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513 Cards in this Set
- Front
- Back
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Nitrates (mechanism, use, toxicity)
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vasodilation
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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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lowering LDL and raising HDL
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Cholestyramine, colestipol, colesevelam (mechanism, use, toxicity)
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Inhibits reabsorption of bile acids
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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 Lipoprotein lipase
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Digoxin and digitoxin (mechanism, use, toxicity)
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Inhibits Na/K ATPase
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Class 1A antiarrhythmics
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inc. AP duration and QT interval
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Class 1B antiarrhythmics
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dec. AP duration especially in depolarized/ischemia tissue; best following MI
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Class 1C antiarrhythmics
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no effect on AP,
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Class 1 antiarrhythmics (general mechanism and toxicity)
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Blocks Na channels, decreasing the slope of phase 0
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Class 2 antiarrhythmics
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Beta-blockers
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Class 3 antiarrhythmics
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Amiodarone, ibutilide, dofetilide, sotalol; K channel blockers; AIDS
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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;
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Adeosine (mechanism, use, toxicity)
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Inc. K efflux, hyperpolarizing the cell;
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Magnseium (mechanism, use, toxicity)
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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
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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
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increases insulin sensitivity
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Tolbutamide, chlorpropamide
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First-generation sulfonylureas; close beta-cell K channels, causing depolarization and increased insulin release;
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Glyburide, glimepiride, glipizide
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Second-generation sulfonylureas; close beta-cell K channels, causing depolarization and increased insulin release
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Pioglitazone, rosiglitazone
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Thiazolidinediones; activates PPAR-gamma, increasing insulin sensitivity and adiponectin levels;
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Acarbose, miglitol
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Alpha-glucosidase inhibitors; prevent sugar hydrolysis and absorption, reducing blood sugar levels
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Pramlintide
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Amylin analog; reduces glucagon secretion
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Exenatide, liraglutide
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GLP-1 analogues; increase insulin, decrease glucagon secretion
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Linagliptin, saxagliptin, sitagliptin
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DPP-4 inhibitors; increase insulin, decrease glucagon secretion
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Propylthiouracil
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Blocks thyroid peroxidase and 5'-deiodinase; used to treat hyperthyroidism
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Methimazole
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used to treat hyperthyrodism
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Levothyroxine, triiodothyronine
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Thyroid hormone analogs
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Oxytocin
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Used to control uterine hemhorrage
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Demeclocycline
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ADH antagonist used to treat SIADH
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Glucocorticoids
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Inhibits phospholipase A2 activity and expression of COX-2
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Cimetidine and ranitidine
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H2 antagonists; used to treat hyperchloridia
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Bismuth, sucralfate
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Coats ulcer base and protects underlying tissue
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Misoprostol
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PGE1 analog that decreases acid production and increases bicarb production
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Octreotide
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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
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Anti-TNF; used to treat IBD and RA
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Sulfasalazine
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Combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory)
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Ondansetron (mechanism, use, toxicity)
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5-HT3 antagonist; antiemetic
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Metoclopramide
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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
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Activates antithrombin, which inactivates thrombin and Xa; used for immediate coagulation and in pregnant women
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Enoxaparin, dalteparin
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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
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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
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Converts plasminogen to plasmin; used as a thrombolytic
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Aspirin
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Irreversibly inhibits COX-1 and COX-2
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Clopidogrel, ticlodipine, prasugrel, ticagrelor
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Irreversibly blocks ADP receptors on platelets,
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Cilostazol, dipyridamole
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Phosphodiesterase inhibitor, increases cAMP and decreases ADP, preventing platelet degranulation;
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Abciximab, eptifibatide, tirofiban
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GPIIb/IIIa inhibitors, preventing platelet aggregation;
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Methotrexate
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Inhibits dihydrofolate reductase, inhibiting DNA synthesis;
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5-fluorouracil
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Pyrimidine analog that is activated and inhibits thymidylate synthase, inhibiting DNA synthesis;
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Cytarabine
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Pyrimidine analog that inhibits DNA polymerase;
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Azathioprine, 6-mercaptopurine, 6-thioguanine
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Purine analogs that are activated by HGPRT and inhibit purine synthesis
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Dactinomycin (actinomycin D)
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DNA intercalator; used for childhood tumors;
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Doxorubicin (Adriamycin), daunorubicin
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Generates free radicals that cause DNA strand breaks;
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Bleomycin
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Generates free radicals that cause DNA strand breaks
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Cyclophosphamide, ifosfamide
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Crosslinks DNA (must be activated by liver);
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Carmustine, lomustine, semustine, streptozocin
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Used to treat CNS tumors
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Busulfan
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Alkylates DNA
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Vincristine, vinblastine
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Block microtubule polymerization
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Paclitaxel
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Blocks microtubule breakdown
