Pulmonary - Week 3 - Notes

Question 2

Define obstructive lung diseases and list the main disorders

Answer 2

Obstructive lung diseases are conditions that limit airflow primarily by increasing airway resistance or causing loss of elastic recoil. Major disorders include asthma chronic obstructive pulmonary disease COPD which encompasses chronic bronchitis and emphysema bronchiectasis cystic fibrosis and certain small airways diseases

Question 3

Define asthma and summarize its epidemiology and etiology

Answer 3

Asthma is a chronic heterogeneous inflammatory airway disease characterized by variable airway obstruction bronchial hyperresponsiveness and episodes of wheeze breathlessness chest tightness and cough. Epidemiology shows variable prevalence worldwide higher rates in children and young adults and rising incidence in many regions. Etiology involves genetic susceptibility atopy environmental exposures such as allergens tobacco smoke pollution viral infections and occupational triggers

Question 4

Describe the pathophysiology of asthma and correlate with typical histological features

Answer 4

Asthma pathophysiology includes chronic airway inflammation driven by type 2 and non type 2 pathways leading to airway hyperresponsiveness mucus hypersecretion and reversible airway narrowing. Histology shows epithelial shedding goblet cell hyperplasia submucosal gland enlargement airway wall edema and smooth muscle hypertrophy with inflammatory infiltrates rich in eosinophils in type 2 asthma and neutrophils in severe or non type 2 phenotypes

Question 5

List the classic clinical features of asthma and typical presentation patterns

Answer 5

Clinical features include episodic wheeze cough chest tightness and dyspnea often worse at night or in the early morning. Patients may have triggers such as allergens exercise cold air or infections and may display variable airflow limitation with symptom free intervals between exacerbations

Question 6

Explain the evaluation of suspected asthma including key investigations

Answer 6

Evaluation includes clinical history focused on variability and triggers physical examination and objective testing. Spirometry with bronchodilator response is central. Peak expiratory flow monitoring can document variability. Additional testing may include bronchoprovocation testing fractional exhaled nitric oxide allergy testing chest imaging and assessment for alternative diagnoses

Question 7

Describe staging and prognosis of asthma and important severity markers

Answer 7

Staging distinguishes intermittent mild persistent moderate persistent and severe persistent asthma based on symptom frequency lung function and exacerbation risk. Prognosis is generally favorable with appropriate control but poor control steroid dependence frequent exacerbations hospitalization history and fixed airflow obstruction predict worse outcomes

Question 8

Summarize principles of asthma management and long term control strategies

Answer 8

Management aims to achieve symptom control reduce exacerbations and minimize medication adverse effects. Core strategies include inhaled corticosteroids as controllers bronchodilators for relief patient education trigger avoidance vaccination and personalized action plans. Step up or step down therapy is guided by control and exacerbation history

Question 9

Compare bronchodilators and controllers used in asthma and COPD with examples

Answer 9

Short acting beta agonists provide quick relief while long acting beta agonists and long acting muscarinic antagonists serve as maintenance bronchodilators. Controllers include inhaled corticosteroids leukotriene modifiers mast cell stabilizers and biologic agents targeting IgE or interleukins in severe asthma. Methylxanthines have limited use due to narrow therapeutic index

Question 10

Explain mechanism of action and key pharmacology of methylxanthines

Answer 10

Methylxanthines such as theophylline inhibit phosphodiesterase leading to increased intracellular cyclic AMP and cause mild bronchodilation and anti inflammatory effects. They have oral bioavailability hepatic metabolism potential drug interactions and narrow therapeutic range with toxicity manifesting as nausea arrhythmia and seizures

Question 11

Explain mechanism of action and key pharmacology of anticholinergic agents

Answer 11

Anticholinergic agents block muscarinic receptors in the airways reducing vagally mediated bronchoconstriction and mucus secretion. Short acting agents are used for acute relief and long acting agents are used for maintenance particularly in COPD. Systemic absorption is low which limits systemic anticholinergic effects

Question 12

Explain mechanism of action and key pharmacology of corticosteroids in airway disease

Answer 12

Corticosteroids modulate gene transcription to reduce airway inflammation decrease cytokine production and suppress inflammatory cell recruitment. Inhaled formulations provide targeted anti inflammatory effect with lower systemic toxicity while systemic corticosteroids are used for severe exacerbations and short term control

Question 13

Explain mechanism of action and role of mast cell stabilizers

Answer 13

Mast cell stabilizers inhibit mediator release from mast cells after antigen exposure and reduce early allergic bronchospasm. They are used mainly as preventive agents in mild allergic asthma and have minimal side effects but are less potent than inhaled corticosteroids

