections.
   • Medical management may include antibiotics to treat active streptococcal infections, anti-inflammatory medications to reduce inflammation, and medications to manage symptoms and complications such as heart failure and arrhythmias.
   • In severe cases with significant valve dysfunction, surgical intervention such as valve repair or replacement may be necessary to restore normal valve function and improve outcomes.
5. Prevention:
   
   • Prevention of rheumatic fever and subsequent rheumatic valvular heart disease involves early diagnosis and treatment of streptococcal infections with appropriate antibiotics.
   • Secondary prevention strategies, including long-term antibiotic prophylaxis for individuals with a history of rheumatic fever, are recommended to prevent recurrent episodes and progression of valvular disease.

Overall, rheumatic valvular heart disease remains a significant cause of cardiovascular morbidity and mortality, particularly in resource-limited settings where access to healthcare and preventive measures may be limited. Efforts to improve access to healthcare, enhance public health initiatives, and promote early detection and treatment of streptococcal infections are essential for reducing the burden of rheumatic heart disease worldwide.

Question 39

Heaped-up, irregular, calcified masses both within cusps and protruding into
the sinuses of Valsalva, free margins of cusps generally uninvolved

Answer 39

calcific aortic stenosis, degenerative type

Calcific aortic stenosis refers to the narrowing (stenosis) of the aortic valve due to the accumulation of calcium deposits on the valve leaflets. This condition typically occurs as a result of degenerative changes in the valve leaflets over time, leading to thickening, calcification, and reduced mobility of the valve cusps. Calcific aortic stenosis is the most common cause of aortic stenosis in adults and is often associated with aging, although it can also occur in younger individuals with congenital bicuspid aortic valves or other underlying conditions. As the aortic valve becomes progressively narrowed, it obstructs blood flow from the left ventricle to the aorta, leading to increased pressure load on the left ventricle and subsequent symptoms such as chest pain, dyspnea (shortness of breath), syncope (fainting), and heart failure. Severe calcific aortic stenosis can have significant clinical implications and may require intervention, such as aortic valve replacement, to relieve symptoms and improve outcomes.

Question 40

Calcification beginning at free margins of cusps with bicuspid valve or valve
with rudimentary third cusp

Answer 40

calcific aortic stenosis, congenital type

Congenital calcific aortic stenosis refers to the narrowing (stenosis) of the aortic valve due to calcium deposits on the valve leaflets that is present from birth. Unlike the more common degenerative calcific aortic stenosis that develops later in life, congenital calcific aortic stenosis occurs as a result of abnormal development or formation of the aortic valve during fetal development.

This condition is often associated with congenital heart defects, such as a bicuspid aortic valve, in which the valve has two instead of three cusps. The abnormal valve structure predisposes it to early calcification and narrowing, leading to obstruction of blood flow from the left ventricle to the aorta.

Congenital calcific aortic stenosis can manifest with symptoms similar to those of acquired calcific aortic stenosis, including chest pain, dyspnea (shortness of breath), fatigue, syncope (fainting), and heart failure. Management may involve monitoring of the condition and, in severe cases, surgical intervention such as aortic valve repair or replacement to relieve the obstruction and improve symptoms.

Question 41

“Hooding” of the leaflet; rubbery thickening of edge of the leaflet; elongation,
attenuation, or even rupture of chordae tendineae

Answer 41

mitral valve prolapse

Mitral valve prolapse (MVP) is a condition in which the two flaps (leaflets) of the heart’s mitral valve bulge or prolapse into the left atrium during the heart’s contraction (systole). Normally, the mitral valve closes tightly to prevent blood from flowing backward into the left atrium from the left ventricle. However, in MVP, the valve’s leaflets are abnormally floppy or enlarged, which can prevent the valve from closing properly. MVP is often benign and may not cause any symptoms or complications. However, in some cases, it can lead to symptoms such as palpitations, chest pain, shortness of breath, and fatigue. In severe cases, MVP can result in mitral regurgitation, where blood leaks backward into the left atrium, potentially leading to heart murmurs, arrhythmias, and, rarely, infective endocarditis. Treatment for MVP depends on the severity of symptoms and complications and may include medication to manage symptoms or, in rare cases, surgical repair or replacement of the mitral valve.

Question 42

Irregular, hard ring of calcification at the leaflet-myocardial connection

Answer 42

calcification of the mitral valve annulus

Calcification of heart valves can be caused by various factors, including aging, chronic inflammation, certain medical conditions like atherosclerosis, rheumatic fever, endocarditis, and congenital heart defects. If there’s a specific reason you’re asking, I can provide more tailored information.

Question 43

• Plaque-like thickenings of endocardium and valves of the right side of heart
(rarely do lesions involve left-sided structures)

Answer 43

carcinoid heart disease

The term “carcinoid” refers to a type of slow-growing tumor that typically originates in the cells of the neuroendocrine system, which is responsible for producing hormones. Carcinoid tumors can develop in various organs, most commonly in the gastrointestinal tract (such as the stomach, small intestine, or appendix) or in the lungs. These tumors can produce hormones and other substances that can cause a variety of symptoms and complications, depending on their location and the substances they release.

Carcinoid heart disease is a rare condition that occurs in some individuals with carcinoid syndrome, a group of symptoms that result from carcinoid tumors. These tumors produce hormones, including serotonin, which can cause damage to the heart valves, leading to fibrosis and thickening. Carcinoid heart disease primarily affects the right side of the heart and can result in valve dysfunction, heart murmurs, and eventually heart failure if left untreated.

Question 44

Small, friable, irregular, and often multiple vegetations along the lines of
closure of a valve or on the chordae

Answer 44

acute rheumatic endocarditis

In the context of the heart, “vegetation” refers to abnormal growths or masses that form on the heart valves or inner lining of the heart chambers. These growths are typically composed of blood cells, fibrin, and bacteria, and they can develop as a result of infective endocarditis, a serious infection of the heart valves or inner lining of the heart. Vegetations can interfere with the normal functioning of the heart valves and may lead to complications such as valve damage, stroke, or systemic infection if not treated promptly.

Acute rheumatic fever, caused by a bacterial infection with Group A streptococcus bacteria, can lead to rheumatic heart disease, a condition where the heart valves are damaged. When the bacteria infect the heart valves, they can cause inflammation and damage to the valve tissue. This damage can create roughened surfaces on the valves, which can then become a site for the formation of blood clots and vegetation.

Additionally, during acute rheumatic fever, the body’s immune response can lead to the formation of immune complexes, which can deposit on the heart valves and contribute to the development of vegetation. These vegetations can interfere with the normal functioning of the heart valves, potentially leading to complications such as valve stenosis or regurgitation.

Question 45

Large irregular masses overhanging free margins that extend to chordae and
valve leaflets or cusps, with or without abscess, possible valve perforation

Answer 45

infective endocarditis

Infective endocarditis is a serious infection of the inner lining of the heart chambers (endocardium) and heart valves. It typically occurs when bacteria, fungi, or other microorganisms enter the bloodstream and attach to damaged areas of the heart lining or heart valves. Once attached, these microorganisms can multiply and form masses of infected tissue called vegetations. Infective endocarditis can cause damage to the heart valves, leading to complications such as valve dysfunction, heart failure, stroke, and systemic infection. Prompt diagnosis and treatment are essential to prevent serious complications.

The pathophysiology of infective endocarditis involves several key steps:

1. Endothelial Damage: Endothelial damage to the inner lining of the heart (endocardium) can occur due to various factors, such as turbulent blood flow, congenital heart defects, or previous heart surgery. This damage creates sites where microorganisms can adhere.
2. Microbial Adherence: Microorganisms, such as bacteria or fungi, enter the bloodstream from infections elsewhere in the body or through invasive procedures (like dental work or surgery). These microorganisms can then adhere to the damaged areas of the endocardium or heart valves.
3. Formation of Vegetations: Once adhered to the damaged endothelium, the microorganisms begin to multiply, forming masses of infected tissue known as vegetations. These vegetations consist of microorganisms, platelets, fibrin, and other blood components.
4. Inflammatory Response: The presence of microorganisms triggers an inflammatory response in the body, leading to the recruitment of immune cells to the site of infection. This inflammatory process can further damage the heart valves and surrounding tissues.
5. Complications: As the infection progresses, vegetations can grow in size, leading to the destruction of heart valve tissue and the formation of abscesses. Pieces of the vegetation can break off and embolize, traveling through the bloodstream to other organs and causing systemic complications, such as stroke, organ damage, or septicemia.
6. Clinical Manifestations: The clinical manifestations of infective endocarditis can vary widely depending on factors such as the causative microorganism, the location of the infection, and the patient’s underlying health status. Common symptoms include fever, chills, fatigue, heart murmurs, and signs of systemic embolization.

Overall, infective endocarditis is a complex condition involving the interplay of microbial virulence factors, host factors, and immune responses, leading to potentially severe complications if left untreated. Early diagnosis and appropriate antimicrobial therapy are crucial for improving patient outcomes.

Question 46

Small, bland, often single vegetations attached at the line of valve closure

Answer 46

nonbacterial thrombotic (marantic) endocarditis

Nonbacterial thrombotic endocarditis (NBTE), also known as marantic endocarditis, is a condition characterized by the formation of sterile (non-infective) thrombi on the heart valves. The pathophysiology of NBTE involves several key mechanisms:

1. Underlying Hypercoagulable State: NBTE often occurs in the setting of conditions associated with a hypercoagulable state, such as advanced malignancies, autoimmune disorders, or chronic inflammatory diseases. These underlying conditions can promote an imbalance in the coagulation system, leading to increased thrombus formation.
2. Endothelial Injury: Endothelial injury or dysfunction, which can occur due to systemic inflammation, cancer-related factors, or other mechanisms, creates a substrate for thrombus formation. Damaged endothelium exposes subendothelial collagen and tissue factor, initiating the coagulation cascade.
3. Platelet Activation: Activated platelets adhere to the damaged endothelium and aggregate, forming a platelet-rich thrombus. This process is facilitated by the release of von Willebrand factor and other platelet agonists.
4. Thrombus Formation: Thrombin generation and fibrin deposition contribute to the growth and stabilization of the thrombus. The thrombus accumulates on the cardiac valves, particularly on the atrioventricular and mitral valves, where blood flow turbulence is more pronounced.
5. Sterile Nature: Unlike infective endocarditis, NBTE does not involve microbial colonization or infection of the heart valves. Instead, the thrombi are composed of platelets, fibrin, and other blood components, without the presence of bacteria or other microorganisms.
6. Clinical Manifestations: NBTE may be asymptomatic or present with symptoms related to embolization of thrombi to peripheral organs, such as stroke, transient ischemic attacks, or systemic embolism. The clinical course is often characterized by episodic embolic events rather than the systemic symptoms seen in infective endocarditis.

Overall, NBTE represents a manifestation of systemic hypercoagulability and endothelial dysfunction, leading to the formation of sterile thrombi on cardiac valves. Treatment typically involves addressing the underlying hypercoagulable state and anticoagulation therapy to prevent thromboembolic complications.

Question 47

Small to medium-sized vegetations on atrioventricular valves; may be on
both sides of valve leaflets

Answer 47

Libman-Sacks endocarditis

Question 48

MYOCARDIAL INFARCTS
- pathomechanism
• Color changes with time

Answer 48

The pathophysiology of myocardial infarction (MI), commonly known as a heart attack, involves the following key mechanisms:

1. Coronary Artery Occlusion: The majority of MIs result from the sudden occlusion (blockage) of a coronary artery, typically due to the rupture or erosion of an atherosclerotic plaque. Atherosclerosis is a chronic inflammatory process characterized by the accumulation of cholesterol, inflammatory cells, and fibrous tissue within the walls of the coronary arteries. When a plaque ruptures, it exposes its contents to the bloodstream, triggering platelet aggregation and the formation of a blood clot (thrombus) at the site of the rupture.
2. Ischemia: The thrombus obstructs blood flow in the affected coronary artery, leading to a reduction or cessation of blood supply (ischemia) to the myocardium (heart muscle) supplied by that artery. Ischemia deprives the myocardium of oxygen and nutrients, impairing its ability to function properly.
3. Myocardial Injury: Prolonged ischemia results in cellular injury and dysfunction within the affected area of the myocardium. The lack of oxygen and nutrients leads to a disruption of cellular metabolism and the accumulation of metabolic byproducts, such as lactic acid, contributing to cellular damage.
4. Cellular Death (Necrosis): If blood flow is not restored promptly, irreversible cellular damage and death (necrosis) occur within the ischemic myocardium. Necrosis of myocardial cells leads to the release of intracellular contents, including enzymes such as creatine kinase (CK), lactate dehydrogenase (LDH), and cardiac troponins, into the bloodstream.
5. Inflammatory Response: The release of cellular contents triggers an inflammatory response, with the recruitment of inflammatory cells (such as neutrophils and macrophages) to the site of injury. Inflammation contributes to further tissue damage and remodeling of the myocardium.
6. Scar Formation: Over time, the necrotic myocardial tissue is replaced by fibrous scar tissue through a process of wound healing and tissue remodeling. The formation of scar tissue alters the structure and function of the affected area of the heart, leading to potential complications such as ventricular remodeling, heart failure, and arrhythmias.

Overall, myocardial infarction is a complex process involving the interplay of coronary artery occlusion, ischemia, cellular injury and death, inflammation, and tissue remodeling. Early recognition and prompt treatment are critical to minimize myocardial damage and improve patient outcomes.

Color changes with time:
• Less than 4 hours:
• no color change
• 4 to 12 hours:
• occasionally dark mottling
• 12 to 24 hours:
• dark mottling
• red-blue pallor
• 1 to 3 days:
• mottling with yellow-tan center
• 3 to 7 days:
• yellow-tan
• central softening
• hyperemic border
• 7 to 10 days:
• maximally yellow-tan
• progressive softening
• red-tan margins
• 10 to 14 days:
• pale red-gray borders
• 2 weeks to 2 months:
• replacement with firm gray-white scar

Question 49

Yellow, flat spots and streaks

Answer 49

fatty streaks

Fatty streaks are the earliest visible lesions in the development of atherosclerosis, a condition characterized by the accumulation of plaque within the walls of arteries. Fatty streaks consist of lipid-laden foam cells (primarily macrophages) within the intima (inner layer) of arteries, particularly in areas prone to turbulent blood flow, such as arterial bifurcations and curvatures.

These foam cells accumulate low-density lipoprotein (LDL) cholesterol that has been deposited in the arterial wall. Over time, other components such as smooth muscle cells, collagen, and extracellular matrix proteins may contribute to the growth and progression of fatty streaks into more advanced atherosclerotic plaques.

Fatty streaks themselves are not typically associated with significant narrowing or obstruction of the artery, nor do they usually cause symptoms. However, they represent the earliest stage of atherosclerosis and can progress to more advanced lesions if risk factors such as high cholesterol, hypertension, smoking, and diabetes are not addressed. Fatty streaks serve as important indicators of early vascular disease and are a target for preventive interventions to reduce the risk of cardiovascular events such as heart attack and stroke.

Atherosclerosis, the buildup of plaque in the arteries, can lead to myocardial infarction (heart attack) through several mechanisms:

1. Plaque Rupture: Atherosclerotic plaques can become unstable and rupture, exposing the underlying tissue to the bloodstream. This triggers the formation of a blood clot (thrombus) at the site of the rupture. If the clot is large enough, it can obstruct blood flow in the coronary artery, leading to myocardial ischemia and potentially infarction.
2. Coronary Artery Stenosis: As atherosclerosis progresses, plaques can grow in size and cause narrowing (stenosis) of the coronary arteries. This narrowing reduces blood flow to the heart muscle, especially during times of increased demand, such as physical exertion or stress. If the stenosis becomes severe enough, it can lead to myocardial ischemia and infarction.
3. Coronary Artery Spasm: Atherosclerosis can make the coronary arteries more prone to spasm, which can further reduce blood flow to the heart muscle. Spasms can occur spontaneously or be triggered by various factors, including emotional stress, exposure to cold temperatures, or certain medications. Severe spasms can lead to myocardial ischemia and infarction.
4. Microvascular Dysfunction: Atherosclerosis can also affect the smaller blood vessels (microvasculature) within the heart muscle itself. Damage to these vessels can impair the ability of the heart muscle to receive adequate oxygen and nutrients, leading to myocardial ischemia and potentially infarction, even in the absence of significant coronary artery stenosis.

Overall, atherosclerosis contributes to myocardial infarction by reducing blood flow to the heart muscle through plaque rupture, stenosis of the coronary arteries, coronary artery spasm, and microvascular dysfunction. These mechanisms can lead to myocardial ischemia and eventual necrosis (death) of the heart muscle if blood flow is not restored promptly.

Question 50

White to white-yellow plaques protruding into arterial lumen, may coalesce
with neighboring plaques (sectioning reveals firm, white luminal surface with
soft, white-yellow central region)

Answer 50

atheroma

Atheroma refers to a characteristic feature of atherosclerosis, where fatty deposits accumulate within the walls of arteries, forming a raised lesion known as a plaque. These plaques consist of lipids (primarily cholesterol), inflammatory cells, smooth muscle cells, and connective tissue components. Atheromas develop gradually over time and can narrow the arterial lumen, restricting blood flow to vital organs and tissues. Additionally, atheromas can become unstable, leading to plaque rupture and the formation of blood clots, which can trigger serious cardiovascular events such as heart attack or stroke.

Question 51

Atheromas with calcification, ulceration, hemorrhage:

Answer 51

complicated atheroma

The key difference between normal atheroma and complicated atheroma lies in their stability and the presence of additional features or complications:

1. Normal Atheroma (Stable Plaque):
   
   • Normal atheroma refers to stable plaques that are typically asymptomatic and do not cause significant narrowing or obstruction of the artery.
   • These plaques are characterized by the gradual buildup of lipids (cholesterol), inflammatory cells, and connective tissue within the arterial wall.
   • Normal atheromas may not produce symptoms and are often discovered incidentally during imaging studies or autopsies.
   • While stable plaques can contribute to chronic conditions like coronary artery disease (CAD), they are less likely to cause acute complications such as plaque rupture or thrombosis.
2. Complicated Atheroma:
   
   • Complicated atheroma refers to plaques that have undergone changes leading to instability and an increased risk of acute complications.
   • These changes may include thinning of the fibrous cap covering the plaque, increased inflammation, intraplaque hemorrhage, calcification, and the presence of a lipid-rich necrotic core.
   • Complicated atheromas are more prone to rupture or erosion, exposing the plaque’s contents to the bloodstream and triggering thrombus formation.
   • Complications of complicated atheromas can include acute coronary syndrome (unstable angina, myocardial infarction), stroke, peripheral artery disease with acute limb ischemia, or aortic aneurysm rupture.
   • Identifying and managing complicated atheromas are crucial for preventing acute cardiovascular events and reducing the risk of complications.

In summary, while both normal atheroma and complicated atheroma involve the accumulation of plaque within arteries, complicated atheroma is characterized by instability and an increased risk of acute complications such as plaque rupture, thrombosis, and acute cardiovascular events.

Atheromas, the characteristic plaques of atherosclerosis, can lead to several complications:

1. Coronary Artery Disease (CAD): Atheromas in the coronary arteries can cause narrowing or obstruction of blood flow to the heart muscle, leading to angina (chest pain) or myocardial infarction (heart attack).
2. Cerebrovascular Disease: Atheromas in the carotid arteries supplying blood to the brain can increase the risk of stroke by causing plaque rupture or by reducing blood flow to the brain.
3. Peripheral Artery Disease (PAD): Atheromas in peripheral arteries (e.g., in the legs) can cause intermittent claudication (leg pain with walking) or critical limb ischemia (severe leg pain at rest) due to reduced blood flow to the lower extremities.
4. Aneurysm Formation: Atheromas can weaken the walls of arteries, leading to the formation of aneurysms (ballooning of the artery wall). Aneurysms can rupture, causing life-threatening bleeding.
5. Ischemic Heart Disease: Chronic narrowing of coronary arteries due to atheromas can lead to ischemic heart disease, where the heart muscle does not receive enough oxygen-rich blood, resulting in symptoms such as chest pain and shortness of breath.
6. Acute Coronary Syndrome (ACS): Plaque rupture or erosion in coronary arteries can trigger the formation of blood clots, leading to unstable angina or acute myocardial infarction (heart attack).
7. Renal Artery Stenosis: Atheromas in the renal arteries can reduce blood flow to the kidneys, leading to hypertension (high blood pressure) and renal dysfunction.

Overall, atheromas pose significant health risks by compromising blood

Question 52

• Dilation of vessel, often containing thrombus
• Small SPHERICAL dilation
• Large SPHERICAL dilation
• Spindle-shaped dilation

Answer 52

• aneurysm
• berry aneurysm
• saccular aneurysm
• fusiform aneurysm

Question 53

Hematoma extending between layers of artery

Answer 53

arterial dissection

The main difference between a hematoma and hemorrhage lies in their location and the way blood collects:

1. Hematoma:
   
   • A hematoma is a localized collection of blood outside of blood vessels, typically within tissues or an organ.
   • Hematomas often result from trauma or injury that damages blood vessels, causing blood to leak into surrounding tissues and form a pocket of blood.
   • Hematomas can vary in size from small bruises (ecchymosis) to larger collections of blood that can cause swelling and pain.
   • Examples of hematomas include subcutaneous hematomas (beneath the skin), intramuscular hematomas (within muscles), and subdural hematomas (within the skull, between the brain and its outermost covering, the dura mater).
2. Hemorrhage:
   
   • Hemorrhage refers to the active escape or release of blood from a ruptured blood vessel, either internally within the body or externally through a break in the skin.
   • Hemorrhages can occur spontaneously or as a result of trauma, surgery, or underlying medical conditions.
   • Depending on the size and location of the hemorrhage, it can lead to various symptoms, including visible bleeding, bruising, swelling, pain, hypovolemic shock (in severe cases), or organ dysfunction.
   • Examples of hemorrhages include intracerebral hemorrhage (bleeding within the brain), gastrointestinal hemorrhage (bleeding within the digestive tract), and hemorrhagic shock (severe blood loss leading to inadequate tissue perfusion).

In summary, while both hematoma and hemorrhage involve the accumulation or escape of blood from blood vessels, a hematoma refers to a localized collection of blood within tissues or an organ, whereas hemorrhage refers to the active release of blood from a ruptured blood vessel, either internally or externally.

Question 54

Stomach normal

Answer 54

The stomach is in the normal anatomical position; the larger curvature is 21 cm, the
smaller one is 15 cm long, respectively.

The stomach wall is 2-4 mm. in thickness,
moderately firm, and grossly having normal layerings.

The serosal (peritoneal) surface is
smooth and glistening.

The mucosal rugae are preserved.

Otherwise, the mucosa is
grossly intact having smooth surfaces with a normal blood content.

Question 55

Stomach
- Edema and hyperemia
- Mucosal erosion, hemorrhage into gastric wall:

Answer 55

• mild acute gastritis
• severe acute gastritis

Gastritis is a medical condition characterized by inflammation of the lining of the stomach, known as the gastric mucosa. This inflammation can be acute (sudden and short-term) or chronic (long-lasting).

In gastritis, the protective barrier of the stomach lining becomes weakened or damaged, allowing digestive juices, particularly hydrochloric acid and pepsin, to irritate the stomach lining. This irritation leads to symptoms such as:

1. Abdominal pain or discomfort: This can range from mild to severe and may be felt in the upper abdomen.
2. Nausea and vomiting: Some individuals with gastritis may experience nausea or vomiting, especially after eating.
3. Indigestion (dyspepsia): Gastritis can cause symptoms of indigestion, such as bloating, belching, and a feeling of fullness after eating.
4. Loss of appetite: In severe cases or chronic gastritis, individuals may experience a reduced appetite or weight loss.
5. Bleeding: Inflammation of the stomach lining can sometimes lead to erosions or ulcers, which may cause bleeding. This can result in vomiting blood (hematemesis) or passing dark, tarry stools (melena).
6. Other symptoms: Additional symptoms may include a feeling of burning or gnawing in the stomach, excessive gas, or discomfort after consuming acidic or spicy foods

The pathomechanism of gastritis involves a complex interplay of factors that lead to inflammation of the gastric mucosa (the lining of the stomach). Several key mechanisms contribute to the development of gastritis:

1. Helicobacter pylori Infection: The most common cause of gastritis is infection with the bacterium Helicobacter pylori (H. pylori). H. pylori colonizes the stomach lining and triggers an immune response, leading to chronic inflammation. This inflammation damages the gastric mucosa, disrupting its normal protective barrier function.
2. Autoimmune Reaction: Autoimmune gastritis occurs when the body’s immune system mistakenly attacks the cells of the gastric mucosa, specifically the parietal cells that produce hydrochloric acid and intrinsic factor. This autoimmune reaction can lead to inflammation and damage to the gastric mucosa.
3. Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen can irritate the gastric mucosa and disrupt the protective mucosal barrier. This can lead to inflammation and erosion of the stomach lining, resulting in gastritis.
4. Alcohol Consumption: Excessive alcohol consumption can irritate the gastric mucosa, leading to inflammation and damage. Alcohol can also increase stomach acid production, further contributing to mucosal injury and inflammation.
5. Bile Reflux: Bile reflux occurs when bile from the duodenum flows back into the stomach, potentially leading to gastritis. Bile acids can irritate the gastric mucosa and cause inflammation.
6. Chemical Irritants: Exposure to certain chemicals, such as corrosive substances or strong acids and bases, can damage the gastric mucosa and cause gastritis.
7. Stress: While acute stress is unlikely to cause gastritis on its own, it can exacerbate existing gastritis or increase susceptibility to gastritis by impairing the protective mechanisms of the gastric mucosa.

Overall, gastritis develops when the balance between protective factors (such as the gastric mucosal barrier) and damaging factors (such as H. pylori infection, NSAID use, or alcohol consumption) is disrupted, leading to inflammation and injury to the gastric mucosa. The specific pathomechanism may vary depending on the underlying cause of gastritis.

Question 56

Stomach

• Flattening of mucosa with loss of rugal folds and thinning of gastric wall

Answer 56

chronic gastritis

Question 57

Round to oval, sharply punched-out defects with straight walls and smooth,
clean bases generally located along the lesser curvature in the border zone
between corpus and antrum or in the first portion of the duodenum

Answer 57

peptic ulcers

The pathophysiology of peptic ulcers involves a complex interplay of various factors that lead to the erosion of the gastrointestinal mucosa. The primary mechanisms include:

1. Disruption of the Gastric Mucosal Barrier: The stomach and duodenum are lined with a protective layer of mucous membrane that acts as a barrier against the corrosive effects of gastric acid and digestive enzymes. Disruption of this mucosal barrier, either by physical damage or chemical irritation, can expose the underlying tissues to aggressive factors.
2. Increase in Gastric Acid Secretion: Factors such as Helicobacter pylori infection, excessive gastrin production (as seen in Zollinger-Ellison syndrome), or the use of nonsteroidal anti-inflammatory drugs (NSAIDs) can increase the secretion of gastric acid. Elevated levels of gastric acid can overwhelm the protective mechanisms of the gastric mucosa and lead to tissue damage.
3. Decrease in Mucosal Defense Mechanisms: Certain conditions or medications can impair the production of protective mucus or bicarbonate secretion, weakening the mucosal defense mechanisms against gastric acid. This includes H. pylori infection, NSAID use, smoking, and alcohol consumption.
4. Helicobacter pylori Infection: H. pylori is a bacterium that colonizes the stomach lining and releases toxins that damage the mucosal barrier. It also induces an inflammatory response in the gastric mucosa, leading to tissue damage and ulcer formation.
5. Decrease in Gastric Blood Flow: Conditions that reduce blood flow to the stomach lining, such as ischemia, shock, or vasoconstriction, can impair the delivery of oxygen and nutrients to the mucosal cells, leading to tissue damage and ulceration.
6. Imbalance Between Aggressive and Protective Factors: The development of peptic ulcers often results from an imbalance between aggressive factors (such as gastric acid, H. pylori infection, and NSAID use) and protective factors (such as mucous secretion, bicarbonate secretion, and blood flow). When aggressive factors outweigh protective factors, mucosal injury and ulceration occur.

Overall, peptic ulcers develop when the normal mechanisms that protect the gastrointestinal mucosa are disrupted, allowing aggressive factors to damage the underlying tissues. Effective management of peptic ulcers involves addressing the underlying causes, reducing gastric acid secretion, and promoting ulcer healing.

Question 58

Small, superficial ulcers with poorly defined margins, dark brown bases, and
no anatomic predilection

Answer 58

superficial stress ulcers

Question 59

Small sessile polyps

Answer 59

usually hyperplastic

Sessile polyps in the stomach can have various causes, including chronic inflammation, infection with Helicobacter pylori bacteria, genetic factors, and certain lifestyle habits like smoking or heavy alcohol consumption.

They can also be associated with conditions like gastritis, gastric ulcers, or even certain genetic syndromes predisposing individuals to polyp formation.

If you suspect you have them, it’s essential to consult with a healthcare professional for proper diagnosis and management.

Question 60

Exophytic, excavated, diffuse infiltrative tumors

Answer 60

gastric adenocarcinoma

Gastric adenocarcinoma refers to cancer that originates in the glandular cells lining the stomach. It’s the most common type of stomach cancer and typically develops slowly over many years. Risk factors for gastric adenocarcinoma include infection with Helicobacter pylori bacteria, chronic gastritis, smoking, a diet high in salted or smoked foods, and a family history of stomach cancer. Symptoms may include indigestion, abdominal discomfort or pain, unintentional weight loss, nausea, vomiting, and blood in the stool. Early detection and treatment are crucial for improving outcomes. Treatment options may include surgery, chemotherapy, radiation therapy, targeted therapy, and immunotherapy, depending on the stage and characteristics of the cancer.

The pathomechanism of gastric adenocarcinoma involves a complex interplay of genetic, environmental, and lifestyle factors. Here’s a brief overview:

1. Chronic Gastritis: Prolonged inflammation of the stomach lining, often due to Helicobacter pylori infection or other causes, can lead to changes in the gastric mucosa over time. Chronic gastritis can progress to more severe conditions like gastric atrophy and intestinal metaplasia, which are precancerous stages.
2. Helicobacter pylori Infection: This bacterium is a major risk factor for gastric adenocarcinoma. It can cause chronic inflammation, leading to genetic mutations in the gastric epithelial cells and an increased risk of cancer development.
3. Genetic Factors: Certain genetic mutations and alterations can predispose individuals to gastric adenocarcinoma. For example, mutations in tumor suppressor genes (such as TP53) and oncogenes (such as HER2) can promote cancer development.
4. Environmental Factors: Factors such as a diet high in salted, smoked, or pickled foods, as well as low fruit and vegetable intake, have been associated with an increased risk of gastric adenocarcinoma. Smoking, obesity, and certain occupational exposures may also contribute to the development of the disease.
5. Epigenetic Changes: Epigenetic alterations, such as DNA methylation and histone modifications, can affect gene expression patterns in gastric cells, leading to abnormal cell growth and cancer progression.
6. Tumor Microenvironment: The microenvironment surrounding the tumor, including immune cells, fibroblasts, and blood vessels, plays a critical role in tumor growth, invasion, and metastasis.

Overall, gastric adenocarcinoma is a multifactorial disease with a complex pathogenesis involving interactions between genetic susceptibility, environmental exposures, and inflammatory processes within the stomach. Early detection and intervention are essential for improving outcomes in patients with this type of cancer.

Question 61

Duodenum Nornal

Answer 61

Question 62

Intestine
- Small blind outpouchings

Answer 62

diverticula;

• may occur anywhere in gastrointestinal tract but most commonly
seen in the colon along margins of taeniae;
• with diverticulitis, the walls of the diverticula become firm and
thickened and may cause narrowing of the wall of the colon

• Diverticula in the digestive system, such as diverticulosis in the colon, typically develop due to increased pressure within the intestinal walls, leading to the formation of small pouches or outpouchings. This increased pressure can be caused by factors like constipation, straining during bowel movements, a low-fiber diet, or age-related changes in the intestinal wall strength. Over time, these pouches can become inflamed or infected, leading to diverticulitis. Treatment often involves dietary changes, medications, and in severe cases, surgery.

Question 63

Solitary diverticulum on antimesenteric side of terminal ileum

Answer 63

Meckel diverticulum

Meckel’s diverticulum is a congenital anomaly of the gastrointestinal tract that occurs due to incomplete closure of the vitelline duct during embryonic development. Here’s the pathomechanism:

1. Embryonic Development: During embryonic development, the vitelline duct connects the yolk sac to the midgut. Normally, this duct narrows and eventually obliterates by the seventh week of gestation. However, if the closure process is incomplete, a remnant of the duct persists, forming Meckel’s diverticulum.
2. Persistence of Vitelline Duct: In cases where the vitelline duct fails to completely close, a pouch-like protrusion develops from the wall of the small intestine. This pouch, known as Meckel’s diverticulum, typically occurs near the ileocecal valve, although it can occasionally be found elsewhere along the small intestine.
3. Structural Features: Meckel’s diverticulum often contains tissue types normally found in the stomach or pancreas, such as gastric mucosa or pancreatic tissue. This heterotopic tissue can lead to complications such as ulceration, bleeding, or obstruction.
4. Complications: Meckel’s diverticulum is usually asymptomatic, but it can lead to complications such as gastrointestinal bleeding, inflammation (diverticulitis), intestinal obstruction, or the formation of a fistula connecting the diverticulum to adjacent structures.

