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Definition
interferes with cellular metabolism or reproduction; some cause leakage of potassium and magnesium from the cell membrane leading to death of cell; other interfere with DNA synthesis and fungal mitosis |
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anti diarrheal adsorbents MOA |
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Definition
Coat walls of the GI tract, absorbing bacteria or toxins causing diarrhea then eliminating them; results in the removal of the causative agents in stools |
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anti diarrheal anti cholinergic MOA |
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Definition
MOA: Decreased intestinal muscle tone and peristalsis by inhibiting the PSNS, thus slowing movement of fecal material |
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anti diarrheal intestinal flora modifiers MOA |
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Definition
MOA: Suppress the growth of diarrhea-causing bacteria and help to reestablish normal intestinal flora that has been depleted |
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anti diarrheal opiates MOA |
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Definition
MOA:Decrease motility of bowel and relieve rectal spasms; also provide some pain relief |
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Term
laxatives Bulk forming MOA |
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Definition
MOA: absorb water into intestines, distending bowel to initiate reflex bowel activity (act similar to natural fiber in diet), diverticulosis |
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Term
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Definition
MOA: Stool softeners allow more water and fat to be absorbed into stool by lowering surface tension of GI fluids |
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Definition
MOA: increase fecal water content resulting in distention, increased peristalsis, and evacuation |
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Term
laxatives saline laxatives MOA |
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Definition
MOA: increases osmotic pressure in small intestines by inhibiting absorption and increasing water and electrolyte secretions, increases distention, peristalsis, and evacuation |
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Term
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Definition
MOA: stimulate nerves that inervate intestines, increasing peristalsis; also increase fluid in intestines, which increases bulk and softens stools |
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Term
diuretics osmotic diuretics MOA |
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Definition
MOA: Increases osmotic pressure of glomerular filtrate---inhibiting tubular resorption of water and solutes----rapid diuresis results; primary site of action is proximal tubule and descending limb of loop of Henle |
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Term
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Definition
MOA: Site of action is the ascending loop of Henle; inhibits the resorption of sodium and chloride Increases the concentrations of renal prostaglandins—results in dilation of blood vessels in kidneys. lungs and body—antihypertensive effect |
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Term
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Definition
MOA: Site of action ascending loop of Henle and early distal tubule---inhibit tubular resorption of sodium and chloride and potassium—osmotic water loss results |
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Term
potassium sparing diuretics MOA |
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Definition
MOA: Spironolactone-competative antagonist of aldosterone (binds to aldosterone receptors-blocks action)—causes sodium and water excretion and potassium retention; site of action is collecting ducts and distal convoluted tubules |
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Term
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Definition
Heparin- binds to antithrombin III, which turns off activating factors: activated II (thrombin), activataed X, and activated XI--turns off coagulation pathway and prevents clot formation Low molecular weight heparin (enoxaparin)-more specific action on factor X-more predictive response; do not need to monitor PTT levels Warfarin (Coumadin)-inhibits clotting factors II VII, IX, and X- by interfering with the production of Vitamin K, needed for synthesis of clotting factors |
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Term
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Definition
Aspirin- inhibits cyclooxygenase in the platelet irreversibely, which prevents formation of thromboxane (TX), substance that causes blood vessels to constrict and platelets to aggregate; therefore dilation of blood vessels and prevention of platelet aggregation results ; also may have hematologic action altering hepatic synthesis of blood coagulation factors VII, IX, and X Ticlopidine (Ticlid) and Clopidogrel (Plavix)-ADP inhibitors--alters platelet membrane so that does not receive the message to aggregate and form a clot; signal is sent by fibrinogen which attaches to glycoprotein receptor (GPIIb/IIIa) on surface of platelet; 24-48 hours for effect |
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Term
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Definition
aminocaproic acid (Amicar)-forms reversible complex with plasminogen and plasmin. Binds to lysine-binding site of plasminogen, displacing plasminogen from surface of fibrin, thus preventing plasmin from lysing the fibrin clot; only work if clot has formed desmopressin (DDAVP); increases factor VII which anchors platelets to damaged vessels; acts as general endothelial stimulant-stimulates factor VII, prostaglandin I2 and plasminogen-activated release |
