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401 Cards in this Set
- Front
- Back
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Nitrates (mechanism, use, toxicity)
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Cause NO release -> vasodilation (veins >>> arteries); used in angina; fast tolerance, hypotension, flushing, headache
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Adverse effects of statins
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Hepatoxicity and muscle breakdown
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Niacin (mechanism, use, toxicity)
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Inhibits lipolysis and reduces VLDL secretion, lowering LDL and raising HDL; hyperlipidemia; flushing and hyperuricemia
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Cholestyramine, colestipol, colesevelam (mechanism, use, toxicity)
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Inhibits reabsorption of bile acids -> lower LDL with slight increase in HDL; unpigmented gallbladder stones and malabsorption
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Ezetimibe
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Prevents cholesterol reabsorption -> lower LDL
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Fibrates (gemfibrozil + -fibrates) (mechanism, use, toxicity)
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Upregulates LPL -> lower triglycerides, slightly inc. HDL and slightly dec. LDL; myositis and hepatoxicity
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Digoxin and digitoxin (mechanism, use, toxicity)
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Inhibits Na/K ATPase -> indirectly inhibits Na/Ca exchanger -> inc. calcium levels -> inc. contractility; stimulates the vagus; causes cholinergic symptoms and hyperkalemia
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Class 1A antiarrhythmics
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Quinidine, procainamide, and disopyramide; inc. AP duration and QT interval; can cause torsades de pointes, cinchonism (qunidine), procainamide (drug-induced lupus)
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Class 1B antiarrhythmics
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Lidocaine, mexiletine, and tocainide; dec. AP duration especially in depolarized/ischemia tissue; best following MI
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Class 1C antiarrhythmics
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Flecainide, propafenone; no effect on AP, used in ventricular tachycardias; do not use post-MI due to risk for arrhythmias
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Class 1 antiarrhythmics (general mechanism and toxicity)
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Blocks Na channels, decreasing the slope of phase 0 depolarization; toxicity exacerbated by hyperkalemia
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Class 2 antiarrhythmics
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Beta-blockers; reduces cAMP, slowing SA and AV node activity, increases PR interval; adverse effects include impotence, asthma exacerbation, sedation
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Class 3 antiarrhythmics
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Amiodarone, ibutilide, dofetilide, sotalol; K channel blockers; inc. AP duration and QT interval
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Toxicity of amiodarone
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Pulmonary fibrosis, hepatotoxicity, thyroid dysfunction
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Class 4 antiarrhythmics
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Ca channel blockers; verapamil and diltiazem; dec. conduction velocity and inc. PR interval; cause constipation, flushing, and edema
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Adeosine (mechanism, use, toxicity)
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Inc. K efflux, hyperpolarizing the cell; used in supraventricular tachycardias; can cause flushing, hypotension, and chest pain
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Magnseium (mechanism, use, toxicity)
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Used in torsades de pointes and digoxin toxicity
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Treatment for prolactinoma
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Bromocriptine or cabergoline (dopamine agonists)
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Treatment of secondary hyperaldosteronism
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Spironolactone (or other AT2 antagonist)
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Treatment of carcinoid syndrome
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Octreotide (somatostatin analogues)
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Rapid-acting insulins (3)
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Lispro, aspart, and glulisine
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Short-acting insulin (1)
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Regular
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Intermediate-acting insulin (1)
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NPH
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Long-acting insulins (2)
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Glargine and detemir
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Metformin (mechanism, use, toxicity)
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Biguanide; unknown mechanism; increases insulin sensitivity and glycolysis and decreases gluconeogenesis; can cause lactic acidosis (don't use in renal failure patients)
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Tolbutamide, chlorpropamide (mechanism, use, toxicity)
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First-generation sulfonylureas; close beta-cell K channels, causing depolarization and increased insulin release; causes disulfuram-like effects
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Glyburide, glimepiride, glipizide (mechanism, use, toxicity)
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Second-generation sulfonylureas; close beta-cell K channels, causing depolarization and increased insulin release; causes hypoglycemia
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Pioglitazone, rosiglitazone (mechanism, use, toxicity)
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Thiazolidinediones; activates PPAR-gamma, increasing insulin sensitivity and adiponectin levels; causes weight gain, hepatotoxicity, and heart failure
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Acarbose, miglitol (mechanism, use, toxicity)
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Alpha-glucosidase inhibitors; prevent sugar hydrolysis and absorption, reducing blood sugar levels
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Pramlintide (mechanism, use, toxicity)
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Amylin analog; reduces glucagon secretion; causes hypoglycemia
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Exenatide, liraglutide (mechanism, use, toxicity)
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GLP-1 analogues; increase insulin, decrease glucagon secretion; causes pancreatitis
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Linagliptin, saxagliptin, sitagliptin (mechanism, use, toxicity)
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DPP-4 inhibitors; increase insulin, decrease glucagon secretion; causes mild urinary/respiratory infections
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Propylthiouracil (mechanism, use, toxicity)
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Blocks thyroid peroxidase and 5'-deiodinase; used to treat hyperthyroidism; causes agranulocytosis, aplastic anemia, hepatotoxicity
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Methimazole (mechanism, use, toxicity)
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Blocks thyroid peroxidase; used to treat hyperthyrodism; teratogenic
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Levothyroxine, triiodothyronine (mechanism, use, toxicity)
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Thyroid hormone analogs; causes thyrotoxicosis
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Oxytocin (mechanism, use, toxicity)
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Used to control uterine hemhorrage
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Demeclocycline (mechanism, use, toxicity)
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ADH antagonist used to treat SIADH; can cause photosensitivty and bone/teeth abnormalities
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Glucocorticoids (mechanism, use, toxicity)
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Inhibits phospholipase A2 activity and expression of COX-2; used for immune suppression; can cause Cushing's syndrome, adrenal insufficiency (if withdrawn quickly)
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Cimetidine and ranitidine (mechanism, use, toxicity)
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H2 antagonists; used to treat hyperchloridia; cimeditine is a P-450 inhibitor and has antiandrogenic effects, both reduce creatinine secretion
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-prazoles (mechanism, use, toxicity)
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Irreversibly inhibit the H/K pump; used to treat hyperchloridia; increased risk of C. difficile infection and hypomagnesemia
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Bismuth, sucralfate (mechanism, use, toxicity)
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Coats ulcer base and protects underlying tissue
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Misoprostol (mechanism, use, toxicity)
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PGE1 analog that decreases acid production and increases bicarb production; used to prevent NSAID ulcers; abortifacient
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Octreotide (mechanism, use, toxicity)
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Somatostatin analog; used to treat VIPoma and carcinoid syndrome
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Toxicity of long-term antacid use
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Hypokalemia
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Infliximab (mechanism, use, toxicity)
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Anti-TNF; used to treat IBD and RA; can cause activation of latent microbes
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Sulfasalazine (mechanism, use, toxicity)
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Combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory); used to treat IBD; causes oligospermia
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Ondansetron (mechanism, use, toxicity)
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5-HT3 antagonist; used as an antiemetic
