Nitrates (mechanism, use, toxicity) Adverse effects of statins Niacin (mechanism, use, toxicity) Cholestyramine, colestipol, colesevelam (mechanism,

use, toxicity) Ezetimibe Fibrates (gemfibrozil + -fibrates) (mechanism, use, toxicity) Digoxin and digitoxin (mechanism, use, toxicity) Class 1A antiarrhythmics Class 1B antiarrhythmics Class 1C antiarrhythmics Class 1 antiarrhythmics (general mechanism and toxicity) Class 2 antiarrhythmics Class 3 antiarrhythmics Toxicity of amiodarone Class 4 antiarrhythmics Adeosine (mechanism, use, toxicity) Magnseium (mechanism, use, toxicity) Treatment for prolactinoma Treatment of secondary hyperaldosteronism Treatment of carcinoid syndrome Rapid-acting insulins (3) Short-acting insulin (1) Intermediate-acting insulin (1) Long-acting insulins (2) Metformin (mechanism, use, toxicity) Tolbutamide, chlorpropamide (mechanism, use, toxicity) Glyburide, glimepiride, glipizide (mechanism, use, toxicity) Pioglitazone, rosiglitazone (mechanism, use, toxicity) Acarbose, miglitol (mechanism, use, toxicity) Pramlintide (mechanism, use, toxicity)

Cause NO release -> vasodilation (veins >>> arteries); used in angina; fast tolerance, hypotension, flushing, headache Hepatoxicity and muscle breakdown Inhibits lipolysis and reduces VLDL secretion, lowering LDL and raising HDL; hyperlipidemia; flushing and hyperuricemia Inhibits reabsorption of bile acids -> lower LDL with slight increase in HDL; unpigmented gallbladder stones and malabsorption Prevents cholesterol reabsorption -> lower LDL Upregulates LPL -> lower triglycerides, slightly inc. HDL and slightly dec. LDL; myositis and hepatoxicity Inhibits Na/K ATPase -> indirectly inhibits Na/Ca exchanger -> inc. calcium levels -> inc. contractility; stimulates the vagus; causes cholinergic symptoms and hyperkalemia Quinidine, procainamide, and disopyramide; inc. AP duration and QT interval; can cause torsades de pointes, cinchonism (qunidine), procainamide (druginduced lupus) Lidocaine, mexiletine, and tocainide; dec. AP duration especially in depolarized/ischemia tissue; best following MI Flecainide, propafenone; no effect on AP, used in ventricular tachycardias; do not use post-MI due to risk for arrhythmias Blocks Na channels, decreasing the slope of phase 0 depolarization; toxicity exacerbated by hyperkalemia Beta-blockers; reduces cAMP, slowing SA and AV node activity, increases PR interval; adverse effects include impotence, asthma exacerbation, sedation Amiodarone, ibutilide, dofetilide, sotalol; K channel blockers; inc. AP duration and QT interval Pulmonary fibrosis, hepatotoxicity, thyroid dysfunction Ca channel blockers; verapamil and diltiazem; dec. conduction velocity and inc. PR interval; cause constipation, flushing, and edema Inc. K efflux, hyperpolarizing the cell; used in supraventricular tachycardias; can cause flushing, hypotension, and chest pain Used in torsades de pointes and digoxin toxicity Bromocriptine or cabergoline (dopamine agonists) Spironolactone (or other AT2 antagonist) Octreotide (somatostatin analogues) Lispro, aspart, and glulisine Regular NPH Glargine and detemir Biguanide; unknown mechanism; increases insulin sensitivity and glycolysis and decreases gluconeogenesis; can cause lactic acidosis (don't use in renal failure patients) First-generation sulfonylureas; close beta-cell K channels, causing depolarization and increased insulin release; causes disulfuram-like effects Second-generation sulfonylureas; close beta-cell K channels, causing depolarization and increased insulin release; causes hypoglycemia Thiazolidinediones; activates PPAR-gamma, increasing insulin sensitivity and adiponectin levels; causes weight gain, hepatotoxicity, and heart failure Alpha-glucosidase inhibitors; prevent sugar hydrolysis and absorption, reducing blood sugar levels Amylin analog; reduces glucagon secretion; causes hypoglycemia

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Cardio Cardio Cardio Cardio Cardio Cardio Cardio Cardio Cardio Cardio Cardio Cardio Cardio Cardio Cardio Cardio Cardio Endocrine Endocrine Endocrine Endocrine Endocrine Endocrine Endocrine Endocrine Endocrine Endocrine Endocrine Endocrine Endocrine

Exenatide, liraglutide (mechanism, use, toxicity) Linagliptin, saxagliptin, sitagliptin (mechanism, use, toxicity) Propylthiouracil (mechanism, use, toxicity) Methimazole (mechanism, use, toxicity) Levothyroxine, triiodothyronine (mechanism, use, toxicity) Oxytocin (mechanism, use, toxicity) Demeclocycline (mechanism, use, toxicity) Glucocorticoids (mechanism, use, toxicity) Cimetidine and ranitidine (mechanism, use, toxicity) -prazoles (mechanism, use, toxicity) Bismuth, sucralfate (mechanism, use, toxicity) Misoprostol (mechanism, use, toxicity) Octreotide (mechanism, use, toxicity) Toxicity of long-term antacid use Infliximab (mechanism, use, toxicity) Sulfasalazine (mechanism, use, toxicity) Ondansetron (mechanism, use, toxicity) Metoclopramide (mechanism, use, toxicity) Can be used to prevent mast cell degranulation Treatment of lead poisoning Heparin (mechanism, use, toxicity) Enoxaparin, dalteparin (mechanism, use, toxicity) Warfarin (mechanism, use, toxicity) Alteplase, reteplase, tenecteplase (mechanism, use, toxicity)

GLP-1 analogues; increase insulin, decrease glucagon secretion; causes pancreatitis DPP-4 inhibitors; increase insulin, decrease glucagon secretion; causes mild urinary/respiratory infections Blocks thyroid peroxidase and 5'-deiodinase; used to treat hyperthyroidism; causes agranulocytosis, aplastic anemia, hepatotoxicity Blocks thyroid peroxidase; used to treat hyperthyrodism; teratogenic Thyroid hormone analogs; causes thyrotoxicosis Used to control uterine hemhorrage ADH antagonist used to treat SIADH; can cause photosensitivty and bone/teeth abnormalities Inhibits phospholipase A2 activity and expression of COX-2; used for immune suppression; can cause Cushing's syndrome, adrenal insufficiency (if withdrawn quickly) H2 antagonists; used to treat hyperchloridia; cimeditine is a P-450 inhibitor and has antiandrogenic effects, both reduce creatinine secretion Irreversibly inhibit the H/K pump; used to treat hyperchloridia; increased risk of C. difficile infection and hypomagnesemia Coats ulcer base and protects underlying tissue PGE1 analog that decreases acid production and increases bicarb production; used to prevent NSAID ulcers; abortifacient Somatostatin analog; used to treat VIPoma and carcinoid syndrome Hypokalemia Anti-TNF; used to treat IBD and RA; can cause activation of latent microbes Combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (antiinflammatory); used to treat IBD; causes oligospermia 5-HT3 antagonist; used as an antiemetic D2 antagonist; used to increase gut muscle activity and as an antiemetic; causes parkinson signs Cromolyn sodium Dimercaprol and EDTA, succimer in kids Activates antithrombin, which inactivates thrombin and Xa; used for immediate coagulation and in pregnant women; some patients develop antibodies to platelet factor 4 (HIT) 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 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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Endocrine Endocrine Endocrine Endocrine Endocrine Endocrine Endocrine Endocrine GI GI GI GI GI GI GI GI GI GI Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc

