Nitrates (mechanism, use, toxicity)
Cause NO release -> vasodilation (veins >>> arteries); used in angina; fast
tolerance, hypotension, flushing, headache Pharmacology Cardio
Adverse effects of statins Hepatoxicity and muscle breakdown Pharmacology Cardio
Niacin (mechanism, use, toxicity)
Inhibits lipolysis and reduces VLDL secretion, lowering LDL and raising HDL;
hyperlipidemia; flushing and hyperuricemia Pharmacology Cardio Cholestyramine, colestipol, colesevelam
(mechanism, use, toxicity)
Inhibits reabsorption of bile acids -> lower LDL with slight increase in HDL;
unpigmented gallbladder stones and malabsorption Pharmacology Cardio
Ezetimibe Prevents cholesterol reabsorption -> lower LDL Pharmacology Cardio
Fibrates (gemfibrozil + -fibrates) (mechanism, use, toxicity)
Upregulates LPL -> lower triglycerides, slightly inc. HDL and slightly dec. LDL;
myositis and hepatoxicity Pharmacology Cardio
Digoxin and digitoxin (mechanism, use, toxicity)
Inhibits Na/K ATPase -> indirectly inhibits Na/Ca exchanger -> inc. calcium levels -> inc. contractility; stimulates the vagus; causes cholinergic symptoms
and hyperkalemia Pharmacology Cardio
Class 1A antiarrhythmics
Quinidine, procainamide, and disopyramide; inc. AP duration and QT interval; can cause torsades de pointes, cinchonism (qunidine), procainamide
(drug-induced lupus) Pharmacology Cardio
Class 1B antiarrhythmics
Lidocaine, mexiletine, and tocainide; dec. AP duration especially in
depolarized/ischemia tissue; best following MI Pharmacology Cardio Class 1C antiarrhythmics
Flecainide, propafenone; no effect on AP, used in ventricular tachycardias; do
not use post-MI due to risk for arrhythmias Pharmacology Cardio Class 1 antiarrhythmics (general mechanism
and toxicity)
Blocks Na channels, decreasing the slope of phase 0 depolarization; toxicity
exacerbated by hyperkalemia Pharmacology Cardio
Class 2 antiarrhythmics
Beta-blockers; reduces cAMP, slowing SA and AV node activity, increases PR
interval; adverse effects include impotence, asthma exacerbation, sedation Pharmacology Cardio Class 3 antiarrhythmics
Amiodarone, ibutilide, dofetilide, sotalol; K channel blockers; inc. AP duration
and QT interval Pharmacology Cardio
Toxicity of amiodarone Pulmonary fibrosis, hepatotoxicity, thyroid dysfunction Pharmacology Cardio Class 4 antiarrhythmics
Ca channel blockers; verapamil and diltiazem; dec. conduction velocity and
inc. PR interval; cause constipation, flushing, and edema Pharmacology Cardio Adeosine (mechanism, use, toxicity)
Inc. K efflux, hyperpolarizing the cell; used in supraventricular tachycardias;
can cause flushing, hypotension, and chest pain Pharmacology Cardio Magnseium (mechanism, use, toxicity) Used in torsades de pointes and digoxin toxicity Pharmacology Cardio Treatment for prolactinoma Bromocriptine or cabergoline (dopamine agonists) Pharmacology Endocrine Treatment of secondary hyperaldosteronism Spironolactone (or other AT2 antagonist) Pharmacology Endocrine
Treatment of carcinoid syndrome Octreotide (somatostatin analogues) Pharmacology Endocrine
Rapid-acting insulins (3) Lispro, aspart, and glulisine Pharmacology Endocrine
Short-acting insulin (1) Regular Pharmacology Endocrine
Intermediate-acting insulin (1) NPH Pharmacology Endocrine
Long-acting insulins (2) Glargine and detemir Pharmacology Endocrine
Metformin (mechanism, use, toxicity)
Biguanide; unknown mechanism; increases insulin sensitivity and glycolysis and decreases gluconeogenesis; can cause lactic acidosis (don't use in renal
failure patients) Pharmacology Endocrine
Tolbutamide, chlorpropamide (mechanism, use, toxicity)
First-generation sulfonylureas; close beta-cell K channels, causing
depolarization and increased insulin release; causes disulfuram-like effects Pharmacology Endocrine Glyburide, glimepiride, glipizide
(mechanism, use, toxicity)
Second-generation sulfonylureas; close beta-cell K channels, causing
depolarization and increased insulin release; causes hypoglycemia Pharmacology Endocrine Pioglitazone, rosiglitazone (mechanism, use,
toxicity)
Thiazolidinediones; activates PPAR-gamma, increasing insulin sensitivity and
adiponectin levels; causes weight gain, hepatotoxicity, and heart failure Pharmacology Endocrine Acarbose, miglitol (mechanism, use, toxicity)
Alpha-glucosidase inhibitors; prevent sugar hydrolysis and absorption,
reducing blood sugar levels Pharmacology Endocrine
Exenatide, liraglutide (mechanism, use, toxicity)
GLP-1 analogues; increase insulin, decrease glucagon secretion; causes
pancreatitis Pharmacology Endocrine
Linagliptin, saxagliptin, sitagliptin (mechanism, use, toxicity)
DPP-4 inhibitors; increase insulin, decrease glucagon secretion; causes mild
urinary/respiratory infections Pharmacology Endocrine Propylthiouracil (mechanism, use, toxicity)
Blocks thyroid peroxidase and 5'-deiodinase; used to treat hyperthyroidism;
causes agranulocytosis, aplastic anemia, hepatotoxicity Pharmacology Endocrine Methimazole (mechanism, use, toxicity) Blocks thyroid peroxidase; used to treat hyperthyrodism; teratogenic Pharmacology Endocrine Levothyroxine, triiodothyronine (mechanism,
use, toxicity) Thyroid hormone analogs; causes thyrotoxicosis Pharmacology Endocrine
Oxytocin (mechanism, use, toxicity) Used to control uterine hemhorrage Pharmacology Endocrine
Demeclocycline (mechanism, use, toxicity)
ADH antagonist used to treat SIADH; can cause photosensitivty and
bone/teeth abnormalities Pharmacology Endocrine
Glucocorticoids (mechanism, use, toxicity)
Inhibits phospholipase A2 activity and expression of COX-2; used for immune suppression; can cause Cushing's syndrome, adrenal insufficiency (if
withdrawn quickly) Pharmacology Endocrine
Cimetidine and ranitidine (mechanism, use, toxicity)
H2 antagonists; used to treat hyperchloridia; cimeditine is a P-450 inhibitor
and has antiandrogenic effects, both reduce creatinine secretion Pharmacology GI -prazoles (mechanism, use, toxicity)
Irreversibly inhibit the H/K pump; used to treat hyperchloridia; increased risk
of C. difficile infection and hypomagnesemia Pharmacology GI Bismuth, sucralfate (mechanism, use,
toxicity) Coats ulcer base and protects underlying tissue Pharmacology GI
Misoprostol (mechanism, use, toxicity)
PGE1 analog that decreases acid production and increases bicarb production;
used to prevent NSAID ulcers; abortifacient Pharmacology GI Octreotide (mechanism, use, toxicity) Somatostatin analog; used to treat VIPoma and carcinoid syndrome Pharmacology GI
Toxicity of long-term antacid use Hypokalemia Pharmacology GI
Infliximab (mechanism, use, toxicity) Anti-TNF; used to treat IBD and RA; can cause activation of latent microbes Pharmacology GI Sulfasalazine (mechanism, use, toxicity)
Combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid
(anti-inflammatory); used to treat IBD; causes oligospermia Pharmacology GI Ondansetron (mechanism, use, toxicity) 5-HT3 antagonist; used as an antiemetic Pharmacology GI Metoclopramide (mechanism, use, toxicity)
D2 antagonist; used to increase gut muscle activity and as an antiemetic;
causes parkinson signs Pharmacology GI
Can be used to prevent mast cell
