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Medical flashcard set for respiratory pathology, USMLE medical student level. Clean, professional design with a dark navy blue header bar showing "Respiratory Pathology Flashcards" in white bold text. Below, a 2x3 grid of flashcard previews, each card with a colored top strip (alternating teal, orange, purple) and white body. Card titles visible: "Asthma", "Emphysema vs Chronic Bronchitis", "Pneumonia Types", "Lung Cancer", "Sarcoidosis", "TB & ARDS". Each card shows a few bullet points of key facts. Clean minimal medical education style.
Here are your complete respiratory pathology flashcards, sourced directly from Robbins & Kumar Basic Pathology and Robbins/Cotran Pathologic Basis of Disease. Each card has a front question and back answer.
🫁 OBSTRUCTIVE LUNG DISEASES
Card 1 — Asthma: Definition & Hallmarks
Q: What are the four pathologic hallmarks of asthma?
A:
- Intermittent, reversible airway obstruction
- Chronic bronchial inflammation with eosinophils
- Bronchial smooth muscle hypertrophy and hyperreactivity
- Increased mucus secretion
Key: Episodic wheezing, dyspnea, cough - especially nocturnal/early morning Source: Robbins Basic Pathology, Ch. 11
Card 2 — Atopic vs. Nonatopic Asthma
Q: How do atopic and nonatopic asthma differ in mechanism?
A:
| Feature | Atopic | Nonatopic |
|---|---|---|
| Type | Type I IgE-mediated | Non-immunologic |
| Triggers | Allergens (pollen, dander, dust) | Infections, irritants, cold air |
| Cells | Th2 cells, IgE, mast cells | Mast cells, eosinophils |
| Key cytokines | IL-4, IL-5, IL-13 | - |
| Skin test | Wheal-and-flare positive | Negative |
- IL-4/IL-13: drive IgE production from B cells
- IL-5: recruits and activates eosinophils
- IL-13: drives mucus production
Card 3 — Obstructive Lung Disease: Quick Comparison
Q: Fill in the table: What is the anatomic site, pathology, and main symptom for each obstructive disorder?
A:
| Disease | Site | Key Pathology | Symptom |
|---|---|---|---|
| Emphysema | Acinus | Air space enlargement, wall destruction | Dyspnea |
| Chronic bronchitis | Bronchus | Mucous gland hypertrophy, hypersecretion | Cough + sputum |
| Asthma | Bronchus | Smooth muscle hypertrophy, mucus, eosinophils | Episodic wheeze |
| Bronchiectasis | Bronchus | Airway dilation and scarring | Purulent sputum, fever |
| Bronchiolitis | Bronchiole | Inflammatory scarring | Cough, dyspnea |
Card 4 — Emphysema
Q: What is the pathogenesis of emphysema and which type is most common?
A:
- Cause: Tobacco smoke - neutrophils/macrophages release elastases that destroy alveolar walls
- Centriacinar (centrilobular) = most common; affects respiratory bronchioles; upper lobes; smokers
- Panacinar = affects entire acinus; lower lobes; seen in alpha-1 antitrypsin deficiency
- Result: Loss of elastic recoil → air trapping → barrel chest, hyperresonance, pursed-lip breathing
- "Pink puffer" phenotype: dyspnea dominant, near-normal PaCO2
Card 5 — Chronic Bronchitis
Q: What is the clinical and histologic definition of chronic bronchitis?
A:
- Clinical: Productive cough for at least 3 consecutive months in at least 2 consecutive years
- Histology: Hypertrophy and hyperplasia of mucus-secreting glands in the bronchial wall
- Reid index = ratio of mucous gland thickness to total bronchial wall thickness (normal < 0.4; elevated in chronic bronchitis)
- "Blue bloater": cyanotic, hypercapnic, hypoxemic, edematous
- Cause: tobacco smoke, air pollutants
🫁 INFECTIOUS / INFLAMMATORY
Card 6 — Community-Acquired Pneumonia: Key Organisms
Q: Match the clinical scenario to the most likely pneumonia organism.
A:
| Scenario | Organism |
|---|---|
| Most common overall (lobar, rust-colored sputum) | S. pneumoniae |
| Elderly/aspiration-prone, tissue necrosis | K. pneumoniae (currant-jelly sputum) |
| Atypical, "walking pneumonia," cold agglutinins | Mycoplasma pneumoniae |
| Legionnaire's disease, water systems, hyponatremia | Legionella pneumophila |
| Flu-like, exposure to birds/droppings | C. psittaci / H. capsulatum |
| Flu followed by bacterial superinfection | S. aureus |
| Hospital-acquired / ventilator-associated | Gram-negative rods (Pseudomonas, Enterobacteriaceae), S. aureus |
Card 7 — Aspiration Pneumonia
Q: Who gets aspiration pneumonia and what are its features?
