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

Source: https://tracknation.in/story/inflammation-and-repair-for-neet-pg-pathology-leukocyte-steps-mediators-granulomas-phagocyte-defects-wound-healing (TrackNation — free UPSC notes with PYQs)

> NEET PG Pathology: cardinal signs, exudate vs transudate, leukocyte rolling, adhesion, chemotaxis and respiratory burst, mediators and fever, CRP and ESR, LAD, CGD and Chédiak-Higashi, granulomas and giant cells, TB vs sarcoidosis, granulation tissue, keloid vs hypertrophic scar and scurvy, with a diagram, hooks, vignette MCQs and cards.

## Start Here

🎯 **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).

| **Mediator (MeSH/MSD)**

 | **Main action**

 |
| Histamine (from histidine)

 | Vasodilator, bronchoconstrictor

 |
| Bradykinin

 | Arteriolar dilation, more capillary permeability (short-lived)

 |
| Prostaglandins (COX pathway)

 | Potent mediators; PGE2 drives fever

 |
| Leukotrienes (5-lipoxygenase)

 | Immediate hypersensitivity, inflammation

 |
| Platelet-activating factor

 | Platelet aggregation, anaphylactic symptoms

 |
| IL-8 (CXC chemokine)

 | Neutrophil chemotaxis

 |
| IL-1, TNF-α, IL-6

 | Endogenous pyrogens

 |
| C3a, C5a

 | Anaphylatoxins

 |

## 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

| **Phagocyte defect (MSD/MeSH)**

 | **Defect**

 | **Clue**

 |
| Leukocyte adhesion deficiency (AR)

 | β2 integrins (CD11/CD18) → neutrophils cannot leave vessels

 | No pus, high WBC, cord separation > 3 weeks

 |
| Chronic granulomatous disease (> 50% X-linked)

 | No oxidative burst (NADPH oxidase) → ingest but cannot kill

 | Catalase-positive infections, Aspergillus; DHR/NBT test

 |
| Chédiak-Higashi syndrome (AR)

 | Abnormal lysosomes

 | Oculocutaneous albinism, pyogenic infections, lymphoreticular cancers

 |

## 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

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

- Cells + protein vs thin, watery, few cells.

- Selectins.

- Integrins (CD11/CD18).

- IL-8.

- NADPH oxidase → superoxide.

- Vasodilator, bronchoconstrictor.

- Dilation + permeability, short-lived.

- Prostaglandins vs leukotrienes.

- IL-1, TNF-α, IL-6 → PGE2.

- High temperature, set point unchanged.

- Acute-phase protein / red-cell settling.

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

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

- AR; albinism; abnormal lysosomes.

- Activated macrophage.

- Horseshoe nuclei — TB, sarcoid.

- Scattered nuclei.

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

- Capillaries + lymphocytes, macrophages, plasma cells.

- Beyond vs within margins.

- 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

**Answer: (d)** — MeSH definition of inflammation.

**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

**Answer: (c)** — Exudates carry cells and proteins from inflamed vessels.

**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

**Answer: (a)** — Rolling; then chemokine activation and firm adhesion.

**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

**Answer: (c)** — Neutrophils cannot leave vessels; autosomal recessive.

**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

**Answer: (c)** — Chemotaxis follows a chemical gradient.

**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

**Answer: (c)** — Defective in chronic granulomatous disease.

**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

**Answer: (b)** — Catalase-positive organisms; Aspergillus is the leading cause of death.

**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

**Answer: (a)** — More than half of cases are X-linked recessive.

**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

**Answer: (b)** — High incidence of lymphoreticular neoplasms.

**Q10.** Bradykinin contributes to inflammatory swelling by

- (a) arteriolar dilation and increased capillary permeability

- (b) neutrophil chemotaxis only

- (c) platelet aggregation

- (d) fever only

**Answer: (a)** — Potent but short-lived.

**Q11.** Prostaglandins are made from arachidonic acid by the

- (a) kinin system

- (b) cyclooxygenase pathway

- (c) complement cascade

- (d) 5-lipoxygenase pathway

**Answer: (b)** — Leukotrienes come from 5-lipoxygenase.

**Q12.** Leukotrienes are formed from arachidonic acid by

- (a) 5-lipoxygenase

- (b) phospholipase only

- (c) NADPH oxidase

- (d) cyclooxygenase

**Answer: (a)** — Involved in immediate hypersensitivity and inflammation.

**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

**Answer: (d)** — MeSH.

**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)

**Answer: (d)** — They reset the hypothalamic set point.

**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

**Answer: (c)** — Fever requires a reset set point.

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

- (a) flagellin only

- (b) peptidoglycan only

- (c) teichoic acid

- (d) lipopolysaccharide (endotoxin)

**Answer: (d)** — S. aureus toxic shock toxin is another.

**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

**Answer: (a)** — Acute-phase proteins can rise or fall.

**Q18.** The ESR measures

- (a) white cell count

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

- (c) CRP concentration

- (d) platelet function

**Answer: (b)** — MeSH: Blood Sedimentation.

**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

**Answer: (d)** — Caused by infectious and non-infectious agents.

**Q20.** Epithelioid cells in a granuloma are

- (a) epithelial cells

- (b) plasma cells

- (c) neutrophils

- (d) activated macrophages after prolonged antigen stimulation

**Answer: (d)** — They fuse to form giant cells.

**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

**Answer: (a)** — Seen in TB, syphilis, sarcoidosis, deep fungal infection.

**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

**Answer: (c)** — They form around exogenous material.

**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

**Answer: (a)** — Non-caseating granulomas; lungs and lymphatics most often.

**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

**Answer: (b)** — Hypercalciuria may occur even with normal serum calcium.

**Q25.** In suspected sarcoidosis, a raised serum ACE is

- (a) diagnostic

- (b) a marker of TB

- (c) always present

- (d) suggestive but non-specific

**Answer: (d)** — Also raised in hyperthyroidism, diabetes, silicosis, mycobacterial and fungal disease.

**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

**Answer: (d)** — Granulation tissue.

**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

**Answer: (d)** — Found in granulation tissue.

**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

**Answer: (d)** — Hypertrophic scars stay within the wound and may regress.

**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

**Answer: (a)** — MeSH.

**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

**Answer: (b)** — Scurvy: defective collagen in small vessels.

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

- (a) half

- (b) one-third

- (c) two-thirds

- (d) one-tenth

**Answer: (b)** — Main constituent of skin, connective tissue, bone and teeth.

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

- (a) a transudate

- (b) a keloid

- (c) a granuloma

- (d) an abscess

**Answer: (d)** — Usually with signs of infection.

### 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.
