MemoCard lernen mit System

TETRACAINE MOA

Blocks the initiation and conduction of nerve impulses

MORPHINE SULFATE MOA

Alleviates pain through CNS actions Suppresses fear and anxiety centers in brain. Depresses brain stem respiratory centers. Decreases preload and afterload, decreasing myocardial oxygen demand.

PANCURONIUM (Pavulon) MOA

Pancuronium produces complete muscular relaxation by binding to the receptor for acetylcholine at the neuromuscular junction, without initiating depolarization of the muscle membrane. As the concentration of acetylcholine rises in the neuromuscular junction, Pancuronium is displaced and muscle tone is regained.

MAGNESIUM SULFATE MOA

Reduces striated muscle contractions and blocks peripheral neuromuscular transmission by reducing acetylcholinesterase release at the myoneural junction; manages seizures in toxemia of pregnancy; induces uterine relaxation; can cause bronchodilation after beta agonists and anticholinergics have been used.

KETAMINE (Ketalar) pain MOA

Blocks pain receptors and minimizes spinal cord activity, between the thalamus and the limbic system.

DIAZEPAM (Valium)cardio MOA

Potentates inhibitory neurotransmitters. Raises seizure threshold.Induces amnesia and sedation.

DEXTROSE MOA

Rapidly increases serum glucose l

NITROPASTE MOA

Smooth muscle relaxant acting on vascular, bronchial, uterine and intestinal smooth muscle. Dilation of arterioles and veins in the periphery reduces preload and afterload, decreases the workload of the heart and, thereby, myocardial oxygen demand.

ADENOSINE (Adenocard) MOA

slows conduction AV node, interrupt re-entrant pathway neg. chronotrope acts onSA cells, 1st choice PSVT

EPINEPHRINE cardiac MOA

+chrono, +inno,+dromo + automaticity.

KETAMINE (Ketalar) delerium MOA

Blocks pain receptors and minimizes spinal cord activity, between the thalamus and the limbic system.

KETOROLAC (Toradol) MOA

anti-inflammatory acting non-narcotic analgesic activity by inhibiting prostaglandin synthesis.

GLUCAGON beta blcker OD MOA

stabilize cardiac rhythm in beta-blocker overdose.

HYDROMORPHONE (Dilaudid) MOA

synthetic analog morphine

FENTANYL CITRATE (Sublimaze) MOA

narcotic analgesic

FLUMAZENIL (Romazicon) MOA

Flumazenil antagonizes benzodiazepines in CNS. reverse sedation, impairment of recall, and psychomotor impairment produced by benzodiazepines. Will not reverse hypoventilation or antagonize CNS effects of ethanol, barbiturates, or opioids.

MEPERIDINE (Demerol) MOA

Synthetic opioid agonist that acts on opioid receptors to produce analgesia, euphoria, respiratory and physical depression; a schedule II drug with potential for physical dependency and abuse.

GLUCOSE -ORAL MOA

fast glucose

MIDAZOLAM (Versed) MOA

Increased production of GABA, an inhibitory neurotransmitter, causing procedural amnesia; anesthesia; skeletal muscle relaxation. Anxiolytic and sedative / hypnotic properties similar to other benzodiazepines.

SUCCINYLCHOLINE (Anectine) MOA

Ultra short acting depolarizing skeletal relaxant that mimics acetylcholine as it binds with the cholinergic receptors on the motor end plate, producing a phase I block as manifested by fasciculations.

PRALIDOXIME CHLORIDE (2-PAM, Protopam) MOA

Reactivation of cholinesterase to effectively act as an antidote to organophosphate pesticide poisoning. This action allows for destruction of accumulated acetylcholine at the neuromuscular junction.

DOPAMINE (Inotropin) Beta-andregenic MOA

+ inotropy. +chronotropy.

PROCAINAMIDE (Pronestyl) MOA

Suppresses phase IV depolarization in normal ventricular muscle and Purkinje fibers, reducing automaticity of ectopic pacemakers; suppresses reentry dysrhythmias by slowing intraventricular conduction.

HALOPERIDOL (Haldol) MOA

strong antidopaminergic and weak anticholinergic. Acts on the CNS to depress subcortical areas, midbrain, and ascending reticular activating system in the brain.

ASPIRIN MOA

Prostaglandin inhibition Blocks Thromboxane A2 via COX 1. Vaso-Dil via the COX 2 pathway.

RACEMIC EPINEPHRINE MOA

Stimulates alpha-1 receptors reducing subglottic edema in croup by mucosal vascular bed vasoconstriction. Stimulates beta-2 receptors in the smaller airways in lungs causing bronchodilation with relaxation of bronchial smooth muscles. Reduces airway resistance. Useful in treating laryngeal edema; inhibits histamine release.

NOREPINEPHRINE (Levophed) MOA

Potent alpha-agonist resulting in intense peripheral vasoconstriction, positive chronotropic and increased inotropic effect with increased cardiac output. Alpha adrenergic activity resulting in peripheral vasoconstriction and beta-adrenergic activity leading to inotropic stimulation of the heart and coronary artery vasodilation.

LIDOCAINE HCL (2%) MOA

Decreases automaticity by slowing the rate of Phase 4 depolarization.

AMIODARONE (Cordarone) MOA

Class III K channel blocker. Prolongation of Action Potential; non-competitive A and B sympathetic blocker; Ca,Na channel blocking effects.

ETOMIDATE (Amidate) MOA

Short acting hypnotic of the reticular activating system

FUROSEMIDE (Lasix) MOA

Inhibits electrolyte reabsorption promotes excretion of sodium, potassium, chloride

VASOPRESSIN (Pitressin) MOA

Vasopressin acts by direct stimulation of smooth muscle receptors. When given in extremely high doses, it acts as a noradrenergic peripheral vasoconstrictor.