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Metoclopramide (mechanism, use, toxicity)
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D2 antagonist; used to increase gut muscle activity and as an antiemetic; causes parkinson signs
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Can be used to prevent mast cell degranulation
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Cromolyn sodium
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Treatment of lead poisoning
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Dimercaprol and EDTA, succimer in kids
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Heparin (mechanism, use, toxicity)
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Activates antithrombin, which inactivates thrombin and Xa; used for immediate coagulation and in pregnant women; some patients develop antibodies to platelet factor 4 (HIT)
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Enoxaparin, dalteparin (mechanism, use, toxicity)
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Same actions as heparin, but has a longer half-life, does not have to be monitored as closely, and has a reduced risk of HIT
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Warfarin (mechanism, use, toxicity)
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Inactivated gamma-carboxylation of factors II, VII, IX, X, C, and S; used for long-term and non-immediate anticoagulation; can cause tissue necrosis, teratogenic
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Alteplase, reteplase, tenecteplase (mechanism, use, toxicity)
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Converts plasminogen to plasmin; used as a thrombolytic
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Aspirin (mechanism, use, toxicity)
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Irreversibly inhibits COX-1 and COX-2; anti-platelet and anti-inflammatory; gastric ulcers, tinnitus, Reye's syndrome in childhood viral infections
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Clopidogrel, ticlodipine, prasugrel, ticagrelor (mechanism, use, toxicity)
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Irreversibly blocks ADP receptors on platelets, preventing degranulation; used for acure coronary syndrome; ticlodipine causes neutropenia
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Cilostazol, dipyridamole (mechanism, use, toxicity)
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Phosphodiesterase inhibitor, increases cAMP and decreases ADP, preventing platelet degranulation; nausea, headache, facial flushing, hypotension
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Abciximab, eptifibatide, tirofiban (mechanism, use, toxicity)
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GPIIb/IIIa inhibitors, preventing platelet aggregation; bleeding, thrombocytopenia
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Methotrexate (mechanism, use, toxicity)
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Inhibits dihydrofolate reductase, inhibiting DNA synthesis; myelosuppression, macrovesicular fatty change in liver
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5-fluorouracil (mechanism, use, toxicity)
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Pyrimidine analog that is activated and inhibits thymidylate synthase, inhibiting DNA synthesis; myelosuppression, photosensitivity
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Cytarabine (mechanism, use, toxicity)
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Pyrimidine analog that inhibits DNA polymerase; leukopenia, thrombocytopenia, megaloblastic anemia
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Azathioprine, 6-mercaptopurine, 6-thioguanine (mechanism, use, toxicity)
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Purine analogs that are activated by HGPRT and inhibit purine synthesis; toxicity is increased with allopurinol, causes bone marrow, GI, and liver toxicity
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Dactinomycin (actinomycin D) (mechanism, use, toxicity)
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DNA intercalator; used for childhood tumors; myelosuppression
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Doxorubicin (Adriamycin), daunorubicin (mechanism, use, toxicity)
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Generates free radicals that cause DNA strand breaks; dilated cardiomyopathy, myelosuppression, alopecia
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Bleomycin (mechanism, use, toxicity)
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Generates free radicals that cause DNA strand breaks; pulmonary fibrosis with minimal myelosuppression
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Cyclophosphamide, ifosfamide (mechanism, use, toxicity)
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Crosslinks DNA (must be activated by liver); myelosuppression, hemhorragic cystitis (can be minimized with mesna)
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Carmustine, lomustine, semustine, streptozocin (mechanism, use, toxicity)
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Used to treat CNS tumors
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Busulfan (mechanism, use, toxicity)
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Alkylates DNA; pulmonary fibrosis, hyperpigmentation
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Vincristine, vinblastine (mechanism, use, toxicity)
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Block microtubule polymerization; vincristine causes neurotoxicity, vinblastine causes bone marro suppression
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Paclitaxel (mechanism, use, toxicity)
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Blocks microtubule breakdown; myelosuppression
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Cisplatin, carboplatin (mechanism, use, toxicity)
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Crosslinks DNA; nephrotoxicity (minimize with chloride diuresis, amifostine), acoustic n. damage
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Etoposide, teniposide (mechanism, use, toxicity)
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Inhibits topoisomerase II; myelosuppression, GI upset, alopecia
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Hydroxyurea (mechanism, use, toxicity)
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Inhibits ribonucleotide reductase; used in cancers and HbSS disease; bone marrow suppression
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Prednisone (mechanism, use, toxicity)
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Unknown but may trigger apoptosis in dividing cells; Cushingoid symptoms
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Tamoxifen, raloxifene (mechanism, use, toxicity)
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Prevents estrogen receptor binding; used in breast cancer and prevention of osteoporosis; tamoxifen increases the risk of endometrial cancer due to agonist effects
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Trastuzumab (mechanism, use, toxicity)
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Antibody against HER-2 receptor; cardiotoxicity
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Imatinib (mechanism, use, toxicity)
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Antibody against bcr-abl tyrosine kinase
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Rituximab (mechanism, use, toxicity)
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Antibody against CD20; used to treat non-Hodgkin's lymphoma and rheumatoid arthritis
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Vemurafenib (mechanism, use, toxicity)
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B-raf kinase inhibitor (V600 mutation); used in metastatic melanoma
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Bevacizumab (mechanism, use, toxicity)
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Antibody against VEGF
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Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac (mechanism, use, toxicity)
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Reversible COX inhibitor; gastric ulcers, renal ischemia (due to constriction of afferent arteriole)
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Celecoxib (mechanism, use, toxicity)
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Reversible COX-2 inhibitor; anti-inflammatory without damage to gastric mucosa; sulfa allergy, thrombosis
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Acetominophen (mechanism, use, toxicity)
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COX inhibitor in the CNS (not anti-inflammatory); causes hepatic necrosis
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Alendronate (mechanism, use, toxicity)
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Pyrophosphate analog that inhibits osteoclasts; used to treat osteoporosis, hypercalcemia, and Paget's disease; corrosive esophagitis
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Allopurinol (mechanism, use, toxicity)
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Xanthine oxidase inhibitor, reduces production of uric acid
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Febuxostat (mechanism, use, toxicity)
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Xanthine oxidase inhibitor
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Probenecid (mechanism, use, toxicity)
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Inhibits reabsorption of uric acid in PCT
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Colchine (mechanism, use, toxicity)
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Inhibits microtubule polymerization, preventing neutrophil extravasation
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Etanercept (mechanism, use, toxicity)
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TNF-alpha receptor that binds free TNF-alpha
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Infliximab, adalimumab (mechanism, use, toxicity)
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Anti-TNF-alpha antibody
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Latanoprost (mechanism, use, toxicity)
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PGF2 analog that increases the outflow of aqueous humor; can cause darkening of the iris
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Morphine, fentanyl, cofeine, heroin, methadone, meperidine, dextromethorphan, diphenoxylate (mechanism, use, toxicity)
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Mu opioid agonists that open K channels and close Ca channels, inhibting synaptic transmission; addiction, respiratory depression, constipation, miosis
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Butorphanol (mechanism, use, toxicity)
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Mu opioid partial agonist; used to treat severe pain; causes withdrawal if being treated with full agonist