Question 14

Explain mechanism of action and role of beta 2 agonists

Answer 14

Beta 2 agonists stimulate beta 2 adrenergic receptors on airway smooth muscle increasing intracellular cyclic AMP and causing bronchodilation. Short acting agents provide rapid symptom relief and long acting agents are used for maintenance often in combination with inhaled corticosteroids

Question 15

Explain mechanism of action and role of leukotriene modifiers

Answer 15

Leukotriene modifiers block leukotriene pathways either by inhibiting leukotriene synthesis or by antagonizing leukotriene receptors thereby reducing bronchoconstriction mucus production and eosinophilic inflammation. They are oral alternatives or add on therapy in allergic and aspirin sensitive asthma

Question 16

Define COPD and list the main phenotypes

Answer 16

Chronic obstructive pulmonary disease COPD is a preventable and treatable disease characterized by persistent airflow limitation that is usually progressive and associated with enhanced chronic inflammatory response. Main phenotypes include chronic bronchitis emphysema and mixed COPD with frequent exacerbator phenotype and asthma COPD overlap

Question 17

Define chronic bronchitis and summarize its etiology and epidemiology

Answer 17

Chronic bronchitis is clinically defined by productive cough for at least three months in two consecutive years due to mucus hypersecretion and airway inflammation. Etiology commonly includes tobacco smoke occupational exposures and recurrent infections. It is more common in smokers and older adults and contributes to COPD morbidity

Question 18

Describe the pathophysiology of chronic bronchitis and its effects on gas exchange

Answer 18

Pathophysiology involves mucus gland enlargement goblet cell metaplasia airway inflammation and small airway narrowing leading to airflow obstruction airway collapse and trapping. Excess mucus and ventilation perfusion mismatch cause hypoxemia and can lead to hypercapnia in advanced disease

Question 19

Describe pathological features of chronic bronchitis in early and late stages

Answer 19

Early disease shows mucous gland enlargement increased Reid index goblet cell hyperplasia and chronic inflammatory infiltrates. Late stage disease shows airway wall fibrosis smooth muscle hypertrophy and emphysematous changes with chronic changes that may become irreversible

Question 20

Explain clinical features and differential diagnosis of chronic bronchitis

Answer 20

Patients have productive cough dyspnea cyanosis and frequent exacerbations with crackles or wheeze on examination. Differential diagnosis includes bronchiectasis asthma heart failure and infections and requires clinical correlation with imaging and pulmonary function tests

Question 21

Define emphysema and explain main etiologies and epidemiology

Answer 21

Emphysema is destruction of alveolar walls and permanent enlargement of airspaces distal to the terminal bronchiole leading to loss of elastic recoil and airflow limitation. Major etiologies include cigarette smoking alpha one antitrypsin deficiency and environmental pollutants. It is common in older smokers and presents with progressive dyspnea

Question 22

Describe the pathology of emphysema including gross and microscopic features

Answer 22

Grossly emphysematous lungs show hyperinflation blebs and increased lung compliance. Microscopically there is destruction of alveolar septa loss of capillary beds and enlarged airspaces with centriacinar panacinar or paraseptal patterns depending on cause

Question 23

Explain clinical features and differential diagnosis of emphysema

Answer 23

Patients typically present with progressive exertional dyspnea minimal cough and a history of smoking thin body habitus and barrel chest in advanced disease. Differential diagnoses include chronic bronchitis bronchiectasis interstitial lung disease and cardiac causes of dyspnea

Question 24

Describe the evaluation of COPD including key tests and staging

Answer 24

Evaluation includes history risk factor assessment spirometry to confirm persistent airflow limitation with post bronchodilator FEV1 FVC ratio less than 0.70 and classification using symptom scores and exacerbation history. Imaging chest radiograph or CT can show emphysema or other structural changes and arterial blood gas testing may assess gas exchange in advanced disease

Question 25

List possible complications and prognosis factors for COPD

Answer 25

Complications include frequent exacerbations pulmonary hypertension cor pulmonale respiratory failure and increased risk of infections and lung cancer. Prognostic factors include FEV1 degree of dyspnea frequency of exacerbations exercise capacity and comorbidities

Question 26

Define bronchiectasis and summarize its common causes and epidemiology

Answer 26

Bronchiectasis is irreversible dilation of bronchi due to chronic infection and inflammation leading to impaired mucus clearance and recurrent infections. Causes include post infectious damage immune deficiencies cystic fibrosis allergic bronchopulmonary aspergillosis and aspiration. Epidemiology varies with higher prevalence in settings with poor access to care and in patients with predisposing conditions