Overall, Meckel’s diverticulum arises from a developmental anomaly during embryogenesis, where the persistence of the vitelline duct leads to the formation of a pouch-like protrusion from the small intestine. While most cases remain asymptomatic, complications can arise, requiring medical intervention.

Question 64

Answer 64

Focal mucosal hyperemia; enlargement of lymphoid tissues; ulcerations;
hemorrhagic or friable mucosal exudates; pseudomembranes; serosal
surfaces unaffected or covered with serous, fibrinous, or hemorrhagic
exudates
• enterocolitis (however, appearance varies depending on
pathogens)

Enterocolitis refers to inflammation of the small intestine (enteritis) and colon (colitis). The pathophysiology of enterocolitis can vary depending on the underlying cause, but here are some common mechanisms:

1. Infection: Enterocolitis is often caused by bacterial, viral, or parasitic infections. Pathogens such as Escherichia coli, Salmonella, Shigella, Campylobacter, Clostridium difficile, norovirus, and rotavirus can invade the gastrointestinal tract, leading to inflammation. Infection can disrupt the normal balance of gut microbiota, damage the intestinal epithelium, and trigger an inflammatory response.
2. Toxins: Certain bacterial toxins, such as those produced by Clostridium difficile, can directly damage the intestinal mucosa and cause inflammation. These toxins can disrupt epithelial cell function, compromise barrier integrity, and lead to the release of pro-inflammatory mediators.
3. Immune Response: In response to infection or toxin exposure, the immune system mounts an inflammatory response to eliminate the invading pathogens. Immune cells such as macrophages, neutrophils, and lymphocytes release pro-inflammatory cytokines, chemokines, and other mediators, contributing to tissue damage and inflammation.
4. Disruption of Barrier Function: Inflammation and infection can compromise the integrity of the intestinal barrier, allowing pathogens, toxins, and inflammatory molecules to penetrate the mucosal layer and enter the bloodstream. This can lead to systemic effects such as sepsis or septic shock.
5. Altered Motility: Inflammation of the gastrointestinal tract can disrupt normal motility patterns, leading to symptoms such as diarrhea, abdominal cramping, and bloating. Increased intestinal motility may contribute to the spread of pathogens and exacerbate inflammation.
6. Risk Factors: Certain factors, such as antibiotic use, immunosuppression, underlying gastrointestinal disorders (e.g., inflammatory bowel disease), and recent hospitalization, can increase the risk of enterocolitis by disrupting the normal balance of gut microbiota or compromising the host immune response.

Overall, enterocolitis is a complex condition involving interactions between infectious agents, host immune responses, and alterations in intestinal barrier function and motility. Treatment typically focuses on addressing the underlying cause, controlling inflammation, restoring fluid and electrolyte balance, and supporting gastrointestinal healing.

Question 65

Answer 65

Dusky purple-red discoloration of serosal and subserosal tissues; thickened,
rubbery bowel wall; lumen containing sanguineous mucus or frank blood:
• transmural infarct
• if due to arterial occlusions, there is usually a sharp demarcation
from normal
• in venous occlusions, no clear demarcation from adjacent normal
tissue is seen

“Frank blood” refers to blood that is clearly visible to the naked eye, often appearing bright red in color. This term is commonly used in medical contexts, particularly when describing symptoms such as rectal bleeding or hemoptysis (coughing up blood). It indicates that the bleeding is substantial and not occult (hidden). Frank blood can result from various conditions, including gastrointestinal bleeding, trauma, respiratory conditions, or other underlying medical issues. Prompt medical evaluation is typically warranted when frank blood is observed, as it may indicate a serious underlying problem.

Question 66

Mucosal infarct

Answer 66

Dark red or red-purple mucosa, multifocal or continuous with unaffected
serosa:

Question 67

Answer 67

Hyperemia and focal ulceration (early lesion), coalescence of ulcers into
serpentine linear ulcers and fissures along bowel axis, narrowing of the
lumen, thickening of the wall, coarsely textured (“cobblestone”) mucosa with
fissures and intervening normal mucosa (chronic lesions):
• Crohn disease

Crohn’s disease is a chronic inflammatory condition that primarily affects the gastrointestinal tract, although it can involve any part of the digestive system from the mouth to the anus. Here’s an overview of its key aspects:

1. Inflammation: Crohn’s disease is characterized by inflammation of the digestive tract, which can extend through multiple layers of the intestinal wall. This inflammation is typically patchy, with areas of healthy tissue interspersed between affected regions.
2. Symptoms: Common symptoms of Crohn’s disease include abdominal pain, diarrhea (which may be bloody), weight loss, fatigue, fever, and in some cases, complications such as strictures, fistulas, or abscesses. The severity and frequency of symptoms can vary widely among individuals.
3. Etiology: The exact cause of Crohn’s disease is not fully understood, but it is believed to involve a combination of genetic predisposition, environmental factors, and dysregulation of the immune system. Factors such as genetics, smoking, diet, and alterations in gut microbiota may play a role in disease development and progression.
4. Diagnosis: Diagnosis of Crohn’s disease typically involves a combination of medical history, physical examination, imaging studies (such as CT scans or MRIs), endoscopic procedures (such as colonoscopy or upper endoscopy), and laboratory tests (including blood tests and stool studies).
5. Treatment: Treatment for Crohn’s disease aims to reduce inflammation, control symptoms, and prevent complications. This may involve medications such as corticosteroids, immunomodulators, biologic therapies, and/or antibiotics. In some cases, surgery may be necessary to remove damaged portions of the intestine or manage complications.
6. Lifestyle Management: Lifestyle modifications, such as dietary changes, stress management, regular exercise, and smoking cessation, may help manage symptoms and improve overall quality of life for individuals with Crohn’s disease.
7. Chronic Condition: Crohn’s disease is a chronic condition, meaning it requires long-term management and monitoring. While there is no cure, treatment can often effectively control symptoms and reduce inflammation, allowing individuals to lead active and productive lives with proper medical care.

Overall, Crohn’s disease is a complex and challenging condition that requires a multidisciplinary approach involving gastroenterologists, primary care physicians, nutritionists, and other healthcare providers to optimize management and improve outcomes for affected individuals.

Question 68

Answer 68

Broad-based ulceration beginning in rectum and extending proximally;
pseudopolyps created by regenerating mucosa adjacent to areas of
ulceration:
• ulcerative colitis

Ulcerative colitis is a chronic inflammatory bowel disease characterized by inflammation and ulceration of the inner lining of the colon and rectum. Here’s an overview of its pathophysiological mechanisms:

1. Immune Dysregulation: Ulcerative colitis is believed to result from an abnormal immune response in genetically predisposed individuals. The exact trigger is not fully understood, but it is thought to involve a combination of genetic factors, environmental influences, and alterations in the gut microbiota. Dysregulation of immune cells, such as T lymphocytes, dendritic cells, and cytokines, leads to chronic inflammation in the intestinal mucosa.
2. Epithelial Barrier Dysfunction: Dysfunction of the intestinal epithelial barrier plays a crucial role in the pathogenesis of ulcerative colitis. Inflammation disrupts the integrity of the epithelial barrier, allowing luminal antigens, bacteria, and toxins to penetrate the mucosal layer and interact with immune cells in the lamina propria. This triggers an exaggerated immune response, perpetuating inflammation and tissue damage.
3. Microbiota Dysbiosis: Alterations in the composition and function of the gut microbiota are observed in individuals with ulcerative colitis. Dysbiosis, characterized by changes in the relative abundance of certain bacterial species and a decrease in microbial diversity, may contribute to inflammation and disease progression. The interaction between the host immune system and the gut microbiota is complex and can influence the development and course of ulcerative colitis.
4. Inflammatory Mediators: Various inflammatory mediators, including cytokines (such as tumor necrosis factor-alpha, interleukin-1, interleukin-6), chemokines, and adhesion molecules, are involved in the pathophysiology of ulcerative colitis. These molecules promote recruitment and activation of immune cells, vasodilation, increased vascular permeability, and tissue damage, contributing to the characteristic features of inflammation and ulceration seen in the colon and rectum.
5. Vascular and Tissue Changes: Chronic inflammation in ulcerative colitis can lead to vascular changes, such as vasodilation, increased blood flow, and angiogenesis. These changes contribute to tissue edema, ulcer formation, and mucosal injury. Over time, repeated cycles of inflammation and healing may result in structural changes, such as crypt distortion, glandular atrophy, and fibrosis.
6. Clinical Manifestations: The hallmark symptoms of ulcerative colitis include bloody diarrhea, abdominal pain, urgency, tenesmus (the sensation of needing to pass stools even when the bowel is empty), and fecal incontinence. Disease severity can vary widely among individuals, ranging from mild to severe, and may fluctuate over time.

Overall, ulcerative colitis is a complex disorder with multifactorial etiology and pathophysiology. Understanding the underlying mechanisms of inflammation and tissue injury is crucial for developing targeted therapeutic strategies to manage the disease and improve outcomes for affected individuals.

Question 69

Smooth, round, <5-mm sessile lesions on mucosal folds

Answer 69

hyperplastic polyps

Question 70

Answer 70

Irregular pedunculated lesion with slender stalk; occasionally sessile, ovoid, Tubular adenomas are benign tumors that typically develop in the colon. Their pathophysiological mechanism involves abnormal growth of glandular tissue within the mucosal layer of the colon, often as a result of genetic mutations. These mutations can lead to uncontrolled cell proliferation and the formation of the adenomatous polyps. However, the exact pathophysiological mechanisms underlying their development are not fully understood.
or flat:
• tubular adenoma

Question 71

Answer 71

Generally sessile polypoid lesion up to 10cm in diameter:
• villous adenoma

Villous adenomas, like tubular adenomas, are benign tumors that typically occur in the colon. Their pathophysiological mechanism involves the overgrowth of glandular tissue with a characteristic villous architecture. This overgrowth is often driven by genetic mutations, leading to uncontrolled cell proliferation and the formation of the adenomatous polyps. Villous adenomas are distinguished by their finger-like projections, which increase the surface area for absorption and secretion. However, similar to tubular adenomas, the precise pathophysiological mechanisms underlying their development are not fully understood.

Question 72

Answer 72

• Polypoid exophytic mass (generally in proximal and transverse colon)
  adenocarcinoma
• Annular, encircling mass narrowing lumen (generally of distal colon):
  • adenocarcinoma

The pathophysiological mechanism of adenocarcinoma, which is the most common type of colon cancer, involves the transformation of normal glandular cells in the colon into cancerous cells. This transformation typically occurs over a period of time and is influenced by various factors, including genetic mutations, environmental exposures, and lifestyle choices.

Several key steps are involved in the development of adenocarcinoma:

1. Initiation: Genetic mutations or alterations occur in the DNA of normal colon cells, often due to factors such as exposure to carcinogens (e.g., tobacco smoke, certain chemicals) or inherited genetic predispositions.
2. Promotion: The mutated cells undergo further changes, leading to uncontrolled growth and division. This stage may involve the activation of oncogenes (genes that promote cell growth) or the inactivation of tumor suppressor genes (genes that normally inhibit cell growth).
3. Progression: As the abnormal cells continue to divide and accumulate, they may develop additional genetic alterations that confer characteristics of malignancy, such as the ability to invade surrounding tissues and metastasize to distant sites.
4. Angiogenesis: As the tumor grows, it requires a blood supply to sustain its growth. Angiogenesis, the formation of new blood vessels, is stimulated by tumor cells to ensure an adequate oxygen and nutrient supply.
5. Invasion and metastasis: Cancer cells acquire the ability to invade through the walls of the colon and spread to nearby lymph nodes and other organs, such as the liver and lungs, through the bloodstream or lymphatic system. This process enables the cancer to establish secondary tumors at distant sites.

Overall, the pathophysiological mechanism of adenocarcinoma( involves a complex interplay of genetic, molecular, and environmental factors that drive the transformation of normal colon cells into malignant tumors.

Question 73

Answer 73

Intramural or submucosal polypoid or elevated yellow-tan masses or bulbous
swellings of the tip of appendix:
• carcinoid (neuroendocrine) tumor

The pathomechanism of carcinoid neuroendocrine tumors (NETs) of the colon involves the abnormal growth of neuroendocrine cells in the lining of the colon. These cells are responsible for producing various hormones and neurotransmitters.

The exact cause of carcinoid tumors is not always clear, but they can arise from precursor lesions known as neuroendocrine cell hyperplasia. These lesions may progress to form carcinoid tumors due to genetic mutations and other factors.

Carcinoid tumors of the colon can produce hormones such as serotonin, histamine, and others, which can lead to symptoms such as flushing, diarrhea, and abdominal pain. Additionally, these tumors can metastasize to other parts of the body, particularly the liver, which can further complicate the condition.

Overall, the pathomechanism involves the dysregulation of neuroendocrine cell growth and hormone production, but the exact triggers and mechanisms can vary among individuals.

Question 74

Liver normal

Answer 74

The liver is located at a normal anatomical position.

It has regular shape and usual size with 1500 g weight.

The Glisson capsule of the liver is smooth, On cut surfaces, the
consistency is moderately firm with grossly intact lobular architecture and normal portal
structure having an overall reddish-brown color for the lobules.

Question 75

Answer 75

Liver capsule subcapsular hematoma

The pathophysiological mechanism of a subcapsular hematoma involves the accumulation of blood between the capsule of an organ and its parenchyma (functional tissue). This condition often occurs due to trauma or injury to the organ, leading to rupture of small blood vessels within the parenchyma.

Here’s how it typically happens:

1. Trauma or Injury: The organ experiences trauma or injury, such as a direct blow or a penetrating injury. This trauma can disrupt blood vessels within the parenchyma, leading to bleeding.
2. Bleeding: As a result of the trauma, blood vessels within the parenchyma rupture, causing blood to leak out into the surrounding tissue.
3. Subcapsular Accumulation: The blood collects between the capsule (the outer covering) of the organ and the parenchyma, forming a hematoma. In the case of a subcapsular hematoma, the hematoma is located just beneath the organ’s capsule.
4. Compression: As the hematoma enlarges, it may exert pressure on the surrounding tissue and structures, leading to symptoms such as pain, swelling, and potentially compromising the function of the affected organ.

Subcapsular hematomas can occur in various organs, including the liver, spleen, and kidneys, among others. The severity of the hematoma depends on factors such as the extent of the injury, the size of the hematoma, and whether there are associated complications such as ongoing bleeding or organ dysfunction. Immediate medical attention is often required to assess and manage subcapsular hematomas, particularly if they are large or causing significant symptoms.

Question 76

Answer 76

Liver capsule lacerations

The pathophysiological mechanism of liver lacerations involves the tearing or cutting of liver tissue, often due to trauma or injury. This can occur in various situations, such as blunt force trauma (e.g., motor vehicle accidents, falls), penetrating injuries (e.g., gunshot wounds, stab wounds), or medical procedures (e.g., surgery).

Here’s how liver lacerations typically occur:

1. Trauma or Injury: The liver is a highly vascular organ located in the upper right abdomen, making it susceptible to injury during accidents or trauma. Blunt force trauma, such as a direct blow to the abdomen, can cause the liver to collide with the rib cage, leading to lacerations. Penetrating injuries, such as gunshot or stab wounds, can directly damage liver tissue.
2. Tearing or Cutting: The force of the trauma or injury causes the liver tissue to tear or be cut. This can result in varying degrees of damage, ranging from small superficial lacerations to deep, extensive lacerations that involve significant bleeding.
3. Hemorrhage: Lacerations of the liver often result in bleeding due to the rich blood supply of the organ. The severity of bleeding depends on the size and depth of the laceration, as well as the integrity of nearby blood vessels. Significant hemorrhage can lead to hypovolemic shock if not promptly controlled.
4. Inflammatory Response: Following the injury, the body initiates an inflammatory response to repair the damaged tissue. Inflammatory cells, such as neutrophils and macrophages, migrate to the site of injury to remove debris and promote tissue healing.
5. Healing and Repair: Liver tissue has a remarkable ability to regenerate, allowing for the repair of minor lacerations. However, severe or extensive lacerations may require medical intervention, such as surgical repair or supportive measures to control bleeding and prevent complications.

Overall, the pathophysiological mechanism of liver lacerations involves the disruption of liver tissue integrity due to trauma or injury, leading to bleeding and subsequent repair processes initiated by the body. Prompt assessment and management are essential to prevent complications and optimize outcomes in individuals with liver lacerations.

Question 77

Liver capsule possible alternations

Answer 77

• subcapsular hematomas
  • lacerations
  • calcified thrombi

The formation of calcified thrombi on the liver capsule typically occurs in the context of chronic liver disease, particularly in conditions associated with portal hypertension, such as cirrhosis. The pathophysiological mechanism involves several interconnected factors:

1. Portal Hypertension: Chronic liver disease can lead to portal hypertension, which is characterized by increased pressure within the portal venous system. This elevated pressure results from impaired blood flow through the liver due to fibrosis, nodular regeneration, and vascular remodeling associated with conditions like cirrhosis.
2. Portosystemic Collaterals: Portal hypertension leads to the development of portosystemic collaterals—abnormal blood vessels that bypass the liver and connect the portal venous system with systemic veins. These collaterals form as the body attempts to divert blood away from the congested portal circulation.
3. Venous Congestion and Thrombosis: The increased pressure within the portal venous system and the development of portosystemic collaterals contribute to venous congestion within the liver and surrounding structures. This venous congestion predisposes to the formation of thrombi (blood clots) within the hepatic veins, portal veins, and sinusoids.
4. Thrombus Organization and Calcification: Over time, thrombi within the liver and its surrounding structures can undergo organization, during which the clot is gradually replaced by fibrous tissue. In some cases, calcium salts may be deposited within the organized thrombi, leading to calcification. This process is often seen in chronic liver diseases with longstanding portal hypertension.
5. Capsular Involvement: The liver capsule, a fibrous layer that envelops the liver, may become involved in the process of thrombus organization and calcification. Calcified thrombi may adhere to the surface of the liver capsule, leading to the formation of calcified plaques or nodules on its surface.

Overall, the pathophysiological mechanism of calcified thrombi on the liver capsule is closely linked to the development of portal hypertension and its consequences in chronic liver disease. These calcifications serve as radiological markers of longstanding liver pathology and are often observed in conditions such as cirrhosis.

Question 78

Answer 78

Nodularity of capsular surface:
• cirrhosis

Liver cirrhosis is a chronic and progressive condition characterized by the replacement of healthy liver tissue with scar tissue (fibrosis), leading to disruption of liver structure and function. The pathophysiological mechanism of liver cirrhosis involves a complex interplay of various factors, including inflammation, fibrogenesis, and regeneration:

1. Liver Injury and Inflammation: Liver cirrhosis often begins with chronic liver injury, which can result from factors such as chronic viral hepatitis (e.g., hepatitis B or C), alcohol abuse, non-alcoholic fatty liver disease (NAFLD), autoimmune hepatitis, or other causes. Persistent liver injury triggers an inflammatory response, leading to the activation of immune cells (e.g., Kupffer cells, macrophages) and the release of pro-inflammatory cytokines.
2. Fibrogenesis: In response to ongoing liver injury and inflammation, hepatic stellate cells, which are normally quiescent and involved in storing vitamin A, become activated. Activated hepatic stellate cells transform into myofibroblasts, which are responsible for excessive production and deposition of extracellular matrix components, primarily collagen. This process leads to the accumulation of scar tissue (fibrosis) within the liver parenchyma, disrupting the normal architecture and function of the liver.
3. Regenerative Response: As liver injury progresses, there is an attempt by the liver to regenerate and repair damaged tissue. Hepatocytes, the primary functional cells of the liver, undergo proliferation in an effort to replace injured cells. However, this regenerative process is often dysregulated in cirrhosis, leading to the formation of nodules of regenerating hepatocytes surrounded by fibrous septa, a characteristic feature of cirrhotic liver tissue.
4. Vascular Changes: Cirrhosis is associated with significant vascular changes within the liver, including increased resistance to blood flow through the hepatic sinusoids and development of portosystemic shunts (collaterals) due to portal hypertension. These vascular alterations contribute to complications such as ascites, varices, and hepatic encephalopathy.
5. Hepatic Decompensation: As cirrhosis progresses, the liver becomes increasingly dysfunctional, leading to the development of complications such as portal hypertension, hepatic encephalopathy, ascites, jaundice, and coagulopathy. These complications can ultimately result in liver failure and death if left untreated.

Overall, the pathophysiological mechanism of liver cirrhosis involves a cascade of events initiated by chronic liver injury and inflammation, leading to fibrogenesis, impaired regeneration, vascular changes, and ultimately, hepatic decompensation. Understanding these mechanisms is crucial for developing strategies to prevent and manage liver cirrhosis and its complications.

Question 79

Firmer than usual parenchyma but without nodularity liver

Answer 79

Liver fibrosis

Liver fibrosis is the excessive accumulation of scar tissue (extracellular matrix) in the liver in response to chronic injury or inflammation. The pathophysiological mechanism of liver fibrosis involves a complex series of events:

1. Liver Injury: Liver fibrosis typically begins with chronic liver injury caused by various factors such as viral hepatitis (e.g., hepatitis B or C), alcohol abuse, non-alcoholic fatty liver disease (NAFLD), autoimmune hepatitis, or other insults. Persistent injury to hepatocytes (liver cells) triggers an inflammatory response.
2. Inflammation and Activation of Hepatic Stellate Cells: In response to liver injury and inflammation, hepatic stellate cells, which are normally quiescent and involved in storing vitamin A, become activated. Various mediators, including cytokines, chemokines, and growth factors released during inflammation, stimulate the activation of hepatic stellate cells.
3. Transformation into Myofibroblasts: Activated hepatic stellate cells undergo a phenotypic transformation into myofibroblasts, which are the primary cells responsible for producing and depositing extracellular matrix components, such as collagen, in the liver parenchyma.
4. Excessive Extracellular Matrix Deposition: Activated myofibroblasts produce and secrete large amounts of extracellular matrix proteins, primarily collagen, leading to the accumulation of scar tissue within the liver. This excessive deposition of collagen disrupts the normal liver architecture and impairs liver function.
5. Remodeling of Liver Tissue: As fibrosis progresses, the liver tissue undergoes remodeling, with the formation of fibrous septa that separate regenerative nodules of hepatocytes. This architectural distortion further impairs liver function and can ultimately lead to cirrhosis if left untreated.
6. Hepatic Decompensation: Advanced fibrosis can result in hepatic decompensation, characterized by the development of complications such as portal hypertension, ascites, varices, hepatic encephalopathy, and liver failure.

Overall, the pathophysiological mechanism of liver fibrosis involves a dynamic process of chronic liver injury, inflammation, activation of hepatic stellate cells, excessive extracellular matrix deposition, tissue remodeling, and ultimately, liver dysfunction. Understanding these mechanisms is essential for the development of therapies aimed at preventing or reversing liver fibrosis and its progression to cirrhosis.

Liver damage can progress through several stages, ranging from mild inflammation and scarring to severe fibrosis and cirrhosis. Here are the typical stages of liver damage:

1. Inflammation: The initial stage of liver damage often involves inflammation, characterized by the presence of immune cells within the liver tissue. This inflammation can result from various causes, such as viral infections (e.g., hepatitis B or C), alcohol abuse, fatty liver disease, autoimmune conditions, or exposure to toxins.
2. Fatty Liver (Steatosis): In some cases, liver damage may progress to the accumulation of fat within liver cells, a condition known as fatty liver or steatosis. This can occur due to factors such as obesity, insulin resistance, excessive alcohol consumption, or certain medications.
3. Fibrosis: Prolonged inflammation and injury to the liver can lead to the accumulation of scar tissue (fibrosis) within the liver parenchyma. Fibrosis represents the body’s attempt to repair damaged tissue but, if left unchecked, can progress to more severe stages of liver damage.
4. Cirrhosis: Cirrhosis is the advanced stage of liver damage characterized by extensive fibrosis and distortion of liver architecture. In cirrhosis, the liver tissue becomes nodular and lumpy due to the formation of regenerative nodules surrounded by fibrous septa. Cirrhosis is irreversible and can lead to significant impairment of liver function.
5. Complications of Cirrhosis: As cirrhosis progresses, it can lead to various complications, including portal hypertension, ascites (accumulation of fluid in the abdominal cavity), hepatic encephalopathy (brain dysfunction due to liver failure), varices (enlarged and swollen veins in the esophagus and stomach), coagulopathy (impaired blood clotting), jaundice (yellowing of the skin and eyes), and hepatocellular carcinoma (a type of liver cancer).

It’s important to note that liver damage can progress at different rates depending on factors such as the underlying cause, individual genetics, lifestyle factors, and the presence of comorbidities. Early detection and intervention are crucial for preventing or slowing the progression of liver damage and its associated complications. Regular monitoring, lifestyle modifications (such as maintaining a healthy weight, limiting alcohol consumption, and avoiding liver-toxic medications), and appropriate medical treatment can help manage liver disease and improve outcomes.

Question 80

Answer 80

• Yellow-tan, greasy parenchyma:
• fatty change

The pathophysiological mechanism of fatty liver, also known as hepatic steatosis or fatty liver disease, involves the abnormal accumulation of fat within liver cells (hepatocytes). While small amounts of fat in the liver are normal, excessive accumulation can lead to liver dysfunction and damage. Here’s how it typically occurs:

1. Increased Hepatic Lipid Uptake: Fatty liver often begins with an imbalance between the uptake and metabolism of lipids (fats) in the liver. This can be triggered by various factors such as insulin resistance, obesity, metabolic syndrome, excessive dietary intake of fats or carbohydrates, alcohol consumption, or certain medications.
2. Increased Lipid Synthesis: Under conditions of excess calorie intake or impaired metabolism, the liver may increase the synthesis of fatty acids from dietary carbohydrates (de novo lipogenesis) or through the uptake of circulating free fatty acids. This leads to an accumulation of triglycerides within hepatocytes.
3. Decreased Lipid Export: In addition to increased lipid synthesis, fatty liver can also result from impaired export of lipids from the liver. This can occur due to dysfunction of lipid export pathways, such as very-low-density lipoprotein (VLDL) secretion, or alterations in adipose tissue metabolism.
4. Oxidative Stress and Lipid Peroxidation: Excessive accumulation of triglycerides within hepatocytes can lead to oxidative stress, characterized by an imbalance between the production of reactive oxygen species (ROS) and antioxidant defenses. Oxidative stress can cause damage to cellular structures and promote lipid peroxidation, further exacerbating liver injury.
5. Inflammation and Hepatocyte Injury: The presence of excessive fat within hepatocytes can trigger an inflammatory response, characterized by the activation of immune cells and the release of pro-inflammatory cytokines. This inflammation can lead to hepatocyte injury and apoptosis (cell death), contributing to liver damage and fibrosis.
6. Progression to Steatohepatitis and Fibrosis: In some individuals, fatty liver can progress to non-alcoholic steatohepatitis (NASH), a more severe form of liver disease characterized by inflammation and liver cell injury. Over time, ongoing inflammation and injury can lead to the development of liver fibrosis, cirrhosis, and ultimately, liver failure.

The pathophysiological mechanism of fatty liver is complex and multifactorial, involving interactions between genetic, metabolic, environmental, and lifestyle factors. Early detection and intervention are crucial for preventing the progression of fatty liver disease to more severe liver complications. Lifestyle modifications such as weight loss, dietary changes, regular exercise, and avoidance of alcohol can help improve liver health and prevent further liver damage.

Question 81

Answer 81

Yellow-tan parenchyma when fresh, green after fixation:
• cholestasis

Cholestasis is a condition characterized by impaired bile flow from the liver to the duodenum, leading to the accumulation of bile within the liver and bloodstream. The pathophysiological mechanism of cholestasis involves various factors that disrupt normal bile formation, secretion, and flow. Here’s how it typically occurs:

1. Hepatocellular Cholestasis: Cholestasis can occur at the level of hepatocytes (liver cells), where bile is synthesized and secreted. Hepatocellular cholestasis can result from conditions such as hepatitis, drug-induced liver injury, genetic disorders (e.g., progressive familial intrahepatic cholestasis), or hepatocellular carcinoma. In these conditions, hepatocyte dysfunction impairs the synthesis, transport, or secretion of bile components.
2. Canalicular Cholestasis: Bile synthesized by hepatocytes is transported to the bile canaliculi, small ductules located between adjacent hepatocytes, where it is collected and ultimately flows into the bile ducts. Canalicular cholestasis occurs when there is impairment of bile secretion into the canaliculi. This can result from genetic mutations affecting canalicular transporters (e.g., bile salt export pump, multidrug resistance-associated protein 2) or acquired conditions such as drug-induced cholestasis.
3. Intrahepatic Bile Duct Cholestasis: Bile flows from the bile canaliculi into the intrahepatic bile ducts, where it is further modified and transported towards the larger bile ducts. Intrahepatic bile duct cholestasis can occur due to obstruction or inflammation of the intrahepatic bile ducts, as seen in conditions such as primary sclerosing cholangitis, primary biliary cholangitis, or biliary strictures.
4. Extrahepatic Bile Duct Cholestasis: Bile exits the liver through the extrahepatic bile ducts, which merge to form the common bile duct. Extrahepatic bile duct cholestasis can result from obstruction of the bile ducts by gallstones, tumors (e.g., pancreatic cancer, bile duct cancer), inflammation (e.g., cholangitis), or compression from adjacent structures.
5. Bile Accumulation and Retention: Regardless of the site of cholestasis, the common feature is the accumulation of bile within the liver parenchyma and bloodstream. This can lead to the retention of bile constituents, including bile acids, bilirubin, cholesterol, and phospholipids, which can have toxic effects on hepatocytes and other tissues.
6. Clinical Manifestations: Cholestasis can manifest clinically as jaundice (yellowing of the skin and eyes), pruritus (itching), pale stools, dark urine, and hepatomegaly (enlarged liver). Complications of cholestasis may include liver injury, fibrosis, cirrhosis, and impaired fat-soluble vitamin absorption.

Overall, the pathophysiological mechanism of cholestasis involves disruptions in bile formation, secretion, and flow at various levels within the liver and biliary tract, leading to bile accumulation and associated clinical manifestations. Treatment aims to address the underlying cause of cholestasis and alleviate symptoms to prevent further liver damage.

Question 82

Firm nodules 3cm or less in diameter

Answer 82

• micronodular cirrhosis due to alcoholic liver disease
• primary and secondary biliary cirrhosis
• glycogenosis type IV
• Indian childhood cirrhosis
• galactosemia and congestive (cardiac) cirrhosis

Question 83

Firm nodules greater than 3cm in diameter:

Answer 83

• macronodular cirrhosis due to alcoholic liver disease
• viral hepatitis
• drug-induced injury
• hepatotoxins
• various hereditary diseases including
• Wilson disease
• hereditary tyrosinemia
• α1-antitrypsin deficiency

Question 84

Firm nodules showing approximately equal numbers of micronodules and macronodules

Answer 84

mixed micronodular and macronodular cirrhosis caused by
• alcoholic cirrhosis and diseases causing macronodular cirrhosis
listed previously

Question 85

Answer 85

Multiple diffuse cysts:
• polycystic liver disease

Polycystic liver disease (PLD) is a genetic disorder characterized by the presence of multiple cysts in the liver. The pathophysiological mechanism of PLD involves mutations in genes associated with the development and regulation of cell proliferation, differentiation, and fluid secretion. Here’s how it typically occurs:

1. Genetic Mutation: PLD can be inherited in an autosomal dominant manner, meaning that a mutation in a single copy of the responsible gene is sufficient to cause the disease. Mutations in several genes have been associated with PLD, including PRKCSH, SEC63, GANAB, and PRKACA, among others. These genes encode proteins involved in various cellular processes, such as cell signaling, protein folding, and vesicular trafficking.
2. Dysregulated Cell Proliferation: Mutations in genes associated with PLD can lead to dysregulated cell proliferation within the liver, resulting in the formation of numerous cysts. The exact mechanisms underlying cyst formation are not fully understood but may involve aberrant activation of signaling pathways that promote cell growth and division.
3. Fluid Secretion and Cyst Expansion: Cysts in PLD are lined by epithelial cells that actively secrete fluid into the cyst cavity. The secretion of fluid is thought to be driven by ion transport mechanisms, including chloride secretion and water movement. As fluid accumulates within the cysts, they gradually expand in size, leading to enlargement of the liver.
4. Compression of Surrounding Tissue: As cysts enlarge, they can exert pressure on surrounding liver tissue and structures, leading to displacement of normal liver parenchyma and compression of adjacent blood vessels, bile ducts, and hepatic parenchyma. This can result in symptoms such as abdominal pain, early satiety, nausea, and complications such as portal hypertension or bile duct obstruction.
5. Hepatic Fibrosis: In some cases, PLD may be associated with hepatic fibrosis, particularly in individuals with more severe disease or concurrent polycystic kidney disease (PKD). Hepatic fibrosis involves the accumulation of scar tissue within the liver, which can further impair liver function and contribute to complications such as portal hypertension or liver failure.

Overall, the pathophysiological mechanism of PLD involves genetic mutations that lead to dysregulated cell proliferation and fluid secretion within the liver, resulting in the formation and expansion of cysts. While PLD is generally considered a benign condition, it can cause significant morbidity and may require treatment to alleviate symptoms and prevent complications.

