Module 6.2 Pulmonary Disorders Flashcards
How does paroxysmal nocturnal dyspnea occur?
This occurs when individuals with heart failure or lung disease wake up at night gasping for air and must sit up or stand to relieve the dyspnea.
What causes (physiologically) the symptoms associated with paroxysmal nocturnal dyspnea?
- When patients are lying down flat, this position redistributes body water, causes the abdominal contents to exert pressure on the diaphragm, and decreases the efficiency of the respiratory muscles.
- There is increased pressure in the bronchial arteries, leading to airway compression, along with interstitial pulmonary edema that leads to increased airway resistance
- This causes patients to wake up gasping for air to relieve the dyspnea.
What is consolidation?
Occurs when inflammation causes the alveoli to fill with fluid, pus, and microorganisms.
What is hypoxemia?
It is caused by reduced oxygenation of arterial blood (reduced PaO2) caused by respiratory alterations.
What causes hypoxemia?
Hypoxemia results from problems with one or more of the major mechanisms of oxygenation:
- Oxygen delivery to the alveoli
- Oxygen content of the inspired air
- Ventilation of the alveoli
- Diffusion of oxygen from the alveoli into the blood
- The balance between alveolar ventilation and perfusion (V/Q mismatch) MOST COMMON CAUSE OF HYPOXEMIA
- Diffusion of oxygen across the alveolocapillary membrane
- Perfusion of pulmonary capillaries
What can cause hypoxemia at the capillary level?
- Normally, alveolocapillary lung units receive almost equal amounts of ventilation and perfusion
- Hypoxemia caused by inadequate ventilation of well perfused areas of the lung (low V/Q), is called shunting.
- Occur with atelectasis, asthma from bronchoconstriction, pulmonary edema, and pneumonia when the alveoli are filled with fluid.
- Causes a right to left shunt
- Hypoxemia caused by poor perfusion of well-ventilated areas of the lung (high V/Q), is called alveolar dead space
- Commonly caused by a pulmonary embolus that impairs blood flow to a segment of the lung
What is asthma?
A chronic inflammatory disorder of the bronchial mucosa that causes bronchial hyperresponsiveness, construction of the airways, and variable airflow obstruction that is reversible
Describe the pathophysiological cause of asthma
- Airway epithelial exposure to an antigen initiates an innate & adaptive immune response
- Patho is related to hyperresponsive lower airways and inflammation to a stimulus (trigger).
- The response has two parts and early phase & a late phase.
- Triggers can include allergens, exercise, cold air, microorganisms
What happens during the early asthmatic response?
During the early response, Th2 cells release various cytokines, mast cells degranulate, and eosinophils release toxic substances that cause tissue injury. Together with various other cells an acute inflammatory response occurs causing vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction, and tenacious mucus secretion from goblet cells, narrowing the airways and obstructing airflow
What happens during the late asthmatic response?
- Begins 4-8 hours after the early response
- Chemotactic recruitment of lymphocytes, eosinophils, and neutrophils during the early response causes a latent release of inflammatory mediators, again causing bronchospasm, edema, and mucus secretion obstructing airflow.
- Leukotrienes released by mast cells contribute to prolonged smooth muscle contraction
- Eosinophil mediators cause tissue injury, fibroblast proliferation, and airway scarring
- Left untreated, causes irreversible airway damage, called airway remodeling.
What are the clinical manifestations of asthma?
bronchospasms, airway edema, and mucus plugs causing cough, wheeze, and dyspnea.
What role does acetylcholine play during and after an asthma attack?
- Acetylcholine acts on the airway smooth muscle, which induces bronchoconstriction, airway smooth muscle thickening, and the modulation of cytokine and chemokine production by these cells
- It induces cell responses associated with airway wall remodeling and triggers proinflammatory cytokine release by structural cells of the airway wall, including airway epithelial cells, airway fibroblasts, and the airway smooth muscle itself.
- These mechanisms promote airway inflammation and remodeling, including airway smooth muscle thickening.
What is emphysema?
- It is the abnormal permanent enlargement of gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis
- The major mechanism of airflow limitation in emphysema is loss of elastic recoil.
Describe the pathophysiological cause of emphysema
- Caused by destruction of alveoli through the breakdown of elastin within the septa by an imbalance between proteases and antiproteases, oxidative stress, and apoptosis of lung structural cells
- The apoptosis of alveolar cells reduces the surface area for gas exchange, producing large air spaces within the lung parenchyma (bullae)
- These changes lead to a V/Q mismatch
- Expiration becomes difficult b/c of loss of elastic recoil → air trapping → ↑WOB, leading to hypoventilation and hypercapnia.
Describe centriacinar emphysema
- Septal destruction occurs in the respiratory bronchioles and alveolar ducts, usually in the upper lobes of the lung.
- This tends to occur in smokers with chronic bronchitis
What are the clinical manifestations associated with emphysema?
- barrel chest, dyspnea, no cough, very little sputum, pt is thin, tachypnea with prolonged expiration uses accessory muscles for respiration, hyperresonant sounds on percussion.
How does smoking contribute to the development of emphysema?
- The inhalation of cigarette smoke causes inflammation of the airway epithelium causing eventual destruction of the alveolar septa and loss of elastic recoil in bronchial walls
What is bronchitis?
