MCQs on the Pathophysiology of Asthma, Chronic Obstructive Pulmonary Disease (COPD), and Tuberculosis

For GPAT, NIPER, AIIMS Pharmacist, Railway Pharmacist, SSC, ESIC, and State Pharmacist Examinations.

Short Notes (Easy to Remember)

1. Bronchial Asthma

Asthma is a chronic inflammatory disease of the airways characterized by reversible airway obstruction, bronchial hyperresponsiveness, and mucus hypersecretion.

Easy Memory Trick

Asthma = "3 B's"

• Bronchospasm

• Bronchial inflammation

• Blocked airway by mucus

Pathophysiology (Flow Chart)

Allergen/Irritant → IgE production → Mast cell activation → Release of histamine, leukotrienes & prostaglandins → Bronchoconstriction + Mucosal edema + Mucus secretion → Airway narrowing → Wheezing, cough & dyspnea

Early Phase Mediators

• Histamine

• Leukotrienes (LTC₄, LTD₄, LTE₄)

• Prostaglandin D₂

Exam Point
Leukotrienes are the most potent bronchoconstrictors.

Late Phase Response

Occurs 4–8 hours after allergen exposure.

Characterized by:

• Eosinophil infiltration

• Airway edema

• Tissue damage

• Airway remodeling

Airway Remodeling Includes

• Thickened basement membrane

• Goblet cell hyperplasia

• Smooth muscle hypertrophy

• Increased mucus glands

Important Cells

• Mast cells

• Eosinophils

• Th2 lymphocytes

• Macrophages

High-Yield Facts

• Airflow obstruction is reversible.

• Eosinophilia is common.

• IgE mediates allergic asthma.

• Histamine causes immediate bronchoconstriction.

• Leukotrienes produce prolonged bronchospasm.

• Status asthmaticus is a medical emergency.

2. Chronic Obstructive Pulmonary Disease (COPD)

COPD is a progressive, irreversible airflow limitation caused mainly by chronic bronchitis and emphysema.

Easy Memory Trick

COPD = "2 Diseases = CB + E"

• Chronic Bronchitis

• Emphysema

Chronic Bronchitis

Productive cough for ≥3 months/year for 2 consecutive years.

Pathophysiology

Smoking → Chronic irritation → Mucus gland enlargement → Goblet cell hyperplasia → Excess mucus production → Airway obstruction

Features

• Productive cough

• Cyanosis

• Hypercapnia

• Hypoxemia

Remember

Blue Bloater = Chronic Bronchitis

Emphysema

Permanent enlargement of air spaces distal to terminal bronchioles with destruction of alveolar walls.

Pathophysiology

Smoking → Neutrophil activation → Elastase release → Alveolar wall destruction → Loss of elastic recoil → Air trapping

Features

• Dyspnea

• Barrel chest

• Weight loss

• Minimal cough

Remember

Pink Puffer = Emphysema

Protease-Antiprotease Theory

Smoking → ↑ Proteases → ↓ Alpha-1 Antitrypsin Activity → Alveolar Destruction

Alpha-1 Antitrypsin Deficiency

Causes panacinar emphysema, especially in the lower lobes.

COPD Facts

• Airflow limitation is irreversible.

• Smoking is the most important risk factor.

• Chronic bronchitis → mucus hypersecretion.

• Emphysema → alveolar destruction.

• Hyperinflated lungs produce a barrel-shaped chest.

Differences Between Asthma and COPD

• Feature Asthma COPD

• Airflow obstruction Reversible Irreversible

• Age Young Older adults

• Cause Allergy Smoking

• Main inflammatory cell Eosinophils Neutrophils

• IgE Increased Usually normal

• Bronchodilator response Good Partial

• Airway remodeling Present Present (different pattern)

3. Tuberculosis (TB)

Tuberculosis is a chronic granulomatous infectious disease caused by Mycobacterium tuberculosis.

