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NTRUHS 2K23 PATHOLOGY CHEAT SHEET

PAPER 1 + PAPER 2 - QUICK REVISION

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PAPER 1

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• Programmed cell death - cell shrinks, chromatin condenses, apoptotic bodies form, phagocytosed without inflammation
• Intrinsic pathway: mitochondria releases cytochrome C → caspase activation (triggered by DNA damage, p53)
• Extrinsic pathway: death receptors (Fas/TNFR) → caspase 8 activation
• Key players: Bcl-2 (anti-apoptotic), Bax (pro-apoptotic), caspases (executioners)
• Other modes of death: Necrosis, Autophagy, Pyroptosis (caspase-1, inflammatory), Necroptosis (programmed necrosis)

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• Necrosis: cell swells, membrane ruptures, inflammation present, enzymatic digestion
• Types of necrosis:
  • Coagulative - most organs, infarcts, architecture preserved (ghost cells)
  • Liquefactive - brain infarcts, bacterial abscesses (pus)
  • Caseous - TB, cheese-like, no architecture
  • Fat necrosis - pancreas/breast, calcium soap deposits
  • Fibrinoid - vessels in malignant HTN/immune vasculitis
  • Gangrenous - dry (coagulative) vs wet (liquefactive superinfection)

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• Cardinal signs: Rubor, Calor, Dolor, Tumor, Functio laesa
• Vascular events: Transient vasoconstriction → vasodilation → increased permeability → stasis
• Cellular events: Margination → Rolling (selectins) → Adhesion (integrins/ICAM) → Transmigration → Chemotaxis → Phagocytosis
• Chemotaxis agents: C5a, LTB4, IL-8, bacterial products
• Phagocytosis: Recognition (opsonins: IgG, C3b) → Engulfment → Killing (ROS, MPO, NO)
• Fate of acute inflammation: Resolution / Suppuration / Fibrosis / Chronic inflammation
• Morphological types: Serous, Fibrinous, Suppurative (abscess/empyema), Ulcerative, Membranous, Pseudomembranous

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• Mechanism: ↑ hydrostatic pressure / ↓ oncotic pressure / ↑ vascular permeability / lymphatic obstruction / Na retention
• Exudate vs Transudate:

• Cardiac oedema: ↑ venous hydrostatic P + ↑ aldosterone → Na/water retention → dependent pitting oedema + ascites

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• After long bone fractures or liposuction (48-72 hrs delay)
• Pathogenesis: fat globules → lungs → systemic → petechiae, respiratory failure, neurological signs
• Classic triad: Hypoxia + neurological changes + petechial rash
• Diagnosis: Sudan III / Oil Red O stain for fat in urine/sputum

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• Type I hypersensitivity, IgE mediated
• Sequential events: Antigen → IgE on mast cells → degranulation → histamine, leukotrienes → vasodilation, bronchoconstriction
• Features: urticaria, angioedema, bronchospasm, hypotension
• Treatment: Epinephrine

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• Commonest cause: Gram negative bacteria (endotoxin/LPS)
• Also: Gram positive (exotoxins), fungi
• Pathogenesis: LPS → macrophage activation → TNF-α, IL-1, IL-6 → systemic inflammatory response → widespread vasodilation → hypotension → multi-organ failure
• Stages: Warm (hyperdynamic) → Cold (hypodynamic) → Irreversible

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• Type I: IgE binds Fc receptor on mast cells → cross-linking by antigen → release of histamine (preformed) + leukotrienes/PGs (newly synthesized)

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• Autoimmune, females 20-40 yrs
• Key antibodies: ANA (most sensitive), Anti-dsDNA + Anti-Sm (most specific)
• Features: butterfly rash, photosensitivity, polyarthritis, serositis, renal, neuro, hematological
• Lupus nephritis WHO classes (ISN/RPS):
  • Class I: Normal
  • Class II: Mesangial
  • Class III: Focal (<50% glomeruli)
  • Class IV: Diffuse (>50% glomeruli) - worst prognosis - "wire loop" lesions
  • Class V: Membranous - nephrotic syndrome
  • Class VI: Sclerosing

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• CD4+ T cell count: Normal >500; AIDS <200 cells/µL
• Pathogenesis: HIV gp120 binds CD4 + coreceptors (CCR5/CXCR4) → viral entry → reverse transcriptase → integration → CD4 depletion
• AIDS-defining illnesses: PCP (Pneumocystis), CMV retinitis, Toxoplasma encephalitis, Cryptococcal meningitis, Kaposi sarcoma, MAC infection
• Window period: ~3 weeks (RNA detectable), ~6 weeks (p24 antigen), ~12 weeks (antibodies)

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• Extracellular deposition of misfolded proteins in beta-pleated sheet configuration
• Types: Primary (AL - light chains, myeloma), Secondary (AA - chronic inflammation, TB, RA), Familial (TTR), Senile, Dialysis-related (β2 microglobulin)
• Morphology: Waxy, firm organs - "lardaceous spleen"
• Staining: Congo red → apple-green birefringence under polarized light; PAS positive; Thioflavin T fluorescence

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• Primary complex (Ghon complex): subpleural focus + hilar lymph nodes
• Microscopy: Caseating granuloma with central necrosis, epithelioid cells, Langhans giant cells, lymphocytes
• Diagnosis: Sputum AFB (ZN stain - red bacilli on blue background), Culture (gold standard - Lowenstein-Jensen), CBNAAT/GeneXpert, Mantoux test, IGRA
• Manifestations: Pulmonary (most common), miliary TB, TB meningitis, Pott's disease, intestinal TB, genitourinary TB

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• Mycobacterium leprae - infects peripheral nerves and skin
• Ridley-Jopling classification:

• Lepromatous microscopy: Foamy macrophages (Virchow cells) packed with bacilli (Globi), no granulomas
• Stain: Modified ZN / Fite-Faraco stain

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• Philadelphia chromosome: t(9;22) → BCR-ABL fusion gene → constitutive tyrosine kinase activity
• Features: Massive splenomegaly, leukocytosis (all stages of myeloid cells), low LAP score
• Blood: ↑ WBC with full myeloid series, basophilia, eosinophilia
• Bone marrow: hypercellular
• Treatment: Imatinib (TKI)
• Blast crisis: transformation to AML/ALL

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• Adults predominantly
• Blasts >20% in bone marrow (WHO criteria)
• Auer rods: pathognomonic (pink needle-shaped inclusions in cytoplasm)
• FAB M3 (APML): t(15;17), PML-RARα, DIC, treat with ATRA
• Markers: MPO+, CD13, CD33, CD117
• Poor prognosis: complex karyotype, FLT3 mutation

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• Most common childhood leukemia
• Lymphoblasts with condensed chromatin, no Auer rods
• L1 (small), L2 (large), L3 (Burkitt-like)
• B-ALL: CD19, CD10 (CALLA), TdT+
• T-ALL: CD3, CD7, TdT+
• t(12;21) - best prognosis (children); Philadelphia chromosome - worst prognosis
• CNS involvement common