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Cisplatin, carboplatin
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Crosslinks DNA
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Etoposide, teniposide
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Inhibits topoisomerase II
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Hydroxyurea
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Inhibits ribonucleotide reductase and increases HbF;
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Prednisone
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Unknown but may trigger apoptosis in dividing cells
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Tamoxifen, raloxifene
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Prevents estrogen receptor binding
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Trastuzumab
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Antibody against HER-2 receptor
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Imatinib
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bcr-abl tyrosine kinase
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Rituximab
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Antibody against CD20
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Vemurafenib
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B-raf kinase inhibitor -metastatic melanoma
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Bevacizumab
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VEGF
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Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac
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Reversible COX inhibitor
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Celecoxib
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COX-2 inhibitor
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Acetominophen
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COX inhibitor in the CNS
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Alendronate
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Pyrophosphate analog that inhibits osteoclasts
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Allopurinol
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Xanthine oxidase inhibitor
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Febuxostat
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Xanthine oxidase inhibitor
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Probenecid
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Inhibits reabsorption of uric acid in PCT
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Colchine
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Inhibits microtubule polymerization, preventing neutrophil extravasation
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Etanercept
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TNF-alpha receptor that binds free TNF-alpha
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Infliximab, adalimumab
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Anti-TNF-alpha
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Latanoprost
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PGF2 analog that increases the outflow of aqueous humor
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Morphine, fentanyl, cofeine, heroin, methadone, meperidine, dextromethorphan, diphenoxylate
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Mu opioid agonists that open K channels and close Ca channels, inhibting synaptic transmission
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Butorphanol
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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
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Weak opioid agonist that inhibits serotonin and NE reuptake
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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
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Increases Na channel inactivation and inhibits glutamate release
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Carbamazepine
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Increases Na channel inactivation
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Lamotrigine
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Blocks Na channels
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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)
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Estrogen receptor agonist at bone, inhibits osteoclast activity and stimulates osteoblast activity; used to treat osteoporosis
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Anastrozole, exemestane (mechanism, use, toxicity)
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Aromatase inhibitors; used in breast cancer
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Mifepristone (mechanism, use, toxicity)
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Progesterone receptor antagonist, given with misoprostol for abortion; abortifacient; bleeding, abdominal pain
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Terbutaline (mechanism, use, toxicity)
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Beta-2 agonist, inhibits uterine contractions
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Tamsulosin (mechanism, use, toxicity)
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Alpha-1 antagonist; used to treat BPH
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Sildenafil, vardenafil (mechanism, use, toxicity)
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Phosphodiesterase 5 inhibitors, causing inc. cGMP levels and smooth muscle relaxation; used in erectile dysfunction; impaired blue-green vision, contradindicated with nitrates
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Danazol (mechanism, use, toxicity)
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Partial androgen receptor agonist; used to treat endometriosis and hereditary angioedema; weight gain, acne, hirsutism, low HDL, hepatoxicity
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Treat methemoglobinemia with
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Methylene blue
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Diphenhydramine, dimenhydrinate, chlorpheniramine (mechanism, use, toxicity)
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(First generation) H1 antagonists; used in allergies, motion sickness, insomnia; sedation, antiadrenergic, antiserotonergic, and antimuscarinic effects due to CNS penetration
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Loratadine, fexofenadine, desloratadine, cetrizine (mechanism, use, toxicity)
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H1 antagonists, 2nd gen; used in allergies; less fatigue than 1st gen antihistamines due to decreased CNS penetration
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Albuterol (mechanism, use, toxicity)
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Short-acting beta-2 agonist; asthma
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Salmeterol, formoterol (mechanism, use, toxicity)
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Long-acting beta-2 agonist; asthma; tremor, arrhythmias
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Theophylline (mechanism, use, toxicity)
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Phosphodiesterase inhibitor, increases cAMP and causes bronchodilation; asthma; cardiotoxicity, neurotoxicity
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Ipratropium (mechanism, use, toxicity)
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Muscarinic antagonist, prevents bronchoconstriction; asthma and COPD
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Beclomethasone, fluticasone (mechanism, use, toxicity)
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Inhibit cytokine synthesis, reducing inflammation due to asthma; 1st line for chronic asthma
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Montelukast, zafirlukast (mechanism, use, toxicity)
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Leukotriene receptor antagonists; especially useful in aspirin-induced asthma
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Zileuton (mechanism, use, toxicity)
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Inhibits activity of 5-lipoxygenase, inhibiting leukotriene production; reduces inflammation
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Omalizumab (mechanism, use, toxicity)
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Anti-IgE antibody; used in refractory allergic asthma
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Guaifenesin (mechanism, use, toxicity)
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Thins respiratory secretions
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N-acetylcysteine (mechanism, use, toxicity)
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Loosens mucus plugs; used in CF patients and as an antidote to acetominaphen posioning
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Bosentan (mechanism, use, toxicity)
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Antagonizes endothelin-1 receptors, reducing vascular resistance in the pulmonary vessels; used in pulmonary hypertension
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Dextromethorphan (mechanism, use, toxicity)
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Antagonizes NMDA receptors, inhibiting coughing; produces opioid effects in large doses and carries mild abuse potential
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Pseudoephedrine, phenylephrine (mechanism, use, toxicity)
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Alpha-1 agonists that reduce edema and nasal congestion; rhinitis; hypertension, quick tolerance (recurrence of symptoms despite continued treatment)
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Difference in competitive vs noncompetitve inhibitors?
