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USMLE - Cell Injury

USMLE - Goljan, Chapter 1 Cell Injury

QuestionAnswer
ischemia not enough blood flow to an area
hypoxemia decreased PaO2 (O2 dissolved in plasma)
If one has anemia, what would you expect PaO2 and SaO2 to be? both should be normal; you just have less RBC's overall
PaO2 O2 dissolved in plasma
SaO2 O2 bound to Hb
If pt has methemoglobinemia, what would you expect PaO2 and SaO2 to be? PaO2 normal, decreased SaO2 because metHb has an oxidized heme group, which can't bind O2
What should you think of when you see "chocolate colored blood"? methemoglobinemia
With metHb, would you expect cyanosis to improve when 100% O2 administered? No
What are the treatments for metHb? Methylene blue --> activates MetHb reductase; Ascorbic acid --> deoxidizes the heme group so Hb can bind O2 again
If pt has CO poisoning, what would you expect PaO2 and SaO2 to be? normal PaO2; decreased SaO2 because CO competes with O2 for binding sites on Hb
How do you treat CO poisoning? 100% O2
why are free radicals bad? degrade nucleic acids --> damage DNA; damages lipids in cell membranes
what neutralizes O2-derived free radicals? superoxide dismutase
Three compounds that can neutralize peroxide (H2O2) free radicals superoxide dismutase; glutathione peroxidase; catalase
What can neutralize free radicals generated by taking acetominophen? glutathione peroxidase
What do vitamin anti-oxidants do? block the formation of free radicals and degrade free radicals
Name some vitamin anti-oxidants ascorbic acid, vitE, B carotenes
What drug is the most common cause of fulminant hepatitis? When would this happen? Acetominophen. When GSH (glutathione) is depleted in the liver -- you need glutathione to conjugate/break down acetominophen.
In acetominophen-induced hepatitis, where would you see the necrosis around the central veins
How would you treat acetominophen-induced hepatitis? give N-acetylcysteine, which increases synthesis of glutathione, which neutralizes the free radicals
Hereditary hemochromatosis body absorbs too much Fe from food; excess Fe stored in liver, heart, pancreas; intracellular Fe --> OH free radicals --> damage cells
hemosiderin the form of Fe in the blood
hemosiderosis too much Fe in body's storage; abnormal accumulation of Fe
What happens when cytochrome c is released from mitochondria? Apoptosis
What can cause release of cytochrome c from mitochondria? Alcohol, salicylates (aspirin), increase Ca2+ in cytosol
Where is the CYP450 enzyme system located? smooth ER of liver cells
What can alcohol, barbuturates and phenytoin do to the smooth ER of liver cells? SER hyperplasia
What is the result of SER hyperplasia in liver cells? increased CYP450 activity --> increase drug metabolism --> decreased therapeutic drug levels in blood
What do PPI's and macrolides do to the CYP450 system? Inhibits CYP450 --> decreased drug metabolism --> higher than expected therapeutic drug levels
Inclusion-cell disease hydrolytic enzymes destined for primary lysosomes are NOT marked with mannose 6-phosphate like they're supposed to be --> primary lysosomes don't contain the appropriate hydrolytic enzymes --> accumulation of undigested substrates in the cytosol
What are the sx's of inclusion-cell disease? psychomotor retardation and early death
Gaucher's disease lysosomal storage disease; deficiency of the enzyme glucocerebrosidase, leading to an accumulation of its substrate, the fatty substance glucocerebroside in lysosomes; autosomal recessive
what is ubiquitin? marker for intermediate filament degradation
What are Mallory bodies and where do you find them? damaged (ubiquinated) intermediate filaments in hepatocytes -- see hyaline inclusions on slides; seen in alcoholic liver disease
What are Lewy bodies and where do you find them? damaged neurofilaments in idiopathic Parkinson's dz (eosinophilic cytoplasmic inclusions in the degenerating substantia nigra)
what is the most common cause of fatty change in the liver? alcohol
Kernicterus damage to the brain centers of infants caused by increased levels of bilirubin; Rh-induced hemolytic dz in newborns --> fat-soluble unconjugated bilirubin --> enters basal ganglia nuclei in brain --> permanent damage
Xanthelasma Yellow plaque on eyelid (like Ba Ngoai); cholesterol in macrophages
Von Gierke's glycogenosis Deficiency of G6P --> excess of glycogen in hepatocytes and renal tubular cells
Addison's disease destruction of the adrenal cortex --> hypocortisol --> increased ACTH --> excess melanin--> diffuse pigmentation of skin and mucosa
What is the difference between ferritin and hemosiderin? Ferritin is major SOLUBLE iron storage protein and can be measured in serum; hemosiderin is INSOLUBLE product of ferritin degradation in lysosomes and is NOT in serum.
