Aromatase inhibitors used in postmenopausal women with breast cancer, MOA: prevent estrogen surge --> prevent LH surge --> prevent ovulation, MOA: PGE2 analog --> cervical dilation and uterine contraction, MOA: alpha1-antagonist --> inhibit smooth muscle contraction, MOA: inhibit cGMP phosphodiesterase --> INC cGMP --> relaxes smooth muscle in corpus cavernosum, increase blood flow --> erection, Toxin: Acetylcholinesterase inhibitor, organophosphates, Toxin: Antimuscarinic, anticholinergic agents, Antidote: stop dig, normalize K, lidocaine, anti-dig Fab fragments, Mg, Antidote: CaEDTA, dimerocaprol, succimer, penicillamine, Antidote: dimerocaprol, succimer, penicillamine, Antidote: nitrite, hydroxycobalamin, thiosulfate, Toxin: Methanol, ethylene glycol (antifreeze). I can tell you about what I found out to be most useful ( I haven't taken the exam yet, though). For pharmacology principles, you can use the basic principles of flashcard making here. What are the first line drugs for tonic-clonic seizures? Today, in this article we are going to share with you free PDF download of USMLE Pharmacology and Treatment Flashcards. Start studying Pharmacology for Step 1. Download . Each card covers a specific disease or drug, with high-yield facts in bold. Also, you can check out the most popular USMLE Step 1 resources. Authored by best-selling medical educator Dr. Conrad Fischer and noted pharmacology expert Dr. Arthur Prancan, Master the Boards: USMLE Step 1 Pharmacology Flashcards give you a streamlined review of the 200 medications most often found on the test, addressing the following frequently asked questions:What are the most likely clinical applications of drugs in each class?What is the mechanism ⦠Lange Pharm seems quite popular, but what do you guys thinks of "Kaplan Medical USMLE Pharmacology and Treatment Flashcards" by Conrad Fischer. The USMLE Step 1 Pharmacology Flashcard Series and the companion PowerPoint presentations are intended to clearly and succinctly review high-yield USMLE Step 1 pertinent information on 5 major areas of Medical Pharmacology. Please select the correct language below. USMLE Step 1 Pharmacology Review Flash Cards. Download . Learn vocabulary, terms, and more with flashcards, games, and other study tools. What is the first-line anti-epileptic for prophylaxis of status seizures? Sign up today! With over 2,600 practice questions, in-depth explanations, flash cards & more, we can help you master the exam to help you become a better clinician. The result is the most COMPREHENSIVE, well-organized, convenient, and effective collection of USMLE Step 1 flashcards available anywhere. Start studying USMLE STEP 1 Pharmacology. Add to folder[?] There is an uptake of glucose by the carri... Use LEFT and RIGHT arrow keys to navigate between flashcards; Use UP and DOWN arrow keys to flip the card; audio not yet available for this language, How do Vmax differe between competitive and noncompetitive inhibitors, How do Km differ between competitive and noncompetitive inhibitors, how are pharmacodynamics affected by competitive inhibitors, how are pharmacodynamics affected by noncompetitive inhibitors, what is the formula for volume of distribution, amount of drug in the body/plasma drug concentration, where is a low volume of distribution held, where is a medium volume of distribution held, where is a high volume of distribution held, - rate of elimination of drug/plasma drug conc, how many half-lifes does it take to reach steady state, how are maintence and loading dose affected in renal and liver disease, maintence dose decreases and loading dose is unchanged, what are three examples of zero order drugs, what is rate of elimation equal to in first order reaction, how does target plasma concentration change during first order reactions, What three things occur during phase 1 metabolism and what metabolites are made, What three things occur during phase 2 metabolism and what metabolites are made, - acetylation, glucuronidation, sulfation, what is the effect of a competitive antagonisist, - shifts curve to right and decreases potency with no change in efficacy, what is the effect of a noncompetitive antagonist, - shifts curve down and decreases efficacy, - acts at same site as full agonist but with reduced maximal effect and decreased efficacy, substance that produces the opposite physiologic effect of an agonist but does not act at the same receptor, what is the formula for therapeudic index, what are the adrenal medulla and sweat glands innervated by, cholinergic fibers and the sympathetic NS, what type of receptors are muscarinic ACh receptors, what are the three major functions of alpha 1 receptors, - icnreased vascular smooth muscle contraction, what are the two main functions of alpha 2 receptors, what are the four main functions of Beta 1 receptors, what are the seven main functions of Beta 2 receptors, what are the two functions of M2 receptors, decrease in heart rate and contractility of atria, What are the six major functions of M3 receptors, what are the major function of D1 receptors, what is the main function of D2 receptors, - modulates transmitter release especially in the brain, what are the four main functions of H1 receptors, - increase in nasal and bronchial mucus production, What is the main function of H2 