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Pulmonology Case Study 22 — Patient Yu., 72 years old

Question 1: Leading Syndromes (with symptom explanation)

This patient presents with three leading syndromes that together point to a combined pulmonary and metabolic pathology:

A. Syndrome of Focal (Lobar) Pulmonary Consolidation (right lower lobe pneumonia)

Symptom/Sign	Pathophysiological explanation
Shortness of breath at rest, RR 26/min, shallow	Alveolar consolidation reduces functional lung surface area → hypoxemia → compensatory tachypnea
Right hemithorax lagging behind in breathing	Splinting of the affected side due to pleuritic irritation/inflammatory exudate
Dull percussive sound (right, below scapular angle, intercostals 8–9)	Air replaced by inflammatory exudate → increased tissue density → dullness on percussion
Weakened vesicular breathing in that zone	Consolidation attenuates transmission of air-entry sounds
Moist, finely bubbly rales (crepitations) in same zone	Reinflation of exudate-filled alveoli during inspiration produces fine crackles
T° 37.4°C (low-grade fever)	Cytokine release (IL-1, IL-6, TNF-α) from inflammatory focus — note: blunted febrile response in diabetics and the elderly

B. Syndrome of Pulmonary Emphysema / COPD (background)

Symptom/Sign	Explanation
Barrel-shaped chest	Chronic air trapping → increased antero-posterior diameter
Boxy (tympanic) sound on upper-zone percussion	Hyperinflated alveoli → increased resonance
Single dry rales in upper zones	Partial bronchial obstruction with secretions in chronically narrowed airways
Chronic dry cough	Excessive mucus, airway remodelling

C. Diabetic Ketoacidosis (DKA) / Decompensated Diabetes Mellitus Type 2

Symptom/Sign	Explanation
Acetone smell from mouth	Beta-oxidation excess → ketone body (acetoacetate → acetone) production
Polydipsia (3 L/day), polyuria	Hyperglycaemia → osmotic diuresis; thirst from hyperosmolarity
General weakness, sleepy face expression	Cellular energy deficit (glucose cannot enter cells without insulin); metabolic acidosis depresses CNS
Dry skin	Dehydration from osmotic diuresis
Acrocyanosis	Poor peripheral perfusion; low cardiac output
Tachycardia 104/min, BP 110/60 mmHg	Dehydration → reduced preload → compensatory tachycardia; muted heart tones suggest pericardial/metabolic effect
Condition worsened 3 days after hypothermia	Cold exposure → stress response → counter-regulatory hormones (cortisol, catecholamines) → insulin resistance → ketogenesis

Question 2: Differential Diagnosis of the Leading (Pulmonary) Syndrome

The leading pulmonary syndrome is right-sided focal consolidation with dullness, weakened vesicular breathing, and moist rales. The differential includes:

Condition	Arguments FOR	Arguments AGAINST
Community-acquired pneumonia (CAP) ✅ Most likely	Acute onset (3 days), right lower lobe dullness + moist crackles + lagging hemithorax, fever, tachycardia, history of diabetes (immunocompromised), worsening after cold exposure	—
Pulmonary tuberculosis	Elderly patient, could deny contact; upper-lobe involvement is classic	Denies TB contact; acute course; predominantly lower lobe; upper zones show emphysematous (boxy) sound — not infiltrate
Pleural exudative effusion	Dullness + absent/weakened breath sounds	Moist rales are present (effusion typically eliminates breath sounds entirely); no mediastinal shift described
Lung cancer with post-obstructive pneumonia	Age 72, chronic cough	No hemoptysis; acute onset after cold; no weight loss mentioned
Pulmonary embolism with infarction	Tachycardia, dyspnea, acrocyanosis	No pleuritic chest pain, no hemoptysis; moist rales rather than a pleural rub; fever + crackles favor infection

Conclusion: Community-acquired pneumonia (right lower lobe) is the most justified diagnosis.