degranulation Cromolyn sodium Pharmacology Heme/Onc
Treatment of lead poisoning Dimercaprol and EDTA, succimer in kids Pharmacology Heme/Onc
Heparin (mechanism, use, toxicity)
Activates antithrombin, which inactivates thrombin and Xa; used for immediate coagulation and in pregnant women; some patients develop
antibodies to platelet factor 4 (HIT) Pharmacology Heme/Onc Enoxaparin, dalteparin (mechanism, use,
toxicity)
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 Pharmacology Heme/Onc
Warfarin (mechanism, use, toxicity)
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 Pharmacology Heme/Onc
Alteplase, reteplase, tenecteplase
(mechanism, use, toxicity) Converts plasminogen to plasmin; used as a thrombolytic Pharmacology Heme/Onc Aspirin (mechanism, use, toxicity)
Irreversibly inhibits COX-1 and COX-2; anti-platelet and anti-inflammatory;
gastric ulcers, tinnitus, Reye's syndrome in childhood viral infections Pharmacology Heme/Onc Clopidogrel, ticlodipine, prasugrel, ticagrelor
(mechanism, use, toxicity)
Irreversibly blocks ADP receptors on platelets, preventing degranulation; used
for acure coronary syndrome; ticlodipine causes neutropenia Pharmacology Heme/Onc Cilostazol, dipyridamole (mechanism, use,
toxicity)
Phosphodiesterase inhibitor, increases cAMP and decreases ADP, preventing
Abciximab, eptifibatide, tirofiban (mechanism, use, toxicity)
GPIIb/IIIa inhibitors, preventing platelet aggregation; bleeding,
thrombocytopenia Pharmacology Heme/Onc
Methotrexate (mechanism, use, toxicity)
Inhibits dihydrofolate reductase, inhibiting DNA synthesis; myelosuppression,
macrovesicular fatty change in liver Pharmacology Heme/Onc 5-fluorouracil (mechanism, use, toxicity)
Pyrimidine analog that is activated and inhibits thymidylate synthase,
inhibiting DNA synthesis; myelosuppression, photosensitivity Pharmacology Heme/Onc Cytarabine (mechanism, use, toxicity)
Pyrimidine analog that inhibits DNA polymerase; leukopenia,
thrombocytopenia, megaloblastic anemia Pharmacology Heme/Onc Azathioprine, mercaptopurine,
6-thioguanine (mechanism, use, toxicity)
Purine analogs that are activated by HGPRT and inhibit purine synthesis; toxicity is increased with allopurinol, causes bone marrow, GI, and liver
toxicity Pharmacology Heme/Onc
Dactinomycin (actinomycin D) (mechanism,
use, toxicity) DNA intercalator; used for childhood tumors; myelosuppression Pharmacology Heme/Onc Doxorubicin (Adriamycin), daunorubicin
(mechanism, use, toxicity)
Generates free radicals that cause DNA strand breaks; dilated cardiomyopathy
(Dexrazoxone, an iron chelator, prevents this), myelosuppression, alopecia Pharmacology Heme/Onc Bleomycin (mechanism, use, toxicity)
Generates free radicals that cause DNA strand breaks; pulmonary fibrosis with
minimal myelosuppression Pharmacology Heme/Onc
Cyclophosphamide, ifosfamide (mechanism, use, toxicity)
Crosslinks DNA (must be activated by liver); myelosuppression, hemhorragic
cystitis (can be minimized with mesna) Pharmacology Heme/Onc Carmustine, lomustine, semustine,
streptozocin (mechanism, use, toxicity) Used to treat CNS tumors Pharmacology Heme/Onc
Busulfan (mechanism, use, toxicity) Alkylates DNA; pulmonary fibrosis, hyperpigmentation Pharmacology Heme/Onc Vincristine, vinblastine (mechanism, use,
toxicity)
Block microtubule polymerization; vincristine causes neurotoxicity, vinblastine
causes bone marro suppression Pharmacology Heme/Onc
Paclitaxel (mechanism, use, toxicity) Blocks microtubule breakdown; myelosuppression Pharmacology Heme/Onc Cisplatin, carboplatin (mechanism, use,
toxicity)
Crosslinks DNA; nephrotoxicity (minimize with chloride diuresis, amifostine),
acoustic n. damage Pharmacology Heme/Onc
Etoposide, teniposide (mechanism, use,
toxicity) Inhibits topoisomerase II; myelosuppression, GI upset, alopecia Pharmacology Heme/Onc Hydroxyurea (mechanism, use, toxicity)
Inhibits ribonucleotide reductase and increases HbF; used in cancers and
HbSS disease; bone marrow suppression Pharmacology Heme/Onc Prednisone (mechanism, use, toxicity) Unknown but may trigger apoptosis in dividing cells; Cushingoid symptoms Pharmacology Heme/Onc Tamoxifen, raloxifene (mechanism, use,
toxicity)
Prevents estrogen receptor binding; used in breast cancer and prevention of osteoporosis; tamoxifen increases the risk of endometrial cancer due to
agonist effects. Raloxifene = no increase in endometrial cancer. Pharmacology Heme/Onc Trastuzumab (mechanism, use, toxicity) Antibody against HER-2 receptor; cardiotoxicity Pharmacology Heme/Onc Imatinib (mechanism, use, toxicity) Antibody against bcr-abl tyrosine kinase Pharmacology Heme/Onc Rituximab (mechanism, use, toxicity)
Antibody against CD20; used to treat non-Hodgkin's lymphoma and
rheumatoid arthritis Pharmacology Heme/Onc
Vemurafenib (mechanism, use, toxicity) B-raf kinase inhibitor (V600 mutation); used in metastatic melanoma Pharmacology Heme/Onc
Bevacizumab (mechanism, use, toxicity) Antibody against VEGF Pharmacology Heme/Onc
Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac (mechanism, use,
toxicity)
Reversible COX inhibitor; gastric ulcers, renal ischemia (due to constriction of
afferent arteriole) Pharmacology Musculoskeletal
Celecoxib (mechanism, use, toxicity)
Reversible COX-2 inhibitor; anti-inflammatory without damage to gastric
mucosa; sulfa allergy, thrombosis Pharmacology Musculoskeletal Acetominophen (mechanism, use, toxicity) COX inhibitor in the CNS (not anti-inflammatory); causes hepatic necrosis Pharmacology Musculoskeletal
Alendronate (mechanism, use, toxicity)
Pyrophosphate analog that inhibits osteoclasts; used to treat osteoporosis,
hypercalcemia, and Paget's disease; corrosive esophagitis Pharmacology Musculoskeletal Allopurinol (mechanism, use, toxicity) Xanthine oxidase inhibitor, reduces production of uric acid Pharmacology Musculoskeletal
Probenecid (mechanism, use, toxicity) Inhibits reabsorption of uric acid in PCT Pharmacology Musculoskeletal Colchine (mechanism, use, toxicity) Inhibits microtubule polymerization, preventing neutrophil extravasation Pharmacology Musculoskeletal Etanercept (mechanism, use, toxicity) TNF-alpha receptor that binds free TNF-alpha Pharmacology Musculoskeletal Infliximab, adalimumab (mechanism, use,
toxicity) Anti-TNF-alpha antibody Pharmacology Musculoskeletal
Latanoprost (mechanism, use, toxicity)
PGF2 analog that increases the outflow of aqueous humor; can cause
darkening of the iris Pharmacology Neurology
Morphine, fentanyl, cofeine, heroin, methadone, meperidine, dextromethorphan,
diphenoxylate (mechanism, use, toxicity)
Mu opioid agonists that open K channels and close Ca channels, inhibting
synaptic transmission; addiction, respiratory depression, constipation, miosis Pharmacology Neurology Butorphanol (mechanism, use, toxicity)
Mu opioid partial agonist; used to treat severe pain; causes withdrawal if
being treated with full agonist Pharmacology Neurology Tramadol (mechanism, use, toxicity)
Weak opioid agonist that inhibits serotonin and NE reuptake; increases risk for
seizures Pharmacology Neurology
First-line therapy for simple partial seizures Carbamazepine Pharmacology Neurology
First-line therapy for complex partial