Converts plasminogen to plasmin; used as a thrombolytic Irreversibly inhibits COX-1 and COX-2; anti-platelet and anti-inflammatory; Aspirin (mechanism, use, toxicity) gastric ulcers, tinnitus, Reye's syndrome in childhood viral infections Clopidogrel, ticlodipine, prasugrel, ticagrelor Irreversibly blocks ADP receptors on platelets, preventing degranulation; used (mechanism, use, toxicity) for acure coronary syndrome; ticlodipine causes neutropenia Cilostazol, dipyridamole (mechanism, use, Phosphodiesterase inhibitor, increases cAMP and decreases ADP, preventing toxicity) platelet degranulation; nausea, headache, facial flushing, hypotension

Abciximab, eptifibatide, tirofiban (mechanism, use, toxicity) Methotrexate (mechanism, use, toxicity) 5-fluorouracil (mechanism, use, toxicity) Cytarabine (mechanism, use, toxicity)

Azathioprine, 6-mercaptopurine, 6thioguanine (mechanism, use, toxicity) Dactinomycin (actinomycin D) (mechanism, use, toxicity) DNA intercalator; used for childhood tumors; myelosuppression Doxorubicin (Adriamycin), daunorubicin Generates free radicals that cause DNA strand breaks; dilated cardiomyopathy (mechanism, use, toxicity) (Dexrazoxone, an iron chelator, prevents this), myelosuppression, alopecia Generates free radicals that cause DNA strand breaks; pulmonary fibrosis with Bleomycin (mechanism, use, toxicity) minimal myelosuppression Cyclophosphamide, ifosfamide (mechanism, Crosslinks DNA (must be activated by liver); myelosuppression, hemhorragic use, toxicity) cystitis (can be minimized with mesna) Carmustine, lomustine, semustine, streptozocin (mechanism, use, toxicity) Used to treat CNS tumors Busulfan (mechanism, use, toxicity) Alkylates DNA; pulmonary fibrosis, hyperpigmentation Vincristine, vinblastine (mechanism, use, Block microtubule polymerization; vincristine causes neurotoxicity, vinblastine toxicity) causes bone marro suppression Paclitaxel (mechanism, use, toxicity) Blocks microtubule breakdown; myelosuppression Cisplatin, carboplatin (mechanism, use, Crosslinks DNA; nephrotoxicity (minimize with chloride diuresis, amifostine), toxicity) acoustic n. damage Etoposide, teniposide (mechanism, use, toxicity) Inhibits topoisomerase II; myelosuppression, GI upset, alopecia Inhibits ribonucleotide reductase and increases HbF; used in cancers and Hydroxyurea (mechanism, use, toxicity) HbSS disease; bone marrow suppression Prednisone (mechanism, use, toxicity) Unknown but may trigger apoptosis in dividing cells; Cushingoid symptoms Prevents estrogen receptor binding; used in breast cancer and prevention of Tamoxifen, raloxifene (mechanism, use, osteoporosis; tamoxifen increases the risk of endometrial cancer due to toxicity) agonist effects. Raloxifene = no increase in endometrial cancer. Trastuzumab (mechanism, use, toxicity) Antibody against HER-2 receptor; cardiotoxicity Imatinib (mechanism, use, toxicity) Antibody against bcr-abl tyrosine kinase Antibody against CD20; used to treat non-Hodgkin's lymphoma and Rituximab (mechanism, use, toxicity) rheumatoid arthritis Vemurafenib (mechanism, use, toxicity) B-raf kinase inhibitor (V600 mutation); used in metastatic melanoma Bevacizumab (mechanism, use, toxicity) Antibody against VEGF Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac (mechanism, use, Reversible COX inhibitor; gastric ulcers, renal ischemia (due to constriction of toxicity) afferent arteriole) Reversible COX-2 inhibitor; anti-inflammatory without damage to gastric Celecoxib (mechanism, use, toxicity) mucosa; sulfa allergy, thrombosis Acetominophen (mechanism, use, toxicity) COX inhibitor in the CNS (not anti-inflammatory); causes hepatic necrosis Pyrophosphate analog that inhibits osteoclasts; used to treat osteoporosis, Alendronate (mechanism, use, toxicity) hypercalcemia, and Paget's disease; corrosive esophagitis Allopurinol (mechanism, use, toxicity) Xanthine oxidase inhibitor, reduces production of uric acid Febuxostat (mechanism, use, toxicity) Xanthine oxidase inhibitor

GPIIb/IIIa inhibitors, preventing platelet aggregation; bleeding, thrombocytopenia Inhibits dihydrofolate reductase, inhibiting DNA synthesis; myelosuppression, macrovesicular fatty change in liver Pyrimidine analog that is activated and inhibits thymidylate synthase, inhibiting DNA synthesis; myelosuppression, photosensitivity Pyrimidine analog that inhibits DNA polymerase; leukopenia, thrombocytopenia, megaloblastic anemia 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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Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc Heme/Onc

Pharmacology Musculoskeletal Pharmacology Musculoskeletal Pharmacology Musculoskeletal Pharmacology Musculoskeletal Pharmacology Musculoskeletal Pharmacology Musculoskeletal

Probenecid (mechanism, use, toxicity) Colchine (mechanism, use, toxicity) Etanercept (mechanism, use, toxicity) Infliximab, adalimumab (mechanism, use, toxicity)

Inhibits reabsorption of uric acid in PCT Inhibits microtubule polymerization, preventing neutrophil extravasation TNF-alpha receptor that binds free TNF-alpha Anti-TNF-alpha antibody PGF2 analog that increases the outflow of aqueous humor; can cause darkening of the iris

Pharmacology Musculoskeletal Pharmacology Musculoskeletal Pharmacology Musculoskeletal Pharmacology Musculoskeletal Pharmacology Pharmacology Pharmacology Pharmacology Pharmacology Pharmacology Pharmacology Pharmacology Neurology Neurology Neurology Neurology Neurology Neurology Neurology Neurology

Latanoprost (mechanism, use, toxicity) Morphine, fentanyl, cofeine, heroin, methadone, meperidine, dextromethorphan, Mu opioid agonists that open K channels and close Ca channels, inhibting diphenoxylate (mechanism, use, toxicity) synaptic transmission; addiction, respiratory depression, constipation, miosis Mu opioid partial agonist; used to treat severe pain; causes withdrawal if Butorphanol (mechanism, use, toxicity) being treated with full agonist Weak opioid agonist that inhibits serotonin and NE reuptake; increases risk for Tramadol (mechanism, use, toxicity) seizures First-line therapy for simple partial seizures Carbamazepine First-line therapy for complex partial seizures Carbamazepine First-line therapies for tonic-clonic seizures (3) Carbamazepine, phenytoin, valproate First-line therapy for absence seizures Ethosuximide 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, Phenytoin (mechanism, use, toxicity) teratogenic, drug-induced lupus, P450 inducer Increases Na channel inactivation; first-line for simple, complex, and tonicclonic seizures and trigeminal neuralgia; agranulocytosis, aplastic anemia, Carbamazepine (mechanism, use, toxicity) P450 inducer, SIADH, liver toxicity Blocks Na channels; used for simple, complex, and tonic-clonic seizures; Lamotrigine (mechanism, use, toxicity) Steven-Johnson syndrome Inhibits Ca channels; used for simple, complex, and tonic-clonic seizures, Gabapentin (mechanism, use, toxicity) migraine prophylaxis, peripheral neuropathy, bipolar disorder; ataxia Blocks Na channels and increases GABA secretion; used for simple, complex, and tonic-clonic seizures and migraine prevention; mental dulling, kidney Topiramate (mechanism, use, toxicity) stones, weight loss Increases GABA channel action; first-line for simple, complex, and tonic-clonic Phenobarbital (mechanism, use, toxicity) seizures in children; P450 inducer Increases Na channel inactivation and increases GABA levels; first-line for tonic-clonic seizures, used for simplex, complex, tonic-clonic, and myoclonic Valproate (mechanism, use, toxicity) seizures; hepatotoxicity, neural tube defects, weight gain, tremor Blocks thalamic Ca channels; first-line for absence seizures; GI distress, Ethosuximide (mechanism, use, toxicity) Steven-Johnson syndrome Increases frequency of GABA channel opening; first-line for status epilepticus (diazepam, lorazepam), used for eclampsia seizures (diazepam, lorazepam), Benzodiazepines (mechanism, use, toxicity) anxiety, alcohol withdrawl, sleep walking, night terrors; sedation Tiagabine (mechanism, use, toxicity) Inhibits GABA reuptake; used for simple and complex seizures Irreversibly inhibits GABA transaminase, increasing GABA concentration; used Vigabatrin (mechanism, use, toxicity) for simple and complex seizures Levetriacetam (mechanism, use, toxicity) Unknown mechanism; used for simple, complex, and tonic-clonic seizures Phenobarbital, pentobarbial, thiopental, Increase duration of GABA channel opening; induction of anesthesia, sedative; secobarbital (mechanism, use, toxicity) CNS depression, P450 inducer, contraindicated in patients with porphyrias

