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coagulative necrosis
denaturation of structural and enzymatic proteins (in ischemia)
  • Karyolysis: nuclear fading
  • Frayed PM
  • Ghost outlines of dead cells
Liquefactive necrosis
Complete digestion of dead cells to gelatinous mass caused by:
  • Bacterial infections that elaborate toxins
  • Fungal and bacterial infxns that elicit intense inflammation
  • Ischemic-hypoxic death of CNS
caseous necrosis
distinctive form of coagulative necrosis - cheesy appearance In TB and certain fungal infxns - forms granuloma
gangrenous necrosis
necrosis of a body part involves epidermis, dermis, subcutis, and deeper tissues dry: w/o infxn wet: w/ infxn
mitochondrial damage
damage --> high conductance channel --> loss of protons --> dec ATP --> NECROSIS   Inc permeability allows leak of cytochrome c
loss of Ca homeostasis
0.1 μm in cell 1300 μm out of cell Inside inc with injury which opens mitochondrial permeability transition pore
  Formed by normal processes 3 antioxidant enzymes break them down
  • -SOD: O2 --> H2O2
  • Glutathione peroxidase (mito): OH --> H2O2 -      -> H2O + O2
  • Catalase (peroxisome): H2O2 --> H2O + O2
Vitamins A, C, and E also help inhibit or inactivate ROS's Fe and Cu storage proteinsminimize OH• production
Ischemia-Reperfusion injury
1)Incoming O2 allows conversion of built up hypoxanthine to urate with superoxide byproduct - SOD produces H2O   2) superoxide + H2O2 = OH   3) O2 allows conversion of hypoxanthine to urate --> O2   Inflammation is amplified
Acetominophen Overdose
Therapeutic dose: 250-500 mg Toxic Dose: 15-25 g If too much is administered, glutathione in the liver cannot metabolize NAPQI (toxic metabolite of Acetominophen) quick enough and NAPQI binds proteins damaging cell membranes and mito --> liver cell necrosis 2-4 days Treat with N-acetylcysteine (precurser to glutathione)
Mitochondrial (Intrinsic) apoptotic pathway
Cell injury stimulates Bcl-2 --> Bax, Bak --> Mito --> cytochrome c --> initiator caspases --> executioner caspases --> endonuclease activation and breakdown of cytoskeleton
Death Receptor (Extrinsic) Apoptotic Pathway
Fas (CD95) and TNF receptor interactions --> adaptor proteins --> initiator caspases --> executioner caspases --> endonucleas activation and breakdown of cytoskeleton
FLIP - protein that inhibits death-receptor pathway by binding to procaspase-8
Initiator Caspases
c-8 (extrinsic) C-9 (Mito)
Executioner Caspases
c-3, c-6, and c-7
Bcl regulation of apoptosis
Bcl-2 and Bcl-x inhibit MPT and leakage of cyto c
lack of survival signals or irritation --> activation of BH3-only proteins (Bim, Bid, Bad) --> Bax and Bak activation which insert into mito memb to create ctyochrome c pore --> caspase activation
Cause of Disease
Sequence of events from initial stimulus to expression of a disease
Molecular Changes
Biochemical alterations in cells
Morphologic Changes
Structural alterations in cells and tissues
Clinical Manifestations
Symptoms and signs of disease that result from functional abnormalities
5 causes of pathologic atrophy
  • Dissue
  • Denervation
  • Decreased blood supply
  • Malnutrition
  • Pressure
Mechanism of Atrophy
Ubiquitin-proteosome pathway --> increased rate of protein degradation
  • Protein binds ubiquitin
  • is degraded in proteosome
Mechanism of Metaplasia
Genetic reprogramming of stem cells to differentiate into a different mature cell type
Morphological changes of reversible injury
  • Blebs
  • Swelling
  • Eosinophilia
  • Shrinkage (pyknosis)
  • Smudged chromatin
  • Increased basophilia
  • Lose microvilli
  • Mildly dilated mitochondria
Morphological changes in necrosis
  • Ruptured cytoplasmic membranes
  • Advanced nuclear pyknosis
  • fading of nuclear basophilia (karyolysis)
  • Swollen mitochondria
3 mechanisms that promote phagocytosis of apoptotic cells
  • Phosphatidylserine abnormally expressed on outer leaflet
  • Apoptotic cells express thrombospondin
  • Apoptotic bodies coated by Abs and C1q
Types of intracellular accumulations
Excess cellular constituent
  • H2O
  • Lipid
  • CHO
Abnormal substance (endogenous or exogenous) Pigments (endogenous or exogenous)
  • Carbon
  • Ink
  • Lipofuscin
  • Melanin
  • Iron
  • Bilirubin
Mechanisms of intracellular accum
  • Abnml metabolism
  • Defect in protein folding, transport
  • Lack of enzyme
  • Ingestion of indigestible materials
Dystrophic Calcifications
Local deposition in nonviable (dead or damaged) tissue despite nml serum Ca level
Metastatic calcification
Deposition in nml, viable tissues secondary to hypercalcemia
  • Excess PTH in parathyroid adenoma
  • PTH-related protein secreted by Malignant neoplasm of lung
  • Destruction of bone in primary bone CA
  • Vit D disorders --> inc absorption of Ca in gut
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