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47 Cards in this Set
- Front
- Back
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What is hypertrophy, where is it seen and what is the pathogenesis?
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Increase in size
Nondividing cells, sk mm, myocardium Increase stress = increase growth |
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What is hyperplasia, where is it seen and what is the pathogenesis?
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Increase in # of cells
Dividing cells, glands, epidermis, bone marrow Cells from G0-G1 by hormones |
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What is atrophy, where is it seen and what is the pathogenesis?
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Decrease in size and number
Aging- brain, liver, kidneys, heart, bone, mm Dec workload, disuse, pressure, dec blood supply Net loss of intracellular protein, inc degradation by proteosome |
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What is metaplasia, where is it seen and what is the pathogenesis?
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REVERSIBLE change of adult cell to a different phenotype
Squamous, glandular, osseous Change in stressors to the cell causes change |
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What do all cells that ARE NOT squamous cells become with metaplasia?
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Squamous
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Which vitamin is needed to maintain specialized epithelium?
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Vit A
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What is the only example of columnar metaplasia in the notes?
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Barrett metaplasia of the distal esophagus
Response to chronic acid reflux from stomach into esophagus Columnar replaces squamous |
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What is dysplasia?
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Premalignant change
Disordered growth of cells with atypical nuclear morphology |
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What is morphology of myocardial hypertrophy? What is the difference between reversible and irreversible morphology?
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Cells increase in size, nuclei increase in size, cells take a "boxy" shape from chronic hemodynamic stress
Reversible change - fatty change, cell swelling Irreversible change - cell death infarct |
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What is the difference between concentric and eccentric myocardial hypertrophy?
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C - from inc in pressure
E - from inc in blood volume |
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What adaptive changes are seen in sm mm? What tissues are involved?
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Inc cell cytoplasm + hypertrophy
Arterioles, viscera, intestines, myometrium |
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Cause and consequence of hypertrophies smooth ER of hepatocytes?
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Response of hepatocytes to CYP drugs, induced by prolonged exposure to the drug, results in subtheraputic response of other drugs
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Define Keloid, Hypertrophic scar, Warts, Psoriasis
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Keloid - excess collagen by fibroblasts
HS - Increase in myofibroblasts Warts - HPV infection of squamous cell induces growth by E6, E7 Psoriasis - proliferation of epidermal squamous cells by inflammatory cytokines |
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Describe function of proteosome
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Selective destruction of the cell protein, ubiquitin attaches to the protein to be destroyed
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Define apoptosis
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Nuclear compaction --> cell shrinkage --> loss of membrane potential --> nuclear fragmentation + blebs
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Define autophagy
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Cellular autodigestion, cytoplasmic vacuolization + lipofuscion granules
Starvation --> formation of autophagosomes --> vacuolization of cytoplasm --> substrate exhaustion --> more vacuoliztion --> cell death |
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Define necrosis
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Opening of the plasma channels --> extracellular fluid influx --> cell swelling, leakage, rupture
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Describe morphology of reversibly injured cells
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ATP depleted
Hydropic swelling Fatty change (lipid vacuoles in cytoplasm |
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When does reversible damage to a cell become irreversible?
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When mitochondria damage becomes irreversible and when membrane stability is lost
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What is gangrene and what is the difference between wet and dry?
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Mixture of ischemia and infection
Wet - infection superimposed in ischemia Dry - ischemia predominates |
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Describe the morphology of caseous necrosis
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Central white cheesy area, granular amorphous cells, cavitates
Monocyte macrophages form giant cells = epithelioid macrophage |
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What are the pathways that create:
-swelling, blebs -nuclear clumping -lipid deposits |
Swelling - Dec Na pump, inc Ca/H20/Na in, inc K out = swelling
Nuclear clumping - inc anaerobic glycolysis, inc lactic acid, dec pH = nuclear clumping Lipid deposits - detachment of ribosomes, dec PRO synthesis = lipid deposits |
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What is the mechanism of cell injury due to mitochondrial injury?
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Inc Ca, ROS --> Dec ATP, H+ released, can't make ATP = necrosis
Inc Ca, ROS --> Cytochrome C released --> apoptosis |
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What are the 3 exogenous chemical sources of ROS's?