Easy Memory Trick

TB = "3 G's"

• Granuloma

• Giant cells

• Ghon focus

Pathophysiology

Inhalation of bacilli → Alveolar macrophages engulf bacilli → Bacteria survive inside macrophages → T-cell activation → Cytokine release → Granuloma formation → Caseous necrosis

Granuloma Contains

• Epithelioid cells

• Langhans giant cells

• Lymphocytes

• Fibroblasts

Caseous Necrosis

Classic pathological feature of tuberculosis.

Primary TB

• Ghon focus

• Hilar lymph node involvement

• Ghon complex

Secondary TB

Occurs due to reactivation.

Usually affects:

• Upper lobe (apex)

• Causes cavitation

Immune Response

Type IV (Delayed) hypersensitivity

Important cytokines:

• IFN-γ

• TNF-α

• IL-12

Important Cells

• Macrophages

• CD4⁺ T cells

• Giant cells

Facts

• Acid-fast bacillus

• Aerobic organism

• Slow-growing bacterium

• Intracellular pathogen

• Granuloma formation is protective.

• Cavitary lesions occur in secondary TB.

One-Liners for Competitive Examinations

Asthma

• Asthma is a reversible obstructive airway disease.

• IgE mediates allergic asthma.

• Eosinophils are the predominant inflammatory cells.

• Leukotrienes are the strongest bronchoconstrictors.

• Histamine mediates the early asthmatic response.

• Airway remodeling occurs in chronic asthma.

COPD

• Smoking is the leading cause of COPD.

• COPD causes irreversible airflow limitation.

• Chronic bronchitis causes mucus hypersecretion.

• Emphysema destroys alveolar walls.

• Alpha-1 antitrypsin deficiency causes panacinar emphysema.

• Chronic bronchitis = Blue bloater.

• Emphysema = Pink puffer.

Tuberculosis

• Mycobacterium tuberculosis is an acid-fast bacillus.

• Tuberculosis produces caseating granulomas.

• Langhans giant cells are characteristic of TB granulomas.

• Primary TB forms the Ghon complex.

• Secondary TB commonly affects the lung apex.

• Immunity against TB is mediated by Type IV delayed hypersensitivity.

• IFN-γ is the key cytokine for macrophage activation.

• TNF-α is essential for maintaining granuloma integrity.

Previous-Year Exams

Asthma

• Reversible airway obstruction

• IgE-mediated hypersensitivity

• Eosinophils and leukotrienes are frequently tested

• Airway remodeling in chronic disease

COPD

• Smoking as the primary cause

• Difference between chronic bronchitis and emphysema

• Alpha-1 antitrypsin deficiency

• Blue bloater vs. Pink puffer

Tuberculosis

• Caseous necrosis

• Ghon focus and Ghon complex

• Langhans giant cells

• Type IV hypersensitivity

• IFN-γ and TNF-α in granuloma formation

• Secondary TB involving the apical lung regions

MCQs

1. Asthma is primarily characterized by:

A. Permanent airflow obstruction
B. Reversible airway obstruction
C. Destruction of alveolar walls
D. Fibrosis of lung tissue

Answer: B. Reversible airway obstruction

Explanation: Asthma is a chronic inflammatory disease of the airways characterized by reversible bronchoconstriction, airway inflammation, and hyperresponsiveness.

2. Which immune cells play the most important role in allergic asthma?

A. Neutrophils
B. Basophils
C. Eosinophils
D. Platelets

Answer: C. Eosinophils

Explanation: Eosinophils release inflammatory mediators such as leukotrienes and major basic protein, causing airway damage and bronchoconstriction.

3. IgE-mediated asthma is classified as:

A. Type I hypersensitivity
B. Type II hypersensitivity
C. Type III hypersensitivity
D. Type IV hypersensitivity

Answer: A. Type I hypersensitivity

Explanation: Allergic asthma is mediated by IgE antibodies bound to mast cells, leading to immediate hypersensitivity reactions.

