General pathology and principles
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Objective description: CLASS-C | show 🗑
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Process: -itis | show 🗑
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Process: -osis, -opathy | show 🗑
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show | Disorders of growth
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Degree types | show 🗑
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Duration types | show 🗑
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Distribution types | show 🗑
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Mild degree | show 🗑
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Moderate degree | show 🗑
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Severe degree | show 🗑
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show | change not clinically detectable
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show | rapid onset, lasts hours, exudative, few cells
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Acute | show 🗑
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subacute | show 🗑
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chronic | show 🗑
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chronic-active | show 🗑
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etiologic diagnosis | show 🗑
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morphologic dx | show 🗑
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Players in cell injury | show 🗑
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show | membrane transport, protein synthesis, lipogenesis, phospholipid turnover
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cytoplasmic calcium activates: | show 🗑
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Effects of mitochondrial damage | show 🗑
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Effects of oxygen and ROS damage | show 🗑
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Reversible hypoxia steps | show 🗑
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show | 1. Degranulation of RER (loss of ribosomes)
2. Moderate to severe mitochondrial swelling
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Irreversible ischemic injury steps | show 🗑
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show | condensation of molecular material (calcium sink in mitochondria leads to mineralization and dissolution)
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show | destructive fragmentation of nucleus
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karyolysis | show 🗑
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show | continued cell death following reperfusion. 1. cells are structurally intact but have lethal functional changes; 2. new injuring processes are initiated; perhaps elaboration of ROS
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show | Superoxide anion (O2-); singlet oxygen (O); hydroxyl radical (OH); nitric oxide (NO); hydrogen peroxide (H2O2)
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Fenton Reaction | show 🗑
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Haber-Weiss Reaction | show 🗑
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show | Inactivates superoxide (forming H2O2 + O2), preventing ROS damage. 1. Mg SO in mitochondria; 2. Cu Zn SOD in cytosol
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show | Inactivates H2O2 --> O2 + 2H2O
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show | Inactivates H2O2 and hydroxyl radical (GSSG (disulfide bond) + 2H2O) - can measure glutathione to assess oxidative stress
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show | Vitamin A, E (membrane antioxidant - prevents lipid peroxidation), C (water soluble); Caeruloplasmin (binds Cu2+); transferrin, lactoferrin, ferritin, hemosiderin (iron bound by protein prevents Fenton Rxn)
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4 morphologic patterns of necrosis | show 🗑
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Coagulative necrosis: gross | show 🗑
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show | hypereosinophilic "ghost cells" (tissue architecture intact)
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Coagulative necrosis: cause | show 🗑
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Liquefactive necrosis: gross | show 🗑
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Liquefactive necrosis: histo | show 🗑
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show | usually bacterial, or tissues with little stoma (e.g. CNS)
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Caseous necrosis: gross | show 🗑
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Caseous necrosis: histo | show 🗑
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Caseous necrosis: cause | show 🗑
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Fat necrosis: gross | show 🗑
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show | lightly basophilic, smudgy saponified material, sometimes with granulomatous inflammation
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Fat necrosis: cause | show 🗑
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Gangrene: cause | show 🗑
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Gangrene: typical location | show 🗑
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show | coagulative
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show | liquefactive, with tissue digestion by opportunistic bacteria (often w/ gas production)
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show | "rotting"- enzymatic degradation and protein denaturation by host enzymes (typically w/ microbial enzyme involvement)
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4 tissue types which undergo rapid autolytic change | show 🗑
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show | temperature, glycogen stores, pH of muscle
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show | microscopic appearance = eosinophilic, homogeneous, glassy material (intracellular or extracellular)
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show | edema fluid, fibrin, amyloid
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show | any protein with fibrils measuring 7.5-10.0nm with a beta-pleated sheet configuration will take on the histologic appearance referred to as "amyloid" (aka "beta-fibrilloses")
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amyloid: morphology | show 🗑
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show | formed from Ig light chains
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show | formed from serum amyloid A (SAA), an acute phase reactavt stains blue-black w/ iodine followed by sulfuric acid (typically follows chronic inflammation)
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AF amyloid | show 🗑
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show | formed from a variety of hormone and hormone-like receptors
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Lipofuscin (pigment) | show 🗑
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carbon (pigment) | show 🗑
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biological pigments | show 🗑
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show | artifact of tissue processing (blackish - can resemble hemosiderin)
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show | incidental pigmentation of tissues in pigmented animals; pleura and meninges most commonly infected
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***Reactive melanosis/hyperpigmentation | show 🗑
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***Pseudomelanosis | show 🗑
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show | lighter brown granular pigment; represents large accumulations of iron and apoferritin (together called ferritin)
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hematoidin (pigment) | show 🗑
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bilirubin (pigment) | show 🗑
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dystrophic calcification | show 🗑
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show | mineralization in living tissue; excess Ca and P in the blood precipitate (exceed max saturation); commonly seen in gastric mucosa, blood vessels, basement membranes in the lungs and kidney (i.e. sites of acid exchange)
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metastatic calcification: causes | show 🗑
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necrosis | show 🗑
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apoptosis, pyroptosis, pyronecrosis, autophagy, and oncosis | show 🗑
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cell death producing inflammation | show 🗑
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show | apoptosis, autophagy
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show | tissues undergoing physiologic or post-pathologic atrophy; embryonic tissues
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show | hematopoietic cell lines (termination of inflammation, self-reactive T cells), cells killed by T cells (AI, viral infection, cells with DNA damage, cells injured by hypoxia, irradiation, hyperthermia, toxins, and drugs
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show | necrosis
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necrosis vs. apoptosis: which has membrane alterations? | show 🗑
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necrosis vs. apoptosis: which is active? | show 🗑
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show | apoptosis
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show | necrosis
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necrosis vs. apoptosis: which undergoes karyolysis? | show 🗑
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necrosis vs. apoptosis: which appears as cytoplasmic eosinophilia? | show 🗑
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show | 1. extrinsic pathway
2. intrinsic pathway (mitochondria)
3. perforin/granzyme pathway (activate T cells)
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Final result of all three types of initiation phase of apoptosis | show 🗑
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show | absence of growth factors, hormones, or cytokines; loss of apoptotic suppression
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apoptosis intrinsic pathway: intracellular signals - positive factors | show 🗑
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apoptotic changes in mitochondrial membrane | show 🗑
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show | 1. CD8 T cell recognizes foreign antigen on cell surface
2. secretion of perforin forming pore in target cell surface
3. secretion of Granzyme B which activates caspases
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apoptosis: DNA damage-mediated | show 🗑
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show | DNA proofreading enzyme. Can initiate apoptosis in event of irreparable DNA damage (prevention of neoplastic cell proliferation)
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show | point where initiation pathways (w/ initiator caspases 8, 9, 10) converge; activation of ENDONUCLEASES AND PROTEASES
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show | externalized to apoptotic cell surface - signal non-inflammatory phagocytic recognition and phagocytosis
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pyroptosis | show 🗑
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autophagy | show 🗑
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show | 1. neoplasia
2. autoimmune disease - insufficient apoptosis of auto-reactive cells
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show | 1. neurodegenerative disorders
2. exacerbation of damage in ischemic injury (e.g. ischemia-reperfusion)
3. virus-induced lymphocyte depletion in acquired immune deficiency syndromes
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