RESP Flashcards
1
Q
What is the definition of asthma?
A
Chronic inflammatory condition of the lungs characterized by reversible airway obstruction, hyperresponsiveness, and inflammation.
2
Q
What are the types of asthma?
A
- Extrinsic (Atopic, Allergic): Triggered by allergens like dust, pollen, or animal dander.
- Intrinsic (Non-Atopic): Not allergy-related; often starts in adulthood and triggered by respiratory infections or irritants.
3
Q
What are the causes of airway narrowing in asthma?
A
- Smooth muscle contraction.
- Thickened airway walls from inflammation and swelling.
- Increased mucus production clogging the airways.
4
Q
What cells and mediators are involved in asthma?
A
- Dendritic cells.
- Th2 lymphocytes.
- Eosinophils.
- Mast cells.
- Cytokines (e.g., IL-4, IL-5), histamine, and leukotrienes.
5
Q
What are common triggers of asthma?
A
- Allergens: Dust, pollen, mold, animal dander.
- Irritants: Tobacco smoke, air pollution, strong odors.
- Other triggers: Cold air, exercise, viral infections, medications (e.g., NSAIDs, beta-blockers).
6
Q
What are the symptoms and signs of asthma?
A
- Symptoms: Intermittent shortness of breath (SOB), wheezing, chest tightness, and cough.
- Worse at night or early morning.
- Triggered by allergens, exercise, or infections.
- Signs: Bilateral wheezing (expiratory > inspiratory), prolonged expiration time, use of accessory muscles during breathing, cyanosis or ‘silent chest’ in severe cases.
7
Q
How is asthma diagnosed?
A
- Pulmonary Function Tests (PFTs): Show reversible airway obstruction (FEV1 increase ≥12% and 200 mL after bronchodilator).
- Peak Expiratory Flow Rate (PEFR): Useful for monitoring, especially during exacerbations.
- Methacholine Challenge Test: For normal PFTs but high suspicion.
- Skin Prick Test: Identifies allergic causes.
- ABG: Assesses severity (mild hyperventilation to respiratory failure).
8
Q
What are the ABG findings in asthma exacerbations?
A
- Mild: Low CO2, high pH (hyperventilation).
- Moderate: Normal CO2 and pH.
- Severe: High CO2, low pH (respiratory acidosis).
9
Q
What is the stepwise treatment of asthma according to GINA guidelines?
A
- Step 1: Low-dose ICS-formoterol(LABA) as needed or SABA + low does ICS
- Step 2: Daily low-dose ICS or as-needed ICS-formoterol.
- Step 3: Daily ICS-LABA or ICS-LTRA
- Step 4: Medium-dose ICS-LABA (consider adding tiotropium or LTRA).
- Step 5: High-dose ICS-LABA, add low-dose oral steroids if needed.
10
Q
How is acute asthma exacerbation managed?
A
- Oxygen therapy: Maintain SpO2 ≥94%.
- Bronchodilators: Nebulized salbutamol (SABA) and ipratropium bromide.
- Corticosteroids: Oral prednisolone or IV hydrocortisone.
- Magnesium sulfate: IV for severe cases.
- Mechanical ventilation: For respiratory failure (silent chest, cyanosis, exhaustion).
11
Q
What are signs of poor asthma control?
A
- Frequent symptoms (>2 days/week).
- Nighttime awakenings.
- Increased reliever use.
- Activity limitation.
12
Q
What is the difference between asthma and COPD?
A
- Asthma: Reversible airway obstruction, typically in younger individuals, often allergy-associated.
- COPD: Irreversible obstruction, common in older adults with a smoking history.
13
Q
What is COPD?
A
Chronic disease characterized by irreversible airflow limitation, caused by damage to the lungs and airways, typically due to smoking or other irritants.
14
Q
What are the common causes and risk factors for COPD?
A
- Causes: Chronic exposure to harmful particles or gases (e.g., smoking, air pollution).
- Risk factors: Smoking (primary cause), long-term exposure to biomass fuels, occupational dusts and chemicals, genetic factors: Alpha-1 antitrypsin deficiency.
15
Q
What are the symptoms of COPD?
A
- Chronic cough, usually productive.
- Progressive shortness of breath, especially with exertion.
- Wheezing and chest tightness.
- Frequent respiratory infections.
- Fatigue and unintended weight loss in severe cases.
16
Q
What are the two main types of COPD?
A
- Chronic Bronchitis: Defined as chronic productive cough lasting at least 3 months for 2 consecutive years, involves inflammation and increased mucus production in the airways.
- Emphysema: Characterized by destruction of alveolar walls and loss of lung elasticity, leads to hyperinflation, air trapping, and reduced gas exchange.
17
Q
What are the signs of COPD on physical examination?
A
- Barrel-shaped chest (hyperinflation).
- Prolonged expiratory phase.
- Use of accessory muscles for breathing.
- Reduced breath sounds and wheezing.
- Cyanosis and signs of right heart failure in advanced cases.
18
Q
How is COPD diagnosed?