DEXAMETHASONE (Decadron) MOA

surpress inflammation, immunosuppressive

THIAMINE (Vitamin B1) MOA

Combines with ATP to form thiamine pyrophosphate coenzyme, a necessary component for carbohydrate metabolism. The brain is extremely sensitive to thiamine deficiency.

IPRATROPIUM BROMIDE (Atrovent) MOA

Blocks acetylcholine at the parasympathetic sites in bronchial smooth muscle causing bronchodilation.

ALBUTEROL (Proventil, Ventolin) MOA

Selective b-2 agonist stimulates adrenergic receptors/smooth muscle relaxation, bronchdilator, peripheral vasodialtion.

AMYL NITRITE, SODIUM NITRITE, SODIUM THIOSULFATE (Cyanide Antidote Kit) MOA

produces thiocyanate, which is then excreted

DOPAMINE (Inotropin) dopaminergic MOA

dilate renal and splanchnic vasculature at low doses.

OXYGEN MOA

Reverses hypoxemia.

DIAZEPAM (Valium) seizure MOA

Potentates inhibitory neurotransmitters. Raises seizure threshold.Induces amnesia and sedation.

LORAZEPAM (Ativan) MOA

Anxiolytic, anticonvulsant, sedative; suppresses seizure produced by foci in cortex, thalamus and limbic areas.

NALOXONE (Narcan) MOA

Competitive inhibition at narcotic receptor sites. Reverse respiratory depression secondary to depressant drugs. Completely inhibits the effect of morphine.

PROMETHAZINE (Phenergan) MOA

H receptor antagonist that blocks the actions of histamines by competitive antagonism at the H receptor. In addition to antihistamine effects, promethazine also possesses sedative, anti-motion, antiemetic, and considerable anticholinergic activity.

HYDROCORTISONE/METHYLPREDNISOLONE (Solu-Cortef, Solu-Medrol) MOA

Suppresses acute and chronic inflammation Replaces absent glucocorticoids Immunosuppressive

NITROGLYCERIN MOA

Smooth muscle relaxant with dilation of arterioles and veins in the periphery, reduces preload and afterload, decreases the workload of the heart and, thereby, myocardial oxygen demand.

DIPHENHYDRAMINE (Benadryl) MOA

Blocks H receptors; decreases vasodilatation Reverses extrapyramidal reactions.

EPINEPHRINE allergic MOA

bronchial smooth muscle relaxation and dilation of skeletal vasculature Blocks histamine release.

HEPARIN SODIUM MOA

IX, XI, XII, plasmin. Does not lyse existing clots.

VERAPAMIL (Isoptin) MOA

Verapamil inhibits the movement of calcium ions across cell membranes. The slow calcium ion current blocked by verapamil is more important for the activity of the sinoatrial node and atrioventricular node than for many other tissues in the heart. Verapamil decreases atrial automaticity, reduces atrioventricular conduction velocity, and prolongs the atrioventricular nodal refractory period. In addition, verapamil depresses myocardial contractility, reduces vascular smooth muscle tone, and dilates coronary arteries and arterioles in normal and ischemic tissues.

METOPROLOL (Lopressor) MOA

Selective inhibitor of beta1-adrenergic receptors; completely blocks beta1 receptors, with little or no effect on beta 2 receptors at doses <100 mg;

HYDROXOCOBALAMIN (Vitamin B 12) MOA

hydroxocobalamin binds cyanide ions to form cyanocobalamin

DILTIAZEM HCL (Cardizem) MOA

Block influx of calcium ions into cardiac muscle. Arterial and venous vasodilator. Reduces preload and afterload. Reduces myocardial oxygen demand.

KETAMINE (Ketalar) RSI MOA

Blocks pain receptors and minimizes spinal cord activity, between the thalamus and the limbic system.

CALCIUM CHLORIDE / CALCIUM GLUCONATE MOA

inotrope May enhance vent automaticity. Helps stabilize the cell membrane

MANNITOL 20% MOA

Promotes the movement of fluid form the intracellular space to the extracellular space. Decreases cerebral edema and intracranial pressure. Promotes urinary excretion of toxins.

TRANEXAMIC ACID (TXA, Cyklokapron) MOA

Reduces plasminogen activation, mitigating conversion to plasmin.

ONDANSETRON (Zofran) MOA

Selective 5-HT receptor antagonist, blocking serotonin, both peripherally on vagal nerve terminals and centrally in the CNS chemoreceptor trigger zone

GLUCAGON hyperglcemia MOA

Increases blood glucose by stimulating glycolysis.

ROCURONIUM (Zemuron) MOA

Rocuronium produces complete muscular relaxation by binding to the receptor for acetylcholine at the neuromuscular junction, without initiating depolarization of the muscle membrane. As the concentration of acetylcholine rises in the neuromuscular junction, Pancuronium is displaced and muscle tone is regained.

SODIUM BICARBONATE 8.4% MOA

Reacts with hydrogen ions to form water and carbon dioxide

ATROPINE SULFATE MOA

inhibits action of acetylcholine at postganglionic parasympathetic neuroeffector sites.

ACETAMINOPHEN (Tylenol, Ofrimev) MOA

analgesics and antipyretics.

ACTIVATED CHARCOAL MOA

Adsorbs toxic GI

DOPAMINE (Inotropin) Andregic MOA

alpha 1 effects

VECURONIUM (Norcuron) MOA

Vecuronium is an intermediate-acting, non-depolarizing, neuromuscular blocking agent. Non-depolarizing agents produce skeletal muscle paralysis by blockade at the myoneural junction. Unlike depolarizing agents, vecuronium has little agonist activity, with no depolarizing effect at the motor endplate.

Flashcard Info

MOA