Question 86

Answer 86

Swollen, red-purple liver with tense capsule:
• hepatic vein (Budd-Chiari syndrome)
• inferior vena caval thrombosis/obstruction

Budd-Chiari syndrome is a rare condition characterized by the obstruction or narrowing of the hepatic veins, which are the blood vessels that carry blood away from the liver and back to the heart. The pathophysiological mechanism of Budd-Chiari syndrome involves various factors that can lead to the obstruction of hepatic venous outflow. Here’s how it typically occurs:

1. Hepatic Vein Obstruction: The obstruction of hepatic venous outflow can occur at various levels within the hepatic veins or the inferior vena cava (IVC), the large vein that carries blood from the lower body to the heart. The obstruction may be partial or complete and can result from several underlying causes.
2. Thrombosis: One of the most common causes of Budd-Chiari syndrome is the formation of blood clots (thrombosis) within the hepatic veins or the IVC. These clots can arise spontaneously or be triggered by conditions such as hypercoagulable disorders, polycythemia vera, paroxysmal nocturnal hemoglobinuria (PNH), or myeloproliferative neoplasms.
3. Compression: Hepatic vein obstruction can also occur due to external compression of the veins by adjacent structures, such as tumors, cysts, or vascular abnormalities. In rare cases, Budd-Chiari syndrome may be caused by extrinsic compression of the hepatic veins by hypertrophic cardiomyopathy or a dilated right atrium.
4. Congenital Anomalies: Budd-Chiari syndrome can also result from congenital anomalies of the hepatic veins or the IVC, such as membranous webs, venous stenosis, or agenesis of the hepatic segment of the IVC. These structural abnormalities can predispose to venous obstruction and impaired hepatic venous outflow.
5. Hepatic Congestion and Liver Dysfunction: The obstruction of hepatic venous outflow leads to hepatic congestion, causing an increase in sinusoidal pressure within the liver. This can result in hepatomegaly (enlarged liver), hepatic necrosis, fibrosis, and eventually, cirrhosis. The impaired venous drainage also leads to portal hypertension, which can cause complications such as ascites, varices, and hepatic encephalopathy.
6. Clinical Manifestations: Patients with Budd-Chiari syndrome may present with symptoms such as abdominal pain, hepatomegaly, ascites, jaundice, and signs of portal hypertension. The clinical presentation can vary depending on the extent and severity of venous obstruction, the rapidity of onset, and the presence of underlying conditions.

Overall, the pathophysiological mechanism of Budd-Chiari syndrome involves the obstruction or narrowing of hepatic venous outflow, leading to hepatic congestion, liver dysfunction, and complications related to portal hypertension. Treatment typically involves addressing the underlying cause of venous obstruction and may include anticoagulation, thrombolysis, angioplasty, or surgical interventions such as shunting procedures or liver transplantation.

Question 87

Answer 87

Well-demarcated, poorly encapsulated nodules, yellow or slightly lighter than
adjacent parenchyma, often with central, gray, stellate scar:
• focal nodular hyperplasia

The pathophysiological mechanism of focal nodular hyperplasia (FNH) involves abnormal growth and organization of hepatocytes (liver cells) within the liver parenchyma, leading to the formation of characteristic nodules. While the exact cause of FNH is not fully understood, several factors have been implicated in its development:

1. Vascular Anomalies: FNH often occurs in association with vascular abnormalities within the liver, such as arterial malformations or abnormal blood vessel patterns. These vascular anomalies can disrupt normal blood flow within the liver and contribute to the development of FNH nodules.
2. Congenital Factors: There is evidence to suggest that congenital factors may play a role in the pathogenesis of FNH. Some cases of FNH have been reported in infants and children, suggesting that developmental factors may contribute to the formation of FNH lesions.
3. Hormonal Influence: Hormonal factors, particularly estrogen, have been implicated in the development of FNH. FNH is more common in women of childbearing age, and the incidence of FNH tends to increase during pregnancy or with the use of oral contraceptives. Estrogen may stimulate the growth of hepatocytes and promote the development of FNH lesions.
4. Genetic Predisposition: While rare, there may be a genetic predisposition to FNH in some individuals. Familial cases of FNH have been reported, suggesting a potential genetic basis for the development of FNH lesions. However, the specific genes involved in FNH pathogenesis have not been fully elucidated.
5. Regenerative Response: FNH lesions are characterized by the presence of abnormal hepatocyte nodules surrounded by fibrous septa. It is believed that FNH represents a hyperplastic response of hepatocytes to underlying vascular abnormalities or other stimuli. The abnormal hepatocytes proliferate and organize into nodules, often with a central scar or stellate scar.

Overall, the pathophysiological mechanism of FNH involves a complex interplay of vascular abnormalities, hormonal influences, congenital factors, and possibly genetic predisposition. While FNH lesions are typically benign and asymptomatic, they may cause clinical symptoms or complications in some cases. Treatment of FNH is generally not necessary unless complications arise, and surgical resection is usually curative.

Question 88

Diffuse spherical nodules without parenchymal fibrosis

Answer 88

nodular regenerative hyperplasia

Question 89

Answer 89

Pale, yellow-tan or bile-stained nodules, generally subcapsular:
• adenoma

The pathophysiological mechanism of liver adenomas involves the abnormal growth of hepatocytes (liver cells) within the liver parenchyma, leading to the formation of benign tumors. Liver adenomas are typically monoclonal in origin, meaning they arise from a single abnormal cell that undergoes uncontrolled proliferation. While the exact cause of liver adenomas is not fully understood, several factors have been implicated in their development:

1. Hormonal Influence: Hormonal factors, particularly estrogen, play a significant role in the pathogenesis of liver adenomas. Liver adenomas predominantly affect women of childbearing age, and the incidence of adenomas tends to increase during pregnancy or with the use of oral contraceptives. Estrogen may stimulate the growth of hepatocytes and promote the development of adenomatous lesions.
2. Genetic Factors: While most liver adenomas are sporadic, there may be a genetic predisposition to the development of these tumors in some individuals. Mutations in genes involved in cell cycle regulation, tumor suppression, and Wnt/β-catenin signaling pathways have been implicated in the pathogenesis of liver adenomas. For example, mutations in the β-catenin gene (CTNNB1) are commonly found in hepatic adenomas with activation of the Wnt/β-catenin pathway.
3. Metabolic Factors: Metabolic conditions such as obesity, metabolic syndrome, and type 2 diabetes have been associated with an increased risk of liver adenomas. These metabolic conditions are often characterized by insulin resistance and dysregulation of lipid metabolism, which may contribute to the development of adenomatous lesions.
4. Exogenous Factors: Certain exogenous factors, such as exposure to anabolic steroids, androgenic hormones, or environmental toxins, have been implicated in the pathogenesis of liver adenomas. Anabolic steroids, in particular, have been associated with the development of adenomas, likely due to their stimulatory effects on hepatocyte proliferation.
5. Inflammatory Stimuli: Chronic inflammation and liver injury may also play a role in the development of liver adenomas. Inflammatory conditions such as non-alcoholic fatty liver disease (NAFLD), alcoholic liver disease, or chronic viral hepatitis may predispose individuals to the development of adenomatous lesions.

Overall, the pathophysiological mechanism of liver adenomas involves a complex interplay of hormonal, genetic, metabolic, exogenous, and inflammatory factors. While liver adenomas are generally benign, they may grow in size, cause symptoms, or rarely undergo malignant transformation. Treatment options for liver adenomas may include observation, surgical resection, or minimally invasive procedures such as radiofrequency ablation or embolization.

Question 90

Answer 90

Neoplasms paler than adjacent liver to slightly green:
• hepatocellular carcinoma (with fibrous bands: fibrolamellar
hepatocellular carcinoma)

The pathomechanism of hepatocellular carcinoma (HCC), the most common type of primary liver cancer, is multifactorial and involves complex interactions between various genetic, environmental, and viral factors. Here’s an overview of the key mechanisms implicated in the development of HCC:

1. Chronic Liver Disease: The majority of HCC cases develop in the setting of chronic liver disease, particularly liver cirrhosis. Chronic liver diseases such as chronic viral hepatitis (hepatitis B and C), alcoholic liver disease, non-alcoholic fatty liver disease (NAFLD), and autoimmune liver diseases can lead to liver cirrhosis, which significantly increases the risk of HCC development.
2. Hepatocyte Injury and Regeneration: Chronic liver injury and inflammation trigger a cascade of events that promote hepatocyte regeneration. During the process of regeneration, genetic alterations may accumulate in hepatocytes, leading to the dysregulation of cellular processes such as proliferation, apoptosis, and DNA repair, which can predispose to the development of HCC.
3. Viral Hepatitis: Chronic infection with hepatitis B virus (HBV) or hepatitis C virus (HCV) is a major risk factor for HCC. These viruses can directly induce hepatocyte injury and inflammation, promote oxidative stress and DNA damage, and disrupt cellular signaling pathways involved in cell growth and survival. Integration of viral DNA/RNA into the host genome may also contribute to hepatocarcinogenesis by activating oncogenes or inactivating tumor suppressor genes.
4. Hepatocarcinogenesis Pathways: Several molecular pathways have been implicated in the development of HCC, including the Wnt/β-catenin pathway, the PI3K/Akt/mTOR pathway, the Ras/Raf/MEK/ERK pathway, and the p53 pathway. Dysregulation of these pathways can promote uncontrolled cell proliferation, inhibit apoptosis, enhance angiogenesis, and facilitate metastasis, all of which are hallmarks of cancer development.
5. Epigenetic Alterations: Epigenetic modifications such as DNA methylation, histone modifications, and non-coding RNA dysregulation can contribute to HCC pathogenesis by altering gene expression patterns. These alterations can silence tumor suppressor genes or activate oncogenes, promoting tumor initiation and progression.
6. Angiogenesis and Metastasis: As HCC progresses, tumor cells acquire the ability to induce angiogenesis, leading to the formation of new blood vessels that supply nutrients and oxygen to the growing tumor. HCC cells also acquire invasive and metastatic properties, allowing them to spread to adjacent tissues and distant organs, such as the lungs and bones.

Overall, the pathomechanism of HCC is complex and involves a combination of genetic, viral, environmental, and molecular factors that contribute to the initiation, promotion, and progression of liver cancer. Understanding these mechanisms is crucial for the development of effective prevention strategies, early detection methods, and targeted therapies for HCC.

Question 91

Answer 91

Gray-white to pale tan, sometimes gelatinous tumor:
• cholangiocarcinoma

Cholangiocarcinoma (CCA) is a malignancy arising from the epithelial cells lining the bile ducts within the liver (intrahepatic) or outside the liver (extrahepatic). The pathophysiological mechanism of cholangiocarcinoma involves a combination of genetic, environmental, and inflammatory factors. Here’s an overview of the key mechanisms implicated in its development:

1. Chronic Biliary Inflammation: Chronic inflammation of the biliary tract is a major risk factor for the development of cholangiocarcinoma. Conditions associated with chronic biliary inflammation include primary sclerosing cholangitis (PSC), choledochal cysts, biliary stones, recurrent biliary infections, and liver fluke infection (e.g., Opisthorchis viverrini, Clonorchis sinensis). Inflammation can lead to DNA damage, cell proliferation, and alterations in signaling pathways that promote carcinogenesis.
2. Biliary Epithelial Cell Injury and Regeneration: Chronic biliary injury and inflammation can cause repeated cycles of epithelial cell injury and regeneration. During the process of regeneration, genetic alterations may accumulate in biliary epithelial cells, leading to dysregulated cell growth, survival, and differentiation, which can predispose to the development of cholangiocarcinoma.
3. Genetic and Molecular Alterations: Cholangiocarcinoma is characterized by a variety of genetic and molecular alterations that contribute to its pathogenesis. These alterations can affect key signaling pathways involved in cell proliferation, apoptosis, angiogenesis, and metastasis. Common genetic alterations observed in cholangiocarcinoma include mutations in tumor suppressor genes (e.g., TP53, PTEN), oncogenes (e.g., KRAS), and genes involved in chromatin remodeling and DNA repair.
4. Chronic Bile Duct Obstruction: Chronic bile duct obstruction, often due to biliary strictures or bile duct stones, can lead to stasis of bile within the biliary tract. Prolonged bile stasis can promote inflammation, cellular proliferation, and DNA damage in the biliary epithelium, predisposing to the development of cholangiocarcinoma.
5. Biliary Stone Formation: Biliary stones, particularly pigment stones, are associated with an increased risk of cholangiocarcinoma. Chronic inflammation and infection associated with biliary stone disease can contribute to the development of cancerous changes in the biliary epithelium.
6. Liver Fluke Infection: In regions where liver fluke infection is endemic, such as parts of Southeast Asia, chronic infection with liver flukes (e.g., Opisthorchis viverrini, Clonorchis sinensis) is a significant risk factor for cholangiocarcinoma. The parasites can cause chronic inflammation and injury to the biliary epithelium, leading to carcinogenesis over time.

Overall, the pathophysiological mechanism of cholangiocarcinoma is complex and involves a combination of genetic, environmental, and inflammatory factors that contribute to the initiation, promotion, and progression of bile duct cancer. Understanding these mechanisms is crucial for the development of effective prevention, early detection, and treatment strategies for cholangiocarcinoma.

Question 92

Answer 92

Masses with central necrosis and umbilication:
• metastatic neoplasms, generally carcinomas

In the context of liver carcinoma, “umbilication” refers to the appearance of a depression or indentation in the surface of the tumor. This indentation can give the tumor a “belly button” or navel-like appearance, resembling the central depression seen in some skin lesions.

Umbilication in liver carcinoma may result from various factors, such as necrosis or fibrosis within the tumor, leading to a central area of tissue collapse or retraction. It can sometimes be observed on imaging studies (e.g., computed tomography scans) or during surgical exploration of the liver.

While umbilication itself does not have specific diagnostic or prognostic significance, it may be noted as a characteristic feature of certain liver tumors during clinical evaluation or radiological assessment.

Question 93

Gallbladder normal

Answer 93

GALLBLADDER and the common bile duct are in normal anatomical positions, and
their shape and caliber are regular in size.The gallbladder is 7 cm in the greatest diameter.

The thickness of the wall is essentially 1 mm.

Both the serosal and mucosal surface are
smooth and intact, the mucosa is bile-tinted. The lumen is empty.

Question 94

Answer 94

Black calculi, usually <1.5cm in diameter:
• pigment stones (chronic hemolysis, alcoholic cirrhosis, biliary infection,
old age)

The pathophysiological mechanism of pigment stone formation in the gallbladder involves the precipitation and accumulation of insoluble pigment compounds within the bile. Pigment stones are primarily composed of bilirubin, a breakdown product of hemoglobin, and calcium salts. Here’s how pigment stones typically form:

1. Bilirubin Metabolism: Bilirubin is produced when aged or damaged red blood cells are broken down in the spleen and liver. Bilirubin is released into the bloodstream and carried to the liver, where it undergoes conjugation to become water-soluble and more easily excreted into bile.
2. Biliary Stasis: Various factors can lead to stagnation or stasis of bile within the gallbladder, which promotes the precipitation of bilirubin and other constituents. Biliary stasis can occur due to conditions such as prolonged fasting, pregnancy, obesity, rapid weight loss, or medications that impair gallbladder emptying.
3. Increased Bilirubin Production: Conditions associated with increased production of bilirubin, such as hemolysis (excessive breakdown of red blood cells) or certain liver diseases (e.g., cirrhosis, Gilbert syndrome), can contribute to the formation of pigment stones. Excess bilirubin in bile can overwhelm the liver’s capacity to maintain it in a soluble form, leading to precipitation.
4. Bacterial Infection: Bacterial infection within the biliary system, particularly in the setting of biliary tract obstruction or stasis, can promote the hydrolysis of bilirubin conjugates by bacterial enzymes. This can lead to the release of unconjugated bilirubin, which is more prone to precipitation and stone formation.
5. Calcium Salt Deposition: Calcium salts, particularly calcium carbonate and calcium phosphate, can bind to bilirubin and other pigment compounds, forming the solid core of pigment stones. These calcium salts act as nucleating agents, facilitating the aggregation and growth of stone particles.
6. Gallbladder Contraction: Periodic contractions of the gallbladder, particularly during fasting or after meals, can promote the mechanical mixing of bile and facilitate the aggregation of bilirubin and calcium salts into solid stones.

Overall, the pathophysiological mechanism of pigment stone formation in the gallbladder involves a combination of factors that promote the precipitation, aggregation, and deposition of insoluble pigment compounds within the bile. These factors include biliary stasis, increased bilirubin production, bacterial infection, and the presence of calcium salts, which contribute to the formation of pigment stones.

Question 95

Answer 95

Round or faceted, pale yellow calculi with granular surfaces; transection
reveals crystalline radiations:
• cholesterol stones (caused by obesity, high-calorie diet, gastrointestinal
diseases, oral contraceptives, estrogen therapy, drug therapy, old age)

The pathophysiological mechanism of cholesterol stone formation in the gallbladder involves the supersaturation of bile with cholesterol, leading to the precipitation and aggregation of cholesterol crystals. Cholesterol stones are the most common type of gallstones and are primarily composed of cholesterol and smaller amounts of calcium salts and bilirubin. Here’s how cholesterol stones typically form:

1. Cholesterol Saturation: Bile is a complex fluid produced by the liver that aids in the digestion and absorption of dietary fats. Cholesterol is a normal constituent of bile, but when bile becomes supersaturated with cholesterol, it can lead to the formation of cholesterol crystals.
2. Gallbladder Hypomotility: Reduced gallbladder motility or stasis of bile within the gallbladder can contribute to cholesterol stone formation. Hypomotility can occur due to various factors, including prolonged fasting, rapid weight loss, pregnancy, or medications that impair gallbladder contraction.
3. Excess Cholesterol Secretion: Increased secretion of cholesterol by the liver, or impaired hepatic uptake of cholesterol, can result in elevated cholesterol levels in bile. This can occur in conditions such as obesity, insulin resistance, metabolic syndrome, or certain medications.
4. Decreased Bile Acids: Bile acids, produced by the liver, help solubilize cholesterol in bile by forming mixed micelles. Reduced bile acid secretion or impaired micelle formation can lead to cholesterol supersaturation and stone formation.
5. Nucleation: Once bile becomes supersaturated with cholesterol, cholesterol molecules can aggregate and form cholesterol crystals. These crystals serve as nuclei for the further precipitation and growth of cholesterol stones.
6. Gallbladder Contraction: Periodic contractions of the gallbladder, particularly during fasting or after meals, can promote the mechanical mixing of bile and facilitate the aggregation of cholesterol crystals into solid stones.
7. Mucin Gel Layer: The presence of a protective mucin gel layer lining the gallbladder epithelium may promote cholesterol stone formation by providing a scaffold for cholesterol crystal growth and aggregation.
8. Genetic Factors: Genetic predisposition may also play a role in cholesterol stone formation. Some individuals may have genetic variations that affect cholesterol metabolism, bile acid synthesis, or gallbladder function, increasing their susceptibility to cholesterol gallstone formation.

Overall, the pathophysiological mechanism of cholesterol stone formation in the gallbladder involves a combination of factors that promote cholesterol supersaturation, nucleation, and stone growth. These factors include gallbladder hypomotility, excess cholesterol secretion, decreased bile acids, gallbladder contraction, the presence of a mucin gel layer, and possibly genetic factors.

Question 96

Answer 96

Central pure cholesterol or bile core surrounded by variegated black (bile)
and gray-white (cholesterol) layers:
• combined stones (inflammatory reaction to initial pure stone)

The formation of combined stones in the gallbladder, also known as mixed stones, involves a combination of cholesterol and pigment components. The pathophysiological mechanism underlying the formation of combined stones shares features with both cholesterol and pigment stone formation. Here’s how combined stones typically form:

1. Bile Composition: Bile is a complex fluid produced by the liver that consists of water, bile salts, cholesterol, bilirubin, and other organic and inorganic compounds. Changes in the composition of bile, such as alterations in cholesterol and bilirubin levels, can predispose to the formation of combined stones.
2. Cholesterol Supersaturation: Similar to cholesterol stone formation, combined stones may form in bile that is supersaturated with cholesterol. Increased secretion of cholesterol by the liver or decreased bile acid levels can lead to cholesterol supersaturation and the formation of cholesterol crystals.
3. Bilirubin Precipitation: Combined stones also contain pigment components, such as bilirubin and calcium salts. Conditions associated with increased bilirubin levels, biliary stasis, or bacterial infection can promote the precipitation of bilirubin and calcium salts within the gallbladder.
4. Mixed Nucleation: In bile that is supersaturated with both cholesterol and bilirubin, mixed nucleation can occur, leading to the formation of combined stones. Cholesterol crystals may serve as nuclei for the precipitation of bilirubin and calcium salts, resulting in the formation of mixed stones containing both cholesterol and pigment components.
5. Gallbladder Stasis: Reduced gallbladder motility or stasis of bile within the gallbladder can contribute to the formation of combined stones. Conditions such as prolonged fasting, rapid weight loss, pregnancy, or medications that impair gallbladder contraction can increase the risk of combined stone formation.
6. Genetic and Environmental Factors: Genetic predisposition, as well as environmental factors such as diet, obesity, and metabolic syndrome, may also play a role in combined stone formation. These factors can influence bile composition, gallbladder function, and the balance between cholesterol and pigment metabolism.

Overall, the pathophysiological mechanism of combined stone formation in the gallbladder involves a combination of factors that promote cholesterol and bilirubin precipitation, mixed nucleation, and stone growth. These factors include bile composition, gallbladder stasis, genetic and environmental factors, and possibly bacterial infection. Combined stones may exhibit a heterogeneous composition, containing both cholesterol and pigment components, and may present unique challenges in terms of diagnosis and management compared to pure cholesterol or pigment stones.

Question 97

Answer 97

Calculi variegated throughout

mixed stones (inflammation of gallbladder)

Mixed stones, also known as combined stones, in the gallbladder are composed of a mixture of cholesterol, bilirubin (pigment), and calcium salts. The pathophysiological mechanism underlying the formation of mixed stones involves a combination of factors related to both cholesterol and pigment stone formation. Here’s how mixed stones typically form:

1. Bile Composition: Bile is a complex fluid produced by the liver that contains water, bile salts, cholesterol, bilirubin, and other organic and inorganic compounds. Changes in the composition of bile can predispose to the formation of mixed stones.
2. Cholesterol Supersaturation: Similar to cholesterol stone formation, mixed stones may form in bile that is supersaturated with cholesterol. Increased secretion of cholesterol by the liver or decreased bile acid levels can lead to cholesterol supersaturation and the formation of cholesterol crystals.
3. Bilirubin Precipitation: Mixed stones also contain pigment components, such as bilirubin and calcium salts. Conditions associated with increased bilirubin levels, biliary stasis, or bacterial infection can promote the precipitation of bilirubin and calcium salts within the gallbladder.
4. Mixed Nucleation: In bile that is supersaturated with both cholesterol and bilirubin, mixed nucleation can occur, leading to the formation of mixed stones. Cholesterol crystals may serve as nuclei for the precipitation of bilirubin and calcium salts, resulting in the formation of mixed stones containing both cholesterol and pigment components.
5. Gallbladder Stasis: Reduced gallbladder motility or stasis of bile within the gallbladder can contribute to the formation of mixed stones. Conditions such as prolonged fasting, rapid weight loss, pregnancy, or medications that impair gallbladder contraction can increase the risk of mixed stone formation.
6. Genetic and Environmental Factors: Genetic predisposition, as well as environmental factors such as diet, obesity, and metabolic syndrome, may also play a role in mixed stone formation. These factors can influence bile composition, gallbladder function, and the balance between cholesterol and pigment metabolism.

Overall, the pathophysiological mechanism of mixed stone formation in the gallbladder involves a combination of factors that promote cholesterol and bilirubin precipitation, mixed nucleation, and stone growth. Mixed stones may exhibit a heterogeneous composition, containing both cholesterol and pigment components, and may present unique challenges in terms of diagnosis and management compared to pure cholesterol or pigment stones.

Question 98

Answer 98

Infiltrating or exophytic tumor:
• adenocarcinoma

The pathophysiological mechanism of adenocarcinoma of the gallbladder involves the stepwise progression of normal gallbladder epithelial cells to malignant cancer cells. While the exact cause is not fully understood, several factors have been implicated in the development of gallbladder adenocarcinoma:

1. Chronic Inflammation: Chronic inflammation of the gallbladder, often due to conditions such as gallstones or chronic cholecystitis, is a major risk factor for the development of adenocarcinoma. Prolonged inflammation can lead to DNA damage, genetic mutations, and alterations in cellular signaling pathways that promote carcinogenesis.
2. Gallstones: Gallstones, particularly large or calcified stones, can cause chronic irritation and inflammation of the gallbladder epithelium. Gallstones are strongly associated with gallbladder adenocarcinoma, and the presence of gallstones increases the risk of developing this cancer.
3. Gallbladder Polyps: Gallbladder polyps are abnormal growths or protrusions from the gallbladder mucosa. While most gallbladder polyps are benign, some may progress to adenocarcinoma, particularly those that are larger in size or associated with other risk factors.
4. Chronic Infection: Chronic infection with certain pathogens, such as Salmonella typhi or Helicobacter species, has been implicated in the development of gallbladder adenocarcinoma. These infections can cause chronic inflammation and tissue damage, predisposing to malignant transformation.
5. Genetic Factors: Genetic predisposition may also play a role in the development of gallbladder adenocarcinoma. Certain genetic syndromes, such as Lynch syndrome or familial adenomatous polyposis (FAP), are associated with an increased risk of gastrointestinal cancers, including gallbladder cancer.
6. Metabolic Syndrome: Metabolic syndrome, characterized by obesity, insulin resistance, dyslipidemia, and hypertension, is associated with an increased risk of gallbladder adenocarcinoma. The underlying metabolic abnormalities may promote inflammation, oxidative stress, and carcinogenesis in the gallbladder epithelium.
7. Environmental Factors: Environmental factors such as diet, smoking, and exposure to carcinogens may also contribute to the development of gallbladder adenocarcinoma. Diets high in fat and low in fiber, as well as tobacco smoke containing carcinogenic compounds, have been implicated in the pathogenesis of gallbladder cancer.

Overall, the pathophysiological mechanism of gallbladder adenocarcinoma involves a combination of chronic inflammation, gallstones, gallbladder polyps, chronic infection, genetic predisposition, metabolic syndrome, and environmental factors that promote malignant transformation of the gallbladder epithelium. Understanding these mechanisms is crucial for the development of prevention strategies, early detection methods, and targeted therapies for gallbladder adenocarcinoma.

Question 99

Pancreas normal

Answer 99

It has regular shape, and usual size with 80 g. The consistency is moderately firm.

The color is grayish-yellow. The glandular pattern (i.e., the special structure) is preserved

Question 100

Answer 100

Head of pancreas encircling duodenum:
• annular pancreas

An annular pancreas is a rare congenital condition where a ring of pancreatic tissue surrounds the duodenum, the first part of the small intestine. This can cause compression of the duodenum, leading to symptoms like vomiting, abdominal pain, and intestinal blockage.

The pathomechanism of annular pancreas is believed to be due to an abnormality during embryonic development. Normally, the pancreas forms from two buds that arise from the primitive foregut. In annular pancreas, one of these buds fails to fully rotate during embryonic development, leading to the encircling of the duodenum by pancreatic tissue. This abnormal positioning can result in compression of the duodenum, leading to symptoms and complications associated with the condition.

Question 101

Answer 101

Pancreatic tissue in stomach, small intestines, Meckel diverticulum:
• ectopic pancreas

Ectopic pancreas, also known as heterotopic pancreas, is a rare condition where pancreatic tissue is found in locations outside of its usual location in the pancreas. This ectopic tissue typically lacks anatomical and functional connection to the main pancreas. It can be found anywhere along the gastrointestinal tract, most commonly in the stomach and small intestine, but also in the esophagus, duodenum, and even in more distant locations like the liver or lungs. Ectopic pancreas is usually asymptomatic but can occasionally cause symptoms or complications such as abdominal pain, obstruction, or inflammation.

The exact pathomechanism of ectopic pancreas formation is not fully understood, but it is believed to result from abnormal migration and differentiation of pancreatic tissue during embryonic development. During the early stages of development, pancreatic tissue buds from the foregut endoderm and migrates to its normal location in the upper abdomen. However, in cases of ectopic pancreas, some pancreatic tissue may become detached or migrate abnormally, leading to its presence in locations outside of the pancreas. Additionally, genetic and environmental factors may play a role in the development of ectopic pancreas.

Question 102

Answer 102

Fatty replacement:
• cystic fibrosis

Cystic fibrosis (CF) is a genetic disorder that primarily affects the lungs and digestive system. One of the common complications of CF is pancreatic insufficiency, which occurs due to the blockage of the pancreatic ducts by thick mucus, leading to impaired secretion of digestive enzymes from the pancreas into the small intestine.

When the pancreas cannot properly release digestive enzymes, the body is unable to properly digest fats, proteins, and other nutrients. As a result, undigested fats can accumulate in the pancreas, leading to the development of a condition known as fatty pancreas. This accumulation of fat in the pancreas can further impair its function, exacerbating pancreatic insufficiency and contributing to malnutrition and other digestive issues commonly seen in individuals with cystic fibrosis.

Question 103

Answer 103

Fat necrosis (firm, minute, yellow-white deposits becoming chalky white after
calcification), parenchymal necrosis (gray-white areas of softening) and
hemorrhage (blue-black or dark red areas):
• acute pancreatitis

Acute pancreatitis occurs when there is sudden inflammation of the pancreas. The pathomechanism of acute pancreatitis involves a cascade of events triggered by various factors, including:

1. Obstruction of the pancreatic duct: This can be caused by gallstones, excessive alcohol consumption, certain medications, or other factors. When the pancreatic duct is blocked, digestive enzymes produced by the pancreas cannot flow properly into the small intestine, leading to their activation within the pancreas itself.
2. Activation of digestive enzymes: Normally, pancreatic enzymes are inactive within the pancreas and become activated only when they reach the small intestine. However, when the pancreatic duct is obstructed or damaged, these enzymes can become prematurely activated within the pancreas, leading to autodigestion of pancreatic tissue.
3. Inflammatory response: The activation of digestive enzymes within the pancreas leads to tissue damage and triggers an inflammatory response. This inflammatory process can cause further damage to pancreatic tissue, blood vessels, and surrounding organs.
4. Release of pro-inflammatory mediators: In response to tissue injury, immune cells release pro-inflammatory mediators such as cytokines and chemokines, which amplify the inflammatory response and contribute to tissue damage.
5. Systemic complications: In severe cases, inflammation and tissue damage can lead to systemic complications such as organ failure, sepsis, and shock.

Overall, acute pancreatitis is a complex condition with multiple contributing factors, and its pathomechanism involves a combination of pancreatic enzyme activation, inflammation, and tissue damage.

Question 104

Answer 104

Hard parenchyma in lobular distribution with focal areas of calcification;
calculi present in pancreatic ducts:
• chronic pancreatitis

Chronic pancreatitis is a long-term inflammation of the pancreas characterized by progressive and irreversible damage to the pancreatic tissue. This condition can lead to persistent abdominal pain, impaired digestion, malabsorption of nutrients, and other complications.

The pathomechanism of chronic pancreatitis involves a combination of factors, including:

1. Recurrent acute pancreatitis: Chronic pancreatitis often develops as a consequence of repeated episodes of acute pancreatitis. Each episode of acute pancreatitis causes damage to pancreatic tissue and can lead to the development of scar tissue (fibrosis).
2. Obstruction of pancreatic ducts: Similar to acute pancreatitis, chronic pancreatitis can be caused by obstruction of the pancreatic ducts due to factors such as gallstones, strictures, tumors, or anatomical abnormalities. When the pancreatic ducts are obstructed, digestive enzymes produced by the pancreas cannot drain properly, leading to their activation within the pancreas and subsequent tissue damage.
3. Alcohol consumption: Chronic alcohol consumption is a major risk factor for chronic pancreatitis. Alcohol can directly damage pancreatic tissue and impair pancreatic function. It is believed that alcohol-induced pancreatitis may involve oxidative stress, activation of pancreatic enzymes, and inflammatory processes.
4. Genetic factors: In some cases, chronic pancreatitis may have a genetic component. Mutations in genes related to pancreatic function and regulation of inflammation have been associated with an increased risk of developing chronic pancreatitis.
5. Autoimmune factors: In autoimmune pancreatitis, the immune system mistakenly attacks the pancreas, leading to inflammation and tissue damage. Autoimmune pancreatitis is a rare form of chronic pancreatitis and is characterized by elevated levels of certain antibodies and response to immunosuppressive therapy.

Overall, chronic pancreatitis is a complex condition with multiple underlying mechanisms, including recurrent inflammation, obstruction of pancreatic ducts, alcohol consumption, genetic factors, and autoimmune processes. These factors can contribute to progressive damage to the pancreas and the development of chronic symptoms and complications.

Question 105

Answer 105

Hard parenchyma in nonlobular distribution, generally involving head of
pancreas:
• obstructive chronic pancreatitis due to obstruction of the sphincter of
Oddi (cholelithiasis, neoplasia)

Obstructive chronic pancreatitis refers to a specific subtype of chronic pancreatitis where the main underlying cause is the obstruction of the pancreatic ducts. This obstruction can be due to various factors such as gallstones, strictures, tumors, or other anatomical abnormalities.

