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USMLE - Cell Injury
USMLE - Goljan, Chapter 1 Cell Injury
| Question | Answer |
|---|---|
| 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
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