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991 Cards in this Set

  • Front
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Cause NO release -> vasodilation (veins >>> arteries); used in angina; fast tolerance
hypotension, flushing, headache,Nitrates (mechanism, use, toxicity)
Hepatoxicity and muscle breakdown
Adverse effects of statins
Inhibits lipolysis and reduces VLDL secretion
lowering LDL and raising HDL; hyperlipidemia; flushing and hyperuricemia,Niacin (mechanism, use, toxicity)
Inhibits reabsorption of bile acids -> lower LDL with slight increase in HDL; unpigmented gallbladder stones and malabsorption
Cholestyramine, colestipol, colesevelam (mechanism, use, toxicity)
Prevents cholesterol reabsorption -> lower LDL
Ezetimibe
Upregulates LPL -> lower triglycerides
slightly inc. HDL and slightly dec. LDL; myositis and hepatoxicity,Fibrates (gemfibrozil + -fibrates) (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
Digoxin and digitoxin (mechanism, use, toxicity)
Quinidine
procainamide, and disopyramide; inc. AP duration and QT interval; can cause torsades de pointes, cinchonism (qunidine), procainamide (drug-induced lupus),Class 1A antiarrhythmics
Lidocaine
mexiletine, and tocainide; dec. AP duration especially in depolarized/ischemia tissue; best following MI,Class 1B antiarrhythmics
Flecainide
propafenone; no effect on AP, used in ventricular tachycardias; do not use post-MI due to risk for arrhythmias,Class 1C antiarrhythmics
Blocks Na channels
decreasing the slope of phase 0 depolarization; toxicity exacerbated by hyperkalemia,Class 1 antiarrhythmics (general mechanism and toxicity)
Beta-blockers; reduces cAMP
slowing SA and AV node activity, increases PR interval; adverse effects include impotence, asthma exacerbation, sedation,Class 2 antiarrhythmics
Amiodarone
ibutilide, dofetilide, sotalol; K channel blockers; inc. AP duration and QT interval,Class 3 antiarrhythmics
Pulmonary fibrosis
hepatotoxicity, thyroid dysfunction,Toxicity of amiodarone
Ca channel blockers; verapamil and diltiazem; dec. conduction velocity and inc. PR interval; cause constipation
flushing, and edema,Class 4 antiarrhythmics
Inc. K efflux
hyperpolarizing the cell; used in supraventricular tachycardias; can cause flushing, hypotension, and chest pain,Adeosine (mechanism, use, toxicity)
Used in torsades de pointes and digoxin toxicity
Magnseium (mechanism, use, toxicity)
Bromocriptine or cabergoline (dopamine agonists)
Treatment for prolactinoma
Spironolactone (or other AT2 antagonist)
Treatment of secondary hyperaldosteronism
Octreotide (somatostatin analogues)
Treatment of carcinoid syndrome
Lispro
aspart, and glulisine,Rapid-acting insulins (3)
Regular
Short-acting insulin (1)
NPH
Intermediate-acting insulin (1)
Glargine and detemir
Long-acting insulins (2)
Biguanide; unknown mechanism; increases insulin sensitivity and glycolysis and decreases gluconeogenesis; can cause lactic acidosis (don't use in renal failure patients)
Metformin (mechanism, use, toxicity)
First-generation sulfonylureas; close beta-cell K channels
causing depolarization and increased insulin release; causes disulfuram-like effects,Tolbutamide, chlorpropamide (mechanism, use, toxicity)
Second-generation sulfonylureas; close beta-cell K channels
causing depolarization and increased insulin release; causes hypoglycemia,Glyburide, glimepiride, glipizide (mechanism, use, toxicity)
Thiazolidinediones; activates PPAR-gamma
increasing insulin sensitivity and adiponectin levels; causes weight gain, hepatotoxicity, and heart failure,Pioglitazone, rosiglitazone (mechanism, use, toxicity)
Alpha-glucosidase inhibitors; prevent sugar hydrolysis and absorption
reducing blood sugar levels,Acarbose, miglitol (mechanism, use, toxicity)
Amylin analog; reduces glucagon secretion; causes hypoglycemia
Pramlintide (mechanism, use, toxicity)
GLP-1 analogues; increase insulin
decrease glucagon secretion; causes pancreatitis,Exenatide, liraglutide (mechanism, use, toxicity)
DPP-4 inhibitors; increase insulin
decrease glucagon secretion; causes mild urinary/respiratory infections,Linagliptin, saxagliptin, sitagliptin (mechanism, use, toxicity)
Blocks thyroid peroxidase and 5'-deiodinase; used to treat hyperthyroidism; causes agranulocytosis
aplastic anemia, hepatotoxicity,Propylthiouracil (mechanism, use, toxicity)
Blocks thyroid peroxidase; used to treat hyperthyrodism; teratogenic
Methimazole (mechanism, use, toxicity)
Thyroid hormone analogs; causes thyrotoxicosis
Levothyroxine, triiodothyronine (mechanism, use, toxicity)
Used to control uterine hemhorrage
Oxytocin (mechanism, use, toxicity)
ADH antagonist used to treat SIADH; can cause photosensitivty and bone/teeth abnormalities
Demeclocycline (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),Glucocorticoids (mechanism, use, toxicity)
H2 antagonists; used to treat hyperchloridia; cimeditine is a P-450 inhibitor and has antiandrogenic effects
both reduce creatinine secretion,Cimetidine and ranitidine (mechanism, use, toxicity)
Irreversibly inhibit the H/K pump; used to treat hyperchloridia; increased risk of C. difficile infection and hypomagnesemia
-prazoles (mechanism, use, toxicity)
Coats ulcer base and protects underlying tissue
Bismuth, sucralfate (mechanism, use, toxicity)
PGE1 analog that decreases acid production and increases bicarb production; used to prevent NSAID ulcers; abortifacient (used with Mifepristone (RU-486) Progesterone Blocker
Misoprostol (mechanism, use, toxicity)
Somatostatin analog; used to treat VIPoma and carcinoid syndrome
Octreotide (mechanism, use, toxicity)
Hypokalemia
Toxicity of long-term antacid use
Anti-TNF; used to treat IBD and RA; can cause activation of latent microbes
Infliximab (mechanism, use, toxicity)
Combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory); used to treat IBD; causes oligospermia
Sulfasalazine (mechanism, use, toxicity)
5-HT3 antagonist; used as an antiemetic
Ondansetron (mechanism, use, toxicity)
D2 antagonist; used to increase gut muscle activity and as an antiemetic; causes parkinson signs
Metoclopramide (mechanism, use, toxicity)
Cromolyn sodium
Can be used to prevent mast cell degranulation
Dimercaprol and EDTA
succimer in kids,Treatment of lead poisoning
Activates antithrombin
which inactivates thrombin and Xa; used for immediate coagulation and in pregnant women; some patients develop antibodies to platelet factor 4 (HIT),Heparin (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,Enoxaparin, dalteparin (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,Warfarin (mechanism, use, toxicity)
Converts plasminogen to plasmin; used as a thrombolytic
Alteplase, reteplase, tenecteplase (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,Aspirin (mechanism, use, toxicity)
Irreversibly blocks ADP receptors on platelets
preventing degranulation; used for acure coronary syndrome; ticlodipine causes neutropenia,Clopidogrel, ticlodipine, prasugrel, ticagrelor (mechanism, use, toxicity)
Phosphodiesterase inhibitor
increases cAMP and decreases ADP, preventing platelet degranulation; nausea, headache, facial flushing, hypotension,Cilostazol, dipyridamole (mechanism, use, toxicity)
GPIIb/IIIa inhibitors
preventing platelet aggregation; bleeding, thrombocytopenia,Abciximab, eptifibatide, tirofiban (mechanism, use, toxicity)
Inhibits dihydrofolate reductase
inhibiting DNA synthesis; myelosuppression, macrovesicular fatty change in liver,Methotrexate (mechanism, use, toxicity)
Pyrimidine analog that is activated and inhibits thymidylate synthase
inhibiting DNA synthesis; myelosuppression, photosensitivity,5-fluorouracil (mechanism, use, toxicity)
Pyrimidine analog that inhibits DNA polymerase; leukopenia
thrombocytopenia, megaloblastic anemia,Cytarabine (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,Azathioprine, 6-mercaptopurine, 6-thioguanine (mechanism, use, toxicity)
DNA intercalator; used for childhood tumors; myelosuppression
Dactinomycin (actinomycin D) (mechanism, use, toxicity)
Generates free radicals that cause DNA strand breaks; dilated cardiomyopathy(Dexrazoxone
an iron chelator, prevents this), myelosuppression, alopecia,Doxorubicin (Adriamycin), daunorubicin (mechanism, use, toxicity)
Generates free radicals that cause DNA strand breaks; pulmonary fibrosis with minimal myelosuppression
Bleomycin (mechanism, use, toxicity)
Crosslinks DNA (must be activated by liver); myelosuppression
hemhorragic cystitis (can be minimized with mesna, and N-acetylcysteine (NAC)),Cyclophosphamide, ifosfamide (mechanism, use, toxicity)
Used to treat CNS tumors
Carmustine, lomustine, semustine, streptozocin (mechanism, use, toxicity)
Alkylates DNA; pulmonary fibrosis
hyperpigmentation,Busulfan (mechanism, use, toxicity)
Block microtubule polymerization; vincristine causes neurotoxicity
vinblastine causes bone marro suppression,Vincristine, vinblastine (mechanism, use, toxicity)
Blocks microtubule breakdown (by hyperstabilization); myelosuppression
Paclitaxel (mechanism, use, toxicity)
Crosslinks DNA; nephrotoxicity (minimize with chloride diuresis
amifostine), acoustic n. damage (ototoxicity),Cisplatin, carboplatin (mechanism, use, toxicity)
Inhibits topoisomerase II; myelosuppression
GI upset, alopecia,Etoposide, teniposide (mechanism, use, toxicity)
Inhibits ribonucleotide reductase and increases HbF; used in cancers and HbSS disease; bone marrow suppression
Hydroxyurea (mechanism, use, toxicity)
Unknown but may trigger apoptosis in dividing cells; Cushingoid symptoms
Prednisone (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.