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Neurology Neurology Neurology Neurology Neurology Neurology Neurology Neurology Neurology Neurology Neurology Neurology Neurology

Triazolam, oxazepam, midazolam (mechanism, use, toxicity) Barbituates vs. benzodiazepines (mechanism) Zolpidem, zaleplon, eszopiclone (mechanism, use, toxicity) Ketamine (mechanism, use, toxicity) Order of sensory loss when using local anesthetics Succinylcholine (mechanism, use, toxicity) Tubocurarine, -curium drugs (mechanism, use, toxicity)

Short-acting benzodiazepines; more addictive potential Increase duration vs. increase frequency BZ1 subtype GABA channel agonists; used to treat insomnia Blocks NMDA receptor; used as an anesthetic; increases cardiac activity, hallucinations, bad dreams Pain -> temperature -> touch -> pressure ACh receptor agonist, produces sustained depolarization and desensitization; used as a paralytic; hypercalcemia, hyperkalemia, malignant hyperthermia

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Neurology Neurology Neurology Neurology Neurology Neurology Neurology Neurology Neurology Neurology Neurology Neurology

ACh antagonists; used as paralytics Inhibits release of Ca from sarcoplasmic reticulum and skeletal muscle; used Dantrolene (mechanism, use, toxicity) to treat malignant hyperthermia and neuroleptic-malignant syndrome Converted to dopamine by dopa decarboxylase in CNS/inhibits peripheral Levodopa/carbidopa (mechanism, use, dopa decarboxylase activity; used to treat parkinson symptoms; can cause toxicity) arrhythmias and "on/off" phenomenon MAO-B (prefers dopamine for breakdown) inhibitor, inhibits dopamine breakdown; used to treat parkinson symptoms; enhances adverse effects of Selegiline (mechanism, use, toxicity) levodopa Donepezil, galantamine, rivastigmine ACh esterase inhibitors; used to treat Alzheimer's disease; cholinergic (mechanism, use, toxicity) symptoms Agonist at 1B/1D serotonin receptors; used to treat acute migraines and Sumatriptan (mechanism, use, toxicity) cluster headaches; coronary vasospasm High potency antipsychotics that antagonize D2 receptors; used to treat schizoprehnia, psychosis, mania, and Tourette's; hyperprolactinemia, anticholinergic symptoms (dry mouth, constipation), extrapyramidal effects Trifluoperzine, fluphenazine, haloperidol (dyskinesia), neuroleptic malignany syndrome, tardive dyskinesia (mechanism, use, toxicity) (haloperidol) Low potency antipsychotics that antagonize D2 receptors; used to treat Chlorpromazine, thioridazine (mechanism, schizophrenia, psychosis, mania, and Tourette's; corneal deposits use, toxicity) (chlorpromazine), retinal desporits (thioridazine) Olanzapine, clozapine, quetiapine, Atypical antipsychotics with unknown mechnism; used for schizophrenia, risperidone, aripripazole, ziprasidone bipolar disorder, OCD, and others; weight gain (olanzapine, clozapine), (mechanism, use, toxicity) agranulocytosis (clozapine), seizures (clozapine), prolonged QT (ziprasidone) Unknown mechanism; used for bipolar disorder and SIADH; tremor, sedation, Lithium (mechanism, use, toxicity) edema, hypothyroidism, polyuria Agonizes 1A serotonin receptors; used for generalized anxiety disorder; no Buspirone (mechanism, use, toxicity) side effects, but takes 1-2 weeks for improvement Block reuptake of serotonin from the synaptic cleft; depression and others; Fluoxetine, paroxetine, sertraline, citalopram sexual dysfunction, sertonin syndrome (hyperthermia, myoclonus, flushing, (mechanism, use, toxicity) diarrhea, seizures) Venlafaxine, duloxetine (mechanism, use, Block reuptake of NE and serotonin from synaptic cleft; depression, diabetic toxicity) neuropathy (duloxetine); hypertension TCAs, block reuptake of NE and serotonin; depression, bewetting -iptyline, -ipramine, doxepin, amoxapine (imipramine), OCD (clomipramine); convulsions, coma, arrhythmias, sedation, (mechanism, use, toxicity) hypotension, anti-cholinergic effects

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Psychiatry Psychiatry Psychiatry Psychiatry Psychiatry Psychiatry Psychiatry Psychiatry

Inhibit breakdown of NE, serotonin, and dopamine; used for atypical Tranylcypromine, phenelzine, isocarboxazid, depression, anxiety, and hypochondriasis; hypertensive crisis (tyramine in selegiline (mechanism, use, toxicity) wine/cheese), don't use with other serotonin agonists Bupropion (mechanism, use, toxicity) Increases NE and dopamine; used for smoking sensation, depression; seizures Alpha-2 antagonist, increases NE and serotonin release, and serotonin receptor agonist; used for depression; sedation, increased appetite with Mirtazapine (mechanism, use, toxicity) weight gain; Maprotiline (mechanism, use, toxicity) Blocks NE reuptake; used for depression; sedation, hypotension Trazodone (mechanism, use, toxicity) Inhibits serotonin uptake; used for insomnia; pripism Osmotic diuretic; used to treat drug overdose and increased ICP; pulmonary Mannitol (mechanism, use, toxicity) edema, CHF Carbonic anhydrase inhibitor; used for glaucoma, metabolic alklalosis; Acetazolamide (mechanism, use, toxicity) hyperchloremic metabolic acidosis, ammonia toxicity, sulfa allergy Inhibits NKCC channel, preventing urine concentration; used in hypertension, CHF, hypercalcemia; ototoxicity, hypokalemia, hypocalcemia, nephritis, gout, Furosemide (mechanism, use, toxicity) sulfa allergy Inhibits NKCC channel; used in patients with furosemide (sulfa) allergy; Ethacrynic acid (mechanism, use, toxicity) hyperuricemia Inhibits NaCl reabsorption in DCT and increases Ca reabsorption; hypertension Hydrochlorothiazide (mechanism, use, and hypercalcinuria; hyperglycemia, hyperlipidemia, hyperuricemia, toxicity) hypercalcemia, sulfa allergy Spironolactone, eplerenone (mechanism, Aldosterone receptor antagonists; hyperaldosteronism, CHF, hypokalemia; use, toxicity) hyperkalemia (arrhythmias), antiandrogen effects with spironolactone Triamterene, amiloride (mechanism, use, toxicity) Block sodium channels in cortical collecting duct; hyperaldosteronism, CHF ACE inhibitor, leads to reduced angiotensin II levels and decreases GFR; Captopril, enalapril, lisinopril (mechanism, prevents heart remodeling, hypertension, CHF; cough, angioedema, transient use, toxicity) creatinine increase, hyperkalemia Losartan, valsartan (mechanism, use, Angiotensin II receptor antagonists; similar to ACE inhibitors, but do not cause toxicity) cough due to normal metabolism of bradykinin 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 Leuprolide (mechanism, use, toxicity) prostate cancer, fibroids, and precocious puberty; antiandrogenic Finasteride (mechanism, use, toxicity) 5-alpha reductase inhibitor; used for BPH and male-pattern baldness Flutamide (mechanism, use, toxicity) Testosterone receptor antagonist; used in prostate cancer Inhibits 17,20-desmolase, stopping sex steroid synthesis; used to treat Ketoconazole (mechanism, use, toxicity) polycystic ovarian syndrome Partial estrogen agonist in the hypothalamus, increases release of LH and Clomiphene (mechanism, use, toxicity) FSH, stimulating ovulation; used for infertility and PCOS Estrogen receptor antagonist at the breast; used for breast cancer; partial Tamoxifen (mechanism, use, toxicity) agonist at the uterus, can cause endometrial hyperplasia Estrogen receptor agonist at bone, inhibits osteoclast activity and stimulates Raloxifene (mechanism, use, toxicity) osteoblast activity; used to treat osteoporosis Anastrozole, exemestane (mechanism, use, toxicity) Aromatase inhibitors; used in breast cancer Progesterone receptor antagonist, given with misoprostol for abortion; Mifepristone (mechanism, use, toxicity) 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