A
- Spirometry: Post-bronchodilator FEV1/FVC ratio <70% confirms airflow limitation.
- Chest X-ray: Hyperinflated lungs, flattened diaphragm, and increased retrosternal air space.
- ABG: Hypoxemia and hypercapnia in advanced disease.
- CT scan: For detailed imaging in severe cases or suspected complications.
19
Q
What is the GOLD classification of COPD severity?
A
- GOLD 1: Mild (≥80% predicted).
- GOLD 2: Moderate (50-79% predicted).
- GOLD 3: Severe (30-49% predicted).
- GOLD 4: Very severe (<30% predicted).
20
Q
How is stable COPD managed?
A
- Non-Pharmacological: Smoking cessation (most important intervention), pulmonary rehabilitation (exercise training, education), vaccinations (influenza and pneumococcal vaccines).
- Pharmacological: Bronchodilators: Long-acting (LAMA, LABA) are first-line, inhaled corticosteroids (ICS) for frequent exacerbators (eosinophilic phenotype), combined LAMA+LABA or LABA+ICS for moderate to severe COPD, mucolytics for chronic sputum production.
21
Q
How is an acute exacerbation of COPD managed?
A
- Controlled oxygen therapy: Keep SpO2 between 88-92%.
- Bronchodilators: Nebulized salbutamol (SABA) and ipratropium bromide (LAMA).
- Systemic corticosteroids: Prednisolone (oral) or IV methylprednisolone.
- Antibiotics: For bacterial infections (e.g., amoxicillin, doxycycline).
- LMWH for DVT prophylaxis
- Non-invasive ventilation (NIV): For hypercapnic respiratory failure.
- Hospitalization: For severe cases or significant comorbidities.
22
Q
What are complications of COPD?
A
- Respiratory failure.
- acute exacerbation (infection, noncompliance, cardiac problems).
- Pulmonary hypertension and cor pulmonale (right-sided heart failure).
- Secondary polycythemia (increased red blood cells).
23
Q
How is end-stage COPD managed?
A
- Long-term oxygen therapy (LTOT) for patients with chronic hypoxemia.
- Palliative care to address symptoms and improve quality of life.
- Smoking cessation and supportive care remain key.
24
Q
What is bronchiectasis?
A
A condition where the bronchi are permanently widened due to chronic infection and inflammation, leading to mucus buildup and recurrent infections.
25
What are the causes of bronchiectasis?
Post-infectious: Tuberculosis, measles, pertussis, or bacterial pneumonia.
Cystic fibrosis: The most common genetic cause.
Other: Primary ciliary dyskinesia, allergic bronchopulmonary aspergillosis (ABPA), humoral immunodeficiency, autoimmune diseases, or aspiration.
26
What are the symptoms of bronchiectasis?
Persistent cough with large amounts of purulent sputum.
Recurrent respiratory infections.
Dyspnea
pleuritic chest pain
Hemoptysis (coughing up blood).
Recurrent or persistent pneumonia
27
What are the signs of bronchiectasis on examination?
Coarse inspiratory Crackles
wheezing
Clubbing of fingers in severe or advanced disease.
Cyanosis in severe cases.
28
How is bronchiectasis diagnosed?
High-Resolution CT (HRCT): Gold standard showing dilated airways ('tram-track' or 'signet ring' appearance).
Sputum culture: Identifies pathogens like Pseudomonas or Haemophilus.
Pulmonary Function Tests (PFTs): May show an obstructive pattern.
Sweat test & CF genetic assessment > cystic fibrosis
Serum immunoglobulin
29
What are complications of bronchiectasis?
• Pneumonia
• Pleural effusion
• Pneumothorax
• Massive hemoptysis
• Poorer prognosis if lower FEV1 or if infection with pseudomonas
30
How is bronchiectasis managed?
Airway clearance: Daily chest physiotherapy and postural drainage, mucolytic agents.
Infection control: CIPROFLAXCIN FOR PSEUDOMONAS, CO-AMOXICLAV FOR H. INFLUENZA.
Long-term azithromycin, bronchodilators, INHALED corticosteroids.
Surgery: Reserved for localized disease unresponsive to medical therapy.
Vaccinations: Influenza and pneumococcal vaccines to prevent respiratory infections.
31
What is cystic fibrosis?
An autosomal recessive genetic disorder caused by mutations in the CFTR gene, leading to thick, sticky mucus in the lungs, pancreas, and other organs.
32
What are the symptoms of cystic fibrosis?
Respiratory: Chronic cough, recurrent lung infections, shortness of breath.
Digestive: Failure to thrive, steatorrhea (fatty stools), malabsorption.
Other: Male infertility, diabetes
O/E: digital clubbing, coarse inspiratory crackles, hyperinflated lung
33
What are complications of cystic fibrosis?
Chronic respiratory infections (e.g., Pseudomonas aeruginosa, Staphylococcus aureus).
Bronchiectasis.
Respiratory failure.
Pancreatic insufficiency leading to diabetes and malnutrition.
