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General pathology and principles

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Question
Answer
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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