Question 3: Preliminary Diagnosis (with justification)

Main diagnosis:

Right-sided lower-lobe community-acquired pneumonia, moderate severity

Complication:

Acute respiratory failure

Background disease:

Type 2 Diabetes Mellitus, decompensated (diabetic ketoacidosis / hyperglycaemic state), on bucarban (glibenclamide) 2 tablets/day

Co-existing:

COPD / Pulmonary emphysema (chronic obstructive background)

Justification:

Pneumonia: Acute onset after hypothermia; right lower lobe dullness to percussion (intercostals 8–9, scapular–posterior axillary lines); weakened vesicular breathing; mass of moist finely bubbly rales; hemithorax lag; tachypnea (RR 26), tachycardia (HR 104), fever 37.4°C
DKA/decompensation: Acetone breath, polydipsia (3 L/day), polyuria, dry skin, weakness, BP 110/60, HR 104 — in the setting of known Type 2 DM on oral hypoglycaemics; infection is the classic precipitant of DKA
COPD/emphysema: Barrel chest, boxy percussion in upper zones, single dry rales — consistent with long-standing obstructive lung disease, likely a smoker (not stated but implied by emphysematous signs)

Question 4: Examination Plan with Expected Results

Laboratory Tests

Test	Expected Result / Rationale
CBC	Leukocytosis (WBC >10×10⁹/L), left shift (band neutrophilia), elevated ESR — infection
Blood glucose (fasting & random)	Markedly elevated (>13.9 mmol/L in DKA or hyperglycaemic crisis)
Blood ketones / urinalysis (ketones, glucose)	Ketonuria +++, glucosuria; confirms DKA
Blood gas (ABG)	Metabolic acidosis: pH <7.35, low HCO₃⁻ (<18 mmol/L), low PaO₂, low PaCO₂ (compensatory hyperventilation) — BUT shallow breathing limits compensation
Serum electrolytes (Na⁺, K⁺, Cl⁻)	Total body K⁺ depleted (even if serum K⁺ initially normal/high); hyponatraemia possible
Urea, creatinine	Elevated (pre-renal azotaemia from dehydration)
C-reactive protein (CRP) / Procalcitonin	Markedly elevated — bacterial infection marker
HbA1c	>9–10% — chronic poor glycaemic control
Sputum culture & sensitivity	Likely S. pneumoniae, H. influenzae (most common CAP organisms in elderly diabetics)
Blood cultures × 2	May yield bacteraemia — important given moderate-severe CAP
Liver function tests	Baseline before antibiotics; hepatotoxicity risk with some agents

Instrumental Tests

Test	Expected Result
Chest X-ray (PA + lateral)	Homogeneous opacity/infiltrate in right lower lobe (S9–10); possible small parapneumonic effusion; emphysematous changes in upper zones (flattened diaphragm, hyperinflation)
Chest CT (if X-ray ambiguous)	Better characterises consolidation, rules out abscess, empyema, neoplasm
Spirometry / Peak flow	Low FEV₁/FVC (<0.7) confirming obstructive pattern — COPD (perform after acute illness resolves)
ECG	Sinus tachycardia; may show metabolic changes from electrolyte imbalance (flat/inverted T-waves, U-waves if hypokalemia)
Pulse oximetry	SpO₂ likely <94% on room air
Echocardiography	If heart failure or pericarditis suspected (muted heart tones); may show diastolic dysfunction common in diabetics

Question 5: Treatment Plan

Regime

Hospital admission (moderate-severe CAP + decompensated DM = mandatory inpatient)
Semi-Fowler's position (headboard raised — already the patient's forced position; reduces work of breathing)
Bed rest until fever resolves, then gradually mobilise
Oxygen therapy: nasal cannula or mask, target SpO₂ 92–96% (careful in COPD: avoid hypercapnic suppression of hypoxic drive — target lower end 88–92% if severe COPD)

Diet

High-protein, low-carbohydrate diet (given DM decompensation)
Adequate caloric intake (avoid starvation which worsens ketosis)
Fluid: oral rehydration when possible; IV if vomiting

Medications

1. Antibiotic Therapy (for moderate CAP, inpatient, with comorbidities)

Per IDSA-ATS guidelines (Fishman's Pulmonary Diseases, Table 128-6):

Drug	Dose & Route
Ampicillin/sulbactam OR Ceftriaxone (β-lactam)	Ceftriaxone 1–2 g IV once daily
PLUS Azithromycin (macrolide)	500 mg IV/PO once daily × 5 days
Alternative: Respiratory fluoroquinolone monotherapy	Levofloxacin 750 mg IV/PO once daily (also covers atypicals)

Note: In a 72-year-old diabetic patient, a respiratory fluoroquinolone (levofloxacin) is an excellent single-agent option covering S. pneumoniae, H. influenzae, and atypicals — but use with caution (blood glucose monitoring, as fluoroquinolones can cause dysglycaemia).