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• Commonest anemia worldwide
• Causes: Blood loss (most common in adults) > ↓ intake > ↓ absorption
• Pathogenesis: depleted stores → low serum ferritin → low serum iron → high TIBC → microcytic hypochromic anemia
• Peripheral smear: microcytic hypochromic RBCs, pencil cells, target cells, anisocytosis, poikilocytosis
• Labs: ↓ serum iron, ↓ ferritin, ↑ TIBC, ↓ MCV, ↓ MCH

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• α-thal: deletion of α-globin genes (chromosome 16); HbH disease (3 genes deleted); Hydrops fetalis (4 genes deleted)
• β-thal major: no β chains, severe hemolysis, Hb F compensation, crew-cut skull X-ray, splenomegaly; transfusion dependent
• β-thal minor: heterozygous, mild hypochromic microcytic anemia

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• Routes: Lymphatic (carcinomas - first), Hematogenous (sarcomas - bone/lung/liver/brain), Direct seeding (ovary → peritoneum), Transcoelomic
• Steps: Invasion → intravasation → survival in circulation → extravasation → colonization
• EMT (Epithelial-Mesenchymal Transition): cancer cells lose E-cadherin, gain mesenchymal markers
• Common sites by primary: Breast → bone/lung/brain/liver; Lung → brain/adrenals; Colon → liver; Prostate → bone (osteoblastic)

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• B12 or Folate deficiency → impaired DNA synthesis → megaloblasts
• Blood: Macro-ovalocytes, hypersegmented neutrophils (>5 lobes), pancytopenia
• Bone marrow: megaloblasts, giant metamyelocytes, ineffective erythropoiesis
• B12 deficiency: neurological (subacute combined degeneration), glossitis; Folate: no neuro
• Pernicious anemia: autoimmune destruction of parietal cells → lack of intrinsic factor → B12 malabsorption; anti-IF antibodies

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• Remote effects of tumor NOT due to metastasis
• Examples:
  • SIADH - small cell lung cancer
  • PTHrP (hypercalcemia) - squamous cell lung/breast
  • ACTH (Cushing) - small cell lung
  • Trousseau sign (migratory thrombophlebitis) - pancreatic/visceral cancers
  • Eaton-Lambert syndrome - small cell lung
  • Polycythemia - renal cell carcinoma (EPO)
  • Dermatomyositis/polymyositis - various cancers

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• Most common lysosomal storage disorder
• Deficiency: Glucocerebrosidase (beta-glucosidase)
• Accumulation: Glucocerebroside in macrophages
• Gaucher cells: "wrinkled tissue paper" cytoplasm (macrophages in liver/spleen/BM)
• Features: Hepatosplenomegaly, Erlenmeyer flask deformity of femur, bone marrow infiltration, anemia
• Stain: PAS positive

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• Treponema pallidum, 3-10 years after primary infection
• Features: Gummas (granulomatous necrosis in skin/bone/viscera), Cardiovascular syphilis (aortitis → aneurysm, AR), Neurosyphilis (tabes dorsalis, general paresis)
• Gumma: rubbery necrosis, NOT caseous, no AFB, central necrosis with surrounding inflammation
• Aortic aneurysm: syphilis most common cause of thoracic aortic aneurysm; "tree bark" appearance

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• Proteinuria: glomerular (albumin >3.5g/day = nephrotic), tubular, overflow
• Bence-Jones protein: immunoglobulin light chains, in myeloma - precipitates at 40-60°C, dissolves at 100°C
• Physical exam: color, clarity, specific gravity (1.001-1.035), pH, smell, volume
• Casts: RBC casts = glomerulonephritis; WBC casts = pyelonephritis; granular = tubular damage; waxy = chronic renal failure

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• Reversible change: one differentiated cell type → another mature cell type
• Examples:
  • Barrett's esophagus: squamous → columnar (acid reflux) → risk of adenocarcinoma
  • Cervical ectopy: columnar → squamous (transformation zone)
  • Bronchial: columnar → squamous (smokers)
  • Bladder: squamous metaplasia (stones/chronic infection)
  • Osseous metaplasia: soft tissue ossification

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• Ischemic necrosis due to arterial occlusion (or venous in special cases)
• Types: Red (hemorrhagic) - loose tissue/dual supply (lung, intestine, reperfusion); White (anemic) - solid organs (heart, spleen, kidney)
• Factors affecting outcome: rate of occlusion, dual blood supply, vulnerability of tissue (neurons 3-5 min), O2 content, collaterals

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• Dystrophic: dead/necrotic tissue, NORMAL calcium levels; e.g., TB, atherosclerosis, heart valves, psammoma bodies
• Metastatic: NORMAL tissue, ELEVATED calcium levels (hyperPTH, Vit D toxicity, sarcoidosis, myeloma); lung/kidneys/stomach/blood vessels
• Psammoma bodies: laminated, concentric calcification; papillary thyroid Ca, meningioma, ovarian serous carcinoma, mesothelioma

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• Virchow's triad: Endothelial injury + Stasis/turbulent flow + Hypercoagulability
• Pathogenesis: platelet adhesion (vWF) → activation → aggregation (GPIIb/IIIa, fibrinogen) → coagulation cascade
• Arterial thrombus: platelet-rich, white thrombus; venous thrombus: RBC-rich, red thrombus
• Lines of Zahn: alternating pale (platelets+fibrin) and red (RBCs) layers - seen in arterial thrombus

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• Platelet function disorders: Bernard-Soulier (↓GPIb - adhesion defect), Glanzmann's thrombasthenia (↓GPIIb/IIIa - aggregation defect)
• Chemotaxis: directed movement of leukocytes along chemical gradient
• Chemotactic agents: C5a, LTB4, IL-8/CXCL8, fMLP (bacterial), platelet activating factor

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1. Self-sufficiency in growth signals (oncogene activation: Ras, Myc)
2. Insensitivity to anti-growth signals (loss of Rb, p16)
3. Evasion of apoptosis (Bcl-2↑, p53 loss)
4. Limitless replicative potential (telomerase)
5. Sustained angiogenesis (VEGF)
6. Tissue invasion and metastasis (MMPs, ↓E-cadherin)
7. Reprogramming energy metabolism (Warburg effect)
8. Evading immune destruction

• Angiogenesis: tumor >2mm needs blood supply; VEGF, bFGF stimulate new vessel formation; leaky, poorly organized vessels

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• Rickets (Vit D deficiency in children): defective bone mineralization; bowing of legs, rachitic rosary, Harrison's sulcus, craniotabes
• Vit C deficiency (Scurvy): defective collagen synthesis; perifollicular hemorrhages, bleeding gums, hemarthrosis, corkscrew hairs, poor wound healing
• SAM (Severe Acute Malnutrition): Marasmus (calorie+protein) vs Kwashiorkor (protein only - edema, fatty liver, flaky paint dermatosis)

