cell injury II – Flashcards
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| what is the definition of necrosis? |
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| irreversible death of a living cell including eventual compromise of the cell membrane, some form of inflammation, denaturation of intracellular proteins, removal of the cell, (assuming the body survived, occurs via macrophages/enzymatic digestion) |
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| what morphologic changes does a necrotic cell take on in terms of color and phospholipids? |
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| increased eosinophilia and mylelin figures, (destroyed phospholipids mass in the cell) |
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| what morphologic changes does a necrotic cell take on in terms of the nucleus? |
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| nuclear changes: karyolysis, (chromatin broken up+dispersed), pyknosis, (nucleus shrivels), and karyorrhexis, (nucleus broken into larger fragments) |
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| what is reperfusion, what characterizes the type of injury on cells? |
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| reperfusion is blood flowing back to a ischemic tissue after a clot has been cleared, and it is characterized predominately by increased O2 free radicals, as well as changes to the mitochondria and complement pathway, (leading to injury/inflammation) |
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| what kinds of cell injury can be incurred by chemicals? |
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| chemicals can directly combine with molecular components/organelles and destroy them, reactive toxic metabolites, (ex:chemicals converted to metabolites, which can be more harmful than the parent chemical, CCl4->CCl3 in the liver->excessive fat deposition due to breaking down of liver's ability to remove fat, tylenol can be toxic in high levels to the liver) |
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| what is the sequence of changes in cell death/necrosis? |
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| coagulative, liquefactive, caseous, fat |
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| what happens in coagualative necrosis? |
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| the structural outline of the cell is intact however structural/enzymatic proteins become denatured internally+nucleus breaks up and fades, looks like a "ghost", an MI is one example, heart muscle will lose striations - can also be seen in the kidney |
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| if a pt dies of an MI immediately, will coagulation necrosis be visible? |
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| no, it takes some time for coagulation necrosis to take place, (takes time for cells to break down) |
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| what is the difference functionally between necrosis and apoptosis? |
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| necrosis is pathologic, apoptosis can be pathologic or physiologic and portions of it will bleb off forming apoptotic bodies which will ultimately be phagocytized and destroyed |
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| what is the appearance of caseous necrosis? what is an example of a disease which gives this kind appearance? |
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| caseous necrosis, resulting in destruction of the parenchyma. tuberculosis is a prime example |
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| what kind of necrosis refers to focal areas of fat destruction? where might this happen? |
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| fat necrosis. in pancreatitis, enzymes may leak out and start to break down the omentum and other intraabdominal fat. blunt force trauma to fatty areas such as the breast can also result in fat necrosis. |
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| where might you find liquefactive necrosis? what is it? |
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| it may be found in areas of the body with looser parenchyma, producing a liquid-like material - commonly seen in bacterial/fungal infections, may not result in scar tissue formation, and thus a cavity may form. this is often seen in infections of the brain, and also possible in the kidneys. |
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| what are some subcellular responses to cellular injury in terms of the cytoskeleton, lysosomes, mitochondria, SER, and heat shock proteins? |
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| cytoskeletal abnormalities, (micro/intermediate filaments that help maintain integrity of the cell, and if the cell is injured, these filaments accumulate). lysosomal catabolism, (lysosomal membranes can be damaged and the contents leak out), mitochondrial alterations, (pores can forms and Ca can leak out, hypertrophy may occur if they are asked to do a lot of work),SER induction, (if the body is constantly exposed to stimuli such as barbituates, then they may be induced), heat shock proteins, (help fold and degrade proteins, get them out of the way) |
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| what are the 2 kinds of lysosomal catabolism? |
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| heterophagy, (phago/pinocytosis) engulfing something else via pseudopods, and autophagy where the cell is breaking down/phagocytizing an intracellular component |
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| what are reasons the SER might be induced? |
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| metabolism of chemicals, P450 modification, can lead to tolerance of drugs |
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| what abnormalities might occur to the mitochondria and why? |
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| hypertrophy, atrophy, pore formation when stressed. can be advantageous |
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| what cytoskeletal abnormailites can occur in terms of cellular injury? |
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| affected thin filaments can result in defects in locomotion, kartanger's syndrome: abnormal respiratory/sperm tail formation due to this, and intermediate filaments, (mallory body: injured filaments in alcoholic liver disease, neurofibrillary tangles: seen in alzhiemer's) |
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| what are some examples of apoptosis occuring in physiologic states? |
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| cell destruction during embryogenesis, (different cell lines: eliminated, like thymus), hormone dependent involution, cell deletion in proliferating cell populations, (reduce neoplasm possibility) acute inflammatory response, eliminating self-reactive lymphocytes, cell death induced by cytotoxic T cells, (cell death induced in certain toxic cells) |
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| what are some examples of apoptosis in pathologic states? |
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| cell death by injurious stimuli, viral infection, (inserted in to genome, may elict apoptosis), atrophy from duct obstruction, (cells being fed by that duct may die off), cell death in tumors, (however not always enough to clinically clear the tumor) |
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| how does the morphology of apoptosis present? |
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| cell shrinkage, chromatin condensation, cytoplasmic blebs/apoptotic bodies, phagocytosis of apoptotic cells |
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| what are some biochemical features of apoptosis in terms of proteins/DNA/phagocytosis? |
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| enzymes such as capsases cleave proteins, DNA is broken down, and the cell is made ready to be recognized by phagocytes |
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| what is the mechanism of apoptosis in the exstrinsic pathway? |
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| cell suface death receptors, FAS, TNF |
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| what is the mechanism of apoptosis in the intrinsic pathway? |
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| balance of proapoptotic, protective molecules and death inducers |
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| what does the execution phase of apoptosis consist of? |
