Sect 4 Chpt 15 MOA

medication MOA

Acetaminophen (Tylenol)

MOA: Exact mechanism of action has not been fully established; it may work peripherally to block pain impulse generation and inhibit prostaglandin synthesis in the CN leading to its analgesic and antipyretic effort

AcetaZOLAMIDE (Diamox, Diamox Sequels)

MOA: Inhibits hydrogen ion excretion in the renal tubules, increasing sodium, potassium, bicarbonate, and water excretion and producing alkaline diuresis

Acetic Acid (vinegar)

MOA: Otic solution provides an acidic medium during irrigation of the ear that minimizes bacterial and fungal promulgation; may stabilize nematocyst discharge in jellyfish found outside the United States, thereby decreasing pain

Acetylcysteine (Mucomyst, Acetadote)

MOA: restores glutathione concentrations within the liver. Glutathione, an antioxidant, has many actions in the body, including detoxifying substances

Activated Charcoal (Insta-Char, Actidose-Aqua, Liqui-Char)

MOA: Restores glutathione concentrations within the liver. Glutathione, an antioxidant, has many actions in the body, including detoxifying substances

Adenosine (Adenocard)

MOA: Short-acting drug that slow conduction through the AV node; can restore sinus rhythm in patients with SVT and terminate regular tachycardias caused by reentrant AV nodal pathways

Albuterol (Proventil, Ventolin, Proair, Accuneb)

MOA: Selective beta-2 adrenergic agonist that causes bronchial smooth muscle relaxation and inhibits mediator release from mast cells

Alprazolam (Xanax)

MOA: Works in the brain by enhancing the activity of a neurotransmitter called gamma-aminobutyric acid (GABA)

Amiodarone (Cordarone, Pacerone)

MOA: Blocks sodium, potassium, and calcium channels; prolongs the action potential’s duration an delays repolarization; decreases AV conduction and sinoatrial (SA) node function

Antibiotics

MOA: Employ various mechanisms to combat bacterial infections, primarily by either killing bacteria (bactericidal) or inhibiting their growth (bacteriostatic)

Anticoagulants

MOA: Prevent the formation of new clots but do not dissolve existing clots

Antidepressant Agents

MOA: Most work by increasing levels or serotonin, norepinephrine, or dopamine within the brain

Antiplatelet Agents

MOA: Supress platelet aggregation and are used to prevent arterial thrombosis

Aspirin (Acetylsalicylic Acid)

MOA: Prevents thromboxane A2 formation, which causes platelets to clump together (aggregate) and form plugs that cause obstruction or constriction; has antipyretic and analgesic properties

Atropine Sulfate

MOA: Inhibits acetylcholine at postganglionic parasympathetic neuroeffector sites; increases heart rate in symptomatic bradydysrhythmias; reverses muscarinic effects of cholinergic poisoning

Benzocaine Spray (Hurricane)

MOA: Prevents impulse transmission along sensory nerve fibers and at nerve endings

Beta Blocking Agents

MOA: Antagonize the effects of epinephrine on beta adrenergic receptors. Some are selective and some are nonselective. beta-1 selective blockers (atenolol (Tenormin) and metoprolol (Lopressor), are also called cardioselective beta blockers. Use results in slowing of the heart rate and force of contraction. They primarily block beta-1 receptor sites. Nonselective beta blockers such as propranolol (Inderal) antagonize both beta-1 and beta-2 receptors, decreasing hear trate and force of contraction and causing some degree of bronchoconstriction.