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Psychiatry Psychiatry Psychiatry Psychiatry Psychiatry Renal Renal Renal Renal Renal Renal Renal Renal Renal Reproductive Reproductive Reproductive Reproductive Reproductive Reproductive Reproductive Reproductive Reproductive Reproductive Reproductive

Phosphodiesterase 5 inhibitors, causing inc. cGMP levels and smooth muscle relaxation; used in erectile dysfunction; impaired blue-green vision, contradindicated with nitrates Partial androgen receptor agonist; used to treat endometriosis and hereditary Danazol (mechanism, use, toxicity) angioedema; weight gain, acne, hirsutism, low HDL, hepatoxicity Treat methemoglobinemia with Methylene blue (First generation) H1 antagonists; used in allergies, motion sickness, Diphenhydramine, dimenhydrinate, insomnia; sedation, antiadrenergic, antiserotonergic, and antimuscarinic chlorpheniramine (mechanism, use, toxicity) effects due to CNS penetration Loratadine, fexofenadine, desloratadine, H1 antagonists, 2nd gen; used in allergies; less fatigue than 1st gen cetrizine (mechanism, use, toxicity) 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 Phosphodiesterase inhibitor, increases cAMP and causes bronchodilation; Theophylline (mechanism, use, toxicity) asthma; cardiotoxicity, neurotoxicity Ipratropium (mechanism, use, toxicity) Muscarinic antagonist, prevents bronchoconstriction; asthma and COPD Beclomethasone, fluticasone (mechanism, Inhibit cytokine synthesis, reducing inflammation due to asthma; 1st line for use, toxicity) chronic asthma Montelukast, zafirlukast (mechanism, use, toxicity) Leukotriene receptor antagonists; especially useful in aspirin-induced asthma Inhibits activity of 5-lipoxygenase, inhibiting leukotriene production; reduces Zileuton (mechanism, use, toxicity) inflammation Omalizumab (mechanism, use, toxicity) Anti-IgE antibody; used in refractory allergic asthma Guaifenesin (mechanism, use, toxicity) Thins respiratory secretions Loosens mucus plugs; used in CF patients and as an antidote to N-acetylcysteine (mechanism, use, toxicity) acetominaphen posioning Antagonizes endothelin-1 receptors, reducing vascular resistance in the Bosentan (mechanism, use, toxicity) pulmonary vessels; used in pulmonary hypertension Dextromethorphan (mechanism, use, Antagonizes NMDA receptors, inhibiting coughing; produces opioid effects in toxicity) large doses and carries mild abuse potential Alpha-1 agonists that reduce edema and nasal congestion; rhinitis; Pseudoephedrine, phenylephrine hypertension, quick tolerance (recurrence of symptoms despite continued (mechanism, use, toxicity) 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! Ionzied species are trapped in urine and not resorbed. Neutral can be How does ionization relate to urine pH? resorbed. How do you treat overdose of weak acid? Give drug examples. Treat with Bicarb to make neutral. Exp: phenobarbital, methotrexate, aspirin. Sildenafil, vardenafil (mechanism, use, toxicity)

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Reproductive Reproductive Respiratory Respiratory Respiratory Respiratory Respiratory Respiratory Respiratory Respiratory Respiratory Respiratory Respiratory Respiratory Respiratory Respiratory Respiratory Respiratory General General General General General General General General general general

How do you treat overdose of weak base? Give drug examples. What is phase I drug metabolism? What pt. population loses this? What is phase II metaboloism? What population depend on this? What is efficacy? What is potency? What happends to efficacy when a partial agonist and full agonist are mixed? What is therapetuic index? What is a therapeutic window? What are the two types of Nicotonic receptors? What kind of messenger do they use? Alpha-1 sympathetic receptor (G-protein class, major function) Alpha-2 sympathetic receptor(G-protein class, major function) Beta-1 sympathetic receptor(G-protein class, major function) Beta-2 sympathetic receptor(G-protein class, major function) M-1 Parasymp receptor(G-protein class, major function) M-2 Parasymp(G-protein class, major function) M-3 parasymp(G-protein class, major function) What receptor is responsible for miosis and accomadation? What receptor is responsbile for mydriasis? Dopamine D-1 receptor(G-protein class, major function) Dopamine D-2 receptor(G-protein class, major function) Histamine H-1 receptor(G-protein class, major function) histamine H-2 receptor(G-protein class, major function) vasopression V-1 receptor(G-protein class, major function) vasopression V-2 receptor(G-protein class, major function) Which receptors work via Gq -> Phospholipase C ->Pip2->DAG + IP3? DAG causes activation of what? IP3 causes increase in what?

Treat with ammonium chloride. exp: amphetamines. Reduction, Oxidation, hydrolysis with CYP450. Often gives neutral products. Geriatrics lose this phase. Conjugation (Glucuronidation, Acetylation, and Sulfation.) Gives charged products. Geriatrics depend on this, old people have GAS. maximal effect a drug can produce. amount of drug needed for the same effect. DECREASED efficacy. fight for same binding site, full agonist cant exert full effect. LD50/ED50. Median lethal dose divded by median effective dose. Safer drugs have a higher TI. Minimum effective dose to minimum toxic dose. Think of it as range of 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. q, increase: vasc. smooth muscle contraction, pupillary dilator muscle contraction, intestinal and bladder sphincter contaction. i, decrease: sympathetic outflow, insulin release, lipolysis. increase: platlet aggregation. s, increase: heart rate, contractilty, renin release, lipolysis s, vasodilation, brochodilation, increase: heart rate, contractility, lipolysis, insulin release, aqueous humor production. decrease: uterine tone, ciliary muscle tone. q, CNS, enteric nervouse system.

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i, decease: heart rate, contractility of atria pharmacology increase: exocrine gland secretion (tears, gastric, etc), gut peristalsis, bladder contraction, bronchoconstriction, pupillary spinchter contraction, cilliary muscle contraction. pharmacology Parasympathetic M-3. Sympathetic Alpha-1. s, relaxes renal vascular smooth muscle i, modulates transmitter release especially in brain. q, increase: mucus production, contraction of bronchioles, pruritus, pain. a, increase gastric acid secretion q, increase: vascular smooth muscle contraction s, increase water permeability and reabsorption in kidneys. (V2 found in 2 kidneys). H1,Alpha1,V1,M1,M3. (remember HAVe 1 M&M) Protein Kinase C. Calcium -> smouth muscle contraction pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology

Which receptors work via Gi->Adenyly cyclase ->cAMP ->Protein Kinase A? Which receptors work via Gs->adenylyate cyclase ->cAMP->Protein Kinase A? What does protein kinase A do? What are the two classes of cholinomimetics? Bethanechol(mechanism,use,toxicity) Carbachol(mechanism,use,toxicity) Pilocarpine(mechanism,use,toxicity) methacholine(mechanism,use,toxicity) Neostigmine(mechanism,use,toxicity) pyridostigmine(mechanism,use,toxicity) edrophonium(mechanism,use,toxicity) Physostigmine(mechanism,use,toxicity) Donepezil(mechanism,use,toxicity) signs of cholinesterase inhibitor poisoning. treatment. Parathion(mechanism, treatment) Atropine, homatropine, tropicamide (mechanism, use, toxicity). Benztropine(mechanism,use,toxicity) Scopolamine(mechanism,use,toxicity) Ipratropium,tiotropium (mechanism, use, toxicity) Oxybutynin(mechanism,use,toxicity) Glycopyrrolate(mechanism,use,toxicity) Jimson Weed(mechanism, toxicity) Epinephrine(Mechanism, receptors bound, use, toxicity)