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Tramadol (mechanism, use, toxicity)
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Weak opioid agonist that inhibits serotonin and NE reuptake; increases risk for seizures
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First-line therapy for simple partial seizures
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Carbamazepine
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First-line therapy for complex partial seizures
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Carbamazepine
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First-line therapies for tonic-clonic seizures (3)
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Carbamazepine, phenytoin, valproate
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First-line therapy for absence seizures
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Ethosuximide
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Phenytoin (mechanism, use, toxicity)
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Increases Na channel inactivation and inhibits glutamate release; used for simple, complex, and tonic-clonic seizures and status epilecticus prophylaxis; nystagmus, gingival hyperplasia, hirsutism, megaloblastic anemia, teratogenic, drug-induced lupus, P450 inducer
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Carbamazepine (mechanism, use, toxicity)
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Increases Na channel inactivation; first-line for simple, complex, and tonic-clonic seizures and trigeminal neuralgia; agranulocytosis, aplastic anemia, P450 inducer, SIADH, liver toxicity
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Lamotrigine (mechanism, use, toxicity)
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Blocks Na channels; used for simple, complex, and tonic-clonic seizures; Steven-Johnson syndrome
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Gabapentin (mechanism, use, toxicity)
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Inhibits Ca channels; used for simple, complex, and tonic-clonic seizures, migraine prophylaxis, peripheral neuropathy, bipolar disorder; ataxia
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Topiramate (mechanism, use, toxicity)
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Blocks Na channels and increases GABA secretion; used for simple, complex, and tonic-clonic seizures and migraine prevention; mental dulling, kidney stones, weight loss
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Phenobarbital (mechanism, use, toxicity)
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Increases GABA channel action; first-line for simple, complex, and tonic-clonic seizures in children; P450 inducer
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Valproate (mechanism, use, toxicity)
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Increases Na channel inactivation and increases GABA levels; first-line for tonic-clonic seizures, used for simplex, complex, tonic-clonic, and myoclonic seizures; hepatotoxicity, neural tube defects, weight gain, tremor
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Ethosuximide (mechanism, use, toxicity)
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Blocks thalamic Ca channels; first-line for absence seizures; GI distress, Steven-Johnson syndrome
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Benzodiazepines (mechanism, use, toxicity)
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Increases frequency of GABA channel opening; first-line for status epilepticus (diazepam, lorazepam), used for eclampsia seizures (diazepam, lorazepam), anxiety, alcohol withdrawl, sleep walking, night terrors; sedation
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Tiagabine (mechanism, use, toxicity)
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Inhibits GABA reuptake; used for simple and complex seizures
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Vigabatrin (mechanism, use, toxicity)
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Irreversibly inhibits GABA transaminase, increasing GABA concentration; used for simple and complex seizures
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Levetriacetam (mechanism, use, toxicity)
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Unknown mechanism; used for simple, complex, and tonic-clonic seizures
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Phenobarbital, pentobarbial, thiopental, secobarbital (mechanism, use, toxicity)
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Increase duration of GABA channel opening; induction of anesthesia, sedative; CNS depression, P450 inducer, contraindicated in patients with porphyrias
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Triazolam, oxazepam, midazolam (mechanism, use, toxicity)
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Short-acting benzodiazepines; more addictive potential
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Barbituates vs. benzodiazepines (mechanism)
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Increase duration vs. increase frequency
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Zolpidem, zaleplon, eszopiclone (mechanism, use, toxicity)
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BZ1 subtype GABA channel agonists; used to treat insomnia
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Ketamine (mechanism, use, toxicity)
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Blocks NMDA receptor; used as an anesthetic; increases cardiac activity, hallucinations, bad dreams
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Order of sensory loss when using local anesthetics
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Pain -> temperature -> touch -> pressure
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Succinylcholine (mechanism, use, toxicity)
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ACh receptor agonist, produces sustained depolarization and desensitization; used as a paralytic; hypercalcemia, hyperkalemia, malignant hyperthermia
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Tubocurarine, -curium drugs (mechanism, use, toxicity)
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ACh antagonists; used as paralytics
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Dantrolene (mechanism, use, toxicity)
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Inhibits release of Ca from sarcoplasmic reticulum and skeletal muscle; used to treat malignant hyperthermia and neuroleptic-malignant syndrome
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Levodopa/carbidopa (mechanism, use, toxicity)
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Converted to dopamine by dopa decarboxylase in CNS/inhibits peripheral dopa decarboxylase activity; used to treat parkinson symptoms; can cause arrhythmias and "on/off" phenomenon
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Selegiline (mechanism, use, toxicity)
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MAO-B (prefers dopamine for breakdown) inhibitor, inhibits dopamine breakdown; used to treat parkinson symptoms; enhances adverse effects of levodopa
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Donepezil, galantamine, rivastigmine (mechanism, use, toxicity)
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ACh esterase inhibitors; used to treat Alzheimer's disease; cholinergic symptoms
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Sumatriptan (mechanism, use, toxicity)
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Agonist at 1B/1D serotonin receptors; used to treat acute migraines and cluster headaches; coronary vasospasm
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Trifluoperzine, fluphenazine, haloperidol (mechanism, use, toxicity)
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High potency antipsychotics that antagonize D2 receptors; used to treat schizoprehnia, psychosis, mania, and Tourette's; hyperprolactinemia, anti-cholinergic symptoms (dry mouth, constipation), extrapyramidal effects (dyskinesia), neuroleptic malignany syndrome, tardive dyskinesia (haloperidol)
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Chlorpromazine, thioridazine (mechanism, use, toxicity)
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Low potency antipsychotics that antagonize D2 receptors; used to treat schizophrenia, psychosis, mania, and Tourette's; corneal deposits (chlorpromazine), retinal desporits (thioridazine)
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Olanzapine, clozapine, quetiapine, risperidone, aripripazole, ziprasidone (mechanism, use, toxicity)
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Atypical antipsychotics with unknown mechnism; used for schizophrenia, bipolar disorder, OCD, and others; weight gain (olanzapine, clozapine), agranulocytosis (clozapine), seizures (clozapine), prolonged QT (ziprasidone)
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Lithium (mechanism, use, toxicity)
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Unknown mechanism; used for bipolar disorder and SIADH; tremor, sedation, edema, hypothyroidism, polyuria
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Buspirone (mechanism, use, toxicity)
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Agonizes 1A serotonin receptors; used for generalized anxiety disorder; no side effects, but takes 1-2 weeks for improvement
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Fluoxetine, paroxetine, sertraline, citalopram (mechanism, use, toxicity)
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Block reuptake of serotonin from the synaptic cleft; depression and others; sexual dysfunction, sertonin syndrome (hyperthermia, myoclonus, flushing, diarrhea, seizures)
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Venlafaxine, duloxetine (mechanism, use, toxicity)
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Block reuptake of NE and serotonin from synaptic cleft; depression, diabetic neuropathy (duloxetine); hypertension
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-iptyline, -ipramine, doxepin, amoxapine (mechanism, use, toxicity)
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TCAs, block reuptake of NE and serotonin; depression, bewetting (imipramine), OCD (clomipramine); convulsions, coma, arrhythmias, sedation, hypotension, anti-cholinergic effects
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Tranylcypromine, phenelzine, isocarboxazid, selegiline (mechanism, use, toxicity)
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Inhibit breakdown of NE, serotonin, and dopamine; used for atypical depression, anxiety, and hypochondriasis; hypertensive crisis (tyramine in wine/cheese), don't use with other serotonin agonists
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Bupropion (mechanism, use, toxicity)
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Increases NE and dopamine; used for smoking sensation, depression; seizures
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Mirtazapine (mechanism, use, toxicity)