4. Which chemical mediator is mainly responsible for immediate bronchoconstriction in asthma?

A. Histamine
B. Dopamine
C. Serotonin
D. Bradykinin

Answer: A. Histamine

Explanation: Histamine released from mast cells rapidly causes bronchoconstriction, increased mucus secretion, and vasodilation.

5. Airway hyperresponsiveness in asthma is mainly due to:

A. Destruction of alveoli
B. Chronic airway inflammation
C. Pulmonary edema
D. Pleural fibrosis

Answer: B. Chronic airway inflammation

Explanation: Persistent inflammation sensitizes airway smooth muscles, making them excessively responsive to various stimuli.

6. Which cytokine is primarily responsible for eosinophil activation in asthma?

A. IL-1
B. IL-2
C. IL-5
D. IL-10

Answer: C. IL-5

Explanation: IL-5 promotes eosinophil maturation, recruitment, and survival in allergic asthma.

7. Airway remodeling in chronic asthma includes:

A. Thickening of the basement membrane
B. Alveolar destruction
C. Pleural fibrosis
D. Pulmonary embolism

Answer: A. Thickening of the basement membrane

Explanation: Chronic inflammation causes smooth muscle hypertrophy, basement membrane thickening, and goblet cell hyperplasia.

8. Which cells release histamine during an asthmatic attack?

A. Macrophages
B. Mast cells
C. Neutrophils
D. Fibroblasts

Answer: B. Mast cells

Explanation: Cross-linking of IgE on mast cells triggers histamine release.

9. A hallmark feature of bronchial asthma is:

A. Irreversible airway obstruction
B. Airway hyperresponsiveness
C. Pulmonary fibrosis
D. Alveolar hemorrhage

Answer: B. Airway hyperresponsiveness

Explanation: Hyperresponsive airways constrict excessively in response to allergens, cold air, or exercise.

10. Which mediator causes prolonged bronchoconstriction in asthma?

A. Leukotrienes
B. Dopamine
C. Acetylcholine
D. Nitric oxide

Answer: A. Leukotrienes

Explanation: Leukotrienes are potent bronchoconstrictors and contribute to mucus secretion and edema.

Chronic Obstructive Pulmonary Disease (COPD)

11. COPD is mainly caused by

A. Viral infection
B. Cigarette smoking
C. Fungal infection
D. Genetic mutation alone

Answer: B. Cigarette smoking

Explanation: Smoking causes chronic inflammation, oxidative stress, and irreversible airflow limitation.

12. COPD airflow limitation is

A. Completely reversible
B. Irreversible or partially reversible
C. Temporary
D. Due to pulmonary embolism

Answer: B. Irreversible or partially reversible

Explanation: Structural damage to the airways and alveoli causes persistent airflow obstruction.

13. Which enzyme contributes to alveolar destruction in emphysema?

A. Elastase
B. Amylase
C. Pepsin
D. Lipase

Answer: A. Elastase

Explanation: Neutrophil elastase destroys elastic fibers in alveolar walls, producing emphysema.

14. Alpha-1 antitrypsin deficiency predisposes to

A. Asthma
B. Emphysema
C. Tuberculosis
D. Pneumonia

Answer: B. Emphysema

Explanation: Alpha-1 antitrypsin inhibits elastase. Its deficiency allows excessive destruction of alveolar tissue.

15. Chronic bronchitis is clinically defined as a productive cough lasting:

A. 1 month/year for 2 years
B. 2 months/year for 1 year
C. 3 months/year for 2 consecutive years
D. 6 months/year

Answer: C. 3 months/year for 2 consecutive years

Explanation: This is the standard diagnostic definition.

16. The predominant inflammatory cells in COPD are

A. Eosinophils
B. Neutrophils and macrophages
C. Mast cells
D. Basophils

Answer: B. Neutrophils and macrophages

Explanation: COPD inflammation is primarily neutrophilic, unlike asthma.

