General Principles Week 4 REV Flashcards
Topic 1 – Cell Adaptation and Cell Injury
TLO 1.1 Describe the types and mechanisms of cell adaptations with examples
Cell adaptation refers to the ability of cells to respond to various types of stimuli and adverse environmental changes. The four main types of cellular adaptations are:
- Hypertrophy: An increase in the size of individual cells. For example, enlargement of skeletal muscle cells due to exercise.
- Hyperplasia: An increase in the number of cells. For example, an increase in the number of epithelial breast cells during pregnancy.
- Atrophy: A reduction in cell size and number. For example, muscle atrophy due to disuse.
- Metaplasia: Transformation from one type of epithelium to another. For example, Barrett’s esophagus due to chronic gastric acid exposure.
These adaptations can be physiologic (normal) or pathologic (abnormal) depending on the stimulus. Cells adapt to maintain homeostasis and cope with new demands placed on them.TLO
1.2 Describe the types and causes of cell injury
Cell injury can be classified into two main types:
- Reversible cell injury: The cell can recover if the damaging stimulus is removed.
- Irreversible cell injury: The cell cannot recover and will die.
Causes of cell injury include:
**Hypoxia (Lack of Oxygen):
**Ischemia (reduced blood flow)
Anemia (reduced oxygen-carrying capacity of blood)
Carbon monoxide poisoning
**Physical Agents:
**Trauma (mechanical injury)
Extreme temperatures (heat or cold)
Radiation
Electric shock
**Chemical Agents and Drugs:
**Environmental toxins (e.g., pesticides)
Drugs and alcohol
Heavy metals (e.g., lead, mercury)
**Infectious Agents:
**Bacteria
Viruses
Fungi
Parasites
**Immunologic Reactions:
**Autoimmune diseases
Allergic reactions
**Genetic Factors:
**Inherited mutations
Chromosomal abnormalities
**Nutritional Imbalances:
**Deficiencies (e.g., vitamin, protein)
Excesses (e.g., obesity, hypervitaminosis)
**Aging:
**Accumulation of cellular damage over time
Reduced ability of cells to repair themselves
These factors can lead to different types of cell injury, depending on the severity and duration of the exposure. If you need more details about any specific cause, just let me know!
TLO 1.3 Discuss the pathogenesis and features of reversible and irreversible cell injury
Reversible cell injury:
- Characterized by cellular swelling due to failure of the sodium-potassium pump
- Accumulation of fatty acids in the cytoplasm (fatty change)
- Cellular functions are altered but can be restored if the injurious stimulus is removed
TLO 1.3 Discuss the pathogenesis and features of reversible and irreversible cell injury
Irreversible cell injury:
**Pathogenesis of Irreversible Cell Injury
**Membrane Damage
Mitochondrial Dysfunction
Calcium Influx
Reactive Oxygen Species (ROS) Production
Nuclear Changes
**Features of Irreversible Cell Injury
**Cellular Swelling
Loss of Membrane Integrity
Mitochondrial Damage
Nuclear Changes
Increased Calcium Levels
Lysosomal Enzyme Release
The transition from reversible to irreversible injury is marked by the inability to reverse mitochondrial dysfunction and extreme disturbances in membrane function.
TLO 1.4 Compare the cellular features of reversible and irreversible injury
Reversible injury features:
Fatty Changes
Mitochondrial Changes
Endoplasmic Reticulum (ER) Changes
Nuclear Changes
Cellular Swelling
Plasma Membrane Alterations
TLO 1.4 Compare the cellular features of reversible and irreversible injury
Irreversible injury features:
Irreversible injury features:
* Severe mitochondrial damage
* Extensive damage to plasma membrane
* Nuclear changes (pyknosis, karyorrhexis, karyolysis)
* Cytoplasmic blebs rupture
* Lysosomes rupture and release hydrolytic enzymes
The key difference is that in reversible injury, the basic cell structure remains intact and can recover, while in irreversible injury, there is a breakdown of cellular organelles and membranes leading to cell death.
Topic 2 – Irreversible Cell Injury
TLO 2.1 Describe the pathogenesis of different types of necrosis
Necrosis is a form of cell death characterized by cellular swelling, breakdown of organelles, and rupture of cell membranes. The main types of necrosis include:
**Coagulative Necrosis:
**
Pathogenesis: Occurs due to ischemia (reduced blood flow) leading to loss of blood supply. This results in protein denaturation, which preserves the basic cell outlines but makes the tissue firm.
**Liquefactive Necrosis:
**
Pathogenesis: Caused by enzymatic digestion of dead cells. Common in the brain due to its high lipid content and in abscesses due to bacterial infections. Results in a liquid, viscous mass.
