Handwritten medical notes style image on "Cell Injury" for FMGE exam preparation. Neat handwriting on lined white paper with blue ink. Include the following organized sections with headings underlined: CELL INJURY - FMGE HIGH YIELD NOTES 1. CAUSES OF CELL INJURY (with small icons) - Hypoxia & Ischemia (most common) - O2 deprivation → ATP failure - Toxins - alcohol, drugs, CO, insecticides - Infections - bacteria, viruses, fungi, parasites - Immunologic - autoimmune, allergy, chronic inflammation - Genetic - mutations, chromosomal abnormalities - Nutritional - protein-calorie deficiency, vitamin deficiency - Physical agents - trauma, radiation, temperature extremes 2. REVERSIBLE vs IRREVERSIBLE INJURY (two-column table) Reversible: Cell swelling, fatty change, ER dilation, mitochondrial swelling, membrane blebbing, ribosomes detach, chromatin clumping Irreversible: Severe mitochondrial vacuolization, lysosomal rupture, nuclear changes (pyknosis/karyorrhexis/karyolysis), plasma membrane breakdown, cell death 3. MORPHOLOGY OF REVERSIBLE INJURY - Cellular swelling (Hydropic/vacuolar degeneration) - most common - Fatty change (lipid vacuoles) - especially liver - Eosinophilic cytoplasm, myelin figures 4. NECROSIS TYPES (table with star marks) ★ Coagulative - most common, MI, kidney (structure preserved, ghost cells) ★ Liquefactive - brain infarct, abscess (enzymatic digestion) ★ Caseous - TB (cheese-like, granuloma with Langhans giant cells) ★ Fat necrosis - pancreatic enzymes, breast trauma (saponification, chalky deposits) ★ Fibrinoid - autoimmune, hypertension (vessel walls) ★ Gangrenous - limb ischemia (wet/dry) 5. APOPTOSIS vs NECROSIS (comparison table) Apoptosis: Single cells, energy-dependent, chromatin condensation, cell shrinkage, apoptotic bodies, NO inflammation, phosphatidylserine flip, caspase-mediated, phagocytosed by macrophages Necrosis: Groups of cells, passive, nuclear lysis, cell swelling, spillage, INFLAMMATION present 6. APOPTOSIS PATHWAYS Intrinsic (mitochondrial): DNA damage → p53 → BAX/BAK activation → cytochrome c release → caspase-9 → caspase cascade Extrinsic (death receptor): FasL binds Fas (CD95)/TNF-R → caspase-8 → caspase cascade BCL-2 = anti-apoptotic (protects); BAX, BAK = pro-apoptotic 7. ISCHEMIA-REPERFUSION INJURY - Reperfusion after ischemia paradoxically worsens injury - Due to: ROS burst from reperfused blood, neutrophil influx, Ca2+ overload, complement activation 8. FREE RADICAL INJURY (ROS) - Sources: Radiation, metabolism, inflammation, drugs - Effects: Lipid peroxidation, DNA damage, protein crosslinking - Defense: SOD, catalase, glutathione peroxidase, Vit E/C FMGE MNEMONICS at bottom: "CAN LIP" = Coagulative, Always consider Necrosis types, Liquefactive (brain/pus), Caseous (TB), Fat necrosis, Fibrinoid (In vessels), Pan(creas) "PKAL" for nuclear changes in necrosis: Pyknosis → Karyorrhexis → Karyolysis Color code: Red for important points, blue for main text, green for mnemonics, orange boxes for tables

Handwritten medical notes on lined white paper in blue and red ink, neat student handwriting style, for FMGE exam. Title at top in bold underlined: "CELL INJURY - FMGE HIGH YIELD" Section 1 (red underlined heading): CAUSES OF CELL INJURY - Hypoxia/Ischemia - MOST COMMON cause - Toxins (alcohol, CO, drugs) - Infections (bacteria, virus, fungi) - Immunologic (autoimmune, allergy) - Genetic (mutations, chromosomal) - Nutritional (protein-calorie, vitamins) - Physical (trauma, radiation, temperature) Section 2 (red underlined heading): REVERSIBLE INJURY (Sublethal) Morphology: - Cellular swelling = Hydropic/Vacuolar degeneration (MOST COMMON) - Fatty change (lipid vacuoles - mainly liver) - Mitochondrial swelling - ER dilation, ribosome detachment - Membrane blebbing - Chromatin clumping (nuclear) - Myelin figures (phospholipid whorls) Section 3 (red underlined heading): NECROSIS TYPES - HIGH YIELD TABLE drawn as a neat 3-column hand-drawn table with columns: Type | Site | Key Feature Coagulative | Heart, Kidney, Spleen | Ghost cells, structure preserved ← MOST COMMON Liquefactive | Brain, Abscess | Enzymatic digestion, pus Caseous | TB lymph node, lung | Cheese-like, granuloma, Langhans giant cells Fat | Pancreas, Breast | Saponification, chalky Ca2+ deposits Fibrinoid | Blood vessels | Autoimmune, hypertension Gangrenous | Limb | Dry=coagulative; Wet=liquefactive Section 4 (red underlined heading): APOPTOSIS vs NECROSIS Hand-drawn two-column comparison box: APOPTOSIS: Single cells | Energy dependent | Cell shrinkage | Chromatin condensation | Apoptotic bodies | NO inflammation | Caspases involved | Phosphatidylserine flips out NECROSIS: Groups of cells | Passive/energy independent | Cell swelling | Nuclear lysis | Cell spillage | INFLAMMATION | No caspases Section 5 (red underlined heading): APOPTOSIS PATHWAYS Intrinsic (Mitochondrial): DNA damage → p53↑ → BAX/BAK activate → Cytochrome c released → Caspase-9 → Caspase cascade → APOPTOSIS BCL-2 = Anti-apoptotic (inhibits BAX) Extrinsic (Death receptor): FasL + Fas(CD95) / TNF → Caspase-8 → Caspase cascade → APOPTOSIS Section 6 (red underlined heading): NUCLEAR CHANGES IN NECROSIS Pyknosis (nuclear shrinkage/condensation) → Karyorrhexis (fragmentation) → Karyolysis (dissolution) Mnemonic: "PKL" = Pyknosis→Karyorrhexis→Karyolysis Section 7 (green ink): MNEMONICS BOX (boxed with green border) Necrosis types: "CAN LF FiG" = Coagulative, Abscess(Liquefactive), caseouN, Liquefactive-brain, Fat, Fibrinoid, Gangrenous Apoptosis: "SESCA-NIC" = Shrinkage, Energy-dep, Single cell, Chromatin condensation, Apoptotic bodies, No inflammation, caspases Bottom note in small writing: Source: Robbins Basic Pathology