Acute then chronic pancreatitis
Meconium ileus / distal intestinal obstruction syndrome
Liver disease (e.g., biliary cirrhosis).
Infertility (particularly in males).
Osteoporosis.
34
How is cystic fibrosis diagnosed?
Sweat test: Elevated chloride levels (≥60 mmol/L).
Genetic testing: Identifies CFTR gene mutations.
Newborn screening: Includes immunoreactive trypsinogen (IRT) testing.
35
How is cystic fibrosis managed?
Respiratory care: Airway clearance techniques, LONG TERM AZITHROMYCIN, HYPERTONIC SALINE, INHALED MANNITOL, LONG TERM TOBRAMYCIN, RECOMBINANT HUMAN DNASE.
Nutritional support: Pancreatic enzyme replacement, high-calorie diet, fat-soluble vitamins.
Infections: PSEUDOMONAS: CEFATAZIDIME AND TOBRAMYCIN.
Advanced therapies: CFTR modulators (e.g., ivacaftor) for G511D mutations.
INFLUENZA AND pneumococcal VACCINE.
Lung transplant: For end-stage lung disease.
36
What is Obstructive Sleep Apnea?
Cessation of breathing for >10 seconds multiple times during sleep due to upper airway obstruction.
## Footnote
Common in obese patients, large tongue, hypothyroidism, acromegaly, or goiter.
37
What are the risk factors for Obstructive Sleep Apnea?
BMI > 30, neck circumference > 40 cm, metabolic syndrome, male gender, postmenopausal women, family history, age > 40 years, Down syndrome.
38
How is Obstructive Sleep Apnea diagnosed?
Screening Test: Overnight oximetry showing cyclic drops in oxygen saturation.
Sleep Study: >10-15 apneas in 1 hour of sleep confirms diagnosis.
Epworth Sleepiness Scale: Total score >10 suggests a sleep disorder.
## Footnote
Questions assess likelihood of falling asleep in various situations (reading, watching TV, driving, etc.).
39
What treatments are available for Obstructive Sleep Apnea?
Lifestyle modifications: Weight loss, sleep in a lateral position.
Surgical intervention: For obstructions like tonsils, nasal polyps, or facial deformities.
CPAP therapy: A mask during sleep that keeps pharyngeal walls open.
40
What is Central Sleep Apnea, and how does it differ from Obstructive Sleep Apnea?
Central Sleep Apnea (CSA): Apnea due to lack of spontaneous respiratory effort, caused by brain dysfunction. Often seen in heart failure, stroke, or opioid use.
## Footnote
In CSA, there is no respiratory movement. In OSA, respiratory effort is present, but airflow is blocked.
41
What is tuberculosis and how is it transmitted?
Cause: Mycobacterium tuberculosis, an aerobic intracellular pathogen. Transmission: Inhalation of aerosolized droplets from an infected person.
## Footnote
Only active TB patients are contagious.
42
What is primary tuberculosis, and what are its features?
Initial infection, mostly in children or immunocompetent individuals. Often asymptomatic but may cause: Erythema nodosum, pleural effusion, collapse from enlarged lymph nodes. Occurs in the upper lungs.
## Footnote
Key lesion: Ghon focus (granulomatous lesion). Ghon complex = Ghon focus + caseous lesions in lymph nodes.
43
What triggers reactivation TB, and what are the symptoms?
Triggered by immunosuppression: HIV, chemotherapy, steroids, DM, malnutrition, aging. Symptoms: Fever, night sweats, weight loss, cough (dry → purulent → hemoptysis).
## Footnote
Localized to apical areas of lungs. Extrapulmonary involvement: Common in lymph nodes, pleura, GI, GU, spine, kidneys, meninges.
44
What is miliary tuberculosis, and what are its key features?
Definition: Hematogenous dissemination of TB causing tiny nodules in multiple organs. Common sites: Lungs, liver, spleen, CNS, bones, LNs
## Footnote
Diagnosis: Chest X-ray or MRI (tiny nodules). Symptoms: Fever, night sweats, weight loss, organ-specific manifestations.
45
How is tuberculosis diagnosed?
Chest X-ray: Upper lobe infiltrates, cavitation, Ghon complex, Ranke Complex (calcified Ghon complex & fibrosis) .
Sputum analysis: Smear for acid-fast bacilli (Ziehl-Neelsen stain)
culture (definitive but takes 3 weeks)
PCR (rapid).
## Footnote
Extrapulmonary tests: Biopsy or aspiration (lymph nodes, bones, urine, etc.).
CSF analysis: For suspected TB meningitis (high protein, lymphocytosis).
46
What is the treatment protocol for active tuberculosis?
Two phases: Intensive phase (2 months): Isoniazid, Rifampin, Pyrazinamide, Ethambutol. Continuation phase (4-7 months): Isoniazid and Rifampin.
## Footnote
Extended if cavitation, delayed response, or HIV co-infection. Add dexamethasone for CNS or pericardial TB.
Check liver functions before starting treatment
47
What are the side effects of common TB medications?