**Caseous Necrosis:
**
Pathogenesis: Typically seen in tuberculosis infections. The immune response causes a combination of coagulative and liquefactive necrosis, resulting in a cheese-like appearance.
**Fat Necrosis:
**
Pathogenesis: Caused by the release of pancreatic enzymes that digest fat cells (e.g., in acute pancreatitis) or by trauma to fatty tissues. Results in chalky, white areas due to fat saponification.
**Fibrinoid Necrosis:
**
Pathogenesis: Occurs in immune-mediated diseases. Immune complexes and fibrin are deposited in vessel walls, causing a bright pink, fibrin-like appearance on microscopy.
**Gangrenous Necrosis:
**
Pathogenesis: Results from severe hypoxia, often due to ischemia. Can be classified as dry gangrene (coagulative) or wet gangrene (liquefactive) if secondary infection is present.
These pathogenesis mechanisms help explain how different types of necrosis occur and their distinct features.
TLO 2.2 Discuss the morphological features of different types of necrosis
**Coagulative Necrosis:
**Gross Appearance: Firm tissue
Microscopic Appearance: Cell outlines preserved (ghost-like cells), red appearance
**Liquefactive Necrosis:
**Gross Appearance: Liquid, creamy yellow (pus)
Microscopic Appearance: Many neutrophils and cell debris
**Caseous Necrosis:
**Gross Appearance: White, soft, cheesy material
Microscopic Appearance: Fragmented cells and debris surrounded by lymphocytes and macrophages (granuloma)
**Fat Necrosis:
**Gross Appearance: Chalky, white areas
Microscopic Appearance: Shadowy outlines of dead fat cells, sometimes bluish from calcium deposits
**Fibrinoid Necrosis:
**Gross Appearance: Changes too small to see grossly
Microscopic Appearance: Thickened vessel walls, pinkish-red deposits (fibrin-like)
**Gangrenous Necrosis:
**Gross Appearance: Black, dead skin; underlying tissue in varying stages of decomposition
Microscopic Appearance: Initially coagulative necrosis, followed by liquefactive necrosis if infected
TLO 2.3 Discuss the pathogenesis of apoptosis
Apoptosis is a programmed cell death process characterized by:
- Activation of caspase enzymes
- Chromatin condensation and DNA fragmentation
- Cell shrinkage and membrane blebbing
- Formation of apoptotic bodies
There are two main pathways of apoptosis:
- Extrinsic pathway: Triggered by external signals binding to death receptors on the cell surface.
- Intrinsic pathway: Initiated by internal cellular stress, leading to mitochondrial release of cytochrome c.
Both pathways converge on the activation of executioner caspases, which cleave cellular proteins and lead to cell death
TLO 2.4 List examples of physiologic apoptosis
- Embryonic development (e.g., formation of digits)
- Hormone-dependent involution (e.g., endometrial breakdown during menstruation)
- Cell turnover in continuously renewing tissues (e.g., intestinal epithelium)
- Immune system regulation (e.g., deletion of self-reactive T cells)
TLO 2.4 List examples of pathologic apoptosis
**Neurodegenerative Diseases:
**Alzheimer’s disease
Parkinson’s disease
Huntington’s disease
**Viral Infections:
**HIV/AIDS
Hepatitis B and C
**Cancer:
**Tumor regression after chemotherapy
Radiation therapy
**Autoimmune Disorders:
**Systemic lupus erythematosus (SLE)
Type 1 diabetes
**Ischemia-Reperfusion Injury:
**Myocardial infarction (heart attack)
Stroke
These are some situations where apoptosis, or programmed cell death, occurs pathologically and contributes to disease processes.
Topic 3 – Acute Inflammation
TLO 3.1 List the causes and cardinal signs of inflammation
Causes of inflammation:
**Infections:
**Bacteria
Viruses
Fungi
Parasites
**Physical Injury:
**Trauma
Cuts and wounds
Burns
Frostbite
**Chemical Agents:
**Toxins
Irritants
**Immune Reactions:
**Autoimmune diseases (e.g., rheumatoid arthritis)
Allergies (e.g., pollen, pet dander)
**Foreign Bodies:
**Splinters
Dirt
Surgical sutures
**Chronic Conditions:
**Obesity
Chronic infections (e.g., tuberculosis)
**Tissue necrosis
**
Cardinal signs of inflammation (5 classical signs):
Calor (heat)
Dolor (pain)
Rubor (redness)
Tumor (swelling)
Functio laesa (loss of function)
TLO 3.2 Discuss the vascular and cellular events in inflammation
Vascular events:
Vascular events:
1. Vasodilation: Increased blood flow to the affected area
2. Increased vascular permeability: Allows plasma proteins and fluid to enter
TLO 3.2 Discuss the vascular and cellular events in inflammation
Cellular events:
Cellular events:
1. Margination: Leukocytes line up along vessel walls
2. Rolling: Leukocytes roll along endothelium
3. Adhesion: Leukocytes firmly attach to endothelium
4. Transmigration: Leukocytes move through vessel walls into tissues
5. Chemotaxis: Directed movement of leukocytes towards the site of injury
6. Phagocytosis: Ingestion and destruction of microbes and debris
TLO 3.3 Discuss the mediators and outcomes of acute inflammation
Mediators of inflammation:
These mediators work together to produce the signs and symptoms of inflammation, such as redness, heat, swelling, pain, and loss of function.
