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127 Cards in this Set
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Hydralazine
-mech -clinical Use -toxicity |
-mech: increase cGMP -> smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction. -use: Sever HTN, CHF. First-line therapy for hypertension in pregnancy, with methyldopa. Frequently coadministered with a B-blocker to prevent reflex tachycardia.
-Tox: Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina. Lupus-like syndrome. |
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Minoxidil
-mechanism -use -toxicity |
-mech: K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle
-use: severe HTN -toxicity: hypertricosis, pericardial effusion, reflex tachycardia, angina, salt retention |
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calcium channel blockers
-drugs -MOA -Use -toxicity |
Nifedipine, verapamil, diltiazem
-MOA: block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility. Vascular smooth muscle - nifedipine > diltiazem > verapamil. Heart - verapamil > diltiazem > nifedipine. -use: HTN, anfgina, arrhytmias (not nifedipine), Printzmetal's angina, Raynaud's -toxicity: cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation |
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Nitroglycerin, isosorbide dinitrate
-MOA -use -toxicity |
-MOA: vasodilate by releasing nitric oxide in smooth muscle, causing increase in cGMP and smooth muscle relaxation. Dilate veins >> arteries. Decrease preload
-use: angina, pulmonary edema. Also used as an aphrodisiac and erection enhancer. -tox: reflex tachycardia, hypotension, flushing, headache, "Monday disease" in industrial exposure; development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend, resulting in tachycardia, dizziness, and headache on reexposure. |
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Malignant HTN treatment
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nitroprusside: short acting; increase cGMP via direct release of NO. Can cause cyanide toxicity (releases CN)
fenoldopam: dopamine D1 receptor agonist - relaxes renal vascular smooth muscle diazoxide: K+ channel opener - hyperpolarizes and relaxes vascular smooth muscle. Can cause hyperglycemia (reduces insulin release) |
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drugs, MOA and side effects of
-HMG-CoA reductase inhibitors -Niacin -Bile acid resins -Ezetimibe -"fibrates" |
-lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin; really decreases LDL, slight increase in HDL, slight decrease in TG; inhibit cholesterol precurose, mevalonate; SE: hepatotoxicity (increase LFTs), rhabdomyolysis
-niacin: decreases LDL, increases HDL, slight decrease in TG; inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation; SE: red, flushed face, which is decreased by aspirin or long-term use; hyperglycemia (acanthosis nigricans); hyperuricemia (exacerbates gout) -cholestyramine, colestipol, colesevelam: decreases LSL, very slightly increases HDL, very slightly increases TG; prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more; SE: patients hate it- tastes bad and causes GI discomfort, decrease absorption of fat-soluble vitamins; cholesterol gallstones -ezetimibe: decreases LDL; prevent cholesterol reabsorption at small intestine brush border; SE: rare increase in LFTs -gemfibrozil, clofibreate, bezafibrate, fenofibrate: slight decrease in LDL, slight increase in HDL, great decrease in TG; upregulate LPL -> increase TG clearance; SE: myositis, hepatotoxicity (increase LFTs), cholesterol gallstones |
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cardiac glycosides - digoxin
-MOA -use -toxicity -antidote |
-MOA: direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca exchanger/antiport. Increase [Ca}i -> positive inotropy. Stimulates vagus nerve
-Use: CHF (increase CTY); atrial fibrillation (decrease conduction at AV node and depression of SA node) -tox: cholinergic - nausea, vomiting, diarrhea, blurry yellow vision; ECG - increase PR, decrease QT, scooping, T-wave inversion, arrhythmia, hyperK. Worsened by renal failure (decrease excretion), hypoK (permissive for digoxin binding at K-binding site on Na/K ATPase), quinidine (decrease digoxin clearance; displaces digoxin from tissue0binding sites) -antidote: slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg2+ |
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general info about Class 1 antiarhythmics
Class 1A, 1B, and 1C drugs |
Na+ channel blockers; local anesthetics. Sow or block conduction (especially in depolarized cells). Decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells. Are state dependent (selectively depress tissue that is frequently depolarized, eg. fast tachycardia)
1A: quinidine, procainamide, disopyramide 1B: lidocaine, mexiletine, tocainide 1C: flecainide, encainide, propafenone |
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Class IA MOA and toxicity
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increase AP duration, increase effective refractory period (ERP), increase QT interval. Affect both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia.
Tox: quinidine (cinchonism - headache, tinnitus; thombocytopenia; tosades de pointes due to increase QT interval); procainamide (reversible SLE-like syndrome) |
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Class IB MOA and toxicity
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decrease AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue. Useful in acute ventricular arrhythimias (especially post MI) and in digitalis-induced arrhythmias.
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Class IC MOA and toxicity
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No effect on AP duration. Useful in V-tachs that progress to VF and in intractable SVT. Usually used only as last resort in refractory tachyarrhythmias. For patients without structural abnormalities.