M2, Alpha2, D2. (remember MAD 2's.) Beta1, Beta2, D1, H2,V2. increase calcium release in heart and blocks myosin light chain kinase. 1. direct agonsts 2. indirect agonists (anticholinesterases). Direct cholinomimetic. Postop or neurogenic ileus, urinary retention. COPD+asthma exacerbation, peptic ulcers. Direct Cholinomimetic. Identical to Ach. Glaucoma, pupillary contraction, relief of IOP. COPD+asthma exacerbation, peptic ulcers. Direct Cholinomimetic. Stimulates tears, salvia, sweat. Open and closed-angle glaucoma.COPD+asthma exacerbation, peptic ulcers. Direct Cholinomimetic. challenge test of asthma diagnosis. COPD+asthma exacerbation, peptic ulcers. Indirect cholinomimetic agonist. NO cns penetration. Postop and neurogenic ileus, myasthenia gravis, reversal of NMJ block. COPD+asthma exacerbation, peptic ulcers. indirect cholinomimetic agonist. Long acting myasthenia gravis treatment. COPD+asthma exacerbation, peptic ulcers. indirect cholinomimetic agonist. Short acting, for myasthenia gravis diagnosis. COPD+asthma exacerbation, peptic ulcers. indirect cholinomimetic agonist. for anti-cholinergic overdose, crosses BBB. COPD+asthma exacerbation, peptic ulcers. indirect cholinomimetic agonist. Alzheimers disease. COPD+asthma exacerbation, peptic ulcers. DUMBBELSS (diarrhea, urination, miosis, bronchospasm, bradycardia, excitation of skeletal muscle +CNS, lacrimation, sweating, salvia.) tx: atropine + pralidoxime. Irreversible cholinesterase inhibitor, ACH overdose. Tx: atropine + pralidoxime. 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. 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. 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. 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. 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. 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. muscarinic antagonist, causes gardner's pupil (mydriasis). Direct Sympathomemetic. A1,A2,B1,B2. Anaphylaxis, open angle glaucoma, asthma, hypotension.

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Norepinephine(Mechanism, receptors bound, use, toxicity) Isoproterenol(Mechanism, receptors bound, use, toxicity) dopamine(Mechanism, receptors bound, use, toxicity) dobutamine(Mechanism, receptors bound, use, toxicity) Phenylephrine(Mechanism, receptors bound, use, toxicity) Albuterol, salmetrol, terbutaline (Mechanism, receptors bound, use, toxicity) Ritodrine(Mechanism, receptors bound, use, toxicity) Amphetamine (mechanism, use) Epinephrine(Mechanism, use, toxicity) Cocaine (mechanims, use). Why must B-Blockers be avoided in suspected cocaine intoxication? How does norepinephrine cause reflex bradycardia? How does isoproterenol cause reflex tachycardia?

direct sympathomemetic. A1,A2, some B1. used in hypotension but it decrease renal perfusion. Direct sympathomemetic. B1, B2. Used in Torsade de pointe and bradyarryhmia. Can cause tachycardia and worsen cardiac ischemia. 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). Direct sympathomimetic. Mostly B1, little a1,a2,b2. Used in heart failure and cardiac stresstest (ionotrpic and chronotropic) Direct sympathomimetic. A1, A2. Used in hypotension, to cause mydriasis, and rhinitis (decongestant). Direct sympathomimetic. Mostly B2, some b1. Sal = long term ashtma or copd. Albuterol for short term asthma. Terbutaline for to reduce premture uterine contractions. Direct sympathomimetic. B2 only. Used to reduce premature uterine contractions. indirect sympathomimetic. Releases stored catecholamines. Used for narcolepsy, obesity, ADD. indirect sympathomimetic. Releases stored catecholamines. Used for nasal decongestion, urinary incontience, hypotension. direct sympathomimetic. Reuptake inhibitor. Causes vasoconstriction and local anesthesia.

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mixing them can lead to unopposed A1 activation and extreme hypertenion. stimulates A1>B2. Causes increased vasoconstrciton -> increased BP. This causes reflex bradycardia and slowing of HR. Stimulates B2>A1. This cause vasodilation and dropping of BP. B1 is stimulated and causes tachycardia. Centrally acting alpha-2 agonists, this causes LESS peripheral sympathetic Clonidine, alpha-methyldopa(Mechanism, release.Used in hypertension, especially renal disease due to no increase in receptors bound, use) renal blood flow! Phenoxybenzamine(Mechanism, receptors IRREVERSIBLE nonslective alpha blocker. Used in pheochromosytoma BEFORE bound, use, toxicity) surgery! toxic: orhtostatic hypotension, reflec tachycardia. phentolamine(Mechanism, receptors bound, REVERSBILE nonselective alpha blocker. give to patients on MAOI who each use, toxicity) tyramine contraining foods. Prazosin, Terazosin, Doxazosin,Tamsulosin Alpha-1 blocker. Used in hypertension, urinary rentention in BPH. tox: (Mechanism, receptors bound, use, toxicity) orthostatic hypotension, dizziness, headache. Alpha-2 blocker. Used in depression. tox: sedation, hypercholesterolemia, Mirtazapine (mechanism, use, toxicity) increased apetite. Describe what occurs when you alphaBefore blockade: Both epi and phen RAISES BP. After alpha blockade: only epi blockade epi vs. phenylephrine. raises, no change in phenyl. Why: Epi has B binding, phenyl does NOT. Angina - decreases HR and contractility, decreasing oxygen use. MI - decrease mortality. SVT - decrease AV duction. Hypertension - decrease CO and renin Give 6 applications of Beta-blockers in secretion. CHF - slows progression. Glaucoma - decrease secretion of aqueous general. humor. impotence, asthma exacerbation, bradycardia, seizures, sedation, hides give general toxicites of b-blockers hypoglycemia. What are the B1 selective b-blockers? When A BEAM. acebutolol, betaxolol, Esmolol, Atenolol, Metoprolol. Useful in are they useful? comorbid pum. disease. What are the nonselective ( b1 = b2) bPlease Try Not Being Picky. Propranolol, Timolol, Nadolol, Pindolol. B = Bblockers? blocker.

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what are the nonselective a and bantagonists? 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 (hemolysis IS PAIN)isoniazid, sulfonamides, primaquine, aspirin, ibuprofen, causes hemolysis in G6PD-defiect patients nitrofurantoin (females with PMS are on full BLAST mode) Phenytoin, Methotrexate, Sulfa causes megaloblastic anemia 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