- Vasoactive amines (e.g., histamine)
- Plasma proteins (e.g., complement, kinins)
- Lipid mediators (e.g., prostaglandins, leukotrienes)
- Cytokines (e.g., TNF-α, IL-1)
- Chemokines
- Nitric oxide
Histamine:
Released by mast cells and basophils
Causes vasodilation and increased permeability of blood vessels
Prostaglandins:
Produced from arachidonic acid
Cause vasodilation, pain, and fever
Cytokines:
Small proteins released by immune cells
Include interleukins (IL), tumor necrosis factor (TNF), and interferons (IFN)
Regulate immune and inflammatory responses
Leukotrienes:
Produced from arachidonic acid
Cause increased permeability of blood vessels and attract white blood cells (chemotaxis)
Bradykinin:
A peptide that causes vasodilation and increases permeability of blood vessels
Causes pain and smooth muscle contraction
TLO 3.3 Discuss the mediators and outcomes of acute inflammation
Outcomes of acute inflammation:
Outcomes of acute inflammation:
1. Resolution: Complete restoration of normal tissue structure and function
2. Fibrosis: Replacement of damaged tissue with scar tissue
3. Abscess formation: Localized collection of pus
4. Chronic inflammation: Persistent inflammatory response
TLO 3.4 Describe the morphological features of acute inflammation
Morphological features of acute inflammation include:
1. Vascular changes:
- Vascular changes:
* Vasodilation
* Increased blood flow
* Vascular congestion
TLO 3.4 Describe the morphological features of acute inflammation
Morphological features associated with each of these aspects of acute inflammation:
**Vascular Changes:
**Vasodilation:
**Blood vessels widen, leading to increased blood flow.
Causes redness and warmth in the affected area.
**Increased Vascular Permeability:
**Blood vessel walls become more permeable.
Plasma proteins and fluids leak into the surrounding tissue.
Edema:
Fluid Accumulation:
Result of increased vascular permeability.
Causes swelling due to the accumulation of fluid in tissues.
Cellular Infiltrate:
Leukocyte Migration:
White blood cells (mainly neutrophils) move out of blood vessels into the inflamed tissue.
Involves rolling, adhesion, and transmigration of leukocytes.
**Phagocytosis:
***
Immune cells engulf and digest pathogens and debris.
**Fibrin Deposition:
Fibrin Formation:
Fibrinogen leaks from blood vessels and is converted to fibrin.
Fibrin forms a mesh-like structure in the tissue.
Tissue Necrosis:
Cell Death:
Severe or prolonged inflammation can lead to cell injury and death (necrosis).
Accumulation of dead cells and debris in the inflamed area.
These features collectively contribute to the signs and symptoms of acute inflammation, such as redness, heat, swelling, pain, and loss of function.
TLO 3.4 Describe the morphological features of acute inflammation
3. Cellular infiltrate:
- Cellular infiltrate:
* Predominance of neutrophils in early stages
* Later influx of macrophages and lymphocytes
TLO 3.4 Describe the morphological features of acute inflammation
4. Fibrin deposition:
- Fibrin deposition:
* Formation of fibrin networks in exudates
TLO 3.4 Describe the morphological features of acute inflammation
TLO 3.4 Describe the morphological features of acute inflammation
5. Tissue necrosis:
- Tissue necrosis:
* In severe cases, localized tissue destruction
Specific patterns of acute inflammation include:
- Serous inflammation: Protein-rich fluid exudate
- Fibrinous inflammation: Exudate rich in fibrin
- Suppurative (purulent) inflammation: Formation of pus
- Ulcers: Local defects in surface epithelium
Topic 4 – Chronic Inflammation and Wound Healing
TLO 4.1 Describe the pathogenesis and morphological features of chronic inflammation
Pathogenesis of chronic inflammation:
Pathogenesis of chronic inflammation:
* Persistent infection
* Prolonged exposure to toxic agents
* Autoimmune reactions
* Recurrent acute inflammation
TLO 4.1 Describe the pathogenesis and morphological features of chronic inflammation
Morphological features:
- Cellular infiltrate: Predominance of mononuclear cells (lymphocytes, plasma cells, macrophages)
- Tissue destruction: Ongoing damage due to inflammatory mediators
- Repair: Attempts at healing through fibrosis and angiogenesis
- Granulation tissue formation: New blood vessels and fibroblasts
- Fibrosis: Excessive collagen deposition leading to scarring
TLO 4.2 Discuss the morphological features of granulomatous inflammation
Granulomatous inflammation is characterized by:
Granulomatous inflammation is characterized by:
1. Formation of granulomas: Focal collections of activated macrophages
2. Epithelioid cells: Modified macrophages with abundant pink cytoplasm
3. Multinucleated giant cells: Fusion of epithelioid cells
4. Lymphocyte cuff: Surrounding the granuloma
5. Central necrosis: In some cases (e.g., tuberculosis)
6. Fibrosis: Surrounding the granuloma in later stages
Types of granulomas:
- Foreign body granulomas
- Immune granulomas (e.g., tuberculosis, sarcoidosis)
TLO 4.3 Enumerate the complications and factors affecting wound healing
Complications of wound healing:
Complications of wound healing:
1. Excessive scarring or keloid formation
2. Wound dehiscence (separation of wound edges)
3. Infection
4. Chronic non-healing wounds
Factors affecting wound healing:
1. Local factors:
2. Systemic factors:
Factors affecting wound healing:
1. Local factors:
* Infection
* Poor blood supply
* Foreign bodies
* Mechanical stress
2. Systemic factors:
* Age
* Nutrition
* Diabetes
* Medications (e.g., steroids)
* Smoking
* Obesity
* Stress
TLO 4.4 Describe the stages of wound healing
The stages of wound healing are:
- Hemostasis (immediate):
* Vasoconstriction
* Platelet aggregation
* Fibrin clot formation - Inflammatory phase (1-4 days):
* Neutrophil and macrophage infiltration
* Removal of debris and bacteria - Proliferative phase (4-21 days):
* Angiogenesis
* Fibroblast proliferation
* Collagen synthesis
* Granulation tissue formation
* Re-epithelialization - Remodeling phase (21 days to 1 year):
* Collagen reorganization
* Scar maturation
* Gradual regain of tissue strength
Topic 5 – Basics of Neoplasia
TLO 5.1 Define and classify neoplasms
A neoplasm is an abnormal mass of tissue resulting from uncontrolled, excessive growth of cells that persists even after the initial stimulus is removed.
Classification of neoplasms:
Classification of neoplasms:
1. By behavior:
* Benign
* Malignant (cancer)
* Potentially malignant (in situ)
2. By tissue of origin:
Carcinomas: Originate from epithelial tissue (e.g., skin, lining of organs)
Sarcomas: Originate from connective tissue (e.g., bone, muscle, cartilage)
Leukemias: Cancers of the blood-forming cells (white blood cells, red blood cells, platelets)
Lymphomas: Cancers of the lymphatic system (lymph nodes, spleen)
TLO 5.2 Discuss the features of benign neoplasms
Features of benign neoplasms:
- Slow growth rate
- Well-circumscribed and often encapsulated
- Resemblance to tissue of origin (well-differentiated)
- Lack of invasion into surrounding tissues
- No metastasis
- Limited effect on host (unless in a critical location)
- Generally good prognosis
- Often can be surgically removed with low risk of recurrence
TLO 5.3 Discuss the features of malignant neoplasms with examples
Features of malignant neoplasms:
Features of malignant neoplasms:
1. Rapid, uncontrolled growth
2. Poorly circumscribed and invasive
3. Loss of differentiation (anaplasia)
4. Invasion of surrounding tissues
5. Ability to metastasize
6. Significant effect on host health
7. Poor prognosis if untreated
8. High risk of recurrence after treatment
Examples:
* Carcinomas: Lung cancer, breast cancer, colorectal cancer
* Sarcomas: Osteosarcoma, leiomyosarcoma
* Hematologic malignancies: Leukemias, lymphomas
* Brain tumors: Glioblastoma multiforme
TLO 5.4 List the differences between benign and malignant neoplasms
Differences between benign and malignant neoplasms:
- Growth rate: Benign - slow; Malignant - rapid
- Differentiation: Benign - well-differentiated; Malignant - poorly differentiated
- Capsule: Benign - often encapsulated; Malignant - not encapsulated
- Invasion: Benign - no invasion; Malignant - invasive growth
- Metastasis: Benign - no metastasis; Malignant - can metastasize
- Prognosis: Benign - generally good; Malignant - often poor if untreated
- Effect on host: Benign - limited; Malignant - significant
- Recurrence: Benign - rare; Malignant - common
- Nuclear features: Benign - normal; Malignant - abnormal (pleomorphism, hyperchromatism)
- Mitotic activity: Benign - low; Malignant - high, often abnormal
Topic 6 – Molecular Basis of Cancer
TLO 6.1 List the risk factors of cancer with examples
Risk factors for cancer include:
- Genetic factors: Inherited mutations (e.g., BRCA1/2 in breast cancer)
- Age: Increased risk with advancing age
- Tobacco use: Lung, mouth, throat cancers
- Alcohol consumption: Liver, esophageal, breast cancers
- Chronic infections: HPV (cervical cancer), Hepatitis B/C (liver cancer)
