Inflammation and Repair for NEET PG Pathology: Leukocyte Steps, Mediators, Granulomas, Phagocyte Defects, Wound Healing

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🎯 Exam priority: High. Expect: steps of leukocyte emigration and their molecules, mediator actions, pyrogens, the three phagocyte defects by their clues, giant-cell types, caseating vs non-caseating granulomas, and keloid vs hypertrophic scar.

CBME mapping: PA 3.1–3.4, 4.1.

Leukocyte steps, mediators, granulomas, phagocyte defects and healing. Drawn by TrackNation.

Acute Inflammation

• Cardinal signs: pain, heat, redness, swelling and loss of function.

• Exudate: fluid, cells and proteins slowly leaving vessels in inflamed tissue. Transudate: thin, watery, few cells or proteins. Oedema = abnormal fluid in tissues or body cavities.

• Neutrophil journey: rolling on endothelium (selectins) → activation by chemokines, flattening and firm attachment (integrins) → chemotaxis up a chemical gradient (e.g. IL-8) → phagocytosis → killing by the respiratory burst (NADPH oxidase makes superoxide).

Fever and the Acute-Phase Response

• Exogenous pyrogens (e.g. endotoxin, the lipopolysaccharide of Gram-negative bacteria) release endogenous pyrogens — IL-1, TNF-α, IL-6 — and PGE2 resets the hypothalamic thermostat. A rise without a reset set point is hyperthermia, not fever.

• The liver changes acute-phase protein output; CRP rises in inflammation and tissue damage. ESR measures how fast red cells settle. Leukocytosis is a transient rise in white cells. An abscess is a collection of pus.

When Phagocytes Fail

Chronic and Granulomatous Inflammation

• A granuloma is a small nodule of grouped mononuclear phagocytes. Epithelioid cells are macrophages activated by prolonged antigen exposure; they fuse into giant cells.

• Langhans giant cells: nuclei in a peripheral horseshoe — TB, syphilis, sarcoidosis, deep fungal infection. Foreign-body giant cells: nuclei scattered irregularly, around foreign material.

• TB: epithelioid granulomas with caseous centres. Sarcoidosis: non-caseating granulomas, cause unknown, mostly lungs and lymph nodes; macrophages activate vitamin D → hypercalcaemia; ACE may be raised but is non-specific.

Repair and Healing

• Regeneration replaces tissue; repair restores integrity with connective tissue. Granulation tissue = new capillaries with lymphocytes, macrophages and plasma cells on a healing surface. Contractile myofibroblasts work in granulation tissue and in fibrosis. Collagen is about one-third of body protein.

• Keloid: fibroblastic overgrowth that extends beyond the wound margins (earlobes, shoulders, upper arms, chest). Hypertrophic scar: stays within the wound and may regress. Fibrosis: fibrous tissue invading an organ after injury.

• Scurvy (vitamin C deficiency): defective collagen in small vessels — bleeding, spongy gums, anaemia, impaired wound healing.

Traps the Examiner Sets

• Selectins = rolling; integrins = firm adhesion (LAD = CD18).

• CGD: phagocytes engulf but cannot kill; catalase-positive bugs. LAD: no pus and late cord fall.

• Langhans = horseshoe nuclei; foreign-body = scattered nuclei.

• Keloid crosses the wound edge; hypertrophic scar does not.

Memory Hooks & Shortcuts

Shortcuts to lock in this article's numbers and lists. Each one only re-packages facts proven above.

• 🧠 Selectins Slow them, Integrins Imprison them — rolling vs firm adhesion

• 🧠 Eight calls the neutrophils to the fight — IL-8 chemotaxis

• 🧠 CGD: Can Grab, Doesn't digest — CGD mechanism

• 🧠 LAD: Leukocytes Aren't Departing (no pus, late cord) — leukocyte adhesion deficiency

• 🧠 Langhans = Lucky horseshoe — Langhans giant cells

• 🧠 Keloid Keeps going beyond the edge — keloid vs hypertrophic

• 🧠 1, 6 and TNF light the fire — pyrogens

Rapid-Revision Cards

• Cardinal signs

  Pain, heat, redness, swelling, loss of function.

• Exudate vs transudate

  Cells + protein vs thin, watery, few cells.

• Rolling

  Selectins.

• Firm adhesion

  Integrins (CD11/CD18).

• Neutrophil chemokine

  IL-8.

• Respiratory burst

  NADPH oxidase → superoxide.

• Histamine

  Vasodilator, bronchoconstrictor.

• Bradykinin

  Dilation + permeability, short-lived.

• COX vs 5-LOX

  Prostaglandins vs leukotrienes.