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competitive = decrease potency, noncompetitive = decrease efficacy.
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What is Km?
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Inverse relation of affinity of enzyme for its substrate.
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What is Vmax?
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Direct proportion to enzyme concentration
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What is bioavailability?
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Fraction of administered drug that reaches systemic circulation unchanged.
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Time to steady state depends on?
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depends on half-life. Does not depend on frequency or size of dose.
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What is rate of elimination in zero order kinetics?
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constant amount eliminated per time.
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Give three drugs that are zero order eliminated.
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PEA - phenytoin, Ethanol, Aspirin.
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What is the rate of elimination for first order kinetics?
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A constant FRACTION is eliminted, variable by concentration!
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How does ionization relate to urine pH?
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Ionzied species are trapped in urine and not resorbed. Neutral can be resorbed.
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How do you treat overdose of weak acid? Give drug examples.
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Treat with Bicarb to make neutral. Exp: phenobarbital, methotrexate, aspirin.
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How do you treat overdose of weak base? Give drug examples.
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Treat with ammonium chloride. exp: amphetamines.
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What is phase I drug metabolism? What pt. population loses this?
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Reduction, Oxidation, hydrolysis with CYP450. Often gives neutral products. Geriatrics lose this phase.
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What is phase II metaboloism? What population depend on this?
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Conjugation (Glucuronidation, Acetylation, and Sulfation.) Gives charged products. Geriatrics depend on this, old people have GAS.
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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). Can be used in haloperiodal O.D, whihc causes torticolliosis. 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
|
(MAGIC ROCKS in GQ) Macrolides, amiodarone, grapefruit juice, isoniazid, cimetidine, ritonavir actue alcohol use, ciprofloxacin, ketoconazole, sulfonamides, gemfibrozil, quinidine.
|
|
|
lists the sulfa drugs
|
(Popular FACTSSS) probenacid, furosemide, acetazolamide, celecoxib, thiazide, sulfonamide antibiotics, sulfaasalazine, sulfonylureas
|
|
|
Difference between peniciliin G and V.
|
G = IV and IM. V = oral.
|
|
|
Penicillin(mechanism,use,toxicity)
|
Bind penicillin-binding proteins(transpeptidases), block cross linking of peptidoglycans;most effective on G+, also N. Meningitidis, Treponema;hypersensitivy reaction, hemolytic anema.
|
|
|
Oxacillin,Naficillin,Dicloxacillin(mechanism,use,toxicity)
|
bind transpeptidases, penicillanse resistant due to bukly r-group blocking B-Lactamse; S. Aureus, except MRSA; hypersensitivity and interstitial nephritis.
|
|
|
Ampicillin, amoxicillin(mecanism,use,toxicity)
|
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.
|
|
|
Which has better bioavailibility; amoxicllin or ampicillin?
|
amOxicllin has better Oral bioavilability.
|
|
|
What does clavulanic acid do?
|
B-lactamse inhibitor
|
|
|
Ticarcillin,piperacillin(mechanism,use,toxicity)
|
transpeptidase inhibitor but extended spectrum;pseduomonas and g- rods, use with claculanic acid due to B-lactamse suspectibilty; hypersensitivity reaction.
|
|
|
List the B-lactamse inhibitors
|
(CAST) Clavulanic Acid, Sulbactam,Tazobactem.
|
|
|
Cephalosporin(mechanism,use,toxiciity)
|
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.
|
|
|
give use of cefazolin, cephalexin.
|
1st generation cephalosporins. PEcK. Proteus, E.coli,Klebsiella. Cefazolin used preop to prevent A.aureus infections.
|
|
|
give use of cefoxitin, cefaclor,cefuroxime`
|
2nd generation cephalosporins. HEN PEcKs. H.ib, Enterbacter, Neisseria, Proteus, E.coli,Klebsiella, Serratia.
|
|
|
give use of ceftriaxone, cefotaxime,ceftazidime
|
3rd gen. cephalosporins. Serious gram - infections. Ceftriaxone = meningitis and gonorrhea. Ceftazidime = pseudomonas.
|
|
|
give use of cefepime.
|
increased activity against pseudomonas and G+ bugs.
|
|
|
Aztreonam(mechanism,use,toxicty)
|
a monobactem resistant to B-lactamases, prevents binding to PBP3 and is synergistic with aminoglycosides;gram - rods only;very nontoxic, some GI upset.
|
|
|
what transpeptidase inhibitor can be used in penicillin allergy?
|
aztreonam.
|
|
|
imipenem/cilastatin,meropenem,etrapenem,doripenem(mechanism,use,toxicity)
|
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.
|
|
|
Vancomycin(mechanism,use,toxicty)
|
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.
|
|
|
How is redman syndrome prevented in vancomycin use?
|
slow infusion and rate and antihistamines.
|
|
|
How does vancomycin resistant occur?
|
amino acid change of D-ala D-ala to D-ala D-lac.
|
|
|
List antibiotic protein synthesis inhibitors
|
AT 30, CCEL at 50. 30S = Aminoglycosides, Tetracyclines. 50S = Chloramphenicol, Clindamycin, Erythromycin, Linezolid.
