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121 Cards in this Set
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Aldosterone Where is it made?What does it do?Synthesis caused by?
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-endogenous-made in the zone glomerulosa of the adrenal gland-mineralocorticoid-causes increases salt reabsorption and increased K+/H+ excretion in the kidney-sythesis is controlled by angiotensin II and plasma potassium levels
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Cortisol Where is it made?What does it do?Synthesis caused by?
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-endogenous-made in the zona fasciculate & reticularis-glucocorticoid-synthesis controlled by ACTH-90% bound in plasma to corticosteroid binding globulin (CBG) or albumin
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Example of Steroid Drug (5)
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-cortisol-dexamethasone-prednisolone-fludrocortisone-aldosterone
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Metyrapone Agonist, Antagonist, or Synthesis Inhibitor?What does it do?What is it used for?
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-synthesis inhibitor-blocks 11B-hydroxylation, so synthesis is stopped at 11-deoxycortisol, which doesn't inhibit ACTH, so ACTH goes up, causing synthesis and excretion of 17-hydroxycorticoids as 11-deoxycortisol- used as a diagnostic test
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Mifepristone Agonist, Antagonist, or Synthesis Inhibitor?What does it do?What is it used for?
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-competitive progesterone ANTAGONIST-competitive glucocorticoid receptor ANTAGONIST-used to terminate pregnancy and treat Cushing's disease
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SpironolactoneEplerenone Agonist, Antagonist, or Synthesis Inhibitor?What does it do?What is it used for?
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-competitive mineralocorticoid (aldosterone) ANTAGONIST-used as a diuretic-treats HTN, treats/prevents cardiac hypertrophy and heart failure
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Drospirenone Agonist, Antagonist, or Synthesis Inhibitor?What does it do?What is it used for?
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-Progesterone AGONIST -with estrogen, suppress ovulation - hormone replacement therapy in post-meopausal women-mineralocorticoid receptor ANTAGONIST -diuretic -antagonizes salt retaining effect of estrogen-androgen receptor ANTAGONIST
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Prednisolone What does it do:Mechanism of action:Uses:Toxicity:Side effects:Contraindication:
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-corticosteroid-reduces access of cells to target tissues---lymphocytopenia and monocytopenia due to redistribution of cells out of vascular space-interfere with macrophage antigen processing and inhibit binding to Fc factorsUse: -used in combo with other drugs in autoimmune diseases and prevent graft rejectionToxicity: acute adrenal insufficiency on abrupt withdrawal, Cushing's syndromeContraindicated: existing infection
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Azathioprine What does it do:Mechanism of action:Uses:Toxicity:Side effects:Contraindication:
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-prodrug that is metabolized to 6-mercaptopurine-orally active-purine anitmetabolite, inhibits purine biosynthesis and there by DNA synthesis-inhibits de novo and salvage pathwaysUse: inhibit organ transplant rejection, autoimmune diseas (RA)Side effect: bone marrow depression, GI & hepatic toxicity
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Cyclophosphamide What does it do:Mechanism of action:Uses:Toxicity:Side effects:Contraindication:
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-alkylating agent that crosslinks DNA to kill replicating and non replicating cells -toxic effect more pronounced on B cells (suppress humoral immunity)-orally active-used in treatment of autoimmune disease in combo with other drugs (lupus)side effect: bone marrow depression
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Methotrexate What does it do:Mechanism of action:Uses:Toxicity:Side effects:Contraindication:
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-inhibits dihydrofolate reductase, which inhibits folate dependent steps in purine synthesis--inhibits DNA synthesis-blocks de novo purine synthesisuse: treat autoimmune diseases (RA, psoriasis)side effects: hepatic toxicity
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Mycophenolate Mofetil What does it do:Mechanism of action:Uses:Toxicity:Side effects:Contraindication:
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-prodrug metabolized to active mycophenolic acid-lymphocyte selective immunosuppressant-inhibits IMP dehydrogenase, which is necessary for de novo purine synthesis (no effect on salvage pathway) so selectively toxic for lymphocytes who are required to use the de novo pathway-orally activeuse: use with cyclosporine and corticosteroids to prevent renal allograft rejection, treat autoimmune disease (RA, psoriasis)-side effect: infection, leukopenia, anemia-contraindication: do not use during pregnancy--causes miscarriage and congenital malformation
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Cyclosporine What does it do:Mechanism of action:Uses:Toxicity:Side effects:Contraindication:
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-lipophilic peptide antibiotic-binds to cyclophilin (receptor) and inhibits calcium-dependent phosphatase (calcineurin), ultimately blocking the activation of the transcription factor NFAT necessary for IL-2 production-so T cell proliferation and cytotoxicity is inhibited-orally active-use: prevent rejection of transplanted organs (fewer side effects), some autoimmune diseases-side effects: nephrotoxicity (possible in 25-40% of pts), hepatotoxicity
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Tacrolimus What does it do:Mechanism of action:Uses:Toxicity:Side effects:Contraindication:
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-binds to FK binding protein (FKBP) (receptor) and then inhibits calcium-dependent phosphatase (calcineurin), ultimately blocking the activation of the transcription factor NFAT necessary for IL-2 production-so T cell proliferation and cytotoxicity is inhibited-50-100x more potent than cyclosporine-less nephro- and hepatotoxicity
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Sirolimus What does it do:Mechanism of action:Uses:Toxicity:Side effects:Contraindication:
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-inhibits T-cell activation and proliferation downstream of IL-2-binds FKBP-12, binds to and blocks mTOR (kinase involved in cell cycle progression), blocking G1 to S transition-uses: coating of cardiac stents, prevent rejection of transplanted organs, some autoimmune diseases
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Nitroglycerin venous or arterial?mechanism of action:Use:Side effect:
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-relax venous smooth muscle-increase NO, increase cGMP, causes relaxation, decrease preload-venous dominant-use: heart failure-side effect: hypotension
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Nitroprusside venous or arterial?mechanism of action:Use:Side effect:
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-arterial and venous relaxation-increase NO, increase cGMP, causes relaxation, decrease preload and afterload-use: HTN emergencies-side effects: hypotension
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Hydralazine venous or arterial?mechanism of action:Use:Side effect:
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-direct vasodilator-arterial vasodilators-decrease afterload-increase cGMP, decrease Ca2+-use: heart failure, HTN emergency-side effect: hypotension
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Minoxidil venous or arterial?mechanism of action:Use:Side effect:
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-direct vasodilator-arterial vasodilator -decrease afterload-K+atp channel opener, cause hyper polarization and relaxation-use: heart failure, severe HTN-side effect: tachycardia, skin rash, hair growth, fluid retention
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Diazoxide mechanism of action:Use:Side effect:
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-membrane channel dilator-nonselective K channel opener-use: HTN emergencies-side effects: hypoglycemia (activate K channel on Beta cells in pancreas and release insulin)
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VerapamilDiltiazem mechanism of action:Use:Side effect:
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-Ca2+ channel blocker-arterial dilator-decrease contraction of heart (bad for heart failure patients
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MilrinoneInamrinoneCilostazol mechanism of action:Use:Side effect:
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-PDE 3 inhibitor-cause an increase in cAMP, relax smooth muscle, cause contraction in cardiac muscle -inhibit MLC kinase-use: heart failure
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SildenafilTadalafil mechanism of action:Use:Side effect:
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-PDE 5 inhibitors-cause an increase cGMP levels, increase relaxation-use: erectile dysfunction
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Fenoldopam mechanism of action:Use:Side effect:
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-Misc. Vasodilator-Dopamine A1 receptor AGONIST-arterial and venous dilation-use: HTN crisis- increase RBF and Na+ excretion
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Prazosin mechanism of action:Use:Side effect:
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-Misc. Vasodilator-alpha adrenergic blocker-arterial and venous circulation-use: treat HTN
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Atosiban mechanism of action:Use:Side effect:
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-oxytocin receptor antagonist-prevent preterm labor
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Misoprostol mechanism of action:Use:Side effect:
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-PGE 1 analog-used to induce labor-causes cervical ripening and postpartum hemorrhage
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Oxytocin mechanism of action:Use:Side effect:
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-cause uterine contraction-causes concern due to stimulating vasopressin V2 receptor, causing antidiuretic action on fluid balance
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Ergonovine mechanism of action:Use:Side effect:
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-cause uterine contraction-postpartum hemorrhage
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Metoclopramide mechanism of action:Use:Side effect:
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-dopamine receptor ANTAGONIST-5-HT4 receptor AGONIST-use: GI motility (increase lower esophageal tone and peristalsis)-side effect: dystonia
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Bethanechol mechanism of action:Use:Side effect:
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-muscarinic receptor AGONIST-GI motility (increase bladder contractions)-does not cross BBB-not hydrolyzed by cholinesterase-useful in pts with diabetic neuropathy
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Cisapride mechanism of action:Use:Side effect:
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-5-HT4 receptor agonist-use: GI motility-side effect: ventricular arrythmias
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Erythromycin mechanism of action:Use:Side effect:
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-motilin mimetic-increase GI motility
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AlbuterolPirbuterolTertbutalineSalmeterolFormoterol mechanism of action:Use:Side effect:
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-B2 agonist-bronchodilator -increase cAMP/PKA-cardiotoxicity, tachycardia
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IpratropiumTiotropium mechanism of action:Use:Side effect:
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-muscarinic antagonist-decrease mucus secretion
