Pathology is the language of disease — and it shows up on almost every USMLE Step 1 question. Learn these 10 high-yield topics and the mnemonics below, and you will have a strong foundation for exam day.

Top 10 High-Yield Pathology Concepts

  1. Acute vs. chronic inflammation — Acute inflammation is fast (hours to days) and driven by neutrophils; chronic inflammation lasts weeks or more and is driven by lymphocytes and macrophages.

  2. Types of necrosis — There are six main types: coagulative (most organs after ischemia), liquefactive (brain infarcts and abscesses), caseous (TB and fungi), fat (pancreatitis), fibrinoid (immune vessel damage), and gangrenous.

  3. Cell injury reversibility — Reversible cell injury shows cell swelling and fatty change; irreversible injury leads to nuclear changes (pyknosis → karyorrhexis → karyolysis) and cell death.

  4. Benign vs. malignant neoplasia — Benign tumors are well-differentiated, slow-growing, and do not invade or metastasize; malignant tumors are poorly differentiated, grow fast, invade locally, and can spread to distant sites.

  5. Tumor markers — PSA (prostate), AFP (hepatocellular carcinoma, germ cell tumors), β-hCG (choriocarcinoma), CEA (colorectal, pancreatic, gastric), CA-125 (ovarian), and CA 19-9 (pancreatic) are the most tested.

  6. Atherosclerosis — A chronic inflammatory disease of medium and large arteries; plaques form from lipid-laden macrophages (foam cells) in the intima, leading to stenosis, thrombosis, and end-organ ischemia.

  7. Myocardial infarction (MI) evolution — Irreversible injury begins at ~20 minutes of ischemia; coagulative necrosis appears by 24 hours; neutrophils peak at 1–3 days; granulation tissue forms by week 1–2; fibrotic scar is complete by ~6 weeks.

  8. Granulomatous disease — A granuloma is an organized collection of epithelioid macrophages (often with giant cells). Key causes include TB, sarcoidosis, Crohn disease, fungal infections (histoplasma, coccidioides), and foreign body reactions.

  9. Amyloidosis — Abnormal protein (amyloid) deposits in tissues, stains with Congo red, and shows apple-green birefringence under polarized light. AL amyloid is from plasma cells; AA amyloid is from chronic inflammation.

  10. Key inheritance patterns — Autosomal dominant disorders (Marfan, Huntington, familial hypercholesterolemia) often affect structural proteins; autosomal recessive disorders (cystic fibrosis, PKU, sickle cell) often affect enzymes. X-linked recessive disorders (hemophilia A, Duchenne) primarily affect males.

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Mnemonics to Remember Them

1. The 5 Cardinal Signs of Acute Inflammation: "PRISH"

Pain, Redness, Immobility (loss of function), Swelling, Heat

Or the classic Latin version: "CALOR, RUBOR, TUMOR, DOLOR, FUNCTIO LAESA" (heat, redness, swelling, pain, loss of function). These five signs map directly to the vascular changes of acute inflammation: vasodilation causes heat and redness; increased vascular permeability causes swelling; mediators stimulate pain receptors; and all together they impair function.

2. Transudate vs. Exudate: "PILS"

To remember that exudates have Protein, Inflammatory cells, LDH, and Specific gravity all elevated (above transudate levels):

Exudate = Everything elevated

Use Light's criteria on exams: exudate if any one of these is true — fluid:serum protein > 0.5, fluid:serum LDH > 0.6, or fluid LDH > 2/3 the upper limit of serum LDH. Transudate is caused by hydrostatic/oncotic forces (heart failure, cirrhosis, nephrotic syndrome); exudate is caused by infection, malignancy, or inflammation.

3. Causes of Granulomas: "ABCDE + SF"

Allergic bronchopulmonary aspergillosis · Berylliosis · Crohn disease · De Quervain thyroiditis · Eosinophilic granulomatosis · Sarcoidosis · Fungi (histoplasma, coccidioides) — and always remember TB as the classic infectious cause.

The key teaching point: caseating granulomas = TB (and some fungi); non-caseating granulomas = sarcoidosis and most others.

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