General pathology and principles
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| show | Color, location, appearance, size, shape, consistency
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| show | Inflammatory
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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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| show | focal, multifocal, locally or regionally extensive, disseminated, diffuse
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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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| show | recurrent bouts of active inflammation superimposed on chronic inflammation
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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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| show | phospholipases, proteases, ATPases, endonucleases
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| show | increased Ca, oxidative stress, phospholipid breakdown and breakdown products. Results in Mitochondrial Permeability Transition (MPT), cytochrome C leakage, loss of membrane potential
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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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| Irreversible injury: karyorrhexis | show 🗑
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| show | dissolution of cell nucleus
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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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| Reactive Oxygen Species (5) | show 🗑
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| show | Pro-oxidative: transition metals (Fe or Cu) catalyze reactions generating reactive oxygen species (OH. and OH-) (hemostasis during surgery can increase Fe in tissue and cause oxidative injury)
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| show | Pro-oxidative: antioxidant defenses are overwhelmed, superoxide and hydrogen peroxide interact to form hydroxyl radical (OH.) and hydroxide (OH-)
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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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| Coagulative necrosis: histo | show 🗑
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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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| Liquefactive necrosis: cause | show 🗑
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| Caseous necrosis: gross | show 🗑
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| Caseous necrosis: histo | show 🗑
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| show | specific immuno-pathologic phenomenon; mycobacterial cell walls
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| show | chalky or mineralized
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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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| show | ischemia
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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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| show | adrenal, CNS, liver, gut
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| Rigor mortis: influencing factors | show 🗑
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| show | microscopic appearance = eosinophilic, homogeneous, glassy material (intracellular or extracellular)
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| Extracellular protein deposits: three examples | show 🗑
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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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| AL amyloid | show 🗑
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| AA amyloid | show 🗑
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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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| show | "antracosis" - lung, urban environments, incidental
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| biological pigments | show 🗑
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| acid-hematin (pigment) | show 🗑
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| show | incidental pigmentation of tissues in pigmented animals; pleura and meninges most commonly infected
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| show | chronically inflamed skin
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| show | postmortem artifact: production of hydrogen sulfide by bacteria with subsequent reaction with iron in hemoglobin to form insoluble iron sulfide (particularly seen in peritoneal and retroperitoneal cavity due to high levels of bacteria in gut)
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| hemosiderin (pigment) | show 🗑
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| show | light yellow variant of hemosiderin that occurs during wound resolution as iron is removed from hemosiderin by macrophages
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| show | greenish yellow pigment, usually not granular; seen within hepatocytes, bile canaliculi, and renal tubular epithelium
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| show | mineralization of dead or dying cells; membrane vesicles form as cell membranes break down and these serve as a nidus for mineral deposition (often seen w/ granulomatous inflammation w/ casseation, e.g. TB)
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| metastatic calcification | show 🗑
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| metastatic calcification: causes | show 🗑
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| show | passive, degradative, from fatal cell injury
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| show | programmed cell death
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| cell death producing inflammation | show 🗑
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| cell death without inflammation | show 🗑
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| In which tissues does apoptosis normally occur? | show 🗑
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| What cells are typically subject to apoptosis? | show 🗑
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| necrosis vs. apoptosis: which has mitochondrial and ER changes? | show 🗑
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| show | necrosis (apoptosis has blebbing only)
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| show | apoptosis
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| necrosis vs. apoptosis: which has DNA damage? | show 🗑
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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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| show | Execution pathway: caspase 3 activation leading to cellular degradation and formation of apoptotic bodies
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| apoptosis intrinsic pathway: intracellular signals - negative factors | show 🗑
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| show | radiation, toxins, hypoxia, hyperthermia, viral infections, free radicals
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| show | Mitochondrial Permeability Transmission (MPT) - release of pro-apoptotic proteins from intermembrane space (including CYTOCHROME C) into cytosol - initiation of caspase cascade
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| apoptosis - perforin/granzyme pathway | show 🗑
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| show | 1. damage to DNA results in elaboration of p53 (proofreading enzyme)
2. p53 stops cell cycles to allow DNA repair
4. if DNA damage is too great, p53 initiates apoptosis
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| p53 | show 🗑
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| Executioner caspases | show 🗑
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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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| two disorders associated with decreased apoptosis | show 🗑
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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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