seizures Carbamazepine Pharmacology Neurology
First-line therapies for tonic-clonic seizures
(3) Carbamazepine, phenytoin, valproate Pharmacology Neurology
First-line therapy for absence seizures Ethosuximide Pharmacology Neurology
Phenytoin (mechanism, use, toxicity)
Increases Na channel inactivation and inhibits glutamate release; used for simple, complex, and tonic-clonic seizures and status epilecticus prophylaxis;
nystagmus, gingival hyperplasia, hirsutism, megaloblastic anemia,
teratogenic, drug-induced lupus, P450 inducer Pharmacology Neurology
Carbamazepine (mechanism, use, toxicity)
Increases Na channel inactivation; first-line for simple, complex, and tonic-clonic seizures and trigeminal neuralgia; agranulocytosis, aplastic anemia,
P450 inducer, SIADH, liver toxicity Pharmacology Neurology Lamotrigine (mechanism, use, toxicity)
Blocks Na channels; used for simple, complex, and tonic-clonic seizures;
Steven-Johnson syndrome Pharmacology Neurology
Gabapentin (mechanism, use, toxicity)
Inhibits Ca channels; used for simple, complex, and tonic-clonic seizures,
migraine prophylaxis, peripheral neuropathy, bipolar disorder; ataxia Pharmacology Neurology
Topiramate (mechanism, use, toxicity)
Blocks Na channels and increases GABA secretion; used for simple, complex, and tonic-clonic seizures and migraine prevention; mental dulling, kidney
stones, weight loss Pharmacology Neurology
Phenobarbital (mechanism, use, toxicity)
Increases GABA channel action; first-line for simple, complex, and tonic-clonic
seizures in children; P450 inducer Pharmacology Neurology
Valproate (mechanism, use, toxicity)
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 Pharmacology Neurology Ethosuximide (mechanism, use, toxicity)
Blocks thalamic Ca channels; first-line for absence seizures; GI distress,
Steven-Johnson syndrome Pharmacology Neurology
Benzodiazepines (mechanism, use, toxicity)
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 Pharmacology Neurology Tiagabine (mechanism, use, toxicity) Inhibits GABA reuptake; used for simple and complex seizures Pharmacology Neurology Vigabatrin (mechanism, use, toxicity)
Irreversibly inhibits GABA transaminase, increasing GABA concentration; used
for simple and complex seizures Pharmacology Neurology Levetriacetam (mechanism, use, toxicity) Unknown mechanism; used for simple, complex, and tonic-clonic seizures Pharmacology Neurology
Phenobarbital, pentobarbial, thiopental, secobarbital (mechanism, use, toxicity)
Increase duration of GABA channel opening; induction of anesthesia, sedative;
Triazolam, oxazepam, midazolam
(mechanism, use, toxicity) Short-acting benzodiazepines; more addictive potential Pharmacology Neurology Barbituates vs. benzodiazepines
(mechanism) Increase duration vs. increase frequency Pharmacology Neurology
Zolpidem, zaleplon, eszopiclone
(mechanism, use, toxicity) BZ1 subtype GABA channel agonists; used to treat insomnia Pharmacology Neurology Ketamine (mechanism, use, toxicity)
Blocks NMDA receptor; used as an anesthetic; increases cardiac activity,
hallucinations, bad dreams Pharmacology Neurology
Order of sensory loss when using local
anesthetics Pain -> temperature -> touch -> pressure Pharmacology Neurology
Succinylcholine (mechanism, use, toxicity)
ACh receptor agonist, produces sustained depolarization and desensitization;
used as a paralytic; hypercalcemia, hyperkalemia, malignant hyperthermia Pharmacology Neurology Tubocurarine, -curium drugs (mechanism,
use, toxicity) ACh antagonists; used as paralytics Pharmacology Neurology
Dantrolene (mechanism, use, toxicity)
Inhibits release of Ca from sarcoplasmic reticulum and skeletal muscle; used
to treat malignant hyperthermia and neuroleptic-malignant syndrome Pharmacology Neurology Levodopa/carbidopa (mechanism, use,
toxicity)
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 Pharmacology Neurology
Selegiline (mechanism, use, toxicity)
MAO-B (prefers dopamine for breakdown) inhibitor, inhibits dopamine breakdown; used to treat parkinson symptoms; enhances adverse effects of
levodopa Pharmacology Neurology
Donepezil, galantamine, rivastigmine (mechanism, use, toxicity)
ACh esterase inhibitors; used to treat Alzheimer's disease; cholinergic
symptoms Pharmacology Neurology
Sumatriptan (mechanism, use, toxicity)
Agonist at 1B/1D serotonin receptors; used to treat acute migraines and
cluster headaches; coronary vasospasm Pharmacology Neurology
Trifluoperzine, fluphenazine, haloperidol (mechanism, use, toxicity)
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) Pharmacology Psychiatry
Chlorpromazine, thioridazine (mechanism, use, toxicity)
Low potency antipsychotics that antagonize D2 receptors; used to treat schizophrenia, psychosis, mania, and Tourette's; corneal deposits
(chlorpromazine), retinal desporits (thioridazine) Pharmacology Psychiatry Olanzapine, clozapine, quetiapine,
risperidone, aripripazole, ziprasidone (mechanism, use, toxicity)
Atypical antipsychotics with unknown mechnism; used for schizophrenia, bipolar disorder, OCD, and others; weight gain (olanzapine, clozapine),
agranulocytosis (clozapine), seizures (clozapine), prolonged QT (ziprasidone) Pharmacology Psychiatry Lithium (mechanism, use, toxicity)
Unknown mechanism; used for bipolar disorder and SIADH; tremor, sedation,
edema, hypothyroidism, polyuria Pharmacology Psychiatry Buspirone (mechanism, use, toxicity)
Agonizes 1A serotonin receptors; used for generalized anxiety disorder; no
side effects, but takes 1-2 weeks for improvement Pharmacology Psychiatry Fluoxetine, paroxetine, sertraline, citalopram
(mechanism, use, toxicity)
Block reuptake of serotonin from the synaptic cleft; depression and others; sexual dysfunction, sertonin syndrome (hyperthermia, myoclonus, flushing,
diarrhea, seizures) Pharmacology Psychiatry
Venlafaxine, duloxetine (mechanism, use, toxicity)
Block reuptake of NE and serotonin from synaptic cleft; depression, diabetic
neuropathy (duloxetine); hypertension Pharmacology Psychiatry -iptyline, -ipramine, doxepin, amoxapine
(mechanism, use, toxicity)
TCAs, block reuptake of NE and serotonin; depression, bewetting (imipramine), OCD (clomipramine); convulsions, coma, arrhythmias, sedation,
Tranylcypromine, phenelzine, isocarboxazid, selegiline (mechanism, use, toxicity)
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 Pharmacology Psychiatry Bupropion (mechanism, use, toxicity) Increases NE and dopamine; used for smoking sensation, depression; seizures Pharmacology Psychiatry
Mirtazapine (mechanism, use, toxicity)
Alpha-2 antagonist, increases NE and serotonin release, and serotonin receptor agonist; used for depression; sedation, increased appetite with
weight gain; Pharmacology Psychiatry
Maprotiline (mechanism, use, toxicity) Blocks NE reuptake; used for depression; sedation, hypotension Pharmacology Psychiatry Trazodone (mechanism, use, toxicity) Inhibits serotonin uptake; used for insomnia; pripism Pharmacology Psychiatry
Mannitol (mechanism, use, toxicity)
Osmotic diuretic; used to treat drug overdose and increased ICP; pulmonary
edema, CHF Pharmacology Renal
Acetazolamide (mechanism, use, toxicity)