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• Adenosine deaminase (ADA) deficiency most common cause
• No T cells and B cells (combined), severe infections from birth
• Reticular dysgenesis: most severe
• Features: susceptibility to ALL infections (viral, bacterial, fungal, protozoal)
• Omenn syndrome: leaky SCID

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• Lipids: fatty change (steatosis) - liver - alcoholism/obesity; Oil Red O stain
• Glycogen: diabetes, glycogen storage diseases; PAS positive
• Proteins: Russell bodies (Ig in plasma cells), Mallory bodies (keratin in hepatocytes)
• Pigments:
  • Exogenous: Carbon (anthracosis), Tattoo pigment, Silica
  • Endogenous: Lipofuscin (wear-and-tear, brown), Melanin, Hemosiderin (Prussian blue stain), Bilirubin

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• Systemic activation of coagulation → widespread microthrombi → consumption of clotting factors + platelets → bleeding
• Causes: Sepsis, Obstetric complications (abruptio placentae, AFE), Malignancy (APML M3), Massive trauma, Snake bite
• Labs: ↑PT, ↑aPTT, ↑D-dimer, ↓fibrinogen, ↓platelets, schistocytes on smear
• Treatment: Treat underlying cause + FFP + platelets + cryoprecipitate

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• Direct acting: alkylating agents, nitrosamines
• Procarcinogens need metabolic activation (CYP450)
• Classic example: Aniline dyes → bladder Ca; Aflatoxin B1 → HCC; Asbestos → mesothelioma

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• Sources: paint, batteries, contaminated water
• Mechanism: inhibits heme synthesis (ALA dehydratase, ferrochelatase) → sideroblastic anemia
• Features: Burton's lines (blue-black gingival line), peripheral motor neuropathy (wrist drop), encephalopathy in children
• Labs: basophilic stippling of RBCs, ↑ALA in urine, ↑blood lead level
• Treatment: DMSA, EDTA chelation

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• Trisomy 21 (95% - non-disjunction), Translocation (4%), Mosaicism (1%)
• Risk increases with maternal age
• Features: simian crease, hypotonia, epicanthic folds, flat face, gap between 1st-2nd toe, intellectual disability
• Associated: ASD/VSD (most common heart defect), duodenal atresia ("double bubble"), Hirschsprung's, leukemia (ALL), early Alzheimer's

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• Primary intention: clean edges, minimal tissue loss; Secondary intention: large defect, granulation tissue, contracture
• Phases: Hemostasis (0-1hr) → Inflammation (1-3 days) → Proliferation (3-21 days: granulation, angiogenesis, collagen) → Remodeling (21 days - 2 years: type III → type I collagen)
• Key cells: Platelets (initiate) → Macrophages (most important for healing) → Fibroblasts (collagen) → Myofibroblasts (contraction)
• Factors delaying: Infection, Poor blood supply, Malnutrition (protein/Vit C/Zinc deficiency), Steroids, DM, Foreign body
• Complications: Keloid (beyond wound margins, Type III collagen), Hypertrophic scar (within), Contracture, Dehiscence, Ulceration

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• X-ray: punched-out lytic lesions ("raindrops on skull"), pathological fractures, Erlenmeyer flask of spine
• Bone marrow: >10% plasma cells (abnormal); Russell bodies, "clock-face" chromatin
• Diagnosis: M-spike on SPEP, Bence-Jones proteinuria, bone marrow biopsy
• CRAB: Hypercalcemia, Renal failure, Anemia, Bone lesions

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• Acute hemolytic (most dangerous): ABO mismatch → intravascular hemolysis; fever, hypotension, flank pain, hemoglobinuria
• Febrile non-hemolytic: most common reaction; cytokines/anti-HLA antibodies; fever/chills
• Allergic: urticaria → anaphylaxis (IgA deficiency)
• TRALI: transfusion-related acute lung injury; within 6 hrs; non-cardiogenic pulmonary edema
• Investigation: re-crossmatch, DAT, urinalysis, repeat blood group
• Bombay blood group (hh): lack H antigen; can only receive Bombay blood; anti-H antibodies

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• 22-23 gauge needle, no anesthesia needed
• Applications: palpable lumps (thyroid, breast, lymph node, salivary gland)
• Advantages: quick, cheap, minimal complications, can avoid surgery
• Limitations: cannot assess architecture, sampling error, insufficient material
• Bethesda system for thyroid; BIRADS for breast reporting

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• Actinomyces israelii (gram positive, branching filamentous bacterium - NOT a true fungus)
• Sites: Cervicofacial (most common - lumpy jaw), Thoracic, Abdominopelvic
• Pathology: woody hard induration, sinus tracts, sulfur granules (yellow, macroscopic colonies)
• Gram stain: gram positive branching filaments
• Treatment: Prolonged penicillin

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• Neoplasia: autonomous, purposeless, excessive proliferation of cells
• Benign vs Malignant:

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• WBC >50,000/µL reactive (non-neoplastic) response
• Causes: severe infection (TB, pertussis), hemolysis, malignancy
• vs CML: LAP score HIGH in leukemoid (LOW in CML); no Philadelphia chromosome; no basophilia
• Smear: mature granulocytes predominate, toxic granulation, Dohle bodies

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• Focal collection of activated macrophages (epithelioid cells) ± giant cells ± lymphocytes
• Types: Caseating (TB, histoplasma), Non-caseating (sarcoidosis, Crohn's, berylliosis, foreign body)
• Giant cell types: Langhans (TB - nuclei at periphery), Foreign body (nuclei scattered), Touton (xanthoma - foam cells periphery)
• Pathogenesis: persistent antigen + T-cell activation → macrophage activation → IL-12 → Th1 response

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• AA released from membrane phospholipids by phospholipase A2
• COX pathway → Prostaglandins (PGE2, PGI2 - vasodilation, pain, fever) + Thromboxane A2 (platelet aggregation, vasoconstriction)
• LOX pathway → Leukotrienes: LTB4 (chemotaxis), LTC4/D4/E4 (bronchoconstriction, vascular permeability = "slow reacting substances")
• Lipoxins: anti-inflammatory, produced from AA via LOX

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PAPER 2

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• Group A Streptococcal pharyngitis → autoimmune cross-reaction (molecular mimicry)
• Jones criteria (Major): Carditis, Polyarthritis, Chorea, Erythema marginatum, Subcutaneous nodules
• Minor: fever, elevated ESR/CRP, prolonged PR interval
• Aschoff bodies: pathognomonic granulomas in heart (fibrinoid necrosis with Aschoff cells/Anitschkow cells)
• Mitral stenosis: most common late complication