receptors, Wha tis the main function of V1 receptors, increase vascular smooth muscle contraction, what is the main function of V2 receptors, - Increase in H2O permeability and reabsorption in the collecting tubules of the Kidney, What drug blocks choline uptake by cholinergic neurons, What block conversion of choline to ACh in the cholinergic neurons, what blacks ACH vesicle binding in cholinergic receptors preventing its release, what blocks conversion of tyrosine to DOPA, what blocks uptake of norepi into vesicles in Noradrenergic neurons, what blocks NE vesicle binding in Noradrenergic neurons to prevent the release of NE, what increases NE vesicle binding in noradrenergic neurons, what three things block NE reuptake by Noradrenergic receptors, direct cholinomimetic agent used for postoperative and neurogenic ileus and urinary retention, - activates bowel and bladder smooth muscle, Direct cholinomimetic agent used for the treatment of glaucoma, to promote pupillary contraction and relief of intraocular pressure, Direct cholinomimetic agent that is a potent stimulator of sweat, tears, and saliva, what are are the two main functionos pilocarpine, contacts ciliary muscle of eye and pupillary sphincter, what drug is used for the challenge test for diagnosis of asthma, stimulates muscarinic receptors in airway when inhaled, what are the four main direct agonists for cholinomimetic agents, what are the five indirect cholinomimetic agents, Indirect cholinomimetic agonist is used to treat postoperative and neuro genic ileus and urinary retetion, Myasthenia gravis, reversal of neuromuscular junction blockade, what two anticholinesterases dont penetrate the CNS, what are the two actions of pyridostigmine, what is the clinical application for Pyridostigime, what drug is short acting for diagnosis of Myasthenia gravis, what drug is used to treat atropine OD and glaucoma, physostigmine Anticholinesterase inhibitor, Anticholinesterase used to treat glaucoma, increases endogenous ACh, what three things should be watched for with choliomimetic agents, - exacerbation of COPD, Asthma and peptic ulcers, what is the antidote for cholinesterase inhibitor poisoning, what normally causes cholinesterase inhibitor poisoning, what are the symptoms of cholinesterase inhibitor poisioning, what three muscarinic antagonists treat the eye, what is the function of muscarnic antagonists on the eye, what two muscarinic antagonists treat the CNS, - Benztropine for Parkinson's and scopolamine for motion sickness, what muscarinic antagonist drug treats motion sickness, what muscarinic antagonist drug treates parkison's disease, what muscarnic antagonist is used to treat the respiratory system, what two muscarinic antagonists treat the genitourinary tract, what is the function of oxybutynin and glycopyrrolate, - reduce urgency in mild cystitis and reduce bladder spasms, what three muscarinic antagonists are used for the GI tract, what are methscopolamine, pirenzepine and propantheline used to treat, what are the the six main atributes of atropine toxicity, - increased temp due to decreased sweating, what can atropine cause in men with prostatic hyperplasia, what are the four main atributes of hexamethonium toxicity, Main treatment indications for epinephrine, anaphylaxis, open angle glaucoma, asthma, hypotension- increases HR and SBP while decreasing DBP resulting in a widening of pulse pressure, - hypotension increases both SBP and DBp so now pulse pressure widening, decreases HR, D1=D2 > B >alpha, requires increasing doses to get B and alpha, shock by improving renal perfusion; inotropic and chronotropic for treating heart failure, highest affinity for Beta1, used to treat heart failure, inotropic but not chronotropic, cardiac stress testing, what drug is used for cardiac stress testing, what receptors are targeted for dobutamine, what sympathomimetic drug is used for pupillary dilation, vasoconstriction and nasal decongestion, what receptors are targeted with phenylephrine, what two sympathomimetic drugs are used to treat acute asthma, what drug beta agonist is used for long term treatment of asthma, what two drugs is used to reduce premature uterine contractions, terbutaline and ritodrine - target Beta2 receptors terbutaline also has B1, indirect sympathomimetic, precursor for various sympathetic molecules, cleared by MAO, MAO-inhibitors can decrease clearance and cause HTN, what indirect sympathomimetic is used to treat narcolepsy, obesity and ADD, amphetamine - indirect general agonist, releases stored catecholamines, what indirect sympathomimetic is used to treat nasal decongestion, urinary incontinence and hypotension, - Ephedrine - indirect general sympathomimetic, releases stored catecholamines, what indirect sympathomimetic causes vasoconstriction and local anesthesia, cocaine - general agonist, uptake inhibitor, what are the three main indirect sympathomimetics, what is the mechanism of action for amphetamiene, wha tis the mechanism of action for ephedrine, what is the mechanism of action for cocaine, what is the mechanism for sympathoplegics, centrally acting alpha-2 agonists, decrease central adrenergic outflow, what is the application for sympathoplegics, - hypertension especially with renal disease because there is no decrease in blood flow to kidney, what