Pulmonary Pathophysiology Flashcards
1) What is forced spirometry and what does it measure?
2) What is FEV1, FVC and what is the normal FEV1/FVC ratio?
3) What changes in FEV1 or FVC is seen in obstructive lung diseases?
4) What changes in FEV1 or FVC is seen in restrictive lung diseases?
1) Deep breath and then forced exhale into spirometer. Measures volume as a function of time
2) FEV1: Forced expiratory volume in the first second. FVC: Forced vital capacity (How much a person can expire maximally)
Normal ratio is 70-80%
3) Decreased FEV1, Air cannot get out, ratio is below normal
4) Decreased FVC and FEV1, Air cannot get in, ratio is normal or higher
1) What is bacterial pneumonia and mention some bacteria that usually causes it?
2) What are the different “things” used to classify the different types of pneumonia?
3) Describe the disease course of pneumococcal pneumonia
4) What is Legionnaire disease?
5) Describe primary atypical pneumonia incl. clinical manifestations
1) Infection in the lower airways by microbes. S. pneumoniae, H. Influenzae, S. Aureus
2) Setting (Community-/ Hospital acquired), Type of agent (Typical/ Atypical), Location (Lobar/ Bronchopneumonia)
3) 1. Edema Alveoli fill with excess fluid. 2. Red hepatization RBCs, neutrophils, fibrin fill airspaces -> solic airspaces. 3. Gray hepatization RBCs are broken down -> Gray appearance. Firm lungs. 4. Resolution Exudate is digested, ingested or coughed up.
4) Water with pathogen is aerosolized and then inhaled. Malaise, weakness, fever, dry cough, diarrhea, CNS disturbances.
5) M. pneumoniae. Damage to epithelial + defence of respiratory tract -> Increased risk of secondary bacterial infection. Symptoms Fever, headache, muscle ache, dry cough
1) Causes of primary lung cancers
2) Describe Small Cell Lung Cancer
3) What are the 3 types of Non-small cell lung cancers and what characterizes them?
4) What are the clinical manifestations of primary lung cancers?
1) More than 80% are caused by smoking, other: asbestos, genetics.
2) Small round/oval cells. Grows in clusters. Produces polypeptide hormones -> Can produce paraneoplastic syndromes. Caused by smoking. Bad prognosis.
3) Squamous Cell Carcinoma Men + smoking. Affects central bronchi. Paraneoplastic syndrome (Hypercalcemia). Adenocarcinoma Most common type. Women + non-smokers. Originates in bronchiolar/alveolar tissue -> peripheral location. Large Cell Carcinoma Large, polygonal cells. Periphery of lung. Poor prognosis.
4) Due to lung involvement (Chronic cough, shortness of breath, wheezing). Local spread/metastasis. Paraneoplastic manifestations. General Weight-loss, anorexia
1) What is RDS?
2) Who gets RDS?
3) What are the clinical manifestations?
1) Respiratory Distress Syndrome. Pulmonary immaturity + No surfactant -> alveolar collapse.
2) Premature infants, Infants with mothers on insulin, Infants born by cesarean birth
3) Signs within 24 hours of delivery. Central cyanosis, Difficulty breathing
1) What is cystic fibrosis and who are diagnosed with it (age group)?
2) Pathophysiology of cystic fibrosis
3) What are the clinical manifestations of cystic fibrosis?
1) Children are diagnosed. Autosomal recessive disorder in CFTR gene -> misfolded CFTR protein
2) CFTR normally pumps Cl- into mucus. Abnormal CFTR -> Na+ and water is drawn out of mucus (in lungs and other) -> mucus is thick -> Increased risk of infections + Obstruction of airways. Also affects pancreas -> pancreatic exocrine deficiency
3) Accumulation of mucus in bronchi, decreased clearance, lung infections. Pulmonary inflammation. Pancreatic exocrine deficiency -> Malabsorption + diarrhea. Diabetes can develop
1) What is asthma?
2) Risk factors of asthma
3) Pathophysiology of asthma
4) Describe an acute asthma attack
5) Describe a prolonged asthma attack
1) Episodes of airway obstruction, bronchial hyperreactivity, airway inflammation
2) Genetic predisposition to IgE response against allergens, Family history, Allergies.