Bumetanide (Bumex)

MOA: A potent loop diuretic with a rapid onset and short duration of action. Inhibits the reabsorption of sodium ad chloride in the ascending limb of the loop of Henle

Calcium Chloride

MOA: Mineral component of bones and teeth; cofactor in enzymatic reactions and affects the secretory activity of endocrine and exocrine glands; essential for neurotransmission, blood clotting, and contraction of cardiac, smooth, and skeletal muscles

Calcium Gluconate

MOA:L Mineral component of bones and teeth; cofactor in enzymatic reactions and affects the secretory activity of endocrine and exocrine glands; essential for neurotransmission, blood clotting, and contraction of cardiac, smooth, and skeletal muscles

Cimetidine (Tagamet)

MOA: Blocks the effects of histamine at H2 receptors of gastric parietal cells, leading to a reduction of gastric acid volume and gastric acidity

Dexamethasone Sodium Phosphate (Decadron)

MOA: Suppresses acute and chronic inflammation; immunosuppressive effects

Dextrose

MOA: Rapidly increases serum glucose levels. Short-term osmotic diuresis

Diazepam (Valium, Diastat AcuDial)

MOA: Appears to act on part of the limbic system, as well as on the thalamus and hypothalamus, to induce a calming effect; inhibits GABA receptors in the CNS, reducing neuron excitability; raises the seizure threshold; induced amnesia and sedation

Digoxin (Lanoxin)

MOA: Binds to the Na+/K+ ATPase pump and inhibits its activity

Diltiazem (Cardizem, Dilacor, Diltiaz)

MOA: Inhibits extracellular calcium ion influx across membranes of myocardial cells and vascular smooth muscle cells, resulting in inhibition of cardiac and vascular smooth muscle contraction and thereby dilating the main coronary and systemic arteries; no effect on serum calcium concentrations; substantial inhibitory effects on the cardiac conduction system, acting principally at the AV node, with some effects at the SA node. Less- negative inotropic effects than verapamil

DiphenhydrAMINE (Benadryl)

MOA: Blocks H1 receptors in the respiratory tract, blood vessels, and GIsmooth muscle; reverses extrapyramidal reactions

DOBUTamine Hydrochloride (Dobutrex)

MOA: Synthetic catecholamine that primarily stimulates beta-1 receptors, with minor stimulation of beta-2 and alpha-1 receptors. Increases myocardial contractility and stroke volume, resulting in increased cardiac output with modest chronotropic effects. Increases renal blood flow secondary to increased cardiac output

DOPamine Hydrochloride (Inotropin)

MOA: Immediate metabolic precursor to norepinephrine with mixed alpha adrenergic, beta adrenergic, and dopaminergic effects that are dose-dependent. At doses of 1 to 2 mcg/kg/min, causes vasodilation in the renal, mesenteric, coronary, and intracerebral vascular beds that is thought to result from stimulation of dopamine receptors. At doses of 2 to 1- mcg/kg/min, DOPamine stimulates beta-1 receptors, increasing myocardial contractility and enhancing cardiac impulse conduction. At infusion rates of 10 to 20 mcg/kg/min, DOPamine stimulates alpha receptors, resulting in vasoconstriction, increased systemic vascular resistance, and a rise in BP. Vasoconstriction occurs first in the skeletal muscle vascular beds, but is evident in the renal and mesenteric vessels with increasing doses. At dosages greater than 20 mcg/kg/min, alpha stimulation predominates, and resultant vasoconstriction may compromise circulation in the limbs

Droperidol (Inapsine)

MOA: Produces marked tranquilization and sedation; reduces motor activity and anxiety; also possesses adrenergic-blocking antifibrillatory, antihistaminic, and anticonvulsive properties

Epinephrine (Adrenalin, EpiPen, AsthmaNefrin)

MOA: Catecholamine with strong alpha adrenergic, strong beta-1, and moderate beta-2 effects. Effects of alpha stimulation result in systemic vasoconstriction, increasing peripheral vascular resistance. Effects of beta-1 stimulation result in increases in heart rate, myocardial contractility, cardiac output, and myocardial oxygen demand. Effects of beta-2 stimulation result in bronchial smooth muscle relaxation. Secondary relaxation effect on the smooth muscle of the stomach, intestine, uterus, and urinary bladder

Etomidate (Amidate)

MOA: Ultra-short-acting hypnotic that produces rapid sedation with minimal cardiovascular or respiratory depression

Famotidine (Pepcid)

MOA: Inhibits the volume and concentration of gastric secretions

Fentanyl Citrate (Sublimaze)

