Unit #7 Respiratory Disorders Flashcards
What is the etiology of pneumothorax – tension pneumothorax?
Characterized by accumulation of air in the pleural space.
- Spontaneous pneumothorax occurs mainly in tall, thin men between ages 20-40 years with no underlying disease factors.
- Smoking increases the risk of spontaneous pneumothorax
- Secondary pneumothorax occurs as a result of complications from pre-existing pulmonary disease (ex. asthma emphysema, cystic fibrosis)
What is the pathogenesis of pneumothorax – tension pneumothorax?
Spontaneous pneumothorax results from rupture of small subpleural blebs in the apices. When air enters the pleural space, the lungs collapse and the rib cage springs out.
- Subpleural blebs occur as a result of negative mechanical pressures in the upper third of the upright lung field.
- Secondary pneumothorax occurs as a complication from an underlying disease and may be due to rupture of a cyst or bleb.
- Tension pneumothorax results from build-up of air under pressure in the pleural space. Air enters the pleural space through inspiration but cannot escape on expiration.
What is the clinical manifestation of pneumothorax – tension pneumothorax?
- Tachycardia
- Decreased or absent lung sounds on affected side
- Hyperresonance
- Sudden chest pain on affected side
- Chest radiograph in tension pneumothorax shows a mediastinal shift.
What is the etiology of pulmonary hypertension?
Defined as a sustained increase in pulmonary artery pressure above 25 mm Hg systolic resting and above 30 mm Hg systolic with exercise. In primary pulmonary hypertension the cause is unknown but can be associated with use of appetite-suppressant drugs, HIV, and portal hypertension of cirrhosis. In secondary pulmonary hypertension the cause is associated with a known disease process. Increased blood flow, increased resistance to blood flow, and increased left atrial pressure.
What is the pathogenesis of pulmonary hypertension?
Chronic exposure to (increased left atrial pressure, increased pulmonary vascular resistance, and increased pulmonary blood flow).
- These result in morphologic changes within the arterial lumen (walls thicken initially because of tissue hypoxia, acidosis, or both)
- As the process intensifies, internals layers of artery become fibrotic.
What is the clinical manifestation of pulmonary hypertension?
Varies according to the severity/duration of the underlying pathologic process.
- Exercise intolerance is often the earliest clinical symptoms
- Patient may also experience; syncope (loss of consciousness), increasing dyspnea, chest pain on exertion, fatigue, hemoptysis (coughing up of blood from respiratory system), and pulmonary edema.
What is the etiology of pulmonary embolism?
Three physiologic factors that predispose patients to thrombus formation (1)venous stasis (sluggish blood flow), (2) hypercoagulability, and (3) damage to venous walls
-Most common risk factors include: immobility, pregnancy, heart failure, and estrogen use.
What is the pathogenesis of pulmonary embolism?
Thrombi are dislodged from their point of origin by multiple mechanism including direct trauma, exercise and muscle action, and changes in blood flow
- Once it is dislodged, they travel to the pulmonary vasculature
- Impact of pulmonary emboli depends on the size and cross-sectional area of circulatory impairment
- Arterial pressure increases because of vasoconstriction from actual mechanical obstruction of blood vessels and the release of serotonin and neural sympathetic stimulation
What is the clinical manifestation of pulmonary embolism?
- Depends on size of emboli
- Initial symptoms may be restlessness, apprehension, and anxiety
- Most common symptom is dyspnea
- Tachycardia
- Severe chest pain (associated with medium-massive sized emboli)
- Can lead to heart failure, shock, and respiratory arrest
What is the etiology of asthma?
- Lung disease characterized by an airway obstruction that is reversible (but not completely in some patients)
- Airway inflammation and increased airway reactivity to a variety of stimuli
- Most cases of asthma can be triggered both by allergens and stimuli, such as exercise and exposure to cold air.
- Asthma is associated with the release of inflammatory chemicals from mast cells in the airways
- Mechanisms stimulating mast cell release are allergic, IgE mediated triggers for extrinsic/allergic asthmas
- In intrinsic/non-allergic asthmas occurs in patients with no history of allergy.
- In exercise induced asthmas heat loss, water loss, and increased osmolarity of the lower respiratory mucosa are believed to stimulate mediator release from basophils and tissue mast cells.
What is the pathogenesis of asthma?
- Inflammation of the airway contributes to acute bronchospasm, mucosal edema, mucous plug formation, and airway wall remodelling.