-tox: proarrhythmic, espically post-MI (contraindicated). Significantly prolongs refreactory period in AV node. |
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Class II antiarrhythmics
-MOA -use -tox |
Beta blockers: propranolol, esmolol, metoprolol, atenolol, timolol
-MOA: decrease cAMP, decrease Ca current. Suppress abnormal pacemakers by decrease slope of phase 4. AV node particularly sensitive - increase PR interval. Esmolol very short acting -Use: V-tach, SVT, slowing ventricular rate during atrial fibrillation and atrial flutter. -toxicity: Impotence, exacerbation of asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia. Metoprolol can cause dyslipidemia. Treat overdose with glucagon. |
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Class III antiarrhythmics
-MOA -toxicity |
K+ channel blockers: sotalol, ibutilide, bretylium, dofetilide, amiodarone
-MOA: increase AP duration, increase ERP. Used when other antiarrhythmics fail. Increase QT interval. -Toxicity: torsades de pointes, excessive B block; ibutilide - torsades; bretylium - new arrhytmias, hypotension; amiodarone - pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/grey) resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF) Amiodarone has class I, II, III, and IV effects because it alters the lipid membrane. |
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Class IV antiarrhythmics
-MOA -toxicity |
Ca2+ channel blockers: verapamil, diltiazem
-MOA: primarily affect AV nodal cels. Decrease conduction velocity, increase ERP, increase PR interval. Used in prevention of nodal arrhythmias (eg. SVT) -tox: constipation, flushing, edema, CV effect (CHF, AV block, sinus node depression) |
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adenosine
K+ Mg2+ |
adenosine: increase K+ out of cells -> hyperpolarizing the cell + decrease ICa. Drug of choice in diagnosing/abolishing SVT. Ver short acting (~15 sec). Toxicity including flushing, hypotension, chest pain. Effects blocked by theophylline.
K+: depresses ectopic pacemakers in hypokalemia (eg. digoxin toxiciy) Mg2+: effective in torsades de points and digoxin toxicity |
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Insulin
-drugs -action -clinical use -toxicities |
-Lispro (short-acting), Aspart (short-acting), Regular (short-acting), NPH (intermediate), Glargine (long-acting), Detemir (long-acting)
-MOA: Bind insulin receptor (tyrosin kinase activity). Liver: increase glucose stored as glycogen; Muscle: increase gylcogen and protein synthesis, K+ uptake; Fat: aids TG storage -Use: Type I DM, type II DM; also life-threatening hypokalemia and stress-induced hyperglycemia -toxicity: hypoglycemia, hypersensitivity reaction (very rare) |
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sulfonylureas
-drugs -action -clinical use -toxicities |
-First generation: tolbutamide, chlorpropamide; Second generation: glyuride, glimepiride, glipizide
-MOA: Close K+ channel in B-cell membrane, so cell depolarizes -> triggering of insulin release via increase Ca2+ influx -Use: Stimulate release of endogenous insulin in type 2 DM. Require some islet function, so useless in type I DM. -Tox: First gen: disulfiram-like effects; Second gen: hypoglycemia |
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Metformin
-MOA -Use -Toxicity |
-MOA: exact mechanism unknown; possibly decrease gluconeogenesis, increase glycolysis, decrease serum glucose levels. Overall acts as insulin sensitizer.
-Use: Used as oral hypoglycemic. Can be used in patients without islet function. -Tox: Most grave adverse effect is lactic acidosis (contraindicated in renal failure) |
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Glitazones/Thiazolidinediones
-drugs -MOA -Use -Tox |
Pioglitazone, Rosiglitazone
-MOA: increase insulin sensitivity in peripheral tissue -Use: Used as monotherapy in type 2 DM or combined with above agents -Tox: weight gain, edema. Hepatotoxicity, CV toxicity |
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alpha-glucosidase inhibitors
-drugs -MOA -Use -Tox |
Acarbose, Miglitol
-MOA: Inhibit intestinal brush-border alpha-glucosideases. Delayed sugar hydrolysis and glucose absorption lead to decrease postprandial hyperglycemia -Use: Used as monotherapy in type II DM or combo with above agents -Tox: GI disturbances |
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Pramlintide
-MOA -Use -Tox Exenatide -MOA -Use -Tox |
-MOA: decrease glucagon
-Use: Type 2 DM -Tox: Hypoglycemia, nausea, diarrhea -MOA: increase insulin, decrease glucagon release -Use: Type II DM -Tox: Nausea, vomiting, pancreatitis |
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Orlistat
-MOA -Use -Tox |
-MOA: Alters fat metabolism by inhibiting pancreatic lipases
-Use: Long-term obesity management (in conjunction with modified diet) -Tox: Steatorrhea, GI discomfort, reduced absorption of fat-soluble vitamins, headache |
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Sibutramine
-MOA -Use -Tox |
-MOA: Sympathomimetic serotonin and NE reuptake inhibitor
-Use: short-term and long-term obesity management -hypertension and tachycardia |
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Propylthiouracil, methimazole
-MOA -Use -Tox |
-MOA: Inhibit organification of iodide and coupling of thyroid hormone synthesis; Propylthiouracil also decrease peripheral conversion of T4 to T3
-Use: Hyperthyroidism -Tox: Skin rash, agranulocytosis (rare), aplastic anemia |
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Levothyroxine, tiiodothyronine
-MOA -Use -Tox |
-MOA: thyroxine replacement
-Use: Hypothyroidism, myxedema -Tox: tachycardia, heat intolerance, tremors, arrhythmias |
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Clinical use of:
-GH -Somatostatin (octreotide) -Oxytocin -ADH (desmopressin) |
-GH: GH deficiency, Turner's syndrome
-Somatostatin (octreotide): Acromegaly, carcinoid, gastrinoma, glucagonoma -Oxytocin: stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage -ADH (desmopressin): pituitary (central, not nephrogenic) DI |
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Demeclocycline
-MOA -Use -Tox |
-MOA: ADH antagonist (member of tetracycline family)
-Use: SIADH -Tox: Nephrogenic DI, photosensitivity, abnormalities of bone and teeth |
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Glucocorticoids
-drugs -MOA -Use -Tox |
hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone
-MOA: Decrease the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX-2 -Use: Addison's disease, inflammation, immune suppression, asthma -Tox: Iatrogenic Cushings syndrome: buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes (if chronic) |
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H2 blockers
-drugs -MOA -Use -Tox |
Cimetidine, ranitidine, famotidine, nizatidine
-MOA: reversible block of histamine H2 receptors -> decrease H+ secretion by parietal cells -Use: peptic ulcer, gastritis, mild esophageal reflux -Tox: cimetidine is a potent inhibitor of P450; it also has antiandrogenic effects (prolactin release gynecomastia, impotence, decrease libido in males); can cross BBB (confusion, dizziness, headaches) and placenta. Both cimetidine and ranitide decrease renal excretion of creatinine. Other H2 blockers are relatively free of these effects |
