Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
43 Cards in this Set
- Front
- Back
|
Statins:
Mechanism AE's Special Considerations |
Competitive inhibition of HMG CoA Reductase, which prevents cholesterol synthesis
AE: Hepatotoxicity, myopathy/myalgia SC's: Simvastatin 80 can't be started unless you've been on Simvastsatin for a year Do not mix with fibrates |
|
|
A starting dose of any statin will provide a ___ percent reduction in LDL, whereas subsequent dose increases will only provide an additional ___.
|
Starting dose: 30% reduction in LDL
Subsequent increase: 6-7% reduction in LDL, 50% increase in AEs |
|
|
Which statins have the most drug interactions? Why?
|
Atorvastatin
Simvastatin Lovastatin bc of interaction with CYP3A$ |
|
|
Which statin is considered the drug of choice if concerned about drug interactions or AEs?
|
Pravastatin (doesn't get metabolized through CYP pathways; metabolized by Sulfation)
|
|
|
What is the most potent statin?
|
Rosuvastatin
|
|
|
Gemfibrozil:
Primary mechanism |
Stimulation of lipoprotein lipase
|
|
|
Fibrates:
Identifying Prefix/Suffix Mechanism AEs Special Considerations |
-fibr-
ex: gemFIBRozil, fenoFIBRate, fenoFIBRIc acid Mech: Decreases TGs by up-regulating lipoprotein lipase AEs: Inc'd liver function tests Special Considerations: Do not use with statin (risk > benefit) unless TG>500 |
|
|
Treating [LDL/TG] is not associated with positive clinical outcomes.
|
Treating TGs is not associated wtih positive clinical outcomes
|
|
|
Bile Acid Resins:
Identifying Prefix/Suffix Mechanism AEs Special Considerations |
Begins with Coles or Choles, ex:
COLEStipol, COLESevelam, CHOLEStyramine Mech: Prevents intestinal reabsorption of bile acids (req'd for cholesterol synthesis) which decreases LDL AE's: GI effects Special: Decreased absorption of fat soluble vitamins |
|
|
Which bile acid resin has been approved for use in DM?
|
Colesevelam
|
|
|
Ezetimibe:
Mechanism AEs Special Considerations |
Ezetimibe = Zetia
Mech: Inhibits intestinal absorption of exogenous cholesterol to lower LDL (no mortality data; has not been demonstrated to improve clinical outcomes in combination with statins!) AE's: Diarrhea Special: Does not affect cholesterol made by liver |
|
|
Niacin:
Mechanism of Action AEs Special Consideration |
Niacin: inhibits lipolysis in adipose tissue, rescudes hepatic VLDL secretion into circulation; both result in increased HDL
AEs: Flushing Special: Careful when giving to pts w/hx DM and gout |
|
|
Class I Antiarrhythmics:
General Mechanism of Action A vs B vs C Effects and AEs List A, B, and C drugs |
Class I Anti's: Sodium channel blockers--slow or block conduction, esp in depolarized cells
IA: Increase AP and refractory period IB: Decrease AP period IC: No change in AP IA: Double Quarter Pounder Disopyramide Quinidine--torsades de pointes Procainamide--reversible Lupus-like syndrome 1B: Lettuce Tomatoes Fries Pickles; CV depression, CNS related AEs Lidocaine Tocainide Mexiletine Phenytoin 1C: Fries Please; Proarrhythmics Felacainide Propafenone |
|
|
What is torsades de pointes?
