pt13 Flashcards

(50 cards)

1
Q

What is the most common cause of community-acquired lobar pneumonia?

A

Streptococcus pneumoniae

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2
Q

Name two patient groups at risk for bronchopneumonia.

A

Infants, elderly, and patients with chronic debilitating disease or immunosuppression

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3
Q

What are the cardinal clinical features of bacterial pneumonia?

A

Cough with purulent or “rusty” sputum, dyspnoea, pyrexia; signs of consolidation and pleural rub

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4
Q

Which bedside tests help confirm consolidation in pneumonia?

A

Dullness to percussion over the affected area and bronchial breath sounds on auscultation

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5
Q

What immediate management is indicated for community-acquired pneumonia?

A

Empirical antibiotics without waiting for culture results; modify once sensitivities available

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6
Q

List two complications of untreated bacterial pneumonia.

A

Lung abscess formation and empyema (pleural effusion with infected exudate)

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7
Q

Describe the Ghon complex in primary tuberculosis.

A

A combination of a peripheral lung granuloma and ipsilateral hilar lymph node involvement, often healing with calcification

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8
Q

What changes characterize secondary (post-primary) pulmonary TB?

A

Reactivation in apical lung zones with caseating necrosis in larger granulomas and fibrous scarring

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9
Q

How is miliary tuberculosis distinguished pathologically?

A

Hematogenous dissemination forming numerous small granulomas (“millet seed” pattern) in multiple organs

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10
Q

What prophylaxis and treatment regimen is used for TB?

A

BCG vaccination for prevention; combination therapy of 3–4 anti-TB drugs for 6–9 months to prevent resistance

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11
Q

What four features characterise COPD?

A

Poorly reversible airflow limitation, progressive course, persistent inflammatory response, includes chronic bronchitis and emphysema

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12
Q

At what age and in which population is COPD most commonly symptomatic?

A

Rarely symptomatic before middle age; common in UK smokers (18% of male, 14% of female smokers)

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13
Q

What is the dominant causal agent in COPD and a notable rare genetic cause?

A

Cigarette smoking; α₁-antitrypsin deficiency causes early-onset emphysema

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14
Q

Describe the pathological changes in chronic bronchitis.

A

Chronic airway inflammation (predominantly lymphocytes), enlarged mucus-secreting glands, airway narrowing and mucus hypersecretion

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15
Q

Describe the pathological changes in emphysema.

A

Destruction and dilatation of lung tissue distal to terminal bronchioles, loss of elastic recoil, air trapping and bullae formation

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16
Q

What are the hallmark symptoms and signs of severe COPD?

A

Cough, sputum, breathlessness, wheeze; severe cases show tachypnoea, accessory muscle use, hyperinflation, poor expansion, cyanosis, cor pulmonale

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17
Q

Which lung function test abnormalities confirm COPD?

A

↓ FEV₁ and ↓ FEV₁/FVC ratio

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18
Q

What chest X-ray and blood gas findings support COPD?

A

Hyperinflated lungs on X-ray; arterial blood gases may show hypoxia and hypercapnia

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19
Q

What are the mainstays of COPD treatment?

A

Smoking cessation; bronchodilators (β₂-agonists, antimuscarinics), corticosteroids, antibiotics, management of respiratory failure and cor pulmonale

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20
Q

What is the 5-year prognosis for severe COPD with breathlessness?

A

Approximately 50% mortality within five years

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21
Q

What three characteristics define asthma?

A

Variable airflow limitation (often reversible), airway hyper-responsiveness, chronic bronchial inflammation

22
Q

How does asthma epidemiology vary geographically?

A

Increasing prevalence overall; more common in developed countries, much rarer in Far Eastern countries

23
Q

What are the two major aetiological categories in asthma?

A

Atopic/allergic (IgE-mediated) and non-atopic (intrinsic hyper-responsiveness to stimuli)

24
Q

Which cells and processes drive asthma pathogenesis?