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Alpha-2 antagonist, increases NE and serotonin release, and serotonin receptor agonist; used for depression; sedation, increased appetite with weight gain;
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Maprotiline (mechanism, use, toxicity)
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Blocks NE reuptake; used for depression; sedation, hypotension
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Trazodone (mechanism, use, toxicity)
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Inhibits serotonin uptake; used for insomnia; pripism
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Mannitol (mechanism, use, toxicity)
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Osmotic diuretic; used to treat drug overdose and increased ICP; pulmonary edema, CHF
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Acetazolamide (mechanism, use, toxicity)
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Carbonic anhydrase inhibitor; used for glaucoma, metabolic alklalosis; hyperchloremic metabolic acidosis, ammonia toxicity, sulfa allergy
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Furosemide (mechanism, use, toxicity)
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Inhibits NKCC channel, preventing urine concentration; used in hypertension, CHF, hypercalcemia; ototoxicity, hypokalemia, hypocalcemia, nephritis, gout, sulfa allergy
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Ethacrynic acid (mechanism, use, toxicity)
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Inhibits NKCC channel; used in patients with furosemide (sulfa) allergy; hyperuricemia
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Hydrochlorothiazide (mechanism, use, toxicity)
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Inhibits NaCl reabsorption in DCT and increases Ca reabsorption; hypertension and hypercalcinuria; hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy
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Spironolactone, eplerenone (mechanism, use, toxicity)
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Aldosterone receptor antagonists; hyperaldosteronism, CHF, hypokalemia; hyperkalemia (arrhythmias), antiandrogen effects with spironolactone
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Triamterene, amiloride (mechanism, use, toxicity)
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Block sodium channels in cortical collecting duct; hyperaldosteronism, CHF
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Captopril, enalapril, lisinopril (mechanism, use, toxicity)
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ACE inhibitor, leads to reduced angiotensin II levels and decreases GFR; prevents heart remodeling, hypertension, CHF; cough, angioedema, transient creatinine increase, hyperkalemia
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Losartan, valsartan (mechanism, use, toxicity)
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Angiotensin II receptor antagonists; similar to ACE inhibitors, but do not cause cough due to normal metabolism of bradykinin
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Leuprolide (mechanism, use, toxicity)
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GnRH analog that acts as an agonist in pulsatile doses and an antagonist in continuous doses; used as an agonist for infertility and an antagonist for prostate cancer, fibroids, and precocious puberty; antiandrogenic
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Finasteride (mechanism, use, toxicity)
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5-alpha reductase inhibitor; used for BPH and male-pattern baldness
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Flutamide (mechanism, use, toxicity)
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Testosterone receptor antagonist; used in prostate cancer
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Ketoconazole (mechanism, use, toxicity)
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Inhibits 17,20-desmolase, stopping sex steroid synthesis; used to treat polycystic ovarian syndrome
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Clomiphene (mechanism, use, toxicity)
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Partial estrogen agonist in the hypothalamus, increases release of LH and FSH, stimulating ovulation; used for infertility and PCOS
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Tamoxifen (mechanism, use, toxicity)
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Estrogen receptor antagonist at the breast; used for breast cancer; partial agonist at the uterus, can cause endometrial hyperplasia
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Raloxifene (mechanism, use, toxicity)
|
Estrogen receptor agonist at bone, inhibits osteoclast activity and stimulates osteoblast activity; used to treat osteoporosis
|
|
|
Anastrozole, exemestane (mechanism, use, toxicity)
|
Aromatase inhibitors; used in breast cancer
|
|
|
Mifepristone (mechanism, use, toxicity)
|
Progesterone receptor antagonist, given with misoprostol for abortion; abortifacient; bleeding, abdominal pain
|
|
|
Terbutaline (mechanism, use, toxicity)
|
Beta-2 agonist, inhibits uterine contractions
|
|
|
Tamsulosin (mechanism, use, toxicity)
|
Alpha-1 antagonist; used to treat BPH
|
|
|
Sildenafil, vardenafil (mechanism, use, toxicity)
|
Phosphodiesterase 5 inhibitors, causing inc. cGMP levels and smooth muscle relaxation; used in erectile dysfunction; impaired blue-green vision, contradindicated with nitrates
|
|
|
Danazol (mechanism, use, toxicity)
|
Partial androgen receptor agonist; used to treat endometriosis and hereditary angioedema; weight gain, acne, hirsutism, low HDL, hepatoxicity
|
|
|
Treat methemoglobinemia with
|
Methylene blue
|
|
|
Diphenhydramine, dimenhydrinate, chlorpheniramine (mechanism, use, toxicity)
|
(First generation) H1 antagonists; used in allergies, motion sickness, insomnia; sedation, antiadrenergic, antiserotonergic, and antimuscarinic effects due to CNS penetration
|
|
|
Loratadine, fexofenadine, desloratadine, cetrizine (mechanism, use, toxicity)
|
H1 antagonists; used in allergies; less fatigue than other antihistamines due to decreased CNS penetration
|
|
|
Albuterol (mechanism, use, toxicity)
|
Short-acting beta-2 agonist; asthma
|
|
|
Salmeterol, formoterol (mechanism, use, toxicity)
|
Long-acting beta-2 agonist; asthma; tremor, arrhythmias
|
|
|
Theophylline (mechanism, use, toxicity)
|
Phosphodiesterase inhibitor, increases cAMP and causes bronchodilation; asthma; cardiotoxicity, neurotoxicity
|
|
|
Ipratropium (mechanism, use, toxicity)
|
Muscarinic antagonist, prevents bronchoconstriction; asthma and COPD
|
|
|
Beclomethasone, fluticasone (mechanism, use, toxicity)
|
Inhibit cytokine synthesis, reducing inflammation due to asthma
|
|
|
Montelukast, zafirlukast (mechanism, use, toxicity)
|
Leukotriene receptor antagonists; especially useful in aspirin-induced asthma
|
|
|
Zileuton (mechanism, use, toxicity)
|
Inhibits activity of 5-lipoxygenase, inhibiting leukotriene production; reduces inflammation
|
|
|
Omalizumab (mechanism, use, toxicity)
|
Anti-IgE antibody; used in refractory allergic asthma
|
|
|
Guaifenesin (mechanism, use, toxicity)
|
Thins respiratory secretions
|
|
|
N-acetylcysteine (mechanism, use, toxicity)
|
Loosens mucus plugs; used in CF patients and as an antidote to acetominaphen posioning
|
|
|
Bosentan (mechanism, use, toxicity)
|
Antagonizes endothelin-1 receptors, reducing vascular resistance in the pulmonary vessels; used in pulmonary hypertension
|
|
|
Dextromethorphan (mechanism, use, toxicity)
|
Antagonizes NMDA receptors, inhibiting coughing; produces opioid effects in large doses and carries mild abuse potential
|
|
|
Pseudoephedrine, phenylephrine (mechanism, use, toxicity)
|
Alpha-1 agonists that reduce edema and nasal congestion; rhinitis; hypertension, quick tolerance (recurrence of symptoms despite continued treatment)
|
|
|
Difference in competitive vs noncompetitve inhibitors?
|
competitive = decrease potency, noncompetitive = decrease efficacy.
|
|
|
What is Km?
|
Inverse relation of affinity of enzyme for its substrate.
|
|
|
What is Vmax?
|
Direct proportion to enzyme concentration
|
|
|
What is bioavailability?
|
Fraction of administered drug that reaches systemic circulation unchanged.
|
|
|
Time to steady state depends on?
|
depends on half-life. Does not depend on frequency or size of dose.
|
|
|
What is rate of elimination in zero order kinetics?
|
constant amount eliminated per time.
|
|
|
Give three drugs that are zero order eliminated.
|
PEA - phenytoin, Ethanol, Aspirin.
|
|
|
What is the rate of elimination for first order kinetics?
|
A constant FRACTION is eliminted, variable by concentration!
|
|
|
How does ionization relate to urine pH?
|
Ionzied species are trapped in urine and not resorbed. Neutral can be resorbed.
|
|
|
How do you treat overdose of weak acid? Give drug examples.
|
Treat with Bicarb to make neutral. Exp: phenobarbital, methotrexate, aspirin.
|
|
|
How do you treat overdose of weak base? Give drug examples.
|
Treat with ammonium chloride. exp: amphetamines.
|
|
|
What is phase I drug metabolism? What pt. population loses this?
|
Reduction, Oxidation, hydrolysis with CYP450. Often gives neutral products. Geriatrics lose this phase.
|
|
|
What is phase II metaboloism? What population depend on this?
|
Conjugation (Glucuronidation, Acetylation, and Sulfation.) Gives charged products. Geriatrics depend on this, old people have GAS.
|
|
|
What is efficacy?
|
maximal effect a drug can produce.
|
|
|
What is potency?
|
amount of drug needed for the same effect.
|
|
|
What happends to efficacy when a partial agonist and full agonist are mixed?
|
DECREASED efficacy. fight for same binding site, full agonist cant exert full effect.
|
|
|
What is therapetuic index?
|
LD50/ED50. Median lethal dose divded by median effective dose. Safer drugs have a higher TI.
|
|
|
What is a therapeutic window?
|
Minimum effective dose to minimum toxic dose. Think of it as range of use.
|
|
|
What are the two types of Nicotonic receptors? What kind of messenger do they use?
|
1. Nicotinic - Ligang gated Na/K channels. Two nicotinic types: Nm(NMJ) and Nn(autonomic ganglia. 2. Muscarinic - G-proteins. 5 types, M1-M5.
|
|
|
Alpha-1 sympathetic receptor (G-protein class, major function)
|
q, increase: vasc. smooth muscle contraction, pupillary dilator muscle contraction, intestinal and bladder sphincter contaction.
|
|
|
Alpha-2 sympathetic receptor(G-protein class, major function)
|
i, decrease: sympathetic outflow, insulin release, lipolysis. increase: platlet aggregation.
|
|
|
Beta-1 sympathetic receptor(G-protein class, major function)
|
s, increase: heart rate, contractilty, renin release, lipolysis
|
|
|
Beta-2 sympathetic receptor(G-protein class, major function)
|
s, vasodilation, brochodilation, increase: heart rate, contractility, lipolysis, insulin release, aqueous humor production. decrease: uterine tone, ciliary muscle tone.
|
|
|
M-1 Parasymp receptor(G-protein class, major function)
|
q, CNS, enteric nervouse system.
