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