A

Eosinophils, T-lymphocytes, macrophages and mast cells release mediators causing bronchoconstriction, inflammation and airway remodelling

25
Give three common precipitating factors for asthma attacks.
Occupational sensitizers (e.g. isocyanates), viral infections/cold air/exercise, airborne Aspergillus spores (rare)
26
What are the typical clinical features of an asthma attack?
Episodic wheezing, shortness of breath, chest tightness; on exam, reduced chest expansion, prolonged expiration, bilateral polyphonic wheezes
27
Which diagnostic tests support asthma?
Lung function showing variable airflow limitation (PEFR or FEV₁), bronchodilator reversibility (>15% FEV₁ improvement), bronchial provocation (histamine/methacholine), skin-prick allergy testing
28
What are first-line pharmacological treatments for asthma?
Short-acting β₂-agonist bronchodilators; inhaled corticosteroids for chronic inflammation
29
Name two add-on therapies for difficult-to-control asthma.
Leukotriene receptor antagonists, chromones, long-acting β₂-agonists, immunosuppressants (e.g., anti-IgE)
30
What proportion of primary lung tumours are bronchial carcinomas?
95% of primary lung tumours
31
What is the 5-year survival rate for primary lung cancer?
Less than 10%
32
List the four main histological types of bronchial carcinoma.
Squamous cell, small cell, adenocarcinoma, large cell undifferentiated carcinoma
33
What are the major risk factors for lung cancer?
Smoking (dominant), occupational carcinogens, pulmonary fibrosis
34
What are common presenting symptoms of lung cancer?
Persistent cough, chest pain, haemoptysis, weight loss
35
Which imaging and pathological investigations confirm lung cancer?
Chest X-ray and CT reveal masses; biopsy and cytology provide histological diagnosis
36
How does treatment differ between non-small cell and small cell lung cancer?
Non-small cell: surgical resection if early; small cell: chemotherapy with or without radiotherapy (often disseminated)
37
Name two targeted therapies recently developed for lung cancer.
EGFR tyrosine kinase inhibitors (for EGFR-mutant tumours), ALK inhibitors (for ALK-rearranged tumours)
38
What are the principal functions of the kidney?
Eliminating waste, regulating fluid/electrolyte and acid–base balance, and endocrine functions (prostaglandins, erythropoietin, 1,25-(OH)₂-D₃, renin)
39
What symptoms suggest renal tract disease?
Dysuria, haematuria, urinary retention, altered urine volume (polyuria or oliguria), and flank pain
40
Which four kidney structures are commonly involved in renal diseases?
Glomeruli, tubules, interstitium, and blood vessels
41
What is nephritis, and what are its main subtypes?
Inflammation of any part of the kidney: glomerulonephritis, interstitial nephritis, and pyelonephritis
42
How is glomerulonephritis classified?
Primary (kidney-predominant, e.g., post-streptococcal GN) vs. secondary (systemic diseases, e.g., SLE)
43
What immune mechanisms can injure the glomerulus?
In situ immune-complex formation; deposition of circulating complexes; anti-GBM antibodies; cell-mediated damage
44
What are the pathological features of acute proliferative glomerulonephritis?
Diffuse hypercellularity, basement-membrane thickening, hyalinisation and sclerosis
45
What are the clinical features of acute nephritic syndrome?
Haematuria, proteinuria, hypertension, periorbital oedema, oliguria, and uraemia
46
How is acute nephritic syndrome managed?
Supportive care, salt restriction, diuretics, vasodilators for hypertension, fluid-balance monitoring, and fluid restriction if oliguric
47
What key defect underlies nephrotic syndrome?
Glomerular basement-membrane damage causing loss of electrostatic and physical barriers to protein filtration
48
What are the diagnostic criteria for nephrotic syndrome?
Proteinuria >3.5 g/24 h, serum albumin <30 g/L, hyperlipidaemia, and oedema
49
How does hypoalbuminaemia lead to oedema in nephrotic syndrome?
↓ Plasma oncotic pressure → hypovolaemia → RAAS activation → sodium and water retention → oedema
50
Why does hyperlipidaemia occur in nephrotic syndrome?
↑ Hepatic lipoprotein synthesis (compensation) and ↓ catabolism of circulating lipids