- It is a hypersecretion of mucus and chronic productive cough that continues for at least 3 months of the year, for at least 2 consecutive years
Describe the pathophysiological cause of bronchitis
- Inspired irritants result in airway inflammation, with infiltration of neutrophils, macrophages, and lymphocytes to the bronchial wall.
- Tabacco smoke directly injures airway epithelial cells
- Continual bronchial inflammation → bronchial edema & increases size & # of goblet cells → Thick, mucus is produced
- The mucus cannot be cleared because of the impaired ciliary function (they were damaged by the previous inflammation)
- ↓ ciliary function → ↑ susceptibility to pulmonary infection → more airway injury
- Airways collapse early in expiration, trapping gas in the distal portions of the lung = ventilation/perfusion mismatch = hypoventilation = increased Paco2 and hypoxemia.
What are the clinical manifestations of bronchitis?
- ↓’d exercise tolerance
- wheezing
- SOB
- Productive cough
- ↓’d FEV
- Frequent pulmonary infections
What is pneumonia?
It is an acute/chronic infection of the lower respiratory tract caused by bacteria, viruses, fungi, protozoa, or parasites.
Describe the pathophysiological cause of bacterial pneumonia
- Aspiration of oropharyngeal secretions containing bacteria leads to the bacteria depositing in the lower respiratory tract
- Innate and Adaptive immunity kick in:
- In the innate immunity: The complement system marks bacteria for destruction & neutrophils attempt to phagocytize microbes, release inflammatory mediators & immune complexes that damage the alveoli.
- Alveolar macrophages in the lower respiratory tract can recognize bacteria and they present the foreign antigens to T & B-cells activating the adaptive immunity.
- Inflammatory cytokines and cells are released that cause alveolar edema, which creates a medium for the multiplication of bacteria and aids in the spread of infection to adjacent portions of the lung
- The involved lobe undergoes consolidation, fibrin deposition to the area causes the tissues to become gray.
- Macrophages clean up by digesting any remaining bacteria, fibrin threads and are removed by the lymphatic vessels.
Describe the pathophysiological cause of viral pneumonia
- Is usually a complication of upper respiratory infection in which the virus spreads to the lower respiratory tract. The virus destroys ciliated epithelial cells and invades goblet cells and bronchial mucous glands.
- Sloughing of destroyed bronchial epithelium impairs mucous clearance by cilia. Bronchial cells are edematous and infiltrated with leukocytes. Like all viral infections, this infection is self-limiting, but there is the potential for secondary bacterial infection.
What is the difference between bacterial and viral pneumonia?
- Viral: In adults, this infection is much milder than bacterial infections. Affected individuals are much less toxic with minimal fever, no respiratory distress, and less mucus production. The infection is generalized throughout the lung.
- Bacterial: infections tend to localize in one area or lobe of the lung. They tend to develop and progress rapidly. The affected individual usually has a toxic appearance with fever and malaise. There is a moist and usually productive cough with purulent mucous. Children may only be able to cough up and swallow mucus. There may be respiratory distress and hypoxia.
What is tuberculosis?
An infection caused by Mycobacterium tuberculosis, an acid-fast bacillus that usually affects the lungs, but may invade other body systems
Describe the pathophysiological cause of Tuberculosis
- Tb is highly contagious and is transmitted from person-to-person in airborne droplets. They are inhaled by others and lodge in the lung periphery (usually in the upper lobe).
- Once in the lung, the bacteria multiply causing nonspecific pneumonitis. Some migrate through the lymphatics and initiate an immune response.
- Because m. tuberculosis is a relatively slow-growing bacterium, the body can mount defenses before it becomes pathogenic. Inflammation in the lung attracts neutrophils, and alveolar macrophages (cell-mediated response).
- These white blood cells seal off colonies of bacilli, forming granulomatous lesions called tubercles. Infected tissues in the tubercle die, creating areas of caseous necrosis. Collagenous scar tissue grows around the tubercle. The bacilli are now isolated and the tuberculosis is dormant.
- If the immune system is impaired or if live bacilli escape into the bronchi, active disease occurs. The infection can spread via blood and lymph to other organs.
What are the clinical manifestations of tuberculosis?
- May be asymptomatic
- Symptoms may develop gradually
- Immune suppressed, debilitated, malnourished, very young or elderly persons may experience rapid disease progression
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Manifestations include:
- Fatigue
- Weight loss
- Lethargy
- Anorexia
- Low grade fever (especially in the late afternoon)
- Night sweats
- Productive cough (chronic and worsening)
What is cystic fibrosis?
It is an inherited autosomal recessive disorder that is associated with defective epithelial chloride ion transport.
Describe the pathophysiological cause of cystic fibrosis
- Characterized by abnormal secretions that cause obstructive problems within the respiratory, digestive, and reproductive tracts.
- Lungs:
- thick secretions are difficult to clear from the airway
- There is an increased number and size of goblet cells
- Recurrent infections develop with inflammatory responses
- Decline in respiratory function with eventual death
- thick secretions are difficult to clear from the airway
- Pancreas:
- Secretions obstruct ducts
- Pancreatic enzymes don’t enter duodenum
- Impaired digestion of protein and fat, malabsorption