Isoniazid: Polyneuropathy (give Vitamin B6), allergic reactions.
Rifampin: Stains body secretions orange/pink, induces liver enzymes.
Pyrazinamide: Hyperuricemia, gout, rash. Contraindicated in pregnancy.
Ethambutol: Optic neuritis (check visual acuity).
48
How is latent TB detected and treated?
Tests: Purified protein derivative (PPD) skin test or interferon-gamma release assay (IGRA). Positive PPD based on induration size: 5 mm: High-risk (e.g., HIV, close contacts).
## Footnote
10 mm: Moderate risk (e.g., healthcare workers, immigrants). 15 mm: Low risk. Treatment: Isoniazid for 9 months.
49
What is pneumonia, and how is it classified?
Definition: Inflammation of lung tissue (alveolar space or interstitial tissue), typically bacterial. Types: Community-acquired pneumonia (CAP): Typical (S. pneumoniae, H. influenzae), atypical (Mycoplasma, Legionella, etc.).
## Footnote
Hospital-acquired pneumonia: Occurs >48 hours after hospitalization.
50
What are the risk factors for pneumonia?
Extremes of age (<16 or >65), smoking, alcohol use, underlying lung diseases (COPD, bronchiectasis), immunosuppression (HIV, steroids, DM), recent viral respiratory infection, hospitalization or surgery.
51
What are the symptoms and diagnostic methods for pneumonia?
Symptoms: Fever, cough (productive or dry), pleuritic chest pain, dyspnea. Physical signs: Dullness to percussion, bronchial breath sounds, pleural rub.
## Footnote
Diagnosis: Chest X-ray (lobar or patchy infiltrates), sputum analysis (Gram stain, culture), CBC (high WBC for bacterial pneumonia).
52
What are the complications of pneumonia?
Pulmonary complications: Lung abscess, pleural effusion, empyema, acute respiratory failure (severe cases). Systemic complications: Septicemia (bloodstream infection).
53
What is the CURB-65 severity score, and how is it used?
Criteria (1 point each): Confusion, urea > 7 mmol/L, respiratory rate > 30/min, blood pressure < 90/60 mmHg, age > 65 years.
## Footnote
Score interpretation: 0–1: Low risk → Outpatient treatment, 2: Moderate risk → Hospitalization, ≥3: Severe pneumonia → ICU admission.
54
How is pneumonia managed?
Supportive care: Analgesia for pleuritic pain, oxygen therapy if hypoxemic, IV fluids for dehydration. Antibiotic therapy: Outpatient CAP: Macrolide (e.g., clarithromycin). And amoxicillin
## Footnote
Inpatient CAP: Macrolide + ceftriaxone or respiratory fluoroquinolones.
55
What investigations are used to diagnose pneumonia?
Chest X-ray: Confirms consolidation and assesses severity. Sputum analysis: Gram stain and culture to identify pathogens. Blood tests: CBC: Elevated WBC in bacterial pneumonia.
## Footnote
CRP/ESR: Markers of inflammation, blood cultures: Rule out sepsis in severe cases.
56
What is the definition of a lung abscess?
A localized collection of pus and necrotic tissue within lung parenchyma caused by microbial infection, often seen with an air-fluid level on chest X-ray.
57
What is the pathophysiology of a lung abscess?
Aspiration (most common) of food or oropharyngeal secretions leads to pneumonia and/or obstruction of smaller airways, causing localized suppurative inflammation and necrosis, resulting in abscess formation within 1–2 weeks.
58
What are the common causes of a lung abscess?
Aspiration pneumonia (anaerobic bacteria like Peptostreptococcus, Prevotella, and Fusobacterium), bacterial pneumonia (e.g., S. aureus, Klebsiella, tuberculosis), bronchial obstruction (tumor, foreign body), conditions like cystic fibrosis, bronchiectasis, and septic emboli.
59
What are the clinical features of a lung abscess?
Persistent or worsening pneumonia, foul-smelling purulent sputum, fever, hemoptysis, anorexia, weight loss, fatigue, pleuritic chest pain, night sweats, finger clubbing, and dullness to percussion over the affected area.
60
How is a lung abscess investigated?
Bacteriological analysis using transtracheal aspiration, bronchoscopy, or percutaneous transthoracic aspiration (gram stain, culture, sensitivity).
Chest X-ray showing a spherical cavity with thick irregular walls and air-fluid levels.
CT chest with IV contrast to confirm the diagnosis and rule out differentials.
CBC showing elevated WBC.
61
How is a lung abscess treated?
Broad-spectrum antibiotics covering aerobic and anaerobic gram-positive and gram-negative bacteria (e.g., cefuroxime and metronidazole). Surgical drainage is occasionally required.
62
What is the definition of empyema?
A collection of pus in the pleural cavity, often caused by untreated bacterial pneumonia or ruptured lung abscess.
63
What are the common causes of empyema?
Complication of bacterial pneumonia (most common), spread from other infection sites (e.g., mediastinitis, abscess).
64
What are the clinical features of empyema?