Tamoxifen, raloxifene (mechanism, use, toxicity)
Antibody against HER-2 receptor; cardiotoxicity
Trastuzumab (mechanism, use, toxicity)
Antibody against bcr-abl tyrosine kinase
Imatinib (mechanism, use, toxicity)
Antibody against CD20; used to treat non-Hodgkin's lymphoma and rheumatoid arthritis
Rituximab (mechanism, use, toxicity)
B-raf kinase inhibitor (V600E mutation); used in metastatic melanoma; B-RAF =proto-oncogene
Vemurafenib (mechanism, use, toxicity)
Antibody against VEGF (used Colon cancer
Wet AMD),Bevacizumab (mechanism, use, toxicity)
Reversible COX inhibitor; gastric ulcers
renal ischemia (due to constriction of afferent arteriole),Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac (mechanism, use, toxicity)
Reversible COX-2 inhibitor; anti-inflammatory without damage to gastric mucosa; sulfa allergy
thrombosis,Celecoxib (mechanism, use, toxicity)
COX inhibitor in the CNS (not anti-inflammatory); causes hepatic necrosis
Acetominophen (mechanism, use, toxicity)
Pyrophosphate analog that inhibits osteoclasts; used to treat osteoporosis
hypercalcemia, and Paget's disease; corrosive esophagitis,Alendronate (mechanism, use, toxicity)
Xanthine oxidase inhibitor
reduces production of uric acid,Allopurinol (mechanism, use, toxicity)
Xanthine oxidase inhibitor
Febuxostat (mechanism, use, toxicity)
Inhibits reabsorption of uric acid in PCT
Probenecid (mechanism, use, toxicity)
Inhibits microtubule polymerization
preventing neutrophil extravasation,Colchine (mechanism, use, toxicity)
TNF-alpha receptor that binds free TNF-alpha; Decoy receptor mimicking inactivating effects of soluble TNF
Etanercept (mechanism, use, toxicity)
Anti-TNF-alpha antibody
Infliximab, adalimumab (mechanism, use, toxicity)
PGF2 analog that increases the outflow of aqueous humor; can cause darkening of the iris
Latanoprost (mechanism, use, toxicity)
Mu opioid agonists that open K channels and close Ca channels
inhibting synaptic transmission; addiction, respiratory depression, constipation, miosis,Morphine, fentanyl, cofeine, heroin, methadone, meperidine, dextromethorphan, diphenoxylate (mechanism, use, toxicity)
Mu opioid partial agonist; used to treat severe pain; causes withdrawal if being treated with full agonist
Butorphanol (mechanism, use, toxicity)
Weak opioid agonist that inhibits serotonin and NE reuptake; increases risk for seizures
Tramadol (mechanism, use, toxicity)
Carbamazepine
First-line therapy for simple partial seizures
Carbamazepine
First-line therapy for complex partial seizures
Carbamazepine
phenytoin, valproate,First-line therapies for tonic-clonic seizures (3)
Ethosuximide
First-line therapy for absence seizures
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,Phenytoin (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,Carbamazepine (mechanism, use, toxicity)
Blocks Na channels; used for simple
complex, and tonic-clonic seizures; Steven-Johnson syndrome,Lamotrigine (mechanism, use, toxicity)
Inhibits Ca channels; used for simple
complex, and tonic-clonic seizures, migraine prophylaxis, peripheral neuropathy, bipolar disorder; ataxia,Gabapentin (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,Topiramate (mechanism, use, toxicity)
Increases GABA channel action; first-line for simple
complex, and tonic-clonic seizures in children; P450 inducer,Phenobarbital (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,Valproate (mechanism, use, toxicity)
Blocks thalamic Ca channels; first-line for absence seizures; GI distress
Steven-Johnson syndrome,Ethosuximide (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,Benzodiazepines (mechanism, use, toxicity)
Inhibits GABA reuptake; used for simple and complex seizures
Tiagabine (mechanism, use, toxicity)
Irreversibly inhibits GABA transaminase
increasing GABA concentration; used for simple and complex seizures,Vigabatrin (mechanism, use, toxicity)
Unknown mechanism; used for simple
complex, and tonic-clonic seizures,Levetriacetam (mechanism, use, toxicity)
Increase duration of GABA channel opening; induction of anesthesia
sedative; CNS depression, P450 inducer, contraindicated in patients with porphyrias,Phenobarbital, pentobarbial, thiopental, secobarbital (mechanism, use, toxicity)
Short-acting benzodiazepines; more addictive potential
Triazolam, oxazepam, midazolam (mechanism, use, toxicity)
Increase duration vs. increase frequency
Barbituates vs. benzodiazepines (mechanism)
BZ1 subtype GABA channel agonists; used to treat insomnia
Zolpidem, zaleplon, eszopiclone (mechanism, use, toxicity)
Blocks NMDA receptor; used as an anesthetic; increases cardiac activity
hallucinations, bad dreams,Ketamine (mechanism, use, toxicity)
Pain -> temperature -> touch -> pressure
Order of sensory loss when using local anesthetics
ACh receptor agonist
produces sustained depolarization and desensitization; used as a paralytic; hypercalcemia, hyperkalemia, malignant hyperthermia,Succinylcholine (mechanism, use, toxicity)
ACh antagonists; used as paralytics
Tubocurarine, -curium drugs (mechanism, use, toxicity)
Inhibits release of Ca from sarcoplasmic reticulum and skeletal muscle; used to treat malignant hyperthermia and neuroleptic-malignant syndrome
Dantrolene (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
Levodopa/carbidopa (mechanism, use, toxicity)
MAO-B (prefers dopamine for breakdown) inhibitor
inhibits dopamine breakdown; used to treat parkinson symptoms; enhances adverse effects of levodopa,Selegiline (mechanism, use, toxicity)
ACh esterase inhibitors; used to treat Alzheimer's disease; cholinergic symptoms
Donepezil, galantamine, rivastigmine (mechanism, use, toxicity)
Agonist at 1B/1D serotonin receptors; used to treat acute migraines and cluster headaches; coronary vasospasm
Sumatriptan (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),Trifluoperzine, fluphenazine, haloperidol (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),Chlorpromazine, thioridazine (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),Olanzapine, clozapine, quetiapine, risperidone, aripripazole, ziprasidone (mechanism, use, toxicity)
Unknown mechanism; used for bipolar disorder and SIADH; tremor
sedation, edema, hypothyroidism, polyuria,Lithium (mechanism, use, toxicity)
Agonizes 1A serotonin receptors; used for generalized anxiety disorder; no side effects
but takes 1-2 weeks for improvement,Buspirone (mechanism, use, toxicity)
Block reuptake of serotonin from the synaptic cleft; depression and others; sexual dysfunction
sertonin syndrome (hyperthermia, myoclonus, flushing, diarrhea, seizures),Fluoxetine, paroxetine, sertraline, citalopram (mechanism, use, toxicity)
Block reuptake of NE and serotonin from synaptic cleft; depression
diabetic neuropathy (duloxetine); hypertension,Venlafaxine, duloxetine (mechanism, use, toxicity)
TCAs
block reuptake of NE and serotonin; depression, bewetting (imipramine), OCD (clomipramine); convulsions, coma, arrhythmias, sedation, hypotension, anti-cholinergic effects,-iptyline, -ipramine, doxepin, amoxapine (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,Tranylcypromine, phenelzine, isocarboxazid, selegiline (mechanism, use, toxicity)
Increases NE and dopamine; used for smoking sensation
depression; seizures,Bupropion (mechanism, use, toxicity)
Alpha-2 antagonist
increases NE and serotonin release, and serotonin receptor agonist; used for depression; sedation, increased appetite with weight gain;,Mirtazapine (mechanism, use, toxicity)
Blocks NE reuptake; used for depression; sedation
