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98 Cards in this Set
- Front
- Back
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What adaptations are reversible?
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atrophy, hypertrophy, hyperplasia and metaplasia
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What adaptations are irreversible?
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agenesis, aplasia, hypoplasia, neoplasia
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What does atrophy mean?
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decrease in cell size and volume
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What are some examples of physiologic atrophy?
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notochord, thryglossal duct, decrease in size of thymus
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What are some ways that pathologic atrophy can occur
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1. diuse
2. denervation 3. decreased blood supply 4. nutrition 5. loss of endocrine stimulation 6. aging 7. pressure |
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What does ubiquitin do to the cells and atrophy?
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binds to proteins slated for removal; by removing cells decreasing cell size
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When is a residual body left behind?
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it is the undigestable material after autophagy of cell organelles in atrophy
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When are blood vessels smaller than normal?
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hypoplastic state
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What is hyperplasia?
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increase in number of cells
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What is hypertrophy?
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increase in size of cell
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What is an example of when hyperplasia takes place?
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endometrium and parathryoid; removing half the liver "compensatory"
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Increasing kinase activity is mechanism for what?
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hypertrophy
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What is metaplasia?
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change in differentiation of cells, forming tissue not normally present
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Example of metaplasia?
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squamous metaplasia; transformation of different epithelium into stratified squamous epithelium
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What is the condition where mucus-secreting columnar epithlium are found in the esophagus?
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Barrett's esophagus
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What are some things that can cause cell injury?
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hypoxia
physical agents chemicals and drugs microbiologic agents immunologica reactions genetic factors nutritional factors aging |
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What happens when cells are injured?
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loss of ability to generate ATP, generation of ROS, defects in membrane permeability, increased intracellular Ca
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What are the essential cellular components that can be injured?
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aeorbic respiration, cell membrane, protein synthesis, nucleus
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Examples of reversible cell injury
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hydropic change
fatty change hyaline degeneration inclusions and deposits |
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How does hypoxia cause a reversible cell injury?
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by decreasing ATP there is a decrease in cell membrane transport so net flux of water and Na and cell swells
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What does decrease oxidative phosphorylation do to cells?
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causes injury because it increases the glyoltic pathway and get lactic acid accumulation which leads to decrease in pH
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What does detachment of ribosomes from the RER lead to?
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decreased protein synthesis and reversible change
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How are blebs created?
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altered cytoskeletal; swollen protruding area is a bleb
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When is cell death inevitable?
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unrecoverable mitochondria damage and severe cell membrane damage
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What does an influx of Ca cause?
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irreversible injury; activates phospholipases which damage membranes
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Is loss of phospholipids from the membranes reversible?
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NO
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What is the significant problem with damaged cell membranes?
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leakage of intracytoplasmic contents
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What allows for diagnosis of liver failure?
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AST and ALT enzymes
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What do CK and troponin in blood indicate?
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mycocardial damage
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What do lipase and amylase in the blood indicate?
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pancreatic necrosis
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What is a morphological change of the mitochondria as a result of irreversible damage?
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marked swelling and dense body formation
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What do damaged lysosomes do?
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release enzymes and the digestion of cell components
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What is karyloysis?
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nucleus fades away
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What is pyknosis?
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hard and dark nucleus
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What is karyorrehexis?
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random breakup of nucleus
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What happens in a reperfusion injury?
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increased O2 free radicals; inflammation can be increased by ischemic injury, C' activated and cytokines are generated
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What are free O2 radicals?
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reactive molecular species that are derived from O2 and contain a single, unpaired electron
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How are free radicals formed?
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1.absorption of radiant energy
2.enzymatic change of exogenous chemicals 3. reduction-oxidation rxn 4. Fe or Cu contribute e- 5. NO |
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What acts as a catalyst for free radical formation
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Fe and Cu
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How is a hydroxyl radical formed?
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ferrous iron reacts with H2O2
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Examples of free radicals?
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superoxide anion
H2O2 hydroxyl radical |
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What is peroxynitrite?
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superoxide + NO
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What are 2 ways that free radicals cause injury?
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can combine with other molecules and disrupt structure and function or set up auto-catalytic rxns
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How does CCl4 cause injury?
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may react with P450 oxidases to form CCl3 which can damage RER and inhibit protein synthesis
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When can lipid peroxidation occur?
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when CCl4 reacts with lipid radicals
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What can be the end result of lipid peroxidation?
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fatty liver or inactivation of mitochondria, cell enzymes and denaturation of proteins
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How is free radical injury prevented?
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Vitamin E and A; sequestration of Fe and Cu; SOD, catalase and glutahthione peroxidase
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example of coagulative necrosis
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myocardial infraction
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liquefactive necrosis
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abscess
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enzymatic fat necrosis
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acute pancreatis
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caseous necrosis
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TB granuloma
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What is coagulation necrosis?