Very ill appearance with fever, increased neutrophils, malaise, weight loss, and finger clubbing.
65
How is empyema investigated?
Bacteriological investigation of specimens obtained via transtracheal aspiration, bronchoscopy, or percutaneous transthoracic aspiration.
66
How is empyema treated?
Antibiotics covering aerobic and anaerobic bacteria (e.g., cefuroxime and metronidazole). Tube drainage or rib resection to drain the empyema cavity.
67
What is the definition of pleural effusion?
An abnormal accumulation of fluid in the pleural cavity between the visceral and parietal pleurae, impairing lung expansion.
68
What are the common types of pleural effusion?
Transudate: Fluid due to disruption of hydrostatic forces, as seen in congestive heart failure or cirrhosis. Exudate: Fluid due to inflammation or lesions in blood/lymph vessels, as seen in infections or malignancies.
69
What are common causes of exudative pleural effusion?
Pulmonary TB, pneumonia (most common cause), bronchial carcinoma, pulmonary infarction, collagen diseases (SLE, RA), lymphoma, sarcoidosis, and pulmonary embolism.
70
What are common causes of transudative pleural effusion?
Congestive heart failure, cirrhosis of the liver, nephrotic syndrome, hypoproteinemia, Meigs syndrome (right pleural effusion, ascites, ovarian fibroma).
71
What criteria are used to classify pleural effusion as an exudate?
Light's criteria: Pleural fluid protein > 0.5 × serum protein. Pleural fluid LDH > 0.6 × serum LDH. Pleural fluid LDH > 2/3 of the upper normal serum LDH.
72
Effusion rarely consist of what?
blood (hemothorax) red, bloody; pus (empyema); lymph (chylothorax) milky and white.
73
What are the clinical features of pleural effusion?
Dyspnea, dry nonproductive cough (w/ infx productive), pleuritic chest pain, reduced chest expansion, diminished or absent breath sounds, dullness to percussion, and decreased tactile fremitus.
74
How is pleural effusion investigated?
Chest X-ray: Blunting of the costophrenic angle, opacity, meniscus sign.
Thoracentesis: Fluid analysis for protein, LDH, glucose, pH, Gram stain, cytology.
Ultrasound: Locates fluid for thoracentesis and assesses septations.
CT scan: Detects underlying causes like malignancies or infections.
Biopsy (definitive diagnosis): tb smear, culture, histology.
75
How is pleural effusion treated?
Transudative effusion: Treat the underlying cause (e.g., diuretics for CHF).
Exudative effusion: Antibiotics for parapneumonic effusion. Drainage for empyema (via chest tube). Surgical lysis of adhesions in empyema. Intrapleural injection of thrombolytic agents (streptokinase/urokinase). Pleurodesis for empyema/malignancy.
76
What is ARDS?
ARDS is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs, leading to noncardiogenic pulmonary edema and severe hypoxemia.
77
What are the causes of ARDS?
Direct lung injury: Pneumonia, gastric aspiration, inhalation injury, vasculitis.
Systemic causes: Sepsis (most common), shock, multiple transfusions, severe trauma, drug overdose.
78
What is the pathophysiology of ARDS?
Neutrophil activation → Inflammatory cytokine release (TNF-alpha, IL-1). Increased alveolar-capillary membrane permeability → Pulmonary edema. Surfactant dysfunction → Alveolar collapse. Formation of hyaline membranes → Impaired gas exchange → Hypoxemia.
79
What are the diagnostic criteria for ARDS? (Berlin Definition)
Acute onset (within 1 week of a known insult). Bilateral diffuse pathy/homogeneous pulmonary infiltrates on CXR. PCWP <18 mmHg. PaO2/FiO2 ratio <300: Mild: 200-300; Moderate: 100-200; Severe: <100.
80
What are the clinical features of ARDS?
Dyspnea, tachypnea, tachycardia. Cyanosis and refractory hypoxemia. Bilateral fine inspiratory crackles. Pulmonary edema without cardiogenic cause. Multi-organ failure & hemodynamic instability are cause of death in severe cases.
81
How is ARDS investigated?
CXR: Bilateral pulmonary infiltrates. ABG: Severe hypoxemia (PaO2/FiO2 <300). Pulmonary artery catheter: PCWP <18 mmHg (excludes cardiogenic pulmonary edema).
82
What is the treatment for ARDS?
ICU admission & supportive care. Mechanical ventilation (low tidal volume, high PEEP, FiO2 titration). Prone positioning. Fluid restriction & diuretics (if pulmonary edema present). Vasodilators (inhaled NO, prostacyclin) for pulmonary hypertension. Treatment of underlying cause (e.g., antibiotics for sepsis). DONT GIVE STEROIDS.
83
What is respiratory failure?
Impairment in gas exchange causing hypoxemia (PaO2 < 60 mmHg) with or without hypercapnia (PaCO2 > 50 mmHg).
84
What are the types of respiratory failure?