3) Airway obstruction, bronchial hyperreactivity, airway inflammation (inflammatory cells in lungs + damage to epithelium). T2H cells respond to allergen -> B-cells produce IgE
4) Bronchospasm, edema, mucus plugging. Long expiration due to obstruction.
5) Air is trapped behind occluded (mucus) + narrow (bronchospasm) airways -> Hyperinflation. More energy is needed to breath. Accessory muscles are required -> Dyspnea, fatigue
1) What is COPD?
2) Etiologies of COPD
3) General pathophysiology and for the 2 types of COPD
4) Clinical manifestations in “general” and for the 2 types
1) Chronic Obstructive Pulmonary Disease. Chronic + recurrent obstruction of airflow
2) Smoking, hereditary deficiency in AAT, Asthma, fumes
3) General Inflammation + fibrosis of bronchial wall, Hypertrophy of submucosal glands, Hypersecretion of mucus -> Airway obstruction. Loss of elastic lung tissue -> Decreased area of gas exchange + Decreased flow rate
Emphysema Loss of lung elasticity + large airways due to breakdown of elastin by enzymes. 2 reasons: Smoking -> Increased inflammatory cells -> release of proteases -> not enough antiproteases -> Destruction of elastic fibers. AAT disorder -> less protection -> Destruction of elastic fibers
Chronic Bronchitis Airway obstruction with hypertrophy and hypersecretion of mucus. Men + smoking. Chronic productive cough
4) General Fatigue, cough, exercise intolerance, sputum production, dyspnea.
Emphysema - Pink puffer No cyanosis, use of extra muscles for breathing, barrel chest, pursed lips
Chronic Bronchitis - Blue bloater Cyanosis, fluid retention
1) What are restrictive lung diseases?
2) Etiology of restrictive lung diseases
3) Manifestations
1) Inflammation + Fibrotic changes in lung tissue -> Stiff lungs -> Decreased total lung capacity (Hard to expand despite normal airways)
2) Pneumoconiosis (Coal, asbestos, fumes), Hypersensitivity pneumonitis (Dust, molds), Sarcoidosis (Systemic disease where granulomas are formed around pathogen by immune cells)
3) Dyspnea, Tachypnea, Cyanosis, No wheezing, Increased respiratory rate, Non-productive cough, FEV1/FVC is normal or increased. Advanced Hypoxemia at rest
1) What is a pulmonary embolism?
2) Etiology of most common reason for a pulmonary embolism
3) Pathogenesis of pulmonary embolism
4) Clinical manifestations of pulmonary embolism
1) Usually blood clots from venous system that becomes lodged in a pulmonary blood vessel when it moves through the right ventricle into the pulmonary circulation. Can also be: Injected air, fat from bone marrow, amniotic fluid during birth
2) DVT. Virchow triangle: Venous stasis (Bedrest, long flights), Venous endothelial injury (Trauma, surgery), Hypercoagulability states (Cancer, oral contraceptives, pregnancy)
3) Depends on size and location. Big embolus -> Pulmonary hypertension + right sided heart failure. Obstruction of blood flow in lungs -> bronchoconstriction -> Decreased gas exchange
4) Chest pain, Dyspnea, Increased respiratory rate
1) What is pulmonary hypertension and what are the 2 categories? Which one is most common?
2) Describe Pulmonary arterial hypertension including definition, etiology and manifestations
3) What can cause secondary pulmonary hypertension?
1) Increased pressure in the pulmonary arterial system. Primary (Pulmonary arterial hypertension - PAH) and Secondary Pulmonary Hypertension (most common)
2) Abnormal proliferation + contraction of vessel smooth muscle, abnormal coagulation, fibrosis. Etiology Genetic, Collagen vascular disease, Drugs, HIV. Clinical manifestations Increased pulmonary arterial pressure + normal left ventricular pressure. Shortness of breath, exercise intolerance
3) COPD or Restrictive Pulmonary Disease -> Hypoxemia -> Constriction of pulmonary vessels
Heart valve disorders -> Increased left atrial pressure
Chronic thromboembolic disorder