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TheophyllineAminophylline mechanism of action:Use:Side effect:
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Methylzanthine bronchodilators-phosphodiesterase 3 inhibitor-adenosine receptor antagonism--decrease inflammation and increase mucus clearance
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Losartan Mechanism of action:Route of admin:Uses:Side Effects:Contraindications:
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-competitive angiotensin II receptor ANTAGONIST-selective for the AT1 receptor subtype-causes a decrease in aldosterone release, decrease vasoconstriction, decrease sympathetic activation-use: treat HTN, improve heart failure (decrease preload and after load, decrease aldosterone)-diuretics enhance their actions-orally active-contraindicated in pregnancy-side effects: dizziness, cough, angioedema-
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CaptoprilEnalaprilLisinopril Mechanism of action:Route of admin:Uses:Side Effects:Contraindications:
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-ACE inhibitor-inhibits angiotensin II formation and bradykinin degredation (vasodilator)-orally active-reduce BP without increasing HR-hypotension possible for pts on diuretics or volume depleted-uses: treat essential HTN, improve heart failure (decrease preload and after load, increase CO)-enalopril and lisinopril are prodrugs, long duration of action-decrease aldosterone release, can cause hyperkalemia-side effects: rash, proteinuria, cough, angioedema
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Aliskiren Mechanism of action:Route of admin:Uses:Side Effects:Contraindications:
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-renin inhibitor-potent active site, non peptide inhibitor-orally active-long lasting, 1x/day dosing-uses: treat HTN-antihypertensive effect enhanced by diuretic, converting enzyme inhibitor or angiotensin antagonist-decrease plasma angiotensin II and aldosterone concentration-side effects: fatigue, headache, GI symptoms
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SpironolactoneEplerenone Mechanism of action:Route of admin:Uses:Side Effects:Contraindications:
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-competitive aldosterone antagonist at mineralocorticoid receptor- diuretic- orally active- decrease mortality from heart failure-used with thiazide or loop diuretic to treat HTN or edema
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PropanololMetoprolol Mechanism of action:Route of admin:Uses:Side Effects:Contraindications:
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-Beta-adrenergic blockers-decrease renin release by blocking B1 receptors-decreases HTN
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FenoldopamDopamineAtriopeptins Type of diuretic/where they work:Mechanism of action:Use:Side effect:
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-vasodilators-decrease the filtration fraction which maintaining GRF, so increase RBP-decrease FF, reduces protein concentration in peritubular capillaries, reduced hydroosmotic forces allow more Na+ and H2O to leak back into the tubule, so net increase in Na+ exrecretion-weak diuretic (compensatory Na+ reabsorption downstream)- hypertensive crisis, dopamine may be used to increase RBF during shock
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Mannitol Type of diuretic/where they work:Mechanism of action:Use:Side effect:Admin route:
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-osmotic diuretic-freely filtered at glomerulus, works throughout tubule-limited reabsorption by tubule and not metabolized by the kidney-non reabsorbed solute limits H2O reabsorption, so decreased Na+ concentration due to more water to dilute out, so overall less Na+ reabsorbed-increase Na/K exchange in distal tubule, increased K excretion-increased excretion of Na+ K+ Cl- H2O- IV admin-used for edema, glaucoma, acute renal failure
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Acetazolamide Type of diuretic/where they work:Mechanism of action:Use:Side effect:Admin route:
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-carbonic anhydrase inhibitor-secreted into proximal tubule by organic acid transporter (OAT)-no H+/HCO3- production, so Na+(in)/H+(out) counter transporter has no H+, so Na+ stays in tubule and no excretion of H+ so urine pH increases-K+ excretion of Na+ K+ HCO3- H2Oside effects: metabolic acidosis (due to bicarb excretion), hypokalemia-uses: glaucoma, alkalinize urine (drug toxicity)-altitude sickness, anticonvulsant
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FurosemideBumetanideEthacrynic acid Type of diuretic/where they work:Mechanism of action:Use:Side effect: Admin route:
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-Loop diuretic-Inhibit the Na+-K+-2Cl- transporter-secreted in proximal tubule by OAT-acts on both CORTICAL and MEDULLARY segments of ascending limb-POTENT DIURETIC- 20-30% of filtered load of Na+ excreted-increase RBF and increase GFR-increase K+ excretion in distal tubule-can't concentration/dilute urine-increased excretion of Na+ K+ Cl- H20-rapid onset (15min) short duration (2-3hr)-uses: manage edema due to heart, hepatic or renal disease-side effects: hypokalemia, hyperglycemia (furosemide) ototoxicity, volume depletion
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ChlorothiazideHydroclorothiazideMetolazone Type of diuretic/where they work:Mechanism of action:Use:Side effect:Admin route:
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-Thiazide diuretic-inhibit the Na+/Cl- symporter-secreted in the proximal tubule by organic acid transporter (OAT)-act on the cortical diluting segment of ascending limb-intermediate activity (8-10%)-impairs ability to produce dilute urine-urine volume increased, increased excretion of Na+ Cl- K+ (hypertonic urine)-rapid onset (1hr) and long duration-uses: edema due to CHF, HTN, management of hypercalciuria-side effects: hypokalemia, hyperuricemia, hyperglycemia
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SpironolactoneEplerenone Type of diuretic/where they work:Mechanism of action:Use:Side effect:Admin route:
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-K+ sparing diuretic-aldosterone ANTAGONIST-acts on distal tubule as a competitive antagonist of aldosterone (blocks the receptor)-urine volume increases, increase Na+ excretion, decrease K+ excretion-long duration-uses: HTN, refractory edema, primary aldosteronism-used with thawed or loop diuretic to enhance diuretic effect and reduce K+ loss-side effects: hyperkalemia, gynecomastia (spironolactone)
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TriamtereneAmiloride Type of diuretic/where they work:Mechanism of action:Use:Side effect:Admin route:
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-Na+ channel inhibitor (ENaC)-K+ sparing diuretic-inhibit entry of Na+ into principle cells, Na+/K+ exchange does not occur-increase urine volume, increase Na+ excretion, decrease K+ excretion-weak diuretic, 2-3% of filtered load-used with thiazide or loop diuretic to enhance diuretic effect with less K+ loss-use: treat edema or HTN-side effect: hyperkalemia, azotemia (increase BUN)
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Dinoprostone What is is?Use:Administration:Mechanism:Side Effects:
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-PGE2 analog-Use: cervical ripening in pregnancy-cervical gel-mech: promote ripening of cervix through activation of collagenase--breaks down collagen, relax cervical smooth muscle, EP4 receptor use 2: terminate early pregnancy/abortion-vaginal suppository-uterine contraction via EP1/3 receptor side effects: GI related (nausea/vomiting/diarrhea), fever, uterine rupture
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Carboprost What is it?Use:Administration:Mechanism:Side Effects:
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-PGF2a analoguse: terminate pregnancy during 2nd trimester between 13 and 20 wks, and to control postpartum hemorrhage not responding to conventional treatment methodsmech: stimulate uterine contractility by action at FP receptoradmin: IM injectionside effects: GI related (nausea/vomiting/diarrhea), fever, uterine rupture
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Misoprostol What is it?Use:Administration:Mechanism:Side Effects:
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-PGE1 analog-use: replacement therapy for prevention of ulcers caused by long-term admin of NSAIDs-orally active, 4x a daymech: decrease gastric acid secretion by sim EP3 receptor on parietal cells, decrease cAMP, increase mucin and bicarb, increase mucous blood flowside effect: diarrhea, miscarriagedo not use during pregnancy!
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Alprostadil What is it?Use:Administration:Mechanism:Side Effects:
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-PGE1 analog-use 1: erectile dysfunction-intracavernous injection/intra urethral-mech: increase cAMP, relax smooth muscle of corpus cavernosum side effect: pain at injection site, priapism -use 2: maintain patent ductus arteriosus-infused intravenously-mech: cAMP mediated relaxation of ductus arteriosus smooth muscleside effect: apnea in 10% of neonates
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Epoprostenol What is it?Use:Administration:Mechanism:Side Effects:
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-PGI2- used to treat primary pulmonary HTN (rare)- continuous IV infusion- mech: cAMP mediated dilation of pulmonary artery vasc. smooth muscle- side effect: nausea/vomiting, headache, flushing
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Bimatoprost What is it?Use:Administration:Mechanism:Side Effects:
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-PGF2a-use: glaucoma-ophthalmic solution-mech: increase outflow of aqueous humor-side effect: eye redness, itching, permanent change in eye color use 2: eyelash hypotrichosis-ophthalmic solution-increase percent and duration of hairs in the growth phaseside effect: excess, unwanted hair growth, brown iris pigmentation, eye redness, itchiness
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Histamine cell source:physiological response:mechanism:pharmacology:
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-biogenic amine-source: mast cells, basophils-response: vasodilation, increase vascular permeability, pain-mech: activate GPCRs--activate signaling pathway-pharm: antihistamines (H1 antagonist)
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Bradykinin cell source:physiological response:mechanism:pharmacology:
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-peptide-source: endothelial cells (lumen of blood vessel)-response: vasodilation, increase micro vessel permeability, pain-mech: activate GPCRs-pharm: BK receptor ANT being tested
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Complement System cell source:physiological response:mechanism:pharmacology:
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-plasma proteins-source: synthesized by liver, circulate in blood-response: chemotaxis, promote release of mediators from neutrophils, increase vascular permeability-mech: complement protein complexes, cause osmotic lysis, activate GPCRs, mast cell degranulation
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C-Reactive Protein cell source:physiological response:mechanism:pharmacology:
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-plasma protein-source: produced by liver in response to cytokines and by adipocytes-response: "acute phase reactant", activate complement cascade, mediates phagocytosis, *marker for inflammation-mech: bind to phosphatidylcholine in bacteria and damaged cells, calcium dependent binding
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Cytokines cell source:physiological response:mechanism:pharmacology:
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-secreted proteins, ex IL-1 and TNF alpha-source: nearly all inflammatory cells-response: stimulate acute phase reactants, TNFa: fever, sepsisIL-1: fever, fibroblast & lymphocyte proliferationmech: bind to specific receptors to induce gene expression of numerous proteins thru activation of transcription factors-increase cyclooxyrgenase (fever) and lipoxygenases-increase adhesion molecule-induce collagenases (fibrosis)pharm: Etanercept, Infliximab
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Adenosine cell source:physiological response:mechanism:pharmacology:
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-purine nucleoside-source: all cells-response: increase extracellularly during injury and has anti-inflammatory effect to inhibit cytokine action-receptor specific (can be pro-inflammatory)mech: activate GPCRs
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Cell Adhesion Molecules (CAMs) cell source:physiological response:mechanism:pharmacology:
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-integrins, selectinssource: endothelial cells, platelets, leukocytesresponse: -leukocyte adhere to endothelium is integral to repair process -endothelial adhesion molecules contribute to recruitment of activated plateletsmech: mediate contact btwn 2 cells or btw cells and extracellular matrix, "contact" molecules, Ca2+ dependent
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Prostaglandins cell source:physiological response:mechanism:pharmacology:
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-pro-inflammatory-source: all cells-response: vasodilation/vasoconstriction, pain, fever, platelet aggregation (tromboxane)-PGE1/PGE2 directly increase blood flow and indirectly enhance edema formationmech: activate specific GPCRspharm: NSAIDs (block prostaglandins)
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Leukotrienes cell source:physiological response:mechanism:pharmacology:
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-pro-inflammatory-source: macrophages, neutrophils-response: increase vascular permeability, bronchoconstrictionmech: activate GPCRpharm: Zileuton, Zafirlukast
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Gluccocorticoids cell source:physiological response:mechanism:pharmacology:
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-anti-inflammatory-source: adrenal cortex-response: inhibit cytokines, inhibit phospholipase A, inhibit cyclooxygenase 2, inhibit cell adhesion molecules-mech: activation of nuclear receptors-pharm: steroid --most potent and effective agents for controlling chronic inflammatory diseases
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Zafirlukast
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-cysteinyl leukotriene receptor ANT-competitive antagonist of leukotriene receptors-orally active-metabolized by CYP2C9/3A4-inhibits cys-LTs at receptor (LTs still synthesized)-minimal side effectsuse- prophylactic treatment of mild asthma
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Zileuton
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-inhibits 5-lipoxygenase, inhibiting the synthesis of leukotrienes-orally active-metabolized by CYP enzymes-inhibits production of cys-leukotrienes (decreasing bronchoconstriction and LTB4 (chemotaxis))-few adverse effects, increase liver enzymesuse: prophylactic treatment of mild asthma
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Etanercept
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-receptor analog-prevent TNF-alpha binding
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Infliximab
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-monoclonal antibody-binds to TNF-alpha, preventing it from binding the receptor
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Verapamil Class:Type of binding:Tissue it binds:Use:Absorption/half-life:Side effects/contraindications:
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-Phenylalkylamine- use-dependent binding-preferentially act on cardiac cells (block myocardium and SA and AV node)-can also cause vasodilation in vascular smooth muscle-used to treat supra ventricular arrhythmias (slow SA node firing/reduce AV node conduction)-undergoes extensive first-pass metabolism-short half life (3-6hr)-side effect: constipation, worse CHF (negative inotropic effect), produce AV block, sinus bradycardia
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Diltiazem Class:Type of binding:Tissue it binds:Use:Absorption/half-life:Side effects/contraindications:
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-Benzothiazepine- use-dependent binding -preferentially act on cardiac cells (block myocardium and SA and AV node)-can also cause vasodilation in vascular smooth muscle-used to treat angina (reduce cardiac workload, block SA node firing, reduce cardiac afterload, dilate coronary arteries), supra ventricular arrhythmias-short half life (3-6hr)-possible AV conduction disturbances/heart block (less likely), sinus bradycardia
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Nifedipine Class:Type of binding:Tissue it binds:Use:Absorption/half-life:Side effects/contraindications:
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-1,4 Dihydropyridin- voltage-dependent-preferentially act on arterial muscle cells, have little effect on veins-causes potent arterial vasodilation (decrease afterload)-used fro angina (due to vasodilatory effects on coronary arteries), hypertension (can cause reflex bradycardia, use with beta blocker)-high percent of protein binding-short half life (3-6hr)-side effect: hypotension, headache, flushing and peripheral edema
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Amlodipine Class:Type of binding:Tissue it binds:Use:Absorption/half-life:Side effects/contraindications:
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-1,4 dihydropyridine- voltage-dependent -preferentially act on arterial muscle cells, have little effect on veins-causes potent arterial vasodilation (decrease afterload)-treat hypertension (slow acting, so less reflex tachycardia)-high percent of protein binding-long half life, 1x/day dosing-side effect: hypotension, headache, flushing and peripheral edema
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Buspirone agonist or antagonist:receptor bound:use:side effect:
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-agonist-5HT2 receptor-potent hallucinogen
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lysergic acid diethylamide (LSD) agonist or antagonist:receptor bound:use:side effect:
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-partial agonist-5HT 1A receptor-anti-anxiety agent
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sumatriptan agonist or antagonist:receptor bound:use:side effect:
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-agonist-5HT 1D receptor on cerebral blood vessels-promote vasoconstrictions of dilated cerebral blood vessels-use: treat migraine headaches, stop existing headache-side effects: n/v, angina, dizziness, flushing
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Fluoxetine agonist or antagonist:receptor bound:use:side effect:
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-indirect agonist-serotonin specific reuptake inhibitor (SSRI)-block active repute of serotonin into neurons-increase serotonin in synapse-use: treat affective disorders, OCD, panic attacks
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Phenelzine agonist or antagonist:receptor bound:use:side effect:
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-indirect agonist-monoamine oxidase inhibitor (MAOI)-block metabolism of serotonin, NE, DA-use: treat depression and narcolepsy-side effect: hypertensive crisis
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Duloxetine agonist or antagonist:receptor bound:use:side effect:
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-partial agonist-serotonin/NE reuptake inhibitor (SNRI)use: major depressive disorder, neuropathic pain
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Cyproheptadine agonist or antagonist:receptor bound:use:side effect:
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-antagonist-5HT2 antagonist-histamine H1 antagonist-use: skin allergies--> pruritis and urticaria, treat carcinoid
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Ondansetron agonist or antagonist:receptor bound:use: side effect:
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-antagonist-5HT3 antagonist-treat chemo induced n/v-acts on both GI and brain receptors-IV and oral form
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Alosetron agonist or antagonist:receptor bound:use:side effect:
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-selective 5HT3 antagonist-treatment with diarrhea predominant IBS who have failed to respond to conventional therapy-can produce severe GI adverse effects
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Cromolyn mechanism:route:side effects:use:
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-inhaled anti-inflammatory agent-stabilizes mast cell membrane, prevent histamine release-inhaled-safe drug/few side effects-preventative management of asthma, allergic rhinitis, conjunctivitis
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Omalizumab mechanism:route: side effects:use:
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-monoclonal antibody-bind IgE, so there is less IgE present to normally bind to and sensitizes mast cells-subcutaneous administration-side effect: anaphylaxis, bleeding related effects-use: allergic asthma
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Diphenhydramine mechanism:use: side effects:
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-1st generation H1 antagonist-used for allergies, motion sickness, early stage Parkinson's, non-rx sleeping tab-side effect: sedation (get across BBB)
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Dimenhydrinate mechanism:use: side effects:
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-1st generation H1 antagonist-used for motion sickness, vestibular disturbances-side effect: sedation (get across BBB)
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Chlorpheniramine mechanism:use: side effects:
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-1st generation H1 antagonist-used for allergies-side effect: sedation (get across BBB)less sedation, more potent
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Promethazine mechanism:use: side effects:
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-1st generation H1 antagonist-used for motion sickness, chemo n/v-side effect: sedation (get across BBB)
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Fexofenadine mechanism:use: side effects:
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-2nd generation H1 antagonist-does not cross BBB, less sedation effects-use: allergies
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Loratadine mechanism:use: side effects:
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-2nd generation H1 antagonist-does not cross BBB, less sedation effects-use: allergies
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Desloratadine mechanism:use: side effects:
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-2nd generation H1 antagonist-does not cross BBB, less sedation effects-use: allergies
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Cetirizine mechanism:use: side effects:
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-2nd generation H1 antagonist-does not cross BBB, less sedation effects--this has the most sedative effects -use: allergies
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Cimetadine mechanism:use: side effects:
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-competitive histamine at H2 receptor antagonist-inhibit gastric acid secretion from parietal cell-use: treat uncomplicated GERD-side effects: diarrhea, drowsiness** inhibits P450 enzymes, increase drug half-lives -long term use at high dose causes gynecomastia and impotence
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Ranitidine mechanism:use: side effects:
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-competitive histamine at H2 receptor antagonist-inhibit gastric acid secretion from parietal cell-use: treat uncomplicated GERD-side effects: diarrhea, drowsiness
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Famotidine mechanism:use: side effects:
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-competitive histamine at H2 receptor antagonist-inhibit gastric acid secretion from parietal cell-use: treat uncomplicated GERD-side effects: diarrhea, drowsiness
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Aspirin (Acetylsalicylic acid) mechanism:anti-inflammatory, analgesia, antipyretic?use: side effects:contraindications:
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-irreversible inhibitor of COX 1 and COX 2 (acetylates a serine group)-anti-inflammatory, analgesia, antipyretic -use: fever, low intensity pain, inflammatory disorder, CV disease (anti-platelet affect)-side effects: gastric irritation (inhibit COX1/cytoprotective PGs), increase bleeding time (platelets can't make TxA2 for their lifetime), hypersensitivity (leukotriene shuttling), decrease RBF/GFR (decrease vasodilatory PGs), Reyes syndrome -contraindicated in pregnancy: may prolong labor, decrease uterine contractions (decreased labor inducing PGs)
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Ibuprofen mechanism:anti-inflammatory, analgesia, antipyretic?use: side effects:contraindications:
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-reversible inhibitor of COX 1 and COX 2-half-life: 2 hrs-anti-inflammatory, antipyretic, analgesic-side effects: GI effects, hypersensitivity, kidney, blood, drug interactions-use: inflammatory diseases and rheumatoid disorders, juvenile RA, fever, dysmenorrhea, oestoarthritis, injection--induce closure of a patent ductus arteriousus
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Naproxen mechanism:anti-inflammatory, analgesia, antipyretic?use: side effects:contraindications:
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-reversible inhibitor of COX 1 and COX 2-half-life: 14 hrs-anti-inflammatory, antipyretic, analgesic-side effects: GI effects, hypersensitivity, kidney, blood, drug interactions-use: osteoarthritis, acute gout, tendonitis, dysmenorrhea, fever
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Indomethacin mechanism:anti-inflammatory, analgesia, antipyretic?use: side effects:contraindications:
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-reversible inhibitor of COX1 and COX 2-half-life 3hrs-anti-inflammatory, analgesic, antipyretic-side effects: frequent adverse rxns, GI toxicity, severe frontal headaches-use: actue gouty arthritis, RA, IV form used in neonates to close patent ductus arteriousus-not routinely used to treat pain/fever
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Ketorolac mechanism:anti-inflammatory, analgesia, antipyretic?use: side effects:contraindications:
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-reversible inhibitor of COX1 and COX 2-analgesic and antipyretic-use: short term management of moderate to severe acute pain req analgesia at the opioid level
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Nabumetone mechanism:anti-inflammatory, analgesia, antipyretic?use: side effects:contraindications:
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-active metabolite is reversible inhibitor of COX 1 and COX2 (COX 2 > COX 1)-long half-life-anti-inflammatory, analgesicside effect: well tolerated, less GI effectsuse: osteoarthritis, RA
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Piroxicam mechanism:anti-inflammatory, analgesia, antipyretic?use: side effects:contraindications:
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-reversible inhibitor of COX 1 and COX2-half-life 50hrs-anti-inflammatory, antipyretic, analgesic-side effect: GI toxicity-use: RA and osteoarthritis
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Sulfasalazine mechanism:anti-inflammatory, analgesia, antipyretic?use: side effects:contraindications:
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-mesalamine is the active component-mechanism of action not clear-local effect in GI to inhibit the inflammatory responseside effects: occur in 10-45%, headache, n/v, fatigue, allergic rxnuse: mild to moderate active ulcerative colitis, RA and ankylosing spondylitis
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Celecoxib mechanism:anti-inflammatory, analgesia, antipyretic?use: side effects:contraindications:
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-contain a sulfonamide side chain-inhibit COX 2--bind to distinct hydrophilic side pocket region close to COX 2 binding site-metabolized via P450 2C9-antipyretic, analgesic, anti-inflammatoryside effects: hypersensitivity, GI irritation, ulceration and bleeding, increase risk of MI and strokecontraindication: prior NSAID hypersensitivity, hx of GI disease, do not give after a CABGuse: sign and symptoms of RA/osteoarthritis, primary dysmenorrhea, management of acute pain, decrease intestinal polyps
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Acetaminophen (Tylenol) mechanism:anti-inflammatory, analgesia, antipyretic?use: side effects:contraindications:
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-mechonism not well understood (NO affinity for COX1 or COX 2)-half-life 2 hrs-analgesic and antipyretic (NOT anti-inflammatory)-use: treatment of mild to moderate pain and feverside effects: well tolerated at normal doses, no GI effectshepatic toxicity after high doses of drug, accumulation of highly reactive intermediatesymptoms: n/v, abd pain, 24hrs to see liver damage
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Heparin mech:route:monitering:adverse rxn:use:contraindication:
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-highly negative charge (sulfated)-mech: induces a conformation change in antithrombin, giving it a higher affinity for Xa and thrombin, which it inactivates**does not affect the synthesis of clotting factors-route: IV admin-does not cross the placenta (can be used in pregnancy!)-monitor with an aPTT-immediate onset of action when given IV-adverse rxn: bleeding, heparin induced thrombocytopenia-use: DVT/PE, acute MI, hemodialysis-contraindication: active bleed, uncontrolled HTN
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EnoxaparinDalteparin mech:route:monitering:adverse rxn:use:contraindication:
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-low molecular weight heparin- mech: bind to antithrombin, causing a conformation change, increasing the binding of Xa, which antithrombin can inactivate-given IV or subQ-cleared by the kidneys!-longer half-life compared to heparinadverse effects: less incidence of bleeding, thrombocytopenia less likelyuse: acute DVT, prophylaxis of DVT, acute MI, hip replacement sxcontraindication: active bleeding, uncontrolled HTN, renal impairment
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Lepirudin mech:route:monitering:adverse rxn:use:contraindication:
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-direct thrombin inhibitor, bind to thrombin catalytic site and to exosite 1-administered IV-excreted by kidneys-adverse effects: bleedinguse: alternative to heparin in pt undergoing coronary angioplasty or cardiopulmonary bypass sxcontraindication: bleeding, recent sx, uncontrolled HTN, renal disease
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Bivalirudin mech:route:monitering:adverse rxn:use:contraindication:
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-direct thrombin inhibitor, bind to thrombin catalytic site and exosite 1-administered IV-excreted by kidney-adverse effects: bleedinguse: alternative to heparin in pts undergoing coronary angioplasty or cardiopulmonary bypass sxcontraindication: active bleeding, renal disease, uncontrolled HTN
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Fondaparinux mech:route:monitering:adverse rxn:use:contraindication:
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-antithrombin mediated selective inhibition of factor Xa -subQ injection- adverse effects: bleedinguse: prophylaxis of DVT, alternative to heparin in pt with hx of HITcontraindication: bleeding, renal impairment
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Protamine sulfate mech:route:monitering:adverse rxn:use:contraindication:
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-heparin antagonist/antidote-positive charge, binds with high affinity to negatively charged heparin, forming inactive complex-use: reverse heparin after bypass
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warfarin mech:route:monitering:adverse rxn:use:contraindication:
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-structural analog to vit K, targets VKORC1-S-warfarin prevents reductive metabolism of the inactive vit k oxide back to its active reduced form, which is needed to activate coagulation factors II, VII, IX, X (causes inactivated coagulation factors to be produced)-monitoring: PT and INR 2-3-oral admin-adverse rxn: bleedingTERATOGENIC-do not use during pregnancyuse: treat venous thromboembolitic disease anecdote: admin vitamin K (competitive inhibition) or frozen fresh plasma (FFP) CYP2C9 responsible for metabolism
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Dabigatran mech:route:monitering:adverse rxn:use:contraindication:
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-new oral anticoagulant (NOAC)-prodrug converted to active dabigatran, prodrug is a substrate for P-gp (pumps drug back into GI lumen)-oral admin-reversible, direct binding to both FREE thrombin and FIBRIN BOUND thrombin
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Rivaroxaban mech:route:monitering:adverse rxn:use:contraindication:
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-new oral anticoagulant (NOAC)-direct factor Xa inhibitor (prevent prothrombin to thrombin conversion)-oral admin-metabolism by both kidney and liver-adverse effects: bleedinguse: prophylaxis of DVT
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Tissue plasminogen activator (t-PA)
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-endogenous, synthesized by vascular endothelial cells-binds to fibrin/plasminogen complex, converts plasminogen to active form plasmin, which then cleaves fibrin (break down clot)
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Alteplase mech:route:monitering:adverse rxn:use:contraindication:
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-exogenous, drug-binds to fibrin/plasminogen complex, converts plasminogen to active form plasmin, which then cleaves fibrin (break down clot)-continuous IV admin-adverse effects: systemic lytic state results from systemic formation of plasmin-use: acute MI, treat PE or DVT, treat stroke within first 3 hourscontraindication: active bleeding, hx of CVA, uncontrolled HTN, pregnancy
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Aminocaproic acid what is it:mech:use:
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-synthetic lysine analog, binds to lysine binding site of plasminogen and plasmin, blocking the binding of plasmin to fibrin-use: decreasing hemorrhage after surgical procedure
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Aspirin mech:route:monitering:adverse rxn:use:contraindication:
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-mech: irreversible inhibition of platelet COX 1 and COX 2 (COX 1 in the platelet), block TxA2 production, inhibit platelet aggregation-adverse effects: bleeding, GI irritation-use: MI prophylaxis, acute phase of ischemic stroke, acute MI, unstable angina
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Dipyridamole mech:route:monitering:adverse rxn:use:contraindication:
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mech: phosphodiesterase inhibition/blockade of uptake of adenosine, increase cAMP--inhibit platelet aggregation-oral admin-adverse effects: headache, GI upset, dizzinessuse: prevention of thromboembolitic in pt with prosthetic valve
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Clopidogrel, Ticlopidine, Prasugrel, Ticagrelor mech:route:monitering:adverse rxn:use:contraindication:which are prodrugs?
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mech: inhibit ADP binding to the P2Y12 receptor, decrease platelet activation and aggregation-clopidegrel, ticlopidine, ticlopidine--PRODRUGS-ticagrelor--REVERSIBLE-prasugrel--higher potency, more rapid onset, more consistent level of platelet inhibition than clopidogreladverse effects: increase risk of bleeding, TICLOPIDINE may cause severe neutropenia
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Abciximabmech: adverse effects:use:
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-Fab fragment of monoclonal antibody, binds to GP IIb/IIIa-prevents platelet aggregation by binding to receptor and inhibiting fibrinogen binding and cross linking of platelets-IV adminadverse effects: bleeding, thrombocytopenia, hypotension, bradycardia-use: prevent platelet aggregation
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Eptifibatidemech:adverse effects:use:
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mech: competitive reversible inhibitor of fibrinogen binding to GP IIb/IIIaadverse effects: bleeding, use cautiously in pts with renal dysfunctionuse: pt with unstable angina, MI, prevent coronary thrombosis
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