Type 1 (Hypoxemic): Low PaO2, normal/low PaCO2 (e.g., ARDS, pneumonia, PE). Type 2 (Hypercapnic): High PaCO2, ± hypoxemia (e.g., COPD, neuromuscular disorders).
85
What are the causes of Type 1 respiratory failure?
V/Q mismatch (e.g., pulmonary edema, pulmonary embolism). Shunting (e.g., ARDS, pulmonary edema). Diffusion impairment (e.g., interstitial lung disease).
86
What are the causes of Type 2 respiratory failure?
Hypoventilation (e.g., COPD, obesity hypoventilation, neuromuscular diseases). Increased CO2 production (e.g., sepsis, DKA, hyperthermia).
87
What are the clinical features of respiratory failure?
Dyspnea, tachypnea, tachycardia. Use of accessory muscles. Cyanosis. Signs of CO2 retention: Asterixis, bounding pulse, warm peripheries.
88
What investigations confirm respiratory failure?
ABG: Hypoxemia (PaO2 < 60), hypercapnia (PaCO2 > 50 in Type 2).
CXR: To identify underlying cause.
Pulmonary function tests: In chronic cases.
PaO2/FIO2 ratio: Used to define respiratory impairment in ARDS.
FEV1: useful to assess patients with acute asthma attacks.
89
What are the treatment options for respiratory failure?
Oxygen therapy: Venturi mask in COPD (controlled FiO2). High-flow oxygen in hypoxemic patients. Non-invasive ventilation (NIV): CPAP for Type 1 respiratory failure. BiPAP for COPD with acidosis (pH < 7.35, PaCO2 > 50 mmHg). Mechanical ventilation if NIV fails. Treat underlying cause (e.g., bronchodilators for COPD, diuretics for pulmonary edema).
90
What are the indications for mechanical ventilation in respiratory failure?
Respiratory distress not responsive to oxygen. pH <7.25 due to respiratory acidosis. PaO2 <50 mmHg despite high-flow oxygen. Severe fatigue and respiratory exhaustion.
91
What is the definition of pneumothorax?
The presence of air in the pleural cavity, leading to lung collapse.
92
What are the types of pneumothorax?
Spontaneous pneumothorax: Primary: Occurs in healthy individuals (commonly tall, young males).
Secondary: Occurs in individuals with underlying lung disease (e.g., COPD, asthma).
Traumatic pneumothorax: Due to penetrating chest injuries.
Tension pneumothorax: A life-threatening condition where air enters the pleural space but cannot exit.
93
What are the clinical features of pneumothorax?
Sudden-onset chest pain, dyspnea, hyperresonance on percussion, diminished or absent breath sounds, and in tension pneumothorax, tracheal deviation to the opposite side.
94
How is pneumothorax diagnosed?
Chest X-ray: Reveals a visible pleural line, absence of lung markings beyond it, and in tension pneumothorax, mediastinal shift. Ultrasound: Useful for rapid bedside diagnosis. CT scan: For small or occult pneumothoraces and to evaluate underlying lung pathology.
95
How is pneumothorax managed?
Small pneumothorax: Observation with oxygen therapy. Large or symptomatic pneumothorax: Needle aspiration or chest tube insertion. Tension pneumothorax: Immediate needle decompression followed by chest tube insertion.
96
What are the complications of pneumothorax?
Respiratory failure, tension pneumothorax, pleural adhesions, recurrent pneumothorax, and cardiovascular collapse in severe cases.
97
What is pulmonary embolism (PE)?
Occlusion of the pulmonary vasculature by a blood clot, commonly arising from deep vein thrombosis (DVT). It is a medical emergency that can lead to sudden death.
98
What are the sources of emboli in PE?
Leg veins (DVT), pelvic veins, upper extremity veins, and the right chamber of the heart.
99
What are other risk factors for pulmonary embolism?
Cancer & malignancy, HRT & pregnancy, recent long-haul flights, history of prior thromboembolic events, genetic thrombophilias, advanced age >60, cardiac disease, obesity, nephrotic syndrome, surgery, trauma, central venous catheterization.
100
What is Virchow’s Triad?
The three main risk factors for thrombosis: Venous stasis, endothelial injury, hypercoagulability.
101
What are the symptoms of PE?
Dyspnea, pleuritic chest pain, cough, hemoptysis, syncope, tachycardia, tachypnea, and in severe cases, shock or circulatory collapse.
102
How is PE diagnosed?
Gold Standard: CT pulmonary angiogram. V/Q scan if CT is contraindicated. D-dimer to rule out PE in low-risk cases. ABG shows respiratory alkalosis. ECG may show sinus tachycardia. Chest X-ray is often normal. Lower extremity ultrasound to detect DVT.
103
How is PE managed?
Stable patients: Anticoagulation for 3-6 months. If anticoagulation contraindicated: IVC filter. Unstable patients: Thrombolytic therapy or surgical/catheter-based embolectomy.
104
What is interstitial lung disease (ILD)?
A group of lung disorders characterized by inflammation and fibrosis of the lung interstitium, leading to impaired gas exchange.