- Environmental toxins: Asbestos (mesothelioma), UV radiation (skin cancer)
- Diet: High red meat consumption (colorectal cancer)
- Obesity: Increased risk for various cancers including breast and colon
- Lack of physical activity: Increased risk for colon and breast cancers
- Hormonal factors: Prolonged estrogen exposure (breast cancer)
- Immunosuppression: Increased risk of various cancers
- Occupational exposures: Certain chemicals, radiation
TLO 6.2 Discuss the mechanism of action of oncogenes, tumor suppressor genes and DNA repair genes with examples
Oncogenes:
- Mechanism: Gain-of-function mutations in proto-oncogenes lead to increased cell proliferation or survival
- Examples:
1. RAS: Constitutively active in many cancers, promoting cell growth and survival
2. MYC: Overexpressed in various cancers, enhancing cell proliferation
3. HER2/neu: Amplified in some breast cancers, leading to increased cell division
Tumor suppressor genes:
- Mechanism: Loss-of-function mutations result in uncontrolled cell growth
- Examples:
1. TP53: “Guardian of the genome,” regulates cell cycle and apoptosis
2. RB: Controls cell cycle progression
3. APC: Regulates cell adhesion and signal transduction in colon cells
DNA repair genes:
- Mechanism: Mutations lead to genomic instability and accumulation of mutations
- Examples:
1. BRCA1/2: Involved in double-strand break repair, mutations increase breast and ovarian cancer risk
2. MLH1/MSH2: Mismatch repair genes, mutations cause Lynch syndrome
3. XPA/XPC: Nucleotide excision repair genes, mutations cause xeroderma pigmentosum
TLO 6.3 Discuss angiogenesis and metastasis of malignant tumors
Angiogenesis:
- Definition: Formation of new blood vessels to supply the tumor
- Process:
1. Tumor cells release pro-angiogenic factors (e.g., VEGF)
2. Endothelial cells are activated and proliferate
3. New blood vessels form and grow towards the tumor - Importance: Essential for tumor growth beyond 1-2 mm and facilitates metastasis
- Therapeutic target: Anti-angiogenic drugs (e.g., bevacizumab) can inhibit tumor growth
Metastasis
- Definition: Spread of cancer cells from primary site to distant organs
- Steps in metastasis:
1. Local invasion: Cancer cells break through basement membrane
2. Intravasation: Cells enter blood or lymphatic vessels
3. Survival in circulation: Cells resist immune attack and mechanical stress
4. Extravasation: Cells exit vessels at distant sites
5. Colonization: Cells adapt and grow in new environment
- Factors influencing metastasis:
- Epithelial-mesenchymal transition (EMT)
- Matrix metalloproteinases (MMPs)
- Adhesion molecules
- Chemokines and their receptors
* Common metastatic sites: Lungs, liver, bones, brain
TLO 6.4 Classify carcinogens and describe the mechanism of action of chemical carcinogens
Classification of carcinogens:
- Chemical carcinogens
- Physical carcinogens (e.g., radiation, asbestos)
- Biological carcinogens (e.g., viruses)
Chemical carcinogens can be further classified as:
- Direct-acting carcinogens
- Indirect-acting carcinogens (procarcinogens)
Mechanism of action of chemical carcinogens:
Chemical carcinogenesis is a multi-step process involving initiation, promotion, and progression. Initiation involves the initial DNA damage caused by the carcinogen. Promotion stimulates the growth of initiated cells. Progression involves further genetic and epigenetic changes that lead to the development of a malignant tumor.
- Initiation:
* Carcinogen or its metabolite interacts with DNA
* Forms DNA adducts or causes mutations
* Examples: Alkylating agents, polycyclic aromatic hydrocarbons (PAHs)
- Initiation:
- Promotion:
* Stimulates proliferation of initiated cells
* Does not directly damage DNA
* Examples: Phorbol esters, phenobarbital - Progression:
* Accumulation of additional genetic changes
* Leads to increased growth and invasive potential
Mechanism of action of chemical carcinogens:
Specific mechanisms:
Specific mechanisms:
1. Direct DNA damage: Alkylating agents form DNA adducts
2. Metabolic activation: Procarcinogens (e.g., benzo[a]pyrene) are activated by cytochrome P450 enzymes
3. Generation of reactive oxygen species: Leads to oxidative DNA damage
4. Epigenetic changes: Altered DNA methylation or histone modifications
5. Interference with DNA repair: Some carcinogens inhibit DNA repair mechanisms
This is for informational purposes only. For medical advice or diagnosis, consult a professional.