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• Most common: LAD occlusion → anterior wall infarct
• Sequential histology:
  • 0-4 hrs: No change (EM shows mitochondrial swelling)
  • 4-12 hrs: Coagulation necrosis begins, wavy fibers
  • 12-24 hrs: Neutrophilic infiltration
  • 1-3 days: Macrophage infiltration
  • 3-10 days: Granulation tissue
  • 2 weeks: Fibrosis begins
  • 2+ months: Dense scar
• Enzymes: Troponin I/T (gold standard, rises 3-6 hrs, persists 7-14 days); CK-MB (rises 6 hrs, normalizes 72 hrs - for reinfarction)
• Complications: Arrhythmia (most common, first 24hrs), Heart failure, Cardiogenic shock, Ventricular rupture (3-5 days), Dressler syndrome (2-10 weeks)

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• Acute (S. aureus) vs Subacute (Strep viridans on damaged valves)
• Vegetations: mitral > aortic; large, irregular, destructive
• Janeway lesions (non-tender palmar/plantar macules), Osler nodes (tender finger nodules), Roth spots (retinal hemorrhage), splinter hemorrhages
• Duke criteria: major (positive blood cultures, echocardiology vegetation) + minor
• Complications: emboli, abscess, valve destruction, mycotic aneurysm

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• Causes: Smoking (#1), asbestos, radon, chromium
• Types:
  • Squamous cell (central, hilar, cavitates) - Keratin pearls, intercellular bridges; PTHrP hypercalcemia
  • Adenocarcinoma (peripheral, non-smokers, women) - gland formation; most common in non-smokers; EGFR mutations
  • Small cell/oat cell (central, aggressive, neuroendocrine) - SIADH, ACTH, Eaton-Lambert; Kulchitsky cells; never surgical
  • Large cell (peripheral, undifferentiated, diagnosis of exclusion)
• Pancoast tumor: apex → Horner syndrome + brachial plexus
• Staging: TNM; solitary pulmonary nodule < 3cm (coin lesion)

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• Permanent enlargement of airspaces distal to terminal bronchioles with wall destruction
• Types:
  • Centrilobular (centriacinar): center of lobule, smoking, upper lobes
  • Panacinar: entire lobule, α1-antitrypsin deficiency, lower lobes
  • Paraseptal: adjacent to pleura, spontaneous pneumothorax in young
  • Paracicatrical: around scars
• Pathogenesis: protease-antiprotease imbalance → elastin destruction
• Gross: hyperinflated lungs, barrel chest, "pink puffer"

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• Lobar pneumonia: Streptococcus pneumoniae (Diplococcus)
• Stages:
  1. Congestion (24 hrs): vascular congestion, edema fluid, few bacteria
  2. Red hepatization (2-4 days): RBCs + fibrin + PMN; lung liver-like
  3. Grey hepatization (4-8 days): PMN + fibrin; RBCs lysed
  4. Resolution (8-10 days): enzymatic digestion, macrophages clear debris
• Complications: Empyema, Lung abscess, Organizing pneumonia, Septicemia, Meningitis
• Bronchopneumonia: patchy, bilateral, lower lobes; H. influenzae, S. aureus, Klebsiella

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• Crohn's morphology: Cobblestone mucosa, creeping fat, skip lesions, string sign on barium, rose thorn ulcers

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• Adenoma → carcinoma sequence (FAP: APC gene, chromosome 5q)
• Microsatellite instability pathway: HNPCC (Lynch syndrome) - MLH1, MSH2
• Morphology: left colon - annular ("apple-core" on barium), right colon - polypoid fungating mass
• Spreads to liver first (portal drainage)
• Dukes staging (or TNM): A - mucosa; B - through muscularis; C - lymph nodes; D - distant mets

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• H. pylori (90% duodenal, 70% gastric ulcers) + NSAIDs
• H. pylori: disrupts mucus, ↑ gastrin, ↓ somatostatin
• Gastric ulcer: lesser curvature, antrum; chronic - punched out, smooth edges, radiating folds
• Duodenal ulcer: 1st part, anterior wall (more common - perforation); posterior wall (bleeds - gastroduodenal artery)
• Complications: Bleeding (most common), Perforation, Obstruction (pyloric stenosis), Malignant change (gastric only)

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• Cirrhosis: diffuse fibrosis + nodular regeneration → loss of normal architecture
• Classification: Micronodular (<3mm - alcohol, hemochromatosis), Macronodular (>3mm - viral hepatitis), Mixed
• Alcoholic liver disease: Fatty change → Alcoholic hepatitis (Mallory bodies, neutrophilic infiltrate) → Cirrhosis
• Mallory-Denk bodies: perinuclear eosinophilic inclusions (damaged keratin)
• HCC: chronic HBV/HCV, cirrhosis, aflatoxin; AFP marker; Bile production by tumor cells (pathognomonic)

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• Causes: Gallstones (#1), Alcohol (#2), Trauma, Drugs, Hypercalcemia, Hyperlipidemia
• Pathogenesis: premature activation of trypsinogen → autodigestion
• Morphology: fat necrosis (chalky white deposits = calcium soap), hemorrhagic necrosis, "ground glass" appearance on CT
• Labs: ↑ serum amylase (first), ↑ lipase (more specific, lasts longer)
• Complications: pseudocyst (most common), abscess, ARDS, DIC, hypocalcemia

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• 2-3 weeks after throat/skin infection (Group A Strep)
• Type III hypersensitivity - immune complex deposition
• Nephritic syndrome: hematuria, hypertension, oliguria, mild proteinuria
• LM: hypercellular glomeruli ("flea-bitten kidney")
• IF: "lumpy-bumpy" granular pattern (IgG, C3)
• EM: subepithelial humps

• Rapid deterioration of renal function
• Crescents = proliferating parietal epithelial cells + fibrin in Bowman's space
• Types: Type I (anti-GBM - Goodpasture's - linear IF), Type II (immune complex - PSGN), Type III (ANCA - Wegener's/MPA - pauci-immune, negative IF)

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• Most common renal tumor in adults; male > female; 6th-7th decade
• VHL gene mutation; clear cell type most common
• Gross: upper pole, bright yellow, golden-yellow cut surface (lipid-rich)
• Microscopy: clear cells (abundant clear cytoplasm - glycogen/lipid), "chicken wire" vasculature
• Classic triad: hematuria + flank pain + palpable mass (only 10% show all three)
• Paraneoplastic: polycythemia (EPO), hypercalcemia (PTHrP), Stauffer syndrome (liver dysfunction)
• Spread: invades renal vein → IVC → right atrium ("tumor thrombus")

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• HPV (high risk: 16, 18) → squamocolumnar junction (transformation zone)
• CIN I → CIN II → CIN III → Invasive carcinoma
• Most common: Squamous cell carcinoma (80%); Adenocarcinoma (15%)
• Screening: Pap smear (from 21 yrs or 3 yrs after sexual debut); Bethesda system reporting
• Colposcopy + biopsy for confirmation
• Vaccination: Gardasil (4-valent: 6,11,16,18) or Cervarix (bivalent: 16,18) or 9-valent