• Endogenous pyrogens

  IL-1, TNF-α, IL-6 → PGE2.

• Hyperthermia

  High temperature, set point unchanged.

• CRP / ESR

  Acute-phase protein / red-cell settling.

• LAD

  AR; CD18; no pus; cord > 3 weeks.

• CGD

  > 50% X-linked; catalase+; DHR/NBT.

• Chédiak-Higashi

  AR; albinism; abnormal lysosomes.

• Epithelioid cell

  Activated macrophage.

• Langhans

  Horseshoe nuclei — TB, sarcoid.

• Foreign-body giant cell

  Scattered nuclei.

• Sarcoidosis

  Non-caseating; vitamin D activation; ACE non-specific.

• Granulation tissue

  Capillaries + lymphocytes, macrophages, plasma cells.

• Keloid vs hypertrophic

  Beyond vs within margins.

• Scurvy

  Collagen defect; gums, bleeding, poor healing.

Sources

Facts in this article were checked against these documents.

• Medical Subject Headings (MeSH) scope notes — US National Library of Medicine, accessed 2026 (link)

• MSD Manual Professional: Fever; Chronic Granulomatous Disease; Leukocyte Adhesion Deficiency; Sarcoidosis; Keloids; Vitamin C Deficiency — Merck & Co. (MSD Manuals), reviewed 2025–26 (link)

• MSD Manual Professional: Complement System; Tuberculosis — Merck & Co. (MSD Manuals), reviewed 2025–26 (link)

• Competency Based Undergraduate Curriculum, Pathology (PA 3–4) — National Medical Commission, 2024

Test Yourself: Practice Questions

Thirty-two questions in NEET PG style, most of them clinical vignettes.

Practice Questions (NEET PG pattern)

Original questions written in the style of the exam: +4 for a correct answer, −1 for a wrong one. Every answer was checked against the sources listed above. NEET PG papers are not published by NBEMS, so these are not past-paper questions.

Q1. The classic signs of acute inflammation are

• (a) fever only

• (b) pallor, cold and numbness

• (c) itching and scaling

• (d) pain, heat, redness, swelling and loss of function

Q2. Fluid from a patient's swollen ankles is thin and watery with very few cells and little protein. It is

• (a) an exudate

• (b) pus

• (c) a transudate

• (d) chyle

Q3. The first loose contact of neutrophils with inflamed endothelium, in which they tumble along the vessel wall, depends mainly on

• (a) selectins

• (b) integrins

• (c) immunoglobulins

• (d) collagen

Q4. An infant has recurrent infections without pus, a persistently high white count and the umbilical cord fell off after 4 weeks. The defect is in

• (a) lysosomes

• (b) NADPH oxidase

• (c) β2 integrins (CD11/CD18) — leukocyte adhesion deficiency

• (d) complement C5

Q5. The chemokine that chiefly draws neutrophils to a site of acute inflammation is

• (a) IL-10

• (b) IL-4

• (c) IL-8 (a CXC chemokine)

• (d) interferon-γ

Q6. Neutrophils kill ingested bacteria by a sudden rise in oxygen use that makes superoxide. The enzyme is

• (a) myeloperoxidase alone

• (b) cyclooxygenase

• (c) NADPH oxidase (respiratory burst)

• (d) lysozyme

Q7. A boy has recurrent abscesses and lung granulomas; cultures grow Staphylococcus aureus and Aspergillus. The DHR test shows no oxidative burst. The diagnosis is

• (a) complement C5 deficiency

• (b) chronic granulomatous disease

• (c) Chédiak-Higashi syndrome

• (d) leukocyte adhesion deficiency

Q8. In chronic granulomatous disease, phagocytes

• (a) ingest bacteria but fail to kill and digest them

• (b) are absent

• (c) cannot leave blood vessels

• (d) cannot ingest bacteria

Q9. A child with oculocutaneous albinism has recurrent pyogenic infections; many cell types contain abnormal lysosomes. The diagnosis is

• (a) Down syndrome

• (b) Chédiak-Higashi syndrome (autosomal recessive)

• (c) chronic granulomatous disease

• (d) leukocyte adhesion deficiency

Q10. Bradykinin contributes to inflammatory swelling by

• (a) arteriolar dilation and increased capillary permeability

• (b) neutrophil chemotaxis only

• (c) platelet aggregation

• (d) fever only

Q11. Prostaglandins are made from arachidonic acid by the

• (a) kinin system

• (b) cyclooxygenase pathway

• (c) complement cascade

• (d) 5-lipoxygenase pathway

Q12. Leukotrienes are formed from arachidonic acid by

• (a) 5-lipoxygenase

• (b) phospholipase only

• (c) NADPH oxidase

• (d) cyclooxygenase

Q13. A phospholipid mediator from platelets, basophils and macrophages that causes platelet aggregation and anaphylactic hypotension is