17. Emphysema primarily involves destruction of

A. Bronchi
B. Alveolar walls
C. Pleura
D. Trachea

Answer: B. Alveolar walls

Explanation: Destruction of alveolar septa reduces gas exchange surface area.

18. The major cause of airflow obstruction in chronic bronchitis is

A. Pulmonary edema
B. Excess mucus production
C. Pleural effusion
D. Alveolar hemorrhage

Answer: B. Excess mucus production

Explanation: Goblet cell hyperplasia and mucus gland enlargement obstruct airways.

19. "Blue bloater" is commonly associated with

A. Asthma
B. Chronic bronchitis
C. Emphysema
D. Pulmonary fibrosis

Answer: B. Chronic bronchitis

Explanation: Patients develop cyanosis due to chronic hypoxemia.

20. "Pink puffer" refers to patients with

A. Tuberculosis
B. Emphysema
C. Bronchitis
D. Pneumonia

Answer: B. Emphysema

Explanation: Patients maintain oxygenation by hyperventilation and appear thin with pursed-lip breathing.

Tuberculosis (TB)

21. Tuberculosis is caused by

A. Streptococcus pneumoniae
B. Mycobacterium tuberculosis
C. Haemophilus influenzae
D. Staphylococcus aureus

Answer: B. Mycobacterium tuberculosis

Explanation: TB is caused by the acid-fast bacillus Mycobacterium tuberculosis.

22. Transmission of tuberculosis occurs mainly through

A. Contaminated food
B. Blood transfusion
C. Airborne droplets
D. Mosquito bites

Answer: C. Airborne droplets

Explanation: TB spreads by inhalation of droplet nuclei expelled during coughing or sneezing.

23. Which immune cells engulf Mycobacterium tuberculosis after infection?

A. Neutrophils
B. Macrophages
C. Eosinophils
D. Platelets

Answer: B. Macrophages

Explanation: Macrophages phagocytose the bacilli, but the organism can survive intracellularly.

24. Granuloma formation in tuberculosis is mainly mediated by

A. B lymphocytes
B. T lymphocytes
C. Platelets
D. RBCs

Answer: B. T lymphocytes

Explanation: Cell-mediated immunity activates macrophages and forms granulomas to contain infection.

25. Caseous necrosis is a characteristic feature of

A. Asthma
B. COPD
C. Tuberculosis
D. Bronchiectasis

Answer: C. Tuberculosis

Explanation: Caseous necrosis appears as soft, cheese-like necrotic tissue within granulomas.

26. Which hypersensitivity reaction is involved in TB pathology?

A. Type I
B. Type II
C. Type III
D. Type IV

Answer: D. Type IV

Explanation: Delayed-type (cell-mediated) hypersensitivity causes tissue damage and granuloma formation.

27. Which cytokine activates macrophages in tuberculosis?

A. IL-4
B. IL-10
C. Interferon-γ
D. IL-5

Answer: C. Interferon-γ

Explanation: IFN-γ released by Th1 cells activates macrophages to kill intracellular mycobacteria.

28. The primary lesion of tuberculosis is known as

A. Aschoff body
B. Ghon focus
C. Mallory body
D. Councilmanic body

Answer: B. Ghon focus

Explanation: A Ghon focus is the initial subpleural lesion formed during primary pulmonary TB.

29. Which component of the immune system is most important in controlling tuberculosis?

A. Humoral immunity
B. Cell-mediated immunity
C. Complement system
D. Platelet activation

Answer: B. Cell-mediated immunity

Explanation: Th1 lymphocytes and activated macrophages are essential for controlling TB infection.

30. Which of the following best explains latent tuberculosis?

A. Complete elimination of bacteria
B. Active bacterial multiplication
C. Dormant bacteria contained within granulomas
D. Infection limited to the blood

Answer: C. Dormant bacteria contained within granulomas

Explanation: In latent TB, viable bacilli persist within granulomas without causing active disease but may reactivate when immunity declines.