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• Estrogen excess (anovulatory cycles, PCOS, obesity, exogenous estrogen)
• Simple → Complex → Atypical (most premalignant) → Endometrial carcinoma
• Risk: atypical complex hyperplasia → 30% risk of Ca

• Complete mole: 46XX (paternal), no fetus, all villi abnormal, high β-hCG, "snowstorm" on USG
• Partial mole: 69XXY (triploid), fetal parts present, some villi abnormal
• Risk of gestational trophoblastic neoplasia: complete 2-3%; partial <1%

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• HAV/HEV: feco-oral, acute only, no chronicity (HEV dangerous in pregnancy)
• HBV: parenteral/sexual/vertical; HBsAg, HBeAg, anti-HBc; Window period (anti-HBc only positive)
• HCV: parenteral (#1 cause transfusion hepatitis); high chronicity (80%)
• Histology: lobular hepatitis; Councilman bodies (acidophil bodies = apoptotic hepatocytes)
• Chronic viral hepatitis: portal inflammation + interface hepatitis (piecemeal necrosis) + fibrosis → cirrhosis
• Ground glass hepatocytes in HBsAg carriers

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• Most common female cancer; BRCA1 (chromosome 17), BRCA2 (chromosome 13)
• Invasive ductal carcinoma NOS: most common (70-80%)
• Morphology: scirrhous (hard, gritty), fibrous stroma, "dimpling" of skin
• Paget's disease of nipple: intraepidermal spread of carcinoma cells from underlying DCIS/invasive Ca; Paget cells (large, pale cells with halo)
• Fibroadenoma: most common benign tumor; young women; mobile, well-circumscribed
• Prognostic factors: lymph node status (#1), tumor size, ER/PR/HER2 (ER+/PR+ = good, HER2+ = Herceptin)

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• Epiphysis of long bones (distal femur, proximal tibia most common); 20-40 yrs
• Gross: soap bubble appearance; extends to articular cartilage
• Microscopy: multinucleated giant cells (osteoclast-like) evenly distributed + mononuclear stromal cells
• X-ray: eccentric, lytic, no periosteal reaction, "soap bubble"
• Bone tumor classification: Benign (Osteoma, Osteochondroma, Giant cell tumor) → Malignant (Osteosarcoma, Chondrosarcoma, Ewing's sarcoma)

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• MPGN (Type I): subendothelial deposits (HBV, HCV); "tram-track" appearance (double contour GBM); hypocomplementemia

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• Germ cell tumors (95%): Seminoma + Non-seminomatous (embryonal, yolk sac, teratoma, choriocarcinoma)
• Seminoma: most common; radiosensitive; αFP normal, β-hCG slight ↑
• Microscopy: large clear cells with central nucleus + fibrous septa with lymphocytes
• Non-seminomatous: AFP raised in yolk sac tumor; β-hCG raised in choriocarcinoma
• Classic triad: painless testicular enlargement + AFP/β-hCG + chest X-ray (lung mets)

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• Microscopy: Orphan Annie eye nuclei (ground glass), nuclear grooves, Psammoma bodies, papillary architecture

• Amyloid deposits in stroma; Congo red positive

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• Type 1: autoimmune destruction of beta cells (HLA DR3/DR4); insulitis; absolute insulin deficiency
• Type 2: insulin resistance + relative deficiency; islet amyloid (amylin/IAPP deposits)
• Late complications (from chronic hyperglycemia → non-enzymatic glycation + osmotic damage):
  • Macrovascular: atherosclerosis (MI, stroke, PVD)
  • Microvascular: Diabetic nephropathy (Kimmelstiel-Wilson nodules), Retinopathy (neovascularization), Neuropathy
  • Others: Cataracts, Infections (foot ulcers, mucormycosis), Xanthomas

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• 2nd most common benign parotid tumor; bilateral in 10%; smokers
• Microscopy: double layer of oncocytic epithelium + dense lymphoid stroma with germinal centers
• Technetium-99m scan: "hot" nodule (oncocytes concentrate Tc)

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• Acute: ascending infection (E. coli 85%); flank pain, fever, pyuria, WBC casts; cortical abscesses
• Chronic: recurrent infections + VUR → scarring, tubular atrophy, interstitial fibrosis; "thyroid-like" tubules (colloid casts)
• Xanthogranulomatous pyelonephritis: Proteus, obstructive uropathy; foam cells, orange-yellow masses

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• Acute: hematogenous (children - metaphysis); S. aureus most common; sickle cell - Salmonella
• Pathogenesis: bacteria lodge in metaphysis → inflammation → pus → periosteal elevation → avascular necrosis
• Morphology: Sequestrum (dead bone) + Involucrum (new bone around) + Cloaca (sinus tract)
• Chronic: persistence of Sequestrum; Brodie's abscess (localized intraosseous abscess)

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• Benign; arises from arachnoid cap cells; spinal cord + intracranial
• WHO Grade I (most), Grade II, Grade III (anaplastic)
• Microscopy: whorls, psammoma bodies, meningothelial cells
• Location: parasagittal, sphenoid ridge, olfactory groove
• MRI: dural tail sign; enhances uniformly with contrast

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• Coal macule → Coal nodule → Progressive massive fibrosis (PMF)
• Caplan syndrome: CWP + rheumatoid arthritis
• Pathogenesis: carbon + silica → macrophage activation → fibrosis

• Malignant tumor of mesothelium; strongly associated with asbestos (crocidolite worst)
• Pleural most common; long latency (20-40 years)
• Microscopy: biphasic (epithelioid + sarcomatous); calretinin+, CK5/6+, WT-1+
• Prognosis: very poor

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• Gram-negative curved rod; urease positive
• Antral gastritis → Chronic active gastritis → Gastric ulcer
• Causes: Chronic gastritis (Type B), Gastric ulcer, Gastric carcinoma (intestinal type), MALT lymphoma
• Morphology: chronic active gastritis; neutrophil infiltration + lymphoid follicles ("follicular gastritis"); intestinal metaplasia (premalignant)

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• Excess cortisol; Cushing disease = pituitary ACTH excess (most common cause)
• Features: central obesity, moon face, buffalo hump, purple striae, hirsutism, hypertension, diabetes, osteoporosis, immunosuppression
• Causes: Exogenous steroids (#1) > Pituitary adenoma > Adrenal adenoma > Ectopic ACTH (small cell lung)
• Diagnosis: midnight cortisol, 24hr urinary free cortisol, overnight dexamethasone suppression test

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• PBC: autoimmune destruction of small intrahepatic bile ducts; anti-mitochondrial antibodies (AMA M2); middle-aged women
• Features: pruritus, jaundice, xanthelasma, elevated ALP
• Pathology: granulomatous destruction of bile ducts → "florid duct lesion" → cirrhosis

• Alcohol: acetaldehyde toxicity → ↑ NADH → inhibit fatty acid oxidation → fat accumulation
• Stain: Oil Red O (frozen sections); Sudan III; H&E shows clear vacuoles
• NASH: metabolic syndrome + steatohepatitis without alcohol

