Pathology · Short notes

Inflammation and Repair: Short Notes & Cheat Sheet

Acute and chronic inflammation, leukocyte recruitment, chemical mediators, granulomas, regeneration and fibrosis, and wound healing.

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Short notes

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How neutrophils leave blood vessels

Each step uses different molecules, which is why defects at any step cause recurrent infections.

Acute inflammation

Cardinal signs: redness (rubor), heat (calor), swelling (tumor), pain (dolor) and loss of function (functio laesa).
Vascular changes: vasodilation and increased permeability (histamine acts first), producing a protein-rich exudate. A transudate is protein-poor fluid from pressure changes.
Neutrophils are the main cells. They move by margination, rolling (selectins), firm adhesion (integrins), transmigration (diapedesis) and chemotaxis (C5a, LTB4, IL-8).
Phagocytosis is helped by opsonins (IgG, C3b).
Outcomes: complete resolution, abscess formation, healing by fibrosis, or progression to chronic inflammation.

Mediators and chronic inflammation

Histamine and serotonin (preformed), prostaglandins and leukotrienes (made on demand), bradykinin (pain, permeability), complement (C3a and C5a are anaphylatoxins; C5b–9 forms the membrane attack complex).
Cytokines IL-1, IL-6 and TNF cause fever and stimulate the liver to make acute-phase proteins such as CRP.
Chronic inflammation involves macrophages, lymphocytes and plasma cells, with ongoing tissue damage and fibrosis.
Granulomas are collections of epithelioid macrophages, often with Langhans giant cells. Caseating granulomas suggest TB; non-caseating ones suggest sarcoidosis.

Repair and wound healing

Labile cells (epithelium, bone marrow) divide continuously; stable cells (liver, kidney) can divide when needed; permanent cells (neurons, heart muscle) cannot, so damage heals by scarring.
Primary intention: clean wounds with close edges (surgical incisions). Secondary intention: large gaps, more granulation tissue and wound contraction by myofibroblasts.
Granulation tissue is new capillaries (angiogenesis, driven by VEGF) plus fibroblasts. Type III collagen is laid down first and later replaced by type I.
Scar strength reaches about 70–80% of normal by about 3 months and never fully recovers.
Healing is delayed by infection (the most important local factor), poor blood supply, diabetes, steroids, malnutrition (protein, vitamin C, zinc) and foreign bodies.
Keloids extend beyond the wound edges; hypertrophic scars stay within them.

Cheat sheet

High-yield facts in one place. Cover the right-hand column and test yourself.

Mediators

Mediator	Main effect
Histamine	Vasodilation, ↑ permeability (early)
Prostaglandins	Vasodilation, pain, fever
Leukotriene B4	Neutrophil chemotaxis
LTC4/D4/E4	Bronchospasm, permeability
Bradykinin	Pain, permeability
C5a	Chemotaxis, anaphylatoxin
C3b	Opsonisation
IL-1, IL-6, TNF	Fever, acute-phase response

Cell types in repair

Type	Examples · regeneration
Labile	Epithelium, marrow · continuous
Stable	Hepatocytes, renal tubules · when stimulated
Permanent	Neurons, cardiac muscle · none; scar forms

Memory aids

Roll with Selectins, Stick with Integrins: Neutrophils roll using selectins and adhere firmly using integrins.

Exam traps

Exudate is protein-rich (inflammation); transudate is protein-poor (pressure changes).
Heart muscle cannot regenerate, so a myocardial infarct heals by scar.
Granulation tissue is not granulomatous inflammation; the names are easily confused.
Wound strength never returns fully to 100% of normal.

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