31. Which of the following best explains why asthma is considered a reversible obstructive lung disease?

A. Airway fibrosis completely resolves after treatment.
B. Bronchial smooth muscle contraction and inflammation can be reversed, restoring airflow.
C. Alveolar destruction regenerates after bronchodilator therapy.
D. Pulmonary fibrosis decreases airway resistance.

Answer: B

Explanation: The hallmark of asthma is reversible bronchoconstriction due to smooth muscle contraction and inflammation. Structural airway remodeling in chronic asthma may become partially irreversible.

32. A patient with allergic asthma is exposed to pollen. Which event occurs first?

A. Eosinophil infiltration
B. Goblet cell hyperplasia
C. Cross-linking of IgE molecules on mast cells
D. Airway remodeling

Answer: C

Explanation: The immediate phase begins with allergen-induced cross-linking of IgE on mast cells, triggering degranulation.

33. Which finding is most likely to be present in COPD but not in asthma?

A. Bronchoconstriction
B. Airway inflammation
C. Permanent destruction of alveolar septa
D. Mucus hypersecretion

Answer: C

Explanation: Permanent destruction of alveolar walls (emphysema) is characteristic of COPD, not asthma.

34. Which mediator contributes most to the late-phase asthmatic response?

A. Histamine
B. Leukotrienes
C. Dopamine
D. Serotonin

Answer: B

Explanation: Leukotrienes are potent mediators responsible for prolonged bronchoconstriction, edema, and eosinophil recruitment.

35. Why are eosinophils considered more damaging than mast cells during chronic asthma?

A. They produce IgE.
B. They release cytotoxic proteins that injure airway epithelium.
C. They produce surfactant.
D. They destroy alveolar macrophages.

Answer: B

Explanation: Major basic protein and eosinophil cationic protein damage airway epithelium, promoting airway hyperresponsiveness.

36. A smoker develops emphysema despite normal pulmonary blood flow. Which pathological event primarily causes reduced gas exchange?

A. Bronchial smooth muscle hypertrophy
B. Alveolar wall destruction
C. Increased mucus secretion
D. Bronchial edema

Answer: B

Explanation: Loss of alveolar septa decreases the surface area available for oxygen diffusion.

37. Which statement best distinguishes emphysema from chronic bronchitis?

A. Emphysema mainly affects the bronchi.
B. Chronic bronchitis primarily destroys alveoli.
C. Emphysema primarily damages alveoli, whereas chronic bronchitis mainly affects conducting airways.
D. Both diseases exclusively involve bronchioles.

Answer: C

Explanation: Emphysema destroys alveoli, while chronic bronchitis involves mucus gland enlargement and airway inflammation.

38. Which mechanism explains airflow limitation in emphysema?

A. Increased surfactant production
B. Loss of elastic recoil causing airway collapse during expiration
C. Bronchospasm due to histamine
D. Pleural fibrosis

Answer: B

Explanation: Destruction of elastic tissue causes small airways to collapse during expiration.

39. Which patient is most likely to develop emphysema at an early age despite never smoking?

A. Patient with chronic asthma
B. Patient with Alpha-1 antitrypsin deficiency
C. Patient with allergic rhinitis
D. Patient with pulmonary edema

Answer: B

Explanation: Alpha-1 antitrypsin normally inhibits elastase. Deficiency causes unchecked alveolar destruction.

40. Which pathological process is common to both asthma and COPD?

A. Caseous necrosis
B. Chronic airway inflammation
C. Granuloma formation
D. Alveolar calcification

Answer: B

Explanation: Both diseases involve airway inflammation, although the predominant inflammatory cells differ.