- Strong association with the ADAM33 gene with asthmatic bronchial hyper-responsiveness.
- In allergic asthmas, an IgE-mediated response is common and is mansifested by elevated IgE levels, allergic rhinitis, eczema, a positive family history of asthmas, and attacks associate with seasonal, environmental or occupational exposure.
- Mechanism for action is initiated by exposure to a specific antigen that has previously sensitized mast cells in airway mucosa. When the antigen reacts with the antibody on the surface of the mast cell, packets of chemical mediators that are released include histamine, slow-reacting substances of anaphylaxis, prostaglandins, bradykinins, serotonin, and others.
What is the clinical manifestation of asthma?
- Common symptoms include wheezing, feelings of tightness in the chest, dyspnea, cough, and increased sputum production
- Some patients have chronic dry cough, and others have a productive cough
What is the etiology of acute bronchitis?
- Acute inflammation of the trachea and bronchi by a variety of viruses (ex. Influenza)
- There are also some non-viral causes and things like heat, smoke inhalation, allergic reactions, and inhalation of irritants.
- Acute bronchitis differs from bronchiolitis in the size of the airways affected (trachea and bronchi as opposed to small bronchiole)
What is the pathogenesis of acute bronchitis?
-Airways become inflamed and narrowed from capillary dilation, swelling from exudation of fluid, infiltration with inflammatory cells, increased mucus secretion, loss of ciliary function, and loss of portions of the ciliated epithelium.
What is the clinical manifestation of acute bronchitis?
- Cough may be productive or non-productive
- Requires only supportive treatment
- Associated symptoms include low-grade fever, substernal chest discomfort, sore throat, postnasal drip, and fatigue.
What is the etiology of chronic bronchitis?
-Major causes are cigarette smoking, repeated airway infections, genetic predisposition, and inhalation of physical or chemical irritants
-Diagnosed by hypersecretion of bronchial mucus and a chronic or recurrent productive cough of more than 3 months’ duration and occurring each year for 2 or more successive years in patients in whom other causes have been excluded.
Patients with chronic bronchitis and emphysema, airway obstruction is persistent and irreversible.
What is the pathogenesis of chronic bronchitis?
- Chronic inflammation and swelling of the bronchial mucosa resulting in scarring, increased fibrosis of the mucous membrane, hyperplasia of bronchial mucous glands and goblet cells.
- Hypertrophy of mucosal glands and goblet cells lead to increased mucous production (mucus then combines with purulent exudate to form bronchial plugs)
- Often the inflammatory and fibrotic changes extend into the surrounding alveoli. The narrowed airways and the mucous plugs prevent proper oxygenation .
- May appear as the “blue bloater”, because of the pathophysiological process of oxygen desaturation (cyanosis) and edema associated with right-sided heart failure.
What is the clinical manifestation of chronic bronchitis?
- Shortness of breath on exertion
- Excessive amount of sputum
- Chronic cough
- Evidence of excess body fluids (edema, hypervolemia)
- Cyanosis (late sign)
What is the etiology of emphysema?
- Destructive changes of the alveolar walls and abnormal enlargement of the distal air sacs.
- Frequently associated with chronic bronchitis
- Causes of emphysema include: smoking, air pollution, and certain occupations (ex. welding, mining, working with asbestos).
- May also follow bacterial lung infections
What is the pathogenesis of emphysema?
- Associated with the release of proteolytic enzymes from inflammatory cells such as neutrophils and macrophages.
- Smoking causes damage in two ways (1) leads to inflammation in the lung tissue, thus initiating a chain of events leading to the release of proteolytic enzymes that directly damage alveolar tissue and (2) it inactivates antitrysin, which normally acts to protect the lung parenchyma
- With the loss of alveolar walls, there is also a marked reduction in pulmonary capillary bed (essential for O2 and Co2 exchange between alveolar air and capillary blood)
- Loss of elastic tissue in lungs, which leads to a decrease in the size of the smaller bronchioles.
- Loss of lung tissue leads to a loss of radial traction, which normally holds the airways open.
What is the clinical manifestation of emphysema?
- Exertional dyspnea (major symptom)
- Decreased ability to consume adequate calories
- Use of accessory muscles to breathe
- Use of pursed-lip breathing in an effort to exhale more air over a longer period of time before the small airways collapse.
What is the etiology of bronchiectasis?