Carbonic anhydrase inhibitor; used for glaucoma, metabolic alklalosis;
hyperchloremic metabolic acidosis, ammonia toxicity, sulfa allergy Pharmacology Renal
Furosemide (mechanism, use, toxicity)
Inhibits NKCC channel, preventing urine concentration; used in hypertension, CHF, hypercalcemia; ototoxicity, hypokalemia, hypocalcemia, nephritis, gout,
sulfa allergy Pharmacology Renal
Ethacrynic acid (mechanism, use, toxicity)
Inhibits NKCC channel; used in patients with furosemide (sulfa) allergy;
hyperuricemia Pharmacology Renal
Hydrochlorothiazide (mechanism, use, toxicity)
Inhibits NaCl reabsorption in DCT and increases Ca reabsorption; hypertension and hypercalcinuria; hyperglycemia, hyperlipidemia, hyperuricemia,
hypercalcemia, sulfa allergy Pharmacology Renal
Spironolactone, eplerenone (mechanism, use, toxicity)
Aldosterone receptor antagonists; hyperaldosteronism, CHF, hypokalemia;
hyperkalemia (arrhythmias), antiandrogen effects with spironolactone Pharmacology Renal Triamterene, amiloride (mechanism, use,
toxicity) Block sodium channels in cortical collecting duct; hyperaldosteronism, CHF Pharmacology Renal Captopril, enalapril, lisinopril (mechanism,
use, toxicity)
ACE inhibitor, leads to reduced angiotensin II levels and decreases GFR; prevents heart remodeling, hypertension, CHF; cough, angioedema, transient
creatinine increase, hyperkalemia Pharmacology Renal
Losartan, valsartan (mechanism, use, toxicity)
Angiotensin II receptor antagonists; similar to ACE inhibitors, but do not cause
cough due to normal metabolism of bradykinin Pharmacology Renal
Leuprolide (mechanism, use, toxicity)
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 Pharmacology Reproductive Finasteride (mechanism, use, toxicity) 5-alpha reductase inhibitor; used for BPH and male-pattern baldness Pharmacology Reproductive Flutamide (mechanism, use, toxicity) Testosterone receptor antagonist; used in prostate cancer Pharmacology Reproductive Ketoconazole (mechanism, use, toxicity)
Inhibits 17,20-desmolase, stopping sex steroid synthesis; used to treat
polycystic ovarian syndrome Pharmacology Reproductive
Clomiphene (mechanism, use, toxicity)
Partial estrogen agonist in the hypothalamus, increases release of LH and
FSH, stimulating ovulation; used for infertility and PCOS Pharmacology Reproductive Tamoxifen (mechanism, use, toxicity)
Estrogen receptor antagonist at the breast; used for breast cancer; partial
agonist at the uterus, can cause endometrial hyperplasia Pharmacology Reproductive Raloxifene (mechanism, use, toxicity)
Estrogen receptor agonist at bone, inhibits osteoclast activity and stimulates
osteoblast activity; used to treat osteoporosis Pharmacology Reproductive Anastrozole, exemestane (mechanism, use,
toxicity) Aromatase inhibitors; used in breast cancer Pharmacology Reproductive
Mifepristone (mechanism, use, toxicity)
Progesterone receptor antagonist, given with misoprostol for abortion;
abortifacient; bleeding, abdominal pain Pharmacology Reproductive Terbutaline (mechanism, use, toxicity) Beta-2 agonist, inhibits uterine contractions Pharmacology Reproductive Tamsulosin (mechanism, use, toxicity) Alpha-1 antagonist; used to treat BPH Pharmacology Reproductive
Sildenafil, vardenafil (mechanism, use, toxicity)
Phosphodiesterase 5 inhibitors, causing inc. cGMP levels and smooth muscle relaxation; used in erectile dysfunction; impaired blue-green vision,
contradindicated with nitrates Pharmacology Reproductive Danazol (mechanism, use, toxicity)
Partial androgen receptor agonist; used to treat endometriosis and hereditary
angioedema; weight gain, acne, hirsutism, low HDL, hepatoxicity Pharmacology Reproductive
Treat methemoglobinemia with Methylene blue Pharmacology Respiratory
Diphenhydramine, dimenhydrinate, chlorpheniramine (mechanism, use, toxicity)
(First generation) H1 antagonists; used in allergies, motion sickness, insomnia; sedation, antiadrenergic, antiserotonergic, and antimuscarinic
effects due to CNS penetration Pharmacology Respiratory Loratadine, fexofenadine, desloratadine,
cetrizine (mechanism, use, toxicity)
H1 antagonists, 2nd gen; used in allergies; less fatigue than 1st gen
antihistamines due to decreased CNS penetration Pharmacology Respiratory Albuterol (mechanism, use, toxicity) Short-acting beta-2 agonist; asthma Pharmacology Respiratory Salmeterol, formoterol (mechanism, use,
toxicity) Long-acting beta-2 agonist; asthma; tremor, arrhythmias Pharmacology Respiratory Theophylline (mechanism, use, toxicity)
Phosphodiesterase inhibitor, increases cAMP and causes bronchodilation;
asthma; cardiotoxicity, neurotoxicity Pharmacology Respiratory Ipratropium (mechanism, use, toxicity) Muscarinic antagonist, prevents bronchoconstriction; asthma and COPD Pharmacology Respiratory Beclomethasone, fluticasone (mechanism,
use, toxicity)
Inhibit cytokine synthesis, reducing inflammation due to asthma; 1st line for
chronic asthma Pharmacology Respiratory
Montelukast, zafirlukast (mechanism, use,
toxicity) Leukotriene receptor antagonists; especially useful in aspirin-induced asthma Pharmacology Respiratory Zileuton (mechanism, use, toxicity)
Inhibits activity of 5-lipoxygenase, inhibiting leukotriene production; reduces
inflammation Pharmacology Respiratory
Omalizumab (mechanism, use, toxicity) Anti-IgE antibody; used in refractory allergic asthma Pharmacology Respiratory
Guaifenesin (mechanism, use, toxicity) Thins respiratory secretions Pharmacology Respiratory
N-acetylcysteine (mechanism, use, toxicity)
Loosens mucus plugs; used in CF patients and as an antidote to
acetominaphen posioning Pharmacology Respiratory
Bosentan (mechanism, use, toxicity)
Antagonizes endothelin-1 receptors, reducing vascular resistance in the
pulmonary vessels; used in pulmonary hypertension Pharmacology Respiratory Dextromethorphan (mechanism, use,
toxicity)
Antagonizes NMDA receptors, inhibiting coughing; produces opioid effects in
large doses and carries mild abuse potential Pharmacology Respiratory Pseudoephedrine, phenylephrine
(mechanism, use, toxicity)
Alpha-1 agonists that reduce edema and nasal congestion; rhinitis; hypertension, quick tolerance (recurrence of symptoms despite continued
treatment) Pharmacology Respiratory
Difference in competitive vs noncompetitve
inhibitors? competitive = decrease potency, noncompetitive = decrease efficacy. Pharmacology General What is Km? Inverse relation of affinity of enzyme for its substrate. Pharmacology General
What is Vmax? Direct proportion to enzyme concentration Pharmacology General
What is bioavailability? Fraction of administered drug that reaches systemic circulation unchanged. Pharmacology General Time to steady state depends on? depends on half-life. Does not depend on frequency or size of dose. Pharmacology General What is rate of elimination in zero order
kinetics? constant amount eliminated per time. Pharmacology General
Give three drugs that are zero order
eliminated. PEA - phenytoin, Ethanol, Aspirin. Pharmacology General
What is the rate of elimination for first order
kinetics? A constant FRACTION is eliminted, variable by concentration! Pharmacology General How does ionization relate to urine pH?
