USMLE

Description:	Comprehensive Pharm 9
Category:	USMLE
Created by:	Asclepius on 2008-10-22

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