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can lead to adrenocortical insufficiency can causes gynecomastia causes hot flashes causes hypergylcemia causes hypothyroidism causes fat redistribution causes gingival hyperplasia causes gout causes myopathies causes osteoporosis causes photosensitivty causes rash/SJS cause drug induced lupus causes teeth problems causes tendonitis, tendon rupture, tooth damage causes diabetes insipidus causes fanconi's syndome causes hemorrhagic cystits causes interstital nephritis causes SIADH causes cinchonism causes parkinson-like syndome causes seizures causes tardive dyskinesia acts like an anti-muscarinic can cause a disulfiram like reaction can cause nephro/ototoxicity list p450 inducers list p450 inhibitors lists the sulfa drugs Difference between peniciliin G and V. Penicillin(mechanism,use,toxicity) Oxacillin,Naficillin,Dicloxacillin(mechanism, use,toxicity) Ampicillin, amoxicillin(mecanism,use, toxicity)

glucocorticoid withdrawl via HPA suppression `(Some drugs create awkward knockers) spironolactone, digitalis, cimetidine, chronic alcohol use, ketoconazole estrogen, clomophene niacin, tacrolimus, protease inhibitor, HCTZ, corticosteriods lithium, amiodarone, suldonamides glucocoricoids, protease inhibitors phenytoin, verpamil furosemide, thiazides, niacin, cyclosporine fibrates, niacin, colchine, hydroxychloroquine, interferon-alpha, penicillamine, statins, glucocorticoids corticosteroids, heparin (SAT for a PHOTO) Sulfonamides, amiodarone, tetracycline penicillin, ethosuximide, carbamazepine, sulfa drugs, lamotrigine, allopurinol, phenytoin, phenobarbital Hydralazine, isonizid, procainamine, phenytoin tetracyclines fluoroquinolones lithium, demeclocycline expired tetracycline Cyclophosamide, ifosfamide methicllin, NSAID, furosemide carbamazepine, cyclophosamide Quinidine, qunine antipsychotics, resperine, metoclopramide (with seizures, I BITE My tongue) isoniazid, Buproprion, imipenem, Tramadol, Enflurane, Metoclopramide antipsychotics Atropine, TCA, H1-blocker, neuoleptics metronidazole, some cephalosporins, procarbazine, 1st gen sulphonoureas aminoglycosides, vancomycin, loop dieuetics, cisplatin (Momma Barb Steals Phen-phen and Refuses Greasy Carbs Chronically) Modafinil, Barbiturates, St. John wart, phenytoin, rifampin, griseofulvin, carbamazepine, chronic alcohol use. (MAGIC ROCKS in GQ) Macrolides, amiodarone, grapefruit juice, isoniazid, cimetidine, ritonavir actue alcohol use, ciprofloxacin, ketoconazole, sulfonamides, gemfibrozil, quinidine. (Popular FACTSSS) probenacid, furosemide, acetazolamide, celecoxib, thiazide, sulfonamide antibiotics, sulfaasalazine, sulfonylureas G = IV and IM. V = oral. Bind penicillin-binding proteins(transpeptidases), block cross linking of peptidoglycans;most effective on G+, also N. Meningitidis, Treponema; hypersensitivy reaction, hemolytic anema. bind transpeptidases, penicillanse resistant due to bukly r-group blocking BLactamse; S. Aureus, except MRSA; hypersensitivity and interstitial nephritis. 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? What does clavulanic acid do? Ticarcillin,piperacillin(mechanism,use, toxicity) List the B-lactamse inhibitors Cephalosporin(mechanism,use,toxiciity) give use of cefazolin, cephalexin. give use of cefoxitin, cefaclor,cefuroxime` give use of ceftriaxone, cefotaxime, ceftazidime give use of cefepime. Aztreonam(mechanism,use,toxicty) what transpeptidase inhibitor can be used in penicillin allergy?

amOxicllin has better Oral bioavilability. B-lactamse inhibitor transpeptidase inhibitor but extended spectrum;pseduomonas and g- rods, use with claculanic acid due to B-lactamse suspectibilty; hypersensitivity reaction. (CAST) Clavulanic Acid, Sulbactam,Tazobactem. 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. 1st generation cephalosporins. PEcK. Proteus, E.coli,Klebsiella. Cefazolin used preop to prevent A.aureus infections. 2nd generation cephalosporins. HEN PEcKs. H.ib, Enterbacter, Neisseria, Proteus, E.coli,Klebsiella, Serratia. 3rd gen. cephalosporins. Serious gram - infections. Ceftriaxone = meningitis and gonorrhea. Ceftazidime = pseudomonas. increased activity against pseudomonas and G+ bugs. 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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aztreonam. pharmacology broad spectrum, B-lactamase resistent but imipenem needs cilastatin to imipenem/cilastatin,meropenem,etrapenem, inhibit renal dehydropeptidase. later carbepenems do not;G+ cocci,G- rods, doripenem(mechanism,use,toxicity) anerobes. used only in life threating events;skin rash, CNS toxicity, seizures. pharmacology inhibits cell wall binding peptidoglycan formation by binding D-ala percursors, is bacterialcidal; G+ only, especially for multidrug resistant onces;NOT Vancomycin(mechanism,use,toxicty) nephrotoxicity, ototoxicity, thrombophlebitis, red man syndrome. pharmacology How is redman syndrome prevented in vancomycin use? slow infusion and rate and antihistamines. pharmacology How does vancomycin resistant occur? amino acid change of D-ala D-ala to D-ala D-lac. pharmacology AT 30, CCEL at 50. 30S = Aminoglycosides, Tetracyclines. 50S = List antibiotic protein synthesis inhibitors Chloramphenicol, Clindamycin, Erythromycin, Linezolid. pharmacology Gentamicin, neomycin, amikacin, aminoglycosides, bacterialcidal, block translocation but require oxygen for tobramycin,streptomycin(mechanism,use, uptake;ineffective in anaerobes,use in gram - rod infections and before bowel toxicity) surgery; nephrotoxicty, NMJ block, ototoxicity, teratogen. pharmacology how does resistenace to aminoglycosides transferase enzymes that inactivate the drug by acetylation, phosphorylation, occur? or adenylation. pharmacology bacteriostatic, prevents aminoacyl-tRNA binds;Borrela, M. Pneuomo, Rickettsia, Chlamysia; can't take with milk, antacids, iron because ions bind it, tetracycline, doxycycline, demecycline, GI distress, discoloration of teeth, inhibition of bone growth, contraindication minocycline(mechanism, use, toxicity) in pregnancy. pharmacology how does resistance to tetracyclines occur? decrease uptake into cells or increased efflux by pumps. pharmacology bacteriostatic, blocks translocation; atypical pneumonias, chlamydia, gram + Azithromycin, clarithromycin, erythromycin cocci; MACRO: increased Motility, arrhythmia, Cholestatic hepatitis, Rash, (mechanism,use,toxicity) eOsinophilia. pharmacology how does resitance to macrolides occur? methylation of 23s rRNA binding site. pharmacology Bacterialstatic, blocks peptidlytransferase; Meningitis in adults, used in power countries due to being cheap; dose dependent anemia, dose independent Chloramphenicol(mechanism,use,toxicity) aplastic anemia, gray baby syndrome. pharmacology

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plasmid-encoded acetyltransferase. Bacteriostatic. Blocks peptide transfer; anaerobic infections in lung infections clindamycin(mechanism,use,toxicity) and oral anerobes; C. Diff infection, fever, diarrhea. Bacteriostatic, PABA metabolites inhibit dihydropteroate synthase; Gram +, GSulfamethoxazole(SMX), sulfisoxazole, , Nocardia, Chlamydia, UTI; hypersensitivty, hemolysis in G6PD, nephrotoxic, sulfadiazine(mechanism, use, toxicity) kernicterus, displaces other drugs from albumin. how does resistance to sulfonamides occur? altered bacterial dihydropteroate or increased PABA synthesis. Bacteriostatic, inhibits bacterial dihydrofolate reductase, blocks folate synthesis; used in UTI, PCP (prophylacis and treatment), shigella, salmonella; Trimethoprim(mechanism,use,toxicity) megaloblastic anemia, leukopenia, granulocytopenia. 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 ciprofloxacin, norfloxacin, levofloxacin, etc... rupture, superinfections, don't give to kids or pregnant women due to (mechanism, use, toxicity) 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 bacterialcidal, forms free radical toxic metabolites that damge bacterial DNA damage; (GET GAP) Giardia, Entamoeba, trichomonas, Gardnerella, Metronidazole(mechanism, use, toxicity) Anaerobes, Pylori; causes disulfiram like reaction, headache, metallic taste. 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 Isoniazid(mechanism,use,toxicity) antagonist. inhibits DNA-dependent RNA polymerase; TB, Leprosy, prophylaxis in Rifampin(mechanism,use,toxicity) meningococcus and Hib type B; hepatotox, p450 inducer, orange body fluids. Pyrazinamide(mechanism, use, toxicity) unknown; TB; hyperuricemia, hepatotoxic. decreased carbohydrate polymerization of TB cell wall, blocks Ethambutol(mechanism,use,toxicity) arabinosyltransferase; TB; optic neuropathy(red-green color blindness_ binds fungal ergosterol, causes holes in membranes; use in systemtic and CNS mycoses infections; fever/chills, hypotension, arrythmias, nephrotoxic, IV Amphotericin B(mechanism, use, toxicity) phlebitis, must supplement K and MG. binds fungal ergosterol;topical only due to high toxicity, used for oral thrush nystatin(mechanism,use,toxicty) and topical diaper rash or vaginal candidiasis. Fluconazole, ketoconazole, clotrimazole, inhibits fungal ergosterol synthesis by binding p450;Fluconazole for itraconazole, voriconazole(mechanism, use, suppression of cryptococcus in AIDs patients, itraconazle for blasto, coccio, toxicity) histo. inhibits fungal DNA and RNA synthesis by conversion to 5FU; used in systemic Flucytosine(mechanism, use, toxicity) fungal infections, especially cryptococcus; bone marrow suppression. Caspofungin, micafungin(mechanism, use, inhibits fungal cell wall synthesis by inhibiting B-glucan synthesis; invasive toxicity) aspergillosis, candida; flushing via histamine releae. inhibits fungal squalene epoxidase; treat dermatophytes - toe nail infection terbinafine(mechanism,use,toxicity) especially;abnormal LFT, visual disturbances. interferes with microtubules, stops mitosis in fungi;deposits in keratin so used in superficial infections, stops dermatophytes; teratogenic, carcinogenic, Griseofulvin(mechanism,use,toxicity) confusion, p450 inducer. Pyrimethamine use toxoplasmosis

