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USMLE

Comprehensive Pharm 9

QuestionAnswer
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
 

 



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