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AEMT class > Drug Action > Flashcards

Drug Action Flashcards

1
Q

Acetazolamide

A

Action: Inhibits hydrogen ion excretion in renal tubule,
increasing sodium,
potassium,
bicarbonate,
and water excretion and producing alkaline diuresis

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2
Q

Acetaminophen

A

Action: May work peripherally to block pain impulse generation; may also inhibitprostaglandin synthesis in CNS

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3
Q

Acetic acid

A

Mechanism of action: Provides an acidic medium
during irrigation of the ear that minimizes
bacterial and fungal promulgation,
Stabilizes nematocyst discharge in non-United States jellyfish, thus decreasing pain

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4
Q

Acetylcysteine

A

Mechanism of action: Lowers mucus viscosity,
restores glutathione concentrations within
the liver,
Acts as sulfhydryl group donor to restore liver glutathione; may also scavenge free radicals to prevent delayed hepatotoxicity as antioxidant; encourages sulfation pathway of metabolism for acetaminophen

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5
Q

Activated Charcoal

A

Mechanism of action: Adsorbs toxic substances
from the GI tract
Absorbs a variety of drugs and chemicals (e.g., physical binding of a molecule to the surface of charcoal particles); desorption of bound particles may occur unless the ratio of charcoal to toxin is exceptionally high

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6
Q

Adenosine

A

Mechanism of action: Slows conduction through
the AV node; can interrupt reentrant AV nodal
pathways

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7
Q

Albuterol

A

Mechanism of action: Selective beta-2 agonist
that stimulates adrenergic receptors of the
sympathomimetic nervous system. Results in
smooth-muscle relaxation in the bronchial tree
and peripheral vasculature

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8
Q

Amiodarone

A

Mechanism of action: Blocks sodium, potassium,
and calcium channels; prolongs the action
potential and repolarization; decreases AV
conduction and sinoatrial (SA) node function

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9
Q

Amyl Nitrite

A

Mechanism of action: Converts hemoglobin to
methemoglobin, which reacts with cyanide and
chemically binds with it, preventing any toxic
effects

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10
Q

Aspirin

A

Mechanism of action: Prevents the formation
of thromboxane A2, which causes platelets to
clump together (aggregate) and form plugs that
cause obstruction or constriction; has antipyretic
and analgesic properties

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11
Q

Atropine

A

Mechanism of action: Inhibits the action of
acetylcholine at postganglionic parasympathetic
neuroeffector sites. Increases heart rate in
symptomatic bradydysrhythmias
Competitively inhibits the action of acetylcholinesterase on autonomic effectors innervated by postganglionic nerves

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12
Q

Calcium Chloride

A

Mechanism of action: Increases cardiac contractile
state (positive inotropic effect). May enhance
ventricular automaticity
Bone mineral component; cofactor in enzymatic reactions, essential for neurotransmission, muscle contraction, and many signal transduction pathways

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13
Q

Calcium Gluconate

A

Mechanism of action: Counteracts the toxicity of
hyperkalemia by stabilizing the membranes
of the cardiac cells, reducing the likelihood of
fibrillation
Bone mineral component; cofactor in enzymatic reactions, essential for neurotransmission, muscle contraction, and many signal transduction pathways

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14
Q

Cimetidine

A

Mechanism of action: Blocks the effects of
histamine at H2 receptors of gastric parietal cells,
leading to a reduction of gastric acid volume
and gastric acidity

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15
Q

Dexamethasone

A

Action: Potent glucocorticoid with minimal to no mineralocorticoid activity Decreases inflammation by suppressing migration of polymorphonuclear leukocytes (PMNs) and reducing capillary permeability; stabilizes cell and lysosomal membranes, increases surfactant synthesis, increases serum vitamin A concentration, and inhibits prostaglandin and proinflammatory cytokines; suppresses lymphocyte proliferation through direct cytolysis, inhibits mitosis breaks down granulocyte aggregates, and improves pulmonary microcirculation

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16
Q

Diazepam

A

Action: Modulated postsynaptic effects of GABA-A transmission, increasing presynaptic inhibition. It appears to act on the part of the limbic system, as well as on the thalamus and hypothalamus, to induce a calming effect

