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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 |