Flashcards in 4/9 Biochem Deck (182)
Which enzyme is absent in Pompe's disease?
-does it present w/hypoglycemia?
alpha-1,4-glucosidase (acid maltase).
-no it does not present w/hypoglycemia.
Fragile X syndrome
-defect affecting the ______ & expression of the _____ gene.
Are Power and sample size related?
Yes, directly related.
-inc. sample size leads to inc. power of a study.
Why does hyponatremia (ie. from thiazides) lead to lithium toxicity?
B/c PCT will then try to resorb more Na and will resorb lithium as well bc of the similar structure. So you'll be resorbing too much lithium.
-lithium has a narrow therapeutic index.
If splenic art is blocked, which arteries that come off of it have poor anastomoses?
-what does the T stand for?
-what are the main Sxs of esophageal dysmotility?
-what will barium study show of esophagus?
-heartburn, regurg, dysphagia.
-dilated esophagus & absent parastalsis
"corkscrew esophagus" seen in what disease?
diffuse esophageal spasm
-mechanism behind esophageal dysmotility?
fibrous replacement of muscularis.
Coronary steal syndrome
-what is the key?
-most often seen w/which drugs?
Key is that collaterals will form distal to the block, and the tissue fed by the blocked areas will be releasing vasodilators due to the ischemia.
-if you give a coronary vasodilator, now the other cornaries (in healthy parts) are also vasodilated, so more blood shunted to them and less blood to ischemic areas!
*seen w/coronary artery vasodilators - adenosine, dipyridamole.
Selective coronary artery vasodilators: name 2:
How many hours of fasting can glycogen stores last before they're depleted?
12 to 18 hours.
-then gluconeo takes over.
-whats the most common cause?
-Tx for prevention?
Phenytoin and valproate inhibit intestinal absorption of which vitamin?
-can lead to what birth defects?
-can lead to neural tube defects.
-deriv of which aortic arch?
6th aortic arch.
-seen in what?
-what is it?
-ventricular compliance reduced via an external force.
-endothelial cells display what?
-neutros display what?
-sialyl lewis acid
-what will you see histologically?
mononuclear, parenchymal infiltration w/well-developed germinal centers.
Infection, pain, sleep deprivation.
-what will blood glucose levels be? inc or dec?
-therefore, will these precipitate a hypoglycemic state in a diabetic?
-typically due to catecholamine release.
-no they will not.
-will stimulate glycogenolysis & gluconeo.
-pt will return to consciousness in 10-15 min.
Purely ketogenic AAs:
Lysine and Leucine
-the onLy pureLy ketogenic amino acids.
-Ketogenic = producing acetoacetate or its precursors.
-Glucogenic = producing TCA intermediates or pyruvate
Inc. serum alanine starting in infancy.
-inc. intake of ketogenic nutrients (e.g., high fat content or inc. lysine and leucine).
Malate to OAA
-what happens in alcoholics?
-Malate to OAA = make NADH. So in alcoholics w/high NADH, opposite rx takes place, OAA => malate, producing NAD+.
-since you need OAA for gluconeo, this inhibits gluconeo, which is why alcoholics get resting hypoglycemia.
Tender loving care for nancy enzymes:
PDH, alpha-KG-DH, branched chain DH.
*these all req thiamine.
*transketolase ONLY req thiamine.
Substrate level phosphorylation steps:
Rotenone, cyanide, antimycin A, CO.
-how do they poison us?
Electron transport inhibitors.
-how does it poison us?
ATP synthase inhibitor.
-2,4-Dinitrophenol (used illicitly for weight loss).
-aspirin (fevers often occur after aspirin overdose).
-thermogenin in brown fat.
Electron transport chain
-protons pumped into which part of the mito?
-where is the ADP made into ATP?
-ATP made in mito matrix, the ATP synthase is in inner-mito membrane.
-where is this enzyme found?
-also kidney & intestinal epithelium.