SMLE Medicine Flashcards

24 sample cards from the Medicine deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Define chronic obstructive pulmonary disease (COPD).

   A chronic, largely irreversible airflow limitation caused by chronic bronchitis and/or emphysema, usually due to a noxious exposure — most commonly cigarette smoke — producing persistent respiratory symptoms.

2. What spirometry criterion confirms an obstructive pattern in COPD?

   A post-bronchodilator $\frac{FEV_1}{FVC} < 0.70$, indicating airflow limitation that is not fully reversible.

3. Contrast the classic 'pink puffer' and 'blue bloater' phenotypes of COPD.

   Pink puffer (emphysema-predominant): thin, marked dyspnea, pursed-lip breathing, relatively normal blood gases. Blue bloater (chronic bronchitis-predominant): overweight, cyanosis, cough with sputum, hypoxemia/hypercapnia, and cor pulmonale.

4. Define chronic bronchitis clinically.

   A productive cough present for at least 3 months in each of 2 consecutive years, in the absence of other explanations.

5. Which genetic deficiency causes early-onset emphysema, especially in non-smokers?

   Alpha-1 antitrypsin ($\alpha_1$-antitrypsin) deficiency, which allows unopposed neutrophil elastase to destroy alveolar tissue, classically causing panacinar, basal-predominant emphysema.

6. What is the only intervention proven to reduce mortality and slow decline in COPD (besides smoking cessation)?

   Long-term oxygen therapy (LTOT) in patients with chronic resting hypoxemia ($PaO_2 \leq 55\ \text{mmHg}$, or $\leq 59\ \text{mmHg}$ with cor pulmonale/polycythemia), used $\geq 15$ hours/day. Smoking cessation is the single most effective intervention overall.

7. What target oxygen saturation range is recommended during a COPD exacerbation, and why?

   $88$-$92\%$. Excessive oxygen can blunt hypoxic respiratory drive and worsen ventilation-perfusion matching, causing $CO_2$ retention and respiratory acidosis in chronic $CO_2$ retainers.

8. List the core pharmacologic management of an acute COPD exacerbation.

   Short-acting bronchodilators (SABA + short-acting antimuscarinic), systemic corticosteroids (e.g., prednisolone ~5 days), antibiotics if increased sputum purulence/volume, controlled oxygen, and non-invasive ventilation (BiPAP) for hypercapnic respiratory failure.

9. Define asthma.

   A chronic inflammatory airway disease characterized by reversible airflow obstruction, bronchial hyperresponsiveness, and airway inflammation, producing episodic wheeze, cough, chest tightness, and dyspnea.

10. How does spirometry demonstrate reversibility in asthma?

    An obstructive pattern ($\downarrow FEV_1/FVC$) that improves after a bronchodilator, defined as an increase in $FEV_1$ of $\geq 12\%$ AND $\geq 200\ \text{mL}$.

11. What is the preferred controller therapy foundation for asthma, and why not SABA alone?

    Inhaled corticosteroids (ICS), often combined with a long-acting beta-agonist (LABA) as needed or maintenance. SABA-only treatment is discouraged because it controls symptoms without treating underlying inflammation and is linked to increased exacerbation and mortality risk.

12. List the clinical features that classify an asthma attack as life-threatening.

    $PEF < 33\%$ predicted, $SpO_2 < 92\%$, silent chest, cyanosis, poor respiratory effort, bradycardia/arrhythmia/hypotension, exhaustion, confusion, or a normal/rising $PaCO_2$ (a sign of impending respiratory failure).

13. In an acute severe asthma exacerbation, what does a normal or rising PaCO2 indicate?

    Impending respiratory failure. Early in an attack $PaCO_2$ is low from hyperventilation; a normalizing or rising $PaCO_2$ signals the patient is tiring and cannot maintain ventilation — a critical warning sign.

14. Outline the emergency treatment of acute severe asthma.

    High-flow oxygen (target $SpO_2\ 94$-$98\%$), nebulized SABA (salbutamol) plus ipratropium, systemic corticosteroids, and IV magnesium sulfate for severe/life-threatening cases; escalate to ICU if not improving.

15. Name the classic asthma triad known as Samter's triad (aspirin-exacerbated respiratory disease).

    Asthma, nasal polyps, and aspirin (NSAID) sensitivity.

16. Contrast asthma and COPD on reversibility, age of onset, and typical trigger.

    Asthma: largely reversible airflow obstruction, often childhood onset, atopy/allergen triggers, eosinophilic inflammation. COPD: largely irreversible obstruction, onset usually after age 40, smoking-related, neutrophilic inflammation.

17. Define pneumonia.

    An acute infection of the lung parenchyma (alveoli and distal airways) causing consolidation, typically presenting with fever, cough, sputum, dyspnea, and pleuritic chest pain.

18. What is the most common bacterial cause of community-acquired pneumonia (CAP)?

    Streptococcus pneumoniae (pneumococcus).

19. What does the CURB-65 score assess, and what do its components stand for?

    It estimates CAP severity and guides admission. Confusion, Urea $> 7\ \text{mmol/L}$, Respiratory rate $\geq 30$, Blood pressure (systolic $< 90$ or diastolic $\leq 60\ \text{mmHg}$), Age $\geq 65$. Each scores 1 point; $0$-$1$ outpatient, $2$ consider admission, $\geq 3$ hospital/ICU assessment.

20. Differentiate typical from atypical pneumonia.

    Typical (e.g., S. pneumoniae): abrupt high fever, productive purulent sputum, lobar consolidation. Atypical (e.g., Mycoplasma, Legionella, Chlamydophila): gradual onset, dry cough, prominent extrapulmonary symptoms, and diffuse/interstitial infiltrates with milder-looking chest exam ('walking pneumonia').

21. Which organism causes pneumonia associated with hyponatremia, GI symptoms, and exposure to contaminated water systems?

    Legionella pneumophila (Legionnaires' disease). Diagnosis is aided by the urinary Legionella antigen test.

22. Distinguish hospital-acquired pneumonia (HAP) from community-acquired pneumonia (CAP) by definition.

    HAP develops $\geq 48$ hours after hospital admission; CAP is acquired outside the hospital or within the first 48 hours of admission. HAP more often involves gram-negative bacilli, S. aureus (including MRSA), and resistant organisms.

23. Which pathogen classically causes 'currant jelly' sputum and cavitating pneumonia, especially in alcoholics/diabetics?

    Klebsiella pneumoniae — associated with thick red-brown ('currant jelly') sputum, upper-lobe involvement, and abscess/cavity formation.

24. What is the empiric outpatient antibiotic approach for community-acquired pneumonia in an otherwise healthy adult?

    A macrolide (e.g., azithromycin) or doxycycline; amoxicillin is also used. For patients with comorbidities, a respiratory fluoroquinolone or a beta-lactam plus a macrolide is preferred to cover typical and atypical organisms.

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