Mechanism of Action

Question 1

Mechanism of Action Fentanyl

Answer 1

Potent, short-acting, synthetic narcotic agonist analgesic. Principle actions are analgesia and sedation. Inhibits ascending pain pathways in CNS, increases pain threshold, and alters pain perception by binding to opiate receptors.

Question 2

MOA ketorolac (Toradol)

Answer 2

Reversibly blocks the action of cyclooxygenase which in turn prevents the formation of prostaglandins. Ketorolac causes analgesia equivalent to that of morphine sulfate.

Question 3

MOA morphine sulfate

Answer 3

A naturally occurring opiate which acts on opiate receptors in the
brain, providing sedation and analgesia. Additionally, its
vasodilatory properties (which are caused by mast cell
degranulation and histamine release) increase peripheral venous
capacity and decrease venous return to the heart. This reduces
cardiac workload, decreases myocardial oxygen demand, and
decreases pulmonary venous congestion.

Question 4

MOA nitrous oxide (Nitronox)

Answer 4

CNS depressant with analgesic properties.

50/50 mixture of nitrous oxide and oxygen.

Question 5

MOA proparacaine (Alcaine)

Answer 5

Provides topical anesthesia to eye by preventing the transmission
of nerve impulses by inhibiting the sodium channels along a nerve pathway, thus interrupting the action potential.

Question 6

MOA activated charcoal (Actidose)

Answer 6

A fine black powder that acts by binding and adsorbing ingested
drugs/toxins/chemicals present in the gastrointestinal tract. This
inhibits their absorption and thus, bioavailability. It acts as an
efficient adsorber due to its large surface area. Once bound, the combined complex is excreted from the body in the feces.

Question 7

MOA Cyanide antidote kit (Lily kit)

Answer 7

Cyanide (CN) binds to iron (Fe) in mitochondria disrupting their
ability to enter the citric acid cycle associated with aerobic
metabolism and thus the cell does not produce an adequate
amount of ATP. Amyl nitrite and sodium nitrite oxidize the Fe in
hemoglobin creating methemoglobin, which is unable to bind to
oxygen. CN then is able to bind to the methemoglobin instead of
the Fe in the mitochondria creating cyanmethemoglobin. Sodium
thiosulfate then converts the cyanmethemoglobin into thiocyanate,
sufite, and hemoglobin. The thiocyanate and sulfite are then
excreted.

Question 8

MOA hydroxocobolamin (CyanoKit)

Answer 8

Hydroxocobolamin is the precursor to vitamin B12 (cyancobolamin). When exposed to hydroxocobolamin, the cyanide attaches itself to form vitamin B12. It is then safely excreted in the urine.

Question 9

MOA flumazenil (Romazicon)

Answer 9

Competitive inhibition of benzodiazepine receptors in the CNS. It blocks both the sedative and anticonvulsant actions of benzodiazepines.

Question 10

MOA Mark-1 kit (NAAK: Nerve Agent Antidote Kit)

Answer 10

Atropine counters the parasympathetic response from muscarinic
receptor over-stimulation associated with organophosphate and
nerve agent poisoning, thus alleviating “SLUDGEM” symptoms

Question 11

MOA naloxone (Narcan)

Answer 11

Competes for, and displaces, narcotic molecules from opiate receptors in the brain.

Question 12

MOA adenosine (Adenocard)

Answer 12

A naturally occurring nucleoside that decreases conduction
through the AV node and interrupts AV and SA re-entry pathways
thus restoring normal sinus rhythm in patients with SVT.

Question 13

MOA amiodarone (Cordarone)

Answer 13

Amiodarone is a unique Class III antidysrhythmic that acts directly on all cardiac tissues. It prolongs the duration of the action potential and refractory period (by blocking potassium channels) without significantly affecting the resting membrane potential. It also blocks sodium channels. The IV form relaxes vascular smooth muscle, decreases peripheral vascular resistance and increases coronary blood flow. Additionally, it blocks the effects of sympathetic stimulation

Question 14

MOA digoxin (Lanoxin)

Answer 14

Increases cardiac contractile force and cardiac output. Reduces
edema associated with congestive heart failure by reducing left
ventricular diameter and decreasing venous pressure thereby
hastening the reduction of peripheral and pulmonary edema.
Slows AV conduction reducing rapid atrial rates in A-Fib and
A-Flutter.