hypotension,Maprotiline (mechanism, use, toxicity)
Inhibits serotonin uptake; used for insomnia; pripism
Trazodone (mechanism, use, toxicity)
Osmotic diuretic; used to treat drug overdose and increased ICP; pulmonary edema
CHF,Mannitol (mechanism, use, toxicity)
Carbonic anhydrase inhibitor; used for glaucoma
metabolic alklalosis; hyperchloremic metabolic acidosis, ammonia toxicity, sulfa allergy,Acetazolamide (mechanism, use, toxicity)
Inhibits NKCC channel
preventing urine concentration; used in hypertension, CHF, hypercalcemia; ototoxicity, hypokalemia, hypocalcemia, nephritis, gout, sulfa allergy; mimics Barter's Disease,Furosemide (mechanism, use, toxicity)
Inhibits NKCC channel; used in patients with furosemide (sulfa) allergy; hyperuricemia
Ethacrynic acid (mechanism, use, toxicity)
Inhibits NaCl reabsorption in DCT and increases Ca reabsorption; hypertension and hypercalcinuria; hyperglycemia
hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy; Mimics Gitelman's disease,Hydrochlorothiazide (mechanism, use, toxicity)
Aldosterone receptor antagonists; hyperaldosteronism
CHF, hypokalemia; hyperkalemia (arrhythmias), antiandrogen effects with spironolactone,Spironolactone, eplerenone (mechanism, use, toxicity)
Block sodium channels in cortical collecting duct; hyperaldosteronism
CHF; used to tx Liddle's Dx,Triamterene, amiloride (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,Captopril, enalapril, lisinopril (mechanism, use, toxicity)
Angiotensin II receptor antagonists; similar to ACE inhibitors
but do not cause cough due to normal metabolism of bradykinin,Losartan, valsartan (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,Leuprolide (mechanism, use, toxicity)
5-alpha reductase inhibitor; used for BPH and male-pattern baldness
Finasteride (mechanism, use, toxicity)
Testosterone receptor antagonist; used in prostate cancer
Flutamide (mechanism, use, toxicity)
Inhibits 17
20-desmolase, stopping sex steroid synthesis; used to treat polycystic ovarian syndrome,Ketoconazole (mechanism, use, toxicity)
Partial estrogen agonist in the hypothalamus
increases release of LH and FSH, stimulating ovulation; used for infertility and PCOS,Clomiphene (mechanism, use, toxicity)
Estrogen receptor antagonist at the breast; used for breast cancer; partial agonist at the uterus
can cause endometrial hyperplasia,Tamoxifen (mechanism, use, toxicity)
Estrogen receptor agonist at bone
inhibits osteoclast activity and stimulates osteoblast activity; used to treat osteoporosis,Raloxifene (mechanism, use, toxicity)
Aromatase inhibitors; used in breast cancer
Anastrozole, exemestane (mechanism, use, toxicity)
Progesterone receptor antagonist
given with misoprostol for abortion; abortifacient; bleeding, abdominal pain,Mifepristone (mechanism, use, toxicity)
Beta-2 agonist
inhibits uterine contractions,Terbutaline (mechanism, use, toxicity)
Alpha-1 antagonist; used to treat BPH
Tamsulosin (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,Sildenafil, vardenafil (mechanism, use, toxicity)
Partial androgen receptor agonist; used to treat endometriosis and hereditary angioedema; weight gain
acne, hirsutism, low HDL, hepatoxicity,Danazol (mechanism, use, toxicity)
Methylene blue
Treat methemoglobinemia with
(First generation) H1 antagonists; used in allergies
motion sickness, insomnia; sedation, antiadrenergic, antiserotonergic, and antimuscarinic effects due to CNS penetration,Diphenhydramine, dimenhydrinate, chlorpheniramine (mechanism, use, toxicity)
H1 antagonists
2nd gen; used in allergies; less fatigue than 1st gen antihistamines due to decreased CNS penetration,Loratadine, fexofenadine, desloratadine, cetrizine (mechanism, use, toxicity)
Short-acting beta-2 agonist; asthma
Albuterol (mechanism, use, toxicity)
Long-acting beta-2 agonist; asthma; tremor
arrhythmias,Salmeterol, formoterol (mechanism, use, toxicity)
Phosphodiesterase inhibitor
increases cAMP and causes bronchodilation; asthma; cardiotoxicity, neurotoxicity, Inhibits adenosine (puringeric inhibit AC--> decrease cAMP), proarrythmic (increases cAMP),Theophylline (mechanism, use, toxicity)
Muscarinic antagonist
prevents bronchoconstriction; asthma and COPD,Ipratropium (mechanism, use, toxicity)
Inhibit cytokine synthesis
reducing inflammation due to asthma; 1st line for chronic asthma,Beclomethasone, fluticasone (mechanism, use, toxicity)
Leukotriene receptor antagonists; especially useful in aspirin-induced asthma
Montelukast, zafirlukast (mechanism, use, toxicity)
Inhibits activity of 5-lipoxygenase
inhibiting leukotriene production; reduces inflammation,Zileuton (mechanism, use, toxicity)
Anti-IgE antibody; used in refractory allergic asthma
Omalizumab (mechanism, use, toxicity)
Thins respiratory secretions
Guaifenesin (mechanism, use, toxicity)
Loosens mucus plugs; used in CF patients and as an antidote to acetominaphen poisoning; also used in cyclophosphmide toxicity of hemorrhagic cystitis
N-acetylcysteine (mechanism, use, toxicity)
Antagonizes endothelin-1 receptors
reducing vascular resistance in the pulmonary vessels; used in pulmonary hypertension,Bosentan (mechanism, use, toxicity)
Antagonizes NMDA receptors
inhibiting coughing; produces opioid effects in large doses and carries mild abuse potential,Dextromethorphan (mechanism, use, toxicity)
Alpha-1 agonists that reduce edema and nasal congestion; rhinitis; hypertension
quick tolerance (recurrence of symptoms despite continued treatment),Pseudoephedrine, phenylephrine (mechanism, use, toxicity)
competitive = decrease potency
noncompetitive = decrease efficacy.,Difference in competitive vs noncompetitve inhibitors?
Inverse relation of affinity of enzyme for its substrate.
What is Km?
Direct proportion to enzyme concentration
What is Vmax?
Fraction of administered drug that reaches systemic circulation unchanged.
What is bioavailability?
depends on half-life. Does not depend on frequency or size of dose.
Time to steady state depends on?
constant amount eliminated per time.
What is rate of elimination in zero order kinetics?
PEA - phenytoin
Ethanol, Aspirin.,Give three drugs that are zero order eliminated.
A constant FRACTION is eliminted
variable by concentration!,What is the rate of elimination for first order kinetics?
Ionzied species are trapped in urine and not resorbed. Neutral can be resorbed.
How does ionization relate to urine pH?
Treat with Bicarb to make neutral. Exp: phenobarbital
methotrexate, aspirin.,How do you treat overdose of weak acid? Give drug examples.
Treat with ammonium chloride. exp: amphetamines.
How do you treat overdose of weak base? Give drug examples.
Reduction
Oxidation, hydrolysis with CYP450. Often gives neutral products. Geriatrics lose this phase.,What is phase I drug metabolism? What pt. population loses this?
Conjugation (Glucuronidation
Acetylation, and Sulfation.) Gives charged products. Geriatrics depend on this, old people have GAS.,What is phase II metaboloism? What population depend on this?
maximal effect a drug can produce.
What is efficacy?
amount of drug needed for the same effect.
What is potency?
DECREASED efficacy. fight for same binding site
full agonist cant exert full effect.,What happends to efficacy when a partial agonist and full agonist are mixed?
LD50/ED50. Median lethal dose divded by median effective dose. Safer drugs have a higher TI.
What is therapetuic index?
Minimum effective dose to minimum toxic dose. Think of it as range of use.
What is a therapeutic window?