what causes grey baby syndrome? How does resistance to chloramphenicol occur?

use of chloramphenicol in premature infants, they lack UDO-glucuronyltransferase.

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trypanosoma brucei trypanosoma cruzi leshmaniasis blocks formation of heme into hemozoin. Heme accumulates and is toxic to Chloroquine(mechanism,use,toxicity) plasmodia;used on all species but falciparum(too much resitance); retinopathy quinidine use lifethreatening malaria artemether/lumifantrine use p. falciparum killing inihibits influenza neuraminidase, stops progeny release; treamt of influenze a Zanamivir,oseltamivir(mechanism,use) and b inhibits sythesis of guanine nucleotides by competitvely inhibiting IMP Ribavarin(mechanism,use,toxicity) dehydrogenase; RSV, chronic hep C; hemolytic anemia, severe teratogen Guanosine analog, inhibits viral DNA polymerase; monophosphorylated by Acyclovir,valacyclovir(mechanism, use, thymidine kinase in HSV/VZV so active in lesions and encephalitis, good for toxicity) prophylaxis, Famciclovir use used in herpes zoster active infections mechanism for resistance to acyclovir mutated viral thymidine kinase guanosine analog, 5'-monophosphate formed by CMV viral kinase, inhibits Ganciclovir,valgangciclovir(mechanism,use, viral DNA polymerase;CMV infections;leukopenia,neutopenia, toxicity) thrombocytopenia,renal toxicity mechanism for resistance to acyclovir mutated CMV DNA polymerase or lack of viral kinase viral DNA polymerase inhibitor, binds to pyrofosphate binding site, doesn't need viral kinase activation;CMV retinitis when ganciclovir fails and acyclovir Foscarnet(mechanism,use,toxicity) restitant HSV; nephrotoxic mechanism for resistance to foscarnet mutated DNA polymerase inhibits DNA polymerase, doesn't require activiation by viral kinase; CMV retenitis, acyclovir resistant HSV; nephrotoxic(coadminister with probenacid cidofovir(mechanism,use,toxicity) 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 all end in -NAVIR! stops HIV mRNA cleavage into functional parts; inhibitors hyperglycemia, GI upset, lipodystrophy. Ritonavir does what to be a "booster" inhibits cytochrome p-450, boosting concentration of other drugs. (NRTI)competitively blocks binding of nucleotide to reverse transcriptase, only Tenofovir, emtricitabine, abacavir, tenofovir doesn't need to be activated;all NRTIs, zidovidine used in pregnancy lamivudine, zidovudine, didansoine, to reduce fetal transmision; bone marrow suppression, lactic acidosis, stavudine(mechanism,use,toxicity peripheral neuropathy. (NNRTI) bind at a site different from NRTIs, no don't require activation don't Nevirapine, Efavirenz, Delavirdine compete with nucleotides; bonow marrow suppression, peripheral neuropathy, (mechanism,use,toxicity) lactic acidosis, inhibits integrase, which stops HIV integration into host cells;HIV; Raltegravir(mechanism,use,toxicity) hypercholesterolemia 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 Interferons(mechanism,use,toxicity) -NADPH oxidase defiency; neutropenia, myopathy. SAFe Children Take Really Good Care. sulfonamides(kericterus), aminoglycosides(ototox), fluoroquinolones(cartilage damage), Clarithromycin What antibiotics must be avoided in (embryotoxic), Tetracycline(teeth,bone damage),Ribavarin(teratogenic), pregnancy? Griseofulvin(teratogenic),Chloramphenicol(grey baby) cause direct toxicity to nerves vincristine and paclitaxil By what mechanism does isoniazid cause B6 isoniazid structurally similar to B6, which causes renal excretion of B6 and (pyridoxine) loss? competes for B6 binding sites.

suramin and melarsoprol use nifurtimox use sodium stibogluconate use

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What medications can be given before Amphotercin B infusion to lessen side effects? Does digoxin cause hyper or hypokalemia? which states increases patient susceptibility to digoxin toxicity? list signs of ammonia overdose cause restrictive lung disease Contrast urine Ca with loop diuretics and thiazides What is a sensitive indicator of alcohol abuse? What is the treatment for delirium tremens? Why is the naloxone-buprenorphine combo used for heroin addiction treatment?
What is neuroleptic malignant syndrome? What is the treatment? What is tardive dyskinesa? Is it reversible? What is serotonin syndrome? what is the treatment? What can long term Phenactin use cause? What are the teratogenic effects of ACE inhibitors? What are the teratogenic effects of alkylating agents? What are the teratogenic effects of aminoglycosides? What are the teratogenic effects of carbamazepine? What are the teratogenic effects of diethylstilbestrol? What are the teratogenic effects of folate antagonists? What are the teratogenic effects of lithium? What are the teratogenic effects of phenytoin? What are the teratogenic effects of tetracyclines What are the teratogenic effects of thalidomide What are the teratogenic effects of valproate? What are the teratogenic effects of warfarin? At what time period is a fetus most susceptable to teratogens? What are the teratogenic effects of vitamin a? What are the teratogenic effects of cocaine? What are the teratogenic effects of smoking? What drug is the leading cause of birth defects and mental retardation? What are the toxicities of Loop diuretics? What are the toxicites of HCTZ? By what mechanisms do thiazides and loop diutetics cause metabolic alkalosis? What drugs can stimulate prolactin secretion? What is a difference in the mechanism of PTU and methimazole? Can sulfonylureas be used in type 1 DM? What drugs can be used to treat type 1 AND 2 DM? What drug is used to prevent tumor lysis urate neuropathy?

antihistamines and antipyretics. digoxin causes hyperkalemia. HOWEVER, a HYPOkalemic state increses patient susceptibility to digoxin toxicity. ataxia, slurred speech, somnolence, vomiting bleomycin, busulfan, amiodarone, methotrexate loop diuretics: increased urine Ca via decreased reabsorption. thiazides: decreased urine Ca. Serum gamma-glutamyltransferase. benzodiazepenes The naloxone is only active if inected, making it hard to abuse the combo.
rigidity, myoglobinuria, autonomic instability. seen with antipsychotics overdose. treatment: dantrolene and bromocriptine (d2 agonist) sterotypical oral-facial movements, from long term antipsychotic use. often NOT reversible. occurs with any drug that increases serotonin (MAO inhibitor, SNRI, TCA) hyperthermia, confusion, myoclonus, cardio collapse, flushing. tx: cyproheptadine (5ht antagonist) Translitional cell carcinoma of the bladder renal damage absence of digits, toes CV VIII toxicity neural tube defects, craniofacial defects vaginal clear cell adenocarcinoma, congenital mullerian anomalies neural tube defects ebstein's anomaly -> atrialized right ventricle fetal hydantoin syndrome->microcephaly,dysmorphic face discolored teeth limb defects like flipper arms inhibitor of maternal folate absorption ->neural tube defects bone deformities, fetal hemorrhage, abortion 3rd -8th week. extremely high risk for spontaneous abortion placental abruption, developmental abnormalities preterm labor, placental problems, ADHD alcohol (OH DANG) Ototox, hypokalemia, dehydration, allergy(sulfa), Nephritis, Gout (hyperGLUC) hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia. 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. OCP and dopemaine antagonists (antipsychotics) PTU disables peroxidase AND 5'-deiodinase. Methimazole only inhibits peroxidase. NO, they require some islet function to release insulin. type 1 - those cells are dead. Insulins, amylin analongs(pramlintide). allopurinol stops urate crystal collection -> no gout.