105
What are the causes of ILD?
Idiopathic: Idiopathic pulmonary fibrosis. Exposure-related: Hypersensitivity pneumonitis, pneumoconioses, radiation pneumonitis. substance induced ILD (drugs- MAN)
Secondary to underlying disease: Connective tissue diseases, granulomatous diseases, infectious diseases, alveolar filling disease.
106
What are the clinical features of ILD?
Progressive dyspnea on exertion, nonproductive cough, fine inspiratory crackles, clubbing, signs of pulmonary hypertension and right heart failure.
107
How is ILD diagnosed?
Chest X-ray shows reticulonodular pattern. PFTs show restrictive pattern. HRCT may show honeycombing. Lung biopsy may be necessary.
108
What is the distribution of upper lobe fibrosis caused by?
ARCHSS: sarcoidosis, hypersensitivity pneumonitis, silicosis, radiation, ankylosing spondylitis, coal worker pneumoconioses.
109
What is the distribution of lower lobe fibrosis caused by?
Idiopathic pulmonary fibrosis, asbestosis.
110
What is Idiopathic Pulmonary Fibrosis (IPF)?
Common type of ILD, usually seen in late 60s, more common in males. Features: Progressive dyspnea, nonproductive cough, clubbing, fine basal crackles. Diagnosis: CXR/HRCT shows subpleural honeycombing. Treatment: Pirfenidone, Nintedanib, lung transplantation.
111
What is Pneumoconioses?
Due to occupational exposures. Features: Progressive dyspnea, cough, restrictive PFTs. Diagnosis: CXR/HRCT shows nodular opacities. Treatment: Supportive care, remove exposure.
112
What is Connective Tissue Disease-associated ILD?
Secondary to conditions like systemic sclerosis, rheumatoid arthritis, SLE. Features: Dyspnea, systemic signs. Diagnosis: Autoantibodies, HRCT, biopsy if needed. Treatment: Immunosuppressants.
113
How is ILD treated?
Idiopathic pulmonary fibrosis: Pirfenidone, Nintedanib, lung transplant. Exposure-related: Remove exposure, steroids if necessary. Connective tissue disease ILD: Immunosuppressants. Supportive care: Oxygen therapy, pulmonary rehabilitation.
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What is sarcoidosis?
A multisystem granulomatous disease of unknown cause, often affecting the lungs.
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What are the key immunopathological features of sarcoidosis?
Noncaseating granulomas, increased CD4 helper T-cells, hypercalcemia due to increased vitamin D production.
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What are the clinical features of sarcoidosis?
50% asymptomatic. Fatigue, dyspnea, nonproductive cough, eye involvement (uveitis), skin manifestations (erythema nodosum)
lofgren syndrome & heerfordt syndrome
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How is sarcoidosis diagnosed?
Hypercalcemia
High ACE
Bronchoalveolar lavage high CD4
Restrictive pattern
Chest X-ray staging: Stage 1: BHL, Stage 2: BHL + pulmonary infiltrates, Stage 3: pulmonary infiltrates only, Stage 4: pulmonary fibrosis. Biopsy shows noncaseating granulomas.
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How is sarcoidosis treated?
Observation if asymptomatic. Steroids for symptomatic patients: prednisolone. For long term control Steroid-sparing agents: Methotrexate, azathioprine.
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What is hypersensitivity pneumonitis?
A lung disorder caused by an exaggerated immune response to inhaled antigens.
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What are the clinical features of hypersensitivity pneumonitis?
Acute: Fever, malaise, dyspnea, cough. Chronic: Progressive dyspnea, weight loss, clubbing.
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How is hypersensitivity pneumonitis diagnosed?
IgG & IgA antibodies against the antigen, neutrophilia and eosinophilia, CXR shows upper zone nodular flurry nodular infiltrates.
HRCT reticular nodular pattern with ground glass appearance.
Bronchoalaveloar lavage high CD8
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How is hypersensitivity pneumonitis treated?
Avoid antigen exposure. Corticosteroids for severe cases.
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What is asbestosis?
Asbestosis is lung parenchymal fibrosis caused by prolonged inhalation of asbestos dust. It usually presents 15-20 years after exposure.
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What are the occupational exposures associated with asbestosis?
Builders, plumbers, and shipyard workers are commonly exposed to asbestos.
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How is asbestosis diagnosed?
Through history of exposure, CXR showing pleural thickening and diaphragmatic calcification, confirmed by HRCT.
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What are the complications of asbestosis?
Pleural effusion, pleural thickening, mesothelioma, and lung adenocarcinoma.
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What are the clinical features of asbestosis?
Long latent period, exertional dyspnea, dry or productive cough, digital clubbing, bilateral fine basal end-inspiratory rales.
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What does CXR show in asbestosis?
Hazy infiltrates with bilateral linear opacities, possibly pleural plaques in lower lung regions.
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What is the treatment for asbestosis?
Cessation of exposure, oxygen therapy, immunization against influenza and pneumococcal pneumonia, antimicrobial treatment for respiratory infections.