A:
- At risk: Debilitated patients, impaired gag/swallowing (post-stroke), unconscious patients
- Mechanism: Gastric acid (chemical) + polymicrobial bacteria
- Organisms: Aerobes > anaerobes (mixed flora)
- Complications: Often necrotizing; lung abscess is common in survivors
- Lower lobes most affected (gravity-dependent)
- Note: Microaspiration (in GERD) ≠ pneumonia, but can exacerbate lung disease
Card 8 — Tuberculosis: Primary vs. Secondary (Reactivation)
Q: Contrast primary and secondary TB in an immunocompetent host.
A:
| Feature | Primary TB | Secondary (Reactivation) TB |
|---|---|---|
| Prior exposure | None | Yes |
| Location | Subpleural focus + hilar nodes (Ghon complex) | Lung apices |
| Lesion type | Usually heals; calcified Ghon focus | Cavitary lesion |
| Symptoms | Usually asymptomatic | Fever, night sweats, hemoptysis |
| Immune state | Competent = contained | Competent but weakened |
- Hallmark: Caseating granulomas (Langhans giant cells + CD4+ Th1 response)
- Immunodeficiency (HIV) → miliary TB, meningitis (progressive forms)
- Stain: Ziehl-Neelsen (acid-fast, carbol fuchsin)
Card 9 — ARDS (Acute Respiratory Distress Syndrome)
Q: What are the key features, histology, and clinical outcomes of ARDS?
A:
- Triggers: Sepsis, trauma, aspiration, pancreatitis, severe pneumonia
- Onset: 85% of cases within 72 hours of insult
- Histology (DAD - diffuse alveolar damage):
- Acute phase: alveolar collapse + distension, pink hyaline membranes lining alveoli
- Healing phase: resorption of membranes, alveolar septal thickening, reactive type II pneumocytes
- Imaging: Bilateral ground-glass opacities on CT
- Prognosis: ~40% mortality; death usually from underlying cause or superinfection, not respiratory failure itself
🫁 INTERSTITIAL / DIFFUSE LUNG DISEASES
Card 10 — Sarcoidosis
Q: What are the defining features of sarcoidosis?
A:
- Hallmark: Non-necrotizing (non-caseating) epithelioid granulomas with Schaumann and asteroid bodies
- Driver: CD4+ Th1 cells; elevated IL-2, IFN-γ
- Unique: Higher prevalence in nonsmokers (rare for a lung disease)
- Distribution: Granulomas follow lymphatic routes - peribronchovascular, subpleural
- Organs: Lung (90%), hilar lymph nodes (75-90%), skin (25% - erythema nodosum), eyes (uveitis), heart
- Blood: Low circulating CD4+ T cells, elevated ACE
- 5-15% progress to honeycomb lung fibrosis
- Lymph nodes: firm, rubbery, non-matted, non-necrotic (unlike TB)
Card 11 — Idiopathic Pulmonary Fibrosis (IPF)
Q: What is the morphologic pattern and clinical course of IPF?
A:
- Pattern: Usual Interstitial Pneumonia (UIP) - temporal and spatial heterogeneity, subpleural/basal predominant
- Histology: Alternating areas of normal lung + fibrosis + honeycombing; fibroblastic foci
- Key feature: Progressive, irreversible fibrosis - median survival ~3 years from diagnosis
- Symptoms: Progressive dyspnea, dry cough, bilateral basal crackles, clubbing
- Treatment: Antifibrotics (pirfenidone, nintedanib) slow decline; lung transplant is only cure
- Differs from sarcoidosis: IPF has fibrosis without granulomas
Card 12 — Hypersensitivity Pneumonitis (Extrinsic Allergic Alveolitis)
Q: What distinguishes hypersensitivity pneumonitis from asthma?
A:
- HP: Type III (immune complex) + Type IV (cell-mediated) hypersensitivity to inhaled organic antigens
- Examples: Farmer's lung (thermophilic actinomycetes in hay), Bird-fancier's lung (avian proteins)
- Histology: Lymphocytic alveolitis + non-caseating granulomas + bronchiolitis
- Key difference from asthma: HP involves alveoli and interstitium; asthma is airway-centric
- Acute: Fever, dyspnea, crackles 4-6 hours after exposure (resolves with avoidance)
- Chronic: Irreversible fibrosis if exposure continues
🫁 LUNG TUMORS
Card 13 — Lung Cancer: Four Major Subtypes
Q: What are the four major histologic types of lung cancer and their key associations?
A:
| Type | % | Location | Key Association |
|---|---|---|---|
| Adenocarcinoma | ~40% (most common) | Peripheral | Nonsmokers, women; EGFR, ALK mutations; lepidic growth |
| Squamous Cell Carcinoma | ~25-30% | Central (hilar) | Heavy smokers; PTH-rP (hypercalcemia); cavitates |
| Small Cell Carcinoma (SCLC) | ~15% | Central | Strongest smoking link; neuroendocrine; ACTH/ADH production; TP53 + RB mutations |
| Large Cell Carcinoma | ~10% | Peripheral | Diagnosis of exclusion; poor prognosis |
Card 14 — SCLC vs. NSCLC: The High-Yield Comparison
Q: Compare SCLC and NSCLC across histology, markers, mutations, and treatment.
