Mechanism of Action Flashcards
ABCIXIMAB
mechanism of action
- 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.
ACETYLSALICYLIC ACID, ASPIRIN, ASA
mechanism of action
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.
ACETYLSALICYLIC ACID, ASPIRIN, ASA (EMT Administration)
mechanism of action
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.
ADENOSINE
mechanism of action
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.
ALBUMIN, normal serum 5% / 25%
mechanism of action
Exerts oncotic pressure, which expands volume of circulating blood and maintains cardiac output.
ALUTEROL SULFATE
mechanism of action
ß agonist (primarily ß2); relaxes bronchial smooth muscle, resulting in bronchodilation; also relaxes vascular and uterine smooth muscle; decreases airway resistance
AMIODARONE
mechanism of action
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).
ATROPINE SULFATE
mechanism of action
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.
BUMETANIDE
mechanism of action
Inhibits electrolyte reabsorption in the ascending loop of Henle leading to diuresis
CALCIUM CHLORIDE
mechanism of action
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
CALCIUM GLUCONATE GEL, 2.5%
mechanism of action
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.
CHARCOAL, ACTIVATED (without sorbitol)
mechanism of action
Pharmacological: Physical binding (adsorption) of toxins from GI tract.
Clinical effects: Prevents/reduces systemic absorption of toxins.
CIMETIDINE
mechanism of action
Competitively inhibits action of histamine at the H2 at receptor sites of parietal cells, decreasing gastric acid secretion.
DEXAMETHASONE SODIUM PHOSPHATE
mechanism of action
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.
DEXTROSE 50%
mechanism of action
Pharmacological: Aerobic metabolic substrate (ATP production).
Clinical effects: Reverses CNS effects of hypoglycemia by rapidly increasing serum glucose levels.
Provides short-term osmotic diuresis.
DIAZEPAM
mechanism of action
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.
DILTIAZEM
mechanism of action
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.
DIPHENHYDRAMINE HCL
mechanism of action
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.
DOPAMINE
mechanism of action
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
EPINEPHRINE AUTO-INJECTOR
mechanism of action
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.
EPINEPHRINE HCL
mechanism of action
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
EPTIFIBATIDE
mechanism of action
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.