|
|
|
Gentamicin, neomycin, amikacin,tobramycin,streptomycin(mechanism,use,toxicity)
|
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.
|
|
|
how does resistenace to aminoglycosides occur?
|
transferase enzymes that inactivate the drug by acetylation, phosphorylation, or adenylation.
|
|
|
tetracycline, doxycycline, demecycline,minocycline(mechanism, use, toxicity)
|
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.
|
|
|
how does resistance to tetracyclines occur?
|
decrease uptake into cells or increased efflux by pumps.
|
|
|
Azithromycin, clarithromycin, erythromycin(mechanism,use,toxicity)
|
bacteriostatic, blocks translocation; atypical pneumonias, chlamydia, gram + cocci; MACRO: increased Motility, arrhythmia, Cholestatic hepatitis, Rash, eOsinophilia.
|
|
|
how does resitance to macrolides occur?
|
methylation of 23s rRNA binding site.
|
|
|
Chloramphenicol(mechanism,use,toxicity)
|
Bacterialstatic, blocks peptidlytransferase; Meningitis in adults, used in power countries due to being cheap; dose dependent anemia, dose independent aplastic anemia, gray baby syndrome.
|
|
|
what causes grey baby syndrome?
|
use of chloramphenicol in premature infants, they lack UDO-glucuronyl-transferase.
|
|
|
How does resistance to chloramphenicol occur?
|
plasmid-encoded acetyltransferase.
|
|
|
clindamycin(mechanism,use,toxicity)
|
Bacteriostatic. Blocks peptide transfer; anaerobic infections in lung infections and oral anerobes; C. Diff infection, fever, diarrhea.
|
|
|
Sulfamethoxazole(SMX), sulfisoxazole, sulfadiazine(mechanism, use, toxicity)
|
Bacteriostatic, PABA metabolites inhibit dihydropteroate synthase; Gram +, G-, Nocardia, Chlamydia, UTI; hypersensitivty, hemolysis in G6PD, nephrotoxic, kernicterus, displaces other drugs from albumin.
|
|
|
how does resistance to sulfonamides occur?
|
altered bacterial dihydropteroate or increased PABA synthesis.
|
|
|
Trimethoprim(mechanism,use,toxicity)
|
Bacteriostatic, inhibits bacterial dihydrofolate reductase, blocks folate synthesis; used in UTI, PCP (prophylacis and treatment), shigella, salmonella; megaloblastic anemia, leukopenia, granulocytopenia.
|
|
|
ciprofloxacin, norfloxacin, levofloxacin, etc...(mechanism, use, toxicity)
|
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.
|
|
|
how does resistance to fluroquinolones occur?
|
mutation in DNA gyrase or efflux pumps.
|
|
|
What groups are susceptible to fluorquinolone tendon rupture?
|
older than 60 or taking prednisone
|
|
|
Metronidazole(mechanism, use, toxicity)
|
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.
|
|
|
Isoniazid(mechanism,use,toxicity)
|
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.
|
|
|
Rifampin(mechanism,use,toxicity)
|
inhibits DNA-dependent RNA polymerase; TB, Leprosy, prophylaxis in meningococcus and Hib type B; hepatotox, p450 inducer, orange body fluids.
|
|
|
Pyrazinamide(mechanism, use, toxicity)
|
unknown; TB; hyperuricemia, hepatotoxic.
|
|
|
Ethambutol(mechanism,use,toxicity)
|
decreased carbohydrate polymerization of TB cell wall, blocks arabinosyltransferase; TB; optic neuropathy(red-green color blindness_
|
|
|
Amphotericin B(mechanism, use, toxicity)
|
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.
|
|
|
nystatin(mechanism,use,toxicty)
|
binds fungal ergosterol;topical only due to high toxicity, used for oral thrush and topical diaper rash or vaginal candidiasis.
|
|
|
Fluconazole, ketoconazole, clotrimazole, itraconazole, voriconazole(mechanism, use,toxicity)
|
inhibits fungal ergosterol synthesis by binding p450;Fluconazole for suppression of cryptococcus in AIDs patients, itraconazle for blasto, coccio, histo.
|
|
|
Flucytosine(mechanism, use, toxicity)
|
inhibits fungal DNA and RNA synthesis by conversion to 5FU; used in systemic fungal infections, especially cryptococcus; bone marrow suppression.
|
|
|
Caspofungin, micafungin(mechanism, use, toxicity)
|
inhibits fungal cell wall synthesis by inhibiting B-glucan synthesis; invasive aspergillosis, candida; flushing via histamine releae.
|
|
|
terbinafine(mechanism,use,toxicity)
|
inhibits fungal squalene epoxidase; treat dermatophytes - toe nail infection especially;abnormal LFT, visual disturbances.
|
|
|
Griseofulvin(mechanism,use,toxicity)
|
interferes with microtubules, stops mitosis in fungi;deposits in keratin so used in superficial infections, stops dermatophytes; teratogenic, carcinogenic, confusion, p450 inducer.