MOA: Binds to opioid receptors, producing analgesia, euphoria, respiratory depression, and sedation

Fibrinolytic Agents

MOA: activate the body’s natural fibrinolytic system which breaks down blood clots by converting plasminogen to plasmin, an enzyme that degrades fibrin, the protein that forms the meshwork of a blood clot

Furosemide (Lasix)

MOA: Inhibits NA+-K+-2Cl- (NKCC2) cotransport (sodium-potassium-chloride cotransport) in the loop of Henle; Blocks reabsorption of sodium, potassium, and chloride from the filtered fluid back into the bloodstream, increases urine output

Glucagon (GlucaGen)

MOA: Increases blood glucose level by stimulation the breakdown of stored glycogen to glucose (glycogenolysis) and inhibiting the synthesis of glycogen from glucose (glycogenesis). Unknown mechanism of stabilizing cardiac rhythm in beta blocker overdose. Minimal positive inotropic and chronotropic responses. Decreases GI motility and secretions

Glucose, Oral (Insta-Glucose)

MOA: After absorption in the GI tract, glucose becomes distributed to the tissues, increasing circulating blood glucose levels.

Glycoprotein IIb/IIIa Inhibitors

MOA: Block the binding of fibrinogen to glycoprotein IIb/IIIa receptors on the surfaces of platelets, thereby inhibiting platelet aggregation

Haloperidol (Haldol)

MOA: Antagonizes dopamine-1 and dopamine-2 receptors in the brain; depresses the reticular activating system and inhibits release of hypothalamic and hypophyseal hormones

Helium Gas Mixture (Heliox)

MOA: Reduces airflow resistance within the bronchial tree in patients with obstructive lung disease; may also reduce the work of breathing and improve pulmonary gas exchange efficiency

HydrALAZINE (Apresoline)

MOA: Relaxes arteriolar, but not venous, smooth muscle. Thought to interfere with calcium movement in vascular smooth muscle, which is responsible for vasoconstriction, resulting in lower BP

Hydrocortisone Sodium Succinate (Solu-Cortef)

MOA: Anti-inflammatory; immunosuppressive with salt-retaining actions

HYDROmorphone (Dilaudid)

MOA: Opioid agonist-analgesic of opioid receptors; inhibits ascending pain pathways, thereby altering the response to pain; increases the pain threshold; produces analgesia, respiratory depression, and sedation

Hydroxocobalamin (Cyanokit)

MOA: A synthetic, injectable form of vitamin B12 (cobalamin) that binds with cyanide to form nontoxic cyanocobalamin, preventing its toxic effects; excreted renally

Ibuprofen (Advil, Motrin)

MOA: Inhibits prostaglandin synthesis, thereby reducing swelling, pain, and fever

Insulin

MOA: Regulates blood glucose levels by facilitating glucose uptake into cells—-does this by binding to insulin receptors on cell surfaces, triggering a cascade of intracellular events that ultimately lead to increased glucose transport into cells, particularly in muscle and fat tissue. It also inhibits glucose production in the liver and promotes glucose storage as glycogen

Ipratropium Bromide (Atrovent)

MOA: Antagonizes the action of acetylcholine on bronchial smooth muscle, resulting in bronchodilation

Isopropyl Alcohol

MOA: In addition to its role as an antiseptic, may be used as an antiemetic. Although its mechanism of action as an antiemetic is not certain, isopropyl alcohol may influence neurotransmission at several sites that activate the chemoreceptor trigger zone

Ketamine (Ketalar)

MOA: Blocks pain receptors and minimizes spinal cord activity, affecting the brain’s association pathways between the thalamus and the limbic system

Ketorolac Tromethamine (Toradol)

MOA: Potent analgesic that inhibits prostaglandin synthesis; does not have any sedative or anxiolytic properties

Levalbuterol (Xopenex)

MOA: Stimulates beta-2 receptors resulting in smooth muscle relaxation of the bronchial tree and peripheral vasculature

Lidocaine Hydrochloride (Xylocaine)