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• Chronic inflammatory airways disease; reversible bronchoconstriction
• Atopic (extrinsic): Type I hypersensitivity; IgE + mast cells + Th2 (IL-4, IL-5, IL-13)
• Non-atopic (intrinsic): infection/irritants
• Early phase (<30 min): histamine, leukotrienes (LTC4/D4/E4) → bronchoconstriction, mucus
• Late phase (4-8 hrs): eosinophil infiltration, further inflammation
• Morphology: Charcot-Leyden crystals (eosinophil granules), Curschmann's spirals (mucus plugs), Creola bodies

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• Stable plaque: large lipid core + thick fibrous cap + calcification; less likely to rupture
• Unstable (vulnerable) plaque: large lipid core + thin fibrous cap + inflammatory cells (macrophages/foam cells) at shoulders; prone to rupture → ACS
• Morphology: fatty streak → fibrous plaque → atheroma (lipid core with necrotic center + fibrous cap + foam cells + calcification)
• Foam cells: lipid-laden macrophages (from oxidized LDL uptake via scavenger receptors)

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• Gluten sensitivity (gliadin) → T-cell mediated mucosal damage
• Anti-tissue transglutaminase (anti-tTG) - most sensitive; anti-endomysial (most specific); anti-gliadin
• Morphology: villous atrophy + crypt hyperplasia + increased intraepithelial lymphocytes (>25 per 100 enterocytes)
• Risk: lymphoma (EATL - enteropathy-associated T-cell lymphoma), adenocarcinoma small bowel

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• Benign: Pleomorphic adenoma (most common overall, most in parotid), Warthin's tumor
• Malignant: Mucoepidermoid carcinoma (most common malignant), Adenoid cystic carcinoma
• Pleomorphic adenoma: mixed tumor; epithelial + mesenchymal (chondromyxoid stroma); firm, mobile
• Microscopy: epithelial cells in duct-like structures + myoepithelial cells + chondroid/myxoid stroma
• Risk: malignant transformation (carcinoma ex pleomorphic adenoma); recurrence if enucleated

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• Actinic (solar) keratosis → SCC; Bowen's disease (SCC in situ)
• Dysplastic nevi → melanoma

• Leukoplakia (white patch, cannot be wiped off) - most common; epithelial dysplasia
• Erythroplakia (red patch) - higher malignant potential than leukoplakia
• Oral submucous fibrosis (betel nut)
• Syphilitic glossitis

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• WHO Grade IV; most common and most malignant brain tumor in adults
• "Butterfly" pattern crossing corpus callosum
• Microscopy: pseudopalisading necrosis + microvascular proliferation (glomeruloid vessels); GFAP+
• IDH wildtype (primary GBM - de novo); IDH mutant (secondary - from lower grade astrocytoma)

• Most common intraocular tumor in children; RB1 gene (chromosome 13q14) - two-hit hypothesis
• Familial (bilateral) vs sporadic (unilateral)
• Microscopy: Flexner-Wintersteiner rosettes (tumor cells around central lumen)
• Leukocoria (white pupillary reflex = cat's eye reflex)

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• Permanent dilation of bronchi/bronchioles due to destruction of muscular and elastic walls
• Causes: Cystic fibrosis (#1 in West), post-infection (TB, measles, pertussis), ABPA, Kartagener syndrome (immotile cilia)
• Morphology: cylindrical, varicose, saccular (most severe)
• Lower lobes most common; "tram-track" on plain X-ray; "signet ring" on HRCT
• Features: chronic productive cough with copious purulent sputum, hemoptysis, recurrent pneumonia

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• Cholesterol stones: most common (80%); associated with female/fat/forty/fertile/fair
• Pigment stones: Black (hemolysis - unconjugated bilirubin), Brown (infection/stasis - conjugated bilirubin)
• Complications: Biliary colic, cholecystitis, Mirizzi syndrome, Charcot's triad (cholangitis), Courvoisier's law, Gallstone ileus, cholangiocarcinoma

• Calcium oxalate (most common, radiopaque), Struvite (triple phosphate = staghorn calculus - Proteus urease), Uric acid (radiolucent), Cystine
• Staghorn calculus: fills entire renal pelvis + calyces; Proteus/Klebsiella (urease organisms)

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• Restrictive pattern: ↓TLC, ↓FVC, FEV1/FVC normal/increased
• UIP (Usual Interstitial Pneumonia)/IPF: honeycomb fibrosis, temporal heterogeneity; lower lobes; poor prognosis
• NSIP: more uniform inflammation/fibrosis; better prognosis; associated with CTD (scleroderma, polymyositis)
• DIP: smoking-related; macrophages fill alveoli; better prognosis with steroid
• Sarcoidosis: non-caseating granulomas; bilateral hilar lymphadenopathy; ACE↑; Schaumann bodies, asteroid bodies

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• Dysgerminoma (equivalent to seminoma): LDH/PLAP markers
• Yolk sac tumor: AFP marker; Schiller-Duval bodies (perivascular glomeruloid structures)
• Choriocarcinoma: β-hCG marker
• Mature cystic teratoma (dermoid cyst): most common benign GCT; contains hair, teeth, sebaceous material; from all 3 germ layers; Rokitansky protuberance; risk of SCC transformation

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• Metabolic syndrome (obesity, DM, hyperlipidemia) → insulin resistance → hepatic fat accumulation → oxidative stress → inflammation → fibrosis
• Histology same as alcoholic hepatitis but no alcohol history

• Complications: Esophageal varices (rupture = most dangerous), Ascites, Splenomegaly, Caput medusae, Hepatic encephalopathy, Hepatorenal syndrome

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• Most common cause of hypothyroidism in iodine-sufficient areas
• Autoimmune: anti-TPO (anti-microsomal), anti-thyroglobulin antibodies
• Pathogenesis: Th1-mediated destruction of thyroid follicles
• Morphology: lymphocytic infiltration + germinal centers + Hurthle cell change (oxyphilic metaplasia of follicular cells)
• Risk: Primary thyroid lymphoma (B-cell, MALT type)

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• Most common primary malignant bone tumor (excluding myeloma)
• Bimodal: 2nd decade (primary) + elderly (secondary to Paget's/radiation)
• Metaphysis of long bones (distal femur, proximal tibia); "skip lesions"
• X-ray: Codman's triangle (periosteal elevation), sunburst pattern
• Microscopy: malignant osteoid/bone formation by sarcoma cells
• Types: Osteoblastic, Chondroblastic, Fibroblastic, Telangiectatic

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• Most common skin cancer (and most common cancer overall); sun-exposed areas; face
• Locally invasive, RARELY metastasizes ("rodent ulcer")
• Risk: UV light (UVB), arsenic, immunosuppression
• Microscopy: nests of basaloid cells with peripheral palisading + retraction artifact
• Morpheaform: most aggressive subtype
• Gorlin syndrome: multiple BCCs + odontogenic keratocysts + rib anomalies (PTCH1 mutation)