2. Diabetes Management (switch from oral agent to insulin — mandatory in acute illness/DKA)

Drug	Dose
Short-acting insulin (actrapid / regular insulin)	0.1 U/kg/h IV infusion (DKA protocol); OR subcutaneous regimen: 4–6 U before each meal (titrate to blood glucose)
Isotonic saline (0.9% NaCl)	1 L over first hour IV, then 250–500 mL/h — rehydration
Potassium chloride	Add to IV fluids once serum K⁺ <5.5 mmol/L (typically 20–40 mEq/L of IV fluid)

Bucarban (glibenclamide/glyburide) should be held during acute illness — sulfonylureas are not safe during DKA, severe infection, or significant caloric restriction.

3. Bronchodilator Therapy (for COPD/obstructive component)

Drug	Dose
Salbutamol (albuterol) inhaler via spacer or nebuliser	2.5 mg nebulised q4–6h PRN
Ipratropium bromide (anticholinergic)	0.5 mg nebulised q6–8h

4. Mucolytics / Expectorants

Drug	Dose
Ambroxol (Ambrobene)	30 mg PO/IV TID

5. Antipyretics / Analgesics (if T° >38.5°C or discomfort)

Drug	Dose
Paracetamol (Acetaminophen)	500–1000 mg PO/IV q6h PRN

6. Thromboprophylaxis (inpatient, elderly, diabetic, immobile)

Drug	Dose
Enoxaparin (LMWH)	40 mg SC once daily

7. Proton Pump Inhibitor (gastric protection — stress ulcer prophylaxis)

Drug	Dose
Omeprazole	20 mg PO/IV once daily

Monitoring

Blood glucose every 1–2 hours during IV insulin infusion
Electrolytes (K⁺, Na⁺) every 4–6 hours initially
SpO₂ continuous
Repeat chest X-ray at 48–72 hours if not improving
Follow-up spirometry after discharge (COPD assessment)

Summary of Preliminary Diagnosis:

Right-sided community-acquired lower-lobe pneumonia (moderate) + Decompensated Type 2 Diabetes Mellitus (DKA-precipitating infection) against a background of pulmonary emphysema/COPD.

Sources: Fishman's Pulmonary Diseases and Disorders (IDSA-ATS CAP Table 128-6); Goldman-Cecil Medicine; Harrison's Principles of Internal Medicine 22E; Washington Manual of Medical Therapeutics.

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Test 2 — V.1 — Full Answers

1. COPD is a disease primarily characterized by:

B) Irreversible airflow limitation

COPD is defined by persistent, not fully reversible airflow obstruction, confirmed by post-bronchodilator FEV1/FVC < 0.7. (Miller's Anesthesia; Fishman's Pulmonary Diseases)

2. How are spirometry results evaluated?

B) By predicted (reference) values

Spirometry results are interpreted by comparing the patient's measured values against predicted normal values based on age, sex, height, and ethnicity.

3. How many subtypes of muscarinic receptors are known in human bronchi?

B) 3

Three muscarinic receptor subtypes (M1, M2, M3) are present in the airways. M3 receptors on smooth muscle mediate bronchoconstriction; M2 receptors (prejunctional) act as autoreceptors limiting acetylcholine release.

4. In bronchial asthma, spirometry parameters:

B) Are never abnormal — ❌ This is wrong. Correct answer: C) Are sometimes normal (between attacks)

Between attacks, spirometry can be completely normal. During an attack, obstructive pattern is seen (reduced FEV1, reduced FEV1/FVC). In severe persistent asthma there may be persistent abnormalities.