|
|
|
Pyrimethamine use
|
toxoplasmosis
|
|
|
suramin and melarsoprol use
|
trypanosoma brucei
|
|
|
nifurtimox use
|
trypanosoma cruzi
|
|
|
sodium stibogluconate use
|
leshmaniasis
|
|
|
Chloroquine(mechanism,use,toxicity)
|
blocks formation of heme into hemozoin. Heme accumulates and is toxic to plasmodia;used on all species but falciparum(too much resitance); retinopathy
|
|
|
quinidine use
|
lifethreatening malaria
|
|
|
artemether/lumifantrine use
|
p. falciparum killing
|
|
|
Zanamivir,oseltamivir(mechanism,use)
|
inihibits influenza neuraminidase, stops progeny release; treamt of influenze a and b
|
|
|
Ribavarin(mechanism,use,toxicity)
|
inhibits sythesis of guanine nucleotides by competitvely inhibiting IMP dehydrogenase; RSV, chronic hep C; hemolytic anemia, severe teratogen
|
|
|
Acyclovir,valacyclovir(mechanism, use, toxicity)
|
Guanosine analog, inhibits viral DNA polymerase; monophosphorylated by thymidine kinase in HSV/VZV so active in lesions and encephalitis, good for prophylaxis,
|
|
|
Famciclovir use
|
used in herpes zoster active infections
|
|
|
mechanism for resistance to acyclovir
|
mutated viral thymidine kinase
|
|
|
Ganciclovir,valgangciclovir(mechanism,use,toxicity)
|
guanosine analog, 5'-monophosphate formed by CMV viral kinase, inhibits viral DNA polymerase;CMV infections;leukopenia,neutopenia,thrombocytopenia,renal toxicity
|
|
|
mechanism for resistance to acyclovir
|
mutated CMV DNA polymerase or lack of viral kinase
|
|
|
Foscarnet(mechanism,use,toxicity)
|
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
|
|
|
mechanism for resistance to foscarnet
|
mutated DNA polymerase
|
|
|
cidofovir(mechanism,use,toxicity)
|
inhibits DNA polymerase, doesn't require activiation by viral kinase; CMV retenitis, acyclovir resistant HSV; nephrotoxic(coadminister with probenacid and IV saline to reduce toxicity).
|
|
|
HAART consist of what?
|
[2 NRTI] +[1 NNRTI OR 1 protease inhibitor OR 1 integrase inhibitor]
|
|
|
give mechanism and toxicity of protease inhibitors
|
all end in -NAVIR! stops HIV mRNA cleavage into functional parts; hyperglycemia, GI upset, lipodystrophy.
|
|
|
Ritonavir does what to be a "booster"
|
inhibits cytochrome p-450, boosting concentration of other drugs.
|
|
|
Tenofovir, emtricitabine, abacavir, lamivudine, zidovudine, didansoine, stavudine(mechanism,use,toxicity
|
(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.
|
|
|
Nevirapine, Efavirenz, Delavirdine(mechanism,use,toxicity)
|
(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,
|
|
|
Raltegravir(mechanism,use,toxicity)
|
inhibits integrase, which stops HIV integration into host cells;HIV;hypercholesterolemia
|
|
|
Interferons(mechanism,use,toxicity)
|
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.
|
|
|
What antibiotics must be avoided in pregnancy?
|
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)
|
|
|
cause direct toxicity to nerves
|
vincristine and paclitaxil
|
|
|
By what mechanism does isoniazid cause B6(pyridoxine) loss?
|
isoniazid structurally similar to B6, which causes renal excretion of B6 and competes for B6 binding sites.
|
|
|
What medications can be given before Amphotercin B infusion to lessen side effects?
|
antihistamines and antipyretics.
|
|
|
Does digoxin cause hyper or hypokalemia? which states increases patient susceptibility to digoxin toxicity?
|
digoxin causes hyperkalemia. HOWEVER, a HYPOkalemic state increses patient susceptibility to digoxin toxicity.
|
|
|
list signs of ammonia overdose
|
ataxia, slurred speech, somnolence, vomiting
|
|
|
cause restrictive lung disease
|
bleomycin, busulfan, amiodarone, methotrexate
|
|
|
Contrast urine Ca with loop diuretics and thiazides
|
loop diuretics: increased urine Ca via decreased reabsorption. thiazides: decreased urine Ca.
|
|
|
What is a sensitive indicator of alcohol abuse?
|
Serum gamma-glutamyltransferase.
|
|
|
What is the treatment for delirium tremens?
|
benzodiazepenes
|
|
|
Why is the naloxone-buprenorphine combo used for heroin addiction treatment?
|
The naloxone is only active if inected, making it hard to abuse the combo.
|
|
|
What is neuroleptic malignant syndrome? What is the treatment?
|
rigidity, myoglobinuria, autonomic instability. seen with antipsychotics overdose. treatment: dantrolene and bromocriptine (d2 agonist)
|
|
|
What is tardive dyskinesa? Is it reversible?
|
sterotypical oral-facial movements, from long term antipsychotic use. often NOT reversible.
|
|
|
What is serotonin syndrome? what is the treatment?
