Pharm9 - Pharm9 Flashcards
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