|
|
|
M-2 Parasymp(G-protein class, major function)
|
i, decease: heart rate, contractility of atria
|
|
|
M-3 parasymp(G-protein class, major function)
|
increase: exocrine gland secretion (tears, gastric, etc), gut peristalsis, bladder contraction, bronchoconstriction, pupillary spinchter contraction, cilliary muscle contraction.
|
|
|
What receptor is responsible for miosis and accomadation?
|
Parasympathetic M-3.
|
|
|
What receptor is responsbile for mydriasis?
|
Sympathetic Alpha-1.
|
|
|
Dopamine D-1 receptor(G-protein class, major function)
|
s, relaxes renal vascular smooth muscle
|
|
|
Dopamine D-2 receptor(G-protein class, major function)
|
i, modulates transmitter release especially in brain.
|
|
|
Histamine H-1 receptor(G-protein class, major function)
|
q, increase: mucus production, contraction of bronchioles, pruritus, pain.
|
|
|
histamine H-2 receptor(G-protein class, major function)
|
a, increase gastric acid secretion
|
|
|
vasopression V-1 receptor(G-protein class, major function)
|
q, increase: vascular smooth muscle contraction
|
|
|
vasopression V-2 receptor(G-protein class, major function)
|
s, increase water permeability and reabsorption in kidneys. (V2 found in 2 kidneys).
|
|
|
Which receptors work via Gq -> Phospholipase C ->Pip2->DAG + IP3?
|
H1,Alpha1,V1,M1,M3. (remember HAVe 1 M&M)
|
|
|
DAG causes activation of what?
|
Protein Kinase C.
|
|
|
IP3 causes increase in what?
|
Calcium -> smouth muscle contraction
|
|
|
Which receptors work via Gi->Adenyly cyclase ->cAMP ->Protein Kinase A?
|
M2, Alpha2, D2. (remember MAD 2's.)
|
|
|
Which receptors work via Gs->adenylyate cyclase ->cAMP->Protein Kinase A?
|
Beta1, Beta2, D1, H2,V2.
|
|
|
What does protein kinase A do?
|
increase calcium release in heart and blocks myosin light chain kinase.
|
|
|
What are the two classes of cholinomimetics?
|
1. direct agonsts 2. indirect agonists (anticholinesterases).
|
|
|
Bethanechol(mechanism,use,toxicity)
|
Direct cholinomimetic. Postop or neurogenic ileus, urinary retention. COPD+asthma exacerbation, peptic ulcers.
|
|
|
Carbachol(mechanism,use,toxicity)
|
Direct Cholinomimetic. Identical to Ach. Glaucoma, pupillary contraction, relief of IOP. COPD+asthma exacerbation, peptic ulcers.
|
|
|
Pilocarpine(mechanism,use,toxicity)
|
Direct Cholinomimetic. Stimulates tears, salvia, sweat. Open and closed-angle glaucoma.COPD+asthma exacerbation, peptic ulcers.
|
|
|
methacholine(mechanism,use,toxicity)
|
Direct Cholinomimetic. challenge test of asthma diagnosis. COPD+asthma exacerbation, peptic ulcers.
|
|
|
Neostigmine(mechanism,use,toxicity)
|
Indirect cholinomimetic agonist. NO cns penetration. Postop and neurogenic ileus, myasthenia gravis, reversal of NMJ block. COPD+asthma exacerbation, peptic ulcers.
|
|
|
pyridostigmine(mechanism,use,toxicity)
|
indirect cholinomimetic agonist. Long acting myasthenia gravis treatment. COPD+asthma exacerbation, peptic ulcers.
|
|
|
edrophonium(mechanism,use,toxicity)
|
indirect cholinomimetic agonist. Short acting, for myasthenia gravis diagnosis. COPD+asthma exacerbation, peptic ulcers.
|
|
|
Physostigmine(mechanism,use,toxicity)
|
indirect cholinomimetic agonist. for anti-cholinergic overdose, crosses BBB. COPD+asthma exacerbation, peptic ulcers.
|
|
|
Donepezil(mechanism,use,toxicity)
|
indirect cholinomimetic agonist. Alzheimers disease. COPD+asthma exacerbation, peptic ulcers.
|
|
|
signs of cholinesterase inhibitor poisoning. treatment.
|
DUMBBELSS (diarrhea, urination, miosis, bronchospasm, bradycardia, excitation of skeletal muscle +CNS, lacrimation, sweating, salvia.) tx: atropine + pralidoxime.
|
|
|
Parathion(mechanism, treatment)
|
Irreversible cholinesterase inhibitor, ACH overdose. Tx: atropine + pralidoxime.
|
|
|
Atropine, homatropine, tropicamide (mechanism, use, toxicity).
|
Muscarinic antagonist. produces mydriasis and cycloplegia. (Atropine also used for bradycardia). Causes hot as a hare, dry as bone, red as beet, blind as bat, mad as a hatter.
|
|
|
Benztropine(mechanism,use,toxicity)
|
Muscarinic antagoist. Parkinsons disease (park my benz). Causes hot as a hare, dry as bone, red as a beet, blind as a bat, mad as a hatter.
|
|
|
Scopolamine(mechanism,use,toxicity)
|
Muscarinic antagonist. Motion sickness. causes hot as a hare, dry as a cone, red as a beet, blind as a bat, mad as a hatter.
|
|
|
Ipratropium,tiotropium (mechanism, use, toxicity)
|
Muscarinic antagonist. COPD, Asthma. Causes hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter.
|
|
|
Oxybutynin(mechanism,use,toxicity)
|
Muscarinic anatagonist. reduces urgency in mild cystitis and reduce bladder spasms. causes hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter.
|
|
|
Glycopyrrolate(mechanism,use,toxicity)
|
Muscarinic anatagonist. IP: given in preop to reduce airway secretions. oral:reduce drooling, peptic ulcer. Can cause hot as a hare, dry as a bone red as a beet, blind as a bat, mad as a hatter.
|
|
|
Jimson Weed(mechanism, toxicity)
|
muscarinic antagonist, causes gardner's pupil (mydriasis).
|
|
|
Epinephrine(Mechanism, receptors bound, use, toxicity)
|
Direct Sympathomemetic. A1,A2,B1,B2. Anaphylaxis, open angle glaucoma, asthma, hypotension.
|
|
|
Norepinephine(Mechanism, receptors bound, use, toxicity)
|
direct sympathomemetic. A1,A2, some B1. used in hypotension but it decrease renal perfusion.
|
|
|
Isoproterenol(Mechanism, receptors bound, use, toxicity)
|
Direct sympathomemetic. B1, B2. Used in Torsade de pointe and bradyarryhmia. Can cause tachycardia and worsen cardiac ischemia.
|
|
|
dopamine(Mechanism, receptors bound, use, toxicity)
|
Direct sympathomimetics. Receptors depend on dose. low = D1, med = D1,B2,B1, high = A1,A2,B1,B2,D1. Used in shock and heart failure (ionotropic and chronotropic).
|
|
|
dobutamine(Mechanism, receptors bound, use, toxicity)
|
Direct sympathomimetic. Mostly B1, little a1,a2,b2. Used in heart failure and cardiac stresstest (ionotrpic and chronotropic)
|
|
|
Phenylephrine(Mechanism, receptors bound, use, toxicity)
|
Direct sympathomimetic. A1, A2. Used in hypotension, to cause mydriasis, and rhinitis (decongestant).
|
|
|
Albuterol, salmetrol, terbutaline (Mechanism, receptors bound, use, toxicity)
|
Direct sympathomimetic. Mostly B2, some b1. Sal = long term ashtma or copd. Albuterol for short term asthma. Terbutaline for to reduce premture uterine contractions.
|
|
|
Ritodrine(Mechanism, receptors bound, use, toxicity)
|
Direct sympathomimetic. B2 only. Used to reduce premature uterine contractions.
|
|
|
Amphetamine (mechanism, use)
|
indirect sympathomimetic. Releases stored catecholamines. Used for narcolepsy, obesity, ADD.