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| proteolytic cascade from capases, and the removal of dead cells via phagocytosis |
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| what are some ways that apotosis can be induced in terms of growth factors, DNA, TNFs, T cells? |
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| growth factor deprivation, DNA damage, or apoptosis by the TNF family of receptors/cytotoxic T lymphocyte mediation |
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| what kinds of things may accumulate in a cell subjected to certain stressors/injury? |
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| normal cellular constituents, (like fat), abnormal substance, (asbestos+carbon, which the body does not have the ability to break down), pigment, (tattoo, hemoglobin etc) |
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| what do heat shock proteins do? what might happen if they cease to function correctly? what is another name for them? |
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| they function as "house keeping" entities that fold other proteins into alpha helices or beta sheets in order to properly function. if heat shock proteins stop working, proteins meant to be folded can accumulate and cause the cell to undergo apoptosis. this problem is implicated in alzhimers, parkinsons, and huntingtons. they are also called "chaperone cells" |
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| what are 3 common kinds of intracellular accumulation? |
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| endogenous substance, (produced at normal or increased rate w/inadequate metabolism), genetic or acquired defects in metabolism transport or secretion, (as in missing enzyme), and deposition of exogenous substance |
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| what is hyaline change? what is it's pattern of accumulation? where might it be seen. |
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| homgenous, glassy, pink change in the cells themselves or extracellular space. it has a nonspecific pattern of accumulation. this might be seen in blood vessels in some instances of cardiovascular disease. |
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| when and where might glycogen accumulate abnormally? |
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| glycogen can accumulated in the proximal convoluted tubules, liver and pancreas in diabetes or glycogen storage diseases |
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| what kinds of exogenous and endogenous pigments can be found accumulating in cells? |
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| exogenously: carbon with anthracosis and tattooing, endogenously: lipofuscin,(aging pigment), melanin, (normal or abnormal -> melanoma), hemosiderin, (breakdown product of hemoglobin) |
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| in instances of malnutrition, why might there be fatty buildup? |
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| if there is not enough protein, it cannot bind to the lipids which allows them to move outside the cell, leaving them to accumulate, (can happen in the liver after heavy drinking) |
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| what happens if there is a genetic mutation in the production of proteins responsible for protein folding or transport, (chaperones)? |
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| an accumulation of abnormal proteins can occur, which can impinge on the functional capabilites of the cell |
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| what is an example of what happens if there is a genetic mutation in the production of enzymes in the cell that break down complex substrates? |
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| lysosomal storage disease where the enzyme is missing that helps break down endogenously produced materials, leading to accumulation |
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| what kinds of accumulation within cells might occur with occupational medicine? |
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| accumulation of indigestible exogenous material like carbon or asbestos |
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| what is one of the more lethal intracellular accumulations in western society? |
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| LDL cholesterol in coronary arteries, which can potentially lead to encroachment and ischemia and possibily an MI |
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| what is an example of protein accumulating in cells? |
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| multiple myeloma, which is a malignancy of plasma cells which produce immunoglobulins which can accumulate |
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| what is steatosis? |
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| accumulation of lipids, it can happen in the liver or heart |
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| what is atherosclerosis? xanthoma? what can happen pathologically with these conditions? |
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| atherosclerosis: accumulation of cholesterol in the lumen of arteries in plaques, (specifically macrophages and smooth muscle cells of the intima show accumulation). xanthoma: intracellular accumulation of cholesterol in skin cells around the eyes. in the worst cases these can lead to inflammation and necrosis |
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| what are russel bodies? |
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| excessive amounts of secretory proteins |
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| why might there be protein accumulation in the proximal convoluted tubules? |
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| in renal disease, proteins leak out and some accumulate in the PCTs |
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| what are 2 kinds of pathologic calcifications? |
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| dystrophic and metastatic |
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| what happens with dystrophic calcification? |
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| previously injured organs, (areas of necrosis), gain Ca accumulation, (intra and extracellularly) resulting in further disruption and structural change. serum Ca levels are generally normal, but it can be accentuated by hypercalcemia |
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| what happens with metastatic calcification? where are common areas for this to occur? |
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| deposition of Ca on otherwise normal organs and structures because serum Ca levels are high, (hypercalcemia), rarely produce significant organ disfunction. metastatic calcification occurs commonly in the gastric mucosa, kidneys, and lungs |
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| what kinds of things can happen with cellular aging? |
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| structural and biochemical changes such as oxidative damage and abnormally folded proteins. replicative senescence occurs to limit cell division over time. accumulation of genetic damage, higher likelihood or malignancy or wearing down of repair cells resulting in states like arthritis |
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| what is serous cell injury? |
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| inflammation that resembles serum, straw colored and protein poor. what you see if you burn your finger on a stove, serous fluid will fill the blister |
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| what is fibrinous cell injury? |
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| due to increased vascular permeability and accumulation of fibrin, has more proteins |
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| what is suppurative cell injury? |
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| associated with abcesses and pus, where the pus is an accumulation of white blood cells that have essentially "lost the battle" and an abscess is the process of walling that off, (liquefactive necrosis may be seen here) |
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| what does ulcerative cell injury refer to? |
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| eroded epithelium, often seen in gastric epithelium or on the extremities of diabetics |