41. Which event allows Mycobacterium tuberculosis to survive inside macrophages?

A. Production of IgE
B. Prevention of phagosome-lysosome fusion
C. Activation of complement
D. Destruction of neutrophils

Answer: B

Explanation: M. tuberculosis inhibits phagosome-lysosome fusion, enabling intracellular survival.

42. Why does granuloma formation benefit the host?

A. It destroys antibodies.
B. It localizes infection and prevents bacterial spread.
C. It enhances bacterial multiplication.
D. It promotes neutrophil apoptosis.

Answer: B

Explanation: Granulomas wall off the bacilli and limit dissemination.

43. Reactivation of tuberculosis most commonly occurs because

A. The bacteria mutate into a virulent form.
B. Cell-mediated immunity becomes weakened.
C. Humoral immunity increases.
D. IgE production decreases.

Answer: B

Explanation: Decline in T-cell-mediated immunity permits dormant bacilli to reactivate.

44. Which feature distinguishes tuberculosis from bacterial pneumonia?

A. Presence of neutrophils
B. Granuloma with caseous necrosis
C. Productive cough
D. Fever

Answer: B

Explanation: Caseating granulomas are characteristic of tuberculosis.

45. Which immune response is most effective against tuberculosis?

A. IgM antibodies
B. Cell-mediated immunity
C. Complement activation
D. Mast cell degranulation

Answer: B

Explanation: Th1 lymphocytes activate macrophages via IFN-γ.

46. Which disease is most likely to show reversible airflow obstruction?

A. COPD
B. Emphysema
C. Asthma
D. Tuberculosis

Answer: C

47. A patient has increased eosinophils in sputum. Which diagnosis is most likely?

A. Tuberculosis
B. Chronic bronchitis
C. Asthma
D. Emphysema

Answer: C

48. Which inflammatory cell predominates in COPD?

A. Mast cells
B. Basophils
C. Neutrophils
D. Plasma cells

Answer: C

49. Which disease primarily affects gas exchange by reducing alveolar surface area?

A. Asthma
B. Chronic bronchitis
C. Emphysema
D. Tuberculosis

Answer: C

50. Which disease is associated with Type IV hypersensitivity?

A. Asthma
B. COPD
C. Tuberculosis
D. Pulmonary edema

Answer: C

51.Assertion (A): Asthma is characterized by reversible airway obstruction.

Reason (R): Bronchial smooth muscle contraction and airway inflammation are reversible in most patients.

A. Both A and R are true, and R is the correct explanation.
B. Both A and R are true, but R is not the correct explanation.
C. A is true, but R is false.
D. A is false, but R is true.

Answer: A

Explanation: Airway obstruction in asthma is largely reversible because bronchospasm and inflammation respond to treatment.

52.

Assertion (A): COPD patients usually respond less completely to bronchodilators than asthma patients.

Reason (R): COPD involves irreversible structural damage to airways and alveoli.

A. Both A and R are true, and R is the correct explanation.
B. Both are true, but R is not the explanation.
C. A is true, but R is false.
D. A is false, but R is true.

Answer: A

53.

Assertion (A): Alpha-1 antitrypsin deficiency predisposes to emphysema.

Reason (R): Alpha-1 antitrypsin inhibits neutrophil elastase.

A. Both A and R are true, and R is the correct explanation.
B. Both are true, but R is not the explanation.
C. A is true, but R is false.
D. A is false, but R is true.

Answer: A

54.

Assertion (A): Tuberculosis is controlled mainly by antibodies.

Reason (R): Cell-mediated immunity is more important than humoral immunity against intracellular pathogens.

A. Both A and R are true.
B. A is true, but R is false.
C. A is false, but R is true.
D. Both A and R are false.

Answer: C

Explanation: Antibodies play a limited role against M. tuberculosis. Cell-mediated immunity is the primary defense.

55.

Assertion (A): Histamine is responsible for the immediate phase of allergic asthma.

Reason (R): Histamine is released following mast cell degranulation after IgE cross-linking.

