Pharm3 - Pharm3 Flashcards

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1
Q

what are the symptoms of organophosphate poisoning

A

DUMBBELSS Diarrhea Urination Miosis Bradycardia Bronchospasm Excitation of skel muscle Lacrimation Sweating Salivation

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2
Q

antidote to organophosphate poisoning

A

atropine + pralidoxime

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3
Q

what is pralidoxime

A

antagonist used to regenerate active cholinesterase

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4
Q

MOA of epi in tx of glaucoma

A

increases outflow of aqueous humor

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5
Q

MOA brimonidine in tx of glaucoma

A

(alpha agonist) decreases aqueous humor synth

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6
Q

MOA beta blockers in tx of glaucoma

A

decreases aqueous humor secretion

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7
Q

MOA acetazolamide in tx of glaucoma

A

decreas aqueous humor secretion d/t decreaed HCO3

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8
Q

MAO cholinomimetics in tx of glaucoma

A

increased outflow of aqueous humor

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9
Q

which drug should be used in a glaucoma emergency

A

pilocarpine (direct ACh mimetic)

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10
Q

MOA latanoprost in tx of glaucoma

A

PGF-alpha, increases outflow of aqueous humor

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11
Q

which glaucoma drugs decrease the synth of aqueous humor?

A

beta-blockers brimonidine acetazolamide

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12
Q

which glaucoma drugs increase outflow of aqueous humor?

A

epi cholinomimetics PGF2alpa (latanoprost)

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13
Q

MOA atropine

A

muscarinic antagonist

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14
Q

toxicity of atropine

A

dry as a bone hot as a hare mad as a hatter red as a beet blind as a bat

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15
Q

Effects Nitrates have on: EDV BP Contractility HR Ejection time MV O2

A

down down up (reflex) up (reflex) down down

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16
Q

Effects B-blockers have on: EDV BP Contractility HR Ejection time MV O2

A

up down down down up down

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17
Q

effects b-blockers + nitrates have on: EDV BP Contractility HR Ejection time MV O2

A

no effect, or down down little, no effect down little/no effect down a lot!

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18
Q

MOA CCBs

A

block voltage dependent ca channels of cardiac and smooth muscle, reducing muscle contractility

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19
Q

In decreasing effect, which CCBs have most effect on vascular smooth muscle?

A

nifedipine > diltiazem > verapemil

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20
Q

in decreasign effeect, which CCBs have most effect on heart?

A

verapamil > diltiazem > nifedipine

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21
Q

which CCB can’t be used for arrhythmias?

A

nifedipine

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22
Q

toxicity of CCBs

A

cardiac depression flushing peripheral edema dizziness constipation

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23
Q

which CCB is most similar to nitrates in effect?

A

nifedipine (makes sense… nifedipine works most strongly on vascular smooth muscle)

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24
Q

which CCB is most similar to b-blockers in effect?

A

verapamil (makes sense… verapamil works most strongly on heart)

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25
Q

MOA statins?

A

HMG-CoA reductase inhibitors blocks formation of cholesterol from HMG-CoA

26
Q

MOA niacin

A

blocks the export of cholesterol from the hepatocyte to the blood

27
Q

MOA bile resins

A

binds cholesterol in the gut so they can’t get to the hepatocytes

28
Q

MOA ezetimibe

A

cholesterol absorption blocker so, prevents cholesterol from entering hepatocytes from gut

29
Q

MOA fibrates

A

increases action of lipoprotein lipase, encouraging the breakdown of VLDL –> LDL also decreases hepatic synthesis and secretion of VLDL increases HDL by decreasing TG (results from decreased VLDL) –> decresaed exchange of cholestreryl esters from HDL

30
Q

which cholesterol agents affect endogenous production of cholesterol?

A

fibrates niacin lovastatin

31
Q

which cholesterol agents affect absorption of exogenous cholesterol

A

ezetimibe bise acid resins

32
Q

effects of statins on: LDL HDL TGs

A

down A LOT up down

33
Q

effects of niacin on LDL HDL TGs

A

down a lot (not as much as statins) up A LOT down

34
Q

effects of bile acid resins on LDL HDL TGs

A

down a lot (not as much as statins) none slightly UP

35
Q

effects of ezetimibe on LDL HDL TGs

A

down a lot (not as much as statins) none none

36
Q

effects of fibrates on: LDL HDL TGs

A

down a little up DOWN A FRIGGIN TON!

37
Q

what 2 cholesterol drugs, if taken concurrently, will cause rhabdomyolysis

A

statins and fibrates

38
Q

which cholesterol drugs increase LFTs?

A

your lft’s are not SEF (safe) statins ezetimibe fibrates

39
Q

which cholesterol drug –> GI discomfort

A

bile acid resins

40
Q

antidote to dig toxicity

A

anti-dig Fab fragment s slowly normalize K lidocaine cardiac pacer

41
Q

MOA of class I anti-arrhythmics class II? class III? class Iv?

A

Na channel blockers B-blockers K channel blockers CCBs

42
Q

which drugs are in class Ia anti-arrythmics?

A

Quinidine Amiodarone Procainamide Disopyramide

43
Q

which drugs are in the class Ib anti-arrhythmics?

A

I Be with my Lid To Mex(ico) lidocaine tocainide mexiletine

44
Q

which drugs are in the class Ic anti-arrythmics?

A

See (C)! And Can’t (EnCain) We FLEe if we PROP up PHENOMS? encainide flecainide propafenone

45
Q

MOA class IA anti-arrhythmics?

A

increased AP duration increased ERP increased QT interval

46
Q

uses for class IA anti-arrhythmics

A

atrial and ventricular arrhythmias (esp reentrant and ectopic) SVT and VT

47
Q

MOA for class IB anti-arrhythmics

A

decreases AP duration

48
Q

use for class IB anti-arrhythmics

A

acute ventricular arrhythmias, esp post MI

49
Q

MOA for class IC anti-arrhythmics

A

no effect on AP

50
Q

uses for class IC anti-arrhythmics

A

VT –> FV inretractable SVT LAST resort

51
Q

toxicity of quinidine

A

cinchonism (HA, tinnitus, thrombocytopenia, torsades de pointes from increased QT interval)

52
Q

toxiciyt of procainamide

A

SLE-like syndrome (reversible)

53
Q

toxicity of IB anti-arrhythmics?

A

local anesthetic CNS stimulation/depression CV depression

54
Q

toxicity of IC anti-arrhythmics

A

pro-arrhythmic (esp post-MI) prolongs refractory period

55
Q

receptor selectivity for epi?

A

all are equal

56
Q

receptor selectivity for NorE

A

a1 = a2 > b1

57
Q

receptor selectivity for isoproteronol

A

B1=b2

58
Q

receptor selectivity for DA

A

d1 = d2 > B > a

59
Q

receptor selectivity for dobutamine

A

b1 > b2

60
Q

receptor selectivity for phenylephrine

A

a1 > a2

61
Q

receptor selectivity for albuterol

A

b2 > b1

62
Q

receptor selectivity for terbutaline

A

b2 > b1