|
Specific form of vtach
|
|
|
Class I Antiarrhythmics:
A vs B vs C Clinical Uses |
A: Atrial and ventricular arrhythmias
B: Acute ventricular arrhytmias (esp post-MI), digoxin-induced arrhythmias C: Vtachs that progress to VF and only as a LAST resort; DO NOT USE POST MI |
|
|
Cinchonism:
Symptoms Associated Drug Overdose |
Ringing in ears, blurred vision, upset stomach
Confused, delirious behavior Must be quinine overdose, so QUINIDINE |
|
|
Class II Antiarrhythmics: Selectives
Identifying Prefiix/Suffix Mechanism of Action AEs Special Consideration |
Selectively block beta-1 receptors in heart/vascular smooth muscle
ends in -olol and begins with A->M (except CARVEDILOL!) AEs: Dizziness, IMPOTENCE Bradycardia Special: Up regulation of receptors seen in chronic use, so don't abruptly discontinue May mask syx of hypoglycemia! |
|
|
Which Class II Antiarrhytmics decrease mortality in heart failure?
|
Bisoprolol
Metropolol Succinate (XL) Carvedilol |
|
|
Class II Antiarrhythmics: Non-Selectives
Identifying Prefiix/Suffix Mechanism of Action AEs Special Consideration |
ends in -olol and begins with N-->Z (Non-Zelective)
Mech: blocks beta-1 and beta-2 receptors in heart and vas smooth muscle AEs: Dizziness, sleep disturbances Considerations: Increased airway resistance--contraindicated in asthmatics |
|
|
Class II Antiarrhythmics:
Uses of Selectives vs Non-Selectives |
Selectives:
Tachycardia, Angina, Arrhythmias, HTN Non-Selectives: Arrhythmias, Angina, pheo, tremor, migraine prohpylaxis, portal HTN |
|
|
Which Class II Antiarrhythmics have the added benefit of vasodilation? Why?
|
Carvedilol
Labetolol Antagonize beta-1, beta-2, and ALPHA-1 (blocks NE receptors to allow for VASODILATION) |
|
|
Class III Antiarrhythmics:
Mechanism Adverse Effects in Specific Drugs |
MOA: Blocks K+ channels to prolong repolarization; increases AP duration, Absolute Refractory, and QT interval
Sotalol- torsades de pointes Ibutilide - torsades de pointes Bretylium - new arrhythmias, hypotn Amiodarone- pulm fibrosis, hepatotox, hypo/hyperthyroid |
|
|
Which antiarrhytmic has Class I, II, III, and IV activity?
|
Amiodarone
|
|
|
Which Class III Antiarrhythmic has the lowest incidence of Torsades de pointes?
|
Amiodarone; also doesn't have negative inotropic effects
|
|
|
Which Class III Antiarrhythmic also has Class II activity?
|
Sotalol
|
|
|
Class IV Antiarrhythmics:
Subcategories and Identifying Prefix/Suffix Mechanism of Action by Category AE's |
Dihydropyridines: -dipine
Binds L-type Ca2+ channels in vasc smooth muscle Non-dihydropyridines: Diltiazem Verapamil Bind L-type Calcium channels in SA node, AV node, and vascular smooth muscle AE: Peripheral edema, AV block, bradycardia, CHF (non-DHPs) |
|
|
Which Class IV Non-Dihydropyridine exhibits a stronger negative inotropic effect?
|
VERapamil--VERy good
|
|
|
What drug category is the drug of choice for hypertension?
|
Dihydropyridines (-dipines)
|
|
|
Adenosine:
Mechanism of action Use |
Slows AV node conduction and interrupts AV node re-entry pathways
Use for diagnosing/abolishing supraventricular tachycardia Short acting (15 secs) and low toxicity |
|
|
Magnesium:
Use |
Torsades de pointes
Digoxin Toxicity |
|
|
Digoxin:
Mechanism of Action Uses AEs Special Consideration |
MOA:
Direct inhibition of Na/K ATPase STIMULATES VAGUS Uses: CHF (increases contractility), Afib (decreases conduction at AV node and depression of SA node) AE: Cholinergic effects, blurry yellow vision Special: Inc'd risk of toxicity if pt is hypokalemic or has impaired renal fn |
|
|
Nitrates:
Mechanism of Action Uses and Order of Onset AEs Special Consideration |
Mech: Vasodilates by release of NO in smooth muscle (inc'd cGMP and muscle relaxation; decreases preload!)