|
|
|
Epinephrine(Mechanism, use, toxicity)
|
indirect sympathomimetic. Releases stored catecholamines. Used for nasal decongestion, urinary incontience, hypotension.
|
|
|
Cocaine (mechanims, use).
|
direct sympathomimetic. Reuptake inhibitor. Causes vasoconstriction and local anesthesia.
|
|
|
Why must B-Blockers be avoided in suspected cocaine intoxication?
|
mixing them can lead to unopposed A1 activation and extreme hypertenion.
|
|
|
How does norepinephrine cause reflex bradycardia?
|
stimulates A1>B2. Causes increased vasoconstrciton -> increased BP. This causes reflex bradycardia and slowing of HR.
|
|
|
How does isoproterenol cause reflex tachycardia?
|
Stimulates B2>A1. This cause vasodilation and dropping of BP. B1 is stimulated and causes tachycardia.
|
|
|
Clonidine, alpha-methyldopa(Mechanism, receptors bound, use)
|
Centrally acting alpha-2 agonists, this causes LESS peripheral sympathetic release.Used in hypertension, especially renal disease due to no increase in renal blood flow!
|
|
|
Phenoxybenzamine(Mechanism, receptors bound, use, toxicity)
|
IRREVERSIBLE nonslective alpha blocker. Used in pheochromosytoma BEFORE surgery! toxic: orhtostatic hypotension, reflec tachycardia.
|
|
|
phentolamine(Mechanism, receptors bound, use, toxicity)
|
REVERSBILE nonselective alpha blocker. give to patients on MAOI who each tyramine contraining foods.
|
|
|
Prazosin, Terazosin, Doxazosin,Tamsulosin(Mechanism, receptors bound, use, toxicity)
|
Alpha-1 blocker. Used in hypertension, urinary rentention in BPH. tox:orthostatic hypotension, dizziness, headache.
|
|
|
Mirtazapine (mechanism, use, toxicity)
|
Alpha-2 blocker. Used in depression. tox: sedation, hypercholesterolemia, increased apetite.
|
|
|
Describe what occurs when you alpha-blockade epi vs. phenylephrine.
|
Before blockade: Both epi and phen RAISES BP. After alpha blockade: only epi raises, no change in phenyl. Why: Epi has B binding, phenyl does NOT.
|
|
|
Give 6 applications of Beta-blockers in general.
|
Angina - decreases HR and contractility, decreasing oxygen use. MI - decrease mortality. SVT - decrease AV duction. Hypertension - decrease CO and renin secretion. CHF - slows progression. Glaucoma - decrease secretion of aqueous humor.
|
|
|
give general toxicites of b-blockers
|
impotence, asthma exacerbation, bradycardia, seizures, sedation, hides hypoglycemia.
|
|
|
What are the B1 selective b-blockers? When are they useful?
|
A BEAM. acebutolol, betaxolol, Esmolol, Atenolol, Metoprolol. Useful in comorbid pum. disease.
|
|
|
What are the nonselective ( b1 = b2) b-blockers?
|
Please Try Not Being Picky. Propranolol, Timolol, Nadolol, Pindolol. B = B-blocker.
|
|
|
what are the nonselective a and b-antagonists?
|
Carvedilol, labetalol.
|
|
|
What are the partial B-agonists?
|
Pindolol, Acebutolol.
|
|
|
Give treatment for acetaminophen overdose.
|
N-Acetylcysteine (replenishes glutathione).
|
|
|
Give treatment for salicylates overdose.
|
NaHCO3 (alkalinize urine)
|
|
|
give treatment for amphetamines overdose
|
NH4Cl (acidify urine)
|
|
|
Give treatment for antimuscarinic and anticholinergic overdose.
|
Phygostigmine and control the hyperhermia.
|
|
|
Give treatment for b-blocker overdose
|
Glucagon
|
|
|
Give treatment for digitalis overdose
|
(KLAM) normalize K, Lidocaine, Anti-dig fab fragments, Mg2
|
|
|
give treatment for iron overdose.
|
deFEroxamine, deFErasirox.
|
|
|
give treatment for lead overdose
|
CaEDTA, dimercaprol, succimer, penicillamine
|
|
|
give treatment for mercury, arsenix, gold overdose
|
Dimercaprol, succiner
|
|
|
give treatment for copper, arsenic, gold overdose
|
penillamine
|
|
|
give treatment for cyanide
|
nitrite + thiosulfate, hydroxocobalamin
|
|
|
give methemoglobin treatment
|
Methylene blue, vitamin c
|
|
|
Give Carbon monocide treatment
|
100% oxygen or hyperbaric oxygen
|
|
|
give treatment for methanol, ethylene glycol overdose
|
Fomepizole>Ethanol, dialysis
|
|
|
give treatment for opiods overdose
|
naloxone/naltrexone
|
|
|
give treatment for benzodiazepine overdose
|
flumazenil
|
|
|
give treatment for TCA overdose
|
NaHCO3 (alkalinize plasma)
|
|
|
give treatment for heparin overdose
|
protamine
|
|
|
give treatment for warfarin overdose
|
Vitamin K, fresh frozen plasma
|
|
|
give treatment for tPA, Streptokinase, urokinase overdose
|
aminocaproic acid
|
|
|
give treatment for theophylline overdose
|
B-Blockers
|
|
|
give treatment for acetylcholinesterase inhibitors
|
atropine + pralidoxime
|
|
|
causes coronary vasospam
|
cocaine, sumatriptan, ergots
|
|
|
causes cutaneous flushing
|
(VANC) Vancomycin, Adenosine, Niacin, Ca blocker
|
|
|
causes dilated cardiomyopathy
|
doxorubicin, daunorubicin
|
|
|
causes torsades de pointes
|
class III (sotalol) and class Ia (quinidine)
|
|
|
causes agranulocytoisis
|
Clozapine, Carbamazepine, Colchine, Propylthiouracil, Methimazole, Dapsone
|
|
|
causes aplastic anemia
|
chloramphenicol, benzene, NSAIDs, propylthiouracil, methimazole
|
|
|
causes direct coombs positive hemolytic anemia
|
methyldopa, penicillin
|
|
|
causes gray baby syndomr
|
chloramphenicol
|
|
|
causes hemolysis in G6PD-defiect patients
|
(hemolysis IS PAIN)isoniazid, sulfonamides, primaquine, aspirin, ibuprofen, nitrofurantoin
|
|
|
causes megaloblastic anemia
|
(females with PMS are on full BLAST mode) Phenytoin, Methotrexate, Sulfa drugs
|
|
|
Causes thrombotic complications
|
OCPs like estrogen
|
|
|
Causes cough
|
ACE inhibitors
|
|
|
causes pulmonary fibrosis
|
Bleomycin, amiodarone, Busulfan
|
|
|
causes acute cholestatic hepatits, jaundice
|
erthryomycin
|
|
|
causes focal to massice hepatic necrosis
|
Halothane, Amanita Phalloides, Valrpoic acid, Acetaminophen
|
|
|
causes hepatits
|
isoniazid
|
|
|
can lead to pseudomembranous colitis
|
clindamycin, ampicillin
|
|
|
can lead to adrenocortical insufficiency
|
glucocorticoid withdrawl via HPA suppression
|
|
|
can causes gynecomastia
|
`(Some drugs create awkward knockers) spironolactone, digitalis, cimetidine, chronic alcohol use, ketoconazole
|
|
|
causes hot flashes
|
estrogen, clomophene
|
|
|
causes hypergylcemia
|
niacin, tacrolimus, protease inhibitor, HCTZ, corticosteriods
|
|
|
causes hypothyroidism
|
lithium, amiodarone, suldonamides
|
|
|
causes fat redistribution
|
glucocoricoids, protease inhibitors
|
|
|
causes gingival hyperplasia
|
phenytoin, verpamil
|
|
|
causes gout
|
furosemide, thiazides, niacin, cyclosporine
|
|
|
causes myopathies
|
fibrates, niacin, colchine, hydroxychloroquine, interferon-alpha, penicillamine, statins, glucocorticoids
|
|
|
causes osteoporosis
|
corticosteroids, heparin
|
|
|
causes photosensitivty
|
(SAT for a PHOTO) Sulfonamides, amiodarone, tetracycline
|
|
|
causes rash/SJS
|
penicillin, ethosuximide, carbamazepine, sulfa drugs, lamotrigine, allopurinol, phenytoin, phenobarbital
|
|
|
cause drug induced lupus
|
Hydralazine, isonizid, procainamine, phenytoin
|
|
|
causes teeth problems
|
tetracyclines
|
|
|
causes tendonitis, tendon rupture, tooth damage
|
fluoroquinolones
|
|
|
causes diabetes insipidus
|
lithium, demeclocycline
|
|
|
causes fanconi's syndome
|
expired tetracycline
|
|
|
causes hemorrhagic cystits
|
Cyclophosamide, ifosfamide
|
|
|
causes interstital nephritis
|
methicllin, NSAID, furosemide
|
|
|
causes SIADH
|
carbamazepine, cyclophosamide
|
|
|
causes cinchonism
|
Quinidine, qunine
|
|
|
causes parkinson-like syndome
|
antipsychotics, resperine, metoclopramide
|
|
|
causes seizures
|
(with seizures, I BITE My tongue) isoniazid, Buproprion, imipenem, Tramadol, Enflurane, Metoclopramide
|
|
|
causes tardive dyskinesia
|
antipsychotics
|
|
|
acts like an anti-muscarinic
|
Atropine, TCA, H1-blocker, neuoleptics
|
|
|
can cause a disulfiram like reaction
|
metronidazole, some cephalosporins, procarbazine, 1st gen sulphonoureas
|
|
|
can cause nephro/ototoxicity
|
aminoglycosides, vancomycin, loop dieuetics, cisplatin
|
|
|
list p450 inducers
|
(Momma Barb Steals Phen-phen and Refuses Greasy Carbs Chronically)Modafinil, Barbiturates, St. John wart, phenytoin, rifampin, griseofulvin, carbamazepine, chronic alcohol use.