Ionzied species are trapped in urine and not resorbed. Neutral can be
resorbed. Pharmacology general
How do you treat overdose of weak acid?
How do you treat overdose of weak base?
Give drug examples. Treat with ammonium chloride. exp: amphetamines. Pharmacology general What is phase I drug metabolism? What pt.
population loses this?
Reduction, Oxidation, hydrolysis with CYP450. Often gives neutral products.
Geriatrics lose this phase. Pharmacology general
What is phase II metaboloism? What population depend on this?
Conjugation (Glucuronidation, Acetylation, and Sulfation.) Gives charged
products. Geriatrics depend on this, old people have GAS. Pharmacology general
What is efficacy? maximal effect a drug can produce. Pharmacology general
What is potency? amount of drug needed for the same effect. Pharmacology general
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. Pharmacology general
What is therapetuic index?
LD50/ED50. Median lethal dose divded by median effective dose. Safer drugs
have a higher TI. pharmacology general
What is a therapeutic window? Minimum effective dose to minimum toxic dose. Think of it as range of use. pharmacology general 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. pharmacology general Alpha-1 sympathetic receptor (G-protein
class, major function)
q, increase: vasc. smooth muscle contraction, pupillary dilator muscle
contraction, intestinal and bladder sphincter contaction. pharmacology autonomics Alpha-2 sympathetic receptor(G-protein
class, major function)
i, decrease: sympathetic outflow, insulin release, lipolysis. increase: platlet
aggregation. pharmacology autonomics
Beta-1 sympathetic receptor(G-protein class,
major function) s, increase: heart rate, contractilty, renin release, lipolysis pharmacology autonomics 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. pharmacology autonomics
M-1 Parasymp receptor(G-protein class,
major function) q, CNS, enteric nervouse system. pharmacology autonomics
M-2 Parasymp(G-protein class, major
function) i, decease: heart rate, contractility of atria pharmacology autonomics
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. pharmacology autonomics
What receptor is responsible for miosis and
accomadation? Parasympathetic M-3. pharmacology autonomics
What receptor is responsbile for mydriasis? Sympathetic Alpha-1. pharmacology autonomics
Dopamine D-1 receptor(G-protein class,
major function) s, relaxes renal vascular smooth muscle pharmacology autonomics
Dopamine D-2 receptor(G-protein class,
major function) i, modulates transmitter release especially in brain. pharmacology autonomics Histamine H-1 receptor(G-protein class,
major function) q, increase: mucus production, contraction of bronchioles, pruritus, pain. pharmacology autonomics histamine H-2 receptor(G-protein class,
major function) a, increase gastric acid secretion pharmacology autonomics
vasopression V-1 receptor(G-protein class,
major function) q, increase: vascular smooth muscle contraction pharmacology autonomics
vasopression V-2 receptor(G-protein class, major function)
s, increase water permeability and reabsorption in kidneys. (V2 found in 2
kidneys). pharmacology autonomics
Which receptors work via Gq ->
Phospholipase C ->Pip2->DAG + IP3? H1,Alpha1,V1,M1,M3. (remember HAVe 1 M&M) pharmacology autonomics
DAG causes activation of what? Protein Kinase C. pharmacology autonomics
Which receptors work via Gi->Adenyly
cyclase ->cAMP ->Protein Kinase A? M2, Alpha2, D2. (remember MAD 2's.) pharmacology autonomics Which receptors work via Gs->adenylyate
cyclase ->cAMP->Protein Kinase A? Beta1, Beta2, D1, H2,V2. pharmacology autonomics
What does protein kinase A do? increase calcium release in heart and blocks myosin light chain kinase. pharmacology autonomics What are the two classes of
cholinomimetics? 1. direct agonsts 2. indirect agonists (anticholinesterases). pharmacology autonomics Bethanechol(mechanism,use,toxicity)
Direct cholinomimetic. Postop or neurogenic ileus, urinary retention.
COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics Carbachol(mechanism,use,toxicity)
Direct Cholinomimetic. Identical to Ach. Glaucoma, pupillary contraction, relief
of IOP. COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics Pilocarpine(mechanism,use,toxicity)
Direct Cholinomimetic. Stimulates tears, salvia, sweat. Open and closed-angle
glaucoma.COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics methacholine(mechanism,use,toxicity)
Direct Cholinomimetic. challenge test of asthma diagnosis. COPD+asthma
exacerbation, peptic ulcers. pharmacology autonomics
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. pharmacology autonomics
pyridostigmine(mechanism,use,toxicity)
indirect cholinomimetic agonist. Long acting myasthenia gravis treatment.
COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics edrophonium(mechanism,use,toxicity)
indirect cholinomimetic agonist. Short acting, for myasthenia gravis diagnosis.
COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics Physostigmine(mechanism,use,toxicity)
indirect cholinomimetic agonist. for anti-cholinergic overdose, crosses BBB.
COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics Donepezil(mechanism,use,toxicity)
indirect cholinomimetic agonist. Alzheimers disease. COPD+asthma
exacerbation, peptic ulcers. pharmacology autonomics signs of cholinesterase inhibitor poisoning.
treatment.
