USMLE Word Scramble
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USMLE
Comprehensive Pharm 9
| Question | Answer |
|---|---|
| which receptors are associaed with Gq | HAVe 1 M&M H1 alpha 1 V1 M1, M3 |
| which receptors are associated with Gi | MAD 2's M2 alpha 2 D2 |
| which receptors are associated with Gs | B1, B2, D1, H2, V2 |
| major fxns of M2 | decreases HR |
| major fxns of M3 | increase exocrine gland secretion |
| major fxns of D1 | relaxes vascular smooth muscle |
| major fxns of D2 | modulates transmimtter release in brain |
| major fxns of H1 | ubcreases basak abd bronchial mucus production, contraction of bronchioles, pruritis, pain |
| major fxns of H2 | increase gastric acid secretion |
| major fxn of V1 | constricts vascular smooth muscle |
| major fxn of V2 | increas water permeability and reabsorption in CT of kidney |
| MOA hemicholinium | blocks the transport of choline into cholinergic neurons, blocking the production of ACh |
| MOA vesamicol | blocks the transporter that brings Acetyl CoA + Choline CHAT into vesicles |
| MOA botulinum | blocks the release of ACh vesicles |
| MOA metyrosine | blocks conversion of tyrosine into DA |
| MOA reserpine | blocks DA transporter into vesicles that form NE |
| MOA guanethidine | inhiits release of NorE from noraderenergic neurons |
| MOA amphetamine | increase release of NorE from vesicles |
| MOA pralodoxime | reactivates AChE after it's been inhibited by pesticides |
| treatment for salicylate OD | alkalinize urine dialysis |
| treatment of antimuscarinics OD | physostigmine salicyate |
| treatment of b-blocker od | glucagon |
| tx of digitalis od | stop dig normalize K \lidocaine anti-dig Fab fragments Mg |
| tx iron toxicity | deferoxamine (chelating agent) |
| tx fo lead poisoning | EDTA dimercaprol succimer penicillamine |
| tx of arsenic toxicity | dimercaprol succimer |
| tx hg toxicity | dimercaprol succimer |
| tx au toxicity | dimercaproli succimer penicillamine |
| tx cu toxicity | penicillamine |
| tx cn toxicyt | nitrite hydroxocobalamin thiosulfate |
| tx methemoglobin toxicity | methylene blue |
| tx CO toxcity | 100% o2, hyperbaric pressure |
| tx of methanol od | ethanol dialysis fomepizole |
| tx of ethylene glycol od | etoh dialysis foempizole |
| tx of opiod toxicity | nalaxone naltrexone |
| tx of benzo od | flumazenil |
| tx of ca od | NaHCO3 |
| tx of heparin toxicity | protamine sulfate |
| tx of warfarin toxicity | vitamin k ffp |
| x tpa toxicity | aminocaproic acid |
| tx streptokinase toxicity | aminocaproic acid |
| sx of iron od | fever sweating abdominal pains diarrhea cyanosis weakness |
| examples of insulin drugs (and give duration of action) | lispro (short) insulin (short) NPH (intermediate) lente and ultralente (long acting) |
| clinical uses of insulin analogs | DM I life-threatening hyperkalemia (insulin increases K entry into cells) stress induced hyperglycemia |
| examples of 1st generation sulfonylureas | tolbutaminde chlorpropamide |
| examples of 2nd generation sulfonylureas | glyburide glimepiride glipizide |
| MOA sulfonylureas | when glucose enters the cell, the ATP level rises high ATP:ADP closes K channel this causes Ca influx --> insulin release these drugs enoucrage this process by closing k channels (basically stimulates the release of endogenous insulin) |
| uses of sulfonylureas | DM II reqires some islet cell fxn, so useless in DM I |
| toxicity associated with sulfonylureas (1st gen) | diulfuram effects |
| toxicity associated with 2nd generation sulfonylureas | hypoglycemia |
| examples of biguanides | metformin |
| MOA metformin | unknown, but might decrease gluconeogenesis, increase glycolysis and decrease serum glucose levels |
| clinical use of metformin | can be used in pts without islet cell fxn |
| adverse effects of metformin | lactic acidosis |
| MOA glitazones | incresaes target cell response to insulin |
| clinical use for glitazones | DM II |
| toxicity associated with glitazones | weight gain edema hepatotoxicity |
| examples of alpha-glucosidase inhibitors | acarbose miglitol |
| MOA alpha-glucosidase inhibitors | inhibits intestinal brush border alpha-glucosidases delays sugar hydrolysis and glucose absorption decreased post-prandial hyperglycemia |
| clinical use of alpha glucosidase inhibitors | DM II |
Created by:
Asclepius
on 2008-10-22