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52 Cards in this Set
- Front
- Back
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Coagulative necrosis
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Component cells are dead, but the besic tissue architecture is preserved. Firm texture. The injury denatures structural proteins, enzymes --> block proteolysis of dead cells --> eosinophilic, anucleate cells. Characterisitic for infarct.
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Liquefactive necrosis
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Seen in focal bacterial (and fungal) infections, because microbes stimulate the accumulation of inflammatory cells and the enzymes of leukocytes "digest"/liquefy the tissue. Hypoxic death of cells in CNS evokes liq.necr. If the reaction was initiated by acute infl; the material is called pus.
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Gangrenous necrosis
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(not destinctive pattern of cell death)Applied to a limb that has lost blood supplie, and underwent coagulative necrosis in multiple layers. "Wet gangrene" if infection is superimposed by bacteria.
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Caseous necrosis
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Most often in foci of tuberculous infection. Micro: collection of fragmented or lysed cells with amorphus granular apperance. Tissue arcithecture completely obliterated. Often in granuloma.
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Fat necrosis
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Focal areas of fat destruction, typically resutling from release of activated pancreatic lipases into the substance of pandreas and the peritoneal cavity. Occurs in acute pancreatitis. Micro: shadowy outlines of necrotic fat cells with basophilic calcium deposits, surrounded by infl.reaction.
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Fibrinoid necrosis
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Usually seen in immune reaction on blood vessels; immune complex deposits and fibrin = "fibrinoid" (bright pink amorphous apperance in H&E stain)
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Reversible cell changes
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Cell swelling (depletion of ATP, Na leak, water enters) Cytoplasmic Fatty Change (altered lipid metabolism) Blebs on cell surface with loss of microvilli Nuclear chromatin clumping ER swelling / detachment of ribosomes Small densities in mitochondria
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Irreversible cell changes
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Cytoplasmic eosinophilia (loss of ribonucleoproteins) Nuclear shrinkage / pyknosis / karyolysis / karyorrhexis Cell membrane defects and myelin figures Large mitochondrial deposits / swelling of mitochondria Swelling of lysosomes, lysis of ER Loss of coenzymes and RNA If reperfused, influx of calcium; calcification
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Increased Vascular Permeability(soluble inflammatory mediators)
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Histamine PAF Leukotrienes C,D,E Serotonin C3a Bradykinin
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Vasodilatation(soluble inflammatory mediators)
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Prostaglandins E,D,I Serotonin Bradykinin
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Vasoconstriction(soluble inflammatory mediators)
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Thromboxane A2 Leukotrienes C,D,E
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Chemotaxis(soluble inflammatory mediators)
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C5a Interleukin-1 (indirectly) C3a Leukotriene B4 Endotoxin
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Opsinization(soluble inflammatory mediators)
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Fc fragment of IgG C3b
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Smooth Muscle Contraction(soluble inflammatory mediators)
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Bradykinin Leukotrienes
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Platelet Aggregation(soluble inflammatory mediators)
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Thromboxane A2 promotes Prostacyclin inhibits
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Pain(soluble inflammatory mediators)
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Bradykinin PGE2
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Fever(soluble inflammatory mediators)
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Interleukin-1 TNF Prostaglandins
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Morphology: common pattern of cell death resulting form lack of oxygen
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Increased eosinophilia, glassy homogenous apperance (due to loss of glycogen), myelin figures(phospholipid masses form damage cell membr), calcified, discontinuation of membr, dilatation of MIT, nuclear changes culmunating in nuclear dissolution.
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Three patterns of nuclear changes (due to breakdown of DNA and chromatin)
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1. kayolysis: basophilia of the chromatin fade2. pyknosis: nuclear shrinkage and increased basophilia, DNA condenses3. karyorrhexis: the pyknotic nucleus undergoes fragmentation
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Autophagy
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In nutrient-deprived cells, organelles are enclosed in vacoules that fuse with lysosomes. The organelles are digested but in some cases indigestible pigment (e.g lipofucin) remains
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Hypertrophy of SER
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Cell exposed to toxins that are metabolized in the SER show hypertrophy of the ER, a compensatory mechanism to maxmize removal of toxins
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Mitochondrial alternations
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MIT may alter in number, shape size and function. Cellular hypertrophy: increased number of MIT.Atrophy: decreased number.Nutritional deficiencies: megaMIT in hepatocytes.Mitochondrial myopathies: increased numbers of unusually large MIT containing abnormal cristae.
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Cytoskelatal alternations
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Some drugs and toxins interfere with the assembly and functions of cytoskeletal filaments or result in abnormal accumulation of filaments
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Ischemia
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-diminished blood flow to a tissue-most common cause of cell injury-deprivement of nutrients
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Loss of ATP leads to
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failure of many energy-dependent systems;- ion pumps- depletion of oxygen stores- reduction of protein synthesis
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Consequences of hypoxia/ischemia
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1. if oxygen is restored; reversible2. if persistance; irreversible injury and necrosis
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Ischemia-reperfusion injury
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Under certain circumstances , the restoration of blood flow to ischemic but otherwise viable tissues results in exacerbated and accelerated injury. As a result, tissues sustain the loss of cells in addition to those that are irreversibly damaged. Clinically important process in myocardial and cerebral infarctions.