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Term
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Definition
activate conversion of plasminogen to plasmin, which breaks down the thrombus (part of fibrinolytic system which is responsible for dissolving clots) |
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Term
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Definition
block or inhibit action of histamine binds with unoccupied Histamine1 receptors |
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Definition
Adrenergic agents: constrict small blood vessels in nasal area-nasal secretions better able to drain Steriods: aimed at inflammatory response-that is elicited by virus or bacteria-turns off cells or renders then unresponsive |
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Definition
Opioids: direct action on cough center Dextromethorphan-action on cough center Benzonatate-suppresses cough reflex by anesthetizing stretch receptors and preventing cough reflex stimulation in medulla |
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Term
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Definition
Reflex stimuation: loosening and thinning in response to an irritation of GI tract produced by agent (Guaifenesin) Direct stimulation of secretory glands to increase production of respiratory tract fluids (iodinated glycerol and potasium iodide) |
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Term
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Definition
Respiratory med MOA: Inhibits phosphodiesterase (PDE), the enzyme responsible for breaking down cyclic adenosine monophosphate (cAMP); cAMP helps to maintain open airways through smooth muscle relaxation and inhibition of IgR-induced release of chemical mediators responsible for allergic reactions |
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Term
Beta-agonist (sympathomimetics) MOA |
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Definition
Respiratory med sympathomimetics- MOA: Stimulation of B2 adrenergic receptors on lungs--adenylate cyclase activated-needed to make cAMP which causes smooth muscle relaxation-bronchial dilation |
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Term
anti cholenergic respiratory MOA |
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Definition
MOA: Prevents bronchoconstriction by binding to acetylcholine receptors on surface of bronchial tree preventing AcH from binding to receptors (AcH when it binds to receptors on bronchial tree will cause smooth muscle constriction) |
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Term
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Definition
respiratory med MOA: Blocks the action of leukotrienes, one of several chemical substances produced in response to a "trigger" which causes inflammation, bronchoconstriction, mucous production which causes symptoms of coughing, SOB, and wheezing |
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Term
corticosteriods respiratory MOA |
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Definition
MOA: Reduces inflammation by stabilizing cell membranes of neutrophils so inflammation causing substances are not released; stabilizing cell membranes of basophils so histamine is not released; decreasing activity of lymphocytes; and inhibiting macrophage accumulation preventing further inflammation |
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Term
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Definition
respiratory med MOA: Stabilizes cell membranes of cells that releases vacoconstrictive substances (histamine,SRS-A) in response to antigen-antibody reactions |
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Term
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Definition
MOA: Stimulate beta cells of pancreas to secrete insulin, increases insulin sensitivity of cells of the muscle, liver, and fat |
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Term
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Definition
MOA: Decreases glucose production by liver. Decreases intestinal absorption of glucose, and improves insulin sensitivity |
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Term
Angiotensin II receptor antagonist |
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Definition
anti hypertensives block angiotensin receptors, preventing vasoconstriction |
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Term
Adrenergics (anti hypertensive) |
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Definition
MOA stimulation of alpha 2 adrenergic receptors decreases SNS stimulation |
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Definition
directly elicit peripheral vasodilation |
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Term
Calcium Channel blockers ()anti hypertensive) |
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Definition
Prevents calcium from entering and interacting in contraction process resulting in relaxation of coronary and peripheral arteries |
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Term
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Definition
anti lipemic agents Bind with bile, preventing the reabsorption of bile acids from intenstines. stimulates hepatic synthesis of bile acids from cholesterol due to decreased bile acid pool. Decreased cholesterol pool in liver. cholesterol biosynthesis and LDL receptors on liver surface increased. Increased removal of LDL from bloodstream |
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Term
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Definition
anti lipemic agent decreases rate of cholesterol production in the liver by inhibiting HMG-COA reductase the enzyme needed to produce cholesterol. liver then increases number of LDL receptors to increase recycling of LDL for production of steroids, bile acids, and cell membranes. |
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