|
occurs with any drug that increases serotonin (MAO inhibitor, SNRI, TCA) hyperthermia, confusion, myoclonus, cardio collapse, flushing. tx: cyproheptadine (5ht antagonist)
|
|
|
What can long term Phenactin use cause?
|
Translitional cell carcinoma of the bladder
|
|
|
What are the teratogenic effects of ACE inhibitors?
|
renal damage
|
|
|
What are the teratogenic effects of alkylating agents?
|
absence of digits, toes
|
|
|
What are the teratogenic effects of aminoglycosides?
|
CV VIII toxicity
|
|
|
What are the teratogenic effects of carbamazepine?
|
neural tube defects, craniofacial defects
|
|
|
What are the teratogenic effects of diethylstilbestrol?
|
vaginal clear cell adenocarcinoma, congenital mullerian anomalies
|
|
|
What are the teratogenic effects of folate antagonists?
|
neural tube defects
|
|
|
What are the teratogenic effects of lithium?
|
ebstein's anomaly -> atrialized right ventricle
|
|
|
What are the teratogenic effects of phenytoin?
|
fetal hydantoin syndrome->microcephaly,dysmorphic face
|
|
|
What are the teratogenic effects of tetracyclines
|
discolored teeth
|
|
|
What are the teratogenic effects of thalidomide
|
limb defects like flipper arms
|
|
|
What are the teratogenic effects of valproate?
|
inhibitor of maternal folate absorption ->neural tube defects
|
|
|
What are the teratogenic effects of warfarin?
|
bone deformities, fetal hemorrhage, abortion
|
|
|
At what time period is a fetus most susceptable to teratogens?
|
3rd -8th week.
|
|
|
What are the teratogenic effects of vitamin a?
|
extremely high risk for spontaneous abortion
|
|
|
What are the teratogenic effects of cocaine?
|
placental abruption, developmental abnormalities
|
|
|
What are the teratogenic effects of smoking?
|
preterm labor, placental problems, ADHD
|
|
|
What drug is the leading cause of birth defects and mental retardation?
|
alcohol
|
|
|
What are the toxicities of Loop diuretics?
|
(OH DANG) Ototox, hypokalemia, dehydration, allergy(sulfa), Nephritis, Gout
|
|
|
What are the toxicites of HCTZ?
|
(hyperGLUC) hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia.
|
|
|
By what mechanisms do thiazides and loop diutetics cause metabolic alkalosis?
|
1. Volume contraction ->AT II increases ->increased bicarb absorbed in PT. 2. K loss leads to K leaving all cells and thus H entering all cells. 3. in a low K state, H is exchanged instead of K for Na in the CCT leading to paradoxical aciduria.
|
|
|
What drugs can stimulate prolactin secretion?
|
OCP and dopemaine antagonists (antipsychotics)
|
|
|
What is a difference in the mechanism of PTU and methimazole?
|
PTU disables peroxidase AND 5'-deiodinase. Methimazole only inhibits peroxidase.
|
|
|
Can sulfonylureas be used in type 1 DM?
|
NO, they require some islet function to release insulin. type 1 - those cells are dead.
|
|
|
What drugs can be used to treat type 1 AND 2 DM?
|
Insulins, amylin analongs(pramlintide).
|
|
|
What drug is used to prevent tumor lysis urate neuropathy?
|
allopurinol stops urate crystal collection -> no gout.
|
|
|
List acute and chronic gout drugs.
|
acute: NSAID, indomethicin. Chronic: allopurinol, febuxostat, probenacid, colchicine
|
|
|
probenacid(mechanism, use, tox)
|
used in chronic gout; inhibits reabsorption of uric acid in the proximal tubule; inhibits secretion of penicillin; do NOT use in renal dysfunction.
|
|
|
febuxostat(use, mechanism)
|
used in chronic gout, inhibits xanthine oxidase.
|
|
|
Polymixin B(mechanism, use, toxicity)
|
binds to G- cell membrane phospoholipids, disrupting them; only works in g-; peripheral neuropathy, dizziness, nsytagmus, nephrotoxicity.
|
|
|
Methylphenidate, destroamphetamine, methamphetamine(mechanism, use)
|
increase catecholamines at synaptic cleft, especially NE + dopamine; ADHD, nacrolepsy, appetite control
|
|
|
Phytonadione(use)
|
this is vitamin K, used in warfarin overdose
|
|
|
Leucovorin(use,mechanism)
|
folinic acid, it is a metabolite of folic acid; given with methotrexate to replish the body's folate stores.
|
|
|
Protamine sulfate (use, mechanism)
|
antidote to heparin overdose. Protamine is a postive ion that binds to negative heparin, inactivating it.
|
|
|
What is tyramine crisis caused by?
|
When someone taking MAO inhibitors eats hard cheeses and drinks wine, causing a crisis.
|
|
|
Why is phenoxybenzamine prefered over phentolamine for presurgery pheochromocytoma surgery?
|
it has a MUCH longer half life, plus it is irrversible while phentolamine is reversible
|
|
|
Why is Lactulose fed to people with hepatic encephalopathy?
|
It is broken down in the gut into an acid. This acid acts as both as osmotic (draws out some ascites) and also it gets rid of excess ammonia, which is causing the encephalopathy.