Question 15

MOA diltiazem (Cardizem)

Answer 15

Inhibits calcium ion influx through slow channels into cells of
myocardial and arterial smooth muscle. This causes intracellular calcium to remain at sub-threshold levels that are insufficient to stimulate cell excitation and contraction. It reduces peripheral vascular resistance by inhibiting the contractility of vascular smooth muscle which causes dilation of the coronary arteries. It also inhibits coronary artery spasm. Diltiazem also slows SA and AV node conduction without affecting atrial action potential.

Question 16

MOA lidocaine (Xylocaine)

Answer 16

Suppresses depolarization and automaticity in the His-Purkinje
system. Also suppresses ventricular ectopy and increases the ventricular threshold for dysrhythmias; however it decreases
the ventricular threshold for defibrillation.

Question 17

MOA metoprolol (Lopressor, Toprol-XL)

Answer 17

Selective inhibitor of Beta-1 adrenergic receptors located on
cardiac muscle. Completely blocks Beta-1 receptors, with little or no effect on Beta-2 receptors at doses less than 100 mg. Reduces heart rate, cardiac output at rest and during exercise, and lowers BP.

Question 18

MOA procainamide (Pronestyl)

Answer 18

Suppresses atrial and ventricular ectopy by reducing the excitability of the myocardium to electrical stimulation, and reducing conduction velocity in the atria, ventricles and His-Purkinje system. It also increases the duration of the refractory period. Procainamide also produces peripheral vasodilation.

Question 19

MOA verapamil (Isoptin) (Calan)

Answer 19

As a calcium-ion antagonist verapamil causes a relaxation of
vascular smooth muscle and slows conduction through the AV
node. This prevents the reentry mechanism of SVTs and
decreases the rapid ventricular response seen in A-Fib/ Flutter.
Additionally, the myocardial oxygen demand is decreased due to
its negative inotropic effects (vasodilation).

Question 20

MOA ondansetron (Zofran)

Answer 20

A serotonin receptor antagonist that prevents acute emesis by blocking serotonin receptors in the chemoreceptor triggering zone (CTZ) and afferent vagal neurons in the upper GI tract. It does not have prophylactic properties, and therefore has no effect on delayed emesis. It will not cause extrapyramidal syndrome (EPS) or acute dystonic reactions because it does not block dopamine receptors.

Question 21

MOA promethazine (Phenergan)

Answer 21

Decreases nausea by blocking dopamine and H1 receptors associated with vagal stimulation of the emesis center in the
medulla. It also decreases the effects of muscarinic receptors in
the GI thus decreasing gastric secretions and peristalsis.

Question 22

MOA acetaminophen (Tylenol, APAP)

Answer 22

Produces analgesia by elevation of the pain threshold. May block
pain impulses by the inhibition of prostaglandin synthesis.
Antipyretic actions result from inhibition of prostaglandins in the
CNS. Does not possess any anti-inflammatory or antiplatelet
properties.

Question 23

MOA ibuprofen (Advil, Motrin, Nuprin)

Answer 23

Ibuprofen inhibits cyclooxygenase (COX) decreasing production of
prostaglandins thus decreasing pain sensation, fever, and inflammation.

Question 24

MOA diazepam (Valium)

Answer 24

By intensifying the activity of GABA, it suppresses the spread of seizure activity through the motor cortex of the brain. It is effective in the management of stress, anxiety, and alcohol withdrawal due to its sedative properties. Additionally, it is effective as a premedication for minor orthopedic procedures due to its skeletal muscle relaxant properties, and as a premedication for cardioversion because it produces amnesia.