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Proton pump inhibitors
-drugs -MOA -Use |
Omeprazole, lansoprazole
-MOA: irreversibly inhibit H+/K+ ATPase in stomach parietal cels -Use: peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome |
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Bismuth, Sucralfate
-MOA -Use |
MOA: bind to ulcer base, providing physical protection, and allow HCO3- secretion to reestablish pH gradient in the mucous layer
-Use: increase ulcer healing, traveler's diarrhea |
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Misoprostol
-MOA -Use -Tox |
-MOA: PGE1 analog; increase production and secretion of gastric mucous barrier, decrease acid production
-Use: prevention of NSAID-induced peptic ulcers; maintenance of a patent ductus arteriosus. Also used to induce labor -Tox: diarrhea, contraindicated in women of childbearing potential |
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Pirenzepine, propantheline
-MOA -Use Tox |
-MOA: Block M1 receptors on ECL cells (decrease histamine secretion) and M3 receptors on parietal cells (decrease H+ secretion)
-Use: peptic ulcer (rarely used) -Tox: tachycardia, dry mouth, difficulty focusing eyes |
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Overuse of antacids can cause the following problems:
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1. aluminum hydroxide: constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures
2. magensium hydroxide: diarrhea, hyporeflexia, hypotension, cardiac arrest 3. calcium carbonate: hypercalcemia, rebound acid increase All can cause hypokalemia |
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Infliximab
-MOA -Use -Tox |
-MOA: monoclonal antibody to TNF, proinflammatory cytokine
-Use: Crohn's disease, rheumatoid arthritis -Tox: Respiratory infection (including reactivation of latent TB), fever, hypotension |
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Sulfasalazine
-MOA -Use -Tox |
-MOA: combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory). Activated by colonic bacteria
-Use: ulcerative colitis, Crohn's disease -Tox: Malaise, nausea, sulfonamide toxicity, reversible oligospermia |
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Odansetron
-MOA -Use -Tox |
-MOA: 5-HT3 antagonist. Powerful central-acting antiemetic
-Use: control vomiting postoperatively and in patients undergoing cancer chemotherapy -Tox: headache, constipation |
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Metoclopramide
-MOA -Use -Tox |
-MOA: D2 receptor antagonist. Increase resting tone, contractility, LES tone, motility. Does no influence colon transport time
-Use: diabetic and post-surgery gastroparesis -Tox: increase parkinsonian effects. Restlessness, drowsiness, fatigue, depression, nausea, diarrhea. Drug interaction with digoxin and diabetic agents. Contraindicated in patients with small bowel obstruction |
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Lepirudin, bivalirudin
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Hirudin derivatives; directly inhibit thrombin. Used as an alternative to heparin for anticoagulating patients with HIT
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Aspirin (ASA)
-MOA -Use -Tox |
-MOA: acetylates and irreversibly cyclooxygenase (noth COX1 and COX2) to prevent conversion of arachidonic acid to thromboxane A2. Increase bleeding time. No effect on PT, PTT
-Use: Antipyretic, analgesic, anti-inflammatory, antiplatelet drug -Tox: gastric ulceration, bleeding, hyperventilation, Reye's syndrome, tinnitus (CN VIII) |
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Clopidogrel, Ticlopidine
-MOA -Use -Tox |
-MOA: Inhibit platelet aggregation by irreversibly blocking ADP receptors. Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa expression
-Use: Acute coronary syndrome; coronary stenting. Decrease incidence of recurrence of thrombotic stroke -Tox: Neutropenia (ticlopidine) |
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Abcixmiab
-MOA -Use -Tox |
-MOA: monoclonal antibody that binds to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation
-Use: acute coronary syndromes, percutaneous transluminal coronary angioplasty -Tox: bleeding, thrombcytopenia |
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Methotrexate
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-MOA: folic acid analog that inhibits dihydrofolate reductase -> decrease dTMP -> decrease DNA and decrease protein synthesis
-Use: Cancers: leukemias, lymphomas, choriocarinoma, sarcomas; Non-neoplastic: abortion, ectopic pregnancy, rheumatoid arthritis, psoriasis -Tox: Myelosuppression, which is reversible with leucovorin (folinic acid) "rescue"; Macrovesicular fatty change in liver; mucositis; teratogenic |
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5-fluorouracil
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-MOA: Pyrimidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid. This complex inhibits thymidylate synthase -> decrease dTMP -> decrease DNA and decrease protein synthesis
-Use: Colon cancer and other solid tumors, basal cell carcinoma (topical); Synergy with MTX -Tox: Myelosuppression, which not reversible with leucovorin. Overdose: "rescue" with thymidine. Photosensitivity |
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6-mercaptopurine
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-MOA: purine (thiol) analog -> decrease de novo purine synthesis. Activated by HGPRTase
-Use: Leukemias, lymphomas (not CLL or Hodgkins) -Tox: Bone marrow, GI, liver. Metabolized by xanthine oxidase; thus increase toxicity with allopurinol |
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6-thioguanine
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-MOA: same as 6-MP
-Use: acute lymphoid leukemia -Tox: Bone marrow depression, liver. Can be given with allopurinol |
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cytarabine (ara-C)
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-MOA: pyrimidine antagonist -> inhibition of DNA polymerase
-Use: AML, ALL, high-grade non-Hodgkins lymphoma -Tox: leukopenia, thrombocytopenia, megaloblastic anemia |
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Dactinomycin
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-MOA: intercalates in DNA
-Use: Wilms' tumor, Ewing's sarcoma, rhabdomyosarcoma. Used for childhood tumors -Tox: myelsuppression |
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Doxorubicin (Adriamycin), Daunorubicin
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-MOA: generate free radicals. Noncovalently intercalate in DNA -> breaks in DNA -> decrease replication
-Use: Part of the ABVD combination regimen for Hodgkins lymphomas; also for myelomas, sarcomas, and solid tumors (breast, ovary, lung) -Tox: cardiotoxicity (dilated cardiomyopathy); also myelosuppression and marked alopecia. Toxic to tissues with extravasation |
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Bleomycin
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-MOA: G2-phase specific. Induces formation of free radicals, which cause breaks in DNA strands.