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Exogenous chemicals - happens in mitochondria, creates free radicals
Transition metals - Fe + Ca donate/accept free electrons (Fenton Rxn) Nitric Oxide - endothelium, macrophages, neurons |
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What are the 3 pathologic effects of ROS's?
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Lipid peroxidation in membranes
Oxidation modification of proteins DNA lesions |
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Define reperfusion injury
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Reperfusion of ischemic tissue = death of some reversibly injured cells by reenergizing macrophages to create ROS, leading to Ca overload and cell death
Cytokines released from ischemic tissue brings leukocytes |
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Compare and contrast apoptosis and necrosis
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Apoptosis - nuclear condensing, blebs, fragmentation, phagocytic consumption
Necrosis - swelling of ER + mitochondria, blebs, breakdown of membranes, leakage of components, myelin figures |
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What enzyme is the major player in apoptosi, and what does it turn DNA into?
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Caspases activate DNAase's, DNA is cleaved into oligonucleosomes, shown as ladders on agarose gel
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What is the extrinsic pathway of apoptosis?
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TNF and FAS ligands (FAS on lymphocytes)
Caspase 8 activated --> execution caspase cascade |
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What is the intrinsic pathway of apoptosis?
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Cytochrome C out of mitochondria trigger the procaspase in the presence of lack of survival signals , DNA damage, protein misfolding or increased intracellular calcium
Cyto C binds from mitochondria binds to Apaf-1 --> activates caspase 9 |
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What is cytotoxic T-lympho mediated apoptosis
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Immune response to viral infection
CTL injects granzyme into target cell --> apoptosis |
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What is the function of NFkB?
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Inhibitor of apoptosis, favors cell survival
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Which 2 factors inhibit apoptosis and which 2 promote apoptosis?
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Inhibit - BCL-2, BCL-X
Promote - BAK, BAX |
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What are 2 situations of pathologic deficient apoptosis?
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Autoimmune disease
Tumors expressing BCL-1, NFkB |
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What is anthracosis?
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Black carbon accumulation in lungs, mediastinal lymph nodes, NO clinical significance usually
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What is steatosis and what is the difference between hepatic and cardiac?
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Accumulation of lipids, reversible accumulation of triglycerides
Hepatic - Enlarged liver, elevated AST/ALT caused by DM, Obesity, ETOH abuse, toxins/drugs, protein malnutrition, shock/anoxia Cardiac - May be due to hypoxia, ischemia, diptheria toxin |
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Define atherosclerosis and xanthomas
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Atherosclerosis - accumulation of cholesterol in the blood vessels
Xanthomas - foam cell tumors in dermis and tendons |
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Define intracellular protein accumulation in the kidneys, ER and Liver
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Nephrotic - hyaline droplets in renal tubular cells w/ heavy proteinurea
ER - a1-antitrypsin deficiency Liver - alcoholic hyaline |
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What is lipofucsin?
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Wear and tear pigment, insoluble residue of lipid peroxidation
Found in the lysosomes of heart/liver of aging patients |
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What inclusion is diagnosed with prussian blue stain?
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Hemosiderin, partially denatured ferritin w/in lysosomes
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What 3 diseases cause hemosiderin accumulation?
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Hereditary hemachromatosis, Anemias, RBC transfusions
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What is bilirubin?
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Iron free derivative of Iron
Causes jaundice/icterus with excess accumulation |
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What is hyaline change?
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Accumulation of protein
Glassy, pink, eosinophilic |
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Compare dystrophic and metastatic pathologic calcifications
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Dystrophic - deposits in nonviable tissue, serum Ca levels NORMAL, necrosis, atherosclerosis, aging, found in HEART VALVES, nucleus of calcification in dead/dying cells
Metastatic - hypercalcemia (bone destruction) OR hyperphosphatemia (renal failure), may occur in NORMAL tissues (lungs, pulmonary veins, kidneys, gastric mucosa), DARK BLUE stain |
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What is Werner syndrome?
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Finite # of cell divisions, premature aging onset 2nd decade
Lack of HELICASE = DNA damage |
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What is Hutchinson-Gilford syndrome?
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Finite # of cell divisions, life of under 10 years, baldness, defect in the LMNA gene
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What are telomeres and telomerases?
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Telomeres allow for more cell replications, telomerase adds more telomeres and allows for longer cell life
Germ cells, stem cells and cancer cells all have high levels of telomerase and telomeres |
