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Arizona Drug Profiles > Drug MOA's > Flashcards

Drug MOA's Flashcards

1
Q

ASA

A

in small doses blocks thromboxane a2, potent platelet aggregate and vasoconstrictor
decreased platelet aggregation

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2
Q

adenosine

A

slows conduction time through AV node, can interrupt re entrant pathways through AV node
slows sinus rate
larger doses decrease bp by decreasing peripheral resistance

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3
Q

albumin normal serum

A

exerts oncotic pressure, which expands volume of circulating blood and maintains cardiac output

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4
Q

albuterol

A

beta agonist primarily b2, relaxes bronchial smooth muscle, resulting in bronchodilation, also relaxes vascular and uterine smooth muscle, decreases airway resistance

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5
Q

amiodarone

A

multiple effect on NA K and CA channels
prolongs action potential, refractory period
ventricular automaticity K
slows membrane depolarization and impulse conduction NA
negative chronotropic activity in nodal tissue, rate reduction, and antisympathetic acticity CA and Beat blockade
dilates coronary arteries DA Alpha blockade

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6
Q

atropine pharmacological

A

blocks action of ACH as competitive antagonist at muscarinic sites in smooth muscle secretory gland, and CNS
blocks parasympathetic response allows sympathetic to take over
increase in cardiac output, drying of secretions

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7
Q

atropine clinical

A

CV: +chrono, +dromo, slight +ino, increased cardiac output
Resp: decreased mucus production, bronchodilation
GI: decreased secretion, motility
GU: decreased urinary bladder tone
Misc: mydriasis decreased sweat production

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8
Q

bumetanide

A

inhibity electrolyte reabsorption in ascending loop of henle leading to diuresis

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9
Q

calcium chloride

A 
increases ECF ICF calcium levels
stimulates release of catecholamines
\+ino
may enhance ventricular automaticity
inhibits effects of adenosine on mast cells
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10
Q

calcium gluconate gel

A

neutralizes hydrofluoric acid to form calcium fluoride

helps stop fluoride ion from penetrating tissue and bone

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11
Q

activated charcoal

A

pharmacological: physical binding of toxins from GI tract
clinical: prevents/reduces systemic absorption of toxins

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12
Q

cimetidine

A

competitively inhibits action of histamine at h2 sites of parietal cells decreasing gastric acid secretion

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13
Q

dexamethasone sodium phosphate

A

improves lung function and myocardial performance

decrease in pulmonary edema, relaxation of bronchospasm

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14
Q

D50

A

pharm: aerobic metabolic substrate
clinical: reverses CNS effects of hypoglycemia by rapidly increasing serum glucose levels
provides short term osmotic diuresis

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15
Q

diazepam

A 
works on parts of limbic system, thalmus, and hypothalamus producing calming effects
increases seizure threshold
transient analgesia
amnesic
sedative
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16
Q

diltiazem

A

pharm: inhibits calcium ion influx during cardiac depolarization, decreases SA and AV conduction and dilates coronary and peripheral arteries and arterioles
clinical: slows rapid ventricular rate associated with a-fib and flutter, reduces coronary and peripheral vascular resistance

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17
Q

diphenhydramine

A

blocks histamine receptors
decreased capillary permeability and decreased vasodilation, prevention of bronchospasm
some anticholinergic effects

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18
Q

dopamine 1-2 mcg

A

dopaminergic receptors to stimulate cerebral renal and mesenteric vasodilation, HR BP usually unchanged

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19
Q

dopamine 2-10 mcg

A

B1 receptors, increased cardiac output, modest increase in SVR

20
Q

dopamine 10-20 mcg

A

a adrenergic effects, renal mesenteric peripheral arterial and venous vasoconstriction, marked increase in SVR, pulmonary vascula resistance, further increased preload