5. A wheezing expiration is typically heard?

B) Bronchial asthma (also COPD)

Wheezing (expiratory) = hallmark of diffuse bronchospasm/airway narrowing, classic in asthma and COPD exacerbations.

6. Into which category are pneumonias NOT classified etiopathogenetically?

D) Lobar pneumonia

Etiopathogenetic classification divides pneumonia by causative agent (bacterial, viral, fungal, atypical) or by acquisition setting (community-acquired, hospital-acquired, aspiration). "Lobar" is an anatomical/morphological classification, not etiopathogenetic.

7. Pneumonia in severely immunocompromised patients:

D) Atypical (Pneumocystis jirovecii, CMV, fungi)

Severely immunocompromised patients (HIV, transplant, chemotherapy) are predisposed to atypical and opportunistic organisms such as Pneumocystis jirovecii, CMV, Mycobacterium avium, fungi — not classified as typical community-acquired organisms. (Harrison's; Goldman-Cecil Medicine)

8. Lung tissue destruction most commonly develops in pneumonia caused by:

B) Staphylococcus (and Klebsiella)

Staphylococcus aureus is notorious for necrotizing pneumonia with abscess/cavity formation. Klebsiella pneumoniae also causes destructive lobar pneumonia ("currant jelly sputum"). Streptococcus pneumoniae (lobar pneumonia) is less commonly destructive.

9. What auscultatory finding is typical during a bronchial asthma attack?

A) Dry wheezing rales

During an acute asthma attack, diffuse high-pitched (sibilant) and low-pitched (sonorous) dry rales/wheezes are heard bilaterally on expiration — due to diffuse bronchospasm.

10. What causes pain on breathing in lobar (croupous) pneumonia?

D) Pleural friction rub (source of the pain) — but the question asks what CAUSES the pain

Answer: B) Pleural friction rub — In lobar (croupous) pneumonia, the inflammation extends to the visceral pleura → fibrinous pleuritis → the two pleural layers rub against each other during breathing → pleural friction rub and pleuritic chest pain (stabbing, worse on inspiration).

(The correct answer choice that causes the pain is pleural inflammation/pleuritis, evidenced by a pleural friction rub on auscultation.)

11. What FEV1 value is characteristic of severe persistent bronchial asthma?

C) More than 40% but more than 60% — the wording is garbled in the image.

Correct answer: Less than 60% predicted (i.e., between 40–60%)

Per GINA classification:

Mild persistent: FEV1 ≥80% predicted
Moderate persistent: FEV1 60–80% predicted
Severe persistent: FEV1 <60% predicted (some sources use <60%, others <40% for very severe)

The answer that fits "severe persistent" is FEV1 less than 60% (or <60% but >40% for severe, and <40% for very severe).

12. What is the main complaint of patients with bronchial asthma?

A) Attacks of suffocation (paroxysmal dyspnea/wheezing attacks)

The cardinal symptom of bronchial asthma is episodic attacks of breathlessness/suffocation (dyspnea), often with audible wheezing, typically reversible spontaneously or with bronchodilators.

13. What is the main patient complaint in bronchial asthma?

(Same as Q12 — repeated) A) Attacks of suffocation / paroxysmal dyspnea

14. What is the maximum permissible daily dose of prednisolone when relieving status asthmaticus?

A) 720 mg — this is very high (emergency/ICU doses) B) 1000 mg and more C) 360 mg D) 720 mg

Correct answer: B) 1000 mg and more is used in status asthmaticus (life-threatening).

In status asthmaticus (severe refractory bronchospasm), IV methylprednisolone 60–125 mg q6h is standard, which can reach 500–1000 mg/day. Maximum doses up to 1000 mg/day (or more in critical cases) of prednisolone equivalent are permissible in status asthmaticus.