1. Nicotinic - Ligang gated Na/K channels. Two nicotinic types: Nm(NMJ) and Nn(autonomic ganglia. 2. Muscarinic - G-proteins. 5 types
M1-M5.,What are the two types of Nicotonic receptors? What kind of messenger do they use?
q
increase: vasc. smooth muscle contraction, pupillary dilator muscle contraction, intestinal and bladder sphincter contaction.,Alpha-1 sympathetic receptor (G-protein class, major function)
i
decrease: sympathetic outflow, insulin release, lipolysis. increase: platlet aggregation.,Alpha-2 sympathetic receptor(G-protein class, major function)
s
increase: heart rate, contractilty, renin release, lipolysis,Beta-1 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.,Beta-2 sympathetic receptor(G-protein class, major function)
q
CNS, enteric nervouse system.,M-1 Parasymp receptor(G-protein class, major function)
i
decease: heart rate, contractility of atria,M-2 Parasymp(G-protein class, major function)
increase: exocrine gland secretion (tears
gastric, etc), gut peristalsis, bladder contraction, bronchoconstriction, pupillary spinchter contraction, cilliary muscle contraction.,M-3 parasymp(G-protein class, major function)
Parasympathetic M-3.
What receptor is responsible for miosis and accomadation?
Sympathetic Alpha-1.
What receptor is responsbile for mydriasis?
s
relaxes renal vascular smooth muscle,Dopamine D-1 receptor(G-protein class, major function)
i
modulates transmitter release especially in brain.,Dopamine D-2 receptor(G-protein class, major function)
q
increase: mucus production, contraction of bronchioles, pruritus, pain.,Histamine H-1 receptor(G-protein class, major function)
s
increase gastric acid secretion,histamine H-2 receptor(G-protein class, major function)
q
increase: vascular smooth muscle contraction,vasopression V-1 receptor(G-protein class, major function)
s
increase water permeability and reabsorption in kidneys. (V2 found in 2 kidneys).,vasopression V-2 receptor(G-protein class, major function)
H1
Alpha1,V1,M1,M3. (remember HAVe 1 M&M),Which receptors work via Gq -> Phospholipase C ->Pip2->DAG + IP3?
Protein Kinase C.
DAG causes activation of what?
Calcium -> smouth muscle contraction
IP3 causes increase in what?
M2
Alpha2, D2. (remember MAD 2's.),Which receptors work via Gi->Adenyly cyclase ->cAMP ->Protein Kinase A?
Beta1
Beta2, D1, H2,V2.,Which receptors work via Gs->adenylyate cyclase ->cAMP->Protein Kinase A?
increase calcium release in heart and blocks myosin light chain kinase.
What does protein kinase C do?
1. direct agonsts 2. indirect agonists (anticholinesterases).
What are the two classes of cholinomimetics?
Direct cholinomimetic. Postop or neurogenic ileus
urinary retention. COPD+asthma exacerbation, peptic ulcers.,Bethanechol(mechanism,use,toxicity)
Direct Cholinomimetic. Identical to Ach. Glaucoma
pupillary contraction, relief of IOP. COPD+asthma exacerbation, peptic ulcers.,Carbachol(mechanism,use,toxicity)
Direct Cholinomimetic. Stimulates tears
salvia, sweat. Open and closed-angle glaucoma.COPD+asthma exacerbation, peptic ulcers.,Pilocarpine(mechanism,use,toxicity)
Direct Cholinomimetic. challenge test of asthma diagnosis. COPD+asthma exacerbation
peptic ulcers.,methacholine(mechanism,use,toxicity)
Indirect cholinomimetic agonist. NO cns penetration. Postop and neurogenic ileus
myasthenia gravis, reversal of NMJ block. COPD+asthma exacerbation, peptic ulcers.,Neostigmine(mechanism,use,toxicity)
indirect cholinomimetic agonist. Long acting myasthenia gravis treatment. COPD+asthma exacerbation
peptic ulcers.,pyridostigmine(mechanism,use,toxicity)
indirect cholinomimetic agonist. Short acting
for myasthenia gravis diagnosis. COPD+asthma exacerbation, peptic ulcers.,edrophonium(mechanism,use,toxicity)
indirect cholinomimetic agonist. for anti-cholinergic overdose
crosses BBB. COPD+asthma exacerbation, peptic ulcers.,Physostigmine(mechanism,use,toxicity)
indirect cholinomimetic agonist. Alzheimers disease. COPD+asthma exacerbation
peptic ulcers.,Donepezil(mechanism,use,toxicity)
DUMBBELSS (diarrhea
urination, miosis, bronchospasm, bradycardia, excitation of skeletal muscle +CNS, lacrimation, sweating, salvia.) tx: atropine + pralidoxime.,signs of cholinesterase inhibitor poisoning. treatment.
Irreversible cholinesterase inhibitor
ACH overdose. Tx: atropine + pralidoxime.,Parathion(mechanism, treatment)
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.,Atropine, homatropine, tropicamide (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.,Benztropine(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.,Scopolamine(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.,Ipratropium,tiotropium (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.,Oxybutynin(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.,Glycopyrrolate(mechanism,use,toxicity)
muscarinic antagonist
causes gardner's pupil (mydriasis).,Jimson Weed(mechanism, toxicity)
Direct Sympathomemetic. A1
A2,B1,B2. Anaphylaxis, open angle glaucoma, asthma, hypotension.,Epinephrine(Mechanism, receptors bound, use, toxicity)
direct sympathomemetic. A1
A2, some B1. used in hypotension but it decrease renal perfusion.,Norepinephine(Mechanism, receptors bound, use, toxicity)
Direct sympathomemetic. B1
B2. Used in Torsade de pointe and bradyarryhmia. Can cause tachycardia and worsen cardiac ischemia.,Isoproterenol(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).,dopamine(Mechanism, receptors bound, use, toxicity)
Direct sympathomimetic. Mostly B1
little a1,a2,b2. Used in heart failure and cardiac stresstest (ionotrpic and chronotropic),dobutamine(Mechanism, receptors bound, use, toxicity)
Direct sympathomimetic. A1
A2. Used in hypotension, to cause mydriasis, and rhinitis (decongestant).,Phenylephrine(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.,Albuterol, salmetrol, terbutaline (Mechanism, receptors bound, use, toxicity)
Direct sympathomimetic. B2 only. Used to reduce premature uterine contractions.
Ritodrine(Mechanism, receptors bound, use, toxicity)
indirect sympathomimetic. Releases stored catecholamines. Used for narcolepsy
obesity, ADD.,Amphetamine (mechanism, use)
indirect sympathomimetic. Releases stored catecholamines. Used for nasal decongestion
urinary incontience, hypotension.,Epinephrine(Mechanism, use, toxicity)
direct sympathomimetic. Reuptake inhibitor. Causes vasoconstriction and local anesthesia.
Cocaine (mechanims, use).
mixing them can lead to unopposed A1 activation and extreme hypertenion.
Why must B-Blockers be avoided in suspected cocaine intoxication?
stimulates A1>B2. Causes increased vasoconstrciton -> increased BP. This causes reflex bradycardia and slowing of HR.
How does norepinephrine cause reflex bradycardia?
Stimulates B2>A1. This cause vasodilation and dropping of BP. B1 is stimulated and causes tachycardia.
How does isoproterenol cause reflex tachycardia?
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!,Clonidine, alpha-methyldopa(Mechanism, receptors bound, use)
IRREVERSIBLE nonslective alpha blocker. Used in pheochromosytoma BEFORE surgery! toxic: orhtostatic hypotension
reflec tachycardia.,Phenoxybenzamine(Mechanism, receptors bound, use, toxicity)
REVERSBILE nonselective alpha blocker. give to patients on MAOI who each tyramine contraining foods.
phentolamine(Mechanism, receptors bound, use, toxicity)
Alpha-1 blocker. Used in hypertension
urinary rentention in BPH. tox:orthostatic hypotension, dizziness, headache.,Prazosin, Terazosin, Doxazosin,Tamsulosin(Mechanism, receptors bound, use, toxicity)
Alpha-2 blocker. Used in depression. tox: sedation
hypercholesterolemia, increased apetite.,Mirtazapine (mechanism, use, toxicity)
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.,Describe what occurs when you alpha-blockade epi vs. phenylephrine.
Angina - decreases HR and contractility
decreasing oxygen use. MI - decrease mortality. SVT - decrease AV duction. Hypertension - decrease CO and renin secretion. CHF - slows progression. Glaucoma - decrease secretion of aqueous humor.,Give 6 applications of Beta-blockers in general.
impotence
asthma exacerbation, bradycardia, seizures, sedation, hides hypoglycemia.,give general toxicites of b-blockers
A BEAM. acebutolol
betaxolol, Esmolol, Atenolol, Metoprolol. Useful in comorbid pum. disease.,What are the B1 selective b-blockers? When are they useful?
Please Try Not Being Picky. Propranolol
Timolol, Nadolol, Pindolol. B = B-blocker.,What are the nonselective ( b1 = b2) b-blockers?
Carvedilol
labetalol.,what are the nonselective a and b-antagonists?
Pindolol
Acebutolol.,What are the partial B-agonists?
