Mechanism of Action

Question 1

ABCIXIMAB

mechanism of action

Answer 1

• Binds with Glycoprotein (GP) IIb/IIIa receptors on the surface of platelets inhibiting the final common pathway for platelet aggregation.
• Binding with GP IIb/IIIa receptors produces a blockade that interferes with fibrinogen, von Willebrand factor and other platelet aggregation modulators.
• Binding with GP IIb/IIIa receptors effectively prevents the formation of intravascular thrombus and may contribute to the resolution of pre-existing thrombus.

Question 2

ACETYLSALICYLIC ACID, ASPIRIN, ASA

mechanism of action

Answer 2

In small doses aspirin blocks thromboxane A2, a potent platelet aggregate and vasoconstrictor.
This property has led to its use in the acute phase of management of the myocardial infarction.
Decreased platelet aggregation.

Question 3

ACETYLSALICYLIC ACID, ASPIRIN, ASA (EMT Administration)

mechanism of action

Answer 3

In small doses aspirin blocks thromboxane A2, a potent platelet aggregate and vasoconstrictor.
This property has led to its use in the acute phase of management of the myocardial infarction.
Decreased platelet aggregation.

Question 4

ADENOSINE

mechanism of action

Answer 4

Slows conduction time through AV node; can interrupt re-entrant pathways through the AV node.
Slows sinus rate.
Larger doses decrease BP by decreasing peripheral resistance.

Question 5

ALBUMIN, normal serum 5% / 25%

mechanism of action

Answer 5

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

Question 6

ALUTEROL SULFATE

mechanism of action

Answer 6

ß agonist (primarily ß2); relaxes bronchial smooth muscle, resulting in bronchodilation; also relaxes vascular and uterine smooth muscle; decreases airway resistance

Question 7

AMIODARONE

mechanism of action

Answer 7

Multiple effects on sodium, potassium and calcium channels.
Prolongs action potential, refractory period.
Ventricular automaticity (potassium channel blockade).
Slows membrane depolarization and impulse conduction (sodium channel blockade).
Negative chronotropic activity in nodal tissue, rate reduction, and antisympathetic
activity (calcium-blockade).

Question 8

ATROPINE SULFATE

mechanism of action

Answer 8

Pharmacological: Blocks the action of acetylcholine as a competitive antagonist at muscarinic receptor sites in smooth muscle, secretory glands, and the CNS. It works by blocking parasympathetic response and allowing sympathetic response to take over, resulting in an increase in cardiac output and the drying of secretions. Atropine reverses the muscarinic effects of cholinergic poisoning by primarily reversing bronchorrhea and bronchoconstriction. At high enough doses, atropine may have an effect on nicotinic receptors responsible for restlessness, hallucinations, disorientation, and/or delirium.
Clinical:
CV: Increased heart rate (positive chronotropic effect); increased conduction
velocity; increased force of contraction (slight), increase cardiac output. Resp: Decreased mucus production; increased bronchial smooth muscle
relaxation (bronchodilation).
GI: Decreased GI secretion and motility.
GU: Decreased urinary bladder tone.
Misc: Mydriasis (pupillary dilation); decreased sweat production.

Question 9

BUMETANIDE

mechanism of action

Answer 9

Inhibits electrolyte reabsorption in the ascending loop of Henle leading to diuresis

Question 10

CALCIUM CHLORIDE

mechanism of action

Answer 10

Increases extracellular and intracellular calcium levels
Stimulates release of catecholamines
Increases cardiac contractile state (positive inotropic effect)
May enhance ventricular automaticity
Inhibits the effects of adenosine on mast cells

Question 11

CALCIUM GLUCONATE GEL, 2.5%

mechanism of action

Answer 11

Calcium gluconate combines with hydrofluoric acid to neutralize the powerful fluoride ion, forming insoluble calcium fluoride. This helps stop the fluoride ion from penetrating into tissue and bone, preventing further damage. The gel does NOT treat or heal HF burns that have already developed.

Question 12

CHARCOAL, ACTIVATED (without sorbitol)

mechanism of action

Answer 12

Pharmacological: Physical binding (adsorption) of toxins from GI tract.
Clinical effects: Prevents/reduces systemic absorption of toxins.

Question 13

CIMETIDINE

mechanism of action

Answer 13

Competitively inhibits action of histamine at the H2 at receptor sites of parietal cells, decreasing gastric acid secretion.

Question 14

DEXAMETHASONE SODIUM PHOSPHATE

mechanism of action

Answer 14

Improves lung function and myocardial performance: stabilization of lysosomal and cell membranes, inhibition of compliment-induced granulocyte aggregation, rightward shift in oxygen-hemoglobin dissociation curve, inhibition of prostaglandin and leukotriene production, increase in surfactant production, decrease in pulmonary edema, relaxation of bronchospasm.