Chemical carcinogens can cause cancer by damaging DNA, the genetic material within cells. Here’s a simplified explanation of their mechanisms of action:
- Direct DNA Damage:
Direct Interaction: Some chemicals can directly react with DNA, causing:
DNA strand breaks: These disrupt the integrity of the DNA molecule.
DNA cross-linking: Chemical bonds form between different parts of the DNA strand, hindering normal cell function.
Base modifications: Chemical groups can be added to or removed from DNA bases, altering their structure and function.
- Indirect DNA Damage:
Metabolic Activation: Many chemicals are not directly harmful but are converted into reactive metabolites within the body. This often happens in the liver through the action of enzymes called cytochrome P450.
Reactive Metabolites: These activated forms of the chemical can then react with DNA, causing damage.
Key Takeaways:
Chemical carcinogens damage DNA in various ways, leading to mutations that can contribute to cancer development.
Some chemicals directly damage DNA, while others require metabolic activation to become harmful.
These mechanisms disrupt the normal cell cycle and can lead to uncontrolled cell growth and division, the hallmark of cancer.
Examples of chemical carcinogens:
- Tobacco smoke components (e.g., nitrosamines, PAHs)
- Aflatoxin B1 (produced by Aspergillus fungi)
- Vinyl chloride (industrial chemical)
- Benzene (solvent and industrial chemical)
- Arsenic compounds (environmental contaminant)
Chemical carcinogens are substances that can cause cancer by damaging DNA, the genetic material within cells. Here are some examples:
Industrial Chemicals:
Aromatic amines: Found in dyes, rubber, and some pharmaceuticals.
Polycyclic aromatic hydrocarbons (PAHs): Present in tobacco smoke, coal tar, and grilled food.
Vinyl chloride: Used in the production of PVC plastics.
Asbestos: A mineral used in insulation and construction materials.
Formaldehyde: Used in building materials, preservatives, and disinfectants.
Environmental Pollutants:
Air pollution: Includes particulate matter, nitrogen oxides, and other pollutants from vehicle exhaust and industrial emissions.
Water pollution: Contaminated water can contain industrial chemicals, pesticides, and heavy metals.
Soil contamination: Industrial waste and agricultural runoff can contaminate soil with harmful chemicals.
Lifestyle Exposures:
Tobacco smoke: Contains numerous carcinogens, including nicotine, tar, and PAHs.
Alcohol consumption: Excessive alcohol consumption can increase the risk of certain cancers, such as liver cancer.
Dietary factors: Processed meats, excessive red meat consumption, and diets low in fruits and vegetables can increase cancer risk.
Medical Treatments:
Chemotherapy drugs: Some chemotherapy drugs can increase the risk of secondary cancers.
Radiation therapy: High doses of radiation can damage DNA and increase the risk of cancer.
A 65-year-old man is brought to the ER with complaints of chest pain radiating to the left arm. He isdiagnosed to have myocardial infarction due to a block in the left anterior descending artery. Arepresentative section from the myocardial infarct is shown in the image. The infarct shows which typeof necrosis?
a.
Fibrinoid necrosis
b.
Liquefactive necrosis
c.
Caseous necrosis
d.
Coagulative necrosis
e.
Gangrenous necrosis
Coagulative necrosis
Factors that inhibit wound healing include all the following EXCEPT
a.
Advanced age
b.
Smoking
c.
Vitamin C
d.
Presence of foreign body
e.
Immunosuppression
Vitamin C
All of the following are TRUE regarding apoptosis EXCEPT
a.
The apoptotic cell attracts inflammatory cells
b.
It is programmed cell death
c.
The nucleus of the cell undergoes pyknosis
d.
Apoptotic bodies are phagocytosed by macrophages
The apoptotic cell attracts inflammatory cells
A 45-year-old patient diagnosed to have acute appendicitis undergoes appendicectomy. Grossexamination of the appendix will show all of the following EXCEPT
a.
Exudate on the serosa
b.
Fibrosis of the wall
c.
Edema of the wall
d.
Congested blood vessels
Fibrosis of the wall
A pathologist notes fatty change in the liver biopsy of a patient with history of alcohol abuse. This finding is an example of
a.
Apoptosis
b.
Reversible injury
c.
Irreversible injury
Reversible injury
The most common etiologic agent of gas gangrene is
a.
Escherichia coli
b.
Staphylococcus aureus
c.
Streptococcus pyogenes
d.