• (a) IL-8

• (b) histamine

• (c) bradykinin

• (d) platelet-activating factor

Q14. The endogenous pyrogens that cause fever in infection are

• (a) IL-4 and IL-13

• (b) IgE and histamine

• (c) IL-10 and TGF-β

• (d) IL-1, TNF-α and IL-6 (acting through PGE2)

Q15. A patient's temperature is 41 °C but the hypothalamic set point has not been reset. This is

• (a) fever from endogenous pyrogens

• (b) a PGE2-mediated fever

• (c) hyperthermia, not fever

• (d) septic fever

Q16. The classic exogenous pyrogen from Gram-negative bacteria is

• (a) flagellin only

• (b) peptidoglycan only

• (c) teichoic acid

• (d) lipopolysaccharide (endotoxin)

Q17. A plasma protein made by the liver that rises during inflammation and after tissue damage is

• (a) C-reactive protein

• (b) albumin

• (c) prealbumin

• (d) transferrin

Q18. The ESR measures

• (a) white cell count

• (b) the rate at which red cells settle in blood

• (c) CRP concentration

• (d) platelet function

Q19. A granuloma is

• (a) a scar

• (b) a blood clot

• (c) a collection of pus

• (d) a small nodular collection of grouped mononuclear phagocytes

Q20. Epithelioid cells in a granuloma are

• (a) epithelial cells

• (b) plasma cells

• (c) neutrophils

• (d) activated macrophages after prolonged antigen stimulation

Q21. A lymph node granuloma contains multinucleated giant cells with nuclei arranged in a peripheral horseshoe. These are

• (a) Langhans giant cells

• (b) foreign-body giant cells

• (c) Touton cells

• (d) Reed-Sternberg cells

Q22. Around foreign material in the skin, giant cells with many nuclei scattered irregularly in the cytoplasm are

• (a) Langhans giant cells

• (b) megakaryocytes

• (c) foreign-body giant cells

• (d) Reed-Sternberg cells

Q23. A young adult with lung and lymph node involvement has granulomas without central necrosis; tests for infection are negative. The likely diagnosis is

• (a) sarcoidosis

• (b) tuberculosis

• (c) foreign-body reaction

• (d) lymphoma

Q24. A patient with sarcoidosis has hypercalcaemia. The mechanism is

• (a) bone metastases

• (b) macrophages convert vitamin D to its active 1,25 form

• (c) thiazide use

• (d) PTH-related peptide from tumour

Q25. In suspected sarcoidosis, a raised serum ACE is

• (a) diagnostic

• (b) a marker of TB

• (c) always present

• (d) suggestive but non-specific

Q26. The pink, granular tissue on the base of a healing ulcer is made of

• (a) fat cells

• (b) epithelium only

• (c) dense mature collagen only

• (d) new capillaries with lymphocytes, macrophages and plasma cells

Q27. Spindle-shaped cells with contractile proteins that help heal wounds and also appear in fibrosis are

• (a) plasma cells

• (b) epithelioid cells

• (c) mast cells

• (d) myofibroblasts

Q28. Months after ear piercing, a firm scar grows well beyond the edges of the original wound. This is

• (a) a hypertrophic scar

• (b) a granuloma

• (c) granulation tissue

• (d) a keloid

Q29. An elevated scar that stays within the wound margins and later regresses by itself is

• (a) a hypertrophic scar

• (b) fibrosis

• (c) a keloid

• (d) a sarcoma

Q30. A man on a very poor diet has bleeding gums, easy bruising and wounds that will not heal. The defect is in

• (a) clotting factor VIII

• (b) collagen formation (vitamin C deficiency)

• (c) iron absorption

• (d) platelet production

Q31. Collagen makes up about what fraction of total body protein?

• (a) half

• (b) one-third

• (c) two-thirds

• (d) one-tenth

Q32. A localised collection of pus in a tissue is called

• (a) a transudate

• (b) a keloid

• (c) a granuloma

• (d) an abscess

Active Recall

From memory: list the cardinal signs and contrast exudate and transudate; describe neutrophil rolling, adhesion, chemotaxis and killing with their molecules; give the action of each major mediator and the pyrogens; match LAD, CGD and Chédiak-Higashi to their defects; describe granulomas and giant cells in TB and sarcoidosis; and explain granulation tissue, keloids and scurvy.