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18 Cards in this Set
- Front
- Back
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what are the 4 main aspects of a disease?
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Etiology (cause)
Mechanism (Pathology) - what's physicially going wrong as a result Functional abnormalities - what the patient experiences Structural abnormalities - physical objective findings. |
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what are possible pathologies?
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Vindicates -
V = vascular I = inflamatory N = Neoplasia D = degenerative I = Idiopathic/Iatrogenic C = Congenital A = Acquired/metabolic T = Trauma E = environmental S = pSychiatric. |
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What are some forms of necrosis he went over?
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He mentioned that necrotic tissue gets - charged, which attracts Ca++, to give you calcium deposits (also seen in breast cancers).
also mentioned coagulative necrosis, where there'd denaturation but the cell outline is preserved. no proteolysis. Seen in MI's. also, there's liquifaction - looks like enzyme digestion. CNS hypoxia, bacterial/fungal. note that gangrenous is a subset of this also caseious and fat, though he didn't talk about these. |
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compare and contrast reversible and irreversible cell damage.
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Etiologies for both: HIT DIG: hypoxia, ischemia, trauma, drugs, immunology, genetics.
reversible can involve ATP depletion and resulting ion concentration changes, influx of water, swellimg. Also some mito damage, making this worse. On scope, can see fatty vacoules, swelling, mito/er dilation, etc. Irreversible - this probably involves the nucleus and serious disruption to the membranes. Mitos loose cytochrome C and TURNS ON APOPTOTIC PATHWAY. Also get a lot of calcium influx - makes everything, including permeability, worse. C++ makes the lysosomes permeable, endonucleases go to work eating up DNA. Also, because of low 02, loose your terminal electron acceptor and stop being able to get rid of radicals - so RADICALS BUILD UP. Get lipid peroxidation, change proteins, oxidize DNA. |
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what does necrosis look like?
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more basic, so you see greater eosinophilia (red).
empty vacuoles (moth-eaten looking). see calcifications (negatively charged attracts the positive Ca++) karyoloysis (fading of blue nuclear color) and pyknosis (shrinking of DNA). seen in both apoptotic and necrotic death. |
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what are our types of necrosis?
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Coagulative: Standard hypoxia situation. Cells keep their outer structure, harden. Denature everything, but outline remains.
Liquifactive - About enzyme digestion. seen in bacterial/fungal infections. See lots of puss. Graneous. Caseous - like cheese!. seen in tuburculosis infections. Lots of granulomas and inflammation. fragmented, coagulated cells. Fat: if you leak lipases from the pancreas, combines with fat cells, lipid cells die, get lots of fat leaked, FFA's and Ca++ combine and you get lots of SOAP, which begin to kill vessels. Bad news. |
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what's reprofusion injury?
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quickly re-adding blood to an ischemic area can cause more free radicals to be made when the cells aren't ready to deal with them.
free radicals can increase the permeability of mitochondria, causing cell death. also, reprofusion can allow the cytokines from the necrotic tissue to call TONS more WBC's to the area, making inflammation much much worse. |
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chemical insults - mercury chloride, cyanide, carbon tetrachloride, and acetaminophen.
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mercury chloride binds to sulfhydryl groups on the surfaces of cells, can block ATPase transport and damage GI and kidney. Increases membrane permeability.
Cyanide - this blocks oxidative phosphorylation by messing with cyrochrome oxidase. Carbon Tetrachloride - think of free radicals. P450 converts it to a radical, encourages fat breakdown and lots more free radicals. So, it injures the liver pretty seriously . acetaminophen: p450 makes a bad metabolite that's usually processed by glutathione. If you have lots of tylenol, eat up all your glutathione and end up with serious liver damage. |
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what's apoptosis? talk about membranes, inflammation, physiologival Vs. pathological, and molecular mechanisms. examples.
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1. membranes remain intact!
2. NO INFLAMMATION. Can be physiological (like embryo getting rid of webbings, getting rid of infected cells, menses, normal cell death over time, immunological). pathological (if DNA damaged badly, begin apoptosis. Can help depend on P53, which is why damaging it causes cancer. This turns on CAPSPASE!!!) can come from cytotoxic T-cells (via Granzyme B to turn on capspase). TNF can turn on NFkB to up inflammation, in addition to binding TNF receptor which turns on caspase. |
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what do the cells look like?
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shrinked, condensed. Chromatin gets small and dark. eventually phagocytosed.
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what are the pathways this happens through?
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intrinsic/mitochondrial:
mess up mitochondria, leak cytochrome C, activate APAF, caspase, cell death. Also AIF (apoptosis inducing factor) from the mitochondria. extrinsic - death receptor. Fas and TNF bind death receptor, turns on Fas, turns on caspases. phagocytes come in and chew up everything. note that healthy cells express a factor that says "don't eat me" |
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can hypertrophy and hyperplasia be normal?
what's atrophy? |
yes - this is physiologica.
physiological hyperplasia includes hormonal (develping breasts) and compensatory (liver regrowing). both can also be pathological. both seem to be induced by hormones or by growth factors, though with pathologic it's excessive. note that in wound healing, fibroblasts undero hyperplasia and become scar tissue. GF's can be made by WBC's, by viruses. Different from cancer in that hyperplastic cells are subject to influences of GF's and other inhibitors - they play by the rules. Cacners grow in an unregulated manner. atrophy is opposite of hypetrtophy - cells shink but are not dead. loss of protein by ubequitin mediated pathways. also, autopaghy (eating of own contents to find nutrition). |
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is metaplaysia reversible? where does it come from?
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yes!
you're replacing one cell with another better able to stand the stress. happens from reprogramming of stem cells - don't re-differentiate an already differentiated cell. |
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what conditions lead to apoptosis, and which lead to necrosis?
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necrosis happens from the typical things like ischemia, trauma, chemical insults, toxins, etc. lysosomes leak out, eat up the cell, PM degrades, spill out lots of stuff.
apoptosis comes from lack of growth factors, or damage to DNA or lots of proteins. this is an ACTIVE PROCESS that requires energy - so those processes that lead to lack of ATP do NOT cause apoptosis. NOTE - apoptosis isn't always pathologic. NECROSIS IS ALWAYS PATHOLOGIC. |
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what two phenomenon coencide with moving from reversible to irreversible cell injury?
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mitochondrial function which doesn't come back to normal, and severe disruption to membranes in the cell.
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what phenomenon are associated with reversible cell injury?
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fatty deposits in cells that depend on fat (heart and liver).
also, swelling - lack of ion control leads to osmotic changes and cells swell. |
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what's interesting about cytochrome C?
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it's a main protein involved in electron transport.
also, it's leaked from the mitochondria and signals for apoptosis. |
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extra Ca++ is bad - what can it turn on?
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phospholipases that eat membrane.
proteases that eat membrane and proteins. endonucleases that eat DNA ATPases to eat ATP. Ca++ can also turn on caspase and induce cytochrome C to fall out of mitochondria, both turning on apoptosis. |