-Use: Testicular cancer, Hodgkins lymphoma (ABVD) -Tox: Pulmonary fibrosis, skin changes, but minimal myelosuppression |
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Etoposide (VP-16), teniposide
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-MOA: Late S- to G2-phase specific. Inhibits topoisomerase II -> increase DNA degradation
-Use: small cel carcinoma of lung and prostate, testicular carcinoma -Tox: Myelosuppression, GI irritation, alopecia |
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Cyclophosphamide, ifosfamide
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-MOA: covalently X-link (interstrand) DNA at guanine N-7. Require bioactivation by liver
-Use: Non-Hodgkins lymphoma, breast and ovarian carcinomas. Also immunosuppressants -Tox: myelosuppression; hemorrhagic cystitis , which can be partially prevented with mesna |
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Nitrosureas
-drugs -MOA -Use -Tox |
Carmustine, lomustine, semustine, streptozocin
-MOA: require bioactivation. Cross BBB -> CNS -Use: brain tumors (including glioblastoma multiforme) -Tox: CNS toxicity (dizziness, ataxia) |
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Busulfan
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-MOA: aklylates DNA
-Use: CML. Also used for ablating bone marrow in hematopoietic stem cell transplants. -Tox: Pulmonary fibrosis, hyperpigmentation |
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Vincristine, vinblastine
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-MOA: alkaloids that bind tubulin in M phase and bloc polymerization of microtubules so that mitotic spindle cannot form.
-Use: Part of the MOPP (Oncovin [vincristine]) regimen for Hodgkins lymphoma, Wilm's tumor, choriocarinoma -Tox: vincristine: neurotoxicity (areflexia, peripheral neuritis), paralytic ileus; Vinblastine blasts bone marrow (suppression) |
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Paclitaxel, other Taxols
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-MOA: Hyperstabilize polymerized microtubules in M phase so that mitotic spindle cannot break down (anaphase cannot occur)
-use: ovarian and breast carcinomas -Tox: myelosuppression and hypersensitivity |
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Cisplatin, carboplatin
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-MOA: cross-link DNA
-Use: testicular, bladder, ovary, and lung carcinomas -Use: testicular, bladder, ovary, and lung carcinomas -Tox: nephrotoxicity and acoustic nerve damage |
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hydroxyurea
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-MOA: inhibits ribonucleotide reductase -> decrease DNA synthesis (S-phase specific)
-Use: melanoma, CML. sickle cell disease (increase HbF) -Tox: bone marrow suppression, GI upset |
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prednisone
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-MOA: may trigger apoptosis. May even work on nondividing cells.
-Use: most commonly used glucocorticoid in cancer chemotherapy. Used in CLL, Hodgkins lymphoma (part of MOPP). Also an immunosuppressant used in autoimmune diseases. -Tox: Cushing-like symptoms; immunosuppression, cataracts, acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis |
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Tamoxifen, raloxifene
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-MOA: SERMS - receptor antagonists in breast, agonists in bone; block the binding of estrogen to estrogen-receptor-positive cells
-Use: breast cancer. Also useful to prevent osteoporosis -Tox: tamoxifen may increase the risk of endometrial carcinoma via partial agonist effects; "hot flashes"; raloxifene does not cause endometrial carcinoma because it is an endometrial antagonist |
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trastuzumab (herceptin)
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-MOA: monoclonal antibody against HER-2 (erb-B2). Helps kill breast cancer cells that overexpress HER-2, possibly through antibody-dependent cytotoxicity.
-Use: metastatic breast cancer -Tox: cardiotoxicity |
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Imatinib (gleevec)
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-MOA: Philadelphia chromosome bcr-abl tyrosine kinase inhibitor
-Use: CML, GI stromal tumors -Tox: fluid retention |
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NSAIDs
-drugs -MOA -Use -Tox |
Ibuprofen, naproxen, indomethacin, ketorolac
-MOA: Reversibly inhibit COX1 and COX2. Block prostaglandin synthesis -Use: antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA -Tox: renal damage, fluid retention, aplastic anemia, GI distress, ulcers |
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Celecoxib
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-MOA: reversibly inhibit specifically the COX2 isoform, which is found in inflammatory cells and vascular endothelium and mediates inflammation and pain; spares COX1, which helps maintain the gastric mucosa. Thus, should not have corrosive effects of other NSAIDs on the GI lining.
-Use: rheumatoid and osteoarthritis -Tox: increase risk of thrombosis. Sulfa allergy. Less toxicity to GI mucosa (lower incidence of ulcers, bleeding than NSAIDs) |
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Acetaminophen
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-MOA: reversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally.