Question 25

MOA lorazepam (Ativan)

Answer 25

Most potent of the benzodiazepines. It acts as an anxiolytic, sedative, hypnotic, and skeletal muscle relaxant. It intensifies GABA. Because of its short half-life it is the preferred benzodiazepine for the treatment of pediatric seizures.

Question 26

MOA midazolam (Versed)

Answer 26

This short-acting benzodiazepine intensifies activity of GABA. It
also has CNS depressant, anticonvulsant and anterograde
amnestic properties. It also relaxes skeletal muscles and induces
sleep.

Question 27

MOA calcium chloride

Answer 27

Replaces elemental calcium, which is essential for regulating excitation threshold of nerves and muscles. Calcium is also essential for blood clotting mechanisms, maintenance of renal function, and bone tissues. Calcium increases myocardial contractile force and ventricular automaticity. Additionally serves as an antidote for magnesium sulfate and calcium channel blocker toxicity. Calcium chloride has three times as much elemental calcium than calcium gluconate.

Question 28

MOA magnesium sulfate

Answer 28

Physiologic calcium channel blocker and also blocks
neuromuscular transmission. Hypomagnesemia can cause cardiac
dysrhythmias. It is also a CNS depressant effective in the
management of seizures associated with eclampsia or pregnancy.
It does this by decreasing the amount of acetylcholine
liberated from motor nerve terminals. Magnesium is necessary for
many biochemical processes and plays a role in the transmission
of electrical impulses.

Question 29

MOA sodium bicarbonate (NaHCO3)

Answer 29

Given IV, it immediately raises the pH of blood plasma by buffering
excess H+ cations. Excess bicarbonate ions are excreted in the
urine, thus rendering the urine less acidic.

Question 30

MOA glucagon (GlucaGen)

Answer 30

Glucagon is a protein secreted by the alpha cells of the Islets of
Langerhans in the pancreas. It is used to convert stored glycogen in the liver to glucose. Additionally, it inhibits the synthesis of glycogen from glucose. It enhances conventional treatments for calcium channel blocker and beta-blocker overdose by producing a positive inotropic and chronotropic effect on the heart via stimulation of glucagon specific receptors in the myocardium. These receptors are not affected by even massive doses of beta-blockers, thereby reversing hypotension and bradycardia.

Question 31

MOA oxytocin (Pitocin)

Answer 31

By direct action on myofibrils, it causes phasic contraction of the
uterine smooth muscle characteristic of normal delivery. It also
promotes milk “letdown” in nursing mothers. Effective in inducing
labor and uterine contractions following delivery, thereby
controlling postpartum hemorrhage.

Question 32

MOA vasopressin (Pitressin)

Answer 32

Vasopressin possesses pressor and antidiuretic properties.
It increases nephron distal tube reabsorption of water. In
unnaturally high doses, it acts as a non-adrenergic vasoconstrictor
by stimulation of smooth muscle receptors. It is used as an
alternative to epinephrine during CPR.

Question 33

MOA atropine sulfate

Answer 33

Blocks muscarinic acetylcholine receptors thus inhibiting
parasympathetic stimulation. By blocking vagal impulses to the
heart it accelerates SA node discharge, enhances conduction through the AV junction, and increases cardiac output. It is also a potent bronchodilator when bronchoconstriction is caused by increased parasympathetic tone.

Question 34

MOA ipratropium bromide (Atrovent)

Answer 34

Acts directly on the smooth muscle of the bronchial tree by
inhibiting interaction of acetylcholine at receptor sites on the
bronchial smooth muscle, resulting in bronchodilation.

Question 35

MOA albuterol (Proventil, Ventolin)

Answer 35

Selectively stimulates Beta-2 adrenergic receptors increasing
bronchodilation. It produces these results by stimulating adenyl cyclase, which transforms ATP into cAMP. cAMP causes relaxation of bronchial smooth muscle. In therapeutic doses, albuterol also inhibits histamine release from mast cells, reducing mucus secretion.