N-Acetylcysteine (replenishes glutathione).
Give treatment for acetaminophen overdose.
NaHCO3 (alkalinize urine)
Give treatment for salicylates overdose.
NH4Cl (acidify urine)
give treatment for amphetamines overdose
Phygostigmine and control the hyperhermia.
Give treatment for antimuscarinic and anticholinergic overdose.
Glucagon
Give treatment for b-blocker overdose
(KLAM) normalize K
Lidocaine, Anti-dig fab fragments, Mg2,Give treatment for digitalis overdose
deFEroxamine
deFErasirox.,give treatment for iron overdose.
CaEDTA
dimercaprol, succimer, penicillamine,give treatment for lead overdose
Dimercaprol
succiner,give treatment for mercury, arsenix, gold overdose
penillamine
give treatment for copper, arsenic, gold overdose
nitrite + thiosulfate
hydroxocobalamin,give treatment for cyanide
Methylene blue
vitamin c,give methemoglobin treatment
100% oxygen or hyperbaric oxygen
Give Carbon monocide treatment
Fomepizole>Ethanol
dialysis,give treatment for methanol, ethylene glycol overdose
naloxone/naltrexone
give treatment for opiods overdose
flumazenil
give treatment for benzodiazepine overdose
NaHCO3 (alkalinize plasma)
give treatment for TCA overdose
protamine
give treatment for heparin overdose
Vitamin K
fresh frozen plasma,give treatment for warfarin overdose
aminocaproic acid
give treatment for tPA, Streptokinase, urokinase overdose
B-Blockers
give treatment for theophylline overdose
atropine + pralidoxime
give treatment for acetylcholinesterase inhibitors
cocaine
sumatriptan, ergots,causes coronary vasospam
(VANC) Vancomycin
Adenosine, Niacin, Ca blocker,causes cutaneous flushing
doxorubicin
daunorubicin,causes dilated cardiomyopathy
class III (sotalol) and class Ia (quinidine)
causes torsades de pointes
Clozapine
Carbamazepine, Colchine, Propylthiouracil, Methimazole, Dapsone,causes agranulocytoisis
chloramphenicol
benzene, NSAIDs, propylthiouracil, methimazole,causes aplastic anemia
methyldopa
penicillin,causes direct coombs positive hemolytic anemia
chloramphenicol
causes gray baby syndomr
(hemolysis IS PAIN)isoniazid
sulfonamides, primaquine, aspirin, ibuprofen, nitrofurantoin,causes hemolysis in G6PD-defiect patients
(females with PMS are on full BLAST mode) Phenytoin
Methotrexate, Sulfa drugs,causes megaloblastic anemia
OCPs like estrogen
Causes thrombotic complications
ACE inhibitors
Causes cough
Bleomycin
amiodarone, Busulfan,causes pulmonary fibrosis
erthryomycin
causes acute cholestatic hepatits, jaundice
Halothane
Amanita Phalloides, Valrpoic acid, Acetaminophen,causes focal to massice hepatic necrosis
isoniazid
causes hepatits
clindamycin
ampicillin,can lead to pseudomembranous colitis
glucocorticoid withdrawl via HPA suppression
can lead to adrenocortical insufficiency
`(Some drugs create awkward knockers) spironolactone
digitalis, cimetidine, chronic alcohol use, ketoconazole,can causes gynecomastia
estrogen
clomophene,causes hot flashes
niacin
tacrolimus, protease inhibitor, HCTZ, corticosteriods,causes hypergylcemia
lithium
amiodarone, suldonamides,causes hypothyroidism
glucocoricoids
protease inhibitors,causes fat redistribution
phenytoin
verpamil,causes gingival hyperplasia
furosemide
thiazides, niacin, cyclosporine,causes gout
fibrates
niacin, colchine, hydroxychloroquine, interferon-alpha, penicillamine, statins, glucocorticoids,causes myopathies
corticosteroids
heparin,causes osteoporosis
(SAT for a PHOTO) Sulfonamides
amiodarone, tetracycline,causes photosensitivty
penicillin
ethosuximide, carbamazepine, sulfa drugs, lamotrigine, allopurinol, phenytoin, phenobarbital,causes rash/SJS
Hydralazine
isonizid, procainamine, phenytoin,cause drug induced lupus
tetracyclines
causes teeth problems
fluoroquinolones
causes tendonitis, tendon rupture, tooth damage
lithium
demeclocycline,causes diabetes insipidus
expired tetracycline
causes fanconi's syndome
Cyclophosamide
ifosfamide,causes hemorrhagic cystits
methicllin
NSAID, furosemide,causes interstital nephritis
carbamazepine
cyclophosamide,causes SIADH
Quinidine
qunine,causes cinchonism
antipsychotics
resperine, metoclopramide,causes parkinson-like syndome
(with seizures
I BITE My tongue) isoniazid, Buproprion, imipenem, Tramadol, Enflurane, Metoclopramide,causes seizures
antipsychotics
causes tardive dyskinesia
Atropine
TCA, H1-blocker, neuoleptics,acts like an anti-muscarinic
metronidazole
some cephalosporins, procarbazine, 1st gen sulphonoureas,can cause a disulfiram like reaction
aminoglycosides
vancomycin, loop dieuetics, cisplatin,can cause nephro/ototoxicity
(Momma Barb Steals Phen-phen and Refuses Greasy Carbs Chronically)Modafinil
Barbiturates, St. John wart, phenytoin, rifampin, griseofulvin, carbamazepine, chronic alcohol use.,list p450 inducers
(MAGIC ROCKS in GQ) Macrolides
amiodarone, grapefruit juice, isoniazid, cimetidine, ritonavir actue alcohol use, ciprofloxacin, ketoconazole, sulfonamides, gemfibrozil, quinidine.,list p450 inhibitors
(Popular FACTSSS) probenacid
furosemide, acetazolamide, celecoxib, thiazide, sulfonamide antibiotics, sulfaasalazine, sulfonylureas,lists the sulfa drugs
G = IV and IM. V = oral.
Difference between peniciliin G and V.
Bind penicillin-binding proteins(transpeptidases)
block cross linking of peptidoglycans;most effective on G+, also N. Meningitidis, Treponema;hypersensitivy reaction, hemolytic anema.,Penicillin(mechanism,use,toxicity)
bind transpeptidases
penicillanse resistant due to bukly r-group blocking B-Lactamse; S. Aureus, except MRSA; hypersensitivity and interstitial nephritis.,Oxacillin,Naficillin,Dicloxacillin(mechanism,use,toxicity)
bind transpeptidases
wide spectrum and more penicillinase sensitive. combo with claculanic acid to protect from B-lactams;kills enterococci(HELPSS)H.iB, E.coli,Listera,Proteus,Salmonella,Shigella,enterococci;hypersensitivity reaction,rash,pseudomemrane colitis.,Ampicillin, amoxicillin(mecanism,use,toxicity)
amOxicllin has better Oral bioavilability.
Which has better bioavailibility; amoxicllin or ampicillin?
B-lactamse inhibitor
What does clavulanic acid do?
transpeptidase inhibitor but extended spectrum;pseduomonas and g- rods
use with claculanic acid due to B-lactamse suspectibilty; hypersensitivity reaction.,Ticarcillin,piperacillin(mechanism,use,toxicity)
(CAST) Clavulanic Acid
Sulbactam,Tazobactem.,List the B-lactamse inhibitors
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.,Cephalosporin(mechanism,use,toxiciity)
1st generation cephalosporins. PEcK. Proteus
E.coli,Klebsiella. Cefazolin used preop to prevent A.aureus infections.,give use of cefazolin, cephalexin.
2nd generation cephalosporins. HEN PEcKs. H.ib
Enterbacter, Neisseria, Proteus, E.coli,Klebsiella, Serratia.,give use of cefoxitin, cefaclor,cefuroxime`
3rd gen. cephalosporins. Serious gram - infections. Ceftriaxone = meningitis and gonorrhea. Ceftazidime = pseudomonas.
give use of ceftriaxone, cefotaxime,ceftazidime
increased activity against pseudomonas and G+ bugs.
give use of cefepime.
a monobactem resistant to B-lactamases
prevents binding to PBP3 and is synergistic with aminoglycosides;gram - rods only;very nontoxic, some GI upset.,Aztreonam(mechanism,use,toxicty)
aztreonam.
what transpeptidase inhibitor can be used in penicillin allergy?
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.,imipenem/cilastatin,meropenem,etrapenem,doripenem(mechanism,use,toxicity)
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.,Vancomycin(mechanism,use,toxicty)
slow infusion and rate and antihistamines.
How is redman syndrome prevented in vancomycin use?
amino acid change of D-ala D-ala to D-ala D-lac.
How does vancomycin resistant occur?
