Drug Mechanisms Flashcards
Acetaminophen
Exact MOA unknown but it’s thought to inhibit prostaglandins and stimulate serotonigenic pathways in the CNS
Adenosine
Binds with phosphate to prevent the formation of ATP in myocardial cells to slow conduction and interrupt AV reentry pathways
Albuterol
Selectively binds to B-2 adrenergic receptors to cause smooth muscle relaxation in bronchioles, which in turn causes bronchodilation
Alteplase
Binds to fibrin-bound plasminogen at the clot site to convert plasminogen to plasmin. Plasmin digests the fibrin strands of theclot.
Amiodarone
Blocks potassium channels causing prolongation of the action potential duration in all cardiac tissues. Also has blocking action on sodium channels, calcium channels and ?- and ?-adrenergic receptors.
Aspirin
Blocks COX enzymes, thereby inhibiting prostanoids which are responsible for platelet aggregation and without plately aggregation, blood clots effectively form.
Atropine
M2 anticholenergic agonist. Inhibits SA/AV node parasympathetic effects principally through K efflux. Positive chronotropy with no ionotropy.
Calcium Chloride
Calcium channel antagonists block the inward movement of calcium by binding to the L-type ?long-acting? voltage-gated calcium channels in the heart, vascular smooth muscle, and pancreas causing a significant increase in
inotropic force and ventricular automaticity.
Calcium Gluconate
Calcium channel antagonists block the inward movement of calcium by binding to the L-type ?long-acting? voltage-gated calcium channels in the heart, vascular smooth muscle, and pancreas causing a significant increase in
inotropic force and ventricular automaticity.
Cefazolin
binds to 1 or more penicillin-binding proteins, thereby arresting bacterial cell-wall synthesis and inhibiting bacterial replication
Dexamethasone
Supresses migration of neutrophils and decrease lymphocyte colony proliferatio, thus inhibits systhesis of pro-inflammatory enzymes such as cytokines, interleukin, and interferon.
Dextrose 10%
Binds to organophosphates and breaks alkyl phosphate-cholinesterase bond to restore the activity of acetylcholinesterase. Primarily works at the nicotinic receptors
Diazepam
Binds to specific site on GABA Type A receptors to potentiate the effects for GABA resulting in sedation and suppression of convulsions
Diltiazem
Inhibits extracellular calcium ion influx across membranes of myocardial cells and vascular smooth muscle cells with substantial inhibitory effects on cardiac conduction system, acting principally at AV node, with some effects at sinus node
Diphenhydramine
acts as an inverse agonist at the H1 receptor, thereby reversing the effects of histamine on capillaries, reducing allergic reaction symptoms.
Dobutamine
Binds to B-1 adrenergic receptors to increase inotropic force with little effect on chronotropy
Dopamine
Acts as a dopamine A1 & B1 adrenegic receptor site agonist. In a dose dependent fashion, in can increase inotropy, chornotropy, dromotropy, and peripheral vascular resistence.
Droperidol
the exact mechanisim is unknow but it’s main action seems to be as a dopamine D2 and A1 receptor antagonist producing antiemetic and sedative-hypnotic effects
Epinephrine
Non-selectively binds to a1, b1, and b2 adrenergic receptors to increase inotropy, chronotropy, dromotropy, automaticity, peripheral vasoconstriction, and bronchodilation.
Etomidate
binds to and displaces inhibitors of GABA neurotransmitter receptors causing rapidly inducing sedation without histamine release. Rapid sedations with few respiratory or cardiovascular effects.
Fentanyl
Hyperpolarization of interneurons and decreased release of neurotransmitter’s responsible for the pain impulses to the thalamus and cerebral cortex.
Flumazenil
Antagonizes the sedative e?ects of benzodiazepines in the CNS by inhibiting their actions on GABA
Furosemide
Loop diuretic; inhibits reabsorption of sodium and chloride ions at proximal and distal renal tubules and loop of Henle; by interfering with chloride-binding cotransport system, causes increases in water, calcium, magnesium, sodium, and chloride
*medscape
Glucagon
Liver - causes activation of cAMP, causes a cascade of effects ultimatley allows glucose to be released from glycogen polymers
Heart - cAMP increase causes calcium entry with a slight positive chronotropy, inotropy, and dromotropy
Haloperidol
Mesolimbic/mesocortical dopamine (D1/D2) antagonist - inhibits dopamine transmission to the limbic system and prefrontal cortex . reduction in psychotic symptoms (hallucinations, agitation, aggression, disorganized speech)
Heparin
Blocks the conversion of prothrombin to thrombin and prevents the conversion of fibrinogen to fibrin
Hydrocortisone
Supresses migration of neutrophils and decrease lymphocyte colony proliferatio, thus inhibits systhesis of pro-inflammatory enzymes such as cytokines, interleukin, and interferon.
Hydromorphone
Precise method is unknown but thought to act as an Opiod (mu) agonist. Blocking pain receptors in the CNS and also potentially causing euphoria
Ibuprofen
Blocks COX 1&2 enzymes which prevents protaglandin production thereby reducing inflation and pain
Insulin
Promotes glucose transport into the cells of all tissues. Causes and intracellular shift of K & Mg which causes a decrease in the serum of these specific electrolytes
Ipratropium bromide
Inhibits acetylcholine at the muscarinic (m3) receptor sites of bronchial smooth muscle to cause slight bronchodilation and dry respiratory tract secretions
Ketamine
Causes disassociation between cortical and limbic system to result is diassociation of patient from their surroundings. Also causes bronchodialtion
Ketorolac
Blocks COX 1&2 enzymes which prevents protaglandin production thereby reducing inflation and pain. Work peripherally, rather than centrally
Lactated Ringer’s
Provides the body with sodium lacate which assists the body’s natural metabolic processes. Also provide fluid volume in intravascular spaces
Levalbuterol
Selectively binds to ?-2 adrenergic receptors to cause smooth muscle relaxation in bronchioles, which in turn causes bronchodilation
Lidocaine
Sodium channel blocker that prevents the rapid influx of sodium in the cardiac myocyte blunting depolarization during phase 0 of the action potential, thereby increasing the effective threshold potential
Lorazepam
Binds to specific site on GABA Type A receptors to potentiate the effects for GABA resulting in sedation and suppression of convulsions
Magnesium Sulfate
Competes with with calcium at NMJ to affect distribution of calcium uptake and release. Decreases amount of Ach released at motor end plate and slows SA node impulses and conduction time
Mannitol
Increases plasma tonicity whichpromotes water out of the brain parenchyma and into the intravascular space.
