3️⃣ Chronic inflammation

Question 1

What categories cause chronic inflammation?

Answer 1

Persistent infection, immune-mediated (autoimmunity, unknown), prolonged toxins (endogenous/exogenous), granulomatous T-cell–driven.

Question 2

What are macroscopic features of chronic inflammation?

Answer 2

Chronic ulcers, abscess cavities, thickened walls, granulomas, fibrosis.

Question 3

What are the microscopic “three Rs” of chronic inflammation?

Answer 3

Inflammation (mononuclear infiltrate), Injury (tissue destruction), Repair (angiogenesis and fibrosis).

Question 4

Contrast M1 vs M2 macrophages.

Answer 4

M1: IFN-γ–activated, microbicidal, pro-inflammatory; M2: IL-4/IL-13–activated, tissue repair, pro-fibrotic (TGF-β, VEGF).

Question 5

What roles do Th1, Th2, and Th17 cells play?

Answer 5

Th1: IFN-γ → M1 activation; Th2: IL-4/5/13 → M2 activation; Th17: IL-17 → neutrophil recruitment.

Question 6

Which other leukocytes participate in chronic inflammation?

Answer 6

Eosinophils (parasites/allergy), mast cells (histamine, leukotrienes), neutrophils (in some chronic conditions).

Question 7

Define diffuse chronic inflammation.

Answer 7

Widespread mononuclear infiltrate and fibrosis without discrete nodules (e.g. chronic bronchitis, rheumatoid arthritis).

Question 8

Define granulomatous inflammation.

Answer 8

Focal aggregates of epithelioid macrophages and giant cells, rimmed by lymphocytes/fibroblasts (caseating in TB, non-caseating in sarcoidosis).

Question 9

What are the key morphological features of a granuloma?

Answer 9

Epithelioid cells with abundant pink cytoplasm, multinucleate giant cells (Langhans type), lymphocytic cuff, possible central caseous necrosis.

Question 10

How is a granuloma formed?

Answer 10

Persistent antigen → Th1 cells release IFN-γ → macrophage activation → epithelioid transformation and giant cell formation → granuloma walling-off.

Question 11

Explain cirrhosis as chronic inflammation.

Answer 11

Chronic alcohol/viral injury → persistent inflammation → stellate cell–mediated fibrosis → nodular, dysfunctional liver.

Question 12

Explain tuberculosis as chronic inflammation.

Answer 12

Intracellular Mycobacterium tuberculosis → Th1 response → IFN-γ–driven caseating granulomas in lung and lymph nodes.

Question 13

Explain atherosclerosis as chronic inflammation.

Answer 13

Endothelial injury by lipids → monocyte recruitment → foam cell formation → chronic intimal inflammation → fibrous cap and necrotic core plaque.

Question 14

What are sequelae of chronic inflammation?

Answer 14

Fibrosis and organ distortion (e.g. cirrhosis, strictures), loss of function, metaplasia, dysplasia, carcinoma.