Question 36

MOA dobutamine (Dobutrex)

Answer 36

Synthetic catecholamine which acts primarily on Beta-1 and
alpha-adrenergic receptors. Balanced by Beta-2 receptors, it
increases cardiac output via increased inotropic effects and decreases pulmonary wedge pressure (PWP) with little or no effect on BP or heart rate. Dobutamine also increases conduction through the AV node.

Question 37

MOA dopamine (Intropin)

Answer 37

A naturally occurring neurotransmitter and catecholamine which
acts on alpha and beta adrenergic receptors (dose-dependent), and dopaminergic receptors. In therapeutic dosages, dopamine maintains blood flow in the renal and mesenteric vascular beds. It is a positive inotrope, therefore it increases cardiac output and systolic BP.

Question 38

MOA epinephrine (Adrenalin)

Answer 38

naturally-occurring catecholamine that acts directly on the alpha
and beta (more profound) adrenergic receptors.
This causes positive inotropic, dromotropic, and chronotropic
effects as well as increased systemic vascular resistance and BP.

Question 39

MOA aspirin

Answer 39

Aspirin blocks the production of cyclooxygenase (COX), the precurser to Thromboxane A2 (which is the physiological inducer of platelet aggregation). As an anti-inflammatory agent it appears to be involved in the inhibition of prostaglandin synthesis. Its anti-inflammatory actions also contribute to its analgesic effects. Aspirin also acts to reduce fever by causing centrally-mediated peripheral vasodilation and sweating.

Question 40

MOA 50% dextrose in water (D50W or “D50”)

Answer 40

Principal form of glucose used by the body to create energy.

Question 41

MOA diphenhydramine (Benedryl)

Answer 41

Blocks histamine H1 (bronchoconstriction, peripheral vasodilation)
receptors, and blocks acetylcholine receptor sites (anticholinergic).
Also useful in reversing dsytonic reactions caused by certain
antipsychotic medications that block histamine receptor sites
(thorazine, compazine, reglan, haldol, phenergan).

Question 42

MOA furosemide (Lasix)

Answer 42

Rapid-acting potent loop diuretic that inhibits sodium and chloride
reabsorption in the nephron’s loop of Henle. Additionally, its
vasodilatory properties reduce cardiac preload.

Question 43

MOA haloperidol (Haldol)

Answer 43

Causes sedation by decreasing nerve impulse transmission by

blocking dopamine and serotonin receptors in the CNS.

Question 44

MOA methylprednisolone (Solu-Medrol)

Answer 44

Intermediate-acting, synthetic adrenal corticosteroid. Decreases inflammation by reversing increased capillary permeability. This suppresses the migration of leukocytes and fibroblasts to the site of injury. Methylprednisolone also stabilizes lysosomes.

Question 45

MOA nitroglycerin (Nitrostat, Nitro-Bid, Tridil)

Answer 45

Rapid vascular smooth muscle relaxant that increases coronary blood flow and improves perfusion of the ischemic myocardium. This results in decreased venous return to the heart, alleviation of chest pain, and a decrease in preload and afterload in the left ventricle.

Question 46

MOA oxygen

Answer 46

A colorless, odorless, tasteless gas necessary for the breakdown
of glucose into a usable energy form.

Question 47

MOA succinylcholine (Anectine)

Answer 47

Synthetic, ultra short-acting neuromuscular blocking agent.
Succinylcholine is composed of two adjacent acetylcholine
molecules and has a high affinity for acetylcholine receptors. It
causes transient muscle contractions called fasciculations followed
by skeletal muscle paralysis. There is no effect on level of
consciousness.

Question 48

MOA thiamine

Answer 48

It is an essential coenzyme in carbohydrate metabolism, required
for the metabolism of pyruvic acid to acetyl-coenzyme-A.
The brain is extremely sensitive to thiamine deficiency and
chronic alcohol intake interferes with the absorption, intake, and use of thiamine. Wernicke’s syndrome and Korsakoff’s psychosis can result from thiamine deficiency.