-Use: antipyretic, analgesic, but lacking anti-inflammatory properties. Used instead of aspiring to prevent Reye's syndrome in children with viral infection -Tox: Overdose produces hepatic necrosis; acetominophen metabolite depletes glutathione and forms toxic tissue adducts in liver. N-acetylcysteine is antidote - regenerates glutathione |
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bisphosphonates
-drugs -moa -use -tox |
Etidronate, pamidronate, alendronate, risedronate
-MOA: inhibit osteoclastic activity; reduce both formation and resorption of hydroxyapatite -Use: malignancy-associated hypercalcemia, Paget's disease of bone, postmenopausal osteoporosis -Tox: corrosive esophagitis, nausea, diarrhea |
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Gout drugs
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-Colchicine: acute gout; binds and stabilizes tubulin to inhibit polymerization, impairing leukocyte chemotaxis and degranulation. GI side effects, especially if given orally. (note: indomethacin is less toxic, also used in acute gout)
-Probenecid: Chronic gout. Inhibits reabsorption of uric acid in PCT (also inhibits secretion of penicillin) -Allopurinol: Chronic gout. Inhibits xanthine oxidase, decrease conversion of xanthine to uric acid. Also used in lymphoma and leukemia to prevent tumor lysis-associated urate nephropathy. Increase concentration of azathioprine and 6-MP (both normally metabolized by xanthine oxidase) Do not give salicylates. All but the highest doses depress uric acid clearance. |
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Etanercept
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-Recombinant form of human TNF alpha receptor that binds TND
-Use: Rheumatoid arthritis, psoriasis, ankylosing spondylitis |
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Infliximab
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-Anti-TNF alpha antibody
-Use: Crohn's disease, rheumatoid arthritis, ankylosing spondylitis -Tox: predisposes to infections (reactivatoin of latent TB) |
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Adalimumab
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-Directly binds TNF-alpha
-Use: rheumatoid arthritis, psoriasis, ankylosing spondylitis |
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Phenytoin
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-MOA: Use-dependent blockade of Na+ channels; increase refractory period; inhibition of glutamate release from excitatory presynaptic neuron.
-Use: 1st line for tonic-clonic seizures. Simple and complex partial seizures. 1st line prophylaxis for status seizures. -Tox: Nystagmus, ataxia, diplopia, sedation, SLE-like syndrome, induction of CytP450. Chronic use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia (decrease folate absorption). Teratogenic (fetal hydantoin syndrome) |
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Epilepsy uses and mechanism of:
-Carbamazepine -Lamotrigine -Gabapentin -Topiramate -Phenobarbital |
-Carbamazepine: Simple and complex partial seizures. 1st line for tonic clonic. Increase Na+ channel inactivation. Also 1st line for trigeminal neuralgia
-Lamotrigine: Simple and complex partial seizures. Tonic-clonic. Blocks voltage-gated Na+ channels -Gabapentin: Simple and complex partial seizures. Tonic-clonic. Designed as GABA analog, but primarily inhibits HVA calcium channels. Also used for peripheral neuropathy, bipolar disorder -Topiramate: Simple and complex partial seizures. Tonic-clonic. Blocks Na+ channels, increase GABA action -Phenobarbital: Simple and complex partial seizures. Tonic-clonic. Increase GABAa action. First line in pregnant women, children |
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Epilepsy uses and mechanism of:
-Valproid acid -Ethosuximide -Benzodiazepines (diazepam or lorazepam) -Tiagabine -Vigabatrin -Levetiracetam |
-Valproid acid: Simple and complex partial seizures. 1st line for tonic-clonic. Absence seizures. Increase Na+ channel inactivation, increase GABA concentration. Also used for myoclonic seizures
-Ethosuximide: 1st line for absence seizures. Blocks thalamic T-type Ca2+ channels -Benzodiazepines (diazepam or lorazepam): 1st line for acute status epilepticus. Increase GABAa action. Also used for seizures of eclampsia but there 1st line is MgSO4 -Tiagabine: Simple and complex partial seizures. Inhibits GABA reuptake -Vigabatrin: Simple and complex partial seizures. Irreversibly inhibits GABA transaminase -> increase GABA -Levetiracetam: Simple and complex partial seizures. Tonic-clonic. Mechanism unknown; may modulate GABA and glutamate release |
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Epilepsy drug toxicities:
-Benzodiazepams -Carbamazepine -Ethosuximide -Phenobarbital |
-Benzodiazepams: Sedation, tolerance, dependence
-Carbamazepine: Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of P450, SIADH, Stevens-Johnson syndrome -Ethosuximide: GI distress, fatigue, headache, urticaria, Stevens-Johnson syndrome -Phenobarbital: Sedation, tolerance, dependence, induction of cyp450 |
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Epilepsy drug toxicities:
-Valproic acid -Lamotrigine -Gabapentin -Topiramate |
-Valproic acid: GI distress, rare but fatal hepatotoxcity (measure LFTs), neural tube defects in fetus, tremor, weight gain. Contraindicated in pregnancy
-Lamotrigine: Stevens-Johnson syndrome -Gabapentin: Sedation, ataxia -Topiramate: Sedation, mental dulling, kidney stones, weight loss |
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Inhaled anesthetics
-Drugs -MOA -Effects -Tox |
Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide
-MOA: unknown -Effects: Myocardial depression, respiratory depression, nausea/emesis, increase cerebral blood flow (decrease cerebral metabolic demand) -Tox: Hepatotoxicity (halothane), nephrotoxicity (enflurane), malignant hyperthermia (rare), expansion of trapped gas (nitrous oxide) |
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Drugs that are intravenous anesthetics
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Barbiturates: Thiopental
Benzos: Midazolam Arylcyclohexylamines (ketamine) Opiates Propofol |
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Barbiturates as IV anesthetics
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Thiopental - high potency, high lipid solubility, rapid entry into brain. Used for induction of anesthesia and short surgical procedures. Effect terminated by rapid redistribution into tissue and fat. Decrease cerebral blood blow
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Benzos as IV anesthetics
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Midazolam most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics. May cause severe postoperative respiratory depression, decrease BP (treat overdose with flumazenil), and amnesia.
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Arylcyclohexylamines (Ketamine)
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PCP analogs that act as dissociative anesthetics. Block NMDA receptors. Cardiovascular stimulants. Cause disorientation, hallucination, and bad dreams. Increase cerebral blood flow.