AT 30
CCEL at 50. 30S = Aminoglycosides, Tetracyclines. 50S = Chloramphenicol, Clindamycin, Erythromycin, Linezolid.,List antibiotic protein synthesis inhibitors
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.,Gentamicin, neomycin, amikacin,tobramycin,streptomycin(mechanism,use,toxicity)
transferase enzymes that inactivate the drug by acetylation
phosphorylation, or adenylation.,how does resistenace to aminoglycosides occur?
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.,tetracycline, doxycycline, demecycline,minocycline(mechanism, use, toxicity)
decrease uptake into cells or increased efflux by pumps.
how does resistance to tetracyclines occur?
bacteriostatic
blocks translocation; atypical pneumonias, chlamydia, gram + cocci; MACRO: increased Motility, arrhythmia, Cholestatic hepatitis, Rash, eOsinophilia.,Azithromycin, clarithromycin, erythromycin(mechanism,use,toxicity)
methylation of 23s rRNA binding site.
how does resitance to macrolides occur?
Bacterialstatic
blocks peptidlytransferase; Meningitis in adults, used in power countries due to being cheap; dose dependent anemia, dose independent aplastic anemia, gray baby syndrome.,Chloramphenicol(mechanism,use,toxicity)
use of chloramphenicol in premature infants
they lack UDO-glucuronyl-transferase.,what causes grey baby syndrome?
plasmid-encoded acetyltransferase.
How does resistance to chloramphenicol occur?
Bacteriostatic. Blocks peptide transfer; anaerobic infections in lung infections and oral anerobes; C. Diff infection
fever, diarrhea.,clindamycin(mechanism,use,toxicity)
Bacteriostatic
PABA metabolites inhibit dihydropteroate synthase; Gram +, G-, Nocardia, Chlamydia, UTI; hypersensitivty, hemolysis in G6PD, nephrotoxic, kernicterus, displaces other drugs from albumin.,Sulfamethoxazole(SMX), sulfisoxazole, sulfadiazine(mechanism, use, toxicity)
altered bacterial dihydropteroate or increased PABA synthesis.
how does resistance to sulfonamides occur?
Bacteriostatic
inhibits bacterial dihydrofolate reductase, blocks folate synthesis; used in UTI, PCP (prophylacis and treatment), shigella, salmonella; megaloblastic anemia, leukopenia, granulocytopenia.,Trimethoprim(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.,ciprofloxacin, norfloxacin, levofloxacin, etc...(mechanism, use, toxicity)
mutation in DNA gyrase or efflux pumps.
how does resistance to fluroquinolones occur?
older than 60 or taking prednisone
What groups are susceptible to fluorquinolone tendon rupture?
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.,Metronidazole(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.,Isoniazid(mechanism,use,toxicity)
inhibits DNA-dependent RNA polymerase; TB
Leprosy, prophylaxis in meningococcus and Hib type B; hepatotox, p450 inducer, orange body fluids.,Rifampin(mechanism,use,toxicity)
unknown; TB; hyperuricemia
hepatotoxic.,Pyrazinamide(mechanism, use, toxicity)
decreased carbohydrate polymerization of TB cell wall
blocks arabinosyltransferase; TB; optic neuropathy(red-green color blindness_,Ethambutol(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.,Amphotericin B(mechanism, use, toxicity)
binds fungal ergosterol;topical only due to high toxicity
used for oral thrush and topical diaper rash or vaginal candidiasis.,nystatin(mechanism,use,toxicty)
inhibits fungal ergosterol synthesis by binding p450;Fluconazole for suppression of cryptococcus in AIDs patients
itraconazle for blasto, coccio, histo.,Fluconazole, ketoconazole, clotrimazole, itraconazole, voriconazole(mechanism, use,toxicity)
inhibits fungal DNA and RNA synthesis by conversion to 5FU; used in systemic fungal infections
especially cryptococcus; bone marrow suppression.,Flucytosine(mechanism, use, toxicity)
inhibits fungal cell wall synthesis by inhibiting B-glucan synthesis; invasive aspergillosis
candida; flushing via histamine releae.,Caspofungin, micafungin(mechanism, use, toxicity)
inhibits fungal squalene epoxidase; treat dermatophytes - toe nail infection especially;abnormal LFT
visual disturbances.,terbinafine(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.,Griseofulvin(mechanism,use,toxicity)
toxoplasmosis
Pyrimethamine use
trypanosoma brucei
suramin and melarsoprol use
trypanosoma cruzi
nifurtimox use
leshmaniasis
sodium stibogluconate use
blocks formation of heme into hemozoin. Heme accumulates and is toxic to plasmodia;used on all species but falciparum(too much resitance); retinopathy
Chloroquine(mechanism,use,toxicity)
lifethreatening malaria
quinidine use
p. falciparum killing
artemether/lumifantrine use
inihibits influenza neuraminidase
stops progeny release; treamt of influenze a and b,Zanamivir,oseltamivir(mechanism,use)
inhibits sythesis of guanine nucleotides by competitvely inhibiting IMP dehydrogenase; RSV
chronic hep C; hemolytic anemia, severe teratogen,Ribavarin(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,"",Acyclovir,valacyclovir(mechanism, use, toxicity)
used in herpes zoster active infections
Famciclovir use
mutated viral thymidine kinase
mechanism for resistance to acyclovir
guanosine analog
5'-monophosphate formed by CMV viral kinase, inhibits viral DNA polymerase;CMV infections;leukopenia,neutopenia,thrombocytopenia,renal toxicity,Ganciclovir,valgangciclovir(mechanism,use,toxicity)
mutated CMV DNA polymerase or lack of viral kinase
mechanism for resistance to acyclovir
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,Foscarnet(mechanism,use,toxicity)
mutated DNA polymerase
mechanism for resistance to foscarnet
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).,cidofovir(mechanism,use,toxicity)
[2 NRTI] +[1 NNRTI OR 1 protease inhibitor OR 1 integrase inhibitor]
HAART consist of what?
all end in -NAVIR! stops HIV mRNA cleavage into functional parts; hyperglycemia
GI upset, lipodystrophy.,give mechanism and toxicity of protease inhibitors
inhibits cytochrome p-450
boosting concentration of other drugs.,Ritonavir does what to be a "booster"
(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.,Tenofovir, emtricitabine, abacavir, lamivudine, zidovudine, didansoine, stavudine(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,"",Nevirapine, Efavirenz, Delavirdine(mechanism,use,toxicity)
inhibits integrase
which stops HIV integration into host cells;HIV;hypercholesterolemia,Raltegravir(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.,Interferons(mechanism,use,toxicity)
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),What antibiotics must be avoided in pregnancy?
vincristine and paclitaxil
cause direct toxicity to nerves
isoniazid structurally similar to B6
which causes renal excretion of B6 and competes for B6 binding sites.,By what mechanism does isoniazid cause B6(pyridoxine) loss?
antihistamines and antipyretics.
What medications can be given before Amphotercin B infusion to lessen side effects?
digoxin causes hyperkalemia. HOWEVER
a HYPOkalemic state increses patient susceptibility to digoxin toxicity.,Does digoxin cause hyper or hypokalemia? which states increases patient susceptibility to digoxin toxicity?
ataxia
slurred speech, somnolence, vomiting,list signs of ammonia overdose
bleomycin
busulfan, amiodarone, methotrexate,cause restrictive lung disease
loop diuretics: increased urine Ca via decreased reabsorption. thiazides: decreased urine Ca.
Contrast urine Ca with loop diuretics and thiazides
Serum gamma-glutamyltransferase.
What is a sensitive indicator of alcohol abuse?
benzodiazepenes
What is the treatment for delirium tremens?
The naloxone is only active if inected
making it hard to abuse the combo.,Why is the naloxone-buprenorphine combo used for heroin addiction treatment?
rigidity
myoglobinuria, autonomic instability. seen with antipsychotics overdose. treatment: dantrolene and bromocriptine (d2 agonist),What is neuroleptic malignant syndrome? What is the treatment?
sterotypical oral-facial movements
from long term antipsychotic use. often NOT reversible.,What is tardive dyskinesa? Is it reversible?
occurs with any drug that increases serotonin (MAO inhibitor
SNRI, TCA) hyperthermia, confusion, myoclonus, cardio collapse, flushing. tx: cyproheptadine (5ht antagonist),What is serotonin syndrome? what is the treatment?
Translitional cell carcinoma of the bladder
What can long term Phenactin use cause?
renal damage
What are the teratogenic effects of ACE inhibitors?
absence of digits
toes,What are the teratogenic effects of alkylating agents?