drug is an irreversible non-selective alphablocker, - phenoxybenzamine, used to treat pheochromocytoma especially before tumor removal, what drug is a reversible non-selective alphablocker, phentolamine; for patients on MAO-inhibitors who eat tyramine containing foods, what is the toxicity from non-selective alpha blockers, - orthostatic hypotension and reflex tachycardia, what are three alpha 1 selevtive blockers, what are the mains uses of alpha 1 selective blockers, what is the toxicity from alpha-1 selective blockers, what drug is an alpha 2 selective blocker, what are toxicity symptoms from mirtazapine, what 6 applications are beta-blockers used for, What is the effect of beta-blockers for hypertesnionj, what are the effects of beta blockers for angina pectoris, - decrease heart rate and contractility resulting in decreased oxygen consumption, what is the effect of betablockers for MIs, what is the effect of betablockers for SVT, decrease in AV conductioin velocity, class II antiarrhythmic, what is the effect of beta blockers for CHF, decreases secretion of aqueous humor for the treatment of glaucoma, what are the four signs of beta-blocker toxicity, what are the four non-selective beta blocker antagonists, what are the five B1 selective antagonists, what are the two nonselective alpha and beta antagonists, what are Beta one selective antagonists useful for, - patients with comorbid pulmonary disease, what patients should beta-blocker use be cautioned for, what are the three cardiac adverse affects from beta-blocker toxicity, what are the CNS adverse effects from beta-blocker toxicity, what is the treatment for acetaminophen toxicity, - N-acetylcysteine replenishes glutathione, what is the treatment for salicylates toxicity, what is the treatment for Amphetamine toxicity, what is the treatment for acetylcholinesterase inhibitor toxicity, what is the treatment for organophosphate toxicity, what is the treatment for antimuscarnic toxicity, what is the treatmenet for anticholinergic aget toxicity, what is the treatment for beta-blocker toxicity, glucagon increases ionotropy and chronotropy of heart, what is the treatment for Digitalis toxicity, - stop dig, normalize K+, lidocane, anti-dig Fab fragments and magnesium (KLAM), what are the four treatments for lead poisoining, what are the two treatments for mercury, arsenic and gold poisoning, what is the treatment for copper, arsenic, gold poisoning, wha tare the three treatments for cyanide poisining, what iare the two treatments for methemoglobin toxicity, what is the treatment for carbon monoxide poisoning, what are the three treatments for methanol, ethylene glycol posioning, what is the treatment for benzodiazepine OD, what is the treatmetn for tPA and streptokinase toxicity, what is the treatment for Theophylline posioning, What drug causes atropine like side effects, What two drugs cause dilated cardiomyopathy, what five drugs can cause aplastic anemia, what drug can cause direct Coombs-postive hemolytic anemia, what six drugs can cause hemolysis is G6PD deficient pts, what three drugs can cause megaloblastic anemia, what three drugs can cause pulmonary fibrosis, what drug can cause acute cholestatic hepatitis, What three drugs can cause focal to massive hepatic necrosis, What fungus can cause focal to massive hepatic necrosis, What three drugs can cause pseudomembranous colitis, what drug can cause adrenocortical insufficiency, Glucocorticoid withdrawal by HPA suppresion, what three drugs can cause hypothyroidism, what drugs can cause gingival hyperplasia, what three drugs can cause photsensitivity, What 8 drugs can cause rash (stevens - Johnson syndrome), What four drugs can cause SLE-like syndrome, what drugs can cause tendonitis, tendon rupture and cartilage damage in kids, what three drugs can cause interstitial nephritis, What two drugs can cause hemorrhagic cystitis, how do you prevent hemorrhagic cystitis from ifosfamide, what two drugs can cause diabetes insipidus, what three drugs can cause parkinson like syndrome, what four drugs can cause disulfiram like reaction, what drugs can cause nephrotoxicity and neurotoxicity, what four drugs can cause nephrotoxicity/ototoxicity, what can induce and inhibit different isoforms of p-450, what does alcohol dehydrogenase convert ethylene glycol to, what does alcohol dehydrogenase convert methanol to, what does formaldehyde and formic acid cause, what blocks alchol dehydrogenase formation of acetaldehyde, what are the three competitive substrates for ADH, fatty acid oxidation in the liver and conversion of pyruvate to lactate, what does does depletion of NAD+ cause in the liver, what is responsible for the glow seen in some individuals after drinking, - Polymorphism in the gene that codes for acetaldehyde dehydrogenase, what are the 7 possible symptoms associated with sulfa allergies, - antibiotic, protein synthesis inhibitor, {"cdnAssetsUrl":"","site_dot_caption":"Cram.com","premium_user":false,"premium_set":false,"payreferer":"clone_set","payreferer_set_title":"USMLE Step 1 Pharmacology","payreferer_url":"\/flashcards\/copy\/usmle-step-1-pharmacology-6274733","isGuest":true,"ga_id":"UA-272909-1","facebook":{"clientId":"363499237066029","version":"v2.9","language":"en_US"}}.
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