MOA: CARDIAC: Combines with fast sodium channels, thereby inhibiting recovery after repolarization, and decreasing myocardial excitability and conduction velocity. LOCAL ANESTHETIC: Inhibits ion transport across the neuronal membrane, blocking conduction of normal nerve impulses. RSI: May decrease ICP response during laryngoscopy

Lorazepam (Ativan)

MOA: Anxiolytic, anticonvulsant, and sedative effect; suppresses propagation of seizure activity produced by foci in the cortex, thalamus, and limbic areas; inhibits GABA receptors in the CNS, reducing neuron excitability

Magnesium Sulfate

MOA: Depresses the CNS, blocks peripheral neuromuscular transmission, and produces anticonvulsant effects; decreases the amount of acetylcholine released at the end plate by motor nerve impulses, slows the rate of SA node impulse formation in the myocardium, and prolongs conduction time. Promotes calcium, potassium, and sodium movement in and out of cells and stabilizes excitable membranes. Induces uterine relaxation. Can cause bronchodilation after beta agonists and anticholinergics have been administered

Mannitol (Osmitrol)

MOA: Promotes the movement of fluid from the intracellular space to the extracellular space. Decreases cerebral edema and ICP. Promotes urinary excretion of toxins

Meperidine Hydrochloride (Demerol)

MOA: Synthetic opioid analgesic whose effects on the CNS and smooth muscle organs are similar to those of morphine; primarily acts as an analgesic and a sedative

MethylPREDNISolone Sodium Succinate (Solu-Medrol)

MOA: Highly potent synthetic glucocorticoid that suppresses acute and chronic inflammation; potentiates vascular smooth muscle relaxation by beta adrenergic agonists; has few to no mineralocorticoid properties

Metoclopramide (Reglan)

MOA: Blocks dopamine receptors (at high doses) and serotonin receptors in the chemoreceptor trigger zone of the CNS; sensitizes tissues to acetylcholine; increases upper GI motility but not secretions; increases lower esophageal sphincter tone

Midazolam Hydrochloride (Versed)

MOA: Inhibits GABA receptors in the CNS, thereby reducing neuron excitability and causing sedative, anxiolytic, amnesic, and hypnotic effects

Milrinone (Primacor)

MOA: Increases myocardial contractility; has a direct dilating effect on vascular smooth muscle; does not possess beta adrenergic properties

Morphine Sulfate (Roxanol, MS Contin)

MOA: Alleviates pain through CNS action. Suppresses the fear and anxiety centers in the brain. depresses brainstem respiratory centers. Increases peripheral venous capacitance and decreases venous return. Decreases preload and afterload, which decreases myocardial oxygen demand

Naloxone Hydrochloride (Narcan, EVZIO)

MOA: Competitive inhibition at opioid receptor sites. Reverses respiratory depression and sedation secondary to opioids

NIFEdipine (Procardia, Adalat, Nifedical)

MOA: Inhibits movement of calcium ions across cell membranes; inhibits cardiac and vascular smooth muscle contraction, thereby dilating the main coronary and systemic arteries, reducing preload and afterload, and reducing myocardial oxygen demand; does not prolong AV nodal conduction

Nitroglycerin (Nitrostat, Nitrolingual Pumpspray, NitroQuick, Nitro-Bid, Tridil)

MOA: Smooth muscle relaxant, which acts on the vasculature, bronchial, uterine, and intestinal smooth muscle. Dilates peripheral arterioles and veins. Reduces peripheral vascular resistance, preload, and afterload, decreasing the heart’s workload and myocardial oxygen demand

Nitroprusside (Nitropress)

MOA: Arterial and venous vasodilator that reduces afterload, resulting in decreased BP and increased cardiac output

Nitrous Oxide 50:50 (Nitronox)

MOA: Exact mechanism is unknown; the analgesic action is thought to occur by potentiating the release of endogenous endorphins that react with opioid receptors in the CNS and alter the pain threshold

Norepinephrine Bitartrate (Levophed, Levarterenol)