Question 15

DEXTROSE 50%

mechanism of action

Answer 15

Pharmacological: Aerobic metabolic substrate (ATP production).
Clinical effects: Reverses CNS effects of hypoglycemia by rapidly increasing serum glucose levels.
Provides short-term osmotic diuresis.

Question 16

DIAZEPAM

mechanism of action

Answer 16

Acts on parts of the limbic system, the thalamus, and hypothalamus producing calming effects; decreases seizures by increasing the seizure threshold; transient analgesia; amnesic; sedative.

Question 17

DILTIAZEM

mechanism of action

Answer 17

Pharmacological: Inhibits calcium ion influx across cell membranes during cardiac depolarization, decreases SA and AV conduction and dilates coronary and peripheral arteries and arterioles.
Clinical effects: Slows the rapid ventricular rate associated with atrial fibrillation and atrial flutter, and reduces coronary and peripheral vascular resistance.

Question 18

DIPHENHYDRAMINE HCL

mechanism of action

Answer 18

Blocks cellular histamine receptors, but does not prevent histamine release; results in decreased capillary permeability and decreased vasodilation, as well as prevention of bronchospasm.
Has some anticholinergic effects.

Question 19

DOPAMINE

mechanism of action

Answer 19

Effects are dose-dependent:
1-2 mcg/kg/min - Acts on dopaminergic receptors to stimulate cerebral, renal and mesenteric vasculature to dilate; HR and B/P are usually unchanged; may increase urine output

2-10 mcg/kg/min - ß1 stimulant action is primary effect (increases cardiac output and partially antagonizes the a-adrenergic-mediated vasoconstriction. Overall effect is increased cardiac output and only modest increase in systemic vascular resistance (SVR)

10-20 mcg/kg/min - a-adrenergic effects predominate resulting in renal, mesenteric and peripheral arterial and venous vasoconstriction with marked increase in SVR, pulmonary vascular resistance and further increased preload

> 20 mcg/kg/min - Produces hemodynamic effects similar to norepinephrine; may increase HR and O2 demand to undesirable limits

Question 20

EPINEPHRINE AUTO-INJECTOR

mechanism of action

Answer 20

Vasoconstrictor: Acts on alpha adrenergic receptors to counter vasodilation and increased vascular permeability that can lead to loss of intravascular fluid volume and hypotension during anaphylactic reaction.
Bronchodilator: Acts on beta receptors on bronchial smooth muscle to cause bronchial smooth muscle relaxation, which alleviates wheezing and dyspnea.
Alleviates pruritis, urticaria, and angioedema and may be effective in relieving gastrointestinal and genitourinary symptoms associated with anaphylaxis.

Question 21

EPINEPHRINE HCL

mechanism of action

Answer 21

Pharmacological Effects: Direct acting a and ß agonist; a-bronchial, cutaneous, renal, and visceral arterial constriction (increased systemic vascular resistance); ß1-positive inotropic and chronotropic actions (increases myocardial workload and oxygen requirements), increases automaticity and irritability; ß2 bronchial smooth muscle relaxation and dilation of skeletal vasculature.
Other: blocks histamine release
Clinical Effects: Cardiac Arrest-increases cerebral and myocardial perfusion pressure; increases systolic and diastolic blood pressures; increases electrical activity in the myocardium; can stimulate spontaneous contractions in asystole. Bradycardia-increases heart rate, increases BP; Bronchospasm/Anaphylaxis-reverse signs/symptoms

Question 22

EPTIFIBATIDE

mechanism of action

Answer 22

Reversibly binds with Glycoprotein (GP) IIb/IIIa receptors on the surface of platelets inhibiting the final common pathway for platelet aggregation. GP IIb/IIIa receptor blockade interferes with the binding of fibrinogen, von Willebrand factors and other platelet aggregation modulators to the surface of platelets thus preventing aggregation.

Question 23

ETOMIDATE

mechanism of action

Answer 23

Produces hypnosis rapidly causing CNS depression and anesthesia. No analgesic effect.

Question 24

FAMOTIDINE

mechanism of action

Answer 24

Competitively inhibits action of histamine at the H2 at receptor sites of parietal cells, decreasing gastric acid secretion.

Question 25

FENTANYL CITRATE | mechanism of action

Answer 25

Alleviates pain by acting on the pain receptors in the brain; elevates pain threshold. Depresses central nervous system; depresses brainstem respiratory centers; decreases responsiveness to changes in PaC02. Increases venous capacitance (venous pooling) and vasodilates arterioles thereby reducing preload and afterload.