CV VIII toxicity
What are the teratogenic effects of aminoglycosides?
neural tube defects
craniofacial defects,What are the teratogenic effects of carbamazepine?
vaginal clear cell adenocarcinoma
congenital mullerian anomalies,What are the teratogenic effects of diethylstilbestrol?
neural tube defects
What are the teratogenic effects of folate antagonists?
ebstein's anomaly -> atrialized right ventricle
What are the teratogenic effects of lithium?
fetal hydantoin syndrome->microcephaly
dysmorphic face,What are the teratogenic effects of phenytoin?
discolored teeth
What are the teratogenic effects of tetracyclines
limb defects like flipper arms
What are the teratogenic effects of thalidomide
inhibitor of maternal folate absorption ->neural tube defects
What are the teratogenic effects of valproate?
bone deformities
fetal hemorrhage, abortion,What are the teratogenic effects of warfarin?
3rd -8th week.
At what time period is a fetus most susceptable to teratogens?
extremely high risk for spontaneous abortion
What are the teratogenic effects of vitamin a?
placental abruption
developmental abnormalities,What are the teratogenic effects of cocaine?
preterm labor
placental problems, ADHD,What are the teratogenic effects of smoking?
alcohol
What drug is the leading cause of birth defects and mental retardation?
(OH DANG) Ototox
hypokalemia, dehydration, allergy(sulfa), Nephritis, Gout,What are the toxicities of Loop diuretics?
(hyperGLUC) hyperglycemia
hyperlipidemia, hyperuricemia, hypercalcemia.,What are the toxicites of HCTZ?
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.,By what mechanisms do thiazides and loop diutetics cause metabolic alkalosis?
OCP and dopemaine antagonists (antipsychotics)
What drugs can stimulate prolactin secretion?
PTU disables peroxidase AND 5'-deiodinase. Methimazole only inhibits peroxidase.
What is a difference in the mechanism of PTU and methimazole?
NO
they require some islet function to release insulin. type 1 - those cells are dead.,Can sulfonylureas be used in type 1 DM?
Insulins
amylin analongs(pramlintide).,What drugs can be used to treat type 1 AND 2 DM?
allopurinol stops urate crystal collection -> no gout.
What drug is used to prevent tumor lysis urate neuropathy?
acute: NSAID
indomethicin. Chronic: allopurinol, febuxostat, probenacid, colchicine,List acute and chronic gout drugs.
used in chronic gout; inhibits reabsorption of uric acid in the proximal tubule; inhibits secretion of penicillin; do NOT use in renal dysfunction.
probenacid(mechanism, use, tox)
used in chronic gout
inhibits xanthine oxidase.,febuxostat(use, mechanism)
binds to G- cell membrane phospoholipids
disrupting them; only works in g-; peripheral neuropathy, dizziness, nsytagmus, nephrotoxicity.,Polymixin B(mechanism, use, toxicity)
increase catecholamines at synaptic cleft
especially NE + dopamine; ADHD, nacrolepsy, appetite control,Methylphenidate, destroamphetamine, methamphetamine(mechanism, use)
this is vitamin K
used in warfarin overdose,Phytonadione(use)
folinic acid
it is a metabolite of folic acid; given with methotrexate to replish the body's folate stores.,Leucovorin(use,mechanism)
antidote to heparin overdose. Protamine is a postive ion that binds to negative heparin
inactivating it.,Protamine sulfate (use, mechanism)
When someone taking MAO inhibitors eats hard cheeses and drinks wine
causing a crisis.,What is tyramine crisis caused by?
it has a MUCH longer half life
plus it is irrversible while phentolamine is reversible,Why is phenoxybenzamine prefered over phentolamine for presurgery pheochromocytoma surgery?
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.,Why is Lactulose fed to people with hepatic encephalopathy?
Complement inhibitor
used in Paroxysmal Nocturnal Hemoglobinuria.,Eculizumab(mechanism, use)
adenosine analog
used in treatment of hairy cell leukemia,Cladribine(mechanism, use)
Used in treating the M3
promyelocytic subtype of AML.,Trans-retinoic acid(use)
Yes
they lower GFP by stopping efferent arteriole constrinction. Creatinine can increase up to 30% and should peak by 1 weak. This can be BAD in renal artery stenosis, where ACE II is what is keeping the kidney alive.,Is an increase in serum creatinine normal after starting ACE inhibitors?
causes depolarization of cellular membrane; used in invasive MRSA; myopathy
raised CPK, inactivated by pulmonary surfactant,Daptomycin(mechanism, use, toxicity)
chemoreceptor trigger zone (area postrema)
the solitary nucleus, and in the presynpatic vagus nerve.,Ondansetron acts on 5HT3 receptors in what location, in order to decrease nausea?
They cause constriction of the spinchter of oddi -> increased billiary pressures -> billiary colic.
Why must mu agonists be avoided in suspected pancreatic or biliary pain?
trimethoprim
methotrexate, pyrimethamine.,What drugs inhibit dihydrofolate reductase?
partial agonist for nicotinic aCh channels in CNS. fights with ciggeratte nicotine for channel. reduces nicotine withdrawl cravings while attenuating the rewarding effects.
Varenicline(mechanism, use)
antidepressants
What class of drug can precipitate mania in those with bipolar disorder?
Desmopression (sleep enuresis = bed wetting)
What is the treatment for sleep enuresis?
furosemide. TAL of Henlee absorbs the most NA here compared to where over diuretics work. will reduce edema quickly.
In general, what is the best drug to use for edema of any kind?
PTU does. Methimazole does NOT.
Which drug used for hyperthyroidism decreases peripheral T3->T3 conversion?
NO. G cells are under vagal influence but they do not use ACh as a neurotransmitter. Instead
they use GRP.,Can atropine be used to block gastric secretions? why or why not?
Inhibits alcohol dehydrogenase; used as an antidote to methanol or ethylene glycol poisoning.
Fomepizole(mechanism, use)
Inhibits acetaldehyde dehydrogenase
makes acetaldehyde accumulate leading to hanger; used in alcohol abuse.,Disulfiram(mechanism, use)
Benzoate or Phenylbutyrate will bind amino acids and lead to excretion.
What can be given to those suffering from hyperammonia caused by a metabolic derangement?
On first dose
patient gets severe hypotension. Correct this by starting with a small dose.,What is first dose effect, typically seen in A1 blockers?
Isosorbide mononitrate can be swallowed. It has an almost 100% biavailability that way. Others cannot due to first pass metabolism.
Which nitrate can be given PO?
Stops chemotaxis of neutrophils
Colchine stops what specific cell to decrease gout symptoms?
methlydopa
What is the first line drug used to treat hypertension in pregnancy?
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.,Why is MRSA resistant to Naficillin but normal S. Aureus is not?
antibody against F protein
prevents pneumonia from RSV in infants,Palizumab(mechanism, use)
IgG anti-RH antibodies. given to mom at 28 weeks and also at birth
it sticks to the RH antigens in the MOM's blood, keeping her from developing antibodies.,Rhogam(mechanism, use)
COMT blockers
which increase DOPA levels; Both stop peripheral methylation and only Tolcapone stops central methylation; tolcapone causes hepatotoxicity,Entacapone, Tolcapone (mechanism, use, tox)
Constipation
What opioid effect is most resistant to tolerance?
IL 2; used in RCC
metastaic melanoma,Aldesleukin (mechanism, use)
erythropoietin; anemias
especially in renal failure,Epoetin Alfa(mechanism, use)
Fil = GC-SF
Sar = GM-CSF; both used in recovery of bone marrow, aplastic anemia,Filgrastim, Sargramostim (mechanism, use)
hepatitis B and C
Kaposi sarcoma, Leukemias, Malignany Melanoma,alpha-inerferon(use)
Multiple sclerosis
B-Interferon(use)
Chronic Granulamatous disease
gamma-interferon(use)
IL-11; thrombocytopenia
Oprelvekin(mechanism, use)
thrombocytopenia
thromopoietin(use)
antibody to CD3; used in acute transplant rejection
Muromonab-CD3 (mechanism, use)
antibody to digoxin; used as antidote to digoxin intoxication
Digoxin Immune Fab(mechanism, use)
Recombinat version of Urate oxidase
breaks uric acid down into allantoin; use in tumor lysis syndrome and gout,Rasburicase (mechanism, use)
monoclonal anitbody that binds to RANKL and prevents its interaction with RANK
inhibiting osteoclasts; decreases bone loss in bone mets,denosumab(mechanism, use)
It's high water solubility. Things with a high lipid solubility (unconjugated bilirubin) tend to cross the placenta while things with high water solubility(conjugated bilirubin) tend to not. binds albumin = probably lipid soluble
What keeps heparin from crossing the placental barrier?