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• Tumor of adrenal medulla chromaffin cells; secretes catecholamines (epinephrine/norepinephrine)
• Rule of 10s: 10% bilateral, 10% extra-adrenal (paraganglioma), 10% malignant, 10% familial, 10% in children
• Features: hypertensive crises (paroxysmal), headache, palpitations, sweating (triad)
• Diagnosis: 24hr urine catecholamines, metanephrines (best), vanillylmandelic acid (VMA)
• Microscopy: nests ("Zellballen") of large pleomorphic cells; S100+ sustentacular cells; chromogranin+
• Associated: MEN2A/2B, VHL, NF1, SDH mutations

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• Polyp: mucosal protrusion into lumen
• Classification: Neoplastic (adenomatous - tubular, villous, tubulovillous) vs Non-neoplastic (hyperplastic, hamartomatous, inflammatory)
• Villous adenoma: highest malignant potential; "cauliflower"; secretory diarrhea
• Tubular adenoma: most common; lowest malignant risk
• Syndromes:
  • FAP (APC gene, AD): thousands of adenomas → 100% cancer risk by 40s; Gardner syndrome (FAP + osteomas + fibromatosis)
  • Peutz-Jeghers (STK11 gene): hamartomatous polyps + mucocutaneous pigmentation (lips/buccal)

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• Most common primary brain tumor group
• WHO grading:
  • Grade I: Pilocytic astrocytoma (children, cerebellum, excellent prognosis; Rosenthal fibers, biphasic)
  • Grade II: Diffuse astrocytoma (IDH mutant; better prognosis)
  • Grade III: Anaplastic astrocytoma
  • Grade IV: Glioblastoma (see Q37)
• IDH mutation: marker of secondary GBM and lower grade gliomas; better prognosis than IDH wild-type
• GFAP positive

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• HCM: "banana-shaped" LV; LVOT obstruction; MV systolic anterior motion (SAM); disorganized myocyte arrangement

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• Rare fibroepithelial tumor of breast; older women (40-50 yrs)
• "Leaf-like" (phyllodes) stromal projections
• Spectrum: benign, borderline, malignant
• Morphology: hypercellular stroma + epithelial clefts; "leaf-like" architecture
• Vs fibroadenoma: larger, older patient, stromal hypercellularity, mitoses, recurrence
• Malignant phyllodes: stromal sarcomatous change; hematogenous spread (not lymphatic)

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HIGH-YIELD STAINS SUMMARY

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HIGH-YIELD GENETICS SUMMARY

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HIGH-YIELD TUMOR MARKERS

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PATHOLOGY EXAM CHEAT SHEET - PRIORITY RANKED

(NTRUHS 2K23 - Most Important Questions Only)

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TIER 1 - MUST KNOW (Almost certain to appear)

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• Cardinal signs: Rubor, Calor, Dolor, Tumor, Functio laesa
• Vascular events: vasoconstriction → vasodilation → increased permeability → stasis → exudate
• Cellular events: Margination → Rolling (selectins) → Adhesion (integrins/ICAM) → Transmigration → Chemotaxis → Phagocytosis
• Chemotaxis agents: C5a, LTB4, IL-8, bacterial products
• Phagocytosis: opsonins (IgG, C3b) → engulfment → ROS/MPO killing
• Fate: Resolution / Suppuration / Fibrosis / Chronic inflammation
• Morphological types: Serous, Fibrinous, Suppurative, Pseudomembranous

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• LAD occlusion = anterior wall (most common)
• Sequential histology:
  • 0-4 hrs: no change (wavy fibers)
  • 12-24 hrs: neutrophil infiltration
  • 1-3 days: macrophages
  • 3-10 days: granulation tissue
  • 2+ months: dense scar
• Enzymes: Troponin I/T (gold standard, rises 3-6 hrs, lasts 14 days); CK-MB (reinfarction)
• Complications: Arrhythmia (first 24 hrs, most common), Heart failure, Ventricular rupture (3-5 days), Dressler syndrome (2-10 wks)

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• Ghon complex: subpleural focus + hilar lymph nodes = primary complex
• Microscopy: caseating granuloma + epithelioid cells + Langhans giant cells + lymphocytes
• ZN stain: red bacilli on blue background
• Diagnosis: ZN stain, Lowenstein-Jensen culture (gold standard), CBNAAT/GeneXpert, Mantoux
• Manifestations: pulmonary, miliary, Pott's disease, meningitis, intestinal

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• Phases: Hemostasis → Inflammation (1-3 days) → Proliferation (3-21 days) → Remodeling (months)
• Most important cell: Macrophage
• Fibroblasts = collagen; Myofibroblasts = contraction
• Factors delaying: infection, malnutrition (Vit C/Zinc/protein), DM, steroids, poor blood supply
• Complications: Keloid (beyond margins, Type III collagen), Hypertrophic scar (within margins), Contracture

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• Coagulative: most organs, infarcts, ghost cells (architecture preserved)
• Liquefactive: brain, bacterial abscess
• Caseous: TB - cheese-like, no architecture
• Fat necrosis: pancreas/breast, chalky white calcium soap deposits
• Fibrinoid: malignant HTN, immune vasculitis
• Gangrenous: dry (coagulative) vs wet (+ liquefactive)

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• Type I: IgE on mast cells → antigen cross-links → degranulation → histamine (immediate) + leukotrienes (late)

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• Organism: Streptococcus pneumoniae
• Stages: Congestion (24 hrs) → Red hepatization (2-4 days) → Grey hepatization (4-8 days) → Resolution (8-10 days)
• Complications: empyema, lung abscess, septicemia, organizing pneumonia

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• Cirrhosis: diffuse fibrosis + nodular regeneration
• Micronodular (<3mm): alcohol, hemochromatosis; Macronodular (>3mm): viral hepatitis
• Alcoholic progression: Fatty change → Alcoholic hepatitis (Mallory bodies) → Cirrhosis
• HCC: chronic HBV/HCV, aflatoxin; marker = AFP; bile production by tumor (pathognomonic)

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• Routes: Lymphatic (carcinomas), Hematogenous (sarcomas), Transcoelomic (ovary → peritoneum), Direct
• Steps: Invasion → intravasation → survival → extravasation → colonization
• EMT: loss of E-cadherin → mesenchymal change
• Common patterns: Breast → bone/lung/brain; Lung → brain/adrenals; Colon → liver first; Prostate → bone (osteoblastic)

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• HPV 16, 18 → squamocolumnar junction (transformation zone)
• CIN I → II → III → Invasive carcinoma
• Squamous cell (80%), Adenocarcinoma (15%)
• Screening: Pap smear from age 21
• Vaccine: Gardasil (6,11,16,18), Cervarix (16,18), 9-valent

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TIER 2 - HIGH YIELD (Very likely to appear)