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Opiates as IV anesthetic
Propofol as IV anesthetic |
Morphine, fentanyl used with other CNS depressants during general anesthesia
Used for rapid anesthesia induction and short procedures. Less postoperative nausea than thiopental. Potentiates GABAa |
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Local Anesthetics
-drugs -MOA -Use -Toxicity |
Esters - procaine, cocaine, tetracaine; amides - lidocaine, mepivacaine, bupivacaine
-MOA: Block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons. Tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form. -Use: Minor surgical procedures, spinal anethesia. If allergic to esthers, give amides. -Toxicity: CNS excitation, severe cardiovascular toxicity (bupivacine), hypertension, hypotension, and arrhythmias (cocaine) |
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Use of neuromuscular blocking drugs
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Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs autonomic) nicotinic receptor.
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depolarizing neuromuscular drugs
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Succinylcholine (complications include hypercalcemia and hyperkalemia).
Reversal of blockade: Phase I (prolonged depolarization) - no antidote. Block potentiated by cholinesterase inhibitors Phase II (repolarized but blocked) - antidote consists of cholinesterase inhibitors (eg. neostigmine) |
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Nondepolarizing neuromuscular blocking drugs
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Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium.
Competitive - compete with ACh for receptors. Reversal of bloackade - neostigmine, edrophonium, and other cholinesterase inhibitors. |
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treatment for Parkinson's disease
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-Agonize dopamine receptors: Bromocriptine, pergolide (ergot alkaloid and partial dopamine agonist), pramipexole, ropinirole (non-ergot); non-ergots are preferred
-Increase dopamine: Amantadine (may increase dopamine release); also used as an antiviral against influenza A and rubella; toxicity= ataxia; L-dopa/carbidopa (converted to dopamine in CNS) -Prevent dopamine breakdown: Selegiline (selective MOA type B inhibitor); entacapone, tolcapone (COMT inhibitors - prevent L-dopa degradation, thereby increasing dopamien availability) -Curb excess cholinergic activity: Benztropine (antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia) |
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L-dopa/carbidopa
-MOA -Use -Toxicity |
-MOA: increase level of dopamine in brain. Unlike dopamine, L-dopa can cross BBB and is converted by dopa decarboxylase in the CNS to dopamine.
-Use: Parkinsonism -Toxicity: Arrhythmias from peripheral conversion to dopamine. Long-term use can -> dyskinesia following administration, akinesia between doses. Carbidopa, a peripheral decarboxylase inhibitor, is given with L-dopa in order to increase bioavailability of L-dopa in the brain and to limit peripheral side effects. |
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Selegiline
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-MOA: Selectively inhibits MOA-B, which preferally metabolizes dopamine over NE and 5-HT, thereby increasing the availability of dopamine
-Use: adjunctive agent to L-dopa in treatment of Parkinson disease -Tox: May enhance adverse effects of L-dopa |
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Alzheimer's drugs
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-Memantine: NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+); Tox: dizziness, confusion, hallucinations
-Donepezil, galantamine, rivastigmine: Acetylcholinesterase inhibitors. Tox: nausea, dizziness, insomnia |
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Huntington's drugs
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-Disease - increase dopamine, decrease GABA + ACh
-Reserpine + tetrabenazine - amine depleting -Haloperidol - dopamine receptor antagonist |
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Sumatriptan
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-MOA: 5-HT 1B/1D agonist. Causes vasoconstriction, inhibition of trigeminal activation and vasoactive peptide release. Half-life < 2 hours.
-Use: Acute migraine, cluster headache attacks -Toxicity: Coronary vasospasm (contraindicated in patients with CAD or Prinzmetal's angina), mild tingling |
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Methyphenidate
-MOA -Use |
-MOA: NE and DA reuptake inhibitor whose effects are similar to amphetamines, but MOA differ. However, the mechanism for relieving ADHD symptoms is not known.
-Use: ADHD |
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treatment for selected psychiatric conditions:
-alcohol withdrawal -anorexia/bulimia -anxiety -ADHD -atypical depression -bipolar disorder |
-alcohol withdrawal: benzos
-anorexia/bulimia: SSRIs -anxiety: benzos, buspirone, SSRIs -ADHD: methylphenidate (ritalin), amphetamines (dexedrine) -atypical depression: MAO-I, SSRIs -bipolar disorder: "mood stabilizers": lithium, valproic acid, carbamazepine |
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treatment for selected psychiatric conditions:
-depression -depression with insomnia -OCD -panic disorder -PTSD -schizophrenia -Tourette's syndrome -Social phobias |
-depression: SSRIs, SNRIs, TCAs
-depression with insomnia: mirtazapine -OCD: SSRIs, clomipramine -panic disorder: SSRIs, TCAs, Benzos -PTSD: SSRIs -schizophrenia: antipsychotics -Tourette's syndrome: antipsychotics (haloperidol) -Social phobias: SSRIs |
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Typical antipsychotics
-drugs -MOA -Use |
Haloperidol, trifluoperazine, fluphenazine, thioridazine, chlorpromazine; high potency: haloperidol, trifluoperazine, fluphenazine - neurologic side effects; low potency: thioridazone, chlorpromazine - non-neurologic side effects
-MOA: all typical antipsychotics block D2 receptors (increase [cAMP]1) -Use: shizophrenia (primarily positive symptoms), psychosis, acute mania, Tourret's syndrome |
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toxicity of typical antipsychotics
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1. Highly lipid soluble and stored in body fat; thus, very slow to be removed from body
2. Extrapyramidal system (EPS) side effects 3. Endocrine side effects (eg. dopamine receptor antagonism -> hyperprolactinemia -> galactorrhea) 4. Side effects arising from blocking muscarinic (dry mouth, constipation), alpha (hypotension), and histamine (sedation) receptors Other: neuroleptic malignant syndrome (NMS) - rigidity, myoglobinuria, autonomic instability, hyperpyrexia. Treatment: dantrolene, agonists (eg. bromocriptine) Tardive dyskinesia: stereotypic oral-facial movements due to long-term antipsychotic use. Often irreversible Evolution of EPS side effects: 4 hours: acute dystonia; 4 days: akinesia; 4 week: akathisia; 4 months: tardive dyskinesia |
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Atypical antipsychotics
-drugs -MOA -Use -Toxicitiy |
Olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone
-MOA: Block 5-HT2, alpha, H1, and dopamine receptors. -Use: Shizophrenia (for + and - symptoms). Olanzapine is also used for OCD, anxiety disorder, depression, mania, Tourette's syndrome -Tox: Fewer EPS and anticholinergic side effects than traditional antipsychotics. Olanzapine/clozapine may cause significant weight gain. Clozapine may cause agranulcytosis (requires weekly WBC monitoring) |
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Lithium
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-MOA: not established; possibly related to inhibition of phosphoinositol cascade.