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17
Q

Diltiazem

A

Action: Inhibits extracellular calcium ion influx across membranes of myocardial cells and vascular smooth muscle cells, resulting in inhibition of cardiac and cascular smooth muscle contrction and thereby dilating main coronary and systemic arteries; no effect on serum calcium concenrations; substantial inhibitory effects on cardiac conduction system, acting principally at AV node with some effects at the sinus node

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18
Q

Diphenhydramine

A

Action: Histamine H1-receptor antagonist of effector cells in the respiratory tract, blood vessels, and GI smooth muscle

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19
Q

Dopamine

A

Action: Endogenous catecholamine, acting on both dopaminergic and adrenergic neurons. Low dose stimulates mainly dopaminergic receptors, producing renal and mesenteric vasodilation; higher dose stimulates both beta-1-adrenergic and dopaminergic receptors, producing cardiac stimulation and renal vasodilation; large dose stimulates alpha-adrenergic receptors

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20
Q

Droperidol

A

Action: Antiemesis: dopamine receptor blockade in brain, predominantly dopamine-2 receptor.
When reuptake is prevented, a strong antidopaminergic, antiserotonergic response occurs
Droperidol reduces motor activity anxiety and causes sedation; it also possesses adrenergic-blocking, antifibrillatory, antihistaminic, and anticonvulsive properties

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21
Q

Epinephrine

A

Action: Strong alpha-adrenergic effects, which cause an increase in cardiac output and heart rate, a decrease in renal perfusion and peripheral vascular resistance, and a variable effect on BP, resulting in systemic vasoconstriction and increased vascular permeability. Strong beta-1-and moderate beta-2-adrenergic effects, resulting in bronchial smooth muscle relaxation
Secondary relaxation effect on the smooth muscle of stomach, intestine, uterus, and urinary bladder

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22
Q

Famotidine

A

Action: Blocks H2 receptors of gastric parietal cells, leading to inhibition of gastric secretions

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23
Q

Fentanyl

A

Action: Narcotic agonist-analgesic of opiate receptors; inhibits ascending pain pathways, thus altering response to pain; increases pain threshold; produces analgesia, respiratory depression and sedation

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24
Q

Glucagon

A

Action: Insulin antagonist. Stimulates cAMP synthesis to accelerate hepatic glycogenolysis and gluconeogenesis.
Glucagon also relaxes smooth muscles of the GI tract

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25
Q

Haloperidol

A

Action: Antagonizes dopamine-1 and dopamine-2 receptors in the brain; depresses reticularactivating system and inhibits the release of hypothalamic and hypophyseal hormones

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26
Q

Helium Gas Mixture

A

Pharmacology: Less resistant that atmospheric air, which may reduce the pt’s work of breathing by increasing tendency to laminar flow and reducing resistance to turbulent flow

27
Q

Hydralazine

A

Pharmacology: Direct vasodilator at the level of arterioles, with little effect on veins.
Decreases systemic resistance

28
Q

Hydrocortisone succinate

A

Action: Glucocorticoid; elicits mild mineralocorticoid activity and moderate anti-inflammatory effects; controls or prevents inflammation by controlling rate of protein synthesis, suppressing migration of polymorphonuclear leukocytes (PMNs) and fibroblasts, and reversing capillary permeability

29
Q

Hydromorphone

A

Pharmacology: Narcotic agonist-analgesic of opiate receptors; inhibits ascending pain pathways, thus altering response to pain; increases pain the threshold; produces analgesia, respiratory depression, and sedation

30
Q

Hydroxocobalamin

A

Action: Vitamin B12 with hydroxyl group complexed to cobalt which can be displaced by cyanide resulting in cyanocobalamin that is renally excreted

31
Q

Ibuprofen

A

Action: INhibits synthesis of prostaglandins in body tissues by inhibiting at least two cyclooxygenase (COX) isoenzymes, COX-1 and COX-2.
May inhibit chemotaxis, alter lymphocyte activity, decrease proinflammatory cytokine activity, and inhibit neutrophil aggregation; these effects may contribute to anti-inflammatory activity

32
Q

Ipratropium

A

Action: Anticholinergic (parasympatholytic) agent; inhibits vagally mediated reflexes by antagonizing acetylcholine action; prevents an increase in intracellular calcium concentration that is caused by the interaction of acetylcholine with muscarinic receptors on bronchial smooth muscle

33
Q

Isopropyl Alchohol

A

Pharmacology: In addition to its traditional role as an antiseptic, it may be used as antiemetic

34
Q

Ketamine

A

Action: Produces dissociative anesthia.