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• Intrinsic pathway: mitochondria → cytochrome C → caspases (p53 triggers)
• Extrinsic pathway: Fas/TNFR → caspase 8
• Bcl-2 = anti-apoptotic; Bax = pro-apoptotic

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• Misfolded proteins in beta-pleated sheet configuration
• Primary (AL - myeloma), Secondary (AA - TB/RA chronic inflammation), Familial (TTR), Senile
• Congo red stain → apple-green birefringence under polarized light
• Organs: waxy "lardaceous spleen," nephrotic syndrome, cardiomegaly

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• Causes: Sepsis, obstetric (abruptio, AFE), APML (M3), massive trauma, snake bite
• Labs: ↑PT, ↑aPTT, ↑D-dimer, ↓fibrinogen, ↓platelets, schistocytes
• Treatment: treat cause + FFP + platelets + cryoprecipitate

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• t(9;22) → BCR-ABL → constitutive tyrosine kinase
• Massive splenomegaly, leukocytosis (all stages of myeloid), low LAP score, basophilia
• Treatment: Imatinib (TKI)
• Blast crisis = transformation to AML/ALL

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• ANA (most sensitive); Anti-dsDNA + Anti-Sm (most specific)
• Lupus nephritis Class IV (diffuse) = worst, "wire loop" lesions
• Features: butterfly rash, polyarthritis, serositis, renal, neuro, hematological

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• H. pylori (90% DU, 70% GU) + NSAIDs
• Duodenal: 1st part, anterior wall (perforation), posterior wall (bleeds - gastroduodenal artery)
• Gastric: lesser curvature, punched out with smooth edges
• Complications: Bleeding (most common) → Perforation → Obstruction → Malignant change (gastric only)

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• B12 or Folate deficiency → impaired DNA synthesis
• Blood: macro-ovalocytes, hypersegmented neutrophils (>5 lobes), pancytopenia
• B12 deficiency only: subacute combined degeneration of spinal cord
• Pernicious anemia: anti-intrinsic factor antibodies → B12 malabsorption

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• Macrovascular: atherosclerosis (MI, stroke, PVD)
• Microvascular: Nephropathy (Kimmelstiel-Wilson nodules), Retinopathy (neovascularization), Neuropathy
• Type 1: autoimmune, HLA DR3/DR4; Type 2: insulin resistance + islet amyloid (amylin)

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• Invasive ductal carcinoma NOS (most common, 70-80%)
• BRCA1 (chr 17), BRCA2 (chr 13)
• Paget's disease: intraepidermal Paget cells (large, pale with halo) from underlying DCIS
• Prognostic: lymph node status (#1), tumor size, ER/PR/HER2
• Fibroadenoma: most common benign, young women, mobile

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• PSGN: 2-3 weeks after strep infection; lumpy-bumpy IF (IgG, C3); subepithelial humps on EM; nephritic syndrome
• Crescentic GN: Type I (anti-GBM, linear IF - Goodpasture's), Type II (immune complex), Type III (ANCA, pauci-immune)

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TIER 3 - IMPORTANT (Likely to appear)

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• Endothelial injury + Stasis/turbulence + Hypercoagulability
• Arterial thrombus = white (platelet-rich); Venous = red (RBC-rich)
• Lines of Zahn: alternating pale/red layers (arterial thrombus only)

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• CD4 <200 = AIDS; gp120 binds CD4 + CCR5/CXCR4
• AIDS-defining: PCP, CMV retinitis, Toxoplasma, Cryptococcal meningitis, Kaposi sarcoma

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• Peripheral smear: microcytic hypochromic, pencil cells, target cells
• Labs: ↓serum iron, ↓ferritin, ↑TIBC, ↓MCV

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• 2nd decade, metaphysis (distal femur, proximal tibia)
• X-ray: Codman's triangle + sunburst pattern
• Microscopy: malignant osteoid production by sarcoma cells

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• Squamous: central, keratin pearls, PTHrP (hypercalcemia)
• Adenocarcinoma: peripheral, non-smokers, EGFR mutations
• Small cell: SIADH + ACTH + Eaton-Lambert; never surgical
• Pancoast: apex → Horner syndrome

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• VHL gene; clear cells; bright yellow gross appearance
• Classic triad: hematuria + flank pain + mass
• Spreads via renal vein → IVC; polycythemia (EPO)

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1. Self-sufficiency in growth (oncogenes: Ras, Myc)
2. Insensitivity to anti-growth signals (Rb loss)
3. Evasion of apoptosis (Bcl-2↑, p53 loss)
4. Limitless replication (telomerase)
5. Sustained angiogenesis (VEGF)
6. Invasion + metastasis (MMPs, ↓E-cadherin)
7. Warburg effect (aerobic glycolysis)
8. Immune evasion

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• Stain: Fite-Faraco (modified ZN)

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• COX pathway → PGs (PGE2 - pain, fever, vasodilation) + TXA2 (platelet aggregation)
• LOX pathway → LTB4 (chemotaxis) + LTC4/D4/E4 (bronchoconstriction - slow reacting substances)
• NSAIDs block COX; Steroids block phospholipase A2

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• Centrilobular: smoking, upper lobes
• Panacinar: α1-antitrypsin deficiency, lower lobes
• Paraseptal: spontaneous pneumothorax in young
• Pathogenesis: protease-antiprotease imbalance → elastin destruction

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• Most common thyroid cancer (80%); RET/PTC mutation; lymphatic spread
• Microscopy: Orphan Annie eye nuclei + nuclear grooves + Psammoma bodies

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• Chemical: Initiation (irreversible mutation) + Promotion (reversible, clonal expansion)
• UV → pyrimidine dimers → skin cancer; Ionizing → double strand breaks → leukemia
• Microbial: HPV (cervical), EBV (Burkitt's, NPC), HBV/HCV (HCC), H. pylori (gastric Ca, MALT)

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• Trisomy 21; non-disjunction (95%)
• Features: simian crease, hypotonia, flat face, epicanthic folds
• Associated: ASD/VSD (most common cardiac), duodenal atresia, ALL, early Alzheimer's

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• Group A strep → molecular mimicry → autoimmune
• Aschoff bodies (pathognomonic) in heart
• Jones criteria major: Carditis, Polyarthritis, Chorea, Erythema marginatum, Subcutaneous nodules
• Late: mitral stenosis (most common)

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• RB1 gene (chr 13q14); two-hit hypothesis
• Leukocoria (white pupillary reflex)
• Microscopy: Flexner-Wintersteiner rosettes

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• S. aureus most common; sickle cell = Salmonella
• Sequestrum (dead bone) + Involucrum (new bone) + Cloaca (sinus tract)
• Brodie's abscess = localized intraosseous abscess (chronic)

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• After long bone fractures (48-72 hrs delay)
• Triad: Hypoxia + neurological changes + petechial rash
• Stain: Sudan III / Oil Red O

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QUICK REFERENCE TABLES

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