-Use: Mood stabilizer for bipolar disorder; blocks relapse and acute manic events. Also SIADH -Tox: Tremor, sedation, edema, heart block, hypothyroidism, polyuria (ADH antagonist causing nephrogenic DI), teratogenesis. Narrow therapeutic window requires close monitoring of serum levels. |
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Buspirone
-MOA -Use |
-Stimulates 5-HT1A receptors
-Use: generalized anxiety disorder. Does not cause sedation, addiction, or tolerance. Does not interact with alcohol |
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Tricyclic antidepressants
-drugs -MOA -Use -Side effects -Toxicity |
Imipramine, amitriptyline, desipramine, nortriptyline, clomipramine, doxepin, amoxapine
-MOA: block reuptake of NE and serotonin -Use: major depression, bedwetting (imipramine), OCD (clomipramine), fibromyalgia -SE: sedation, alpha-blocking effects, atropine-like (anticholinergic) side effects (tachycardia, urinary retention). Tertiary TCAs (amitriptyline) have more anticholinergic effects than do secondary TCAs (nortriptyline). Desipramine is the least sedating and has lower seizure threshold. -Tox: convulsions, coma, cardiotoxciity (arrhythmias); also respiratory depressoin, hyperpyrexia. Confusion and hallucinations in elderly due to anticholinergic side effects (use nortriptyline). Treatment: NaHCO3 for CV toxicity |
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SSRIs
-drugs -MOA -Use -Toxicity |
Fluoxetine, paroxetine, sertraline, citalopram
-MOA: serotonin-specific reuptake inhibitors -Use: Depression, OCD, bulimia, social phobias; takes 2-3 weeks to have an effect -Tox: Fewer than TCAs. GI distress, sexual dysfunction (anorgasmia). "Serotonin syndrome" with any drug that increases serotonin (MOA-I) - hyperthermia, muscle rigidity, cardiovascular collapse, flushing, diarrhea, seizures. Treatment: cyproheptadine (5-HT2 receptor antagonist) |
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SNRIs
-drugs -MOA -Use -Tox |
Venlafaxine, duloxetine
-MOA: inhibit serotonin and NE reuptake -Use: depression. Venlafaxine is also used in generalized anxiety disorder; duloxetine is also indicated for diabetic peripheral neuropathy. Duloxetine has greater effect on NE -Tox: increase BP most common; also stimulant effects, sedation, nausea |
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Monoamine oxidase (MAO) inhibitors
-drugs -MOA -Use -Tox |
Phenelzine, tranylcypromine, isocarboxazid, selegiline (selective MOA-B inhibitor)
-MOA: nonselective MAO inhibition -> increase levels of amine neurotransmitters -Use: atypical depression, anxiety, hypochondriasis -hypertensive crisis with tyramine ingestion (in many foods, such as wine and cheese) and B-agonists; CNS stimulation. Contraindicated with SSRIs or meperdine (to prevent serotonin syndrome) |
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Buproprion
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Atypical antidepressant. Also used for smoking cessation. Increase NE and dopamine via unknown mechanism. Toxicity: stimulant effects (tachycardia, insomnia), headache, seizure in bulimic patients. No sexual side effects
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Mirtazapine
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Atypical antidepressant. Alpha2-antagonist (increase release of NE and serotonin) and potent 5-HT2 and 5-HT3 receptor antagonist.
Toxicity: sedation, increase appetite, weight gain, dry mouth |
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Maprotiline
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Atypical antidepressant. Blocks NE reuptake.
Toxicity: sedation, orthostatic hypotension |
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Trazodone
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Atypical antidepressant. Primarily inhibits serotonin reuptake. Used for insomnia, as high doses are needed for antidepressant effects.
Toxicity: sedation, nausea, priapism, postural hypotension |
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Mannitol
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-MOA: osmotic diuretic, increase tubular fluid osmolarity, producing increased urine flow
-Use: shock, drug overdose, increase intracranial/intraocular pressure -Tox: pulmonary edema, dehydration. Contraindicated in anuria, CHF |
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Acetazolamide
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-MOA: Carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and reduction in total-body HCO3- stores
-Use: glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness -Tox: hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy |
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Furosemide
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-MOA: sulfonamide loop diuretic. Inhibits cotransport system (Na+, K+, 2Cl-) of thick ascending limb of loop of Henle. Abolishes hypertonicity of medulla, preventing concentration of urine. Increase Ca++ excretion.
-Use: edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema) hypertension, hypercalcemia -Tox: ototoxicity, hypokalemia, dehydration, allergy (sulfa), nephritis (interstitial), gout |
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Ethacrynic acid
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-MOA: Phenoxyacetic acid derivative (not a sulfonamide). Essentially same action as furosemide
-Use: Diuresis in patients allergic to sulfa drugs -Tox: Similar to furosemide; can be used in hyperuricemia, acute gout (never used to treat gout) |
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Hydrochlorothiazide
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-MOA: thiazide diuretic. Inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of the nephron. Decrease Ca2+ excretion.