Blocks N-methyl D-aspartate (NMDA) receptor

35
Q

Ketorolac

A

Action: Inhibits synthesis of prostaglandins in body tissues by inhibiting at least two cyclooxygenase (COX) isoenzymes, COX-1 and COX-2.
May inhibit chemotaxis, alter lymphocyte activity, decrease proinflammatory cytokine activity, and inhibit neutrophil aggregation; these effects may contribute to anti-inflammatory activity

36
Q

Labetalol

A

Pharmacology: Nonselective beta-blockers with intrinsic sympathomimetic activity; also alpha-blocker

37
Q

Lidocaine

A

Action: Class 1b antidysrhythmic; combines with fast sodium channels and thereby inhibits recovery after repolarization, resulting in decreasing myocardial excitability and conduction velocity

38
Q

Lorazepam

A

Action: Desative hypnotic with the short onset of effect and relatively long half-life; by increasing the action of gamma-aminobutyric acid (GABA), which is a major inhibitory neurotransmitter in the brain, lorazepam may depress all levels of the CNS, including limbic and reticular formation

39
Q

Magnesium sulfate

A

Action: Depresses CNS, blocks peripheral neuromuscular transmission, produces anticonvulsant effects, decreases the amount of acetylcholine released at end-plate by a motor nerve impulse. Slows rate of sino-atrial (SA) node impulse formation in the myocardium and prolongs conduction time. Promotes movement of calcium, potassium, and sodium in and out of cells an stabilizes excitablemembranes

40
Q

Methylprednisolone

A

Action: Potent glucocorticoid with minimal to no mineralocorticoid activity
Modulates carbohydrate, protien, and lipid metabolism and maintains fluid and electrolyte homeostasis.
Controls or precents inflammation by controlling the rate of protein synthesis, suppressing migration of polymorphonuclear leukocytes (PMNs) and fibroblasts, reversing capillary permeability, and stabilizing lysosomes at the cellular level

41
Q

Metoclopramide

A

Action: Blocks dopamine receptors (at high dose) and serotonin receptors in chemoreceptors trigger zone of CNS, and sensitizes tissues to acetylcholine; increases upper GI motility by not secretions; increases lower esophageal sphincter tone

42
Q

Metoprolol

A

Action: Blocks response to beta-adrenergic stimulation; cardioselective for beta-1 receptors at low doses, with little or no effect on beta-2 receptors

43
Q

Midazolam

A

Action: Binds receptors at several sites within the CNS, including the limbic system and reticular formation; effects may be mediated through gabba-aminobutyric acid (GABA) receptor system; increase in neuronal membrane permeability to chloride ions enhances the inhibitory effects of GABA; the shift in chloride ions causes hyperpolarization (less excitability) and stabilization of the neuronal membrane

44
Q

Morphine Sulfate

A

Action: Narcotic agonist-analgesic of opiate receptors; inhibits ascending pain pathways, thus altering response to pain; produces analgesia, respiratory depression, and sedation; suppresses cough by acting centrally in the medulla

45
Q

Naloxone

A

Action: Competitive opioid antagonist; synthetic congener of oxymorphone

46
Q

Nifedipine

A

Action: Calcium-channel blocker; inhibits the transmembrane influx of extracellular calcium ions across myocardial and vascular smooth muscle cell membranes without changing serum calcium concentrations; this results in inhibition of cardiac and vascular smooth muscle contraction, dilating main coronary and systemic arteries. Vasodilation with decreased peripheral resistance and increased heart rate