The key difference between obstructive chronic pancreatitis and “normal” chronic pancreatitis lies in the primary cause of pancreatic injury and inflammation. In obstructive chronic pancreatitis, the obstruction of pancreatic ducts plays a central role in initiating and perpetuating the inflammatory process. The obstruction leads to the accumulation of pancreatic enzymes within the pancreas, which causes tissue damage, inflammation, and ultimately, the development of chronic pancreatitis.

In contrast, “normal” chronic pancreatitis may have different underlying causes, such as recurrent episodes of acute pancreatitis, chronic alcohol consumption, genetic factors, or autoimmune processes. While obstruction of pancreatic ducts can also occur in these cases, it may not be the primary initiating factor.

Overall, obstructive chronic pancreatitis is a specific subtype of chronic pancreatitis characterized by the prominent role of pancreatic duct obstruction in its pathogenesis. However, regardless of the underlying cause, chronic pancreatitis is characterized by progressive and irreversible damage to the pancreatic tissue, leading to persistent symptoms and complications.

Question 106

Answer 106

Pancreas

Cystic tumors:
• cystadenoma
• cystadenocarcinoma
• solid cystic tumor

An overview of the pathophysiological mechanisms leading to cystic tumors of the pancreas:

1. Cystadenoma:
   
   • Cystadenomas are benign cystic tumors of the pancreas that typically arise from the epithelial cells lining the pancreatic ducts or acini.
   • The exact pathophysiological mechanism of cystadenoma formation is not fully understood, but it is believed to involve dysregulation of cell growth and proliferation.
   • Some cystadenomas may be associated with genetic mutations, such as mutations in the KRAS oncogene or inactivation of tumor suppressor genes, which can promote uncontrolled cell growth and tumor formation.
2. Cystadenocarcinoma:
   
   • Cystadenocarcinomas are malignant cystic tumors of the pancreas that originate from the epithelial cells lining the pancreatic ducts or acini.
   • Similar to cystadenomas, the exact pathophysiological mechanisms underlying cystadenocarcinoma development are not fully understood.
   • However, cystadenocarcinomas are thought to arise from pre-existing cystadenomas or de novo from dysplastic epithelial cells within the pancreatic ducts.
   • Genetic mutations, such as mutations in the KRAS oncogene, TP53 tumor suppressor gene, and alterations in other oncogenes and tumor suppressor genes, are commonly observed in cystadenocarcinomas and contribute to their malignant transformation.
3. Solid pseudopapillary tumor (Solid cystic tumor):
   
   • Solid pseudopapillary tumors (SPTs) are rare, low-grade malignant tumors of the pancreas that typically occur in young women.
   • The pathophysiological mechanisms underlying SPT formation are not fully understood, but they are believed to arise from pluripotent stem cells within the pancreas.
   • Genetic studies have identified mutations in the CTNNB1 gene, which encodes the beta-catenin protein, as well as other genetic alterations, in solid pseudopapillary tumors.
   • These genetic alterations likely contribute to the aberrant activation of signaling pathways involved in cell growth and proliferation, leading to tumor formation.

Overall, cystic tumors of the pancreas, including cystadenomas, cystadenocarcinomas, and solid pseudopapillary tumors, involve complex interactions between genetic mutations, dysregulated cell growth, and other factors that contribute to their development and progression.

Question 107

Answer 107

Ill-defined, gray-white to gray-yellow, firm mass anywhere in pancreas:
• adenocarcinoma

Adenocarcinoma, the most common type of pancreatic cancer, arises from the ductal cells of the pancreas. Its pathophysiological mechanism involves a series of genetic and molecular alterations that lead to uncontrolled cell growth and tumor formation. Here’s an overview of the pathophysiological mechanisms underlying pancreatic adenocarcinoma:

1. Genetic mutations:
   
   • Adenocarcinoma of the pancreas is associated with several genetic mutations that contribute to its development and progression.
   • One of the most common mutations found in pancreatic adenocarcinoma is the activation of the KRAS oncogene, which occurs in approximately 95% of cases. KRAS mutations lead to the dysregulation of cellular signaling pathways involved in cell proliferation and survival.
   • Other genetic alterations commonly observed in pancreatic adenocarcinoma include mutations in tumor suppressor genes such as TP53, CDKN2A (p16), and SMAD4 (DPC4), which further promote tumor growth and progression.
2. Dysregulated signaling pathways:
   
   • Dysregulation of key signaling pathways is a hallmark of pancreatic adenocarcinoma.
   • Activation of the RAS-MAPK pathway, driven by mutations in the KRAS oncogene, promotes uncontrolled cell proliferation and survival.
   • Dysregulation of the PI3K/AKT/mTOR pathway, often due to mutations in tumor suppressor genes or activation of growth factor receptors, promotes cell growth and survival.
   • Aberrant activation of the WNT/β-catenin signaling pathway, driven by mutations in the CTNNB1 gene or other genetic alterations, contributes to tumor progression and metastasis.
3. Tumor microenvironment:
   
   • The tumor microenvironment plays a crucial role in pancreatic adenocarcinoma progression.
   • Pancreatic tumors are characterized by dense stroma, which consists of fibroblasts, immune cells, and extracellular matrix components.
   • The stroma provides a supportive environment for tumor growth and promotes tumor cell invasion and metastasis.
   • Interactions between tumor cells and stromal components contribute to immune suppression, tumor angiogenesis, and treatment resistance.
4. Inflammatory microenvironment:
   
   • Chronic inflammation is associated with an increased risk of pancreatic adenocarcinoma.
   • Inflammatory mediators, such as cytokines, chemokines, and growth factors, produced in response to tissue injury or infection, promote tumor initiation and progression.
   • Inflammatory cells, including macrophages, neutrophils, and lymphocytes, infiltrate the tumor microenvironment and contribute to tumor growth, invasion, and metastasis.

Overall, pancreatic adenocarcinoma is a complex disease driven by a combination of genetic mutations, dysregulated signaling pathways, and interactions with the tumor microenvironment. Understanding the underlying pathophysiological mechanisms is crucial for the development of targeted therapies and improved treatment strategies for this aggressive malignancy.

Question 108

Encapsulated pale tan to red-brown tumors pancreas

Answer 108

islet cell tumors

Islet cell tumors, also known as neuroendocrine tumors (NETs) of the pancreas, arise from the hormone-producing cells (islet cells) of the pancreas. These tumors can produce various hormones, such as insulin, glucagon, gastrin, somatostatin, and others, leading to a wide range of clinical presentations depending on the hormone produced and the tumor’s functionality. Here’s an overview of the pathophysiological mechanisms underlying islet cell tumors:

1. Genetic mutations:
   
   • Islet cell tumors can be sporadic or occur as part of genetic syndromes such as multiple endocrine neoplasia type 1 (MEN1), von Hippel-Lindau (VHL) syndrome, neurofibromatosis type 1 (NF1), and tuberous sclerosis complex (TSC).
   • MEN1 syndrome, caused by mutations in the MEN1 gene, predisposes individuals to the development of pancreatic neuroendocrine tumors (pNETs) among other endocrine tumors.
   • Mutations in other genes, such as the DAXX and ATRX genes, have been associated with the development of sporadic pancreatic neuroendocrine tumors.
2. Dysregulated cell growth and proliferation:
   
   • Genetic mutations and dysregulation of signaling pathways contribute to uncontrolled cell growth and proliferation in islet cell tumors.
   • The mammalian target of rapamycin (mTOR) pathway is commonly dysregulated in islet cell tumors, promoting cell growth and survival.
   • Dysregulated insulin-like growth factor (IGF) signaling pathways and other growth factor receptors may also contribute to tumor growth.
3. Hormone production and secretion:
   
   • Islet cell tumors can produce hormones such as insulin, glucagon, gastrin, somatostatin, and others, leading to hormonal symptoms and syndromes.
   • Insulinomas, the most common type of functional islet cell tumor, produce excessive insulin, leading to hypoglycemia and related symptoms.
   • Glucagonomas produce excessive glucagon, leading to hyperglycemia, skin rash (necrolytic migratory erythema), weight loss, and other symptoms.
   • Other functional tumors, such as gastrinomas, produce excessive gastrin, leading to gastric acid hypersecretion and the development of peptic ulcers (Zollinger-Ellison syndrome).
4. Metastasis and spread:
   
   • Islet cell tumors have the potential to metastasize, particularly if they are high grade or poorly differentiated.
   • Metastasis may occur to regional lymph nodes, liver, lungs, and other sites, contributing to disease progression and prognosis.

Overall, the pathophysiological mechanisms underlying islet cell tumors involve a complex interplay of genetic mutations, dysregulated signaling pathways, hormone production and secretion, and potential for metastasis. Understanding these mechanisms is important for diagnosis, treatment, and management of patients with islet cell tumors.

Question 109

Kidney normal

Answer 109

The kidneys are in the normal anatomical position, They are symmetrical, same sized.

The kidneys have regular shape and 300 g weight.

The capsule is easily removable.

The surface is smooth, and the 5 mm thick pale brown cortex is well separating from the darker redish-brown medulla.

The amount of the peripelvic adipose tissue is preserved.

The pelvises and the ureters are in the normal anatomical positions, with regular shape and usual caliber.

The blood content of their smooth mucosal surface is usual.

The lumen is empty

Question 110

Answer 110

Fusion of upper or lower poles of kidney:
• horseshoe kidney

Horseshoe kidney is a congenital anomaly in which the kidneys fuse together at the lower poles during fetal development, forming a U-shaped structure. This condition occurs during embryonic development and involves the following pathophysiological mechanism:

1. Abnormal migration and fusion of the kidneys: During early fetal development, the kidneys originate in the pelvic area and ascend to their normal position in the abdomen. In cases of horseshoe kidney, the ascent of the kidneys is hindered, leading to abnormal positioning. As the kidneys ascend, they may fuse together at the lower poles due to their close proximity, resulting in the characteristic U-shaped appearance.
2. Failure of renal fusion:
   
   • Normally, the kidneys undergo fusion and rotation during development to assume their typical position in the abdomen.
   • In horseshoe kidney, fusion occurs but is incomplete, resulting in the formation of a horseshoe-shaped kidney instead of two separate kidneys.
3. Vascular anomalies:
   
   • Horseshoe kidney is often associated with vascular anomalies due to the abnormal positioning and fusion of the kidneys.
   • The renal arteries and veins may have abnormal courses or branching patterns, which can affect blood supply to the kidneys and increase the risk of complications such as renal artery stenosis or renal vein thrombosis.
4. Association with other congenital anomalies:
   
   • Horseshoe kidney is frequently associated with other congenital anomalies, including anomalies of the genitourinary system, such as ureteropelvic junction obstruction, vesicoureteral reflux, or renal dysplasia.
   • Additionally, horseshoe kidney may be associated with anomalies in other organ systems, such as the cardiovascular, musculoskeletal, or gastrointestinal systems, due to shared developmental origins during embryogenesis.

Overall, horseshoe kidney results from a combination of abnormal migration, fusion, and rotation of the kidneys during fetal development. These developmental anomalies lead to the characteristic U-shaped configuration of the kidneys and are associated with various vascular and other congenital anomalies.

Question 111

Answer 111

Bilateral massively enlarged kidneys with multiple dilated cysts (up to 4cm)
filled with clear, turbid, or hemorrhagic fluid:
• autosomal dominant adult polycystic kidney disease

Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder characterized by the progressive development and growth of fluid-filled cysts in the kidneys, leading to renal enlargement, renal dysfunction, and eventually, end-stage renal disease. The pathomechanism of ADPKD primarily involves genetic mutations in either the PKD1 or PKD2 genes, which encode for proteins involved in the regulation of tubular epithelial cell proliferation, differentiation, and fluid secretion in the kidneys. Here’s a detailed overview of the pathophysiological mechanisms underlying ADPKD:

1. Genetic mutations:
   
   • The majority of cases of ADPKD are caused by mutations in the PKD1 gene, located on chromosome 16, which encodes for the protein polycystin-1.
   • A smaller proportion of cases are caused by mutations in the PKD2 gene, located on chromosome 4, which encodes for the protein polycystin-2.
   • Polycystin-1 and polycystin-2 are integral membrane proteins primarily localized to the primary cilium, a microtubule-based organelle protruding from the apical surface of renal tubular epithelial cells.
   • These proteins play crucial roles in the regulation of intracellular calcium signaling, cell-cell and cell-matrix interactions, cell proliferation, apoptosis, and fluid secretion in renal tubules.
   • Mutations in the PKD1 or PKD2 genes lead to abnormal or absent polycystin proteins, disrupting cellular signaling pathways and physiological processes involved in maintaining tubular integrity and renal function.
2. Aberrant cellular signaling:
   
   • Loss of functional polycystin proteins results in dysregulated cellular signaling pathways, including the cAMP, mTOR, and Wnt/β-catenin signaling pathways, among others.
   • Dysregulation of these pathways leads to increased cell proliferation, fluid secretion, and cyst growth in the renal tubules.
   • Aberrant activation of the cAMP pathway, in particular, plays a central role in cystogenesis by stimulating fluid secretion and transepithelial ion transport in renal tubular epithelial cells.
3. Cyst formation and growth:
   
   • The loss of functional polycystin proteins disrupts cell-cell and cell-matrix interactions, leading to abnormal proliferation and dedifferentiation of renal tubular epithelial cells.
   • Cysts initially form from dilation of renal tubules due to fluid accumulation and hyperplasia of tubular epithelial cells.
   • As cysts grow, they compress adjacent renal parenchyma, disrupt normal renal architecture, and impair renal blood flow and urine concentration ability.
4. Inflammatory and fibrotic responses:
   
   • Cyst expansion and compression of surrounding renal tissue lead to activation of inflammatory and fibrotic pathways, contributing to interstitial inflammation, fibrosis, and progressive renal dysfunction.
   • Inflammatory mediators, such as cytokines, chemokines, and growth factors, promote the recruitment of immune cells and the activation of fibroblasts, leading to collagen deposition and fibrotic scarring in the kidney.

Overall, the pathophysiological mechanisms underlying ADPKD involve genetic mutations that disrupt normal cellular processes in renal tubular epithelial cells, leading to dysregulated cell proliferation, fluid secretion, and cyst growth in the kidneys. These cystic changes, along with associated inflammatory and fibrotic responses, ultimately result in progressive renal dysfunction and the development of end-stage renal disease.

Question 112

Answer 112

Cortical and medullary cysts (0.5 to 2cm) containing clear fluid in patients
undergoing dialysis:
• acquired cystic disease

Acquired cystic kidney disease (ACKD) is a condition characterized by the development of multiple fluid-filled cysts in the kidneys, typically occurring in individuals with advanced chronic kidney disease (CKD), particularly those undergoing long-term hemodialysis or peritoneal dialysis. The pathomechanism of ACKD involves a combination of factors related to CKD, dialysis treatment, and other contributing factors:

1. Chronic kidney disease (CKD):
   
   • The underlying renal insufficiency and progressive loss of kidney function in CKD contribute to the development of ACKD.
   • CKD leads to alterations in renal tubular structure and function, including tubular dilation, atrophy, and fibrosis, which create a predisposing environment for cyst formation.
   • Chronic hypoxia, oxidative stress, inflammation, and other pathological processes associated with CKD can also contribute to cystogenesis in the kidneys.
2. Dialysis treatment:
   
   • Long-term hemodialysis and peritoneal dialysis are major risk factors for the development and progression of ACKD.
   • Dialysis treatment imposes hemodynamic and mechanical stress on the kidneys, leading to tubular injury, ischemia-reperfusion injury, and alterations in renal perfusion.
   • Dialysis-related factors, such as repeated vascular access procedures, exposure to bioincompatible dialysis membranes, and fluctuations in extracellular fluid volume, can further exacerbate renal injury and promote cyst formation.
3. Fluid and electrolyte imbalances:
   
   • Dysregulation of fluid and electrolyte balance in CKD and during dialysis treatment can contribute to cystogenesis in the kidneys.
   • Volume overload, electrolyte disturbances (e.g., hyperkalemia), and acid-base imbalances can disrupt renal tubular homeostasis and promote cyst formation.
   • Inadequate clearance of uremic toxins and retention of solutes can also contribute to cellular injury and proliferation in the kidneys, further promoting cyst growth.
4. Uremic toxins and metabolic derangements:
   
   • Accumulation of uremic toxins and metabolic derangements in CKD can promote cellular injury, oxidative stress, and inflammation in the kidneys, contributing to cystogenesis.
   • Uremic toxins, such as indoxyl sulfate, p-cresol sulfate, and advanced glycation end products (AGEs), have been implicated in the pathogenesis of renal fibrosis, tubular injury, and cyst formation.
   • Dysregulation of metabolic pathways, such as glucose and lipid metabolism, can also contribute to cellular dysfunction and cyst formation in the kidneys.

Overall, the pathomechanism of acquired cystic kidney disease involves a complex interplay of factors related to CKD, dialysis treatment, fluid and electrolyte imbalances, uremic toxins, and metabolic derangements. These factors contribute to renal tubular injury, cellular proliferation, and cyst formation in the kidneys, ultimately leading to the development and progression of ACKD in individuals with advanced CKD.

Question 113

Answer 113

Single or multiple thin-walled translucent cortical cysts (1 to >10 cm) filled
with clear fluid:
• simple cysts

Simple renal cysts are fluid-filled sacs that form within the kidneys. They are usually benign and do not cause symptoms unless they grow large or become complicated. The exact cause of simple renal cysts is not fully understood, but several factors may contribute to their formation:

1. Age-related changes: Simple renal cysts become more common with age, suggesting that age-related changes in kidney structure and function may play a role in their development. As individuals age, there may be alterations in renal tubular epithelial cells, leading to the formation of cysts.
2. Obstruction of tubules: Obstruction of renal tubules or small collecting ducts within the kidney may contribute to the development of simple renal cysts. When the flow of urine within the kidney is obstructed, fluid can accumulate and form cysts.
3. Degenerative changes: Degenerative changes in the kidney, such as weakening of the renal parenchyma or atrophy of renal tubules, may predispose individuals to the formation of cysts. These changes can result from aging, chronic kidney disease, or other underlying conditions.
4. Genetic predisposition: There may be a genetic predisposition to the development of simple renal cysts in some individuals. Family history studies have suggested a possible genetic component to the formation of renal cysts, although specific genetic mutations associated with simple renal cysts have not been identified in most cases.
5. Lymphatic or vascular malformations: Malformations of the lymphatic or vascular system within the kidney may contribute to the development of simple renal cysts. These malformations can disrupt normal fluid dynamics within the kidney, leading to cyst formation.

Overall, the exact cause of simple renal cysts is likely multifactorial, involving a combination of age-related changes, obstruction of tubules, degenerative processes, genetic factors, and abnormalities in the lymphatic or vascular system within the kidney. Simple renal cysts are typically benign and do not require treatment unless they cause symptoms or complications.

Question 114

Answer 114

Abscesses in cortex; ulceration of ureteral mucosa; purulent material in
ureteral lumen:
• acute pyelonephritis

Acute pyelonephritis is a bacterial infection of the renal parenchyma and renal pelvis, typically caused by the ascent of bacteria from the lower urinary tract. The pathomechanism of acute pyelonephritis involves several steps:

1. Bacterial colonization: The infection usually begins with the colonization of the lower urinary tract by uropathogenic bacteria, most commonly Escherichia coli. Other pathogens, such as Klebsiella pneumoniae, Proteus mirabilis, and Enterococcus faecalis, can also be responsible.
2. Ascension of bacteria: Bacteria ascend from the urethra and bladder into the upper urinary tract, including the ureters and kidneys. Factors that facilitate bacterial ascent include urinary tract obstructions (e.g., kidney stones, strictures), urinary reflux (retrograde flow of urine from the bladder into the ureters), and instrumentation of the urinary tract (e.g., catheterization).
3. Adherence and invasion: Bacteria adhere to the urothelial lining of the renal pelvis and renal tubules, facilitated by bacterial adhesins and host cell receptors. Once attached, bacteria may invade the urothelial cells and breach the epithelial barrier, allowing access to the renal parenchyma.
4. Inflammatory response: The presence of bacteria in the renal parenchyma triggers an inflammatory response, characterized by the release of pro-inflammatory cytokines (e.g., interleukin-1β, tumor necrosis factor-α) and chemokines. Neutrophils are recruited to the site of infection, leading to tissue infiltration and the formation of pus.
5. Tissue damage: The inflammatory response and immune cell infiltration lead to tissue damage within the renal parenchyma. Neutrophils release reactive oxygen species and proteolytic enzymes, causing direct cellular injury and necrosis. The accumulation of pus and edema further contributes to tissue destruction.
6. Clinical manifestations: The clinical manifestations of acute pyelonephritis include fever, chills, flank pain, dysuria, urinary frequency, and urgency. Systemic symptoms such as nausea, vomiting, and malaise may also occur, reflecting the systemic inflammatory response.
7. Complications: Severe or untreated cases of acute pyelonephritis can lead to complications such as renal abscess formation, sepsis, acute kidney injury, and chronic kidney disease. Prompt diagnosis and appropriate antibiotic therapy are essential to prevent these complications and promote recovery.

Overall, the pathomechanism of acute pyelonephritis involves bacterial colonization, ascension of bacteria into the upper urinary tract, adherence and invasion of renal tissue, inflammatory response, tissue damage, and clinical manifestations of infection. Early recognition and treatment are crucial to prevent complications and promote resolution of the infection.

Question 115

Kidney

Extension of suppurative areas through renal capsule into perinephric fat

Answer 115

perinephric abscess

A perinephric abscess, also known as perirenal abscess, is a collection of pus in the perinephric space surrounding the kidney. It typically arises as a complication of untreated or inadequately treated urinary tract infections, including pyelonephritis. The pathomechanism of perinephric abscess formation involves several steps:

1. Urinary tract infection (UTI): The infection usually begins in the lower urinary tract, commonly the bladder, and may ascend to involve the upper urinary tract, including the kidneys. Bacteria, such as Escherichia coli, Klebsiella pneumoniae, and Proteus mirabilis, are the most common causative agents.
2. Renal infection: Once the bacteria reach the kidneys, they can infect the renal parenchyma and renal pelvis, causing pyelonephritis. In pyelonephritis, inflammation and tissue damage occur within the kidney due to the presence of bacteria and the host immune response.
3. Extension of infection: In some cases, the infection may extend beyond the renal parenchyma and pelvis to involve the surrounding perinephric space. This can occur through direct extension of infection from the kidney or via hematogenous spread from distant sites of infection.
4. Formation of abscess: Within the perinephric space, the infection can lead to the formation of an abscess, which is a localized collection of pus surrounded by inflamed tissue. Pus consists of dead white blood cells, bacteria, and tissue debris.
5. Encapsulation: The abscess may become encapsulated by fibrous tissue, forming a well-defined cavity within the perinephric space. This encapsulation helps to contain the infection and prevent its spread to adjacent structures.
6. Clinical manifestations: Patients with a perinephric abscess may present with fever, chills, flank pain, and tenderness. Other symptoms may include malaise, nausea, vomiting, and signs of systemic inflammation. In severe cases, patients may develop sepsis or septic shock.
7. Imaging findings: Diagnosis of a perinephric abscess is usually confirmed by imaging studies, such as ultrasound, computed tomography (CT) scan, or magnetic resonance imaging (MRI). These imaging modalities can visualize the presence of a fluid collection adjacent to the kidney and help differentiate it from other causes of flank pain.

Overall, the pathomechanism of perinephric abscess formation involves the extension of infection from the kidney to the surrounding perinephric space, leading to the formation of a localized collection of pus. Early recognition and treatment of urinary tract infections can help prevent the development of perinephric abscesses and, associated complications.

Question 116

pyelonephrosis

Answer 116

Suppurative exudate within obstructed renal pelvis, calyces, and ureter

Pyelonephrosis is a condition characterized by the dilation or distension of the renal pelvis and calyces due to obstruction of the urinary tract, typically by a kidney stone, tumor, or stricture. The term combines “pyel-“ referring to the renal pelvis and “nephrosis” meaning kidney disorder. Here’s an overview of the pathophysiological mechanisms and clinical features of pyelonephrosis:

1. Obstruction of urinary flow: The primary cause of pyelonephrosis is the obstruction of urinary flow at the level of the renal pelvis or ureter. This obstruction prevents urine from draining properly from the kidney, leading to an increase in pressure within the renal collecting system.
2. Backflow of urine: As pressure builds up behind the obstruction, urine may back up into the renal pelvis, causing dilation of the renal pelvis and calyces. The severity of dilation depends on the degree and duration of the obstruction.
3. Impaired urine drainage: With continued obstruction, urine stagnates in the affected kidney, providing an ideal environment for bacterial growth and infection. This can lead to pyelonephritis, an infection of the renal parenchyma.
4. Inflammatory response: In response to infection and inflammation, the renal parenchyma may become inflamed and edematous, further contributing to the dilation of the renal pelvis and calyces. The inflammatory process can also impair renal function and lead to systemic symptoms such as fever, chills, and flank pain.
5. Clinical manifestations: Patients with pyelonephrosis may present with symptoms similar to those of pyelonephritis, including fever, chills, flank pain, and urinary symptoms such as dysuria, urgency, and frequency. In severe cases, patients may develop sepsis or septic shock.
6. Diagnostic evaluation: Pyelonephrosis is typically diagnosed through imaging studies such as ultrasound, computed tomography (CT) scan, or magnetic resonance imaging (MRI). These imaging modalities can visualize the dilation of the renal pelvis and calyces, as well as identify the underlying cause of obstruction.
7. Management: Treatment of pyelonephrosis involves relieving the obstruction to restore normal urinary flow and drainage from the affected kidney. This may involve the placement of a ureteral stent or nephrostomy tube to bypass the obstruction. Antibiotic therapy is also initiated to treat any associated infection.

Overall, pyelonephrosis is a serious condition that requires prompt diagnosis and treatment to prevent complications such as renal damage, sepsis, and renal failure. Identifying and addressing the underlying cause of obstruction is essential for successful management of the condition.

Question 117

Answer 117

Gray-white to yellow discoloration of distal pyramids:
• papillary necrosis

Papillary necrosis is a condition characterized by ischemic or necrotic changes in the renal papillae, which are the small projections in the renal medulla where urine collects before entering the ureters. The pathomechanism of papillary necrosis involves several contributing factors:

1. Ischemia: Ischemia, or inadequate blood flow to the renal papillae, is a primary factor contributing to papillary necrosis. Ischemia can result from various conditions, including renal artery stenosis, thromboembolism, vasculitis, or systemic hypoperfusion (e.g., shock). Reduced blood flow deprives the renal papillae of oxygen and nutrients, leading to tissue injury and necrosis.
2. Obstruction: Obstruction of the urinary tract can contribute to papillary necrosis by impeding urine flow and increasing pressure within the renal collecting system. Obstruction can result from kidney stones, tumors, strictures, or compression of the ureters. Increased pressure within the renal papillae can compromise blood flow, exacerbating ischemic injury and promoting necrosis.
3. Toxic injury: Exposure to nephrotoxic agents can also contribute to papillary necrosis. Certain medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs), analgesics (e.g., aspirin, acetaminophen), antibiotics (e.g., sulfonamides), and contrast agents, have been implicated in causing renal papillary injury. These agents can induce direct toxic effects on renal tubular epithelial cells, leading to cellular injury, inflammation, and necrosis.
4. Infection: Infections of the urinary tract, particularly those caused by bacteria, can contribute to papillary necrosis. Bacterial infections, such as pyelonephritis, can lead to inflammation and tissue damage in the renal papillae, promoting necrosis. In addition, bacterial toxins and inflammatory mediators released during infection can exacerbate ischemic injury and worsen tissue damage.
5. Vascular diseases: Certain systemic vascular diseases, such as diabetes mellitus and sickle cell disease, can predispose individuals to papillary necrosis. These conditions can cause microvascular damage and impaired blood flow to the renal papillae, increasing the risk of ischemic injury and necrosis.

Overall, papillary necrosis is a multifactorial condition involving a combination of ischemic injury, obstruction, toxic exposure, infection, and underlying vascular diseases. The interplay of these factors disrupts the normal physiology of the renal papillae, leading to tissue necrosis and the characteristic changes seen in papillary necrosis. Early recognition and management of underlying risk factors are essential for preventing and treating this condition.

Question 118

analgesic nephropathy

Answer 118

Brownish necrotic papillae

Analgesic nephropathy is a kidney disorder caused by long-term, excessive use of certain analgesic medications, particularly nonsteroidal anti-inflammatory drugs (NSAIDs) and combination analgesics containing phenacetin. The pathophysiological mechanism of analgesic nephropathy involves several interrelated factors:

1. Direct tubular toxicity: The primary mechanism of analgesic nephropathy involves direct toxicity to renal tubular cells caused by prolonged exposure to high doses of analgesic medications. Phenacetin, a compound previously used in many analgesic preparations, and its metabolite, acetaminophen (paracetamol), have been implicated in tubular injury. Phenacetin is converted to a toxic metabolite, N-acetyl-p-benzoquinone imine (NAPQI), which can accumulate in renal tubular cells and cause oxidative stress, mitochondrial dysfunction, and cell death.
2. Papillary necrosis: Analgesic nephropathy can lead to papillary necrosis, a condition characterized by ischemic or necrotic changes in the renal papillae. The renal papillae are particularly susceptible to injury due to their high oxygen demand and low blood flow. Ischemia resulting from vasoconstriction and impaired blood flow, combined with direct tubular toxicity, contributes to the development of papillary necrosis.
3. Chronic interstitial nephritis: Prolonged exposure to analgesic medications can lead to chronic interstitial nephritis, characterized by inflammation and fibrosis of the renal interstitium. Chronic interstitial nephritis is thought to result from immune-mediated mechanisms triggered by the release of pro-inflammatory cytokines and chemokines in response to tubular injury.
4. Renal medullary fibrosis: Analgesic nephropathy can also cause fibrosis and scarring in the renal medulla, leading to loss of renal function over time. Fibrosis disrupts the normal architecture of the kidney, impairs tubular function, and contributes to the development of chronic kidney disease (CKD) and end-stage renal disease (ESRD).
5. Renal papillary calcification: Long-term use of analgesic medications has been associated with the development of renal papillary calcification, which can further impair renal function and increase the risk of urinary tract obstruction, infection, and stone formation.

Overall, the pathophysiological mechanism of analgesic nephropathy involves a combination of direct tubular toxicity, papillary necrosis, chronic interstitial nephritis, renal medullary fibrosis, and renal papillary calcification. These pathological changes disrupt renal function and contribute to the progression of kidney damage and decline in renal function over time. Avoidance of excessive analgesic use, particularly of medications containing phenacetin or acetaminophen, is essential for preventing analgesic nephropathy.

Question 119

Answer 119

Coarse or irregular cortical scars, primarily in upper or lower poles; dilation
and blunting of calyces; dilation and thickening of ureters:
• chronic pyelonephritis

Chronic pyelonephritis is a long-standing inflammatory condition of the renal parenchyma and collecting system, usually resulting from recurrent or persistent urinary tract infections (UTIs). The pathophysiological mechanism of chronic pyelonephritis involves a complex interplay of infectious, immunological, and structural factors:

1. Recurrent urinary tract infections (UTIs): Chronic pyelonephritis often begins with acute pyelonephritis, an acute bacterial infection of the renal parenchyma and collecting system. Recurrent or untreated acute pyelonephritis can lead to chronic inflammation and scarring of the renal parenchyma over time.
2. Ascending bacterial infection: The most common route of infection is the ascent of bacteria from the lower urinary tract, typically Escherichia coli, into the upper urinary tract, including the kidneys. Factors that predispose individuals to ascending UTIs include vesicoureteral reflux, urinary tract obstructions (e.g., kidney stones, strictures), and neurogenic bladder dysfunction.
3. Persistent bacterial colonization: In some cases, bacteria may persistently colonize the renal parenchyma or form biofilms within the renal tubules, leading to chronic low-grade inflammation and tissue damage. Bacterial persistence can evade host immune responses and promote the development of chronic pyelonephritis.
4. Inflammatory response: Chronic pyelonephritis is characterized by a sustained inflammatory response within the renal parenchyma and collecting system. Inflammatory mediators, such as cytokines (e.g., interleukin-1β, tumor necrosis factor-α) and chemokines, are released in response to bacterial infection and contribute to tissue damage and fibrosis.
5. Tubulointerstitial fibrosis: Chronic inflammation and tissue injury in the renal parenchyma lead to the activation of fibroblasts and deposition of extracellular matrix proteins, resulting in tubulointerstitial fibrosis. Fibrosis disrupts the normal architecture of the kidney, impairs renal function, and contributes to the progression of chronic kidney disease (CKD).
6. Scarring and renal damage: Chronic pyelonephritis is associated with scarring of the renal parenchyma, dilatation of the renal pelvis and calyces (hydronephrosis), and distortion of the renal architecture. These structural changes can impair renal function, predispose to urinary tract obstruction, and increase the risk of complications such as renal hypertension and chronic kidney disease.
7. Complications: Chronic pyelonephritis can lead to various complications, including renal insufficiency, hypertension, proteinuria, and end-stage renal disease (ESRD). Early recognition and treatment of urinary tract infections, along with management of underlying risk factors, are essential for preventing the progression of chronic pyelonephritis and preserving renal function.