DUMBBELSS (diarrhea, urination, miosis, bronchospasm, bradycardia, excitation of skeletal muscle +CNS, lacrimation, sweating, salvia.) tx: atropine
+ pralidoxime. pharmacology autonomics
Parathion(mechanism, treatment)
Irreversible cholinesterase inhibitor, ACH overdose. Tx: atropine +
pralidoxime. pharmacology autonomics
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. pharmacology autonomics
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. pharmacology autonomics 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. pharmacology autonomics 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. pharmacology autonomics
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. pharmacology autonomics Jimson Weed(mechanism, toxicity) muscarinic antagonist, causes gardner's pupil (mydriasis). pharmacology autonomics Epinephrine(Mechanism, receptors bound,
use, toxicity)
Direct Sympathomemetic. A1,A2,B1,B2. Anaphylaxis, open angle glaucoma,
Norepinephine(Mechanism, receptors bound, use, toxicity)
direct sympathomemetic. A1,A2, some B1. used in hypotension but it
decrease renal perfusion. pharmacology autonomics
Isoproterenol(Mechanism, receptors bound, use, toxicity)
Direct sympathomemetic. B1, B2. Used in Torsade de pointe and
bradyarryhmia. Can cause tachycardia and worsen cardiac ischemia. pharmacology autonomics 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). pharmacology autonomics
dobutamine(Mechanism, receptors bound, use, toxicity)
Direct sympathomimetic. Mostly B1, little a1,a2,b2. Used in heart failure and
cardiac stresstest (ionotrpic and chronotropic) pharmacology autonomics Phenylephrine(Mechanism, receptors bound,
use, toxicity)
Direct sympathomimetic. A1, A2. Used in hypotension, to cause mydriasis,
and rhinitis (decongestant). pharmacology autonomics 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. pharmacology autonomics
Ritodrine(Mechanism, receptors bound, use, toxicity)
Direct sympathomimetic. B2 only. Used to reduce premature uterine
contractions. pharmacology autonomics
Amphetamine (mechanism, use)
indirect sympathomimetic. Releases stored catecholamines. Used for
narcolepsy, obesity, ADD. pharmacology autonomics
Epinephrine(Mechanism, use, toxicity)
indirect sympathomimetic. Releases stored catecholamines. Used for nasal
decongestion, urinary incontience, hypotension. pharmacology autonomics Cocaine (mechanims, use).
direct sympathomimetic. Reuptake inhibitor. Causes vasoconstriction and
local anesthesia. pharmacology autonomics
Why must B-Blockers be avoided in
suspected cocaine intoxication? mixing them can lead to unopposed A1 activation and extreme hypertenion. pharmacology autonomics How does norepinephrine cause reflex
bradycardia?
stimulates A1>B2. Causes increased vasoconstrciton -> increased BP. This
causes reflex bradycardia and slowing of HR. pharmacology autonomics How does isoproterenol cause reflex
tachycardia?
Stimulates B2>A1. This cause vasodilation and dropping of BP. B1 is
stimulated and causes tachycardia. pharmacology autonomics 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! pharmacology autonomics
Phenoxybenzamine(Mechanism, receptors bound, use, toxicity)
IRREVERSIBLE nonslective alpha blocker. Used in pheochromosytoma BEFORE
surgery! toxic: orhtostatic hypotension, reflec tachycardia. pharmacology autonomics phentolamine(Mechanism, receptors bound,
use, toxicity)
REVERSBILE nonselective alpha blocker. give to patients on MAOI who each
tyramine contraining foods. pharmacology autonomics
Prazosin, Terazosin, Doxazosin,Tamsulosin (Mechanism, receptors bound, use, toxicity)
Alpha-1 blocker. Used in hypertension, urinary rentention in BPH. tox:
orthostatic hypotension, dizziness, headache. pharmacology autonomics Mirtazapine (mechanism, use, toxicity)
Alpha-2 blocker. Used in depression. tox: sedation, hypercholesterolemia,
increased apetite. pharmacology autonomics
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. pharmacology autonomics
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. pharmacology autonomics
give general toxicites of b-blockers
impotence, asthma exacerbation, bradycardia, seizures, sedation, hides
hypoglycemia. pharmacology autonomics
What are the B1 selective b-blockers? When are they useful?
A BEAM. acebutolol, betaxolol, Esmolol, Atenolol, Metoprolol. Useful in
comorbid pum. disease. pharmacology autonomics
What are the nonselective ( b1 = b2) b-blockers?
Please Try Not Being Picky. Propranolol, Timolol, Nadolol, Pindolol. B =
what are the nonselective a and
b-antagonists? Carvedilol, labetalol. pharmacology autonomics
What are the partial B-agonists? Pindolol, Acebutolol. pharmacology autonomics
Give treatment for acetaminophen overdose. N-Acetylcysteine (replenishes glutathione). pharmacology overdose
Give treatment for salicylates overdose. NaHCO3 (alkalinize urine) pharmacology overdose
give treatment for amphetamines overdose NH4Cl (acidify urine) pharmacology overdose
Give treatment for antimuscarinic and
anticholinergic overdose. Phygostigmine and control the hyperhermia. pharmacology overdose
Give treatment for b-blocker overdose Glucagon pharmacology overdose
Give treatment for digitalis overdose (KLAM) normalize K, Lidocaine, Anti-dig fab fragments, Mg2 pharmacology overdose
give treatment for iron overdose. deFEroxamine, deFErasirox. pharmacology overdose
give treatment for lead overdose CaEDTA, dimercaprol, succimer, penicillamine pharmacology overdose give treatment for mercury, arsenix, gold
overdose Dimercaprol, succiner pharmacology overdose
give treatment for copper, arsenic, gold
overdose penillamine pharmacology overdose
give treatment for cyanide nitrite + thiosulfate, hydroxocobalamin pharmacology overdose
give methemoglobin treatment Methylene blue, vitamin c pharmacology overdose
Give Carbon monocide treatment 100% oxygen or hyperbaric oxygen pharmacology overdose
give treatment for methanol, ethylene glycol
overdose Fomepizole>Ethanol, dialysis pharmacology overdose
give treatment for opiods overdose naloxone/naltrexone pharmacology overdose
give treatment for benzodiazepine overdose flumazenil pharmacology overdose
give treatment for TCA overdose NaHCO3 (alkalinize plasma) pharmacology overdose
give treatment for heparin overdose protamine pharmacology overdose
give treatment for warfarin overdose Vitamin K, fresh frozen plasma pharmacology overdose
give treatment for tPA, Streptokinase,
urokinase overdose aminocaproic acid pharmacology overdose
give treatment for theophylline overdose B-Blockers pharmacology overdose
give treatment for acetylcholinesterase
inhibitors atropine + pralidoxime pharmacology overdose
causes coronary vasospam cocaine, sumatriptan, ergots pharmacology reactions
causes cutaneous flushing (VANC) Vancomycin, Adenosine, Niacin, Ca blocker pharmacology reactions
causes dilated cardiomyopathy doxorubicin, daunorubicin pharmacology reactions
causes torsades de pointes class III (sotalol) and class Ia (quinidine) pharmacology reactions causes agranulocytoisis Clozapine, Carbamazepine, Colchine, Propylthiouracil, Methimazole, Dapsone pharmacology reactions causes aplastic anemia chloramphenicol, benzene, NSAIDs, propylthiouracil, methimazole pharmacology reactions causes direct coombs positive hemolytic