MOA: Acts predominantly on alpha adrenergic receptors to produce constriction of resistance and capacitance vessels, thereby increasing systemic BP and coronary artery blood flow; also acts on beta-1 receptors. In relatively lower doses, the cardiac-stimulant effect of norepinephrine predominates; with larger doses, the vasoconstrictor effect predominates

Octreotide (Sandostatin)

MOA: Mimics the actions of the naturally occurring hormone, somatostatin, decreasing visceral blood flow and inhibiting the release of serotonin, gastrin, vasoactive intestinal peptide, secretin, motilin, and pancreatic polypeptide

Olanzapine (Zyprexa)

MOA: Exact mechanism has not been determined; may act through a combination of dopamine and serotonin type 2 receptor site antagonism

Ondansetron Hydrochloride (Zofran, Zofran ODT, Zuplenz)

MOA: Blocks the action of serotonin, a natural substance that causes nausea and vomiting. Does not affect dopamine receptors, so it does not cause extrapyramidal symptoms

Oral Antidiabetic (Hypoglycemic) Drugs

MOA: Work through various mechanisms to lower blood glucose levels in people with type 2 diabetes including stimulating insulin release, enhancing insulin’s effectiveness, decreasing glucose production by the liver, and reducing glucose absorption in the intestines

Oxygen

MOA: Reverses hypoxemia

Oxymetazoline (Afrin, Dristan 12-Hour, Vicks Sinus-12 Hour)

MOA: Stimulates alpha adrenergic receptors in the arterioles of the nasal mucosa to produce vasoconstriction

Oxytocin (Pitocin)

MOA: Binds to oxytocin receptor sites on the surface of uterine smooth muscle, increasing the force and frequency of uterine contractions. Causes dilation of vascular smooth muscle, thereby increasing renal, coronary, and cerebral blood flow

Pancuronium Bromide (Pavulon)

MOA: Binds to the receptor for acetylcholine at the neuromuscular junction. Skeletal muscle relaxation proceeds in a predictable order, starting with muscles associated with fine movements (eg, eyes, face, neck), followed by muscles of the limbs, chest, and abdomen, and then the diaphragm; muscle tone returns in the reverse order

Phenylephrine (Neo-Synephrine)

MOA: Stimulates alpha adrenergic receptors in the arterioles of the nasal mucosa to produce vasoconstriction

Phenytoin (Dilantin)

MOA: Blocks voltage-gated sodium channels in neurons—this stabilizes the neuronal membrane and reduces the ability of neurons to fire at high frequencies, thus preventing the spread of abnormal electrical activity that causes seizures. Specifically, phenytoin bind to sodium channels in their inactive state, prolonging the time it takes for them to return to an active state. This effect is ore pronounced in neurons that are firing at high frequencies, which is characteristic of seizure activity

Potassium Iodide (Pima Syrup, SSKI, ThyroSafe, ThyroSheild)

MOA: Potassium iodide (KI) can help block radioactive iodine from being absorbed by the thyroid gland, thereby protecting this gland from radiation injury and reducing the risk of thyroid cancer. It does not keep radioactive iodine from entering the body and cannot reverse the health effects caused by radioactive iodine once the thyroid is damaged. The protection against radioactive iodine provided by KI depends on the time after contamination, the rate of KI absorption, and the dose of radioactive iodine

Pralidoxime (2-PAM, Protopam)

MOA: Binds to organophosphates and breaks their alkyl phosphate-cholinesterase bonds to restore the activity of acetylcholinesterase

PredniSONE (Rayos)

MOA: Primarily involves its conversion to prednisolone, which then interacts with glucocorticoid receptors (GR) inside cells—the activated complex then enters the cell nucleus and influences gene expression, leading to both anti-inflammatory and immunosuppressive effects

Procainamide Hydrochloride (Pronestyl)

MOA: Inhibits recovery after repolarization, resulting in decreased myocardial excitability and conduction velocity. Direct membrane depressant that decreases conduction velocity, prolongs the refractory period, decreases automaticity, and reduces repolarization abnormalities