-Use: Hypertension, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus -Tox: Hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, and hypercalcemia. Sulfa allergy. |
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K+ sparing diuretics
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Spironolactone, Triamterene, Amiloride, eplerenone
-MOA: Spironolactone is a competitive aldosterone receptor antagonist in the cortical collecting tubule. Triamterene and amiloride act at the same part of the tubule by blocking Na+ channels in the CCT -Use: Hyperaldosteronism, K+ depletion, CHF -Toxicity: Hyperkalemia (can lead to arrhythmias), endocrine effects with aldosterone antagonists (eg. spironolactone causes gynecomastia, antiandrogen effects) |
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ACE inhibitors
-drugs -MOA -Use -Toxicity |
Captopril, enalapril, lisinopril
-MOA: Inhibit angiotensin-converting enzyme, reducing levels of angiotensin II and preventing inactivation of bradykinin, a potent vasodilator. Renin release is increased due to loss of feedback inhibition. -Use: Hypertension, CHF, diabetic renal disease -Toxicity: Cough, Angioedema, Proteinuria Taste changes, hypotension, pregnancy problems (fetal renal damage), rash, increased renin, lower angiotensin II. Also hyperkalemia. Avoid with bilateral renal artery stenosis because ACE inhibitors significantly decrease GFR by preventing constriction of efferent arterioles. (Losartan is an angiotensin II receptor antagonist. It is not an ACE inhibitor and does not cause cough) |
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Leuprolide
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-MOA: GnRH analog with agonist properties when used in pulsatile fashion; antagonist properties when used in continuous fashion
-Use: Infertility (pulsatile), prostate cancer (continuous - use with flutamide), uterine fibroids -Toxicity: Antiandrogen, nausea, vomiting |
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Testosterone (methyltestosterone)
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-MOA: Agonist at androgen receptors
-Use: Treat hypogonadism and promote development of secondary sex characteristics; stimulation of anabolism to promote recovery after burn or injury; treat ER-positive breast cancer (exemestane) -Toxicity: Causes masculinization in females; reduces intratesticular testosterone in males by inhibiting release of LH (via negative feedback), leading to gonadal atrophy. Premature closure of epiphyseal plates. Increase LDL, decrease HDL |
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Antiandrogens
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-Finasteride: 5alpha-reductase inhibitor (decrease conversion of testosterone to dihydrotestosterone). Usedful in BPH. Also promotes hair growth - used to treat male-pattern baldness.
-Flutamide: A nonsteroidal competitive inhibitor of androgens at the testosterone receptor. Used in prostate carcinoma. -Ketoconazole: Inhibits steroid synthesis (inhibits desmolase) -Spironolactone: Inhibits steroid binding Ketoconazole and spironolactone are used in the treatment of polycystic ovarian syndrome to prevent hirsutism. Both have side effects of gynecomastia and amenorrhea. |
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Estrogens (ethinyl estradiol, DES, mestranol)
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-MOA: bind estrogen receptors
-Use: hypogonadism or ovarian failure, menstrual abnormalities, HRT in postmenopausal women; use in men with androgen-dependent prostate cancer -Tox: Increase risk of endometrial cancer, bleeding in postmenopausal women, clear cell adenocarcinoma of vagina in females exposed to DES in utero, increased risk of thrombi. Contraindications-ER positive breast cancer, history of DVTs |
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Estrogen partial agonists (selective estrogen receptor modulators - SERMs)
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-Clomiphene: Partial agonist at estrogen receptors in hypothalamus. Prevents normal feedback inhibition and increase release of LH and FSH from pituitary, which stimulates ovulation. Used to treat infertility and PCOS. May cause hot flashes, ovarian enlargement, multiple simultaneous pregnancies, and visual disturbances.
-Tamoxifen: Antagonist on breast tissue; used to treat and prevent recurrence of ER-positive breast cancer -Raloxifene: Agonist on bone; reduces resorption of bone; used to treat osteoporosis |
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Hormone replacement therapy
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Used for relief or prevention of menopausal symptoms (eg. hot flashes, vaginal atrophy) and osteoporosis (increase estrogen, decrease osteoclast activity)
Unopposed estrogen replacement therapy (ERT) increases the risk of endometrial cancer, so progesterone is added. Possible increase CV risk. |
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Anastrozole/exemestane
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Aromatase inhibitors used in postmenopausal women with breast cancer.
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Progestins
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-MOA: bind progesterone receptors, reduce growth, and increase vascularization of endometrium
-Use: Used in oral contraceptives and in the treatment of endometrial cancer and abnormal uterine bleeding |
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Mifepristone (RU-486)
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-MOA: Competitive inhibitor of progestins at progesterone receptors
-Use: Termination of pregnancy. Administered with misoprostol (PGE1) -Toxicity: Heavy bleeding, GI effects (nausea, vomiting, anorexia), abdominal pain |
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Dinoprostone
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PGE2 analog causing cervical dilation and uterine contraction, inducing labor
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Ritodrine/terbutaline
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B2-agonists that relax the uterus; reduce premature uterine contractions
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Tamulosin
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alpha1-antagonist used to treat BPH by inhibiting smooth muscle contraction. Selective for alpha1A,D receptors (found on prostate) vs vascular alpha1B receptors
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Sildenafil, vardenafil
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-MOA: Inhibit cGMP phosphodiesterase, causing increase cGMP, smooth muscle relaxation in the corpus cavernosum, increase blood flow, and penile erection.
-Use: treatment of erectile dysfunction -Tox: headache, flushing, dyspepsia, impaired blue-green color vision. Risk of life-threatening hypotension in patients taking nitrates. |