|
|
|
Eculizumab(mechanism, use)
|
Complement inhibitor, used in Paroxysmal Nocturnal Hemoglobinuria.
|
|
|
Cladribine(mechanism, use)
|
adenosine analog, used in treatment of hairy cell leukemia
|
|
|
Trans-retinoic acid(use)
|
Used in treating the M3, promyelocytic subtype of AML.
|
|
|
Is an increase in serum creatinine normal after starting ACE inhibitors?
|
Yes, they lower GFP by stopping efferent arteriole constrinction. Creatinine can increase up to 30% and should peak by 1 weak. This can be BAD in renal artery stenosis, where ACE II is what is keeping the kidney alive.
|
|
|
Daptomycin(mechanism, use, toxicity)
|
causes depolarization of cellular membrane; used in invasive MRSA; myopathy, raised CPK, inactivated by pulmonary surfactant
|
|
|
Ondansetron acts on 5HT3 receptors in what location, in order to decrease nausea?
|
chemoreceptor trigger zone (area postrema), the solitary nucleus, and in the presynpatic vagus nerve.
|
|
|
Why must mu agonists be avoided in suspected pancreatic or biliary pain?
|
They cause constriction of the spinchter of oddi -> increased billiary pressures -> billiary colic.
|
|
|
What drugs inhibit dihydrofolate reductase?
|
trimethoprim, methotrexate, pyrimethamine.
|
|
|
Varenicline(mechanism, use)
|
partial agonist for nicotinic aCh channels in CNS. fights with ciggeratte nicotine for channel. reduces nicotine withdrawl cravings while attenuating the rewarding effects.
|
|
|
What class of drug can precipitate mania in those with bipolar disorder?
|
antidepressants
|
|
|
What is the treatment for sleep enuresis?
|
Desmopression (sleep enuresis = bed wetting)
|
|
|
In general, what is the best drug to use for edema of any kind?
|
furosemide. TAL of Henlee absorbs the most NA here compared to where over diuretics work. will reduce edema quickly.
|
|
|
Which drug used for hyperthyroidism decreases peripheral T3->T3 conversion?
|
PTU does. Methimazole does NOT.
|
|
|
Can atropine be used to block gastric secretions? why or why not?
|
NO. G cells are under vagal influence but they do not use ACh as a neurotransmitter. Instead, they use GRP.
|
|
|
Fomepizole(mechanism, use)
|
Inhibits alcohol dehydrogenase; used as an antidote to methanol or ethylene glycol poisoning.
|
|
|
Disulfiram(mechanism, use)
|
Inhibits acetaldehyde dehydrogenase, makes acetaldehyde accumulate leading to hanger; used in alcohol abuse.
|
|
|
What can be given to those suffering from hyperammonia caused by a metabolic derangement?
|
Benzoate or Phenylbutyrate will bind amino acids and lead to excretion.
|
|
|
What is first dose effect, typically seen in A1 blockers?
|
On first dose, patient gets severe hypotension. Correct this by starting with a small dose.
|
|
|
Which nitrate can be given PO?
|
Isosorbide mononitrate can be swallowed. It has an almost 100% biavailability that way. Others cannot due to first pass metabolism.
|
|
|
Colchine stops what specific cell to decrease gout symptoms?
|
Stops chemotaxis of neutrophils
|
|
|
What is the first line drug used to treat hypertension in pregnancy?
|
methlydopa
|
|
|
Why is MRSA resistant to Naficillin but normal S. Aureus is not?
|
All S. Aureus has Beta-lactamases. Naficillin fights this. But MRSA has this AND altered penicillin binding proteins, which prevents Naficillin from working in MRSA.
|
|
|
Palizumab(mechanism, use)
|
antibody against F protein, prevents pneumonia from RSV in infants
|
|
|
Rhogam(mechanism, use)
|
IgG anti-RH antibodies. given to mom at 28 weeks and also at birth, it sticks to the RH antigens in the MOM's blood, keeping her from developing antibodies.
|
|
|
Entacapone, Tolcapone (mechanism, use, tox)
|
COMT blockers, which increase DOPA levels; Both stop peripheral methylation and only Tolcapone stops central methylation; tolcapone causes hepatotoxicity
|
|
|
What opioid effect is most resistant to tolerance?
|
Constipation
|
|
|
Aldesleukin (mechanism, use)
|
IL 2; used in RCC, metastaic melanoma
|
|
|
Epoetin Alfa(mechanism, use)
|
erythropoietin; anemias, especially in renal failure
|
|
|
Filgrastim, Sargramostim (mechanism, use)
|
Fil = GC-SF, Sar = GM-CSF; both used in recovery of bone marrow, aplastic anemia
|
|
|
alpha-inerferon(use)
|
hepatitis B and C, Kaposi sarcoma, Leukemias, Malignany Melanoma
|
|
|
B-Interferon(use)
|
Multiple sclerosis
|
|
|
gamma-interferon(use)
|
Chronic Granulamatous disease
|
|
|
Oprelvekin(mechanism, use)
|
IL-11; thrombocytopenia
|
|
|
thromopoietin(use)
|
thrombocytopenia
|
|
|
Muromonab-CD3 (mechanism, use)
|
antibody to CD3; used in acute transplant rejection
|
|
|
Digoxin Immune Fab(mechanism, use)
|
antibody to digoxin; used as antidote to digoxin intoxication
|
|
|
Rasburicase (mechanism, use)
|
Recombinat version of Urate oxidase, breaks uric acid down into allantoin; use in tumor lysis syndrome and gout
|
|
|
denosumab(mechanism, use)
|
monoclonal anitbody that binds to RANKL and prevents its interaction with RANK, inhibiting osteoclasts; decreases bone loss in bone mets
|
|
|
What keeps heparin from crossing the placental barrier?