anemia methyldopa, penicillin pharmacology reactions
causes gray baby syndomr chloramphenicol pharmacology reactions
causes hemolysis in G6PD-defiect patients
(hemolysis IS PAIN)isoniazid, sulfonamides, primaquine, aspirin, ibuprofen,
nitrofurantoin pharmacology reactions
causes megaloblastic anemia
(females with PMS are on full BLAST mode) Phenytoin, Methotrexate, Sulfa
drugs pharmacology reactions
Causes thrombotic complications OCPs like estrogen pharmacology reactions
Causes cough ACE inhibitors pharmacology reactions
causes pulmonary fibrosis Bleomycin, amiodarone, Busulfan pharmacology reactions
causes acute cholestatic hepatits, jaundice erthryomycin pharmacology reactions
causes focal to massice hepatic necrosis Halothane, Amanita Phalloides, Valrpoic acid, Acetaminophen pharmacology reactions
causes hepatits isoniazid pharmacology reactions
can lead to adrenocortical insufficiency glucocorticoid withdrawl via HPA suppression pharmacology reactions can causes gynecomastia
`(Some drugs create awkward knockers) spironolactone, digitalis, cimetidine,
chronic alcohol use, ketoconazole pharmacology reactions
causes hot flashes estrogen, clomophene pharmacology reactions
causes hypergylcemia niacin, tacrolimus, protease inhibitor, HCTZ, corticosteriods pharmacology reactions
causes hypothyroidism lithium, amiodarone, suldonamides pharmacology reactions
causes fat redistribution glucocoricoids, protease inhibitors pharmacology reactions
causes gingival hyperplasia phenytoin, verpamil pharmacology reactions
causes gout furosemide, thiazides, niacin, cyclosporine pharmacology reactions
causes myopathies
fibrates, niacin, colchine, hydroxychloroquine, interferon-alpha, penicillamine,
statins, glucocorticoids pharmacology reactions
causes osteoporosis corticosteroids, heparin pharmacology reactions
causes photosensitivty (SAT for a PHOTO) Sulfonamides, amiodarone, tetracycline pharmacology reactions causes rash/SJS
penicillin, ethosuximide, carbamazepine, sulfa drugs, lamotrigine, allopurinol,
phenytoin, phenobarbital pharmacology reactions
cause drug induced lupus Hydralazine, isonizid, procainamine, phenytoin pharmacology reactions
causes teeth problems tetracyclines pharmacology reactions
causes tendonitis, tendon rupture, tooth
damage fluoroquinolones pharmacology reactions
causes diabetes insipidus lithium, demeclocycline pharmacology reactions
causes fanconi's syndome expired tetracycline pharmacology reactions
causes hemorrhagic cystits Cyclophosamide, ifosfamide pharmacology reactions
causes interstital nephritis methicllin, NSAID, furosemide pharmacology reactions
causes SIADH carbamazepine, cyclophosamide pharmacology reactions
causes cinchonism Quinidine, qunine pharmacology reactions
causes parkinson-like syndome antipsychotics, resperine, metoclopramide pharmacology reactions causes seizures
(with seizures, I BITE My tongue) isoniazid, Buproprion, imipenem, Tramadol,
Enflurane, Metoclopramide pharmacology reactions
causes tardive dyskinesia antipsychotics pharmacology reactions
acts like an anti-muscarinic Atropine, TCA, H1-blocker, neuoleptics pharmacology reactions
can cause a disulfiram like reaction metronidazole, some cephalosporins, procarbazine, 1st gen sulphonoureas pharmacology reactions can cause nephro/ototoxicity aminoglycosides, vancomycin, loop dieuetics, cisplatin pharmacology reactions
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. pharmacology reactions
list p450 inhibitors
(MAGIC ROCKS in GQ) Macrolides, amiodarone, grapefruit juice, isoniazid, cimetidine, ritonavir actue alcohol use, ciprofloxacin, ketoconazole,
sulfonamides, gemfibrozil, quinidine. pharmacology reactions lists the sulfa drugs
(Popular FACTSSS) probenacid, furosemide, acetazolamide, celecoxib,
thiazide, sulfonamide antibiotics, sulfaasalazine, sulfonylureas pharmacology reactions
Difference between peniciliin G and V. G = IV and IM. V = oral. pharmacology micro
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. pharmacology micro 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. pharmacology micro
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
Which has better bioavailibility; amoxicllin or
ampicillin? amOxicllin has better Oral bioavilability. pharmacology micro
What does clavulanic acid do? B-lactamse inhibitor pharmacology micro
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. pharmacology micro
List the B-lactamse inhibitors (CAST) Clavulanic Acid, Sulbactam,Tazobactem. pharmacology micro
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. pharmacology micro give use of cefazolin, cephalexin.
1st generation cephalosporins. PEcK. Proteus, E.coli,Klebsiella. Cefazolin used
preop to prevent A.aureus infections. pharmacology micro give use of cefoxitin, cefaclor,cefuroxime`
2nd generation cephalosporins. HEN PEcKs. H.ib, Enterbacter, Neisseria,
Proteus, E.coli,Klebsiella, Serratia. pharmacology micro give use of ceftriaxone, cefotaxime,
ceftazidime
3rd gen. cephalosporins. Serious gram - infections. Ceftriaxone = meningitis
and gonorrhea. Ceftazidime = pseudomonas. pharmacology micro give use of cefepime. increased activity against pseudomonas and G+ bugs. pharmacology micro
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. pharmacology micro
what transpeptidase inhibitor can be used in
penicillin allergy? aztreonam. pharmacology micro
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. pharmacology micro
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. pharmacology micro How is redman syndrome prevented in
vancomycin use? slow infusion and rate and antihistamines. pharmacology micro
How does vancomycin resistant occur? amino acid change of D-ala D-ala to D-ala D-lac. pharmacology micro List antibiotic protein synthesis inhibitors
AT 30, CCEL at 50. 30S = Aminoglycosides, Tetracyclines. 50S =
Chloramphenicol, Clindamycin, Erythromycin, Linezolid. pharmacology micro 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. pharmacology micro how does resistenace to aminoglycosides
occur?
transferase enzymes that inactivate the drug by acetylation, phosphorylation,
or adenylation. pharmacology micro
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. pharmacology micro
how does resistance to tetracyclines occur? decrease uptake into cells or increased efflux by pumps. pharmacology micro Azithromycin, clarithromycin, erythromycin
(mechanism,use,toxicity)
bacteriostatic, blocks translocation; atypical pneumonias, chlamydia, gram + cocci; MACRO: increased Motility, arrhythmia, Cholestatic hepatitis, Rash,
eOsinophilia. pharmacology micro
how does resitance to macrolides occur? methylation of 23s rRNA binding site. pharmacology micro
Chloramphenicol(mechanism,use,toxicity)
Bacterialstatic, blocks peptidlytransferase; Meningitis in adults, used in power countries due to being cheap; dose dependent anemia, dose independent
what causes grey baby syndrome?
