Pathology II — Inflammation & Repair — USMLE Step 1 Notes
Free, high-yield revision notes for USMLE Step 1. Read here, or drill the same material as questions and flashcards in the app.
These are high-yield revision notes written for first-order recall. A revision aid, not editorially reviewed and not clinical advice — verify against a primary source before relying on anything clinically.
Acute inflammation
- Cardinal signs: rubor, calor, dolor, tumor, functio laesa
- Vascular phase: transient vasoconstriction then vasodilation and increased permeability (histamine, leukotrienes)
- Cellular phase — leukocyte extravasation in order: margination → rolling (selectins) → adhesion (integrins–ICAM-1) → transmigration (PECAM-1) → chemotaxis
- Neutrophil chemoattractants: C5a, LTB4, IL-8, bacterial products
Key cell-defect diseases (map the step to the disease)
- Leukocyte adhesion deficiency 1 (CD18 integrin): no pus, delayed cord separation, neutrophilia
- Chédiak-Higashi (LYST, defective phagosome-lysosome fusion): giant granules, albinism, recurrent infection
- Chronic granulomatous disease (NADPH oxidase): catalase-positive infections, abnormal dihydrorhodamine test
Chemical mediators worth memorising
- Vasodilation: prostaglandins, nitric oxide, histamine
- Pain: bradykinin, PGE2
- Fever: IL-1, IL-6, TNF, PGE2
- Acute-phase reactants (from IL-6): CRP, fibrinogen, hepcidin, ferritin, serum amyloid A
- Negative acute-phase reactant: albumin, transferrin
Chronic inflammation and granulomas
- Cells: lymphocytes, plasma cells, macrophages
- Granuloma: epithelioid macrophages ± giant cells; driven by Th1 and interferon-gamma; TNF maintains it (anti-TNF drugs reactivate TB)
- Caseating (TB, fungi) vs non-caseating (sarcoid, Crohn, berylliosis, cat-scratch, foreign body)
Repair
- Labile (gut, skin, marrow), stable (liver, proximal tubule), permanent (neuron, cardiac, skeletal muscle)
- Granulation tissue = new capillaries + fibroblasts + loose matrix (NOT the same as a granuloma)
- VEGF → angiogenesis; TGF-beta and FGF → fibrosis; excess TGF-beta → keloid
- Vitamin C and zinc needed for collagen cross-linking and wound healing
Acute vs chronic inflammation
- Acute — neutrophil-dominant; vascular (vasodilation, increased permeability) and cellular (margination, rolling on selectins, firm adhesion via integrins, transmigration). Cardinal signs: rubor, calor, tumor, dolor, functio laesa.
- Chronic — macrophages, lymphocytes, plasma cells; tissue destruction and repair concurrently; may form granulomas.
Key mediators
- Histamine (vasodilation, permeability), prostaglandins (pain, fever), leukotrienes (LTB4 chemotaxis; C4/D4/E4 bronchospasm), bradykinin, complement (C3a/C5a anaphylatoxins, C3b opsonin, MAC).
- Cytokines: TNF-alpha and IL-1 (fever, endothelial activation), IL-6 (acute-phase), IL-8 (neutrophil chemotaxis).
- Acute-phase reactants: CRP, ferritin, fibrinogen, hepcidin up; albumin, transferrin down.
Granulomatous disease
- Epithelioid macrophages + giant cells, driven by Th1/IFN-gamma and TNF (anti-TNF reactivates TB). Caseating (TB, fungi) vs non-caseating (sarcoid, Crohn, foreign body).
Wound healing & repair
- Regeneration (labile/stable cells) vs fibrosis (permanent cells → scar). Phases: haemostasis, inflammation, proliferation (granulation tissue, angiogenesis, VEGF/FGF), remodelling (collagen III → I).
- Complications: dehiscence, hypertrophic scar vs keloid (beyond wound margins, collagen excess), contracture. Vitamin C and zinc are needed; steroids impair healing.
Practise this, free
Turn these notes into questions, flashcards and timed blocks. No paywall, no trial, no card.
Open StepSherpa