Question 120

Answer 120

Chronic pyelonephritis with nodular yellow-orange lesions:
• xanthogranulomatous pyelonephritis

Xanthogranulomatous pyelonephritis (XGP) is a rare and severe form of chronic pyelonephritis characterized by the replacement of renal parenchyma with lipid-laden macrophages (xanthoma cells) and granulomatous inflammation. The pathophysiological mechanism of XGP involves a complex interplay of infectious, inflammatory, and immunological factors:

1. Urinary tract obstruction: XGP often occurs in the setting of urinary tract obstruction, which can be caused by various factors such as kidney stones, ureteral strictures, renal tumors, or congenital anomalies. Urinary tract obstruction leads to stasis of urine within the renal pelvis and calyces, predisposing the kidney to recurrent bacterial infections.
2. Chronic bacterial infection: XGP is typically associated with recurrent or persistent urinary tract infections, usually caused by bacteria such as Escherichia coli, Proteus mirabilis, or Klebsiella pneumoniae. Bacterial infection triggers an inflammatory response within the renal parenchyma, leading to tissue damage and activation of macrophages and other immune cells.
3. Impaired bacterial clearance: In XGP, the renal parenchyma may become infiltrated with lipid-laden macrophages (foamy histiocytes), which are characteristic of xanthogranulomatous inflammation. These macrophages are unable to effectively clear the infecting bacteria and may contribute to the chronicity of the infection.
4. Granulomatous inflammation: XGP is characterized by the formation of granulomas, which are aggregates of immune cells (macrophages, lymphocytes, and multinucleated giant cells) surrounded by fibrous tissue. Granulomas are a hallmark of chronic inflammation and represent the host’s attempt to contain the infection.
5. Lipid accumulation: Xanthoma cells, which are lipid-laden macrophages, accumulate within the renal parenchyma and give XGP its characteristic yellow-orange appearance. These lipid-laden macrophages are derived from circulating monocytes and are a histological feature of xanthogranulomatous inflammation.
6. Tissue destruction and fibrosis: Chronic inflammation and tissue damage in XGP lead to destruction of renal parenchyma, fibrosis, and distortion of the renal architecture. As the disease progresses, the affected kidney may become enlarged, nodular, and nonfunctional.
7. Clinical manifestations: Patients with XGP may present with symptoms similar to those of chronic pyelonephritis, including fever, flank pain, hematuria, and recurrent urinary tract infections. In severe cases, complications such as renal abscess formation, perinephric abscess, or sepsis may occur.

Overall, the pathophysiological mechanism of XGP involves chronic bacterial infection, granulomatous inflammation, lipid accumulation, tissue destruction, and fibrosis within the renal parenchyma. Early recognition and treatment of urinary tract obstruction and infection are essential for preventing the progression of XGP and preserving renal function.

Question 121

Answer 121

Normal size or reduced weights; fine, even granular surfaces, cortical
narrowing:
• benign nephrosclerosis due to hypertension
• diabetic nephropathy

Diabetic nephropathy is a progressive kidney disease that occurs as a complication of diabetes mellitus, primarily affecting individuals with type 1 and type 2 diabetes. The pathophysiological mechanism of diabetic nephropathy involves a complex interplay of metabolic, hemodynamic, inflammatory, and fibrotic processes:

1. Hyperglycemia: Chronic hyperglycemia, a hallmark feature of diabetes mellitus, plays a central role in the development and progression of diabetic nephropathy. Elevated blood glucose levels lead to various metabolic derangements, including increased production of advanced glycation end products (AGEs), activation of protein kinase C (PKC) pathways, and overproduction of reactive oxygen species (ROS).
2. Renal hemodynamic changes: Hyperglycemia and dysregulation of the renin-angiotensin-aldosterone system (RAAS) lead to alterations in renal hemodynamics, including glomerular hyperfiltration and increased intraglomerular pressure. Glomerular hyperfiltration contributes to increased filtration of proteins and solutes, placing additional strain on the renal filtration barrier.
3. Glomerular injury: Prolonged exposure to hyperglycemia and hemodynamic stress leads to structural and functional changes within the glomeruli. These changes include thickening of the glomerular basement membrane, mesangial expansion, podocyte injury, and glomerulosclerosis (scarring of the glomeruli). Glomerular injury disrupts the filtration function of the kidneys and leads to proteinuria (excretion of protein in the urine).
4. Tubulointerstitial injury: Diabetic nephropathy is characterized by tubulointerstitial inflammation and fibrosis, which contribute to progressive renal dysfunction. Inflammatory mediators, such as cytokines and chemokines, are released in response to glomerular injury and contribute to tubular cell injury, apoptosis, and interstitial fibrosis.
5. Renal fibrosis: Activation of fibrotic pathways, including transforming growth factor-beta (TGF-β) signaling, leads to the accumulation of extracellular matrix proteins (collagen, fibronectin) in the renal interstitium. Renal fibrosis disrupts the normal architecture of the kidney, impairs tubular function, and contributes to the progression of chronic kidney disease (CKD) and end-stage renal disease (ESRD).
6. Inflammatory and immune responses: In addition to local inflammation within the kidney, systemic inflammatory and immune responses may also contribute to the pathogenesis of diabetic nephropathy. Chronic low-grade inflammation, endothelial dysfunction, and activation of immune cells (macrophages, T cells) have been implicated in the progression of renal injury.

Overall, the pathophysiological mechanism of diabetic nephropathy involves a multifactorial interplay of metabolic, hemodynamic, inflammatory, and fibrotic processes. Early detection and aggressive management of diabetes, along with interventions targeting modifiable risk factors, are essential for preventing the progression of diabetic nephropathy and reducing the burden of chronic kidney disease.

Question 122

Answer 122

Small petechial-type hemorrhages on cortical surface (“flea-bitten”):
• malignant nephrosclerosis

Malignant nephrosclerosis is a severe and rapidly progressive form of hypertensive nephropathy characterized by severe hypertension, renal dysfunction, and histological changes in the kidney. The pathomechanism of malignant nephrosclerosis involves a cascade of events resulting from uncontrolled hypertension and its effects on the renal vasculature and parenchyma:

1. Severe hypertension: Malignant nephrosclerosis typically occurs in individuals with severe and poorly controlled hypertension, often with systolic blood pressure exceeding 180 mmHg and diastolic blood pressure exceeding 120 mmHg. Chronic hypertension leads to sustained elevation in systemic blood pressure, causing damage to blood vessels and organs throughout the body, including the kidneys.
2. Renal vascular changes: Chronic hypertension leads to structural changes in the renal vasculature, including arteriolar sclerosis, hyalinosis (thickening of arteriolar walls), and fibrinoid necrosis (deposition of fibrin within vessel walls). These changes result in narrowing and occlusion of small renal arterioles, impairing renal blood flow and causing ischemia in the renal parenchyma.
3. Renal ischemia: The narrowing and occlusion of renal arterioles reduce blood flow to the renal parenchyma, leading to renal ischemia and hypoxia. Ischemia-induced tissue injury triggers a cascade of cellular and molecular events, including inflammation, oxidative stress, and activation of the renin-angiotensin-aldosterone system (RAAS).
4. Activation of the renin-angiotensin-aldosterone system (RAAS): Renal ischemia stimulates the release of renin from the juxtaglomerular cells of the kidney, initiating the RAAS cascade. Renin converts angiotensinogen to angiotensin I, which is subsequently converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that further narrows renal arterioles, exacerbating renal ischemia.
5. Endothelial dysfunction: Chronic hypertension and renal ischemia lead to endothelial dysfunction, characterized by impaired vasodilation, increased vascular permeability, and pro-inflammatory and pro-thrombotic responses. Endothelial dysfunction contributes to the progression of renal injury and exacerbates hypertension by disrupting normal vascular homeostasis.
6. Renal injury and fibrosis: Prolonged hypertension and renal ischemia result in progressive injury to the renal parenchyma, characterized by tubular atrophy, interstitial fibrosis, and glomerulosclerosis. Fibrotic changes disrupt the normal architecture and function of the kidney, leading to irreversible renal dysfunction and decline in renal function.
7. Clinical manifestations: Patients with malignant nephrosclerosis may present with symptoms such as severe hypertension, headache, visual disturbances, nausea, vomiting, and signs of end-organ damage, including hypertensive retinopathy, encephalopathy, and congestive heart failure.

Overall, the pathomechanism of malignant nephrosclerosis involves a complex interplay of hypertension-induced vascular changes, renal ischemia, activation of the RAAS, endothelial dysfunction, and progressive renal injury and fibrosis. Early recognition and aggressive management of hypertension are essential for preventing the development and progression of malignant nephrosclerosis and reducing the risk of end-stage renal disease.

Question 123

Answer 123

Wedge-shaped, sharply demarcated pale yellow-white areas with hyperemic
borders:
• acute infarcts

Acute infarction of the kidney, also known as renal infarction, occurs when blood flow to a portion of the kidney is abruptly interrupted, leading to tissue ischemia and necrosis. Several underlying causes can result in acute infarction of the kidney:

1. Renal artery thrombosis: Formation of a blood clot (thrombus) within one or more branches of the renal artery can lead to acute renal artery thrombosis and subsequent infarction of the affected renal parenchyma. Renal artery thrombosis may occur spontaneously or as a complication of conditions such as atherosclerosis, vasculitis, or hypercoagulable disorders.
2. Renal artery embolism: Embolization of a blood clot or other material (e.g., cholesterol plaque, tumor fragments) from a distant site can result in acute renal artery embolism and subsequent infarction of the affected renal territory. Common sources of emboli include cardiac sources (e.g., atrial fibrillation, endocarditis), large artery atherosclerosis, or iatrogenic causes (e.g., vascular catheterization).
3. Renal artery dissection: Dissection of the renal artery, often secondary to trauma or spontaneous vascular pathology (e.g., fibromuscular dysplasia), can lead to acute renal artery dissection and compromise renal blood flow. Dissection may result in the formation of intramural hematomas or intimal tears, leading to ischemia and infarction of the affected renal tissue.
4. Renal vein thrombosis: Thrombosis of the renal vein, either in isolation or as an extension of inferior vena cava (IVC) thrombosis, can lead to acute renal vein thrombosis and subsequent renal infarction. Renal vein thrombosis may occur in the setting of hypercoagulable states, nephrotic syndrome, malignancy, or IVC obstruction.
5. Systemic vasculitis: Inflammatory conditions affecting the renal vasculature, such as polyarteritis nodosa, systemic lupus erythematosus (SLE), or antiphospholipid syndrome, can lead to acute vasculitis and compromise renal blood flow, resulting in renal infarction.
6. External compression: External compression of the renal artery or vein by adjacent structures, such as tumors, lymphadenopathy, or retroperitoneal fibrosis, can lead to vascular compromise and renal infarction.
7. Trauma: Blunt or penetrating trauma to the kidney or adjacent structures can result in disruption of the renal vasculature, leading to acute renal infarction.

Overall, acute infarction of the kidney can result from a variety of underlying causes, including vascular thrombosis, embolism, dissection, vasculitis, compression, and trauma. Prompt recognition and management of the underlying cause are essential for preserving renal function and preventing

Question 124

Answer 124

Wedge-shaped depressions with underlying pale gray-white scars:
• remote infarcts

Remote infarcts in the kidney refer to areas of ischemic tissue damage that occur in regions of the kidney distant from the site of vascular occlusion or injury. The pathomechanism of remote infarcts in the kidney involves several potential contributing factors:

1. Collateral circulation: The kidneys have an extensive network of collateral blood vessels that can provide alternative routes for blood flow in the event of partial occlusion or thrombosis of the main renal arteries. However, if the collateral circulation is insufficient to compensate for the loss of blood supply, remote areas of the kidney may become ischemic and vulnerable to infarction.
2. Microvascular dysfunction: In addition to large vessels such as the renal arteries and veins, the kidneys are supplied by a network of smaller blood vessels, including arterioles, capillaries, and venules. Dysfunction of the microvasculature, such as impaired autoregulation, endothelial dysfunction, or microvascular thrombosis, can disrupt blood flow to remote areas of the kidney and predispose them to ischemic injury.
3. Hemodynamic changes: Conditions that affect systemic blood pressure or renal blood flow dynamics can influence the distribution of blood within the kidney and increase the risk of remote infarcts. For example, conditions such as hypertension, hypotension, or renal artery stenosis can alter renal perfusion pressure and contribute to ischemia in vulnerable areas of the kidney.
4. Embolic phenomena: Embolization of thrombi, atheromatous plaques, or other material from distant sites can result in acute arterial occlusion and infarction in remote areas of the kidney. Emboli may originate from cardiac sources (e.g., atrial fibrillation, endocarditis), large artery atherosclerosis, or other systemic sources (e.g., septic emboli).
5. Vascular compression: Compression of the renal vasculature by adjacent structures, such as tumors, cysts, or fibrotic tissue, can compromise blood flow to specific regions of the kidney and predispose them to ischemic injury. Vascular compression may lead to localized infarction or contribute to the development of remote infarcts over time.
6. Vascular dysplasia: Structural abnormalities or developmental defects in the renal vasculature, such as fibromuscular dysplasia or arteriovenous malformations, can disrupt normal blood flow patterns and increase the risk of ischemic injury in remote areas of the kidney.

Overall, the pathomechanism of remote infarcts in the kidney involves a combination of factors that disrupt renal blood flow and predispose vulnerable regions of the kidney to ischemic injury. Identifying and addressing underlying vascular abnormalities or systemic conditions that contribute to renal ischemia are essential for preventing remote infarcts and preserving renal function.

Question 125

Answer 125

Diffuse, pale, ischemic necrosis limited to the cortex:
• diffuse cortical necrosis

Diffuse cortical necrosis (DCN) is a rare but severe condition characterized by widespread ischemic necrosis of the renal cortex, leading to acute kidney injury (AKI) and often resulting in irreversible loss of renal function. The pathomechanism of diffuse cortical necrosis involves a cascade of events that disrupt renal blood flow and lead to extensive tissue ischemia and necrosis:

1. Severe hypoperfusion: The primary cause of diffuse cortical necrosis is severe and prolonged hypoperfusion of the kidneys, leading to global ischemia of the renal cortex. Hypoperfusion can result from various underlying conditions, including severe hypotension, shock (e.g., septic shock, hemorrhagic shock), disseminated intravascular coagulation (DIC), placental abruption, or obstetric complications (e.g., abruptio placentae, severe preeclampsia/eclampsia).
2. Vascular endothelial injury: Severe hypoperfusion and ischemia cause endothelial injury and dysfunction, leading to disruption of the vascular endothelial barrier and impaired regulation of vascular tone. Endothelial injury results in increased vascular permeability, microvascular thrombosis, and activation of coagulation cascades.
3. Microvascular thrombosis: Endothelial injury and activation of coagulation pathways result in the formation of microthrombi within the renal microvasculature, leading to occlusion of small arteries, arterioles, and capillaries. Microvascular thrombosis further exacerbates tissue ischemia and compromises renal blood flow, contributing to the development of diffuse cortical necrosis.
4. Systemic inflammation: Inflammatory mediators released in response to tissue ischemia and endothelial injury contribute to the systemic inflammatory response syndrome (SIRS), further exacerbating vascular dysfunction and tissue injury. Systemic inflammation amplifies the coagulation cascade, promotes microvascular thrombosis, and exacerbates tissue ischemia and necrosis.
5. Activation of renin-angiotensin-aldosterone system (RAAS): Reduced renal perfusion pressure and ischemia activate the renin-angiotensin-aldosterone system (RAAS), leading to vasoconstriction of renal arterioles and redistribution of blood flow away from the renal cortex. Activation of RAAS contributes to renal hypoperfusion and exacerbates tissue ischemia in diffuse cortical necrosis.
6. Acute kidney injury (AKI): The extensive ischemic necrosis of the renal cortex results in acute kidney injury (AKI), characterized by a rapid decline in renal function and oliguria/anuria. AKI may progress to irreversible renal failure if the underlying cause of diffuse cortical necrosis is not promptly identified and treated.

Overall, the pathomechanism of diffuse cortical necrosis involves a complex interplay of severe hypoperfusion, endothelial injury, microvascular thrombosis, systemic inflammation, and activation of vasoactive pathways. Early recognition and management of conditions predisposing to diffuse cortical necrosis are essential for preventing irreversible renal injury and preserving renal function.

Question 126

Papillary adenoma

Answer 126

Small (typically <5mm), pale gray-yellow, encapsulated nodule

Papillary adenomas are benign tumors that typically arise from the epithelial cells lining the renal tubules in the renal cortex. The pathophysiological mechanism underlying the development of papillary adenomas is not fully understood, but several factors may contribute to their formation:

1. Genetic factors: Genetic mutations or alterations in oncogenes or tumor suppressor genes may predispose individuals to the development of papillary adenomas. For example, mutations in the MET oncogene, which encodes the receptor tyrosine kinase MET, have been implicated in the pathogenesis of papillary renal tumors, including papillary adenomas.
2. Chronic kidney disease: Chronic kidney disease (CKD) or long-standing renal injury may create a microenvironment conducive to the development of papillary adenomas. The regenerative response of renal tubular epithelial cells to injury may become dysregulated, leading to the formation of benign proliferative lesions such as papillary adenomas.
3. Von Hippel-Lindau (VHL) disease: VHL disease is a hereditary cancer syndrome characterized by the development of multiple benign and malignant tumors, including renal cell carcinomas (RCCs) and renal cysts. Individuals with VHL disease have an increased risk of developing papillary adenomas, particularly in association with renal cysts.
4. Chronic inflammation: Chronic inflammation within the renal parenchyma, such as that seen in conditions like chronic pyelonephritis or interstitial nephritis, may promote cellular proliferation and the development of papillary adenomas. Inflammatory mediators released during the inflammatory response may stimulate epithelial cell growth and tumor formation.
5. Hormonal factors: Hormonal imbalances or disturbances may influence the growth and development of papillary adenomas. For example, estrogen and androgen receptors are expressed in renal tubular epithelial cells, and hormonal stimulation may promote cell proliferation and tumorigenesis.
6. Environmental factors: Exposure to certain environmental toxins, carcinogens, or nephrotoxic agents may increase the risk of papillary adenoma formation. However, specific environmental factors associated with the development of papillary adenomas have not been clearly identified.

Overall, the pathophysiological mechanism underlying the development of papillary adenomas is likely multifactorial, involving a combination of genetic, environmental, hormonal, and inflammatory factors. Further research is needed to fully elucidate the molecular pathways involved in papillary adenoma formation and progression.

Question 127

renal fibroma

Answer 127

Small (typically <1cm), firm, gray-white lesions in pyramids

Renal fibromas are rare benign tumors composed predominantly of fibrous tissue and are typically found incidentally during imaging studies or surgical procedures. The exact pathophysiological mechanism underlying the development of renal fibromas is not well understood, but several factors may contribute:

1. Genetic predisposition: While the specific genetic factors contributing to renal fibroma development are not well characterized, genetic predisposition may play a role. Certain hereditary syndromes, such as Birt-Hogg-Dubé syndrome, von Hippel-Lindau disease, or tuberous sclerosis complex, are associated with an increased risk of developing renal tumors, including fibromas.
2. Mesenchymal origin: Renal fibromas are thought to arise from the mesenchymal cells within the renal parenchyma, which have the potential to differentiate into fibrous tissue. The exact triggers or stimuli that initiate the proliferation and differentiation of mesenchymal cells into fibromas are not fully understood.
3. Chronic inflammation: Chronic inflammatory conditions within the kidney, such as chronic pyelonephritis or interstitial nephritis, may contribute to the development of renal fibromas. Inflammatory mediators released during the inflammatory response may stimulate the proliferation of fibroblasts and the deposition of fibrous tissue within the renal parenchyma.
4. Hormonal factors: Hormonal imbalances or disturbances may influence the growth and development of renal fibromas. For example, estrogen and androgen receptors are expressed in renal cells, and hormonal stimulation may promote cell proliferation and fibrosis. However, the specific hormonal factors involved in renal fibroma pathogenesis have not been well characterized.
5. Fibrosis: Renal fibromas are characterized by the proliferation of fibroblasts and the deposition of collagen and other extracellular matrix components. Dysregulation of fibrogenic pathways or aberrant wound healing processes within the kidney may lead to the formation of fibromas.
6. Unknown factors: Other unknown factors, such as environmental exposures, toxins, or epigenetic changes, may also contribute to the development of renal fibromas. However, further research is needed to elucidate the specific mechanisms involved.

Overall, the pathophysiological mechanism underlying the development of renal fibromas is likely multifactorial, involving a combination of genetic, environmental, inflammatory, hormonal, and fibrotic factors. Further studies are needed to better understand the molecular pathways involved in renal fibroma pathogenesis.

Question 128

Answer 128

Spherical masses, yellow to gray-white, with foci of hemorrhage, softening,
and discoloration:
• renal cell carcinoma

Renal cell carcinoma (RCC) is the most common type of kidney cancer in adults, and its pathophysiology involves a complex interplay of genetic, molecular, and environmental factors. Here’s an overview of the key mechanisms involved:

1. Genetic predisposition: Certain hereditary syndromes, such as von Hippel-Lindau (VHL) disease, hereditary papillary renal carcinoma, hereditary leiomyomatosis, and Birt-Hogg-Dubé syndrome, are associated with an increased risk of RCC. Mutations or alterations in tumor suppressor genes (e.g., VHL gene), oncogenes (e.g., MET, c-MET), and other genes involved in cell cycle regulation, apoptosis, and angiogenesis play a crucial role in the development of RCC.
2. Loss of VHL function: The VHL gene, located on chromosome 3p25, is a tumor suppressor gene that regulates the degradation of hypoxia-inducible factors (HIFs). Loss of function mutations or inactivation of the VHL gene leads to the stabilization of HIFs, which in turn promotes the transcription of genes involved in angiogenesis (e.g., vascular endothelial growth factor, VEGF) and cell proliferation, contributing to tumor growth and progression.
3. Angiogenesis: RCC tumors are highly vascularized due to the upregulation of angiogenic factors such as VEGF, platelet-derived growth factor (PDGF), and fibroblast growth factor (FGF). Increased angiogenesis promotes the formation of new blood vessels, providing oxygen and nutrients to the growing tumor and facilitating tumor growth and metastasis.
4. Immune evasion: RCC tumors have immunosuppressive mechanisms that allow them to evade immune surveillance and clearance. Tumor cells may express programmed death-ligand 1 (PD-L1), which interacts with programmed cell death protein 1 (PD-1) on immune cells, leading to T-cell exhaustion and inhibition of antitumor immune responses. Immune checkpoint inhibitors targeting the PD-1/PD-L1 pathway have shown efficacy in the treatment of RCC.
5. Tumor microenvironment: The tumor microenvironment plays a critical role in RCC progression and metastasis. Stromal cells, immune cells, and extracellular matrix components interact with tumor cells to modulate tumor growth, invasion, and metastasis. Inflammatory mediators, cytokines, and growth factors released within the tumor microenvironment contribute to tumor progression and therapeutic resistance.
6. Metabolic alterations: RCC tumors exhibit metabolic reprogramming to support their rapid growth and proliferation. Increased aerobic glycolysis (the Warburg effect), altered lipid metabolism, and activation of signaling pathways such as the mammalian target of rapamycin (mTOR) pathway contribute to tumor cell survival and proliferation.

Overall, the pathophysiology of RCC is multifactorial and involves a complex interplay of genetic alterations, dysregulated signaling pathways, angiogenesis, immune evasion, and metabolic reprogramming. Understanding these mechanisms is crucial for the development of targeted therapies and personalized treatment strategies for RCC.

Question 129

Bladder normal

Answer 129

The bladder is in its normal anatomical position in the pelvis.

The wall is 2-4 mm
depending on the contraction state.

It is filled with clear urine.

The inner surface is
irregular and grayish-pale, the area of the trigonum is smooth, the inner orifices of the
ureters are symmetric and open.

The urethra is 2-4 mm thick, the lumen is regular, the
inner lining is smooth and pale.

Question 130

Answer 130

Pouchlike eversions of bladder wall:
• diverticula

Bladder diverticula are outpouchings or sac-like protrusions of the bladder wall, and their pathomechanism involves a combination of structural, functional, and obstructive factors:

1. Bladder outlet obstruction: Chronic bladder outlet obstruction, often due to conditions such as benign prostatic hyperplasia (BPH) in males or pelvic organ prolapse in females, can lead to increased bladder pressure during voiding. This elevated pressure within the bladder can cause weak areas of the bladder wall to bulge outward, forming diverticula.
2. Detrusor muscle dysfunction: Dysfunction of the detrusor muscle, which is responsible for bladder contraction during urination, can contribute to the development of bladder diverticula. Conditions such as neurogenic bladder dysfunction, spinal cord injury, or bladder muscle weakness can impair detrusor function and result in abnormal bladder wall compliance and diverticulum formation.
3. Chronic urinary retention: Prolonged urinary retention, whether due to bladder outlet obstruction, neurogenic bladder dysfunction, or other causes, can lead to distension of the bladder wall and weakening of its structural integrity. Chronic urinary retention increases intravesical pressure and may predispose to diverticulum formation.
4. Congenital factors: In some cases, bladder diverticula may be congenital, resulting from developmental abnormalities or defects in the structure of the bladder wall. These congenital diverticula may be associated with conditions such as bladder exstrophy or congenital bladder diverticula syndromes.
5. Chronic inflammation: Chronic inflammation of the bladder wall, such as that seen in recurrent urinary tract infections (UTIs) or bladder stones, can weaken the bladder wall and predispose to diverticulum formation. Inflammatory processes may disrupt the normal architecture of the bladder wall and promote the development of outpouchings.
6. Trauma: Bladder trauma, such as pelvic fractures or iatrogenic injury during bladder surgery, can lead to focal areas of weakness in the bladder wall, which may subsequently develop into diverticula. Traumatic injuries can disrupt the structural integrity of the bladder wall and alter its compliance and function.
7. Aging: Age-related changes in bladder structure and function, including alterations in bladder compliance and detrusor muscle function, may contribute to the development of bladder diverticula. Age-related changes may increase the susceptibility of the bladder wall to structural abnormalities and outpouchings.

Overall, the pathomechanism of bladder diverticula involves a combination of obstructive, functional, congenital, inflammatory, traumatic, and age-related factors that lead to weakening of the bladder wall and the formation of outpouchings or diverticula. Identifying and addressing underlying causes, such as bladder outlet obstruction or detrusor dysfunction, is essential for managing bladder diverticula and preventing complications such as recurrent UTIs or urinary retention.

Question 131

acute cystitis bladder

Answer 131

Mucosal hyperemia and ulcerations, suppurative exudates

Acute cystitis, which is inflammation of the bladder, typically occurs due to bacterial infection, most commonly by uropathogenic Escherichia coli. The pathomechanism involves several key steps:

1. Bacterial adhesion: Uropathogenic bacteria, such as E. coli, adhere to the urothelial cells lining the bladder wall. Adhesion is facilitated by bacterial surface structures called adhesins, which interact with specific receptors on the urothelial cells.
2. Colonization and proliferation: Once adhered to the urothelial cells, bacteria colonize the bladder epithelium and multiply rapidly. Bacterial proliferation leads to an increase in bacterial load within the bladder.
3. Host immune response: The presence of bacteria triggers an inflammatory response in the bladder wall, mediated by immune cells such as neutrophils, macrophages, and T cells. Cytokines and chemokines are released, leading to recruitment of immune cells to the site of infection.
4. Tissue damage: Inflammatory mediators and bacterial toxins contribute to damage of the urothelial cells and underlying tissues. This results in disruption of the bladder epithelium, loss of barrier function, and exposure of underlying tissues to bacterial invasion.
5. Symptoms: The inflammatory response and tissue damage lead to characteristic symptoms of acute cystitis, including dysuria (painful urination), urinary frequency, urgency, suprapubic discomfort, and hematuria (blood in the urine).
6. Bacterial persistence: Despite the host immune response, bacteria may persist within the bladder epithelium or form intracellular bacterial communities (IBCs), which can evade immune detection and antibiotic treatment. Bacterial persistence contributes to recurrent or chronic cystitis.

Overall, the pathomechanism of acute cystitis involves bacterial adhesion, colonization, host immune response, tissue damage, and symptom development. Prompt diagnosis and appropriate antibiotic therapy are essential for resolving acute cystitis and preventing complications such as recurrent infections or ascending urinary tract infections.

Question 132

chronic cystitis

Answer 132

Red, friable, granular, sometimes ulcerated epithelium

Chronic cystitis, characterized by persistent inflammation of the bladder lasting for more than six weeks, can have various underlying causes and pathomechanisms. Here’s an overview:

1. Recurrent or persistent bacterial infection: Chronic cystitis may result from recurrent or persistent bacterial infections of the bladder. Bacteria, typically uropathogenic Escherichia coli, can adhere to the bladder epithelium, evade host immune responses, and form bacterial reservoirs within the bladder wall or urothelial cells. Chronic bacterial colonization leads to ongoing inflammation and tissue damage.
2. Interstitial cystitis/bladder pain syndrome (IC/BPS): IC/BPS is a chronic inflammatory condition of the bladder characterized by pelvic pain, urinary urgency, frequency, and nocturia. The exact pathophysiology of IC/BPS is not fully understood but likely involves a complex interplay of neurogenic, immunologic, and inflammatory mechanisms. Dysfunctional bladder epithelial barrier, increased permeability, mast cell activation, neurogenic inflammation, and autoimmune processes are thought to contribute to the chronic inflammatory state in IC/BPS.
3. Chemical irritants: Chronic exposure to certain chemical irritants, such as chemicals in perfumes, douches, soaps, or spermicides, can irritate the bladder mucosa and lead to chronic inflammation. Occupational exposures to chemicals or radiation therapy to the pelvic area can also predispose individuals to chronic cystitis.
4. Bladder outlet obstruction: Chronic cystitis may develop secondary to bladder outlet obstruction, such as benign prostatic hyperplasia (BPH) in males or pelvic organ prolapse in females. Bladder outlet obstruction leads to incomplete bladder emptying, urinary stasis, and increased susceptibility to bacterial colonization and chronic inflammation.
5. Neurogenic bladder dysfunction: Neurological conditions affecting bladder function, such as spinal cord injury, multiple sclerosis, or diabetic neuropathy, can lead to neurogenic bladder dysfunction and predispose individuals to chronic cystitis. Dysfunction of bladder innervation and impaired bladder emptying contribute to urinary stasis, bacterial overgrowth, and chronic inflammation.
6. Radiation cystitis: Chronic cystitis may occur as a late complication of pelvic radiation therapy for malignancies such as bladder cancer, prostate cancer, or gynecological cancers. Radiation-induced damage to the bladder epithelium, blood vessels, and connective tissue can lead to chronic inflammation, fibrosis, and vascular changes.
7. Chronic inflammatory conditions: Systemic inflammatory conditions such as lupus erythematosus, Crohn’s disease, or chronic granulomatous infections can involve the bladder and lead to chronic cystitis. Immune-mediated mechanisms, autoimmune reactions, or chronic inflammatory responses contribute to the pathogenesis of cystitis in these conditions.

Overall, the pathomechanism of chronic cystitis is multifactorial and may involve bacterial infection, chemical irritants, bladder outlet obstruction, neurogenic dysfunction, radiation therapy, or underlying inflammatory conditions. Management of chronic cystitis involves identifying and addressing the underlying cause, along with symptomatic treatment to alleviate inflammation and bladder symptoms.

Question 133

Answer 133

Cystitis with soft, yellow, flat mucosal plaques:
• cystitis with malacoplakia

Malacoplakia is a rare inflammatory condition characterized by the presence of distinctive lesions composed of macrophages with basophilic granular cytoplasm (called von Hansemann cells), calcification, and fibrosis. The pathomechanism of malacoplakia involves an impaired immune response, usually in the setting of chronic bacterial infection, typically by gram-negative bacteria such as Escherichia coli. Here’s a breakdown of the key factors involved:

1. Impaired macrophage function: Malacoplakia is primarily a disorder of macrophage function. Macrophages play a crucial role in the innate immune response, particularly in phagocytosis and intracellular killing of bacteria. In malacoplakia, there is impaired macrophage function, leading to defective phagocytosis and incomplete bacterial clearance.
2. Bacterial infection: The pathogenesis of malacoplakia is closely associated with chronic bacterial infection, most commonly by gram-negative bacteria such as Escherichia coli. These bacteria are phagocytosed by macrophages but are not efficiently destroyed due to impaired macrophage function. Instead, they persist within the macrophages, leading to the formation of intracellular bacterial colonies.
3. Defective lysosomal function: Within macrophages, bacteria are typically targeted to lysosomes for degradation. In malacoplakia, there is impaired fusion of lysosomes with phagosomes containing bacteria, leading to the formation of basophilic granules known as Michaelis-Gutmann bodies. These bodies represent undigested bacterial products within macrophages.
4. Chronic inflammation: The presence of persistent bacterial antigens and defective immune responses leads to chronic inflammation within affected tissues. Chronic inflammation further impairs macrophage function and perpetuates the cycle of defective bacterial clearance and tissue damage.
5. Formation of malacoplakia lesions: Over time, chronic inflammation, macrophage dysfunction, and persistent bacterial infection lead to the formation of malacoplakia lesions. These lesions typically consist of aggregates of von Hansemann cells, which are enlarged macrophages containing basophilic granules representing undigested bacteria. Additionally, there may be associated calcification and fibrosis within the lesions.
6. Predisposing factors: Certain predisposing factors may increase the risk of malacoplakia, including immunosuppression (e.g., HIV/AIDS, organ transplantation, corticosteroid therapy), chronic infections (e.g., urinary tract infections, tuberculosis), and conditions associated with impaired macrophage function (e.g., diabetes mellitus, autoimmune diseases).