Methylprednisolone
Supresses migration of neutrophils and decrease lymphocyte colony proliferatio, thus inhibits systhesis of pro-inflammatory enzymes such as cytokines, interleukin, and interferon.
Metoclopramide
Dopamine (D2) R antagonist - inhibits communication from the chemoreceptor trigger zone (which recognizes emetic toxins) to the vomiting center (4th ventricle) of the brain; inhibits gastric SMC relaxation, leading to increased motility of stomach contents into the small intestine
Metoprolol
Binds to and Blocks ?-1 sympathetic receptors which block catecholamines. Causes negative chronotropy, inotropy, dromotropy
Midazolam
Binds to specific site on GABA Type A receptors to potentiate the effects for GABA resulting in sedation and suppression of convulsions
Morphine
Binds to opiate receptors in central nervous system to cause analgesia and euphoria; vasodilation resulting in decreased preload and decreased myocardial oxygen demand
Naloxone
Competitively binds to opiate receptors in the brain, displacing opiates and reversing e?ects of opiates
Nitroglycerin
Nitroglycerin is a pro-drug which must be de-nitrated to form the active metabolite nitric oxide (NO). Then, NO activates the conversion of GTP -cGMP + 2P in vascular smooth muscle cells (VSMC). cGMP activates a cascade of reactions that cause a reduction in intracellular Ca2+, VSMC relaxation (in arterioles) and decreased cardiac preload and afterload.
Norepinephrine
Binds to A1, and B1 adrenergic receptors with more profound A1 effects to cause peripheral vasoconstriction and coronary vasodilation. Primary action is with calcium channels
Normal Saline
Adds water, sodium, and cholride into the body. Provides additional fluid volume in intravascular spaces
Olanzipine
Inhibits synaptic uptake of serotonin and norepinephrine to produce antipsychotic and anticholinergic effects
Ondansetron
Serotonin (5-HT3) R antagonist. Works by blocking blocks serotonin binding to receptors at vagal nerve terminals and postrema “chemoreceptors zone” which inhibits vomiting reflex.
Oxygen
-Enters body via respiratory system-Transported to cells by Hb-Required for efficient breakdown of glucose into usable energy for aerobic metabolism
Oxytocin
Stimulates uterine contractions by causing G-coupled protein receptors to stimulate a rise in intracellular calcium in the uterine myofibrils
Phenylephrine
Binds to A1 adrenergic receptors, second messenger release of calcum in VSMC, causing peripheral vasoconstriction, increasing SVR, increasing BP.
Pralidoxime
Binds to organophosphates and breaks alkyl phosphate-cholinesterase bond to restore the activity of acetylcholinesterase. Primarily works at the nicotinic receptors
Procainamide
Binds to sodium channels which prolongs Phase 0 of the action potential thus decreasing ventricular automaticity. Little effect on atrial tissue. Suppresses intraventricular conduction
Prochlorperazine
Dopamine (D2) R antagonist - inhibits communication from the chemoreceptor trigger zone (which recognizes emetic toxins) to the vomiting center (4th ventricle) of the brain; inhibits gastric SMC relaxation, leading to increased motility of stomach contents into the small intestine; also has weak anticholinergic properties
Propofol
Not well understood….causes global CNS depression by decreasing the dissociation of GABA from the GABA receptors and potentiating the neuro-inhibitory effects of the NT. This keeps the channel open increasing chloride conductance leading to hyperpolarization of the membrane.
Racemic epinephrine
Chemical isomer of epinephrine that stimulates both Alpha and Beta
receptors with a slight preference for Beta2 to cause bronchodilation.
Rocuronium
Binds competively to cholinergic receptors at the motor end plate to antagonize the action of acetylcholine producing skeletal muscle paralysis without e?ectng consciousness
Sodium bicarbonate
Buffers metabolic acidosis and lactic acid buildup in the body by
combining with excessive hydrogen to increase pH
Succinylcholine
combines with cholinergic receptors at the motor nerves to cause depolarization, thus blocking acetylcholine and inhibiting neuromuscular transmission
Terbutaline
Beta-adrenergic receptor agonist that leads to bronchodilation and uterine smooth muscle relaxation. Activation of the beta 2 receptor initials the G-coupled signal transduction pathway. In smooth muscle, elevated levels of cAMP lead to increased levels of PKA. PKA reduces intracellular calcium concentrations and decreases sensitivity to calcium inhibiting myosin light chain phosphorylation and inhibiting smooth muscle contraction
Tetracaine
Sodium channel blocker. Stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of pain impulses, thus causing local anesthetic action
Tranexamic Acid
Forms a complex that displaces plasminogen from fibrin resulting in fibrinolysis
Vecuronium
Binds competively to cholinergic receptors at the motor end plate to antagonize the action of acetylcholine producing skeletal muscle paralysis without e?ecting consciousness
Whole blood
Directly replaces blood volume