- Dilation of bronchial wall
- Either acquired (rare) or congenital
- Obstructive and suppurative (pus-forming) disorder
- Children high risk because of anatomic factors such as small, soft, elastic bronchi (easily damaged by overinflation/distension from infection and inflammation)
What is the pathogenesis of bronchiectasis?
- Recurrent infection and infection of bronchial walls leads to persistent dilation
- Inflammation leads to destruction of walls
- Destructive process leads to loss of ciliated epithelium (turn into squamous cells and pus formation) leading to obstruction.
What is the clinical manifestation of bronchiectasis?
- Productive cough with copious amounts of purulent, foul-smelling, green or yellow sputum (separates into three distinct layers in a sputum cup).
- Other clinical manifestations include: hemoptysis (coughing up blood), fever, night sweats, rhonchi (low-pitched rattling lung sounds), skin pallor, clubbing.
What is the etiology of bronchiolitis?
- Widespread inflammation of bronchioles due to infectious agents
- Also occasionally produced by allergic reactions
- In adults because of smoking, toxic fumes, and immunosuppression
What is the pathogenesis of bronchiolitis?
- Once initiated by the agent, proliferation and necrosis of bronchiolar epithelium occurs (produces obstruction and increased mucus secretion)
- Possible mechanism for airway obstruction include: development of inflammatory exudate, release of chemical mediators, inflammation, goblet cell metaplasia, and increased bronchial muscle mass.
What is the clinical manifestation of bronchiolitis?
- Severity and course range from mild to fatal
- Wheezing related to bronchospasm
- Crackles
- Decreased breath sounds
- Retractions
- Increased sputum
- Dyspnea
- Tachypnea
What is the etiology of cystic fibrosis?
- Autosomal recessive disorder of the endocrine glands
- Most common genetic lung disease in US
- Affects pancreas, intestinal tract, sweat glands, lungs, infertility (male)
- Classified as either an airflow obstruction or a suppurative (pus-forming) disorder.
- Hypersecretion of abnormal, thick mucus that obstructs exocrine glands and ducts is a characteristic finding in this disease.
What is the pathogenesis of cystic fibrosis?
- One genetic defect associated with cystic fibrosis involves deletion of three base pairs in codon 508 (CFTR) that code for phenylalanine on chromosome 7 (CFTR gene becomes dysfunctional) CFTR encodes a membrane chloride channel and is expressed in the sweat glands, the lungs, and pancreas.
- Bronchopulmonary system is also affected by the thick, tenacious mucus that results from failure of chloride channels to function in the apical membranes of the mucosal cells.
- High concentration of DNA in airway secretions increased sputum viscosity
What is the clinical manifestation of cystic fibrosis?
- Typical findings include a history of cough in young adult or child, thick/tenacious sputum, recurrent pulmonary infections, and recurrent episodes of bronchitis
- These eventually lead to pneumonia and bronchiectasis, right-sided heart failure, and exercise intolerance.
- Physical findings include: digital clubbing (late), dyspnea/tachypnea, sternal retractions, unequal lung sounds, barrel chest, depleted fat storage, steatorrhea (fatty stool), anorexia, and decreased growth rate in children.
What is the etiology of fibrotic interstitial lung disease-diffuse interstitial lung disease?
-Thickening of the alveolar interstitium
What is the pathogensis of fibrotic interstitial lung disease-diffuse interstitial lung disease?
Not well understood but is possibly related to an immune reaction that usually begins with injury to the alveolar epithelial or capillary endothelial cells.
- Lung tissue become infiltrated by lymphocytes, macrophages, and plasma cells. Persistent alveolitis may lead to obliteration of alveolar capillaries, reorganization of the lung parenchyma, and irreversible fibrosis. (changes lead to formation of large air-filled sacs (cysts) accompanied by dilated terminal and respiratory bronchioles.
- Pathologic patterns of inflammation in the alveoli include inflammation, fibrosis, and destruction.
- Triggers (ex. tobacco) lead to inflammation and the response is increased inflammatory cells.
- Then, fibroblastic proliferation and deposition of large amounts of collagen follows. (reduced compliance and increased elastic recoil)
- Lung destruction pattern is manifested by loss of alveolar walls
What is the clinical manifestation of fibrotic interstitial lung disease-diffuse interstitial lung disease?
- Progressive dyspnea and non-productive cough (most common)
- Also include: tachypnea, clubbing of nail beds, Cyanosis (later finding), Inability to increase cardiac output with exercise as evidenced by low maximal heart rate.