Prochlorperazine (Compazine)

MOA: Exerts its antiemetic effect by depressing the brain’s chemoreceptor trigger zone; also has moderate anticholinergic and alpha adrenergic receptor blocking effects. Alpha-1 adrenergic receptor blockade produces sedation, muscle relaxation, and cardiovascular effects (eg, hypotension, reflex tachycardia, minor ECG pattern changes)

Promethazine Hydrochloride (Phenergan)

MOA: H1 receptor antagonist; blocks the action (but not the release) of histamine; possesses sedative, antimotion, antiemetic, and anticholinergic activity; potentiates the effects of opioids to induce analgesia

Proparacaine Ophthalmic (Alcaine, Ophthaine)

MOA: Produces local anesthesia by blocking sodium ion channels, thereby stopping cellular depolarization and preventing the action potential development of nerve impulses at the ophthalmic pain nerve cell membrane

Propofol (Diprivan)

MOA: Produces a rapid and brief state of general anesthesia

Proton Pump Inhibitors

MOA: Block the hydrogen/potassium ATPase enzyme system (ie, the gastric proton pump) in the stomach wall, inhibiting the final stage of gastric acid production and limiting the amount of acid produced

Rocuronium Bromide (Zemuron)

MOA: Antagonizes acetylcholine at the motor endplate, producing skeletal muscle paralysis

Sildenafil (Revatio, Viagra)

MOA: Inhibits phosphodiesterase enzyme 5 in lung tissue, which results in relaxation of pulmonary vascular smooth muscle cells and subsequent vasodilation of the pulmonary vasculature

Sodium Bicarbonate

MOA: Reacts with hydrogen ions to form water and carbon dioxide, correcting metabolic acidosis. Increases blood and urinary pH by releasing a bicarbonate ion, which in turn neutralizes hydrogen ion concentrations

Sodium Thiosulfate (Nithiodote)

MOA: Converts cyanide to the less toxic thiocyanate, which is then excreted in the urine

Statins

MOA: decrease the concentrations of serum cholesterol and triglycerides, decrease low-density lipoprotein (LDL) cholesterol, and slightly increase high-density lipoprotein (HDL) cholesterol

Succinylcholine Chloride (Anectine)

MOA: Ultra-short-acting depolarizing skeletal muscle relaxant that mimics acetylcholine. It binds with the cholinergic receptors on the motor endplate, producing a phase 1 block manifested by muscle fasciculations

Tadalafil (Cialis, Adcirca)

MOA: Inhibits phosphodiesterase enzyme 5 in lung tissue, which results in relaxation of pulmonary vascular smooth muscle cells and subsequent vasodilation of the pulmonary vasculature

Tetracaine Ophthalmic Solution (Pontocaine)

MOA: Produces local anesthesia by blocking sodium ion channels, thereby stopping cellulr depolarization and preventing the action potential development of nerve impulses at the ophthalmic pain nerve cell membrane

Thiamine Hydrochloride (Vitamin B1)

MOA: Combines with adenosine triphosphate to form thiamine pyrophosphate, a coenzyme essential for carbohydrate metabolism

Tranexamic Acid (Cyklokapron, Lysteda)

MOA: Inhibits the activation of plasminogen, thereby reducing the conversion of plasminogen to plasmin (which breaks down fibrin clots, fibrinogen, and other plasma proteins). By hindering fibrin’s breakdown, clotting factors and circulating platelet plugs can form a seal (fibrin clot) and reduce bleeding

Vecuronium Bromide (Norcuron)

MOA: Neuromuscular agent with an intermediate duration of action that competes with acetylcholine for receptors at the motor endplate, resulting in neuromuscular blockade

Verapamil Hydrochloride (Isoptin, Calan)

MOA: Slows AV node conduction, shortens the refractory period of accessory pathways, and acts as a negative inotrope and vasodilator

Ziprasidone (Geodon)

MOA: Blocks synaptic reabsorption of serotonin and norepinephrine, binds to alpha adrenergic receptors, dopamine receptors, and serotonin receptors