Cell Injury and Adaptation
🟢 Lite — Quick Review (1h–1d)
Rapid summary for last-minute revision before your exam.
Cell Injury and Adaptation — Key Facts for FMGE Core concept: Cells adapt to stress through hypertrophy, hyperplasia, atrophy, or metaplasia; injury leads to reversible or irreversible damage High-yield point: Know the difference between reversible cell injury (degeneration) and irreversible cell injury (necrosis) ⚡ Exam tip: Necrosis types and their morphological features are frequently tested in FMGE
🟡 Standard — Regular Study (2d–2mo)
Standard content for students with a few days to months.
Cell Injury and Adaptation — FMGE Study Guide
Causes of Cell Injury
Hypoxic Injury
- Ischemia: Reduced blood flow (most common cause in myocardial infarction, stroke)
- Hypoxia: Low oxygen tension (anemia, respiratory diseases)
- Mechanism: Anaerobic glycolysis → ATP depletion → failure of Na⁺/K⁺ pump → cellular swelling
- Reversible if oxygen restored within 6 minutes; beyond 20-30 minutes → irreversible
Free Radical Injury
- Reactive Oxygen Species (ROS): Superoxide (O₂⁻), hydrogen peroxide (H₂O₂), hydroxyl radical (OH•)
- Sources: Normal metabolism, inflammation, radiation, chemicals, metals
- Damage: Lipid peroxidation, protein oxidation, DNA damage
- Antioxidants: Superoxide dismutase, catalase, glutathione peroxidase, vitamins A, C, E
Physical Injury
- Mechanical trauma, temperature extremes, electric shock, radiation
- Burns cause protein denaturation and血流stasis
Chemical Injury
- Direct toxins (cyanide, arsenic)
- Indirect via metabolic activation (CCl₄ → free radicals → liver necrosis)
- Drugs and heavy metals
Biological Injury
- Bacteria, viruses, parasites
- Bacterial toxins (clostridial lecithinase in gas gangrene)
Immunologic Injury
- Hypersensitivity reactions (Type I-IV)
- Autoimmune diseases
Reversible Cell Injury (Cellular Degeneration)
Morphological Features
Cellular swelling:
- Earliest change; due to ATP depletion → Na⁺/K⁺ pump failure
- Microscopically: swollen cells with pale, vacuolated cytoplasm
- Seen in: kidney, liver, heart after ischemic injury
Fatty change (Steatosis):
- Accumulation of triglycerides in cells
- Causes: Alcohol (liver), diabetes, obesity, malnutrition, toxins
- Gross: enlarged, yellow, greasy liver
- Micro: vacuoles pushing nucleus to periphery (zone 3 of liver acinus)
Hydropic change:
- Severe cellular swelling with vacuolation
- Seen in viral infections, toxins
Endoplasmic reticulum dilation:
- Dispersal of ribosomes → decreased protein synthesis
- Seen in toxic injury
Irreversible Cell Injury and Necrosis
Necrosis Types
Coagulative necrosis:
- Protein denaturation predominates over enzymatic digestion
- Architecture preserved for days
- Firm, pale, tissue outline maintained
- Classic example: Myocardial infarction (anoxia)
- Cause: Ischemia (except brain), toxins
Liquefactive necrosis:
- Enzymatic digestion predominates
- Tissue liquefied → abscess or cystic cavity
- Classic examples: Brain infarcts, Staphylococcus aureus abscesses
- Causes: Bacterial infections, hypoxic injury to CNS
Caseous necrosis:
- Cheese-like, crumbly appearance
- Neither architecture preserved nor liquefied
- Classic example: Tuberculosis (granulomatous inflammation)
- Microscopic: amorphous eosinophilic debris with granulomas
Fat necrosis:
- Enzymatic: Pancreatic lipases digest peripancreatic fat → saponification
- Classic example: Acute pancreatitis (calcium soaps appear as chalky white areas)
- Non-enzymatic: Trauma to breast, subcutaneous fat
Fibrinoid necrosis:
- Immune-mediated vascular damage
- Deposition of immune complexes and fibrin in vessel walls
- Examples: Malignant hypertension (kidney), polyarteritis nodosa, rheumatic heart disease
- Microscopic: pink (eosinophilic) deposits in vessel walls
Gangrenous necrosis:
- Dry gangrene: Coagulative necrosis of limb due to ischemia (diabetes, atherosclerosis)
- Wet gangrene: Superimposed infection with liquefactive component; foul-smelling, swollen
Apoptosis vs Necrosis
| Feature | Apoptosis | Necrosis |
|---|---|---|
| Nature | Programmed, physiological | Accidental, pathological |
| Cell size | Shrinks | Swells |
| Nucleus | Pyknosis → Karyorrhexis → Karyolysis | Karyolysis, pyknosis, karyorrhexis |
| Cell membrane | Intact blebs | Ruptures |
| Inflammation | None | Prominent |
| Energy | Active (ATP required) | Passive |
| Examples | Embryogenesis, menstruation, T-cell deletion | Infarction, infection, toxins |
Cell Death in Specific Tissues
Myocardium: Coagulative necrosis → granulation tissue by day 10 → fibrosis by 2 months Brain: Liquefactive necrosis Liver: Fatty change → coagulative necrosis Kidney: Severe ischemia → acute tubular necrosis (ATN)
Cellular Adaptations
Hypertrophy
- Increase in cell size WITHOUT cell division
- Stimulus: Increased workload, hormonal stimulation
- Examples: Left ventricular hypertrophy (HTN), skeletal muscle hypertrophy (exercise), uterine enlargement (pregnancy)
- Mechanism: Increased synthesis of contractile proteins and organelles
Hyperplasia
- Increase in cell NUMBER
- Stimulus: Growth factors, hormones, chronic irritation
- Examples: Endometrial hyperplasia (estrogen), goiter (TSH), skin hyperplasia (wound healing)
- Can be physiological or pathological (endometrial hyperplasia → carcinoma risk)
Atrophy
- Decrease in cell size due to decreased workload, nutrition, or hormonal stimulation
- Examples: Skeletal muscle disuse atrophy, brain atrophy in elderly, thymic atrophy with age
- Mechanism: Autophagy (self-digestion of organelles)
Metaplasia
- Replacement of one differentiated cell type with another
- Stimulus: Chronic irritation/stress (smoking, reflux)
- Examples: Squamous metaplasia of respiratory epithelium (smokers), Barrett’s esophagus (columnar → squamous)
- Often reversible; persistence can lead to dysplasia
Dysplasia
- Abnormal cell growth with loss of uniformity
- Grade: Mild, moderate, severe
- May progress to carcinoma in situ (CIS) → invasive carcinoma
- Important: Dysplasia ≠ carcinoma but is precancerous
Intracellular Accumulations
Lipids: Fatty change (steatosis) - liver, heart, kidney Proteins: Russell bodies (immunoglobulin in plasma cells), Mallory bodies (keratin in alcoholic liver) Glycogen: Glycogen storage diseases, diabetes (renal tubular cells) Pigments: Lipofuscin (aging), hemosiderin (iron overload), melanin, carbon (anthracosis) Calcium: Dystrophic (damaged tissue) vs Metastatic (hypercalcemia)
Pathological Calcification
Dystrophic calcification:
- Calcium deposits in damaged/necrotic tissue
- Normal serum calcium levels
- Examples: atherosclerotic plaques, old tuberculous lesions, damaged heart valves, necrotic tissue
Metastatic calcification:
- Calcium deposits in normal tissues due to hypercalcemia
- Associated with: hyperparathyroidism, vitamin D intoxication, sarcoidosis, renal failure, bone destruction
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