15. Which of the following has no significance in the pathogenesis of bronchial asthma attack?

A) Immediate-type allergic reactions — these DO matter (IgE-mediated) B) Activation of adrenergic receptors — this has NO significance (it is actually inhibition/reduced β₂-adrenergic response, not activation, that contributes) C) Physical exertion — a known trigger D) Chemical irritants — known triggers

Correct answer: B) Activation of adrenergic receptors

Adrenergic (β₂) receptor stimulation is protective/bronchodilatory — it is NOT a pathogenic mechanism. It is the decreased β₂-adrenergic sensitivity, increased cholinergic tone, and mast cell/IgE activation that drive the asthmatic attack.

16. Which of the following are mechanisms of bronchial tree obstruction?

A) Outlet of the bronchial mucosa ❌ (not standard) B) Decrease of bronchial glands C) Drug intake D) Chemical irritants

The classic mechanisms of bronchial obstruction in asthma are:

Bronchospasm (smooth muscle contraction)
Mucosal edema (inflammation)
Hypersecretion of mucus (mucus plugging)

From the listed options, A) Outlet (swelling/edema) of the bronchial mucosa, B) (increased) bronchial gland secretion, and D) Chemical irritants (trigger bronchospasm) are mechanisms. The most correct answer pairing the question is A + B + D — edema of mucosa, excessive secretion of bronchial glands, and bronchospasm from irritants.

17. Which of the following are mucolytic agents?

A) Acetylcysteine ✅ B) Berotec ❌ (fenoterol — β₂-agonist bronchodilator) C) Tetracycline ❌ (antibiotic)

Correct answer: A) Acetylcysteine is a mucolytic (breaks disulfide bonds in mucus glycoproteins). Berotec and tetracycline are NOT mucolytics.

18. Which of the following are mucolytic agents?

(Overlaps with Q17) C) Acetylcysteine ✅

Also mucolytics include: Ambroxol, Bromhexine, Carbocisteine. Prednisolone = corticosteroid; Salbutamol = bronchodilator; Tetracycline = antibiotic — none are mucolytics.

19. Which of the following are NOT bronchodilators?

D) Prednisolone

Bronchodilators include: β₂-agonists (salbutamol/berotec), anticholinergics (ipratropium), xanthines (theophylline/aminophylline).

Salbutamol ✅ bronchodilator
Xanthines ✅ bronchodilator
Cholinomimetics (e.g. acetylcholine) ❌ — cause bronchoconstriction, NOT bronchodilation
Prednisolone — corticosteroid (anti-inflammatory, not a primary bronchodilator)
Anticholinergics ✅ bronchodilator

Correct answer: B) Cholinomimetics (they cause bronchoconstriction, the opposite effect) and D) Prednisolone is not a bronchodilator per se.

20. Which of the following belongs to primary changes in bronchial asthma?

A) Weather dependence — a trigger, not a primary structural change B) Reaction to viral infection — a trigger C) Reaction to house dust — allergenic trigger ✅ (IgE-mediated) D) Reaction to cold air — a trigger

Correct answer: C) Reaction to house dust (Dermatophagoides mite allergen) represents a primary/core allergic (IgE-mediated) mechanism underlying atopic asthma — it is the most fundamental sensitizing trigger in the pathogenesis of allergic bronchial asthma, not merely an exogenous environmental modulator.

(Weather dependence, viral infection, and cold air are non-specific triggers or exacerbating factors rather than primary pathogenetic mechanisms.)

Quick Reference Summary Table

Q	Answer
1	B — Irreversible airflow limitation
2	B — Predicted (reference) values
3	B — 3 subtypes (M1, M2, M3)
4	C — Sometimes normal (between attacks)
5	B — Bronchial asthma
6	D — Lobar (morphological, not etiopathogenetic)
7	D — Atypical (opportunistic in immunocompromised)
8	B — Staphylococcus (necrotizing)
9	A — Dry wheezing rales
10	B — Pleural friction rub (fibrinous pleuritis)
11	FEV1 <60% predicted (severe persistent)
12	A — Attacks of suffocation
13	A — Attacks of suffocation
14	B — 1000 mg and more (status asthmaticus)
15	B — Activation of adrenergic receptors
16	A+B — Mucosal edema + excess mucus secretion
17	A — Acetylcysteine
18	C — Acetylcysteine
19	B — Cholinomimetics (cause bronchoconstriction)
20	C — Reaction to house dust

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