Where is ferritin stored? in bone marrow macrophages and hepatocytes
What is does serum ferritin measure? Amount of ferritin stores in the bone marrow
In Fe-deficiency anemia, what level of ferritin would you expect to see? Decreased
What is the difference between dystrophic and metastatic calcification? Dystrophic calcification is calcification of necrotic tissue (normal serum Ca and Phosphate); metastatic is calcification in normal tissue (elevated serum Ca and P)
What does parathyroid hormone do? Releases Ca into the serum & decreases uptake of P from the kidney (more P is released in the urine). PTH releases Ca from bone marrow, decreases loss of Ca in urine, and stimulates production of VitD so that more Ca can be absorbed in intestines
Why would hypoparathyroidism cause hyperphosphatemia and metastatic calcification? decreased PTH --> increased retention of P (not as much excreted through urine); Ca levels not maintained in the serum --> Ca driven into normal tissues
Difference between atrophy, hypertrophy, and hyperplasia Atrophy - decrease in cell SIZE; hypertrophy - increase in cell SIZE; hyperplasia - increase in cell NUMBER of NORMAL cells
Difference between hyperplasia, metaplasia, dysplasia Hyperplasia - increase in number of NORMAL cells; metaplasia - replacement of one fully differentiated cell type by another (new type is less sensitive to a particular stress); dysplasia - disordered cell growth
What is polycythemia? net increase in the total number of red blood cells in the body (overproduction of RBCs, malignancy, or chronic low O2)
Coagulation necrosis preservation of structural outline of dead cells (but no nuclei); from denaturation of enzymes/proteins inside cell --> autolysis of cell
What kind of necrosis in dry gangrene in pts with diabetes mellitus? coagulation necrosis
what is an infarction? gross manifestation of coagulation necrosis secondary to the sudden occulsion of a vessel
What is a pale/ischemic infarction? coagulation necrosis in dense tissue -- RBCs can't diffuse through
What is a hemorrhagic infarction? coagulation necrosis in loose tissue -- RBCs CAN diffuse through
Liquefactive necrosis necrotic tissue that becomes liquefied due to lysosomal enzymes released by necrotic cells or neutrophils
What type of necrosis in cerebral infarction? Liquefactive (hydrolytic enzymes released by neuroglial cells)
What kind of necrosis in abscess from bacterial infxn? Liquefactive (hydrolytic enzymes from neutrophils)
What kind of necrosis in wet gangrene in pts with diabetes mellitus? It is an anaerobic infxn (i.e. C.perfringens) --> liquefactive
Caseous necrosis acellular and cheese-like; lipid released from cell walls of M.TB and systemic fungi such as Histoplasma after destruction by macrophages
Enzymatic fat necrosis Adipose tissue surrounding acutely inflamed pancreas; pancreatic lipase --> hydrolysis of TG's in fat cells
Fibrinoid necrosis in damaged basement membrane in small vessels
What are caspases? Cysteine proteases that initiate apoptosis
BAX gene pro-apoptosis gene
TP53 gene suppressor gene (aborts apoptosis): temporarily arrests the cell cycle in G1 to repair DNA; if damage is too great --> activate BAX gene --> apoptosis
BCL-2 Gene family inhibits apoptosis (prevent mitochondrial leakage of cytochrome c into the cytosol)
pyknosis Ink dot appearance of nucleus -- indicates cell is undergoing apoptosis
AST (aspartate aminotransferase) mitochondrial enzyme; marker of diffuse liver cell necrosis; increased in alcohol-induced liver dz
ALT (alanine aminotransferase) Marker of diffuse liver cell necrosis; more specific for liver cell necrosis than AST
CK-MB (creatine kinase MB) isoenzyme that is a marker for acute MI or myocarditis
Amylase and lipase are markers for what pathology? acute pancreatitis; lipase more specific because amylase is also increased in salivary gland inflammation such as mumps
Created by: christinapham