Clostridium perfringens
Clostridium perfringens
A 25-year-old male presents to the ER with complaints of productive cough and progressivelyincreasing swelling in the neck for 3 months which has not subsided with multiple courses of antibiotics.He gives a history of low-grade fever, loss of appetite and weight loss. On examination, he has mattedlymph nodes in the right supraclavicular region. Laboratory investigations show elevated ESR and CRP.Sputum AFB, Quantiferon Tb Gold and PCR for tuberculosis is positive. Microscopic examination ofbiopsy from the lymph node is given below. The multinucleate cells shown by the arrow head arederived from the fusion of
a.
Lymphocytes
b.
Neutrophils
c.
Basophils
d.
Eosinophils
e.
Epithelioid cells
Epithelioid cells
A 45-year-old patient diagnosed to have acute appendicitis undergoes appendicectomy. Microscopicexamination of a section from the appendix will show predominantly which type of inflammatory cells?
a.
Lymphocytes
b.
Macrophages
c.
Plasma cells
d.
Neutrophils
Neutrophils
A 72-year-old male was diagnosed with diffuse atherosclerotic cerebrovascular disease (blockage ofblood vessels by atherosclerotic plaques). The brain parenchyma in this patient will show
a.
Hypertrophy
b.
Atrophy
c.
Hyperplasia
d.
Metaplasia
Atrophy
Chemotaxis refers to
a.
Increased random movement of WBC’s
b.
Migration of WBC’s between endothelial cells to the site of inflammation
c.
Unidirectional locomotion of WBC’s directed by chemoattractants
d.
Migration of WBC’s through the basement membrane
Unidirectional locomotion of WBC’s directed by chemoattractants
The multinucleate cell found in TB granuloma is known as
a.
Langhans giant cell
b.
Popcorn giant cell
c.
Langerhans giant cell
d.
Reed Sternberg giant cell
Langhans giant cell
The sequence of cellular events in acute inflammation is
a.
Margination, rolling, transmigration, firm adhesion, chemotaxis, phagocytosis
b.
Margination, rolling, firm adhesion, chemotaxis, transmigration, phagocytosis
c.
Margination, rolling, firm adhesion, transmigration, chemotaxis, phagocytosis
d.
Margination, firm adhesion, rolling, transmigration, chemotaxis, phagocytosis
Margination, rolling, firm adhesion, transmigration, chemotaxis, phagocytosis
A 58-year-old man who presents to the ER with complaints of heart burn and dysphagia undergoesesophagoscopy. Microscopic examination findings of the oesophageal biopsy given shows which typeof adaptive change in the lining epithelium?
a.
Dysplasia
b.
Neoplasia
c.
Anaplasia
d.
Metaplasia
e.
Hyperplasia
Metaplasia
Diapedesis refers to
a.
Migration of RBC’s through the basement membrane
b.
Migration of leukocytes through the vessel wall to the site of inflammation
c.
Aggregation of platelets at the site of injury
Migration of leukocytes through the vessel wall to the site of inflammation
A 36-year-old lady presents with a painful mass in the breast ten days after a fall. Examination of thebreast shows a hard lump. Microscopic examination of the excised lump will show
a.
Caseous necrosis
b.
Fibrinoid necrosis
c.
Coagulative necrosis
d.
Fat necrosis
e.
Liquefactive necrosis
Fat necrosis
Microscopic examination of section from the liver following embolism of the hepatic artery shows ghostcells and increased eosinophilia of hepatocytes. This is a characteristic microscopic feature of
a.
Caseous necrosis
b.
Liquefactive necrosis
c.
Gangrenous necrosis
d.
Fat necrosis
e.
Coagulative necrosis
Coagulative necrosis
The maximum tensile strength of the injured tissue reached on wound healing compared to the normaltissue is
a.
100%
b.
50%
c.
80%
d.
30%
0.8
Non-caseating granulomas are seen in all the following EXCEPT
a.
Sarcoidosis
b.
Hodgkin lymphoma
c.
Crohn disease
d.
Tuberculosis
Tuberculosis
A 50-year-old man who presents to the ER with complaints of chest pain for one day is diagnosed tohave a myocardial infarct. He dies before intervention. Microscopic examination of the infarct will show
a.
Liquefactive necrosis of cardiac myocytes with lymphocyte infiltrate
b.
Caseous necrosis of cardiac myocytes with plasma cell infiltrate
c.
Coagulative necrosis of cardiac myocytes with neutrophil infiltrate
d.
Fibrinoid necrosis of cardiac myocytes with macrophage infiltrate
e.