Overall, the pathomechanism of malacoplakia involves impaired macrophage function, defective bacterial clearance, chronic inflammation, and the formation of characteristic lesions containing von Hansemann cells, calcification, and fibrosis. Treatment typically involves antibiotics to target the underlying bacterial infection and sometimes surgical excision of symptomatic lesions.

Malakoplakia is a rare chronic inflammatory condition characterized by the formation of distinctive lesions typically found in the urogenital tract, although they can occur in other organs as well. These lesions are composed of macrophages with characteristic basophilic granules known as Michaelis-Gutmann bodies. Malakoplakia is often associated with chronic bacterial infection, particularly by gram-negative bacteria such as Escherichia coli, and is considered a disorder of macrophage function. The condition is named from the Greek words “malakos” meaning soft, and “plakos” meaning plaque, due to the soft, plaque-like appearance of the lesions.

Question 134

urethral obstruction

Answer 134

Thickening of bladder wall, enlargement of individual muscle bundles into
trabeculations, crypts, diverticula

Urethral obstruction refers to any condition that impedes or obstructs the flow of urine through the urethra, the tube that carries urine from the bladder to the outside of the body. Various factors can lead to urethral obstruction, including:

1. Benign prostatic hyperplasia (BPH): BPH is a common condition in older men characterized by non-cancerous enlargement of the prostate gland. As the prostate gland enlarges, it can compress the urethra, leading to partial or complete obstruction of urine flow.
2. Urethral strictures: Urethral strictures are narrowings or constrictions of the urethra, often resulting from scar tissue formation due to inflammation, trauma, infection, or prior urethral instrumentation (e.g., catheterization, urethral surgery). Urethral strictures can obstruct urine flow and cause symptoms such as difficulty urinating, weak urinary stream, and urinary retention.
3. Urethral stones: Urethral stones, also known as urethrolithiasis, are mineral deposits that form within the urethra. These stones can obstruct urine flow and cause symptoms such as pain during urination, urinary frequency, urgency, and hematuria (blood in the urine).
4. Urethral tumors: Tumors of the urethra, including benign and malignant growths, can obstruct urine flow if they grow large enough to block the lumen of the urethra. Urethral tumors are relatively rare but can cause symptoms such as urinary obstruction, hematuria, and pelvic pain.
5. Urethral diverticula: Urethral diverticula are outpouchings or sac-like protrusions of the urethral wall. These diverticula can obstruct urine flow and cause symptoms such as difficulty urinating, urinary frequency, urgency, and recurrent urinary tract infections.
6. External compression: External compression of the urethra by adjacent structures, such as pelvic tumors, pelvic organ prolapse, or pregnancy, can lead to urethral obstruction. External compression can cause symptoms such as difficulty urinating, urinary hesitancy, and incomplete bladder emptying.
7. Neurogenic bladder dysfunction: Neurological conditions affecting bladder function, such as spinal cord injury, multiple sclerosis, or diabetic neuropathy, can lead to neurogenic bladder dysfunction and impaired bladder emptying. Neurogenic bladder dysfunction can result in urinary retention and urethral obstruction.
8. Congenital anomalies: Rare congenital anomalies of the urethra, such as urethral valves or urethral atresia, can lead to urethral obstruction in infants and children.

Overall, urethral obstruction can result from a variety of causes, including anatomical, structural, inflammatory, infectious, neoplastic, and neurological factors. Prompt diagnosis and appropriate management are essential to relieve the obstruction, alleviate symptoms, and prevent complications such as urinary tract infections, urinary retention, and kidney damage.

Question 135

transitional cell carcinoma

Answer 135

Papillary, flat, nodular or mixed-pattern tumor:
• transitional cell carcinoma

Transitional cell carcinoma (TCC), also known as urothelial carcinoma, is the most common type of bladder cancer and can also affect the renal pelvis, ureters, and urethra. The pathomechanism of TCC involves a complex interplay of genetic, environmental, and molecular factors. Here’s an overview:

1. Genetic predisposition: Genetic factors play a significant role in the development of TCC. Individuals with a family history of bladder cancer have an increased risk of developing the disease. Mutations or alterations in tumor suppressor genes (e.g., TP53, RB1), oncogenes (e.g., HRAS, FGFR3), and DNA repair genes (e.g., ERCC2) are commonly associated with TCC development.
2. Exposure to carcinogens: Environmental and occupational exposures to carcinogens are major risk factors for TCC. The most well-established carcinogen associated with bladder cancer is cigarette smoking, which contains aromatic amines and polycyclic aromatic hydrocarbons that can be metabolized and excreted in the urine, leading to direct contact with the urothelial lining of the bladder. Other occupational exposures to chemicals such as aromatic amines, arsenic, benzidine, and certain industrial chemicals have also been linked to an increased risk of TCC.
3. Chronic inflammation: Chronic inflammation of the bladder, often due to recurrent urinary tract infections (UTIs), bladder stones, or long-term indwelling catheters, can contribute to the development of TCC. Inflammatory mediators released during chronic inflammation can promote DNA damage, cellular proliferation, and genetic alterations, predisposing to carcinogenesis.
4. Schistosomiasis infection: In regions where schistosomiasis is endemic, chronic infection with Schistosoma haematobium, a parasitic flatworm, can lead to chronic inflammation and squamous metaplasia of the bladder epithelium, increasing the risk of TCC development.
5. DNA damage and genomic instability: Carcinogenesis in TCC involves the accumulation of genetic and epigenetic alterations that disrupt normal cellular processes, leading to uncontrolled proliferation, survival, and invasion of malignant urothelial cells. These alterations include chromosomal abnormalities, gene mutations, DNA methylation changes, and alterations in signaling pathways involved in cell cycle regulation, apoptosis, and DNA repair.
6. Activation of oncogenic pathways: Dysregulation of signaling pathways such as the Ras-MAPK pathway, phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR pathway, and fibroblast growth factor receptor (FGFR) pathway has been implicated in TCC pathogenesis. Activation of these oncogenic pathways promotes cell proliferation, survival, angiogenesis, and metastasis in TCC cells.

Overall, the pathomechanism of transitional cell carcinoma involves a complex interplay of genetic susceptibility, environmental exposures, chronic inflammation, DNA damage, genomic instability, and dysregulation of oncogenic signaling pathways. Understanding these mechanisms is essential for the development of targeted therapies and personalized treatment approaches for TCC.

Question 136

Prostate normal

Answer 136

It has regular shape, and usual size with 23 g weight. The consistency is moderately firm,
the color is pale gray.

The glandular pattern is preserved

Question 137

Acute prostatitis

Answer 137

Soft, spongy gland enlargement, small or coalescing abscesses:
• acute prostatitis

Acute prostatitis is a bacterial infection of the prostate gland, typically caused by gram-negative bacteria such as Escherichia coli, Klebsiella pneumoniae, or Proteus mirabilis. The pathomechanism of acute prostatitis involves several key steps:

1. Bacterial entry: Bacteria gain entry into the prostate gland via ascending infection from the urethra or bladder. This can occur due to urethral instrumentation (e.g., catheterization), urinary tract procedures, or hematogenous spread from distant sites of infection.
2. Bacterial colonization: Once in the prostate gland, bacteria adhere to the epithelial cells lining the prostatic ducts and acini, where they multiply and establish infection. Bacterial colonization triggers an inflammatory response in the prostate tissue.
3. Inflammatory response: The presence of bacteria in the prostate tissue elicits an inflammatory response, characterized by the recruitment of immune cells such as neutrophils, macrophages, and lymphocytes to the site of infection. Inflammatory mediators such as cytokines, chemokines, and prostaglandins are released, leading to tissue inflammation and damage.
4. Prostatic congestion: Inflammation and edema of the prostate gland lead to congestion of prostatic blood vessels, impairing blood flow and causing further tissue damage. Prostatic congestion contributes to the characteristic symptoms of acute prostatitis, including pelvic pain, dysuria (painful urination), and urinary retention.
5. Clinical manifestations: The inflammatory process in the prostate gland results in symptoms such as fever, chills, malaise, perineal or pelvic pain, dysuria, urinary frequency, urgency, and nocturia. Patients may also experience systemic symptoms such as fatigue, myalgias, and headache.
6. Complications: If left untreated, acute prostatitis can lead to complications such as prostatic abscess formation, urinary retention, septicemia, and urosepsis. Prostatic abscesses may require drainage via transrectal ultrasound-guided aspiration or surgical intervention.

Overall, the pathomechanism of acute prostatitis involves bacterial entry and colonization of the prostate gland, triggering an inflammatory response and leading to prostatic congestion, tissue damage, and characteristic clinical symptoms. Prompt diagnosis and appropriate antibiotic therapy are essential to prevent complications and promote resolution of the infection.

Question 138

nodular hyperplasia

Answer 138

Gland enlargement due to nodules of variable color and consistency, white to
yellow or yellow-pink, and soft to firm depending on amount of fibrous tissue:

Nodular hyperplasia of the prostate, also known as benign prostatic hyperplasia (BPH), is a non-cancerous enlargement of the prostate gland that commonly occurs in aging men. The pathomechanism of BPH involves several key factors:

1. Hormonal changes: The development of BPH is strongly influenced by hormonal changes, particularly the age-related increase in dihydrotestosterone (DHT) levels. DHT is a potent androgen that stimulates the growth and proliferation of prostate cells. As men age, there is a gradual increase in the conversion of testosterone to DHT within the prostate gland, leading to prostatic hyperplasia.
2. Androgen receptor activation: DHT binds to androgen receptors located on prostate epithelial cells, leading to the activation of intracellular signaling pathways that promote cell proliferation and survival. The androgen receptor signaling pathway plays a central role in the development and progression of BPH.
3. Stromal-epithelial interactions: BPH is characterized by the proliferation of both epithelial and stromal cells within the prostate gland. Stromal-epithelial interactions, mediated by growth factors, cytokines, and extracellular matrix components, play a crucial role in regulating prostate growth and differentiation. Alterations in these interactions contribute to the development of BPH nodules.
4. Chronic inflammation: Chronic inflammation within the prostate gland has been implicated in the pathogenesis of BPH. Inflammatory mediators released during chronic inflammation, such as cytokines, chemokines, and growth factors, can stimulate prostate cell proliferation and contribute to tissue remodeling and fibrosis.
5. Age-related changes: Aging is the primary risk factor for the development of BPH, with prevalence increasing with advancing age. Age-related changes in prostate structure and function, including alterations in hormone levels, oxidative stress, and cellular senescence, contribute to the pathogenesis of BPH.
6. Genetic and environmental factors: Genetic predisposition and environmental factors may also influence the development of BPH. Family history, ethnicity, obesity, sedentary lifestyle, and dietary factors have been associated with an increased risk of BPH.

Overall, the pathomechanism of nodular hyperplasia of the prostate involves a complex interplay of hormonal, stromal-epithelial, inflammatory, age-related, genetic, and environmental factors. Understanding these mechanisms is important for developing targeted therapies for BPH and improving the management of this common condition in aging men.
• nodular hyperplasia

Question 139

adenocarcinoma of prostate

Answer 139

Single nodule or multifocal areas of gritty, firm yellow or gray-white tissue
arising in peripheral zone, often difficult to distinguish from surrounding
normal prostate:
• adenocarcinoma

Adenocarcinoma is a type of cancer that arises from glandular epithelial cells, which are found in various organs and tissues throughout the body. The pathomechanism of adenocarcinoma involves a series of genetic and molecular changes that lead to uncontrolled growth and proliferation of these cells. Here’s an overview of the key steps involved:

1. Initiation: The initiation of adenocarcinoma typically begins with genetic alterations in normal glandular epithelial cells. These alterations can be caused by various factors, including exposure to carcinogens (such as tobacco smoke, UV radiation, or chemical toxins), viral infections (such as human papillomavirus), or inherited genetic mutations.
2. Tumor suppressor gene inactivation: In the early stages of adenocarcinoma development, mutations or inactivation of tumor suppressor genes, such as TP53, PTEN, or APC, may occur. Tumor suppressor genes normally regulate cell growth and division and prevent the development of cancer. Loss of function mutations in these genes can lead to uncontrolled cell proliferation and tumor formation.
3. Oncogene activation: Concurrent with tumor suppressor gene inactivation, activation of oncogenes may occur. Oncogenes are genes that promote cell growth and division when mutated or overexpressed. Common oncogenes implicated in adenocarcinoma development include KRAS, EGFR, and HER2. Activation of oncogenes can drive aberrant signaling pathways that promote cell proliferation, survival, and tumor growth.
4. Genomic instability: Genetic instability is a hallmark of cancer cells, including adenocarcinoma. Accumulation of additional genetic alterations, such as chromosomal rearrangements, amplifications, and deletions, leads to genomic instability and further drives tumor progression and heterogeneity.
5. Epigenetic changes: Epigenetic alterations, such as DNA methylation, histone modifications, and microRNA dysregulation, play a critical role in regulating gene expression patterns in adenocarcinoma cells. Aberrant epigenetic changes can silence tumor suppressor genes, activate oncogenes, and promote tumor growth and metastasis.
6. Angiogenesis: As the tumor grows, it requires a blood supply to provide oxygen and nutrients and to facilitate metastasis. Angiogenesis, the formation of new blood vessels, is a key step in tumor progression. Adenocarcinomas can secrete angiogenic factors such as vascular endothelial growth factor (VEGF) to promote the formation of new blood vessels from existing vasculature.
7. Invasion and metastasis: In advanced stages, adenocarcinoma cells acquire the ability to invade surrounding tissues and metastasize to distant organs. This process involves various molecular mechanisms, including epithelial-mesenchymal transition (EMT), degradation of extracellular matrix components by matrix metalloproteinases (MMPs), and interactions with the tumor microenvironment.

Overall, the pathomechanism of adenocarcinoma involves a complex interplay of genetic, molecular, epigenetic, and microenvironmental factors that drive the initiation, growth, and progression of the tumor. Understanding these mechanisms is essential for developing targeted therapies and improving outcomes for patients with adenocarcinoma.

Question 140

UTERUS

Answer 140

The uterus is in normal anatomical position.

It has regular shape.

The size of it 3 cm x 6cm x 2.5 cm.

The weight of the uterus is 50 g.

The serosal surface is smooth.

Theectocervix is 2.5 cm in maximum diameter, smooth surfaced, grayish-white.

The cervical channel is 2 cm long, with transparent mucous fluid in it.

The consistency of the myometrium is moderately firm, the thickness of the myometrium
is 1 cm.

The endometrium is less than 1 mm thick. The cavity of the uterus is empty.

Question 141

Uterus cervicitis

Answer 141

Hyperemia, erosions of cervix:
• cervicitis

Cervicitis is an inflammation of the cervix, the lower part of the uterus that connects to the vagina. The pathomechanism of cervicitis involves various infectious and non-infectious factors that contribute to inflammation and irritation of the cervical tissue. Here’s an overview:

1. Infectious agents: Cervicitis is commonly caused by infections with various microorganisms, including bacteria, viruses, fungi, and parasites. The most common infectious agents implicated in cervicitis include:
   
   • Sexually transmitted infections (STIs): Bacterial pathogens such as Chlamydia trachomatis and Neisseria gonorrhoeae are frequent causes of cervicitis, especially in sexually active individuals. Other STIs such as herpes simplex virus (HSV), human papillomavirus (HPV), and Trichomonas vaginalis can also infect the cervix and contribute to inflammation.
   • Non-sexually transmitted infections: Non-sexually transmitted bacterial infections, such as those caused by group B Streptococcus, Mycoplasma genitalium, or Ureaplasma urealyticum, can also lead to cervicitis.
   • Fungal infections: Candida species, which are responsible for vaginal yeast infections, can sometimes cause cervicitis, particularly in women with compromised immune systems.
   • Parasitic infections: Parasites such as Trichomonas vaginalis can infect the cervix and cause inflammation.
2. Sexual activity: Cervicitis is often associated with sexual activity, particularly unprotected intercourse with multiple partners or a new sexual partner. Trauma to the cervix during sexual activity can lead to irritation and inflammation, predisposing to cervicitis.
3. Chemical irritants: Exposure to chemical irritants, such as douches, spermicides, vaginal deodorants, or certain contraceptive methods (e.g., diaphragms, cervical caps), can irritate the cervical mucosa and contribute to cervicitis.
4. Hormonal changes: Fluctuations in hormonal levels, particularly during the menstrual cycle, pregnancy, or menopause, can affect the cervical mucosa and increase susceptibility to inflammation.
5. Allergic reactions: Allergic reactions to latex condoms, lubricants, or other products used during sexual activity can cause cervicitis in some individuals.
6. Autoimmune conditions: In rare cases, autoimmune conditions such as systemic lupus erythematosus (SLE) or Behçet’s disease can affect the cervix and lead to inflammation.
7. Iatrogenic causes: Trauma or injury to the cervix during medical procedures such as cervical biopsies, cervical polypectomies, or childbirth can cause cervicitis.

Overall, the pathomechanism of cervicitis involves a combination of infectious, inflammatory, mechanical, hormonal, and environmental factors that contribute to inflammation and irritation of the cervical tissue. Prompt diagnosis and treatment are essential to alleviate symptoms, prevent complications, and reduce the risk of transmission of sexually transmitted infections.

Question 142

Answer 142

Small, soft, sessile, mucoid polyps:
• endocervical and endometrial polyps

Endocervical and endometrial polyps are benign growths that develop within the cervical canal (endocervical polyps) or the lining of the uterus (endometrial polyps). While the exact pathomechanism of polyp formation is not fully understood, several factors may contribute to their development:

1. Chronic inflammation: Chronic inflammation of the cervical or endometrial epithelium can lead to the formation of polyps. Inflammatory processes may result from infections, hormonal changes, or irritants, which can stimulate abnormal growth and proliferation of cells in the affected tissues.
2. Hormonal factors: Hormonal imbalances, particularly estrogen dominance, are believed to play a role in the development of endometrial polyps. Estrogen stimulates the growth of the endometrial lining, and an imbalance between estrogen and progesterone levels can lead to excessive growth and proliferation of endometrial tissue, predisposing to polyp formation.
3. Endometrial hyperplasia: Endometrial polyps may arise from areas of endometrial hyperplasia, which is characterized by excessive proliferation of the endometrial glands and stroma. Hyperplastic changes can occur in response to hormonal imbalances, chronic inflammation, or other factors, leading to the formation of polypoid structures within the endometrium.
4. Genetic factors: Genetic alterations or mutations in the cells of the cervical or endometrial epithelium may contribute to the development of polyps. While the specific genes involved in polyp formation are not well defined, genetic predisposition may play a role in some cases.
5. Vascular abnormalities: Abnormalities in the blood vessels supplying the cervical or endometrial tissue may contribute to the growth and development of polyps. Vascular malformations or alterations in angiogenic factors may promote angiogenesis and neovascularization within the polyp tissue.
6. Age and reproductive factors: Endometrial polyps are more common in women of reproductive age, particularly those who have had multiple pregnancies or have undergone hormonal therapy. The risk of endometrial polyps also increases with advancing age, possibly due to cumulative hormonal exposures and chronic inflammatory changes.
7. Iatrogenic factors: Trauma or injury to the cervical or endometrial tissue, such as from surgical procedures (e.g., cervical biopsies, curettage) or childbirth, may predispose to the formation of polyps. Mechanical irritation or disruption of the epithelial lining can stimulate abnormal tissue growth and polyp formation.

Overall, the pathomechanism of endocervical and endometrial polyps likely involves a combination of chronic inflammation, hormonal factors, genetic predisposition, vascular abnormalities, and iatrogenic factors. Further research is needed to fully elucidate the underlying mechanisms of polyp formation and to develop targeted strategies for prevention and treatment.

Question 143

Answer 143

Fungating, ulcerating, infiltrating tumors of cervix:
• predominately squamous cell carcinoma

The pathomechanism of squamous cell carcinoma of the cervix, the most common type of cervical cancer, involves a series of steps that lead to the malignant transformation of cervical epithelial cells. Here’s an overview:

1. Human papillomavirus (HPV) infection: The primary risk factor for the development of squamous cell carcinoma of the cervix is persistent infection with high-risk types of HPV, particularly HPV-16 and HPV-18. HPV is a sexually transmitted virus that infects the squamous epithelial cells of the cervix. The virus is transmitted through sexual contact, and persistent infection with high-risk HPV types is necessary for the development of cervical cancer.
2. Viral integration: Following infection with HPV, the viral DNA may integrate into the host cell’s genome. Viral integration disrupts the normal regulation of host cell genes and leads to dysregulation of cell growth, proliferation, and differentiation.
3. Expression of viral oncoproteins: High-risk HPV types encode two oncoproteins, E6 and E7, which play key roles in the pathogenesis of cervical cancer. These viral oncoproteins interfere with the function of tumor suppressor genes and promote the proliferation and survival of infected cells.
   • E6 protein: The E6 protein targets the tumor suppressor protein p53 for degradation, leading to the inhibition of apoptosis (programmed cell death) and allowing the survival of cells with damaged DNA.
   • E7 protein: The E7 protein interacts with and inactivates the retinoblastoma (Rb) protein, leading to the release of E2F transcription factors and promoting cell cycle progression and proliferation.
4. Progression to dysplasia and carcinoma in situ: Persistent infection with high-risk HPV and dysregulation of cellular pathways lead to the development of premalignant lesions, known as cervical intraepithelial neoplasia (CIN) or squamous intraepithelial lesions (SIL). These lesions range from mild dysplasia (CIN1) to severe dysplasia or carcinoma in situ (CIN3). During this stage, the affected epithelial cells undergo progressive genetic and epigenetic changes that drive the transformation to invasive carcinoma.
5. Invasion and metastasis: Invasive squamous cell carcinoma of the cervix develops when dysplastic cells penetrate through the basement membrane and invade the underlying stromal tissue. Once invasive, the carcinoma can spread locally to adjacent tissues, such as the vagina, parametrium, or pelvic sidewall, and metastasize to regional lymph nodes and distant organs.

Overall, the pathomechanism of squamous cell carcinoma of the cervix involves the complex interplay between high-risk HPV infection, viral oncoprotein expression, dysregulation of cellular pathways, and the accumulation of genetic and epigenetic alterations that drive the transformation from normal cervical epithelium to invasive carcinoma. Vaccination against HPV and screening programs for cervical cancer are important strategies for prevention and early detection of this malignancy.

Question 144

Endometrial hemorrhage, nonmenstrual blood in uterine cavity

Answer 144

endometrial hemorrhage due to systemic shock (uterine apoplexy)
• disseminated intravascular coagulation
• coagulopathies

Uterine apoplexy, also known as spontaneous uterine rupture or hemorrhagic infarction of the uterus, is a rare and serious condition characterized by the sudden rupture of the uterine wall and bleeding into the peritoneal cavity. The pathomechanism of uterine apoplexy involves several factors that contribute to the rupture of the uterine tissue:

1. Uterine overdistension: Uterine apoplexy most commonly occurs during pregnancy, particularly in cases of multiple gestation (e.g., twins, triplets) or in women with uterine abnormalities such as uterine fibroids. The uterine wall may become overstretched and weakened due to the excessive size or weight of the fetus(es) or the presence of fibroids, predisposing to rupture.
2. Placental abruption: Placental abruption, the premature separation of the placenta from the uterine wall, can lead to uterine apoplexy. The sudden release of blood into the uterine cavity during placental abruption can cause rapid distension and rupture of the uterine wall.
3. Trauma or injury: Trauma or injury to the abdomen, such as a motor vehicle accident, physical assault, or iatrogenic injury during childbirth (e.g., forceps or vacuum delivery), can cause direct trauma to the uterus and lead to rupture.
4. Uterine pathology: Certain uterine pathologies, such as uterine leiomyomas (fibroids), adenomyosis (endometrial tissue within the uterine muscle), or uterine anomalies (e.g., uterine septum), can weaken the integrity of the uterine wall and increase the risk of rupture.
5. Labor and childbirth: Uterine apoplexy may occur during labor or childbirth, particularly in cases of prolonged or obstructed labor, precipitous labor, or uterine hyperstimulation (e.g., induced or augmented labor with oxytocin). The intense uterine contractions and increased intrauterine pressure during labor can predispose to uterine rupture.
6. Uterine ischemia: Ischemic conditions affecting the uterus, such as uterine artery embolism, acute uterine torsion, or uterine artery rupture, can lead to vascular compromise and necrosis of the uterine tissue, increasing the risk of rupture.
7. Hormonal factors: Hormonal changes associated with pregnancy, childbirth, or hormonal therapies may affect the structural integrity of the uterine wall and predispose to rupture.

Overall, the pathomechanism of uterine apoplexy involves a combination of factors that contribute to the weakening of the uterine wall and the sudden rupture of uterine tissue, leading to hemorrhage into the peritoneal cavity. Uterine apoplexy is a medical emergency that requires prompt diagnosis and intervention to control bleeding, stabilize the patient, and prevent complications such as shock and disseminated intravascular coagulation (DIC).

Question 145

Endometriosis

Answer 145

Red-blue to yellow-brown nodules implanted on serosal surfaces:
• endometriosis; may cause severe scarring

Endometriosis is a chronic condition characterized by the presence of endometrial-like tissue outside the uterus, commonly on pelvic structures such as the ovaries, fallopian tubes, pelvic peritoneum, and bowel. The pathomechanism of endometriosis involves several theories, although the exact cause remains incompletely understood. Here are the key aspects of endometriosis pathophysiology:

1. Retrograde menstruation: The most widely accepted theory is retrograde menstruation, where menstrual blood containing endometrial cells flows backward through the fallopian tubes into the pelvic cavity instead of exiting the body through the cervix. These displaced endometrial cells can implant and grow on pelvic organs and tissues, leading to the formation of endometriotic lesions.
2. Embryonic cell transformation: Another theory suggests that embryonic remnants, such as Müllerian ducts, may undergo transformation into endometrial-like tissue during fetal development. These transformed cells can persist into adulthood and give rise to endometriotic lesions later in life.
3. Lymphatic or vascular dissemination: Endometrial cells may also spread through lymphatic or vascular channels to distant sites in the body, where they implant and proliferate to form endometriotic lesions. This theory proposes that endometriosis can occur in extrapelvic locations, such as the lungs or brain, via hematogenous or lymphatic dissemination.
4. Immune dysfunction: Dysfunction of the immune system may contribute to the development and progression of endometriosis. Abnormalities in immune surveillance and response mechanisms may allow endometrial cells to evade immune recognition and clearance, facilitating their implantation and growth outside the uterus.
5. Genetic and hormonal factors: Genetic predisposition and hormonal factors also play roles in endometriosis pathogenesis. Certain genetic variations may increase susceptibility to endometriosis, while hormonal imbalances, particularly estrogen dominance, can promote the growth and survival of endometriotic lesions.
6. Inflammation and angiogenesis: Endometriotic lesions are characterized by chronic inflammation and increased angiogenesis (formation of new blood vessels). Proinflammatory cytokines and angiogenic factors released by endometriotic lesions promote tissue proliferation, invasion, and the development of a supportive microenvironment for lesion growth.
7. Neurovascular involvement: Endometriotic lesions may infiltrate nerves and blood vessels, causing neuropathic pain and further promoting lesion growth and dissemination.

Overall, endometriosis is a multifactorial condition with complex pathophysiology involving retrograde menstruation, embryonic cell transformation, immune dysfunction, genetic and hormonal factors, inflammation, angiogenesis, and neurovascular involvement. A better understanding of these mechanisms is crucial for the development of targeted therapies and improved management of endometriosis.

Question 146

Answer 146

Enlargement and irregular thickening of uterine wall:
• adenomyosis

Adenomyosis is a condition characterized by the presence of endometrial tissue (the tissue lining the uterus) within the myometrium (the muscular layer of the uterus). The pathomechanism of adenomyosis involves several theories, although the exact cause remains incompletely understood. Here are the key aspects of adenomyosis pathophysiology:

1. Invasion of endometrial tissue: One theory proposes that adenomyosis occurs due to the invasion of endometrial tissue into the myometrium. This invasion may occur through defects or microscopic channels in the endometrial lining, allowing endometrial cells to penetrate into the underlying myometrial tissue.
2. Estrogen-related changes: Estrogen, a female sex hormone, plays a central role in the pathogenesis of adenomyosis. Estrogen promotes the growth and proliferation of endometrial tissue, and women with adenomyosis often exhibit estrogen dominance, characterized by elevated estrogen levels relative to progesterone levels. Estrogen may stimulate the migration and implantation of endometrial cells into the myometrium and contribute to the growth of adenomyotic lesions.
3. Inflammatory and immune factors: Chronic inflammation within the uterus may contribute to the development of adenomyosis. Inflammatory mediators released during menstruation or in response to hormonal fluctuations may disrupt the normal architecture of the endometrium and myometrium, facilitating the invasion of endometrial tissue into the myometrium. Dysfunction of the immune system may also play a role in adenomyosis pathogenesis, allowing aberrant endometrial tissue to evade immune surveillance and establish within the myometrium.
4. Genetic predisposition: Genetic factors may predispose individuals to adenomyosis. Certain genetic variations or mutations may increase susceptibility to adenomyosis by affecting the structure or function of uterine tissues, altering hormone signaling pathways, or modulating immune responses.
5. Hormonal and reproductive factors: Hormonal and reproductive factors, such as parity (number of pregnancies), age at first childbirth, and history of uterine surgeries (e.g., cesarean section, uterine curettage), may influence the risk of adenomyosis. Childbirth and uterine surgeries may disrupt the normal architecture of the uterus and facilitate the implantation of endometrial tissue into the myometrium.
6. Vascular and lymphatic dissemination: Endometrial cells may spread to the myometrium via vascular or lymphatic channels. Disruption of blood vessels or lymphatic vessels during menstruation or uterine procedures may facilitate the dissemination of endometrial tissue into the myometrium.

Overall, adenomyosis is a multifactorial condition with complex pathophysiology involving the invasion of endometrial tissue into the myometrium, estrogen-related changes, inflammation, immune dysregulation, genetic predisposition, and hormonal and reproductive factors. Further research is needed to elucidate the underlying mechanisms of adenomyosis and develop targeted therapies for this common gynecological disorder.

Question 147

Answer 147

Sharply circumscribed, round, firm, gray-white masses that may be
intramural, subserosal, or submucosal:
• leiomyomas

Leiomyomas, also known as uterine fibroids, are benign tumors that arise from the smooth muscle cells of the uterus. The pathophysiological mechanism of leiomyomas involves several interconnected factors:

1. Genetic predisposition: Genetic factors play a significant role in the development of leiomyomas. Certain genetic mutations or alterations are associated with an increased risk of leiomyoma development. For example, mutations in the mediator complex subunit 12 (MED12) gene have been identified in a subset of leiomyomas.
2. Hormonal influences: Hormonal factors, particularly estrogen and progesterone, play a central role in leiomyoma pathogenesis. Estrogen stimulates the growth and proliferation of uterine smooth muscle cells, which contribute to leiomyoma development. Progesterone also influences leiomyoma growth, although its precise role is not fully understood. Estrogen and progesterone receptors are commonly expressed in leiomyomas, indicating their responsiveness to hormonal stimulation.
3. Cellular proliferation and apoptosis imbalance: Leiomyomas are characterized by increased cellular proliferation and decreased apoptosis (programmed cell death). Dysregulation of signaling pathways involved in cell cycle control, apoptosis, and growth factor signaling contributes to the excessive proliferation of smooth muscle cells within leiomyomas.
4. Angiogenesis: Angiogenesis, the formation of new blood vessels, is essential for leiomyoma growth and survival. Leiomyomas are highly vascularized tumors, and angiogenic factors such as vascular endothelial growth factor (VEGF) promote the formation of new blood vessels within leiomyomas, ensuring a constant supply of oxygen and nutrients for tumor growth.
5. Extracellular matrix (ECM) remodeling: Alterations in the ECM, which provides structural support to tissues, contribute to leiomyoma pathogenesis. Leiomyomas exhibit changes in ECM composition, including increased deposition of collagen, fibronectin, and proteoglycans, which contribute to the firm texture of these tumors.
6. Inflammatory mediators: Inflammatory processes and immune dysregulation may also play a role in leiomyoma development and growth. Inflammatory mediators, such as cytokines, chemokines, and growth factors, produced by leiomyoma cells and surrounding stromal cells, contribute to inflammation, fibrosis, and tissue remodeling within leiomyomas.
7. Epigenetic factors: Epigenetic alterations, such as DNA methylation, histone modifications, and microRNA dysregulation, contribute to leiomyoma pathogenesis by regulating gene expression patterns. These epigenetic changes affect various cellular processes, including proliferation, apoptosis, and ECM remodeling, promoting leiomyoma growth and survival.

Overall, the pathophysiological mechanism of leiomyomas involves a complex interplay of genetic, hormonal, cellular, angiogenic, ECM, inflammatory, and epigenetic factors. Understanding these mechanisms is essential for the development of targeted therapies and interventions for leiomyomas.

