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USMLE > Pharm9 - Pharm9 > Flashcards

Pharm9 - Pharm9 Flashcards

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1
Q

which receptors are associaed with Gq

A

HAVe 1 M&M H1 alpha 1 V1 M1, M3

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2
Q

which receptors are associated with Gi

A

MAD 2’s M2 alpha 2 D2

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3
Q

which receptors are associated with Gs

A

B1, B2, D1, H2, V2

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4
Q

major fxns of M2

A

decreases HR

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5
Q

major fxns of M3

A

increase exocrine gland secretion

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6
Q

major fxns of D1

A

relaxes vascular smooth muscle

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7
Q

major fxns of D2

A

modulates transmimtter release in brain

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8
Q

major fxns of H1

A

ubcreases basak abd bronchial mucus production, contraction of bronchioles, pruritis, pain

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9
Q

major fxns of H2

A

increase gastric acid secretion

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10
Q

major fxn of V1

A

constricts vascular smooth muscle

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11
Q

major fxn of V2

A

increas water permeability and reabsorption in CT of kidney

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12
Q

MOA hemicholinium

A

blocks the transport of choline into cholinergic neurons, blocking the production of ACh

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13
Q

MOA vesamicol

A

blocks the transporter that brings Acetyl CoA + Choline CHAT into vesicles

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14
Q

MOA botulinum

A

blocks the release of ACh vesicles

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15
Q

MOA metyrosine

A

blocks conversion of tyrosine into DA

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16
Q

MOA reserpine

A

blocks DA transporter into vesicles that form NE

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17
Q

MOA guanethidine

A

inhiits release of NorE from noraderenergic neurons

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18
Q

MOA amphetamine

A

increase release of NorE from vesicles

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19
Q

MOA pralodoxime

A

reactivates AChE after it’s been inhibited by pesticides

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20
Q

treatment for salicylate OD

A

alkalinize urine dialysis

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21
Q

treatment of antimuscarinics OD

A

physostigmine salicyate

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22
Q

treatment of b-blocker od

A

glucagon

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23
Q

tx of digitalis od

A

stop dig normalize K \lidocaine anti-dig Fab fragments Mg

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24
Q

tx iron toxicity

A

deferoxamine (chelating agent)

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25
tx fo lead poisoning
EDTA dimercaprol succimer penicillamine
26
tx of arsenic toxicity
dimercaprol succimer
27
tx hg toxicity
dimercaprol succimer
28
tx au toxicity
dimercaproli succimer penicillamine
29
tx cu toxicity
penicillamine
30
tx cn toxicyt
nitrite hydroxocobalamin thiosulfate
31
tx methemoglobin toxicity
methylene blue
32
tx CO toxcity
100% o2, hyperbaric pressure
33
tx of methanol od
ethanol dialysis fomepizole
34
tx of ethylene glycol od
etoh dialysis foempizole
35
tx of opiod toxicity
nalaxone naltrexone
36
tx of benzo od
flumazenil
37
tx of ca od
NaHCO3
38
tx of heparin toxicity
protamine sulfate
39
tx of warfarin toxicity
vitamin k ffp
40
x tpa toxicity
aminocaproic acid
41
tx streptokinase toxicity
aminocaproic acid
42
sx of iron od
fever sweating abdominal pains diarrhea cyanosis weakness
43
examples of insulin drugs (and give duration of action)
lispro (short) insulin (short) NPH (intermediate) lente and ultralente (long acting)
44
clinical uses of insulin analogs
DM I life-threatening hyperkalemia (insulin increases K entry into cells) stress induced hyperglycemia
45
examples of 1st generation sulfonylureas
tolbutaminde chlorpropamide
46
examples of 2nd generation sulfonylureas
glyburide glimepiride glipizide
47
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)
48
uses of sulfonylureas
DM II reqires some islet cell fxn, so useless in DM I
49
toxicity associated with sulfonylureas (1st gen)
diulfuram effects
50
toxicity associated with 2nd generation sulfonylureas
hypoglycemia
51
examples of biguanides
metformin
52
MOA metformin
unknown, but might decrease gluconeogenesis, increase glycolysis and decrease serum glucose levels
53
clinical use of metformin
can be used in pts without islet cell fxn
54
adverse effects of metformin
lactic acidosis
55
MOA glitazones
incresaes target cell response to insulin
56
clinical use for glitazones
DM II
57
toxicity associated with glitazones
weight gain edema hepatotoxicity
58
examples of alpha-glucosidase inhibitors
acarbose miglitol
59
MOA alpha-glucosidase inhibitors
inhibits intestinal brush border alpha-glucosidases delays sugar hydrolysis and glucose absorption decreased post-prandial hyperglycemia
60
clinical use of alpha glucosidase inhibitors
DM II

USMLE (16 decks)

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