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Ischemia-reperfusion injury causes
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1. increased generation of ROS from parenchymal and endothelial cells and from infiltrating leukocytes2. inflammation may increase due to influx of leukocytes and plasma proteins3. activation of complement system
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Apoptosis in physiologic situations (def)
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Serves to eliminate cells that are no longer needed and to maintain a steady number of various cell population in tissues
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Examples of apoptosis in physiologic situation
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- the programmed destruction of cells during embryogenesis (implantation, organogenesis, developmental involution, metamorphosis)- involution of hormone-dependent tissues upon hormone deprivation (endometrium)- cell loss in proliferating cell populations- death of cells that have served their function- elimination of potentially harmful self-reavtive lymphocytes- cell death induced by cytotoxic T cells
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Apoptosis in pathological conditions (def) |
Elimination of cells that are genetically altered or injured beyond repair without eliciting a severe host reaction, thus keeping the damage as contained as possible
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Examples poptosis in pathological conditions
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- DNA damage (if injury is mild)- accumulation of misfolded proteins leads to ER stress- pathologic atrophy in parenchymal organs after duct obstruction (pancreas, parotid gl, kidney)
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Main pathways of abnormal IC accumulations (with examples)
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1. abnormal metabolism (fatty liver)2. defect in protein folding, transport (accumulation of abnormal proteins)3. lack of enzyme ( lysosomal storage disease: accumulation of endogenous materials)4. Ingestion of indigestible materials (accumulation of exogenous materials)
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Causes of fatty change
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1. cellular poisoning; bacteria, chemicals (chloroform, alcohol)2. clinical disorders; anorexia (due to anemia, cardiac failure, respiratory disease), DM, chronic malnutrition
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Fatty change in liver due to hypoxia caused by anemia and caridiac failure
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Fatty changes is seen farest away from the blood supplie (hepatic arteriole), around the efferent vein (hepatic venule)
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Fatty change in liver due to poisons, toxins (alcohol, infection, organic solvent)
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Fatty changes is seen nearest the afferent blood supplie (hepatic arteriole and portal venule)
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Patters of lipid deposits in heart
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1. prolonged, moderate hypoxia (as in profound anemia): focal IC fat deposits, creating bands of yellowed myocardium alternating with bands of darker, red-brown, uninvolved heart "tigered effect"2. profound hypoxia or toxic injury (eg diptheria). Uniformly affected myocytes
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Cholesterol and cholesteryl esters deposit in cells
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1.foam cells; macrophages in contact with the lipid debris of necrotic cells or abnormal forms of lipoproteins are filled with phagocytosed lipid2. in atherosclerosis; smooth muscle cells and macroph are filled with chol and chol esters, gives characteristic yellow colour3. Hyperlipidemic syndromes; macroph accumulate IC chol. Xanthomas=clusters of foamy macroph in subepithelial CT of skin or tendons
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Protein deposits in cells
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1. In nephrotic synrdome it is protein leakage across the glomerular filter, and mush larger reabsorbtion: Pink, hyaline cytoplasmic droplets in renal tubular epi.2. Russell bodies: accumulation of newly synthesized Ig in RER of plasma cells3. Mallory body /"alcoholic hyalin": eosinophilic cytoplasmic inclusion du to liver cell injury4. Alzheimer: disrupted neuronal cytoskeleton forms neurofibrillary tangle
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Exogenous pigments
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Carbon: air pollutant, inhaled ->phagocytosed by alveolar macroph. -> transported to regional tracheobronchial LYNAggregates: anthracosisHeavy accumulations may induce emphysema or a fibroblastic reaction that may result in a serious lung diseas; worker's pneumoconiosis
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Endogenous pigments
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LipofuscinMelaninCertain derivates of hemoglobin
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Lipofuscin
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"wear-and-tear pigment". Insoluble brownish-yellow granular IC materials that accumulates in a variety of tissues as a function of age or atrophy. Marker of past free-radical injury. In large amount: brown atrophy
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Melanin
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Brown-black pigment produced in melanocytes in epidermis, act as screen against harmful UV. Basal keratinocytes and dermal macrophages may accumulate the pigment.
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Hemosiderin
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Hb-derived granular yellow-brown pigment, accumulates in whit local or systemic iron excess. Abnormal large amount of ferritin micelles (=iron + apoferritin). Visualized with Prussian blue. Small amounts are physiological in BM, spleen,m liver).
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Local and systemic deposition of hemosiderin
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1. Local excess of iron due to hemorrhage, eg: bruise2. Systemic = hemosiderosis. First in mononclr phagocytes of the BM, spleen, liver, LYN, progressvie accumulation, parenchymal cells in the body(mainly liver, pancreas, heart, endocrine organs) becomes bronzed.
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Hemosiderosis occures in the setting of
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1. increased absorbtion of dietary iron2. impeared utilisation of iron3. hemolytic anemias4. transfusions5. hereditary hemochromatosis
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Dystrophic calcification |
Deposition of calcium in dead or dyning tissues. Occures in the absence of calcium metabolic derangements (ie normal serum levels of calcium). Intra- and/or extracellular basophilic deposits. In time, heterotrophic bone may be formed.
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Metastatic calcification
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Almost always reflects some derangements in calcium metabolism (hypercalcemia). Principally affects the interstitiall tissue of vasculature, kidneys, lungs, and gastric mucosa
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Four major causes of metastatic calcification
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1. increased secretion of parathyroid hormone 2. destruction of bone due to accelerated turn over (eg Paget d), immobilization, tumours3. vitamin D-related disorders (vitD intoxication, sarcoidosis)4. renal failure (phosphate retention leads to 2ndary hyperparathyroidism)
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Cellular aging (def)
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The result of a progressive decline in the proliferative capacity and life span of cells and the effects of continous exposure to exogenous factors that cause accumulation of cellular and molecular damage
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Mechanisms responsible for cellular aging
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- DNA damage- decreased cellular replication (terminal nondividing stage:replicative senescence)(short telomeres)- reduced regenerative capacity of tissue stem cells- accumulation of metabolic damage
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Werner syndrome
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Characterized by mature aging. Cells have reduced life span
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