Question 27

Describe the pathology and etiopathogenesis of bronchiectasis gross and microscopic

Answer 27

Pathology shows gross bronchial dilation plugged airways and sometimes mucus filled cystic spaces. Microscopy reveals chronic inflammation destruction of elastic and muscular components of the bronchial wall and squamous metaplasia with varying degrees of fibrosis

Question 28

Explain clinical features evaluation and differential diagnosis of bronchiectasis

Answer 28

Patients present with chronic productive cough recurrent purulent sputum hemoptysis and frequent respiratory infections. Evaluation includes high resolution CT which is diagnostic sputum culture immunologic testing and tests for underlying causes. Differential diagnoses include COPD cystic fibrosis chronic bronchitis and tuberculosis

Question 29

Summarize management complications and prognosis of bronchiectasis

Answer 29

Management focuses on airway clearance techniques treatment of infections with antibiotics management of underlying disorder and sometimes surgical resection for localized disease. Complications include hemoptysis respiratory failure and cor pulmonale. Prognosis depends on cause severity frequency of infections and response to therapy

Question 30

Describe the CFTR protein function and pathophysiology of cystic fibrosis

Answer 30

CFTR is an ATP gated chloride and bicarbonate channel on epithelial cells that regulates salt and water transport. Defective CFTR causes thick viscous secretions in the lungs pancreas and biliary system leading to chronic airway infection bronchiectasis malabsorption and liver disease

Question 31

Explain clinical features diagnosis criteria and relevant investigations for cystic fibrosis

Answer 31

Clinical features include chronic productive cough recurrent sinopulmonary infections failure to thrive and pancreatic insufficiency. Diagnosis is made by clinical features plus evidence of CFTR dysfunction such as elevated sweat chloride or identification of pathogenic CFTR mutations. Pulmonary function testing imaging microbiology and pancreatic testing are part of evaluation

Question 32

Summarize pharmacologic approaches to cough including antitussives expectorants and demulcents

Answer 32

Antitussives suppress cough center activity and include opioid derivatives and dextromethorphan while expectorants aim to increase secretion clearance and demulcents soothe the pharynx. Treatment choice depends on cough cause with cough suppression used for nonproductive troublesome cough and expectorants used when secretion clearance is desired

Question 33

Describe mechanism uses and adverse effects of codeine and dextromethorphan

Answer 33

Codeine is an opioid that suppresses the cough reflex via central mu receptor agonism and may cause sedation constipation and risk of dependence. Dextromethorphan is a non opioid NMDA receptor antagonist at high doses that suppresses cough and can cause dizziness gastrointestinal upset and at high doses dissociative effects

Question 34

Define obstructive sleep apnea OSA and summarize pathophysiology and clinical features

Answer 34

Obstructive sleep apnea is recurrent upper airway collapse during sleep causing intermittent hypoxia sleep fragmentation and daytime somnolence. Risk factors include obesity craniofacial anatomy and neuromuscular tone alterations. Clinical features include loud snoring witnessed apneas and excessive daytime sleepiness

Question 35

Differentiate obstructive from central sleep apnea and summarize evaluation with polysomnography

Answer 35

Obstructive sleep apnea results from collapse of the upper airway while central sleep apnea results from failure of central respiratory drive. Polysomnography is the diagnostic test that records apneas hypopneas oxygen desaturation and sleep architecture. Treatment differs with CPAP mandibular advancement or surgery for obstructive types and addressing underlying causes for central types

Question 36

Define respiratory acidosis and alkalosis and list common etiologies

Answer 36

Respiratory acidosis results from alveolar hypoventilation leading to elevated PaCO2 common causes include COPD severe asthma respiratory muscle weakness and central depression. Respiratory alkalosis results from alveolar hyperventilation leading to low PaCO2 common causes include anxiety pain high altitude fever and pulmonary embolism

Question 37

Describe the pathophysiology clinical features and management principles for respiratory acid base disorders

Answer 37

Respiratory acid base disorders arise from imbalance in ventilation altering PaCO2 which shifts pH and leads to metabolic compensation over time. Clinical features vary from dyspnea and confusion in acidosis to lightheadedness and paresthesia in alkalosis. Management targets the underlying cause supports ventilation and uses careful correction to avoid rapid shifts in pH

Question 38

Explain high yield exam style approach for pulmonary obstructive disease questions

Answer 38

For exam style questions integrate presenting history physical findings and spirometry patterns correlate phenotypes with risk factors and imaging and apply first line management followed by escalation. Focus on key distinguishing features such as reversibility in asthma persistent obstruction in COPD productive cough in chronic bronchitis and imaging for bronchiectasis