|
|
|
list p450 inhibitors
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(MAGIC ROCKS in GQ) Macrolides, amiodarone, grapefruit juice, isoniazid, cimetidine, ritonavir actue alcohol use, ciprofloxacin, ketoconazole, sulfonamides, gemfibrozil, quinidine.
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lists the sulfa drugs
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(Popular FACTSSS) probenacid, furosemide, acetazolamide, celecoxib, thiazide, sulfonamide antibiotics, sulfaasalazine, sulfonylureas
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Difference between peniciliin G and V.
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G = IV and IM. V = oral.
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Penicillin(mechanism,use,toxicity)
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Bind penicillin-binding proteins(transpeptidases), block cross linking of peptidoglycans;most effective on G+, also N. Meningitidis, Treponema;hypersensitivy reaction, hemolytic anema.
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Oxacillin,Naficillin,Dicloxacillin(mechanism,use,toxicity)
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bind transpeptidases, penicillanse resistant due to bukly r-group blocking B-Lactamse; S. Aureus, except MRSA; hypersensitivity and interstitial nephritis.
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Ampicillin, amoxicillin(mecanism,use,toxicity)
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bind transpeptidases, wide spectrum and more penicillinase sensitive. combo with claculanic acid to protect from B-lactams;kills enterococci(HELPSS)H.iB, E.coli,Listera,Proteus,Salmonella,Shigella,enterococci;hypersensitivity reaction,rash,pseudomemrane colitis.
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Which has better bioavailibility; amoxicllin or ampicillin?
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amOxicllin has better Oral bioavilability.
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What does clavulanic acid do?
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B-lactamse inhibitor
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Ticarcillin,piperacillin(mechanism,use,toxicity)
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transpeptidase inhibitor but extended spectrum;pseduomonas and g- rods, use with claculanic acid due to B-lactamse suspectibilty; hypersensitivity reaction.
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List the B-lactamse inhibitors
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(CAST) Clavulanic Acid, Sulbactam,Tazobactem.
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Cephalosporin(mechanism,use,toxiciity)
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inhibit cell wall synthesis but are less susceptible to B-lactamases, are bactericidal;use depends on generation, there are four;hypersensitivty reactions, vitamin K defiency, increased nephrotoxicity of aminoglycosides.
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give use of cefazolin, cephalexin.
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1st generation cephalosporins. PEcK. Proteus, E.coli,Klebsiella. Cefazolin used preop to prevent A.aureus infections.
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give use of cefoxitin, cefaclor,cefuroxime`
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2nd generation cephalosporins. HEN PEcKs. H.ib, Enterbacter, Neisseria, Proteus, E.coli,Klebsiella, Serratia.
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give use of ceftriaxone, cefotaxime,ceftazidime
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3rd gen. cephalosporins. Serious gram - infections. Ceftriaxone = meningitis and gonorrhea. Ceftazidime = pseudomonas.
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give use of cefepime.
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increased activity against pseudomonas and G+ bugs.
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Aztreonam(mechanism,use,toxicty)
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a monobactem resistant to B-lactamases, prevents binding to PBP3 and is synergistic with aminoglycosides;gram - rods only;very nontoxic, some GI upset.
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what transpeptidase inhibitor can be used in penicillin allergy?
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aztreonam.
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imipenem/cilastatin,meropenem,etrapenem,doripenem(mechanism,use,toxicity)
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broad spectrum, B-lactamase resistent but imipenem needs cilastatin to inhibit renal dehydropeptidase. later carbepenems do not;G+ cocci,G- rods, anerobes. used only in life threating events;skin rash, CNS toxicity, seizures.
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Vancomycin(mechanism,use,toxicty)
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inhibits cell wall binding peptidoglycan formation by binding D-ala percursors, is bacterialcidal; G+ only, especially for multidrug resistant onces;NOT - nephrotoxicity, ototoxicity, thrombophlebitis, red man syndrome.
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How is redman syndrome prevented in vancomycin use?
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slow infusion and rate and antihistamines.
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How does vancomycin resistant occur?
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amino acid change of D-ala D-ala to D-ala D-lac.
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List antibiotic protein synthesis inhibitors
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AT 30, CCEL at 50. 30S = Aminoglycosides, Tetracyclines. 50S = Chloramphenicol, Clindamycin, Erythromycin, Linezolid.
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Gentamicin, neomycin, amikacin,tobramycin,streptomycin(mechanism,use,toxicity)
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aminoglycosides, bacterialcidal, block translocation but require oxygen for uptake;ineffective in anaerobes,use in gram - rod infections and before bowel surgery; nephrotoxicty, NMJ block, ototoxicity, teratogen.
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how does resistenace to aminoglycosides occur?
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transferase enzymes that inactivate the drug by acetylation, phosphorylation, or adenylation.
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tetracycline, doxycycline, demecycline,minocycline(mechanism, use, toxicity)
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bacteriostatic, prevents aminoacyl-tRNA binds;Borrela, M. Pneuomo, Rickettsia, Chlamysia; can't take with milk, antacids, iron because ions bind it, GI distress, discoloration of teeth, inhibition of bone growth, contraindication in pregnancy.
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how does resistance to tetracyclines occur?
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decrease uptake into cells or increased efflux by pumps.
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Azithromycin, clarithromycin, erythromycin(mechanism,use,toxicity)
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bacteriostatic, blocks translocation; atypical pneumonias, chlamydia, gram + cocci; MACRO: increased Motility, arrhythmia, Cholestatic hepatitis, Rash, eOsinophilia.
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how does resitance to macrolides occur?
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methylation of 23s rRNA binding site.
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Chloramphenicol(mechanism,use,toxicity)
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Bacterialstatic, blocks peptidlytransferase; Meningitis in adults, used in power countries due to being cheap; dose dependent anemia, dose independent aplastic anemia, gray baby syndrome.
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what causes grey baby syndrome?
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use of chloramphenicol in premature infants, they lack UDO-glucuronyl-transferase.
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How does resistance to chloramphenicol occur?
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plasmid-encoded acetyltransferase.