Question 148

Fallopian tubes

Small, thin-walled fallopian tube cysts containing serous fluid

Answer 148

paratubal cysts

The term “paratubal cysts” refers to fluid-filled cysts that develop adjacent to the fallopian tubes, often arising from remnants of embryonic structures known as the Wolffian or Müllerian ducts. The pathomechanism of paratubal cysts involves several factors:

1. Embryological remnants: During embryonic development, the Wolffian and Müllerian ducts give rise to the male and female reproductive organs, respectively. Paratubal cysts may develop from remnants of these ducts or adjacent structures that fail to regress completely during fetal development.
2. Fluid accumulation: Paratubal cysts form when fluid accumulates within the remnants of embryonic structures, leading to the formation of cystic structures adjacent to the fallopian tubes. The exact mechanism of fluid accumulation is not fully understood but may involve factors such as secretions from nearby epithelial cells, obstruction of tubal fluid flow, or alterations in fluid reabsorption mechanisms.
3. Hormonal influences: Hormonal factors may contribute to the development or enlargement of paratubal cysts. Changes in hormonal levels, particularly estrogen and progesterone, during the menstrual cycle or pregnancy, may affect the growth and stability of cystic structures in the pelvis.
4. Inflammatory processes: Inflammation within the pelvic cavity, such as pelvic inflammatory disease (PID) or previous pelvic surgeries, may predispose to the formation or enlargement of paratubal cysts. Inflammatory mediators released during inflammatory processes may alter the local microenvironment and contribute to cyst development.
5. Genetic predisposition: Genetic factors may play a role in the development of paratubal cysts. Certain genetic variations or mutations may increase susceptibility to cyst formation or affect the regulation of cell proliferation and differentiation within the pelvic structures.
6. Mechanical factors: Mechanical factors, such as pressure from adjacent structures or changes in intra-abdominal pressure, may influence the formation or growth of paratubal cysts. Increased pressure within the pelvic cavity, for example, due to constipation, pregnancy, or obesity, may contribute to cyst development.

Overall, the pathomechanism of paratubal cysts is multifactorial and likely involves a combination of embryological, hormonal, inflammatory, genetic, and mechanical factors. While paratubal cysts are typically benign and asymptomatic, they may occasionally cause symptoms such as pelvic pain, abdominal discomfort, or reproductive complications, necessitating further evaluation and management.

Question 149

Larger, thin-walled fallopian tube cysts near fimbriated end or in the broad
ligament

Answer 149

hydatids of Morgagni

Hydatids of Morgagni, also known as cysts of Morgagni, are small fluid-filled cysts that develop within the remnants of the Müllerian ducts near the fimbriae of the fallopian tubes. The pathomechanism of hydatids of Morgagni involves several factors:

1. Embryonic remnants: During embryonic development, the Müllerian ducts give rise to the female reproductive organs, including the fallopian tubes, uterus, and upper vagina. Hydatids of Morgagni develop from remnants of the Müllerian ducts or adjacent structures that fail to regress completely during fetal development.
2. Cyst formation: The exact mechanism of cyst formation in the remnants of Müllerian ducts is not fully understood. It is believed that fluid accumulates within these embryonic remnants, leading to the formation of cystic structures known as hydatids of Morgagni. The cysts are typically small and lined with epithelial cells.
3. Hormonal influences: Hormonal factors, particularly estrogen and progesterone, may influence the development or growth of hydatids of Morgagni. Changes in hormonal levels during the menstrual cycle or pregnancy may affect the stability or size of cystic structures within the pelvic cavity.
4. Genetic predisposition: Genetic factors may play a role in the development of hydatids of Morgagni. Certain genetic variations or mutations may increase susceptibility to cyst formation or affect the regulation of cell proliferation and differentiation within the Müllerian duct remnants.
5. Inflammatory processes: Inflammation within the pelvic cavity, such as pelvic inflammatory disease (PID) or previous pelvic surgeries, may predispose to the formation or enlargement of cysts of Morgagni. Inflammatory mediators released during inflammatory processes may alter the local microenvironment and contribute to cyst development.
6. Mechanical factors: Mechanical factors, such as pressure from adjacent structures or changes in intra-abdominal pressure, may influence the formation or growth of hydatids of Morgagni. Increased pressure within the pelvic cavity, for example, due to constipation, pregnancy, or obesity, may contribute to cyst development.

Overall, the pathomechanism of hydatids of Morgagni is multifactorial and likely involves a combination of embryological, hormonal, genetic, inflammatory, and mechanical factors. While hydatids of Morgagni are typically benign and asymptomatic, they may occasionally cause symptoms such as pelvic pain or reproductive complications, necessitating further evaluation and management.

Question 150

Ovaries normal

Answer 150

The ovaries have regular shape.

The size of each 2.5 cm in maximum diameter with 5-5
g weight.

The consistency is firm, the color is gray.

On the cut-surface of them there are
some corpora albicantia.

Question 151

Answer 151

Cysts, usually multiple, with gray, glistening lining and containing clear
serous fluid:
• follicular cysts

Follicular cysts are the most common type of ovarian cysts and typically develop during the menstrual cycle when a follicle fails to rupture or release an egg (ovum) during ovulation. The pathomechanism of follicular cysts involves several key steps:

1. Normal ovarian function: During the menstrual cycle, the ovaries undergo a series of hormonal changes under the influence of the hypothalamic-pituitary-ovarian (HPO) axis. Follicle-stimulating hormone (FSH) stimulates the growth and maturation of ovarian follicles, each containing an immature egg (oocyte).
2. Follicle development: In the early phase of the menstrual cycle, multiple follicles begin to develop in the ovaries in response to FSH stimulation. Each follicle contains an oocyte surrounded by granulosa cells. As the menstrual cycle progresses, one dominant follicle typically matures and becomes ready for ovulation.
3. Ovulation: Under the influence of a surge in luteinizing hormone (LH) triggered by the hypothalamus, the dominant follicle undergoes final maturation and rupture (ovulation), releasing the mature egg into the fallopian tube, where it can be fertilized by sperm.
4. Formation of follicular cysts: In some cases, the dominant follicle fails to rupture and release the egg during ovulation. Instead, the follicle continues to grow and accumulate fluid, forming a cystic structure known as a follicular cyst. Factors that may contribute to the failure of follicle rupture include inadequate LH surge, hormonal imbalances, or disturbances in the normal feedback mechanisms of the HPO axis.
5. Hormonal influences: Hormonal imbalances, particularly alterations in FSH and LH levels, may contribute to the development of follicular cysts. Insufficient LH surge or inadequate luteinization of the follicle may prevent the follicle from rupturing and lead to cyst formation. Conversely, conditions associated with excessive FSH stimulation, such as polycystic ovary syndrome (PCOS), may result in the development of multiple follicular cysts.
6. Functional nature: Follicular cysts are considered functional ovarian cysts because they are part of the normal menstrual cycle and typically resolve spontaneously within a few menstrual cycles. They are usually asymptomatic and do not require intervention unless they become large or cause complications such as rupture or torsion.

Overall, the pathomechanism of follicular cysts involves disturbances in the normal process of follicle development and ovulation, resulting in the formation of cystic structures within the ovaries. While most follicular cysts are benign and resolve spontaneously, monitoring and management may be necessary in cases of symptomatic cysts or complications.

Question 152

luteal cysts

Answer 152

Cysts lined by bright yellow luteal tissue

Question 153

Answer 153

Large ovaries with numerous subcortical cysts (0.5 to 1.5cm in diameter):
• polycystic ovaries

Polycystic ovary syndrome (PCOS) is a complex endocrine disorder characterized by hormonal imbalances, irregular menstrual cycles, and the presence of multiple cysts on the ovaries. The exact pathomechanism of PCOS is not fully understood, but it involves several key factors:

1. Hormonal imbalance: One of the central features of PCOS is hormonal dysregulation, including elevated levels of androgens (male hormones such as testosterone) and luteinizing hormone (LH), and decreased levels of follicle-stimulating hormone (FSH). This hormonal imbalance disrupts normal ovarian function and follicular development, leading to the formation of multiple small follicular cysts on the ovaries.
2. Insulin resistance: Many women with PCOS also have insulin resistance, a condition in which the body’s cells become less responsive to the effects of insulin. Insulin resistance leads to compensatory hyperinsulinemia (elevated insulin levels) as the body attempts to overcome the resistance. Insulin resistance and hyperinsulinemia can contribute to the overproduction of androgens by the ovaries and impair the normal maturation and release of eggs (ovulation).
3. Hyperandrogenism: Elevated levels of androgens, such as testosterone, are a hallmark of PCOS. Hyperandrogenism can result from both ovarian and adrenal sources. The ovaries produce excess androgens in response to increased LH stimulation, while the adrenal glands may also contribute to androgen production. Hyperandrogenism contributes to symptoms such as hirsutism (excessive hair growth), acne, and male-pattern baldness.
4. Disordered folliculogenesis: In PCOS, the normal process of follicular development and ovulation is disrupted. Follicles may develop but fail to mature properly or ovulate, leading to the accumulation of small, immature follicles on the ovaries. These follicles form cystic structures that give the ovaries a characteristic appearance on ultrasound.
5. Gonadotropin dysregulation: Dysregulation of gonadotropin hormones, particularly LH and FSH, is observed in PCOS. Elevated LH levels relative to FSH levels (an elevated LH/FSH ratio) are common and may contribute to the excessive production of androgens by the ovaries and disruption of normal ovarian function.
6. Genetic and environmental factors: Genetic predisposition and environmental factors may also contribute to the development of PCOS. Several genetic variants have been associated with an increased risk of PCOS, although the inheritance pattern appears to be complex. Environmental factors such as obesity, unhealthy diet, sedentary lifestyle, and exposure to endocrine-disrupting chemicals may exacerbate the symptoms of PCOS.

Overall, the pathomechanism of PCOS involves a complex interplay of hormonal, metabolic, and genetic factors that disrupt normal ovarian function, follicular development, and hormonal balance. The exact mechanisms underlying PCOS are still the subject of ongoing research, and further studies are needed to fully elucidate the causes and develop targeted treatments for this common endocrine disorder.

Question 154

Cystic masses with variable solid components

Ovaries

Answer 154

serous cystadenoma

serous cystadenocarcinoma
• mucinous cystadenoma
• mucinous cystadenocarcinoma
• endometrioid carcinoma

Question 155

Answer 155

Unilocular cystic tumors containing hair and sebaceous material:
• benign teratomas

Benign teratomas, also known as mature cystic teratomas or dermoid cysts, are germ cell tumors that contain tissues derived from two or three embryonic germ layers: ectoderm, mesoderm, and endoderm. The pathomechanism of benign teratomas involves several key factors:

1. Embryonic origin: Benign teratomas arise from germ cells, which are specialized cells that give rise to the eggs (ova) in females and spermatozoa in males. During embryonic development, germ cells migrate to the gonads (ovaries in females, testes in males) and differentiate into ova or sperm. However, in some cases, germ cells may aberrantly migrate to other sites in the body or fail to differentiate properly, leading to the formation of teratomas.
2. Pluripotency: Germ cells possess pluripotent properties, meaning they have the potential to differentiate into various cell types representing different embryonic germ layers. Benign teratomas reflect this pluripotency and typically contain a diverse array of tissues derived from ectoderm, mesoderm, and endoderm. These tissues may include skin, hair, teeth, bone, cartilage, neural tissue, and glandular structures.
3. Embryonic development anomalies: The exact mechanisms underlying the development of benign teratomas are not fully understood, but it is believed that anomalies during early embryonic development may contribute to their formation. Factors such as abnormal migration of germ cells, failure of germ cells to differentiate properly, or disturbances in the signaling pathways that regulate germ cell development may predispose to teratoma formation.
4. Immature tissue differentiation: In benign teratomas, germ cells may undergo incomplete or aberrant differentiation, leading to the formation of tissues resembling those found in early embryonic stages. This results in the presence of tissues such as hair follicles, sebaceous glands, and sweat glands within the teratoma.
5. Somatic cell contributions: While germ cells are the primary constituents of teratomas, somatic cells may also contribute to their formation. Somatic cells from surrounding tissues or adjacent structures may become incorporated into the growing teratoma, adding to its complexity and diversity of tissues.

Overall, the pathomechanism of benign teratomas involves anomalies in germ cell development and differentiation during embryonic development, resulting in the formation of tumors containing tissues derived from multiple embryonic germ layers. Despite their benign nature, teratomas can grow and cause symptoms due to their size or location, and surgical removal is often necessary for treatment.

Question 156

Immature malignant teratomas

Answer 156

Large solid tumors with necrosis, hemorrhage, hair, grumous material, bone,
cartilage:
• immature malignant teratomas

Immature malignant teratomas are rare and aggressive tumors that contain embryonic-like tissues resembling those found in early stages of fetal development. Unlike benign teratomas, immature malignant teratomas display malignant characteristics, including rapid growth, invasion into surrounding tissues, and the potential to metastasize. The pathomechanism of immature malignant teratomas involves several key factors:

1. Embryonic origin and pluripotency: Similar to benign teratomas, immature malignant teratomas arise from germ cells that possess pluripotent properties. During embryonic development, these germ cells may undergo abnormal differentiation, leading to the formation of immature tissues representing various embryonic germ layers (ectoderm, mesoderm, and endoderm) within the tumor.
2. Genetic abnormalities: Immature malignant teratomas often harbor genetic abnormalities, including chromosomal abnormalities and gene mutations, that contribute to their malignant behavior. These genetic alterations may affect key signaling pathways involved in cell proliferation, differentiation, and apoptosis, leading to uncontrolled growth and tumor progression.
3. Histological features: Histologically, immature malignant teratomas contain primitive, undifferentiated tissues resembling those found in embryonic or fetal stages of development. These tissues may include immature neuroectodermal elements (such as primitive neural tissue), primitive mesenchymal elements (such as undifferentiated mesenchyme), and immature endodermal elements (such as primitive epithelial structures).
4. Potential for differentiation: Despite their immature appearance, malignant teratomas may demonstrate areas of partial differentiation or focal maturation into more specialized cell types. However, these differentiated areas are often limited, and the tumor as a whole retains a high degree of cellular immaturity and aggressiveness.
5. Clinical behavior: Immature malignant teratomas typically present as large, rapidly growing masses, often with invasive features and a tendency to recur locally after surgical resection. In some cases, immature teratomas may metastasize to distant sites, particularly if they contain highly aggressive components such as primitive neuroectodermal tumors (PNETs) or rhabdomyosarcomas.

Overall, the pathomechanism of immature malignant teratomas involves aberrant differentiation of germ cells during embryonic development, genetic abnormalities, and the presence of immature, undifferentiated tissues within the tumor. These tumors are characterized by their aggressive behavior and potential for metastasis, necessitating prompt diagnosis and aggressive treatment approaches, including surgical resection and adjuvant therapy.

Question 157

Various solid tumors:

Answer 157

germ cell tumors and sex-cord stromal tumors

Germ cell tumors and sex cord-stromal tumors are two broad categories of ovarian neoplasms with distinct pathomechanisms:

1. Germ cell tumors: Germ cell tumors arise from the ovaries’ primordial germ cells, which give rise to ova (eggs). The pathomechanism of germ cell tumors involves various factors:
   • Developmental anomalies: Errors during embryonic development can lead to germ cell abnormalities, such as incomplete migration or abnormal differentiation. These anomalies can predispose germ cells to neoplastic transformation.
   • Genetic factors: Germ cell tumors may be associated with genetic abnormalities, such as chromosomal aberrations or gene mutations. For example, mutations in genes such as OCT3/4, NANOG, and SOX2 have been implicated in the development of germ cell tumors.
   • Hormonal influences: While hormonal factors are not the primary drivers of germ cell tumor development, some tumors may exhibit hormone receptor expression or respond to hormonal stimulation. However, the exact role of hormones in germ cell tumorigenesis is not fully understood.
   • Immune dysregulation: Dysregulation of the immune system may contribute to the development of germ cell tumors. Immune surveillance mechanisms that normally recognize and eliminate abnormal cells may be compromised, allowing neoplastic germ cells to proliferate unchecked.
2. Sex cord-stromal tumors: Sex cord-stromal tumors originate from the ovarian stroma or sex cord cells, which support the development of ovarian follicles and produce sex hormones. The pathomechanism of sex cord-stromal tumors differs from germ cell tumors and involves distinct factors:
   • Hormonal influences: Sex cord-stromal tumors are often hormonally active and may produce estrogen, progesterone, or testosterone. Hormonal imbalances resulting from tumor hormone production can lead to clinical manifestations such as abnormal uterine bleeding, precocious puberty, or virilization.
   • Genetic factors: Some sex cord-stromal tumors may be associated with specific genetic mutations or syndromes. For example, mutations in the FOXL2 gene are commonly found in adult-type granulosa cell tumors.
   • Follicle development abnormalities: Sex cord-stromal tumors may arise from abnormalities in folliculogenesis or the development of ovarian follicles. Dysregulation of signaling pathways involved in follicle development, such as the Wnt/β-catenin pathway, may contribute to tumor initiation and progression.
   • Stromal cell proliferation: Sex cord-stromal tumors may arise from hyperplasia or neoplastic transformation of ovarian stromal cells. Aberrant proliferation of stromal cells can lead to the formation of tumors such as fibromas, thecomas, or fibrothecomas.

Overall, germ cell tumors and sex cord-stromal tumors have distinct pathomechanisms involving developmental anomalies, genetic factors, hormonal influences, and cellular dysregulation. Understanding these mechanisms is crucial for the diagnosis, management, and treatment of ovarian neoplasms.

Question 158

Spleen normal

Answer 158

Question 159

Answer 159

Accessory masses of splenic tissue (splenunculi):
• found in 10% to 15% of autopsies

The presence of accessory masses of splenic tissue, also known as splenunculi, is a relatively common anatomical variation found in 10% to 15% of autopsies. The pathomechanism underlying the development of splenunculi is not fully understood, but several theories have been proposed:

1. Embryonic development anomalies: Splenunculi may arise due to anomalies during embryonic development of the spleen. During fetal development, the spleen forms from mesodermal tissue that migrates to the left upper quadrant of the abdomen. Anomalies or disruptions in this migration process may result in the formation of accessory splenic tissue at sites other than the normal location of the spleen.
2. Splenic lobulation: The spleen undergoes complex lobulation during embryonic development, which involves the formation of multiple lobes separated by connective tissue septa. Anomalies or incomplete fusion of these septa may lead to the formation of isolated splenic nodules or masses, giving rise to splenunculi.
3. Accessory splenic tissue dissemination: Another proposed mechanism is the dissemination of splenic tissue during embryonic development or postnatal life. Fragments of splenic tissue may become detached from the main spleen and implant at distant sites within the abdominal cavity or along the course of the splenic vasculature, forming splenunculi.
4. Trauma or surgical manipulation: Trauma or surgical procedures involving the spleen may lead to the inadvertent dissemination of splenic tissue into adjacent structures or distant sites within the abdomen. For example, splenic trauma or splenectomy may result in the seeding of splenic tissue fragments, leading to the formation of splenunculi.
5. Genetic predisposition: Genetic factors may predispose individuals to the development of splenunculi. Certain genetic variations or mutations may affect the development or migration of splenic tissue during embryonic development, increasing the likelihood of splenunculi formation.

Overall, the pathomechanism of splenunculi likely involves a combination of embryonic developmental anomalies, splenic lobulation abnormalities, dissemination of splenic tissue, trauma, surgical manipulation, and genetic predisposition. While splenunculi are generally considered benign and asymptomatic, they may be associated with an increased risk of complications such as torsion, infarction, or hemorrhage, particularly if they undergo pathological changes or become symptomatic.

Question 160

acute splenitis

Answer 160

The presence of accessory masses of splenic tissue, also known as splenunculi, is a relatively common anatomical variation found in 10% to 15% of autopsies. The pathomechanism underlying the development of splenunculi is not fully understood, but several theories have been proposed:

1. Embryonic development anomalies: Splenunculi may arise due to anomalies during embryonic development of the spleen. During fetal development, the spleen forms from mesodermal tissue that migrates to the left upper quadrant of the abdomen. Anomalies or disruptions in this migration process may result in the formation of accessory splenic tissue at sites other than the normal location of the spleen.
2. Splenic lobulation: The spleen undergoes complex lobulation during embryonic development, which involves the formation of multiple lobes separated by connective tissue septa. Anomalies or incomplete fusion of these septa may lead to the formation of isolated splenic nodules or masses, giving rise to splenunculi.
3. Accessory splenic tissue dissemination: Another proposed mechanism is the dissemination of splenic tissue during embryonic development or postnatal life. Fragments of splenic tissue may become detached from the main spleen and implant at distant sites within the abdominal cavity or along the course of the splenic vasculature, forming splenunculi.
4. Trauma or surgical manipulation: Trauma or surgical procedures involving the spleen may lead to the inadvertent dissemination of splenic tissue into adjacent structures or distant sites within the abdomen. For example, splenic trauma or splenectomy may result in the seeding of splenic tissue fragments, leading to the formation of splenunculi.
5. Genetic predisposition: Genetic factors may predispose individuals to the development of splenunculi. Certain genetic variations or mutations may affect the development or migration of splenic tissue during embryonic development, increasing the likelihood of splenunculi formation.

Overall, the pathomechanism of splenunculi likely involves a combination of embryonic developmental anomalies, splenic lobulation abnormalities, dissemination of splenic tissue, trauma, surgical manipulation, and genetic predisposition. While splenunculi are generally considered benign and asymptomatic, they may be associated with an increased risk of complications such as torsion, infarction, or hemorrhage, particularly if they undergo pathological changes or become symptomatic.

Question 161

congestive splenomegaly

Answer 161

Marked enlargement (1000 to 5000 g), thick and fibrous capsule, firm
parenchyma, gray-red to dark red depending on parenchymal fibrosis,
follicles indistinct:
• congestive splenomegaly

Congestive splenomegaly, also known as passive splenomegaly or congestive enlargement of the spleen, occurs as a result of increased blood flow and congestion within the splenic sinuses. The pathomechanism of congestive splenomegaly is typically secondary to underlying conditions that lead to elevated portal venous pressure or splenic venous congestion. Several factors contribute to the development of congestive splenomegaly:

1. Portal hypertension: Portal hypertension, characterized by increased pressure in the portal venous system, is a primary cause of congestive splenomegaly. Portal hypertension can result from liver cirrhosis, portal vein thrombosis, hepatic venous outflow obstruction (Budd-Chiari syndrome), or congestive heart failure. Increased portal venous pressure leads to congestion within the splenic sinusoids and results in splenomegaly.
2. Splenomegaly in liver cirrhosis: Liver cirrhosis, a common cause of portal hypertension, often leads to congestive splenomegaly. In cirrhosis, fibrotic changes in the liver parenchyma impede blood flow through the liver, causing an increase in portal venous pressure. This elevated pressure is transmitted to the splenic circulation, resulting in splenomegaly.
3. Hepatic venous outflow obstruction: Conditions such as Budd-Chiari syndrome, characterized by obstruction of the hepatic venous outflow tract, can lead to congestion within the liver and elevated portal venous pressure. The resulting portal hypertension contributes to splenic congestion and splenomegaly.
4. Congestive heart failure: In congestive heart failure, impaired cardiac function leads to elevated central venous pressure, including pressure in the hepatic and portal venous systems. Increased venous pressure is transmitted to the splenic circulation, causing splenic congestion and enlargement.
5. Splenomegaly in portal vein thrombosis: Portal vein thrombosis, a condition characterized by the obstruction of the portal vein, can lead to increased pressure in the portal venous system proximal to the thrombus. This elevated pressure contributes to splenic congestion and splenomegaly.
6. Other causes: Congestive splenomegaly may also occur in other conditions associated with elevated venous pressure, such as congestive splenomegaly associated with pregnancy or congestive splenomegaly secondary to inferior vena cava obstruction.

Overall, the pathomechanism of congestive splenomegaly involves increased portal venous pressure or splenic venous congestion, leading to splenic sinusoidal dilatation, congestion, and subsequent enlargement of the spleen. Treatment typically focuses on managing the underlying cause of portal hypertension or venous congestion to alleviate splenic congestion and reduce splenomegaly.

Question 162

Other causes of spelenomegaly

Answer 162

• infections
• lymphoproliferative disorders
• immunologic diseases
• storage diseases
• amyloidosis
• neoplasms

Question 163

acute ischemic infarcts spleen

Answer 163

Pale red, wedge-shaped lesions with fibrin on overlying capsule:
• acute ischemic infarcts

Acute ischemic infarction of the spleen occurs when the blood supply to a portion of the spleen is compromised, leading to tissue necrosis due to inadequate oxygenation and nutrient supply. The pathomechanism of acute ischemic infarct of the spleen typically involves one or more of the following factors:

1. Arterial occlusion: The most common cause of acute splenic infarction is the occlusion of one or more splenic arteries, which supply oxygenated blood to the spleen. Arterial occlusion can occur due to various mechanisms, including embolism (e.g., thrombus or plaque dislodgment), thrombosis (e.g., formation of a blood clot within the splenic artery), or vasculitis (e.g., inflammation and narrowing of the splenic artery).
2. Thromboembolism: Embolism from distant sites, such as the heart (e.g., atrial fibrillation), aorta (e.g., atherosclerosis), or other arteries, can travel through the bloodstream and lodge within the smaller branches of the splenic artery, causing acute arterial occlusion and infarction of the downstream splenic tissue.
3. Vasculitis: Inflammatory conditions affecting the blood vessels, such as vasculitis (e.g., systemic lupus erythematosus, polyarteritis nodosa), can lead to inflammation and narrowing of the splenic arteries, reducing blood flow to the spleen and predisposing to infarction.
4. Hypoperfusion: Acute systemic hypoperfusion or shock states, such as hemorrhagic shock, septic shock, or cardiogenic shock, can lead to reduced blood flow to the spleen and subsequent ischemia. Hypoperfusion may result from decreased cardiac output, blood loss, systemic vasodilation, or impaired vascular tone.
5. Trauma: Traumatic injuries, such as blunt abdominal trauma or penetrating injuries, can directly damage the splenic vasculature or disrupt blood flow, leading to ischemia and infarction of the affected spleen tissue.
6. Hypercoagulable states: Conditions associated with hypercoagulability, such as thrombophilia, malignancy, or autoimmune disorders, can increase the risk of thrombus formation within the splenic vasculature, leading to arterial occlusion and infarction.
7. Vascular abnormalities: Structural abnormalities of the splenic vasculature, such as aneurysms, arteriovenous malformations, or arteriosclerosis, can predispose to thromboembolic events or impaired blood flow, increasing the risk of splenic infarction.

Overall, acute ischemic infarction of the spleen results from a disruption in the normal blood supply to the organ, leading to tissue hypoxia, necrosis, and infarction. The underlying cause of splenic infarction may vary depending on the specific clinical context and predisposing factors. Treatment typically involves supportive measures and addressing the underlying cause of ischemia, such as anticoagulation therapy for thromboembolic events or resuscitation and stabilization in cases of shock.

Question 164

Healing infarcts spleen

Answer 164

Pale yellow, wedge-shaped lesions becoming depressed scars:
• healing infarcts

Healing of infarcts in the spleen involves a complex series of events aimed at removing necrotic tissue, repairing damaged structures, and restoring normal tissue architecture. The pathomechanism of healing infarcts in the spleen typically follows several key steps:

1. Phagocytosis of necrotic tissue: Following an acute infarction, necrotic tissue in the affected area undergoes phagocytosis by macrophages and other phagocytic cells. These cells engulf and digest the debris, clearing the site of necrosis and preparing it for repair.
2. Granulation tissue formation: Granulation tissue, composed of proliferating fibroblasts, new blood vessels (angiogenesis), and inflammatory cells, begins to form within the infarcted area. Angiogenesis is particularly important for restoring blood supply to the healing tissue.
3. Fibrosis and scar formation: Fibroblasts within the granulation tissue deposit collagen fibers, leading to the formation of scar tissue. The scar tissue helps to reinforce the structural integrity of the healed area but may also result in functional impairment, depending on the extent of fibrosis and the location of the infarct.
4. Resolution of inflammation: As healing progresses, the inflammatory response gradually resolves, and the number of inflammatory cells decreases. This allows for the transition from the acute inflammatory phase to the proliferative and remodeling phases of wound healing.
5. Tissue remodeling: The remodeling phase involves ongoing rearrangement and maturation of collagen fibers, as well as continued angiogenesis and tissue restructuring. This process helps to further strengthen the scar tissue and restore the architecture and function of the spleen.
6. Functional recovery: Depending on the size and location of the infarct, functional recovery of the spleen may occur over time as the healing process progresses. However, extensive infarcts or fibrosis may result in permanent loss of splenic function or predispose to complications such as splenic rupture or abscess formation.

Overall, the pathomechanism of healing infarcts in the spleen involves a coordinated series of cellular and tissue-level responses aimed at repairing the damage caused by ischemia and restoring normal tissue structure and function. The process of healing may vary in duration and outcome depending on factors such as the size and severity of the infarct, the presence of underlying conditions, and the effectiveness of the healing response.

Question 165

Septicinfarct spleen

Answer 165

Suppurative, soft, wedge-shaped infarcts:
• septic infarcts

The pathomechanism of septic infarcts in the spleen involves the interplay between microbial infection, immune response, and vascular compromise. It typically follows a sequence of events:

1. Microbial seeding: Septic infarcts in the spleen often occur secondary to bacteremia or fungemia, where microorganisms (bacteria or fungi) are introduced into the bloodstream. These microorganisms may originate from infections at distant sites, such as the lungs (pneumonia), urinary tract (urinary tract infections), abdomen (peritonitis), or endocardium (endocarditis).
2. Hematogenous spread: The microorganisms circulate in the bloodstream and may lodge within the small vessels of the spleen, leading to focal areas of infection. The spleen acts as a filter for blood, trapping microorganisms and facilitating their interaction with immune cells within the splenic tissue.
3. Inflammatory response: The presence of microorganisms within the splenic tissue triggers an inflammatory response, characterized by the recruitment of immune cells (e.g., neutrophils, macrophages) to the site of infection. These immune cells attempt to contain and eliminate the invading microorganisms through phagocytosis and the release of antimicrobial substances.
4. Vascular compromise: The inflammatory response within the splenic tissue may lead to vascular compromise, including vasculitis, thrombosis, or microvascular occlusion. These vascular changes can impair blood flow to affected areas of the spleen, resulting in ischemia and infarction.
5. Infarction and abscess formation: Ischemic necrosis of splenic tissue occurs within the areas affected by vascular compromise, leading to the formation of septic infarcts. The necrotic tissue provides a nidus for bacterial proliferation, facilitating the formation of abscesses within the infarcted areas.
6. Systemic spread: In severe cases, microorganisms and inflammatory mediators may disseminate from the infected spleen into the systemic circulation, leading to systemic manifestations of sepsis, such as fever, hypotension, and organ dysfunction.

Overall, the pathomechanism of septic infarcts in the spleen involves the complex interplay between microbial infection, immune response, and vascular compromise. Prompt diagnosis and treatment of the underlying infection are crucial to prevent further complications and mitigate the risk of systemic spread of infection. Treatment typically involves antimicrobial therapy, supportive care, and occasionally, drainage or surgical intervention for abscesses.

Question 166

Adrenal gland normal

Answer 166

Question 167

Cushing syndrome relation to adrenal gland

Answer 167

Diffusely thickened, yellow cortex contributing to slight or marked bilateral
enlargement:
• diffuse hyperplasia producing Cushing syndrome (hypercortisolism)

Yellow nodules (0.5 to 2.0cm) scattered throughout cortex bilaterally:
• nodular hyperplasia producing Cushing syndrome

Cushing syndrome refers to a group of signs and symptoms caused by prolonged exposure to high levels of cortisol. While cortisol is essential for various physiological functions, excessive cortisol production or administration can lead to adverse effects, including changes in the adrenal glands. The mechanism by which Cushing syndrome causes changes in the adrenal glands involves several key factors:

1. Adrenal hypertrophy: Prolonged exposure to high levels of cortisol stimulates the adrenal glands to undergo hypertrophy, characterized by an increase in the size and mass of the adrenal cortex. This hypertrophy primarily affects the zona fasciculata and zona reticularis, which are responsible for cortisol production.
2. Corticotrophin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) suppression: In cases of endogenous Cushing syndrome, the excessive production of cortisol by the adrenal glands suppresses the release of CRH and ACTH from the hypothalamus and pituitary gland, respectively. This negative feedback mechanism leads to decreased stimulation of the adrenal glands by ACTH, contributing to adrenal atrophy and decreased responsiveness to ACTH stimulation.
3. Adrenal atrophy: Chronic suppression of ACTH secretion and decreased adrenal stimulation result in adrenal atrophy, particularly affecting the zona glomerulosa, which produces aldosterone. The degree of adrenal atrophy may vary depending on the duration and severity of cortisol excess.
4. Functional changes: In addition to structural changes, Cushing syndrome can lead to functional alterations in the adrenal glands. Excessive cortisol production can disrupt the normal feedback mechanisms that regulate cortisol synthesis and secretion, leading to dysregulation of adrenal hormone production. For example, high levels of cortisol can inhibit the production of aldosterone and adrenal androgens while promoting gluconeogenesis and inhibiting immune function.
5. Secondary changes: Chronic cortisol excess can also lead to secondary changes in the adrenal glands, such as the development of adrenal nodules, cysts, or even adenomas. These changes may contribute to further alterations in adrenal function and hormone production.

Overall, the mechanism by which Cushing syndrome causes changes in the adrenal glands involves a complex interplay of hormonal, structural, and functional adaptations in response to chronic cortisol excess. These changes can have significant implications for adrenal function, hormone regulation, and overall health in individuals with Cushing syndrome.