use of chloramphenicol in premature infants, they lack
UDO-glucuronyl-transferase. pharmacology micro
How does resistance to chloramphenicol
occur? plasmid-encoded acetyltransferase. pharmacology micro
clindamycin(mechanism,use,toxicity)
Bacteriostatic. Blocks peptide transfer; anaerobic infections in lung infections
and oral anerobes; C. Diff infection, fever, diarrhea. pharmacology micro Sulfamethoxazole(SMX), sulfisoxazole,
sulfadiazine(mechanism, use, toxicity)
Bacteriostatic, PABA metabolites inhibit dihydropteroate synthase; Gram +, G-, NocardiaG-, ChlamydiaG-, UTI; hypersensitivtyG-, hemolysis in G6PDG-, nephrotoxicG-,
kernicterus, displaces other drugs from albumin. pharmacology micro how does resistance to sulfonamides occur? altered bacterial dihydropteroate or increased PABA synthesis. pharmacology micro
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. pharmacology micro
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. pharmacology micro
how does resistance to fluroquinolones
occur? mutation in DNA gyrase or efflux pumps. pharmacology micro
What groups are susceptible to
fluorquinolone tendon rupture? older than 60 or taking prednisone pharmacology micro
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. pharmacology micro
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. pharmacology micro
Rifampin(mechanism,use,toxicity)
inhibits DNA-dependent RNA polymerase; TB, Leprosy, prophylaxis in
meningococcus and Hib type B; hepatotox, p450 inducer, orange body fluids. pharmacology micro Pyrazinamide(mechanism, use, toxicity) unknown; TB; hyperuricemia, hepatotoxic. pharmacology micro
Ethambutol(mechanism,use,toxicity)
decreased carbohydrate polymerization of TB cell wall, blocks
arabinosyltransferase; TB; optic neuropathy(red-green color blindness_ pharmacology micro
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. pharmacology micro nystatin(mechanism,use,toxicty)
binds fungal ergosterol;topical only due to high toxicity, used for oral thrush
and topical diaper rash or vaginal candidiasis. pharmacology micro 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. pharmacology micro
Flucytosine(mechanism, use, toxicity)
inhibits fungal DNA and RNA synthesis by conversion to 5FU; used in systemic
fungal infections, especially cryptococcus; bone marrow suppression. pharmacology micro Caspofungin, micafungin(mechanism, use,
toxicity)
inhibits fungal cell wall synthesis by inhibiting B-glucan synthesis; invasive
aspergillosis, candida; flushing via histamine releae. pharmacology micro terbinafine(mechanism,use,toxicity)
inhibits fungal squalene epoxidase; treat dermatophytes - toe nail infection
especially;abnormal LFT, visual disturbances. pharmacology micro
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. pharmacology micro
suramin and melarsoprol use trypanosoma brucei pharmacology micro
nifurtimox use trypanosoma cruzi pharmacology micro
sodium stibogluconate use leshmaniasis pharmacology micro
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 pharmacology micro
quinidine use lifethreatening malaria pharmacology micro
artemether/lumifantrine use p. falciparum killing pharmacology micro
Zanamivir,oseltamivir(mechanism,use)
inihibits influenza neuraminidase, stops progeny release; treamt of influenze a
and b pharmacology micro
Ribavarin(mechanism,use,toxicity)
inhibits sythesis of guanine nucleotides by competitvely inhibiting IMP
dehydrogenase; RSV, chronic hep C; hemolytic anemia, severe teratogen pharmacology micro 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, pharmacology micro
Famciclovir use used in herpes zoster active infections pharmacology micro
mechanism for resistance to acyclovir mutated viral thymidine kinase pharmacology micro
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 pharmacology micro
mechanism for resistance to acyclovir mutated CMV DNA polymerase or lack of viral kinase pharmacology micro
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 pharmacology micro
mechanism for resistance to foscarnet mutated DNA polymerase pharmacology micro
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). pharmacology micro HAART consist of what? [2 NRTI] +[1 NNRTI OR 1 protease inhibitor OR 1 integrase inhibitor] pharmacology micro give mechanism and toxicity of protease
inhibitors
all end in -NAVIR! stops HIV mRNA cleavage into functional parts;
hyperglycemia, GI upset, lipodystrophy. pharmacology micro Ritonavir does what to be a "booster" inhibits cytochrome p-450, boosting concentration of other drugs. pharmacology micro
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. pharmacology micro
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, pharmacology micro
Raltegravir(mechanism,use,toxicity)
inhibits integrase, which stops HIV integration into host cells;HIV;
hypercholesterolemia pharmacology micro
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. pharmacology micro
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) pharmacology micro
cause direct toxicity to nerves vincristine and paclitaxil pharmacology reactions
By what mechanism does isoniazid cause B6 (pyridoxine) loss?
isoniazid structurally similar to B6, which causes renal excretion of B6 and
What medications can be given before Amphotercin B infusion to lessen side
effects? antihistamines and antipyretics. pharmacology micro
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. pharmacology cardio list signs of ammonia overdose ataxia, slurred speech, somnolence, vomiting pharmacology overdose
cause restrictive lung disease bleomycin, busulfan, amiodarone, methotrexate pharmacology reactions Contrast urine Ca with loop diuretics and
thiazides
loop diuretics: increased urine Ca via decreased reabsorption. thiazides:
decreased urine Ca. pharmacology renal
What is a sensitive indicator of alcohol
abuse? Serum gamma-glutamyltransferase. pharmacology psych
What is the treatment for delirium tremens? benzodiazepenes pharmacology psych
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. pharmacology psych What is neuroleptic malignant syndrome? What is the
treatment?
rigidity, myoglobinuria, autonomic instability. seen with antipsychotics overdose. treatment:
dantrolene and bromocriptine (d2 agonist) pharmacology psych
What is tardive dyskinesa? Is it reversible? sterotypical oral-facial movements, from long term antipsychotic use. often NOT reversible. pharmacology psych 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) pharmacology psych
What can long term Phenactin use cause? Translitional cell carcinoma of the bladder pharmacology renal
What are the teratogenic effects of ACE inhibitors? renal damage pharmacology reactions
What are the teratogenic effects of alkylating agents? absence of digits, toes pharmacology reactions
What are the teratogenic effects of aminoglycosides? CV VIII toxicity pharmacology reactions
What are the teratogenic effects of carbamazepine? neural tube defects, craniofacial defects pharmacology reactions
What are the teratogenic effects of diethylstilbestrol? vaginal clear cell adenocarcinoma, congenital mullerian anomalies pharmacology reactions
What are the teratogenic effects of folate antagonists? neural tube defects pharmacology reactions
What are the teratogenic effects of lithium? ebstein's anomaly -> atrialized right ventricle pharmacology reactions What are the teratogenic effects of phenytoin? fetal hydantoin syndrome->microcephaly,dysmorphic face pharmacology reactions
What are the teratogenic effects of tetracyclines discolored teeth pharmacology reactions
What are the teratogenic effects of thalidomide limb defects like flipper arms pharmacology reactions
What are the teratogenic effects of valproate? inhibitor of maternal folate absorption ->neural tube defects pharmacology reactions
What are the teratogenic effects of warfarin? bone deformities, fetal hemorrhage, abortion pharmacology reactions
At what time period is a fetus most susceptable to
teratogens? 3rd -8th week. pharmacology reactions
What are the teratogenic effects of vitamin a? extremely high risk for spontaneous abortion pharmacology reactions
What are the teratogenic effects of cocaine? placental abruption, developmental abnormalities pharmacology reactions
What are the teratogenic effects of smoking? preterm labor, placental problems, ADHD pharmacology reactions
What drug is the leading cause of birth defects and
mental retardation? alcohol pharmacology reactions
What are the toxicities of Loop diuretics? (OH DANG) Ototox, hypokalemia, dehydration, allergy(sulfa), Nephritis, Gout pharmacology reactions What are the toxicites of HCTZ? (hyperGLUC) hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia. pharmacology reactions 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. pharmacology reactions
What drugs can stimulate prolactin secretion? OCP and dopemaine antagonists (antipsychotics) pharmacology endocrine
What is a difference in the mechanism of PTU and
methimazole? PTU disables peroxidase AND 5'-deiodinase. Methimazole only inhibits peroxidase. pharmacology endocrine
Can sulfonylureas be used in type 1 DM? NO, they require some islet function to release insulin. type 1 - those cells are dead. pharmacology endocrine
What drugs can be used to treat type 1 AND 2 DM? Insulins, amylin analongs(pramlintide). pharmacology endocrine
What drug is used to prevent tumor lysis urate