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clindamycin(mechanism,use,toxicity)
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Bacteriostatic. Blocks peptide transfer; anaerobic infections in lung infections and oral anerobes; C. Diff infection, fever, diarrhea.
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Sulfamethoxazole(SMX), sulfisoxazole, sulfadiazine(mechanism, use, toxicity)
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Bacteriostatic, PABA metabolites inhibit dihydropteroate synthase; Gram +, G-, Nocardia, Chlamydia, UTI; hypersensitivty, hemolysis in G6PD, nephrotoxic, kernicterus, displaces other drugs from albumin.
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how does resistance to sulfonamides occur?
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altered bacterial dihydropteroate or increased PABA synthesis.
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Trimethoprim(mechanism,use,toxicity)
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Bacteriostatic, inhibits bacterial dihydrofolate reductase, blocks folate synthesis; used in UTI, PCP (prophylacis and treatment), shigella, salmonella; megaloblastic anemia, leukopenia, granulocytopenia.
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ciprofloxacin, norfloxacin, levofloxacin, etc...(mechanism, use, toxicity)
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bactericidal, inhibits DNA gyrase(topo II and IV);G- rods of urinary and GI tracts, Neisseria, some G+;( lones hurt the bones) tenonitis and tendon rupture, superinfections, don't give to kids or pregnant women due to cartilage damage.
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how does resistance to fluroquinolones occur?
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mutation in DNA gyrase or efflux pumps.
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What groups are susceptible to fluorquinolone tendon rupture?
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older than 60 or taking prednisone
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Metronidazole(mechanism, use, toxicity)
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bacterialcidal, forms free radical toxic metabolites that damge bacterial DNA damage; (GET GAP) Giardia, Entamoeba, trichomonas, Gardnerella, Anaerobes, Pylori; causes disulfiram like reaction, headache, metallic taste.
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Isoniazid(mechanism,use,toxicity)
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decrease synthesis of mycolic acids, bacterial catalase peroxidase(KatG) must activate INH; TB drug, only one used as prophylaxis and in latent TB; peripheral neuropathy, hepatoxic, lupis like drug interaction, pyridoxine antagonist.
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Rifampin(mechanism,use,toxicity)
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inhibits DNA-dependent RNA polymerase; TB, Leprosy, prophylaxis in meningococcus and Hib type B; hepatotox, p450 inducer, orange body fluids.
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Pyrazinamide(mechanism, use, toxicity)
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unknown; TB; hyperuricemia, hepatotoxic.
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Ethambutol(mechanism,use,toxicity)
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decreased carbohydrate polymerization of TB cell wall, blocks arabinosyltransferase; TB; optic neuropathy(red-green color blindness_
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Amphotericin B(mechanism, use, toxicity)
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binds fungal ergosterol, causes holes in membranes; use in systemtic and CNS mycoses infections; fever/chills, hypotension, arrythmias, nephrotoxic, IV phlebitis, must supplement K and MG.
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nystatin(mechanism,use,toxicty)
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binds fungal ergosterol;topical only due to high toxicity, used for oral thrush and topical diaper rash or vaginal candidiasis.
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Fluconazole, ketoconazole, clotrimazole, itraconazole, voriconazole(mechanism, use,toxicity)
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inhibits fungal ergosterol synthesis by binding p450;Fluconazole for suppression of cryptococcus in AIDs patients, itraconazle for blasto, coccio, histo.
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Flucytosine(mechanism, use, toxicity)
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inhibits fungal DNA and RNA synthesis by conversion to 5FU; used in systemic fungal infections, especially cryptococcus; bone marrow suppression.
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Caspofungin, micafungin(mechanism, use, toxicity)
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inhibits fungal cell wall synthesis by inhibiting B-glucan synthesis; invasive aspergillosis, candida; flushing via histamine releae.
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terbinafine(mechanism,use,toxicity)
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inhibits fungal squalene epoxidase; treat dermatophytes - toe nail infection especially;abnormal LFT, visual disturbances.
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Griseofulvin(mechanism,use,toxicity)
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interferes with microtubules, stops mitosis in fungi;deposits in keratin so used in superficial infections, stops dermatophytes; teratogenic, carcinogenic, confusion, p450 inducer.
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Pyrimethamine use
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toxoplasmosis
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suramin and melarsoprol use
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trypanosoma brucei
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nifurtimox use
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trypanosoma cruzi
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sodium stibogluconate use
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leshmaniasis
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Chloroquine(mechanism,use,toxicity)
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blocks formation of heme into hemozoin. Heme accumulates and is toxic to plasmodia;used on all species but falciparum(too much resitance); retinopathy
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quinidine use
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lifethreatening malaria
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artemether/lumifantrine use
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p. falciparum killing
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Zanamivir,oseltamivir(mechanism,use)
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inihibits influenza neuraminidase, stops progeny release; treamt of influenze a and b
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Ribavarin(mechanism,use,toxicity)
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inhibits sythesis of guanine nucleotides by competitvely inhibiting IMP dehydrogenase; RSV, chronic hep C; hemolytic anemia, severe teratogen
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Acyclovir,valacyclovir(mechanism, use, toxicity)
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Guanosine analog, inhibits viral DNA polymerase; monophosphorylated by thymidine kinase in HSV/VZV so active in lesions and encephalitis, good for prophylaxis,
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Famciclovir use
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used in herpes zoster active infections
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mechanism for resistance to acyclovir
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mutated viral thymidine kinase
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Ganciclovir,valgangciclovir(mechanism,use,toxicity)
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guanosine analog, 5'-monophosphate formed by CMV viral kinase, inhibits viral DNA polymerase;CMV infections;leukopenia,neutopenia,thrombocytopenia,renal toxicity
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mechanism for resistance to acyclovir
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mutated CMV DNA polymerase or lack of viral kinase
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Foscarnet(mechanism,use,toxicity)
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viral DNA polymerase inhibitor, binds to pyrofosphate binding site, doesn't need viral kinase activation;CMV retinitis when ganciclovir fails and acyclovir restitant HSV; nephrotoxic
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mechanism for resistance to foscarnet
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mutated DNA polymerase
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cidofovir(mechanism,use,toxicity)
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inhibits DNA polymerase, doesn't require activiation by viral kinase; CMV retenitis, acyclovir resistant HSV; nephrotoxic
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HAART consist of what?
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[2 NRTI] +[1 NNRTI OR 1 protease inhibitor OR 1 integrase inhibitor]
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give mechanism and toxicity of protease inhibitors
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all end in -NAVIR! stops HIV mRNA cleavage into functional parts; hyperglycemia, GI upset, lipodystrophy.
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Ritonavir does what to be a "booster"
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inhibits cytochrome p-450, boosting concentration of other drugs.
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Tenofovir, emtricitabine, abacavir, lamivudine, zidovudine, didansoine, stavudine(mechanism,use,toxicity
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(NRTI)competitively blocks binding of nucleotide to reverse transcriptase, only tenofovir doesn't need to be activated;all NRTIs, zidovidine used in pregnancy to reduce fetal transmision; bone marrow suppression, lactic acidosis, peripheral neuropathy.
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Nevirapine, Efavirenz, Delavirdine(mechanism,use,toxicity)
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(NNRTI) bind at a site different from NRTIs, no don't require activation don't compete with nucleotides; bonow marrow suppression, peripheral neuropathy, lactic acidosis,
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Raltegravir(mechanism,use,toxicity)
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inhibits integrase, which stops HIV integration into host cells;HIV;hypercholesterolemia
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Interferons(mechanism,use,toxicity)
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glycoproteins synthesized my virus infected cells, block RNA and DNA virus replication; INFa- chronic hep b and c, Kaposi sarcoma, IFN-b -MS, INF-gamma -NADPH oxidase defiency; neutropenia, myopathy.
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What antibiotics must be avoided in pregnancy?
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SAFe Children Take Really Good Care. sulfonamides(kericterus), aminoglycosides(ototox), fluoroquinolones(cartilage damage), Clarithromycin(embryotoxic), Tetracycline(teeth,bone damage),Ribavarin(teratogenic),Griseofulvin(teratogenic),Chloramphenicol(grey baby)
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