A:
| Feature | SCLC | NSCLC (Adeno/SCC) |
|---|---|---|
| Microscopy | Scant cytoplasm, hyperchromatic nuclei, diffuse sheets | Abundant cytoplasm, glandular/squamous architecture |
| Neuroendocrine markers (chromogranin, synaptophysin, CD56) | Present | Absent |
| Mucin | Absent | Present (adenocarcinoma) |
| TP53 mutations | ~90% | ~50% |
| RB mutations | ~90% | ~20% |
| KRAS mutations | Rare | ~30% (adenocarcinoma) |
| EGFR mutations | Absent | ~20% (adenocarcinoma, nonsmokers) |
| Chemo/RT response | Often complete, but always recurs | Incomplete response |
| Checkpoint inhibitors | Unresponsive | Responsive |
| Surgery | NOT curative (already metastatic at diagnosis) | Curative if localized |
| Median survival with Tx | ~1 year | Varies by stage |
Card 15 — Paraneoplastic Syndromes in Lung Cancer
Q: Match the paraneoplastic syndrome to the lung cancer subtype.
A:
| Syndrome | Mechanism | Cancer Type |
|---|---|---|
| Cushing syndrome (ACTH-like) | Ectopic ACTH production | SCLC |
| SIADH (hyponatremia) | Ectopic ADH production | SCLC |
| Hypercalcemia | PTH-related peptide (PTH-rP) | Squamous cell carcinoma |
| Eaton-Lambert syndrome | Anti-VGCC antibodies | SCLC |
| Clubbing / hypertrophic osteoarthropathy | Unknown mechanism | Adenocarcinoma/SCC |
| Pancoast syndrome (shoulder/arm pain, Horner's) | Apical tumor invading brachial plexus/sympathetic chain | Any (often SCC) |
🫁 VASCULAR / OTHER
Card 16 — Pulmonary Embolism (PE)
Q: What is Virchow's triad and how does it relate to PE?
A:
- Virchow's Triad: Stasis + Endothelial injury + Hypercoagulability
- Source: 95% from deep vein thrombosis (DVT) in legs
- Consequences depend on size:
- Large saddle embolus: sudden death, right heart failure
- Medium: pulmonary infarction (Hampton's hump on CXR), hemoptysis, pleuritis
- Small/recurrent: pulmonary hypertension
- Dx: CT pulmonary angiography (gold standard); D-dimer (sensitive, not specific)
- Rx: Anticoagulation (heparin → warfarin or DOAC); thrombolytics for massive PE
Card 17 — Pleural Effusion: Transudate vs. Exudate
Q: How do you distinguish a transudate from an exudate? (Light's Criteria)
A:
Exudate = ANY ONE of Light's criteria met:
- Pleural fluid protein / serum protein > 0.5
- Pleural fluid LDH / serum LDH > 0.6
- Pleural fluid LDH > 2/3 upper limit of normal serum LDH
| Transudate | Exudate |
|---|---|
| Low protein, low LDH | High protein, high LDH |
| CHF, cirrhosis, nephrotic syndrome | Pneumonia, malignancy, TB, PE |
| Hydrostatic/oncotic cause | Inflammatory/lymphatic cause |
Card 18 — Mesothelioma
Q: What is malignant mesothelioma and what causes it?
A:
- Cause: Asbestos exposure (latency 25-45 years); amphibole fibers (crocidolite) most dangerous
- Location: Pleura (most common), peritoneum, pericardium
- Presentation: Progressive dyspnea, chest pain, recurrent bloody pleural effusion
- Histology: Biphasic - epithelioid + sarcomatoid patterns; mesothelial markers (calretinin, WT-1, CK5/6); negative for CEA (distinguishes from adenocarcinoma)
- Prognosis: Very poor; median survival ~12 months
- Note: Asbestosis (interstitial fibrosis from asbestos) ≠ mesothelioma - both are asbestos-related but distinct diseases
RAPID REVIEW MNEMONICS
| Mnemonic | Meaning |
|---|---|
| "Pink Puffer vs Blue Bloater" | Emphysema (dyspnea, normal O2) vs Chronic Bronchitis (cyanosis, hypercapnia) |
| "EGFR = Ethnic/Female/No-smoking" | Adenocarcinoma EGFR mutations favor Asian women, never-smokers |
| "Ghon = Gone (healed) primary TB" | Ghon complex = subpleural focus + hilar node (primary TB, usually healed) |
| "SCLC = Surgery Contraindicated, Lethal Course" | Metastatic at diagnosis, not surgically curable |
| "ACE is high in Sarcoidosis" | Elevated serum ACE; granulomas produce it |
| "3 months × 2 years = Chronic Bronchitis" | Clinical definition |
| "Asbestosis: Ferruginous bodies, pleural plaques, mesothelioma" | All three are asbestos-related findings |
All content sourced from Robbins & Kumar Basic Pathology, 10e and Robbins, Cotran & Kumar Pathologic Basis of Disease, 10e.
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