16/08/2026
General Pathology — USMLE Buzzwords 🔥
Cellular Adaptation
* ↑ cell size → Hypertrophy
* ↑ cell number → Hyperplasia
* ↓ cell size → Atrophy
* One mature cell type replaced by another → Metaplasia
* Smoking → bronchial squamous metaplasia
* Barrett esophagus → intestinal-type columnar metaplasia
* Exercise → skeletal muscle hypertrophy
* Pregnancy → uterine hypertrophy + hyperplasia
Cell Injury
* ATP depletion → Na⁺/K⁺ pump failure
* Na⁺/K⁺ pump failure → cellular swelling
* Ribosomal detachment → ↓ protein synthesis
* ER dilation → reversible cell injury
* Fat accumulation in liver → steatosis
* Severe mitochondrial damage → irreversible injury
* Ca²⁺ influx → activation of phospholipases/proteases/endonucleases
* ROS → lipid peroxidation + protein/DNA damage
* Reversible injury → cellular swelling + fatty change
Nuclear Changes
* Nuclear shrinkage → Pyknosis
* Nuclear fragmentation → Karyorrhexis
* Nuclear dissolution → Karyolysis
* Pyknosis → karyorrhexis → karyolysis
Necrosis
* Ischemia in most solid organs → Coagulative necrosis
* Myocardial infarction → coagulative necrosis
* Renal infarction → coagulative necrosis
* Splenic infarction → coagulative necrosis
* Brain infarction → Liquefactive necrosis
* Bacterial abscess → liquefactive necrosis
* TB granuloma → Caseous necrosis
* Cheese-like necrosis → caseous necrosis
* Acute pancreatitis → Fat necrosis
* Chalky white deposits → fat necrosis
* Saponification → fat necrosis
* Vasculitis → Fibrinoid necrosis
* Malignant hypertension → fibrinoid necrosis
* Dry gangrene → coagulative necrosis
* Wet gangrene → liquefactive component
* Gas gangrene → Clostridium perfringens
Apoptosis
* Programmed cell death → Apoptosis
* Cell shrinkage → apoptosis
* Chromatin condensation → apoptosis
* Apoptotic bodies → apoptosis
* No significant inflammation → apoptosis
* Intrinsic pathway → Mitochondria
* Cytochrome c release → Caspase-9
* Extrinsic pathway → Fas/TNF receptor
* Fas → Caspase-8
* Executioner caspases → 3, 6, 7
* p53 activation → apoptosis after severe DNA damage
* BCL-2 → inhibits apoptosis
* BAX/BAK → promote apoptosis
Free Radicals
* Superoxide → O₂⁻
* Hydrogen peroxide → H₂O₂
* Hydroxyl radical → OH•
* Superoxide dismutase → O₂⁻ → H₂O₂
* Catalase → H₂O₂ → H₂O + O₂
* Glutathione peroxidase → H₂O₂ → H₂O
* Iron + H₂O₂ → hydroxyl radicals → Fenton reaction
* Reperfusion after ischemia → ROS injury
Acute Inflammation
* Acute inflammation → Neutrophils
* Chronic inflammation → Macrophages + lymphocytes
* First vascular response → Vasodilation
* Increased vascular permeability → Exudation
* Protein-rich fluid → Exudate
* Low-protein fluid → Transudate
* Slow blood flow → Stasis
* Stasis → leukocyte margination
Leukocyte Recruitment
* Rolling → Selectins
* E-selectin → endothelial cells
* P-selectin → endothelial cells/platelets
* L-selectin → leukocytes
* Firm adhesion → Integrins
* Integrins bind ICAM-1/VCAM-1
* Diapedesis → PECAM-1/CD31
* Chemotaxis → movement toward inflammatory signal
* C5a → neutrophil chemotaxis
* LTB4 → neutrophil chemotaxis
* IL-8 → neutrophil chemotaxis
Complement
* C3b → Opsonization
* C3a → Anaphylatoxin
* C5a → Chemotaxis
* C5a → neutrophil activation
* C5b-9 → MAC
* MAC → cell lysis
* C3a + C5a → mast-cell degranulation
Inflammatory Mediators
* Histamine → vasodilation + ↑ vascular permeability
* Bradykinin → Pain
* Bradykinin → vasodilation + ↑ permeability
* PGE₂ → Fever + pain
* TXA₂ → platelet aggregation + vasoconstriction
* PGI₂ → vasodilation + ↓ platelet aggregation
* LTB4 → neutrophil chemotaxis
* LTC4/LTD4/LTE4 → Bronchoconstriction
* IL-1 → Fever
* TNF-α → endothelial activation + fever
* IL-6 → Acute-phase response
* IL-8 → neutrophil chemotaxis
* IFN-γ → Macrophage activation
* TGF-β → Fibrosis
Chronic Inflammation
* Chronic inflammation → macrophages + lymphocytes
* Chronic inflammation → tissue destruction
* Chronic inflammation → fibrosis
* Granuloma → activated macrophages surrounded by lymphocytes
* Epithelioid macrophages → granuloma
* Giant cells → fused macrophages
* IFN-γ → macrophage activation
* TNF-α → granuloma maintenance
High-Yield Healing
* Healing by first intention → clean surgical wound
* Healing by second intention → large wound/tissue loss
* Granulation tissue → new vessels + fibroblasts
* Granulation tissue ≠ granuloma
* VEGF → Angiogenesis
* FGF → fibroblast proliferation
* TGF-β → collagen synthesis + fibrosis
* Type III collagen → early wound
* Type I collagen → mature scar
* Vitamin C deficiency → impaired collagen hydroxylation
* Zinc deficiency → impaired wound healing
* Keloid → scar extends beyond original wound
* Hypertrophic scar → remains within original wound boundaries