Question 168

Conn syndrome changes to adrenal gland

Answer 168

Small (generally solitary and <2 cm), bright yellow, encapsulated masses,
more often on left than right, without overall gland enlargement:
• aldosterone-producing adenomas (Conn syndrome)

Conn syndrome, also known as primary aldosteronism, is characterized by excessive production of aldosterone by the adrenal glands. The primary mechanism underlying Conn syndrome involves the dysregulation of aldosterone secretion, often due to adrenal adenomas (aldosterone-producing adenomas, or APAs) or bilateral adrenal hyperplasia (BAH). Here’s how these changes occur:

1. Aldosterone production: In Conn syndrome, there is inappropriate and excessive production of aldosterone by the adrenal glands. Aldosterone is normally produced by the outer layer of the adrenal glands called the zona glomerulosa. Its primary function is to regulate sodium and potassium balance in the body, primarily in the kidneys.
2. Adrenal adenomas (APAs): In approximately 70-80% of cases of Conn syndrome, aldosterone-producing adenomas (APAs) are responsible for the excess aldosterone production. APAs are benign tumors that autonomously produce aldosterone, independent of the normal regulatory mechanisms. The exact cause of APA development is not fully understood but may involve genetic mutations or alterations in signaling pathways that control aldosterone production.
3. Bilateral adrenal hyperplasia (BAH): In the remaining cases of Conn syndrome, bilateral adrenal hyperplasia (BAH) is the underlying cause. BAH refers to the enlargement of both adrenal glands due to excessive proliferation of aldosterone-producing cells in the zona glomerulosa. The etiology of BAH is multifactorial and may involve genetic predisposition, abnormal hormonal regulation, or other unidentified factors.
4. Renin-angiotensin-aldosterone system (RAAS) activation: The excess aldosterone production in Conn syndrome leads to the activation of the renin-angiotensin-aldosterone system (RAAS). Aldosterone acts on the kidneys to increase sodium reabsorption and potassium excretion, leading to sodium retention, potassium loss, and volume expansion. This results in hypertension, hypokalemia (low potassium levels), metabolic alkalosis, and often, volume expansion.
5. Feedback mechanisms: Normally, the production of aldosterone is tightly regulated by the renin-angiotensin system, potassium levels, and other factors to maintain electrolyte balance and blood pressure. However, in Conn syndrome, these feedback mechanisms are disrupted, leading to persistent aldosterone excess.

Overall, the mechanism of Conn syndrome involves the autonomous production of aldosterone by adrenal adenomas or hyperplasia, resulting in dysregulation of electrolyte balance, volume status, and blood pressure. Treatment typically involves surgical removal of aldosterone-producing adenomas or medical management to control blood pressure and correct electrolyte abnormalities.

Question 169

Answer 169

Bilateral dark red parenchyma:
• massive bilateral adrenal hemorrhage (Waterhouse-Friderichsen
syndrome)

Waterhouse-Friderichsen syndrome (WFS) is a rare and life-threatening condition characterized by adrenal gland hemorrhage typically associated with severe bacterial infections, most commonly meningococcal septicemia caused by Neisseria meningitidis. The pathomechanism of Waterhouse-Friderichsen syndrome involves several key factors:

1. Bacterial infection: The syndrome is usually triggered by overwhelming bacterial sepsis, often due to Neisseria meningitidis, although other bacteria such as Streptococcus pneumoniae and Haemophilus influenzae may also be implicated. These bacteria can cause invasive infections such as meningitis or septicemia, leading to widespread dissemination throughout the bloodstream.
2. Endotoxin release: The bacteria responsible for the infection release endotoxins (lipopolysaccharides) as part of their cell wall structure. These endotoxins trigger a systemic inflammatory response, leading to activation of the coagulation cascade, endothelial dysfunction, and widespread vasodilation.
3. Adrenal gland involvement: The adrenal glands, particularly the adrenal cortex, are highly vascularized and susceptible to damage during severe sepsis. Endotoxins and other inflammatory mediators cause endothelial damage and disrupt the integrity of blood vessels within the adrenal glands.
4. Disseminated intravascular coagulation (DIC): In severe cases of sepsis, the systemic inflammatory response can lead to disseminated intravascular coagulation (DIC), a condition characterized by widespread activation of the coagulation cascade and consumption of clotting factors and platelets. DIC results in microvascular thrombosis, leading to tissue ischemia and organ dysfunction, including adrenal gland hemorrhage.
5. Adrenal hemorrhage: The combination of endothelial damage, coagulation abnormalities, and vasodilation leads to impaired vascular integrity and hemorrhage within the adrenal glands. Adrenal hemorrhage can result in adrenal gland necrosis and acute adrenal insufficiency, contributing to the clinical manifestations of Waterhouse-Friderichsen syndrome.
6. Clinical presentation: Patients with Waterhouse-Friderichsen syndrome typically present with sudden-onset fever, shock, disseminated intravascular coagulation (DIC), and signs of adrenal insufficiency, such as hypotension, hyponatremia, hyperkalemia, and metabolic acidosis. Hemorrhagic skin lesions, purpura, and petechiae may also be present.

Overall, the pathomechanism of Waterhouse-Friderichsen syndrome involves the development of adrenal gland hemorrhage secondary to severe bacterial sepsis, leading to acute adrenal insufficiency and potentially life-threatening shock. Prompt recognition and aggressive management of sepsis and adrenal insufficiency are essential for improving outcomes in affected individuals.

Question 170

Addison disease effect on adrenal gland

Answer 170

Addison’s disease, also known as primary adrenal insufficiency or adrenal insufficiency, is a condition characterized by insufficient production of adrenal hormones, particularly cortisol and often aldosterone, due to damage to the adrenal glands. The effects of Addison’s disease on the adrenal glands include:

1. Adrenal gland atrophy: Chronic destruction of the adrenal cortex, typically caused by autoimmune destruction (autoimmune adrenalitis) but also by other conditions such as tuberculosis, fungal infections, or adrenal hemorrhage, leads to progressive atrophy of the adrenal glands. The adrenal cortex, particularly the zona fasciculata and zona reticularis, undergoes fibrosis and loss of functional tissue.
2. Decreased cortisol production: Cortisol, a glucocorticoid hormone produced by the adrenal cortex, plays a crucial role in regulating metabolism, immune function, stress response, and many other physiological processes. In Addison’s disease, the reduced functional mass of the adrenal glands leads to decreased cortisol production. This results in impaired glucose metabolism, decreased ability to cope with stress, fatigue, weakness, weight loss, hypotension, and other symptoms characteristic of cortisol deficiency.
3. Decreased aldosterone production (if present): In some cases of Addison’s disease, particularly those caused by autoimmune destruction of the adrenal glands, aldosterone production may also be affected. Aldosterone is a mineralocorticoid hormone that regulates sodium and potassium balance, blood volume, and blood pressure. Reduced aldosterone production can lead to sodium loss, potassium retention, dehydration, hypotension, and electrolyte imbalances such as hyponatremia and hyperkalemia.
4. Adrenal crisis: In severe cases of adrenal insufficiency, particularly during times of stress such as illness, surgery, or trauma, the body’s demand for cortisol and aldosterone increases. However, individuals with Addison’s disease lack the ability to mount an appropriate stress response due to insufficient adrenal hormone production. This can lead to adrenal crisis, a life-threatening condition characterized by severe hypotension, electrolyte abnormalities, dehydration, hypoglycemia, and shock.

Overall, Addison’s disease leads to significant impairment of adrenal gland function, resulting in deficiencies of cortisol and aldosterone. These hormonal deficiencies have widespread effects on metabolism, electrolyte balance, cardiovascular function, and stress response, contributing to the clinical manifestations and complications of the disease. Treatment typically involves lifelong hormone replacement therapy to replace deficient adrenal hormones and prevent adrenal crisis.

Question 171

tuberculous or fungal infection
• metastatic carcinoma may also cause chronic adrenocortical
insufficiency

Changes in adrenal gland macroscopicalpy

Answer 171

Effacement of adrenal glands by caseous necrosis or tumor

Question 172

secondary hypoadrenalism adrenal gland

Answer 172

Small, flattened atrophic adrenals with thickened capsule, very thin cortex,
and normal medulla:
• secondary hypoadrenalism

Secondary hypoadrenalism, also known as secondary adrenal insufficiency, occurs when there is a deficiency in adrenocorticotropic hormone (ACTH) production or release from the pituitary gland, leading to decreased stimulation of the adrenal glands and subsequent insufficient cortisol production. The pathomechanism of secondary hypoadrenalism involves several key factors:

1. Pituitary dysfunction: Secondary hypoadrenalism most commonly arises from dysfunction or damage to the pituitary gland, specifically the corticotroph cells that produce ACTH. This dysfunction may result from pituitary tumors (e.g., adenomas), pituitary surgery, radiation therapy, pituitary infarction (e.g., Sheehan syndrome), or other causes of pituitary insufficiency.
2. Decreased ACTH secretion: Pituitary dysfunction leads to decreased secretion or impaired release of ACTH into the bloodstream. ACTH is the primary hormone responsible for stimulating the adrenal glands to produce cortisol. In secondary hypoadrenalism, the diminished ACTH levels result in reduced adrenal gland stimulation, leading to decreased cortisol synthesis and secretion.
3. Adrenal gland atrophy: In the absence of adequate ACTH stimulation, the adrenal glands may undergo atrophy and loss of functional tissue over time. Chronic lack of ACTH signaling leads to decreased adrenal cell proliferation and reduced synthesis of cortisol. Adrenal atrophy may contribute to the persistence of adrenal insufficiency even if ACTH secretion is eventually restored.
4. Preservation of aldosterone production: Unlike primary adrenal insufficiency (Addison’s disease), which often results in deficiencies of both cortisol and aldosterone, secondary hypoadrenalism primarily affects cortisol production while typically sparing aldosterone secretion. This is because aldosterone synthesis is primarily regulated by the renin-angiotensin system rather than ACTH. Therefore, individuals with secondary hypoadrenalism may not experience electrolyte imbalances associated with aldosterone deficiency.
5. Clinical presentation: The clinical presentation of secondary hypoadrenalism is similar to primary adrenal insufficiency and typically includes symptoms such as fatigue, weakness, weight loss, hypotension, hypoglycemia, and decreased stress tolerance. However, individuals with secondary hypoadrenalism may have preserved skin pigmentation (as ACTH levels are low, and melanocyte-stimulating hormone, which shares the same precursor molecule with ACTH, is also low) and may not exhibit hyperpigmentation seen in primary adrenal insufficiency.

Overall, the pathomechanism of secondary hypoadrenalism involves insufficient ACTH production or release from the pituitary gland, resulting in decreased stimulation of the adrenal glands and inadequate cortisol production. Prompt diagnosis and treatment with glucocorticoid replacement therapy are essential to prevent adrenal crisis and alleviate symptoms associated with adrenal insufficiency.

Question 173

Adenocortical adenoma

Answer 173

Yellow to yellow-brown cortical masses, some with hemorrhage, cystic
degeneration, and calcification:
• with adjacent cortex appearing normal
• nonfunctioning adrenocortical adenomas

• with atrophy of adjacent normal cortex
• functioning adrenocortical adenomas

Large yellow masses with hemorrhagic, cystic, and necrotic regions:
• adrenocortical carcinomas

The pathomechanism of adenocortical adenoma, also known as adrenal cortical adenoma, involves the development of a benign tumor within the adrenal cortex. Adenocortical adenomas are typically hormonally active and can produce excessive amounts of cortisol, aldosterone, or less commonly, androgens. Here’s how adenocortical adenomas develop and function:

1. Genetic mutations: Adenocortical adenomas often arise due to genetic mutations or alterations that disrupt the normal regulation of adrenal cell growth and function. Mutations in genes such as PRKAR1A, GNAS, and CTNNB1 have been implicated in the pathogenesis of adrenal adenomas. These mutations can lead to dysregulation of cell proliferation, hormone synthesis, and tumor formation within the adrenal cortex.
2. Autonomous hormone production: Adenocortical adenomas are characterized by autonomous hormone production, meaning they can produce adrenal hormones independently of normal regulatory mechanisms. Depending on the specific genetic alterations and cellular characteristics, adenomas may produce cortisol (causing Cushing’s syndrome), aldosterone (causing primary aldosteronism or Conn syndrome), or androgens (causing virilization).
3. Cortisol-producing adenomas: Cortisol-producing adenomas, also known as cortisol-secreting adenomas or cortisol-producing adrenal adenomas, are the most common type of adrenal adenoma. These tumors typically arise from the zona fasciculata of the adrenal cortex and produce excessive amounts of cortisol. The overproduction of cortisol can lead to the clinical manifestations of Cushing’s syndrome, such as weight gain, central obesity, hypertension, diabetes, and osteoporosis.
4. Aldosterone-producing adenomas: Aldosterone-producing adenomas, also known as aldosteronomas, arise from the zona glomerulosa of the adrenal cortex and produce excessive aldosterone. This leads to primary aldosteronism (Conn syndrome), characterized by hypertension, hypokalemia, metabolic alkalosis, and suppression of plasma renin activity.
5. Androgen-producing adenomas: Androgen-producing adenomas are less common and typically arise from the zona reticularis of the adrenal cortex. These tumors can produce excessive androgens, leading to virilization in women and precocious puberty or masculinization in children.
6. Clinical presentation: The clinical presentation of adenocortical adenoma varies depending on the type of hormone produced and the degree of hormone excess. Patients may present with symptoms related to hormone excess (e.g., Cushing’s syndrome, Conn syndrome, virilization) or may be asymptomatic and incidentally discovered during imaging studies performed for unrelated reasons.

Overall, the pathomechanism of adenocortical adenoma involves genetic mutations or alterations that lead to the development of benign tumors within the adrenal cortex, resulting in autonomous hormone production and hormonal disturbances characteristic of various adrenal disorders. Treatment may involve surgical resection of the adenoma or medical management to control hormone excess and associated symptoms.

Question 174

Adrenal gland

Answer 174

Yellow-tan to gray-pink masses with foci of hemorrhage, necrosis, and cystic
degeneration in larger lesions:
• pheochromocytoma

Pheochromocytoma is a rare neuroendocrine tumor that arises from chromaffin cells in the adrenal medulla or, less commonly, from extra-adrenal chromaffin tissue (referred to as paragangliomas). These tumors produce and release excessive amounts of catecholamines, such as epinephrine, norepinephrine, and dopamine, leading to episodic or sustained hypertension and other symptoms characteristic of catecholamine excess. The pathomechanism of pheochromocytoma involves several key factors:

1. Chromaffin cell proliferation: Pheochromocytomas arise from chromaffin cells, which are neuroendocrine cells located in the adrenal medulla and sympathetic ganglia. These cells are derived from neural crest cells and normally produce catecholamines in response to sympathetic stimulation. In pheochromocytoma, chromaffin cells proliferate abnormally, forming a tumor mass that can secrete excessive amounts of catecholamines.
2. Genetic mutations: Pheochromocytomas can occur sporadically or as part of hereditary syndromes such as multiple endocrine neoplasia type 2 (MEN 2), von Hippel-Lindau (VHL) syndrome, neurofibromatosis type 1 (NF1), and familial paraganglioma syndromes. These syndromes are associated with specific genetic mutations that predispose individuals to the development of pheochromocytomas and other tumors of the endocrine system.
3. Excessive catecholamine production: Pheochromocytomas produce and release excessive amounts of catecholamines, particularly epinephrine, norepinephrine, and dopamine. These catecholamines act as potent vasoactive substances, exerting effects on the cardiovascular system, metabolism, and other physiological processes. The release of catecholamines into the bloodstream leads to episodic or sustained hypertension, tachycardia, palpitations, sweating, headache, and other symptoms of catecholamine excess.
4. Episodic symptoms: Pheochromocytoma-related symptoms often occur in paroxysmal or episodic episodes, known as paroxysmal or episodic catecholamine release. These episodes may be triggered by various factors such as physical exertion, emotional stress, changes in body position, or manipulation of the tumor during surgery. During these episodes, patients may experience sudden and severe hypertension, palpitations, diaphoresis, and other symptoms.
5. Metabolic effects: In addition to its cardiovascular effects, catecholamine excess can also affect metabolism, leading to hyperglycemia, glycogenolysis, lipolysis, and metabolic acidosis. These metabolic effects contribute to symptoms such as weight loss, polyuria, and polydipsia observed in some patients with pheochromocytoma.

Overall, the pathomechanism of pheochromocytoma involves abnormal proliferation of chromaffin cells, genetic predisposition in some cases, and excessive production of catecholamines, leading to episodic or sustained hypertension and other symptoms of catecholamine excess. Prompt diagnosis and management, including surgical resection of the tumor and medical therapy to control blood pressure and catecholamine release, are essential for improving outcomes in patients with pheochromocytoma.

Question 175

External examination normal

Answer 175

The 169 cm long, well nourished, middle-aged caucasian female/male deceased.

His/her skin is intact (i.e., no signs for previous operation, scar, etc) having a pale grayish-white
color.

On the back of the patent skin, at the lowest parts some irregularly shaped,
confluent and well defined livid purple-red (post-mortal) stainings are visible which,
under pressure, become pale.

On the whole body post-mortal rigidity is present.

The skull is having a regular shape, the hair is 15 cm long, wavy, brunette.

The eyelids are closed, the conjunctivae are pale-red; the sclera (on both sides) is white; the pupils are
symmetrical and moderately open, central in position, and round.

The irises are blue, the corneas are transparent, intact. The orifices of the mouth, ears, nose are free of blood,
liquor or any kind of fluid or contaminations.

The teeth are complete/incomplete.

The thorax is well proportional.

The genitals are grossly normal, the anus is clean, free of
blood or intestinal content.

All the extremities are in normal anatomical positions, no
deformities or abnormalities are seen.

Question 176

Neck external examination possible findings

Answer 176

• inspect soft tissues, muscles, and hyoid bone for evidence of trauma
• major arteries and veins for obstruction
• inspect hypopharynx, epiglottis, external larynx, and trachea for
• obstruction
• deviation, or
• compression
• check for trauma
• inspect initial thyroid gland in situ
• palpate cervical spine
• recheck neck mobility


• Lymphadenopathy:
• hyperplasia
• tuberculosis
• lymphoma
• metastatic carcinoma
• Midline neck cysts or sinus tract anterior to trachea or proximal to thyroid:
• thyroglossal cyst or duct
• Gray, yellow-brown homogeneous mass below angle of jaw:
• carotid body tumor

Question 177

Breast external possible findings

Answer 177

Brown to blue, semitranslucent fluid-filled cysts:
• fibrocystic change

• Hard areas without yellow streaks or yellow-white foci:
• sclerosing adenosis

• Masses:

• Firm, pale, sharply demarcated, sometimes with slit-like spaces:
• fibroadenoma

• Hard, sometimes gritty, gray, with radiating edges:

• may be invasive ductal carcinoma (scirrhous carcinoma)

• Firm, glistening, pale gray-blue, homogeneous, often well circumscribed:
• may be colloid (mucinous) carcinoma

• Firm, rubbery, poorly circumscribed:
• may be lobular carcinoma

• Soft, gray-white, fleshy, smooth to slightly irregular borders:
• may be medullary carcinoma

Question 178

Scars external examination

Answer 178

describe characteristics of scars (site, healing, surgical, traumatic)
- measure scars
- describe identifying marks such as tattoos, body piercings

• inspect for evidence of recent medical therapy
• describe needle puncture marks in reasonable detail (may be a clue to
  blood effusions in body cavities)
• describe remote wounds/scars
• note presence of
• endotracheal or nasogastric tube
• indwelling peripheral or central intravascular catheter
• urethral catheter
• feeding tube, and so forth
• do not remove devices until proper placement is ascertained

Question 179

Skin external examination findings

Answer 179

• Decreased elasticity and turgor:
• progressive postmortem change
• Loose skin that wrinkles when pushed with finger:
• weight loss
• Skin color:
• Pallor—exsanguinating hemorrhage
• Yellow—jaundice
• Blue—cyanosis (nail beds, lips, one limb)

• Generalized hyperpigmentation:
• Addison disease

• hemochromatosis
• chronic malaria
• cachexia
• Localized hyperpigmentation:
• Chloasma (melasma)
• pregnancy
• oral contraceptive use
• Addison disease
• Café au lait spots
• neurofibromatosis
• Hypermelanotic papillary or verrucous excrescences
• acanthosis nigricans (about half of adult cases have associated
carcinoma)
• Brown to black spots around mouth, nostrils, eyelids, hands, feet
• Peutz-Jeghers syndrome
• Depigmentation:
• vitiligo
• Pitting, taut shiny skin in dependent areas:
• edema from acute and chronic cardiac and renal failure
• hypoalbuminemia
• allergic reactions
• starvation
• Hemorrhages:
• trauma
• disseminated intravascular coagulopathy (petechiae)
• purpura (coagulopathy)
• senile purpura
• Ulcers:
• varicose ulcers are generally above medial malleolus
• arterial insufficiency
• diabetic ulcers involve toes, heels, lower anterior surface of leg
• ulcers from infections variable with associated cellulitis

Question 180

Back external examination

Answer 180

• inspect/palpate
• check for symmetry
• deformities
• inspect anus

• Curvature of spinal column:
• kyphosis
• lordosis
• scoliosis
• Ulcers:
• pressure sores due to immobility
• Pigmented area, tuft of hair, dimple, fistula:
• spina bifida occulta
• Dimple near anus:
• rectoperineal fistula
• Perianal skin tags or pedunculated masses:
• external hemorrhoids

Question 181

Extremities external examination

Answer 181

• symmetry (measure circumference of asymmetrical limbs)
• edema
• muscle wasting
• ulcers
• masses
• check for joint
• deformities
• swelling
• subluxation
• contracture
• mobility (avoid interpretive errors due to rigor or refrigeration)
• inspect hands/feet;
• note condition of fingernails and toenails
• color of nail beds (cyanosis)
• clubbing
  • Edema of single limb or upper or lower extremities due to
  • venous thrombosis or
  • lymphatic obstruction
  • Atrophy of muscles:
  • upper/lower motor neuron disease
  • muscular dystrophies
  • Joint swelling:
  • connective tissue diseases
  • gout
  • Joint effusions:
  • suppurative arthritis
  • connective tissue diseases
  • Fusiform enlargement of proximal interphalangeal joints;
  • ulnar deviation of hand
  • flexion deformities in elbows/knees
  • subcutaneous nodules on backs of elbows, wrists, and fingers
  • indicate rheumatoid arthritis
  • Tophi:
  • gout
  • Clubbing of fingers without periostosis:
  • idiopathic
  • Clubbing with periostosis:
  • hypertrophic pulmonary osteoarthropathy

Question 182

External genitalia

Answer 182

Abnormalities of urethral orifice:
• epispadias
• hypospadias
• Scrotal/vulvar edema:
• anasarca from any cause (e.g., cardiac or renal failure)
• localized edema from regional venous obstruction
• portal vein obstruction
• pelvic vein thrombosis
• Scrotal/vulvar lymphedema:
• lymphatic blockage (tumors, filariasis)
• Ulcers:
• chancroid
• syphilis
• lymphogranuloma venereum
• herpes
• Warty lesions:
• condyloma
• carcinoma

• Absent testis:
• maldescended (cryptorchism)
• surgically removed
• Testicular atrophy:
• remote infarcts
• healed mumps orchitis
• syphilis, filariasis
• liver failure
• Scrotal swellings or testicular enlargements:
• hematocele
• acute and chronic infections (mumps, tuberculosis, tertiary syphilis)
• neoplasms
• Spermatic cord swellings:
• epididymitis
• hydrocele
• spermatocele
• varicocele
• hematoma
• infections
• tumors
• Uterus protruding from introitus:
• uterine prolapse

Question 183

Abdomen external examination

Answer 183

• contour
• local bulges
• distention
• organomegaly (liver, spleen)
• masses
• discoloration
• abnormal veins
• hernias
• palpate inguinal region for lymphadenopathy

• Masses:
• neoplasms
• Distention:
• ileus
• ascites
• peritoneal carcinomatosis

Question 184

Chest external examination

Answer 184

thoracic symmetry
- pectus deformities
- size
- asymmetry
- consistency
- masses of breasts
- discharge or scaling/excoriation of nipples
- inversion/retraction of nipples
- dimpling or edema of skin
- palpate axilla for lymphadenopathy

• Asymmetry of chest wall:
• rickets
• osteomalacia
• kyphoscoliosis
• rib fractures
• Increased anterior-posterior chest diameter:
• chronic obstructive lung disease
• Chest deformities:
• Pectus carinatum—sternum arches forward (pigeon breast)
• Pectus excavatum—sternum and adjacent costal cartilages curve
backward (funnel chest)

• Gynecomastia—
• estrogen administration
• estrogen, prolactin, or human chorionic gonadotropin–forming tumors
• congenital syndromes with increased estrogen secretion
• decreased androgen secretion, or
• decreased androgen activity
• testicular failure
• liver failure (cirrhosis)
• complications of various therapeutic drugs
• thyrotoxicosis
• idiopathic

• Breast hypertrophy:
• pregnancy
• idiopathic

• Mastitis:
• reddening and edema of overlying skin
• Nipple discharge:
• benign or malignant tumors
• hormonal therapy

• Galactorrhea:
• therapeutic drug complication
• suprahypophyseal or hypophyseal tumor
• ectopic prolactin production (renal or bronchogenic neoplasms)
• hypothyroidism
• Addison disease
• adrenal carcinoma
• polycystic ovarian syndrome
• renal failure
• liver failure

• Scaling and excoriation of nipple:
• Paget disease

• Edema (peau d’orange), dimpling of breast:
• carcinoma

• Palpable breast masses:
• benign and malignant tumors

Question 185

Neck external examination

Answer 185

• symmetry
• mobility
• crepitus
• position of trachea and thyroid
• distention of neck vessels
• palpable cervical lymphadenopathy or masses

• Crepitus of skin:
• subcutaneous emphysema
• Crepitus or increased mobility:
• cervical spine fracture or atlanto-occipital dislocation (if possible, obtain
confirming radiographs prior to dissection)
• Masses:
• lymphadenopathy
• thyroid tumors
• goiter
• other tumors
• Tracheal deviation:
• retrosternal goiter
• lymphadenopathy
• Distention of neck vessels:
• congestive heart failure
• superior vena caval obstruction

Question 186

Head external examination

Answer 186

• head size and shape
• color, amount, and distribution of scalp and facial hair
• fractures of skull and facial bones and swellings of soft tissues
• symmetry of face
• fluid or discharge coming from ears, nose, or mouth
• color of irides
• size and equality of pupils
• color of sclerae
• clarity of corneae and lens
• patency of auditory canal
• patency of nares
• abnormal contents or lesions of oral cavity
• presence, absence, and condition of teeth
• abnormal size, coatings, or lesions of tongue
• lesions of palate and pharynx

• Loss of hair:
• may follow debilitating illnesses
• chemotherapy, or radiation therapy

• Hirsutism:
• virilization in women due to Cushing disease
• masculinizing ovarian tumors
• adrenal hyperactivity, or androgen administration

• Facial edema:
• myxedema
• superior vena cava syndrome (with upper limb edema)
• part of generalized anasarca

• Eyelid edema:
• local infection
• sinusitis
• angioneurotic edema
• renal failure
• cavernous sinus thrombosis
• superior vena cava syndrome

• Corneal ulceration:
• hyperthyroidism
• facial paralysis
• herpes zoster infection

• Corneal haziness:
• acute glaucoma

• Corneal opacification:
• cataract
• injury
• inflammation

• Corneal rings:
• Arcus senilis: ill-defined gray ring just inside cornea
• Kayser-Fleischer ring: green-brown ring just inside cornea, seen in Wilson
disease
• Pigmented nodules of iris (Lisch nodules):
• neurofibromatosis type 1


• Blue sclerae:
• Ehlers-Danlos syndrome
• Subconjunctival hemorrhage from anterior cranial fossa fracture


• Necrosis of nasal tip:
• acute bacterial endocarditis
• Epistaxis:
• hypertension
• coagulation disorder
• nasal trauma
• anterior cranial fossa fracture
• Bloody discharge from auditory canals
• indicates middle fossa skull fracture
• Purulent discharge from auditory canals:
• otitis media or meatal abscess
• Creases in earlobes may indicate vascular disease
• Gingival hemorrhages seen with
• coagulation defects
• periodontitis, or trauma

• Exudates and lesions of the oral cavity and tongue:
• Tough, gray-white adherent membrane over red, ulcerated mucosa
• diphtheria
• White exudates due to candidiasis (thrush)
• Vesicular lesions in
• herpes simplex
• herpangina, and
• aphthous stomatitis
• Severe vesicular eruptions in
• Stevens-Johnson syndrome
• Behçet syndrome, and
• pemphigus

• Gray-white plaques, indurated white fissures in

• leukoplakia
• Network of threadlike, lacy white lines in
• lichen plants
• Hyperplastic gingiva with
• diphenylhydantoin use
• Enlargement of the tongue in
• angioneurotic edema
• Atrophy of tongue in
• pernicious anemia

Question 187

Some postmortem changes

Answer 187

• Drying of skin in areas of abrasion, thermal injury, or ruptured vesicles
within a few hours after death
• Skin becomes dry, wrinkled, and eventually leathery
• Hair loosens
• Apparent lengthening of fingernails due to shrinkage of fingertips
• Eyes dry in 1 to 2 hours;

• if eyelids are open, sclerae sometimes show a dark red-brown
horizontal band along opening (“tache noire”)
• Film appears on cornea; later cornea becomes opacified
• Globes become softened and flattened.

• Obesity: generalized type involves particularly the face, neck, trunk, upper
arms, thighs, and breasts
• Cushing disease or corticosteroid therapy is characterized by moon face,
thick neck with pad of fat over upper thoracic spine, abdominal
obesity with purple striae, and contrasting thin extremities; obesity
associated with portal hypertension involves breasts, pelvis, lower
abdomen

• Cachexia:
• gaunt face
• sunken eyes
• sharp tip of nose
• prominent ribs
• sunken flat abdomen flaring away from costal margins and iliac crests
• wasting of extremities with greatest diameter at knees and elbows
(camel-like limbs)
• hair dull and brittle

Question 188

Rigor mortis:

Answer 188

begins in the jaw muscles; proceeds to the neck, face, and arms and finally
to the lower extremities, with the muscles of the ankles last;
reverses in same order

Question 189

Livor mortis:

Answer 189

• seen in dependent parts both externally and internally
• develops in 30 minutes to 2 hours, reaching maximum at 8 to 18 hours,
depending on local conditions

• becomes “fixed” or nonblanching with time (8 to 12 hours):

• pressure of pooling blood may rupture small vessels, causing “Tardieu
spots” (postmortem purpura or petechial-type hemorrhages)

• may be difficult to see in dark-skinned decedents
• color of postmortem lividity varies

- Distinctive livor mortis colors:


Blue-purple—normal


Black-green—putrefaction; hydrogen sulfide poisoning


Pink, cherry red—cyanide, carbon monoxide, or fluoroacetate
poisoning; moist postmortem environment


Minimal or absent—exsanguination

Question 190

Signs of clinical death

Answer 190

Question 191

Post mortal phenomenom

Answer 191

Question 192

Algor mortis

Answer 192

Question 193

Pallor mortis

Answer 193

Question 194

Livor mortis

Answer 194

Question 195

Livor mortis more

Answer 195

Question 196

Rigor mortis

Answer 196

Question 197

Nysten rule

Answer 197

Question 198

Cruor postmortalis

Answer 198

Question 199

Decompositio postmortalis

Answer 199

Question 200

Mummification

Answer 200

Question 201

Maceration

Answer 201

Question 202

Adipocere

Answer 202

Question 203

Larynx, trachea, esophagus

Answer 203

Question 204

Thyroid gland normal

Answer 204

Question 205

Answer 205

1. Major papilla: Also known as the duodenal papilla or papilla of Vater, the major papilla is a small nipple-like structure located in the second part of the duodenum, where the common bile duct and the pancreatic duct converge and enter the duodenum. It is the point of entry for bile from the common bile duct and pancreatic enzymes from the pancreatic duct into the duodenum. The major papilla is surrounded by the sphincter of Oddi, which regulates the flow of bile and pancreatic secretions into the duodenum.
2. Minor papilla: The minor papilla is a smaller structure located proximal to the major papilla in the duodenum. It serves as an alternative or accessory opening for pancreatic duct drainage into the duodenum. While most pancreatic secretions enter the duodenum through the major papilla, some may also exit through the minor papilla. The minor papilla is less prominent and less commonly used than the major papilla.
3. Ampulla of Vater: The ampulla of Vater, also known as the hepatopancreatic ampulla or the hepatopancreatic duct, is a dilated portion at the confluence of the common bile duct (carrying bile from the liver and gallbladder) and the pancreatic duct (carrying pancreatic enzymes from the pancreas). It is located within the duodenal wall, near the major papilla. The ampulla of Vater is surrounded by the sphincter of Oddi, which controls the release of bile and pancreatic secretions into the duodenum.
4. Sphincter of Oddi: The sphincter of Oddi, also known as the hepatopancreatic sphincter, is a muscular valve located at the confluence of the common bile duct, pancreatic duct, and duodenum. It regulates the flow of bile and pancreatic secretions into the duodenum. The sphincter of Oddi consists of smooth muscle fibers and is under autonomic nervous system control. It relaxes in response to hormonal and neural signals to allow the release of bile and pancreatic enzymes into the duodenum during digestion, and it contracts to prevent reflux of duodenal contents into the bile and pancreatic ducts when digestion is not occurring.