Dense fibrous scar
Coagulative necrosis of cardiac myocytes with neutrophil infiltrate
Reversible Injury
Reversible Injury
Cells Undergo cloudy swelling
Cell Membrane Blebbing
Mitochondria Swollen and vacuolated
Nucleus Clumping of chromatin
Myelin Figures Rare
Endoplasmic Reticulum (ER) Swollen
Lysosomes Intact
Irreversible Injury
Irreversible Injury
Cells Cell death occurs
Cell Membrane Discontinuous
Mitochondria Amorphous density and calcification
Nucleus Pyknosis, karyorrhexis, karyolysis
Myelin Figures Swollen with loss of ribosomes
Endoplasmic Reticulum (ER) Swollen with loss of ribosomes
Lysosomes Ruptured with release of enzymes
Summary of Cellular Events
Cellular Events of Inflammation Caused/Mediated By
Margination Stasis of blood with reduced shear stress on endothelial cells
Rolling and Transient Adhesion Binding of selectins with their ligands
Firm Adhesion and Transmigration Binding of integrins (LFA-1 & VLA-4) to IgS CAMs (ICAM, VCAM, and JAM)
Binding of PECAM molecules
Chemotaxis Bacterial products, cytokines, components of the complement system, and phospholipids
Phagocytosis Interaction of TLRs (on phagocytes) with PAMPs (on the pathogen)
Mediators of Inflammation
Cell Derived Mediators Functions
Vasoactive Amines (Histamine, Serotonin) Vasodilation, increased vascular permeability, and smooth muscle contraction
Nitric Oxide (NO) Smooth muscle relaxation, vasodilation, inhibits platelet function
Cytokines Pro-inflammatory and anti-inflammatory action, functioning of the immune system, hematopoiesis, antiviral action, and acute phase response
Eicosanoids Vasodilation & increased vascular permeability (PGI2 and prostacyclin), vasoconstriction & platelet aggregation (thromboxane, leukotriene)
Reactive Oxygen Species Microbial killing, cell damage, and inflammatory response
Lysosomal Enzymes Increase vascular permeability, chemotaxis of inflammatory cells, activation of complement components, degrade bacteria and extracellular matrix
Platelet Activating Factor (PAF) Vasodilation, platelet activation, increased vascular permeability, and bronchoconstriction
Common Benign Tumors & Their Malignant Counterparts
Common Benign Tumors & Their Malignant Counterparts
Epithelial Tissue
Benign Tumor: Squamous cell papilloma
Malignant Tumor: Squamous cell carcinoma
Connective Tissue
Fibrocyte
Benign Tumor: Fibroma
Malignant Tumor: Fibrosarcoma
Cartilage
Benign Tumor: Chondroma
Malignant Tumor: Chondrosarcoma
Bone
Benign Tumor: Osteoma
Malignant Tumor: Osteosarcoma
Fat
Benign Tumor: Lipoma
Malignant Tumor: Liposarcoma
Bone Marrow
No benign tumor
Malignant Tumor: Leukemia
Lymph Node
Benign Tumor: Lymphoma
Malignant Tumor: Lymphosarcoma
Blood Vessel
Benign Tumor: Hemangioma
Malignant Tumor: Hemangiosarcoma
Muscle Tissue
Smooth Muscle
Benign Tumor: Leiomyoma
Malignant Tumor: Leiomyosarcoma
Skeletal Muscle
Benign Tumor: Rhabdomyoma
Malignant Tumor: Rhabdomyosarcoma
Retinoblastoma gene and TP53 gene mutations are examples of which mechanism that could lead to cancer?
Retinoblastoma gene and TP53 gene mutations are examples of which mechanism that could lead to cancer?
Increasing apoptosis
Proto-oncogenes being converted to oncogenes
Inactivation of tumor suppressor genes (selected)
Mutation in DNA repair genes
Match the neoplasm with its description
Match the neoplasm with its description
Squamous cell carcinoma:
Malignant tumor of epithelial cells
Chondroma:
Benign tumor of cartilage
Osteosarcoma:
Malignant tumor of bone
Leiomyoma:
Benign tumor of smooth muscle
Liposarcoma:
Malignant tumor of adipocytes
Which of the following can cause chronic inflammation? Select all that apply:
Persistent infection
Autoimmune disorder
Acute exposure to an environmental toxin
Chronic exposure to an environmental toxin
Which of the following can cause chronic inflammation? Select all that apply:
☑ Persistent infection
☑ Autoimmune disorder
☐ Acute exposure to an environmental toxin
☑ Chronic exposure to an environmental toxin
What is the convergence point of both the intrinsic and extrinsic pathways of apoptosis?
Executor caspases activated
Initiator caspases activated
Increased BAX and BAK proteins
Fas ligand binding to Fas receptor
Cytochrome c leakage from mitochondria
What is the convergence point of both the intrinsic and extrinsic pathways of apoptosis?
Initiator caspases activated
Match the cell adaptation to its description
Match the cell adaptation to its description
Hypertrophy: Increase in the size of cells
Atrophy: Decrease in the size of cells
Hyperplasia: Increase in the number of cells
Metaplasia: Change to a different cell type
