Flashcards in Mechanism of Action-Table 1 Deck (39):
A colorless odorless, tasteless gas necessary for the breakdown of glucose into a usable energy form.
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
Most potent of the benzodiazapines. It acts as an anxiolytic, sedative, hypnotic, and skeletal muscle relaxant. It intensifies GABA. Because of its short half-life it is the preferred benzodiazapine for the treatment of pediatric seizures.
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.
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 paralysis. There is no effect on level of consciousness.
A 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.
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.
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 defibrilation.
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
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.
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.
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.
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.
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.
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.
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.
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 after-load in the left ventricle.
Nitroglycerin (Nitrostat, Nitro-Bid, Tridil)
Givein 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.
Sodium Bicarbonate (NaHCO3)
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.
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.
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.
Albuterol (Proventil, Ventolin)
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.
Ipratropium Bromide (atrovent)
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.
Principal form of glucose used by the body to create energy.
D50 (50% Dextrose in Water)
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.
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).
Causes sedation by decreasing nerve impulse transmission by blocking dopamine and serotonin receptors in the CNS.
Competes for, and displaces, narcotic molecules from opiate receptors in the brain.
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.
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.
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.
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.
Activated Charcoal (Actidose)
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.
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.
Fentanyl Citrate (Sublimaze)
Reversibly blocks the action of cyclooxygenase which in turn prevents the formation of prostaglandins. Ketorolac causes analgesia equivalent to that of morphine sulfate.
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.
Acetaminophen (tylenol, APAP)
Ibuprofen inhibits cyclooxygenase (COX) decreasing production of prostaglandins thus decreasing pain sensation, fever, and inflammation.
Ibuprofen (Advil, Motrin, Nuprin)