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What is silicosis?
Silicosis is caused by inhalation of silica dust, commonly in mining, glass, pottery making, and sandblasting.
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What is the pathophysiology of silicosis?
Silica dust interacts with aqueous media, producing oxygen radicals that trigger inflammation, leading to pulmonary fibrosis and scarring.
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What are the clinical features of silicosis?
Exertional dyspnea, cough with sputum, increased risk of TB.
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What are the CXR findings in silicosis?
Eggshell calcification of hilar lymph nodes, bilateral diffuse ground-glass opacities, small rounded opacities in the upper lobes, confluent lesions that enlarge over time.
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What are the complications of silicosis?
Chronic bronchitis, progressive massive pulmonary fibrosis, and Caplan syndrome.
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What is the treatment for silicosis?
Supportive care and removal from silica exposure.
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What is coal worker’s pneumoconiosis (CWP)?
A lung disease caused by inhalation of coal dust, leading to pulmonary nodules and fibrosis.
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What are the stages of coal worker’s pneumoconiosis?
Simple CWP: Small pulmonary nodules. Progressive massive fibrosis: Large fibrotic masses (1-10 cm).
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What are the symptoms of coal worker’s pneumoconiosis?
Breathlessness and cough with black sputum.
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What is the pathophysiology of pneumoconiosis?
Inhalation of dust particles leads to phagocytosis by alveolar macrophages, inflammatory reaction, scarring and granuloma formation.
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What are the radiographic features of Coal workers pneumoconiosis?
Honeycombing (cystic lesions in lung parenchyma), irregular thickening of intralobular septa, reticular pattern with ground-glass opacities, traction bronchiectasis.
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What is the treatment for coal worker’s pneumoconiosis?
Supportive care and cessation of coal dust exposure.
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What are the indications for oxygen therapy?
Hypoxia, acute hypotension, breathing inadequacy, trauma (e.g., rebreather mask at 15 L/min in ER), CO poisoning, severe anemia, perioperative period.
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What are the mechanisms of hypoxemia?
V/Q mismatch, right-to-left shunt, impaired diffusion, alveolar hypoventilation.
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What are the dangers of oxygen therapy?
Ignition hazard, respiratory depression (e.g., hypoxic drive in COPD), oxygen toxicity (with high flow for long durations).
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What is the purpose of a humidifier in oxygen therapy?
Prevents drying of mucous membranes and thick sputum formation if oxygen flow exceeds 4 L/min.
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What are the different oxygen delivery devices?
Nasal cannula, simple face mask, Venturi mask, non-rebreather mask, high-flow nasal cannula (HFNC).
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What is non-invasive ventilation (NIV)?
CPAP and BiPAP.
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What is invasive ventilation?
Ventilation provided via a machine attached to an artificial airway (e.g., endotracheal tube).
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What are the indications for pulmonary function tests (PFTs)?
Smoking history, persistent cough or sputum production, history of lung irritant exposure, assessing disease progression, preoperative risk stratification, evaluating disability or impairment.
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How are PFTs performed?
Take normal and deep breaths, exhale quickly and forcefully for at least 6 seconds, repeat test three times for accuracy.
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What do FVC and FEV1 measure?
FVC: Total air exhaled, normal is 80-120% of predicted. FEV1: Air exhaled in 1 second, normal is >80% predicted.
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What patterns are identified in PFTs?
Obstructive: Low FEV1/FVC, reversible with bronchodilator in asthma. Restrictive: Low FVC and FEV1, normal/increased FEV1/FVC.
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What is the methacholine challenge test?
A test for asthma diagnosis when PFTs and other tests are normal. Positive if FEV1 decreases by 20% after methacholine.
154
What is the most common type of primary lung tumor?
Bronchial carcinoma, which accounts for 95% of primary lung tumors.
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What are common metastatic sites for lung cancer?
Primary cancers often metastasize to the lungs from the kidney, prostate, breast, bone, gastrointestinal tract, cervix, or ovary.
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What are the risk factors for lung cancer?
Tobacco smoking, radon exposure, asbestos exposure, secondhand smoke, chronic obstructive pulmonary disease (COPD).
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What are the common symptoms of lung cancer?
Cough, hemoptysis, dyspnea, wheezing, recurrent pneumonia, chest pain, weight loss, hoarseness.
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What is superior vena cava (SVC) syndrome?
Obstruction of the SVC causing prominent jugular venous distension (JVD) and facial swelling.
159
What are paraneoplastic syndromes, and how are they related to lung cancer?
Paraneoplastic syndromes are conditions caused by tumor-secreted hormones or immune responses against the tumor, often associated with lung cancer.
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How is lung cancer diagnosed?
Imaging: CXR or chest CT, biopsy.
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What are the main pathological types of lung cancer?
Small Cell Lung Cancer (SCLC)and Non-Small Cell Lung Cancer (NSCLC- adenocarcinoma, squamous cell carcinoma, large cell carcinoma, bronchial carcinoma tumor) (check table in survival for extra info)