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denaturation of cellular proteins
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Where is "red" infract seen?
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organs with dual blood supply; lung
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What is a "special" type of coagulation necrosis?
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gangrene
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What is liquefactive necrosis?
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initial digestion of cells and tissue predominantes with loss of structure
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What is fat necrosis?
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necrosis of pancreatic cells that contains large amounts of hydrolytic enzymes
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What is caseous necrosis?
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due to mycobacterial or fungal infection and necrotic tissue is formed into a "cheesy" material
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What is fibrinoid necrosis?
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necrosis occurring in arterial walls
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In what diseases is the apoptosis process disrupted or abnormal?
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neoplasia and SLE
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What are some normal apoptotic processes?
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embryogeneis, involution of adult organs, death of immune cells, cell deletion in proliferating cell populations and tumors
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When is apoptosis pathological?
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mild injury, some viral diseases, pathologic atrophy in organs after duct obstruction and cytotoxic T cells
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What are some morphologic changes in apoptosis?
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cell shrinks and detaches from neighbor, blebs form, chromatin condensation, apoptotic bodies form, phagocytosis of apoptotic bodies
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What are some biochemical changes in apoptosis?
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protein cleavage by caspases
DNA breakdown phagocytic recognition |
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3 types of caspases?
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1. interleukin converting enzyme
2. death-signaling/initator 3. executioner |
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What is extrinisic apoptosis?
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initated by members of tumor necrosis factor receptor family; receptor ligand interactions FAS or TNF
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What is intrinisic apoptosis?
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replacement of anti-apoptotic proteins in the mitochondria; withdrawl of growth factors or hormones
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What are some negative signals that initiate apoptosis?
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increased O2 derived radicals, damage to DNA, binding of ligands to specific receptors, or withdrawl of positive signals
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When would you see a councilman body?
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acute hepatitis
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What is the stimuli for necrosis?
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hypoxia or toxins
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stimuli for apoptosis?
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physiological or pathological
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tissue reaction in necrosis?
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inflammation
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tissue reaction in apoptosis?
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no inflammation; phagocytosis of apoptotic body
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Heterophagy?
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uptake by endocytosis; lysosomal catabolism
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Autophagy?
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removal of damaged organelles during injury, remodeling, atrophy or hormonal involution: lysosomal catabolism
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What happens to the SER during injury
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hypertrophy because detoxify more rapidly
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What are some mitochondrial alterations during cell injury?
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increased number in hypertrophy, decreased number in atrophy, megamitochondria in liver disease
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What are some way normal endogenous substances accumulate?
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genetic or aquired defect in metabolism, packaging, transport or secretion of the substance
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How does a gene mutation lead to intracellular accumulation?
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production of abnormally folded protein like alpha-1-antitrypsin
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2 diseases that cause microvesicular fat only?
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Reyes syndrome and acute fatty liver in pregnacy
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What are foamy cells?
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macrophages that have taken up large amounts of cholesterol because they took up cell membranes in areas of necrosis
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Where would could there be an accumulation of proteins?
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kidney
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What does the absence of alpha-1-antitrypsin lead to?
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lung damage
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What does an abnormal alpha-1-antitrypsin protein lead to?
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collects in cytoplasm and can result in liver damage
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What is Fe stored as?
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ferritin
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What is Fe transported as?
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transferrin
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What is hemosiderin?
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product when small amounts of Fe undergo autophagy
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How can excess intracellular cause injury?
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1. can catalyze free radical formaion and lipid peroxidation
2. damage DNA 3. stimulate collagen synthesis |
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What are some conditions where Fe accumulates?
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aplastic anemia, sickle cell, thalassemias, bone marrow transplant
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What is hemochromatosis?
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AR disorder of Fe absorption; deposition in various organs that leads to toxicity
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How is copper excreted?
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via biliary tract so chronic biliary obstruction can lead to copper accumulation in hepatocytes
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Wilson's disease?
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AR disease of Cu accumulation; toxic levels accumulate in the liver and becomes deposited in other tisssues causing hemolysis
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what is diagnostic of wilsons disease?
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keiser frasher rings
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What is dystrophic calcification?
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deposition of Ca in necrotic or chronically traumatized tissue; NORMAL serum Ca levels
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Examples of dystrophic calcification
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fat necrosis, caseous necrosis, walls of blood vessels affected by atherosclerosis
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What is metastatic calcification?
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occurs in conditions of high serum Ca levels with Ca deposits in viable tissue
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Causes of hypercalcemia
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hyperparathyroidism, destruction of bone, vitamin D poisoning, milk-alkali syndrome
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What are the predilected areas associated with alkaline milieu?
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intersistial tissues of gastric mucosa, kidneys, lungs
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How are hyalin and hyaline different?
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hyaline is a adjective describing a homogeneous glassy pink appearance and hyalin is a noun that refers to a substance with a hyaline appearance
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