21
Q

dopamine >20 mcg

A

effects similar to norepi, may increase HR and o2 demand to undesirable levels

22
Q

epi pharmacological

A

A&B agonist, A-increased SVR, B1- +inotropic and chronotropic increases automaticity and irritability
B2- bronchodilation, dilation of skeletal vasculature

23
Q

epi clinical

A

cardiac arrest- increases cerebral and myocardial perfusion pressure, increases bp, increases electrical activity in myocardium
bradycardia- +chrono, increases bp,
reverses s/s of bronchospasm and anaphylaxis

24
Q

etomidate

A

produces hypnosis rapidly causing CNS depression and anesthesia, no analgesic effect

25
Q

fentanyl citrate

A

alleviates pain by acting on pain receptors in brain, elevates pain threshold
depresses CNS, depresses brainstem respiratory centers
increases venous pooling, vasodilates arterioles thus reducing preload and afterload

26
Q

furosemide

A

pharm: inhibits NA K chloride reabsorption in ascending loop of henle, venous pooling and decreased afterload
clinical: diruesis

27
Q

glucagon pharmacological

A

acts only on liver glycogen, converting it to glucose, counteracts effects of insulin, relases gi smooth muscle causing dilation and decreased motility
cardiac inotrope

28
Q

glucagon clinical

A

may reverse hypoglycemia within 4 mins

29
Q

hydroxocobalamin

A

binds to cyanide ions

30
Q

ipratropium bromide

A

anticholinergic agent, antagonizes action of ACH

31
Q

ketamine

A

produces dissociative anesthesia
minimal cardiac depression
bronchodilator, respiratory stimulation frequently seen

32
Q

lidocaine

A

decreases automaticity by slowing rate of spontaneous phase 4 depolarization
terminate re-entry by decreasing conduction in re-entrant pathways
increases v-fib threshold

33
Q

lorazepam

A

high afinity for GABA benzo receptor without displacing GABE

exerts tranquilizing action on CNS

34
Q

magnesium sulfate

A

decreases myocardial irritability and neuromuscular irritability
reduces ventricular irritability
inhibition of muscular excitability

35
Q

solu-medrol

A

thought to stabilize cellular and intracellular membranes

36
Q

midazolam

A

CNS effects mediated through GABA
acts on limbic, thalamic, and hypothlamic levels of CNS producing anxiolytic, sedative, hypnotic, and anticonvulsant effects
capable of producing all levels of CNS depression, from mild sedation to coma

37
Q

morphine

A

acts on pain receptors in brain, elevates pain threshold
depresses CNS, respiratory centers
venous pooling, vasodilates arterioles, reducing preload and afterload
histamine release

38
Q

nitro

A 
smooth muscle relaxant on vascular, uterine, bronchial, and intestinal smooth muscle
decreases preload and afterload
coronary artery vasodilation
increases blood flow to myocardium
decreases myocardial o2 demand
39
Q

norepi

A

stimulates b1 and a1 receptors causing vasoconstriction, increased bp, enhanced contractility and decreased heart rate

40
Q

ondanestron

A

selectively blocks serotonin 5-HT3 receptors located in CNS at chemoreceptor trigger zone and in peripheral nervous syste on nerve terminals of vagus nerve

41
Q

oxytocin

A

binds to oxytocin receptor sites on surface of uterine smooth muscles, increases force and frequency of uterine contractions

42
Q

propofol

A

produces effects by positive modulation of GABA through ligand-gated GABA receptors

43
Q

sodium bicarbonate

A

buffers H+ and increases PH

44
Q

succinylcholine

A

combines with cholinergic receptors of the motor end plate to produce depolarization hydrolyzed by ACHe

45
Q

vasopressin

A

causes vasoconstriction of peripheral, cerebral, pulmonary, and coronary vessels

46
Q

verapamil

A

blocks calcium ion influx results in negative inotropy
coronary and peripheral vasodilation
slows conduction and prolongs refractory period in AV node
slows SA discharge
in summary, decreases myocardial contractile force and slows AV conduction

Arizona Drug Profiles (5 decks)

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