A. Both A and R are true, and R is the correct explanation.
B. Both are true, but R is not the explanation.
C. A is true, but R is false.
D. A is false, but R is true.

Answer: A

56.

Assertion (A): Granuloma formation prevents widespread dissemination of Mycobacterium tuberculosis.

Reason (R): Activated macrophages and T lymphocytes surround infected tissue to contain the bacilli.

A. Both A and R are true, and R is the correct explanation.
B. Both are true, but R is not the explanation.
C. A is true, but R is false.
D. A is false, but R is true.

Answer: A

57.

Assertion (A): Airway remodeling contributes to irreversible airflow limitation in long-standing asthma.

Reason (R): Chronic inflammation causes smooth muscle hypertrophy, subepithelial fibrosis, and basement membrane thickening.

A. Both A and R are true, and R is the correct explanation.
B. Both are true, but R is not the correct explanation.
C. A is true, but R is false.
D. A is false, but R is true.

Answer: A

58.

Assertion (A): Smoking increases the risk of COPD.

Reason (R): Cigarette smoke causes oxidative stress, chronic inflammation, and protease–antiprotease imbalance.

A. Both A and R are true, and R is the correct explanation.
B. Both are true, but R is not the explanation.
C. A is true, but R is false.
D. A is false, but R is true.

Answer: A

59.

Assertion (A): All patients with latent tuberculosis are infectious.

Reason (R): Dormant bacilli remain enclosed within granulomas without active multiplication.

A. Both A and R are true.
B. A is true, but R is false.
C. A is false, but R is true.
D. Both A and R are false.

Answer: C

Explanation: Patients with latent TB are not infectious because the bacteria remain dormant and contained within granulomas.

60.

Assertion (A): Both asthma and COPD are obstructive lung diseases.

Reason (R): Airflow limitation is present in both diseases, but it is largely reversible in asthma and largely irreversible in COPD.

A. Both A and R are true, and R is the correct explanation.
B. Both are true, but R is not the explanation.
C. A is true, but R is false.
D. A is false, but R is true.

Answer: A

Explanation: Both diseases obstruct airflow, but the underlying pathology and reversibility of obstruction differ, making this a key concept frequently tested in competitive examinations.

One-Liners for Competitive Examinations

• Asthma: Reversible airway obstruction with eosinophilic inflammation.

• COPD: Irreversible airflow limitation, most commonly caused by cigarette smoking.

• Asthma: Type I (IgE-mediated) hypersensitivity disease.

• COPD: Predominantly neutrophil- and macrophage-mediated inflammation.

• IL-5: Principal cytokine responsible for eosinophil activation in asthma.

• Histamine: Causes immediate bronchoconstriction during an asthma attack.

• Leukotrienes: Produce prolonged bronchoconstriction and mucus hypersecretion.

• Airway remodeling: Thickened basement membrane, goblet cell hyperplasia, and smooth muscle hypertrophy.

• Emphysema: Destruction of alveolar walls due to protease–antiprotease imbalance.

• Alpha-1 antitrypsin deficiency: Genetic risk factor for early-onset emphysema.

• Chronic bronchitis: Productive cough for ≥3 months/year for 2 consecutive years.

• "Blue bloater": Chronic bronchitis with cyanosis and chronic hypoxemia.

• "Pink puffer": Emphysema with dyspnea, hyperventilation, and weight loss.

• Tuberculosis: Caused by Mycobacterium tuberculosis, an acid-fast bacillus.

• TB transmission: Airborne droplet nuclei.

• Granuloma: Hallmark lesion of tuberculosis formed by activated macrophages and T lymphocytes.

• Caseous necrosis: Characteristic pathological feature of tuberculosis.

• Interferon-γ: Key cytokine for macrophage activation in TB.

• TB immunity: Predominantly cell-mediated (Type IV hypersensitivity).

• Latent TB: Dormant bacilli persist within granulomas and may reactivate when host immunity declines.