Used in transplant anti-rejected
treatment of graft-vs-host disease, and psoriasis; binds calineurin on T cells, stopping IL2 from being expressed, lowering T cell response; nephtrotox and lymphomma risk,cyclosporine(mechanism, use, toxicity)
a retinoid that has immunomodulatory effects
binds nuclear receptors; psorisias and acne; severe teratogen,Isotretinoin, tretinoin, Acitretin(mechanism,use,toxicity
vitamin D analog; used in topical psoariasis treatment
Calcipotrol(mechanism, use)
Inhibits intestinal lipase
decreasing fat absorption; used to treat obesity,Orlistat(mechanism, use)
aspirin. Niacin increases prostaglandin D2. release. asprin blocks this release = lower flushing
giving what drug 30 minutes before Niacin can help reduce flushing?
Prevent growth of intima by inhibiting cellular growth = no restenosis
Paclitaxil or sirolimus are commonly used in cardiac stents. why?
IV magnesium sulfate for seizures
What is the drug used for Pre-eclampsi and ecplamsia?
Protease inhibitor
proteases are overactive in some cancers and can destroy pro-apototic proteins; used in multiple myeloma; peripheral neuropathy,Bortezomib(mechanism,use, toxicity)
Nitroprusside degrades into cyanide. Give thiosulfide to inactivate.
What causes nitroprusside toxicity? What is the antidote?
blocks NMDA-type glutamate receptors; used in alzheimers; confusion
Memantine(mechanism, use, toxicity)
Vitamin E (generic name is alpha-tocopherol)
What vitamin is used in alzheimer's treatment?
Lipid solubility = potency (MAC). Blood solubility = speed of induction.
In gas anesthesias, what is the lipid solubility and the blood solubility?
topical vitamin D analogs
activate nuclear receptors that inhibit keratinocyte proliferation and enhance keratinocyte differentiation; psoriasis,Calcitrol, calcipotriene, tacalcitol (mechanism, use)
monoclocal antibody that binds IL-12 and IL-12 thus inhibiting activation of Th1 cd4+ t cells; used in psoriasis
Usetekinumab(mechanism, use)
MAO-inhbitors (phenelzine) inactive the MAO-I enzymes. It takes 2 weeks for them to get re-synthesized. If both SSRI and MAO-I are active at the same time
serotonin syndrome could occur,Why is it required to wait 14 days after stoping a MAO-i before starting an SSRI?
from leeches
inhibit thrombin; used as an alternative to heparin in HIT.,Lepirudin, Bivalirudin (mechanism, use)
are D2 agonists that DON'T need to be activated like l-dopa does; used in parkinsons and restless leg syndrome
Ropinirole, Pramipexole (mechanism, use)
indirect and direct D agonist
also some anticholingergic functions which reduces tremors,what are the uses of amantidine for parkinsons?
sodium metabisulite
found as a food additive and sanitizer,What compound can cause sickling of sickle cell trait RBC's?
They act on D4 instead of D2 receptors -> no risk of tardive dyskinesia or parkinson's like symptoms
How do atypical antipsychotics avoid causing parkinson's symptoms and tardive dyskinesia?
Celecoxib. It only impairs COX2. COX1 is predominate in platlets.
Which anti-inflammatories will not impair platlet aggregation? why?
binds alpha-4 integrin
which blocks movement of WBC into orgrans;used in crohns and MS; can cause PML and hepatotoxicity.,Natalizumab(mechanism, use, toxicity)
Anti-muscarinics (Benzotropine). Giving dopamine agonists would exacerbate psychosis.
What drugs are preferred in medication induced parkinson's treatment? why?
induction = lower solubility in blood
quicker induction. potency = higher with higher lipid solubility =1/MAC.,What defines induction and potency in gas anesthetics?
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
Pramlintide (mechanism
use, toxicity),Amylin analog; reduces glucagon secretion; causes hypoglycemia 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 platelet degranulation; nausea, headache, facial flushing, hypotension Pharmacology Heme/Onc
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
6-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, 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; 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 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
Febuxostat (mechanism
use, toxicity),Xanthine oxidase inhibitor 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; CNS depression, P450 inducer, contraindicated in patients with porphyrias Pharmacology Neurology
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, hypotension, anti-cholinergic effects Pharmacology Psychiatry
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; used in allergies; less fatigue than other 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 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? Give drug examples.
Treat with Bicarb to make neutral. Exp: phenobarbital, methotrexate, aspirin. Pharmacology general
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
IP3 causes increase in what?
Calcium -> smouth muscle contraction 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). 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, asthma, hypotension. pharmacology autonomics
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 = B-blocker. pharmacology autonomics
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 pseudomembranous colitis
clindamycin, ampicillin 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 reaction,rash,pseudomemrane colitis. pharmacology micro
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 aplastic anemia, gray baby syndrome. pharmacology micro
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-, Nocardia, Chlamydia, UTI; hypersensitivty, hemolysis in G6PD, nephrotoxic, 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
Pyrimethamine use
toxoplasmosis 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 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
benzodiazepines
alcohol withdrawl
ssri
anorexia/bulimia
benzodiazepines
buspirone, ssri,anxiety (3)
methylphenidate
amphetamines, atomoxetine,ADHD (3)
mao inhibitors
ssri,atypical depression (2)
lithium
valproic acid, carbamazepine, atypical antipsychotics,bipolar disorder (4)
ssri
snri, tca,depression (3)
mirtazapine
depression with insomnia
ssri
clomipramine,ocd (2)
ssri
tca, benzodiazepines,panic disorder (3)
SSRI
ptsd
antipsychotics
schizophrenia
antipsychotics (haloperidol)
tourette's syndrome
ssri
social phobia
adhd
narcolepsy, appetite control,cns stimulants clinical use
increased catecholamines at the synaptic cleft (especially NE
dopamine),cns stimulants mechanism
cns stimulant
methylphenidate
cns stimulant
dextroamphetamine
cns stimulant
mixed amphetamine salts
antipsychotic
haloperidol
antipsychotic
trifluoperazine
antipsychotic
fluphenazine
antipsychotic
thioridazine
antipsychotic
chlorpromazine
block dopamine D2 receptors (increases cAMP)
typical antipsychotics mechanism
schizophrenia (positive symptoms)
psychosis, acute mania, tourette's syndrome,typical antipsychotics clinical use (4)
atypical antipsychotic
olanzapine
atypical antipsychotic
clozapine
atypical antipsychotic
quetiapine
atypical antipsychotic
risperidone
atypical antipsychotic
aripiprazole
atypical antipsychotic
ziprasidone
block 5-HT2
doapine, alpha, and H1 receptors,mechanism of atypical antipsychotics
schizophrenia (positive and negative)
atypical antipsychotic clinical use
ocd
anxiety disorder, depression, mania, tourette's syndrome,olanzapine clinical use
mood stabilizer for bipolar disorder
blocks relapse and acute manic events, SIADH,lithium clinical use (3)
not established
related to inhibition of phosphoinositol cascade,lithium mechanism
stimulates 5HT1a receptors
buspirone mechanism
generalized anxiety disorder
buspirone clinical use
increases NE and dopamine via unknown mechanism
bupropion mechanism
smoking cessation
antidepressant,bupropion clinical use (2)
a2 antagonist (increases release of NE and serotonin)
antagonist at 5HT2, 5HT3,mirtazapine mechanism
atypical antidepressant
mirtazapine
atypical antidepressant
bupropion
atypical antidepressant
maprotiline
atypical antidepressant
trazodone
primarily inhibits serotonin reuptake
trazodone mechanism
insomnia (high doses needed for antidepressant effects)
trazodone clinical use
blocks NE reuptake
maprotiline mechanism
block reuptake of NE and serotonin
tricyclic antidepressant mechanism
major depression
fibromyalgia,tricyclic antidepressants general use
bedwetting
imipramine special use
ocd
clomipramine special use
tca
imipramine
tca
amitriptyline
tca
desipramine
tca
nortriptyline
tca
clomipramine
tca
doxepin
tca
amoxapine
ssri
fluoxetine
ssri
paroxetine
ssri
sertraline
ssri
citalopram
serotonin specific reuptake inhibitor
mechanism of ssris
depression
ocd, bulimia, social phobias,clinical use of ssris (4)
cyproheptadine (5HT2 receptor antagonist)
treatment of serotonin syndrome
venlafaxine
duloxetine,snris (generic names) 2
inhibit serotonin and NE reuptake
mechanism of SNRIs
depression
generalized anxiety disorder (venlafaxine); diabetic peripheral neuropathy (duloxetine),clinical use of SNRIs (3)
nonselective MAO inhibition
increases levels of (NE, serotonin, dopamine),mao inhibitors mechanism
atypical depression
anxiety, hypochondriasis,mao inhibitors clinical use (3)
mao inhibitor
phenelzine
mao inhibitor
tranylcypromine
mao inhibitor
isocarboxazid
mao inhibitor (mao-b selective)
selegiline