Question 26

FUROSEMIDE | mechanism of action

Answer 26

Pharmacologic: Inhibits electrolyte reabsorption in the ascending Loop of Henle. Promotes excretion of sodium, potassium, chloride. Vasodilation increases venous capacitance and decreases afterload. Clinical: Diuresis

Question 27

GLUCAGON | mechanism of action

Answer 27

Pharmacologic: Acts only on liver glycogen, converting it to glucose. Counteracts the effect of insulin. Relaxes GI smooth muscle causing dilation and decreased motility. Cardiac inotrope. Clinical effects: May reverse hypoglycemia (if patient has glycogen stored in liver) within 4-8 minutes (could be as long as 15 or more).

Question 28

HEMOSTATIC AGENTS (KAOLIN, CHITOSAN) mechanism of action

Answer 28

Kaolin is an inert mineral and it promotes clotting by two main modes of action: Kaolin promotes the activation of Factor XII (FXII) in the presence of kallikrein and high molecular weight kininogen. Activated FXII initiates the intrinsic clotting pathway via the activation of Factor XI. Activated FXI continues the coagulation pathway that ends with the formation of a fibrin clot. Kaolin promotes the activation of platelet-associated FXI and it is a distinct and separate molecule from plasma FXI. Activated platelet-associated FXI initiates the intrinsic clotting pathway in normal and FXII deficient patients.

Question 29

HYDROXOCOBALAMIN | mechanism of action

Answer 29

The action of hydroxocobalamin in the treatment of cyanide poisoning is based on its ability to bind cyanide ions. Each hydroxocobalamin molecule can bind cyanide ion by substituting it for the hydroxo ligand linked to the trivalent cobalt ion, to form cyanocobalamin, which is then excreted in the urine.

Question 30

INSULIN | mechanism of action

Answer 30

Promotes glucose transport, which stimulates carbohydrate metabolism in skeletal and cardiac muscle and adipose tissue. Also promotes phosphorylation of glucose in liver, where it's converted to glycogen. Directly affects fat and protein metabolism, stimulates protein synthesis, inhibits release of free fatty acids, and indirectly decreases phosphate and potassium

Question 31

IPRATROPIUM BROMIDE | mechanism of action

Answer 31

Anticholinergic (parasympatholytic) agent appears to inhibit vagally-mediated reflexes by antagonizing the action of acetylcholine, the transmitter released from the vagal nerve. (SEE: Notes) Special Notes: Anticholinergics produce preferential dilatation of the larger central airways, in contrast to beta agonists, which affect the peripheral airways. May be more effective used in combination with beta agonists. Should be kept out of light in foil pouch and avoid excessive humidity.

Question 32

KETAMINE HYDROCHLORIC INJECTION | mechanism of action

Answer 32

Pharmacologic Effects: Ketamine is a Class III Phencyclidine (PCP) derivative that is rapid acting in producing a “dissociative” anesthesia in which the patient’s consciousness is detached from their nervous system. Due to its “dissociative” properties, Ketamine is a potent analgesic. Minimal cardiac depression occasionally reported with rapid-high doses. May transiently (within 30-60 seconds) increase heart rate and blood pressure by central sympathetic stimulation. Return to normal values begins almost immediately, and is complete within 15 minutes. Ketamine is a bronchodilator and has minimal to no respiratory depression, with respiratory stimulation frequently seen. Metabolized: The liver microsomal enzyme system metabolizes Ketamine.

Question 33

LIDOCAINE HCL | mechanism of action

Answer 33

Decreases automaticity by slowing the rate of spontaneous phase 4 depolarization. Terminates re-entry by decreasing conduction in re-entrant pathways (by slowing conduction in ischemic tissue, equalizes conduction speed among fibers). Increases ventricular fibrillation threshold.

Question 34

LORAZEPAM | mechanism of action

Answer 34

Agent has high affinity for the gamma-amino butyric acid (GABA) benzodiazepine receptor complex without displacing GABA, (GABA is the major inhibitory neurotransmitter in the brain). It exerts tranquilizing action on the central nervous system.

Question 35

MAGNESIUM SULFATE | mechanism of action

Answer 35

Pharmacology: Second most plentiful intracellular cation; essential to enhance intracellular potassium replenishment and activity of many enzymes; important role in neurochemical transmission and muscular excitability (may decrease acetylcholine released by nerve impulses); decreases myocardial irritability and neuromuscular irritability. Clinical: Cardiac-reduces ventricular irritability, especially when associated with hypomagnesemia; inhibition of muscular excitability.

Question 36

METHYLPREDNISOLONE SODIUM SUCCINATE | mechanism of action

Answer 36

Enters target cells and causes many complex reactions that are responsible for its anti- inflammatory and immunosuppressive effects; thought to stabilize cellular and intracellular membranes.