Use: Relief of angina via decreased preload Onset: Nitroglycerin > isosorbide DInitrate > isosorbide MONOnitrate (veins are affected more than arteries!) AE's: Reflex tach, flushing, hypotn Special: Contraindicated with PDE-5 inhibitors (severe hypotn!) Can develop tolerance |
|
|
Hydralazine:
Mechanism of Action Uses AEs Special Consideration |
Peripheral vasodilation via inc'd cGMP and smooth muscle relaxation; thus reduces AFTERLOAD
Use: SEVERE hypertn, CHF AE: Reflex tach, LUPUS-like syndrome Special: Contraindicated in angina/CAD |
|
|
Nitrates preferentially dilate _____.
|
Veins
|
|
|
Hydralazine preferentially dilates _____.
|
Arterioles over veins (afterload reduction)
|
|
|
Ranolazine:
Mechanism of Action Uses AEs Special Consideration |
Mech: Unknown
Use: Chronic angina AE: Prolonged QT interval, (increased risk of Torsade de pointes). syncope Special: Don't use with renal impairment |
|
|
Aspirin:
Mechanism of Action Uses AEs Special Consideration |
Irreversibly inhibits COX1/2
Use: Antipyretic, Analgesic, Anti-platelet (MI/TIA/Thrombotic Prophylaxis) AE: Gastric ulcers/bleeds, tinnitus Special: Reye's syndrome (careful with kids!) |
|
|
Thienopyridines:
Mechanism of Action Uses AEs by drug Special Consideration |
Mech: Inhibit platelet aggregation by blocking ADP receptors (prevent Glycoprotein IIb/IIIa expression)
Use: Acute Coronary Syndrome, Stenting, Thrombotic Prophylaxis AEs: Ticlopidine: Neutropenia Clopiodgrel, Prasugrel: Bleeding Special: Caution with poor metabolizers of 2C19 |
|
|
Glycoprotein IIb/IIIa inhibition:
Mechanism of Action Uses AEs by drug Special Consideration |
Inhibits aggregation of platelets by antagonizing fibrinogen binding GP IIb/IIIa receptor
Use: Acute Coronary Syndrome, MI, Cath Lab AEs: TiroFIBAn: bleeding, brady, dizzy AbcixIMAB: Hypotn EftiFIBAtide: hypotn, bleeding Special: Tirofiban: can't be used in pts w/ASA allergy |
|
|
Heparin vs Warfarin:
Mechanism Monitoring Administration Toxicity Treatment Time of Effect Onset Use in Pregnancy |
Heparin:
Activates antithrombin (dec'd IIa and Xa) Monitored by PT Given IV/SQ Tox treat w/protamine RAPID anticoag CAN be used in pregnancy Warfarin: Interferes w/synthesis of Vit K clotting factors (II, VII, IX, X) Monitored by PT/INR Given orally Tox treat w/Vit K and frozen plasma 2-3 days before effect CANT be used in pregnancy |
|
|
Direct Thrombin Inhibitors:
Identifying Prefix/Suffix Mechanism of Action Uses AEs Special Consideration |
Ends in -irudin
Except Argatroban, Dabigatran Mech: Binds and inhibits active site on thrombin Use: Heparin induced thrombocytopenia, vascular thromboembolism, DVT, PE, Afib, Cath; no antidotes and SUPER expensive AE's: Bleeding, hemorrhage Special: Argatroban: hepatic elimination; everything else is renal elimination |
|
|
Low Molecular Weight Heparins:
Identifying Prefix/Suffix Uses Mechanism of Action AEs Special Consideration |
End in -PARIN (hePARIN)
Use: DVT, Cath Lab, N/STEMI(!) Mech: Inhibits thrombin, Xa AE: Bleeding, HIT, osteoporosis (chronic) Special: No therapeutic monitoring, can be dosed subcutaneously as outpatient |
|
|
Enzyme Epoxide Reductase is afilliated with ________.
|
Vitamin K; inhibited by warfarin
|