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pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology pharmacology psych psych

micro cardio overdose reactions renal psych psych psych

psych renal reactions reactions reactions reactions reactions reactions reactions reactions reactions reactions reactions reactions reactions reactions reactions reactions reactions reactions reactions

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List acute and chronic gout drugs. probenacid(mechanism, use, tox) febuxostat(use, mechanism) Polymixin B(mechanism, use, toxicity) Methylphenidate, destroamphetamine, methamphetamine(mechanism, use) Phytonadione(use) Leucovorin(use,mechanism) Protamine sulfate (use, mechanism) What is tyramine crisis caused by? Why is phenoxybenzamine prefered over phentolamine for presurgery pheochromocytoma surgery? Why is Lactulose fed to people with hepatic encephalopathy? Eculizumab(mechanism, use) Cladribine(mechanism, use) Trans-retinoic acid(use)

acute: NSAID, indomethicin. Chronic: allopurinol, febuxostat, probenacid, colchicine used in chronic gout; inhibits reabsorption of uric acid in the proximal tubule; inhibits secretion of penicillin; do NOT use in renal dysfunction. used in chronic gout, inhibits xanthine oxidase. binds to G- cell membrane phospoholipids, disrupting them; only works in g-; peripheral neuropathy, dizziness, nsytagmus, nephrotoxicity. increase catecholamines at synaptic cleft, especially NE + dopamine; ADHD, nacrolepsy, appetite control this is vitamin K, used in warfarin overdose folinic acid, it is a metabolite of folic acid; given with methotrexate to replish the body's folate stores. antidote to heparin overdose. Protamine is a postive ion that binds to negative heparin, inactivating it. When someone taking MAO inhibitors eats hard cheeses and drinks wine, causing a crisis.

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MSK MSK MSK micro psych heme/onc

heme/onc heme/onc reactions autonomics GI heme/onc heme/onc heme/onc renal micro GI neuro general neuro psych renal renal endocrine GI neuro neuro general cardio cardio GI repro

it has a MUCH longer half life, plus it is irrversible while phentolamine is reversible 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. Complement inhibitor, used in Paroxysmal Nocturnal Hemoglobinuria. adenosine analog, used in treatment of hairy cell leukemia Used in treating the M3, promyelocytic subtype of AML. Yes, they lower GFP by stopping efferent arteriole constrinction. Creatinine can increase up to Is an increase in serum creatinine normal after starting 30% and should peak by 1 weak. This can be BAD in renal artery stenosis, where ACE II is what ACE inhibitors? is keeping the kidney alive. causes depolarization of cellular membrane; used in invasive MRSA; myopathy, raised CPK, Daptomycin(mechanism, use, toxicity) inactivated by pulmonary surfactant Ondansetron acts on 5HT3 receptors in what location, in chemoreceptor trigger zone (area postrema), the solitary nucleus, and in the presynpatic vagus order to decrease nausea? 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. partial agonist for nicotinic aCh channels in CNS. fights with ciggeratte nicotine for channel. Varenicline(mechanism, use) 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 furosemide. TAL of Henlee absorbs the most NA here compared to where over diuretics work. will any kind? 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 NO. G cells are under vagal influence but they do not use ACh as a neurotransmitter. Instead, or why not? they use GRP. Fomepizole(mechanism, use) Inhibits alcohol dehydrogenase; used as an antidote to methanol or ethylene glycol poisoning. Inhibits acetaldehyde dehydrogenase, makes acetaldehyde accumulate leading to hanger; used in Disulfiram(mechanism, use) 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. Isosorbide mononitrate can be swallowed. It has an almost 100% biavailability that way. Others Which nitrate can be given PO? 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

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Why is MRSA resistant to Naficillin but normal S. Aureus is not? Palizumab(mechanism, use)

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. antibody against F protein, prevents pneumonia from RSV in infants IgG anti-RH antibodies. given to mom at 28 weeks and also at birth, it sticks to the RH antigens in Rhogam(mechanism, use) the MOM's blood, keeping her from developing antibodies. COMT blockers, which increase DOPA levels; Both stop peripheral methylation and only Entacapone, Tolcapone (mechanism, use, tox) 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 Recombinat version of Urate oxidase, breaks uric acid down into allantoin; use in tumor lysis Rasburicase (mechanism, use) syndrome and gout monoclonal anitbody that binds to RANKL and prevents its interaction with RANK, inhibiting denosumab(mechanism, use) osteoclasts; decreases bone loss in bone mets 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 = What keeps heparin from crossing the placental barrier? probably lipid soluble 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 cyclosporine(mechanism, use, toxicity) lymphomma risk a retinoid that has immunomodulatory effects, binds nuclear receptors; psorisias and acne; severe Isotretinoin, tretinoin, Acitretin(mechanism,use,toxicity 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 Protease inhibitor, proteases are overactive in some cancers and can destroy pro-apototic Bortezomib(mechanism,use, toxicity) 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. topical vitamin D analogs, activate nuclear receptors that inhibit keratinocyte proliferation and Calcitrol, calcipotriene, tacalcitol (mechanism, use) enhance keratinocyte differentiation; psoriasis monoclocal antibody that binds IL-12 and IL-12 thus inhibiting activation of Th1 cd4+ t cells; used Usetekinumab(mechanism, use) in psoriasis Why is it required to wait 14 days after stoping a MAO-i MAO-inhbitors (phenelzine) inactive the MAO-I enzymes. It takes 2 weeks for them to get rebefore starting an SSRI? 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. are D2 agonists that DON'T need to be activated like l-dopa does; used in parkinsons and restless Ropinirole, Pramipexole (mechanism, use) leg syndrome

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micro micro repro neuro Neuro heme/onc heme/onc heme/onc heme/onc heme/onc heme/onc heme/onc heme/onc heme/onc heme/onc endocrine heme/onc general heme/onc heme/onc heme/onc GI GI cardio repro heme/onc reactions neuro neuro neuro msK msK neuro heme/onc neuro

pharmacology

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what are the uses of amantidine for parkinsons? What compound can cause sickling of sickle cell trait RBC's? How do atypical antipsychotics avoid causing parkinson's symptoms and tardive dyskinesia? Which anti-inflammatories will not impair platlet aggregation? why? Natalizumab(mechanism, use, toxicity) What drugs are preferred in medication induced parkinson's treatment? why?

indirect and direct D agonist, also some anticholingergic functions which reduces tremors sodium metabisulite, found as a food additive and sanitizer They act on D4 instead of D2 receptors -> no risk of tardive dyskinesia or parkinson's like symptoms Celecoxib. It only impairs COX2. COX1 is predominate in platlets. 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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neuro reactions neuro heme/onc msk psych neuro

Anti-muscarinics (Benzotropine). Giving dopamine agonists would exacerbate psychosis. induction = lower solubility in blood, quicker induction. potency = higher with higher lipid solubility What defines induction and potency in gas anesthetics? =1/MAC.