|
It's high water solubility. Things with a high lipid solubility (unconjugated bilirubin) tend to cross the placenta while things with high water solubility(conjugated bilirubin) tend to not. binds albumin = probably lipid soluble
|
|
|
cyclosporine(mechanism, use, toxicity)
|
Used in transplant anti-rejected, treatment of graft-vs-host disease, and psoriasis; binds calineurin on T cells, stopping IL2 from being expressed, lowering T cell response; nephtrotox and lymphomma risk
|
|
|
Isotretinoin, tretinoin, Acitretin(mechanism,use,toxicity
|
a retinoid that has immunomodulatory effects, binds nuclear receptors; psorisias and acne; severe teratogen
|
|
|
Calcipotrol(mechanism, use)
|
vitamin D analog; used in topical psoariasis treatment
|
|
|
Orlistat(mechanism, use)
|
Inhibits intestinal lipase, decreasing fat absorption; used to treat obesity
|
|
|
giving what drug 30 minutes before Niacin can help reduce flushing?
|
aspirin. Niacin increases prostaglandin D2. release. asprin blocks this release = lower flushing
|
|
|
Paclitaxil or sirolimus are commonly used in cardiac stents. why?
|
Prevent growth of intima by inhibiting cellular growth = no restenosis
|
|
|
What is the drug used for Pre-eclampsi and ecplamsia?
|
IV magnesium sulfate for seizures
|
|
|
Bortezomib(mechanism,use, toxicity)
|
Protease inhibitor, proteases are overactive in some cancers and can destroy pro-apototic proteins; used in multiple myeloma; peripheral neuropathy
|
|
|
What causes nitroprusside toxicity? What is the antidote?
|
Nitroprusside degrades into cyanide. Give thiosulfide to inactivate.
|
|
|
Memantine(mechanism, use, toxicity)
|
blocks NMDA-type glutamate receptors; used in alzheimers; confusion
|
|
|
What vitamin is used in alzheimer's treatment?
|
Vitamin E (generic name is alpha-tocopherol)
|
|
|
In gas anesthesias, what is the lipid solubility and the blood solubility?
|
Lipid solubility = potency (MAC). Blood solubility = speed of induction.
|
|
|
Calcitrol, calcipotriene, tacalcitol (mechanism, use)
|
topical vitamin D analogs, activate nuclear receptors that inhibit keratinocyte proliferation and enhance keratinocyte differentiation; psoriasis
|
|
|
Usetekinumab(mechanism, use)
|
monoclocal antibody that binds IL-12 and IL-12 thus inhibiting activation of Th1 cd4+ t cells; used in psoriasis
|
|
|
Why is it required to wait 14 days after stoping a MAO-i before starting an SSRI?
|
MAO-inhbitors (phenelzine) inactive the MAO-I enzymes. It takes 2 weeks for them to get re-synthesized. If both SSRI and MAO-I are active at the same time, serotonin syndrome could occur
|
|
|
Lepirudin, Bivalirudin (mechanism, use)
|
from leeches, inhibit thrombin; used as an alternative to heparin in HIT.
|
|
|
Ropinirole, Pramipexole (mechanism, use)
|
are D2 agonists that DON'T need to be activated like l-dopa does; used in parkinsons and restless leg syndrome
|
|
|
what are the uses of amantidine for parkinsons?
|
indirect and direct D agonist, also some anticholingergic functions which reduces tremors
|
|
|
What compound can cause sickling of sickle cell trait RBC's?
|
sodium metabisulite, found as a food additive and sanitizer
|
|
|
How do atypical antipsychotics avoid causing parkinson's symptoms and tardive dyskinesia?
|
They act on D4 instead of D2 receptors -> no risk of tardive dyskinesia or parkinson's like symptoms
|
|
|
Which anti-inflammatories will not impair platlet aggregation? why?
|
Celecoxib. It only impairs COX2. COX1 is predominate in platlets.
|
|
|
Natalizumab(mechanism, use, toxicity)
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binds alpha-4 integrin, which blocks movement of WBC into orgrans;used in crohns and MS; can cause PML and hepatotoxicity.
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What drugs are preferred in medication induced parkinson's treatment? why?
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Anti-muscarinics (Benzotropine). Giving dopamine agonists would exacerbate psychosis.
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What defines induction and potency in gas anesthetics?
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induction = lower solubility in blood, quicker induction. potency = higher with higher lipid solubility =1/MAC.
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