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33 Cards in this Set
- Front
- Back
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drugs that can cause torsades |
MRS. QT Can PROLONg M – macrolides; R – Risperidone (antipsychotics); S– Sotalol; Q – Quinidine (along with Class Ia and Class III antiarrhythmic drugs); T – Thiazides; C – Chloroquine; Pro – Protease inhibitors. ON- Ondansetron |
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when would you see pure RBC aplasia (NL platelets and WBCs) |
thymoma, B19 infection, some leukemias |
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GLUT transporters |
1: "RBC": Rbc, Brain, Cornea 2: "two directions" (bidirectional), liver (bidirectional to release glucose in gluconeogenesis), beta islet cells, kidney, small intestine (glut 2 is slow (high Km) to allow other GLUT to have access to glucose first) 3: Brain 4: "need insulin 4 glut4" skeletal musc., adipocytes 5: "five for fructose" spermatocytes, GI (to bring in fructose) |
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relationship btwn wall tension, pressure, radius and wall thickness |
wall tension= Pr/(2t) ("two t on the bottom") P=transmural pressure r= lumen radius t=wall thickness |
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exceptions to the obvious HPA hormone functions: prolactin somatostatin TRH |
prolactin inhibits GnRH (eg during breast feeding high PRL = birth control) (another eg... decreased GnRH -> decreased EST -> osteoporosis in pituitary adenoma) somatostatin inhibits TSH (octreotide as a side fx can cause hypothyroidism) TRH increases prolactin (hypothyroid state-> increased TRH -> increased PRL -> amenorrhea) |
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prl interaction w/ est and prg |
est increases prl secretion but prg blocks prl fx at breast (so no lactation during pregnancy bc prg is high) @ birth, decreased prg allows prl to have fx on breast |
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another cation that fx PTH secretion causes of deficiency of this cation |
Mg2+ (can inc. or dec. pth depending on how low it is) causes ("DADA"): diarrhea, aminoglycosides, diuretics, alcohol abuse |
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rules for hormone receptors |
steroid hormones + thyroid hormone use intracellular vasodilators (bnp/anp, no) use cGMP Insulin and Insulin-like Growth Factor (and other growth factors) use Intrinsic tyrosine kinase (RAS-RAF Mapk pathway) pituitary acidophils (PRL and GH), as well as cytokines (IL2, IL6, etc) use receptor-associated tyrosine kinase (jak-stat pathway) ant pit. basophils ("FLAT") use Gs pathway (cAMP) as do related hormones (hCG~LH/FSH), MSH~ACTH. Also, stimulating hormones (glucagon and epi, etc.). So does PTH (elevated cAMP is one test for primary hyperparathyroidism) IP3 ("1P3") is used by post. pit. hormones (oxytocin and ADH, v1 receptor). other stuff is split between Gs and Gq mechanisms |
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how does thyroid hormone increase metabolic rate? |
increased Na/Katpase |
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4 main functions of thyroid hormones |
"the 4 B's" $Brain maturation $Bone growth $increased Beta1 receptors $increased Basal metabolism (via increased Na/Katpase) -> increased body temp-> heat intolerance |
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prevention of tumor lysis syndrome |
allopurinol (xo inhibitor) rasburicase/pegloticase (synthetic urate oxidase) good hydration |
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where does compliment bind Ab |
in the Fc region near the hinge region (phagocytosis is at the tail of the Fc region) |
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rx to decrease kidney stones |
high fluid intake increased citrate intake (via K+citrate): binds calcium and increases ca excretion |
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why are ca channel blockers effective in cardiac and smooth muscle, but not skeletal |
cardiac and smooth have Ca induced Ca release whereas skeletal does not. |
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tumor markers for neuroblastoma? presentation vs Wilms tumor? |
HVA Bombesin ("bombs blast") Nmyc Nb is irregular that can cross midline ("like an irregular explosion") vs WT, which is more refined ("like Sir Wilms"), ie smooth and unilateral |
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tmt for pheos |
alpha blockade first! (phenoxybenzamine) next, B blockers, then tumor resection |
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hla dr5 |
hashimoto and pernicious anemia |
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tmt for thyroid storm |
propranolol (B block) propylthiouracil (decrease T3/4) Prednisolone (steroids) to decrease Ab production |
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psammoma bodies in... |
Papillary thyroid CA Serous cystadenoma/CA Meningioma Mesothelioma |
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tmt for prolactinoma |
dopamine agonists (bromocriptine or cabergoline) |
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NL suppressors of GH |
somatostatin and elevated glucose |
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drugs that cause nephrogenic DI |
lithium, demeclocycline |
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tmt for nephrogenic DI |
HCTZ, indomethacin, hydration |
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main causes of SIADH |
small cell lung ca cyclophosphamide |
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elevated blood glucose and necrolytic migratory erythema |
glucagonoma |
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jejunal ulcers |
ZE syndrome |
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sulfonylureas |
1st gen: tolbutamide, chlorpropamide 2nd gen: glyburide, glimepiride, glipizide MOA: close K channel in B cells leads to inc. insulin release. sfx: disulfiram like fx (esp 1st gen), hypoglycemia (bc increased insulin), weight gain |
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TZDs |
-glitazone moa: increased insulin sensitivity via PPAR transcription factor. Also increases adiponectin |
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type2 DM drugs that decrease glucagon |
Amylin agalog: pramlintide glp-1: exenatide, liraglutide dpp4 inhibitors: -gliptin |
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octreotide |
somatostatin analogue used to treat: acromegaly, carcinoid, gastrinoma, glucagonoma (decreases GI secretions), esophageal varices (decreases portal pressure) |
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demeclocycline |
tetracycline that is an ADH antagonist use: SIADH tmt can cause nephrogenic DI and other tetracycline toxicities (photosens, teeth/bone abnormalities) |
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falciform ligament |
anterior liver to abd wall (ventral mesentery) contains ligamentum teres (was umbilical vein) |
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hepatic zones (lobular structure) |
zone I nearest portal triad: affected first by viral hepatitis, ingested toxins (already toxic, ie don't have to be metabolized into their toxic form), Fe in hemochromotosis zone III near the central vein (centrilobular): affected 1st by ischemia (oxygenated blood comes in near zone I) think "IIIetabolism" of toxins: contains cytochrome p450 system so acetaminophen and CCl4 are toxic to zone III first. Site of alcoholic hepatitis |