Question 37

MIDAZOLAM HYDROCHLORIDE | mechanism of action

Answer 37

CNS effects are mediated through the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). Acts at the limbic, thalamic, and hypothalamic levels of the CNS, producing anxiolytic, sedative, hypnotic, and anticonvulsant effects. Capable of producing all levels of CNS depression, from mild sedation to coma.

Question 38

MORPHINE SULFATE | mechanism of action

Answer 38

Alleviates pain by acting on the pain receptors in the brain; elevates pain threshold. Depresses central nervous system; depresses brainstem respiratory centers; decreases responsiveness to changes in PaC02. Increases venous capacitance (venous pooling), vasodilates arterioles, reducing preload and afterload. Histamine release.

Question 39

NALMEFENE HCL | mechanism of action

Answer 39

Competitive inhibition at narcotic receptor sites | Reverses respiratory depression secondary to narcotics

Question 40

NALOXONE HCL | mechanism of action

Answer 40

Competitive inhibition at narcotic receptor sites | Reverses respiratory depression secondary to narcotics

Question 41

NITROGLYCERIN | mechanism of action

Answer 41

Smooth muscle relaxant acting on vascular, uterine, bronchial, and intestinal smooth muscle Reduces workload on the heart by causing blood pooling (decreased preload) Arteriolar vasodilation (decreased afterload) Coronary artery vasodilation Increases blood flow to myocardium Decreases myocardial O2 demand

Question 42

NOREPINEPHRINE | mechanism of action

Answer 42

Stimulates beta1 and alpha1 receptors in sympathetic nervous system, causing vasoconstriction, increased blood pressure, enhanced contractility, and decreased heart rate.

Question 43

ONDANSETRON | mechanism of action

Answer 43

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

Question 44

OXYTOCIN | mechanism of action

Answer 44

Binds to oxytocin receptor sites on surface of uterine smooth muscles: increases force and frequency of uterine contractions

Question 45

PHENYLEPHRINE NASAL SPRAY 0.5% | mechanism of action

Answer 45

Stimulates a receptors in the blood vessels of the nasal mucosa which causes their constriction and thereby decreases the risk of nasal bleeding.

Question 46

PROPARACAINE HYDROCHLORIDE OPTHALMIC | mechanism of action

Answer 46

Site of action is at the ophthalmic pain nerve cell membrane. Alleviates pain by limiting the sodium ion permeability in these nerve cell membranes; this elevates the threshold stimulus needed to trigger action potential in these cells. When the action is sufficiently well developed, block of conduction is produced.

Question 47

PROPOFOL | mechanism of action

Answer 47

Sedative-hypnoticagent. Suspected to produce effects by the positive modulation of the inhibitory function of the neurotransmitter gamma aminobutyric acid (GABA) through the ligand-gated GABA receptors

Question 48

RACEMIC EPINEPHRINE | mechanism of action

Answer 48

Alpha-receptor stimulation: causes vasoconstriction, which results in reduction of mucosal and submucosal edema Beta-receptor stimulation: bronchodilation, reduction in airway smooth muscle spasm

Question 49

RANITIDINE | mechanism of action

Answer 49

Competitively inhibits action of histamine at the H2 at receptor sites of parietal cells, decreasing gastric acid secretion.

Question 50

SODIUM BICARBONATE 8.4% | mechanism of action

Answer 50

Buffers H+ and increases pH

Question 51

SUCCINYLCHOLINE | mechanism of action

Answer 51

Combines with cholinergic receptors of the motor end plate to produce depolarization Hydrolyzed by acetylcholinesterase

Question 52

``` THIAMINE HCL (VITAMIN B1) mechanism of action ```

Answer 52

Required for carbohydrate metabolism. Deficiency leads to anemia, polyneuritis, Wernicke's encephalopathy, cardiomyopathy. Administration may reverse symptoms of deficiency, but effects are dependent upon duration of illness and severity of disease.

Question 53

TIROFIBAN | mechanism of action

Answer 53

Reversibly binds with Glycoprotein (GP) IIb/IIIa receptors on the surface of platelets inhibiting the final common pathway for platelet aggregation. GP IIb/IIIa receptor blockade interferes with the binding of fibrinogen, von Willebrand factors and other platelet aggregation modulators to the surface of platelets thus preventing aggregation.

Question 54

VASOPRESSIN | mechanism of action

Answer 54

Causes vasoconstriction (pressor effect) of peripheral, cerebral, pulmonary, and coronary vessels

Question 55

VERAPAMIL HCL | mechanism of action

Answer 55

Blocks calcium ion influx into cardiac and smooth muscle cells causing a depressant effect on the contractile mechanism resulting in negative inotropy. Reduces contractile tone in vascular smooth muscle resulting in coronary and peripheral vasodilation. Slows conduction and prolongs refractory period in the AV node due to calcium channel blocking. Slows SA node discharge. In summary, decreases myocardial contractile force and slows AV conduction.