47
Q

Nitrous Oxide

A

Action: It’s analgesic mechanism of action is described as an opioid and may involve several spinal neuromodulators. The anxiolytic effect is similar to that of benzodiazepine and may involve gamma-aminobutyric (GABA) receptors. The anesthesia mechanism may involve GABA and possibly N-methyl-D-aspartate receptors as well. In general, the effect of nitrous oxide ceases as soon as the inhalation stops, with no residual effect

48
Q

Nitroglycerin

A

Action: Organic nitrate, which causes systemic venodilation, decreasing preload. Cellular mechanism: nitrate enters vascular smooth muscle and is concerted to nitric oxide (NO), leading to cyclic guanosine monophosphate (cGMP) activation and vasodilation. Relaxes smooth muscle via dose-dependent dilation of arterial and venous beds to reduce both preload and afterload and myocardial O2 demand. It also improves coronary collateral circulation. Lower BP, increases heart rate, occasional paradoxical bradycardia

49
Q

Norepinephrine

A

Action: Strong beta-1 and alpha-adrenergic effects and moderate beta-2 effects, which increase cardiac output and heart rate, decrease renal perfusion and peripheral vascular resistance and cause variable BP effects

50
Q

Olanzapine

A

Action: May act through a combination of dopamine and serotonin type 2 receptor site antagonism

51
Q

Ondansetron

A

Action: Mechanism not fully characterized; selective 5-HT3 receptor antagonist; binds to 5-HT3 receptors both in periphery and CNS, with primary effects in the GI tract. It does not affect dopamine receptors and therefore does not cause extrapyramidal symptoms

52
Q

Oxymetazoline

A

Action: Alpha-adrenergic agonist; stimulates alpha-adrenergic receptors and produces vasocontraction in the arterioles of the nasal mucosa

53
Q

Potassium iodide

A

Action: As thyroid protective agent: systemically circulating potassium iodide is readily taken up by thyroid gland by sodium/iodide transporter in the basal membrane; blocking the thyroid uptake of radioactive isotopes of iodine; concentration gradient of the thyroid gland to plasma is 20-50:1

54
Q

Pralidoxime chloride (2-PAM)

A

Action: Binds to organophosphates and breaks alkyl phosphate-cholinesterase bond to restore and activity of acetylcholinesterase

55
Q

Procainamide

A

Action: Class la (membrane-stabilizing) antidysrhythmic agent; inhibits recovery after repolarization, decreasing myocardial excitability and conduction velocity. Direct membrane depressant that decreases conduction velocity prolongs refractoriness, decreases automaticity, and reduces repolarization abnormalities

56
Q

Prochlorperazine

A

Action: Antiemetic: antidopaminergic effect, blocking dopamine receptors in the brain, blocking vagus nerve in GI tract.
Antipsychotic: blocking mesolimbic dopamine receptors and blocking alpha-adrenergic receptors (D1 and D2) in the brain

57
Q

Sildenafil

A

Action: Inhibits PDE-5 increasing cyclic guanosine monophosphate (cGMP) to allow smooth-muscle relaxation

58
Q

Sodium Bicarbonate

A

Action: Increases blood and urinary pH by releasing a bicarbonate ion, which in turn neutralizes hydrogen ion concentrations

59
Q

Sodium Nitrite

A

Action: Nitrites create methemoglobins to bind to cyanide

60
Q

Sodium Thiosulfate

A

Action: Thiosulfate is a sulfur donor utilized by rhodenase to convert cyanide to less toxic thiocyanate

61
Q

Sorbitol

A

Action: Polyalcoholic sugar with hyperosmotic effects

62
Q

Tadalafil

A

Action: Pulmonary arterial hypertension (PAH): inhibits PDE-5, increasing cyclic guanosine monophosphate (cGMP) to allow relaxation of pulmonary vascular smooth muscle cells and vasodilation of pulmonary vasculature

63
Q

Ziprasidone

A

Action: Acts as an antagonist at dopamine-2 and serotonin type 1 and 2 (5HT1D, 5HT2A) receptors; acts as an agonist at serotonin 5HT1A receptor; moderately inhibits the reuptake of norepinephrine and serotonin; has alpha-blocking and antihistaminic activity

AEMT class (14 decks)

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