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;
48 Cards in this Set
- Front
- Back
|
Quinidine
|
Class 1A antiarrhythmic; Na-channel blocker
- 1A's also block K channels BAD DRUG!!! It has pro-arrhythmic effects -causes muscarinic blocade --> increases HR and AV conduction -reflex tachycardia d/t vasodilation from alpha block - In A-fib, use in combo w/ digoxin to slow AV conduction SE: cinchonism, hypotension, prolonged QT --> Torsades DDI: hyper-K enhances effect; increases Digoxin tox by displacing it from protein binding -Quinidine is a weak base --> antacids greatly increase absorption and toxicity |
|
|
Procainamide
|
Class 1A Na+ channel blocker
- 1As also block K channels PK: Less muscarinic and no alpha block (compared to quinidine) - Phase II metab --> SLE w/ slow acetylators (the "P" in HIP) AE: drug-induced SLE -Thrombocytonpenia, agranulocytosis -Torsades (NAPA, active metabolite, increases ADP --> extends drug life, but also causes Torsades) |
|
|
What is unique about Class 1B drugs' MOA from other antiarrhythmetics?
|
Most antiarrhythmics work during the AP. Class 1Bs work between the AP.
They target inactivated Na-channels, which also allows them to target damaged or ischemic tissue |
|
|
Lidocaine
|
Class 1B antiarrhythmic Na-channel blocker
Use: Post-MI, open-heart surgery - Antidote to Digoxin toxicity! PK: IV only to avoid 1st pass SE: CNS tox (seizures); least cardiotoxic of the antiarrhythmics |
|
|
Mexiletine
|
Class 1B Na-channel Blocker
Same as lidocaine, but comes in oral form |
|
|
Flecainide
|
Class 1C Na-channel blocker
-Targets fast Na channels, esp His-Purkinje fibers -Not effect on APD and no ANS effects SE: rarely used d/t pro-arrhythmic effects when used post-MI or prophylactically in VT |
|
|
Which beta blockers are used as antiarrhythmics?
|
Class II antiarrhythmics:
Propranolol (non-selective) Acebutolol & esmolol (B1 selective) Use: Prophylaxis post-MI and in SVTs -Esmolol (IV) for Tx of acute SVT Sotalol: classified as a Class III AA --> used to Tx life-threatening arrhythmias |
|
|
Amiodarone
|
Class III antiarrhythmic: K+ channel blocker
Used in any arrhythmia; mimics classes I-IV PK: t1/2 > 80 days; binds extensively to tissues SE: pulmonary fibrosis, phototoxicity, corneal deposits, hepatic necrosis; Blue skin pigmentation and thyroid dysfunction d/t iodine in drug **No Torsades risk!** |
|
|
Sotalol
(CV use) |
Class III antiarrhythmic: K-channel blocker
MOA: decreases K channel, slowing phase 4 - B1 blockade decreases HR and AV conduction Use: Life-threatening arrhythmias (esp. Torsades) |
|
|
Verapamil
Diltiazem (antiarrhythmic effects) |
Class IV Ca-channel blockers
MOA: Decrease phase 0 & 4 - decrease SA and AV node activity Use: Antiarrhythmic - SVTs; HTN; Angina SE: constipation (verapamil), flushing, AV block DDI: Additive AV block w/ BB and digoxin; Verapamil displaces dig from TBPs |
|
|
Clonidine
|
alpha-2 agonist
Use: HTN (powerful ↓ in SANS, ↓ TPR and HR) - Opiate withdrawal SE: CNS depression and edema DDI: Tricyclic antidepressants decrease the antihypertensive effects of a2-Ag |
|
|
Methyldopa
|
alpha-2 agonist
Use: HTN (powerful ↓ in SANS, ↓ TPR and HR) - HTN in pregnancy! SE: Hemolytic anemia (+ Coombs test) -CNS depression and edema DDI: Tricyclic antidepressants decrease the antihypertensive effects of a2-Ag |
|
|
Reserpine
|
Use: HTN
MOA: destroys vessicles - ↓ CO and TPR (d/t ↓ NE) - ↓ NE, DA, and 5-HT in CNS SE: Severe depression (depletes amines); Edema; Increased GI secretions |
|
|
Guanethidine
|
Use: HTN
MOA: Accumulates in nerved endings via reuptake --> binds vesicles --> Inhibits NE release SE: Diarrhea, edema DDI: tricyclic antidepressants block reuptake, therefore block guanethidine's action |
|
|
Which alpha-1 blockers are used to Tx HTN?
|
Prazosin, doxazosin, terazosin
Use: HTN, BPH SE: "First dose" syncope and orthostatic hypotention; urinary incontinence Advantage - good for lipid profile (↓ LDL & ↑ HDL) |
|
|
Pneumonic for antiarrhythmic drugs classes
|
I - Saved - Sodium
II - By - Beta blocker III - Pharm - Potassium IV - Class - Calcium |
|
|
Adenosine
|
Antiarrhythmic (unclassified)
MOA: activates adenosine receoptors (heart/lungs) --> Gi-coupled decrease in cAMP --> increased K efflux (hyperpolarization) Use: DOC for paroxysmal SVTs and AV nodal arrhythmias -along w/ valsalva and carotid massage Administered IV d/t half life < 10 sec SE: Flushing, sedation, dyspnea (this one can stop the heart for a few seconds!) DDI: antagonized by methyzanthines (theophylline and caffeine) |
|
|
Magnesium
(CV effects) |
Antiarrhythmic (unclassified)
Used to Tx torsades |
|
|
Orthostatic hypotension occurs with drugs that cause (vasodilation/venodilation)?
|
Venodilation
|
|
|
Hydralazine
|
Direct-acting vasodilator
Use: moderate-severe HTN MOA: Arteriole-specific dilation via NO -no venodilation --> no orthostatic hypoTN SE: SLE in slow acetylators (Phase II) -edema -reflex tachycardia |
|
|
Nitroprusside
|
Direct-acting vasodilator
Use: DOC for hypertensive emergencies (IV use) MOA: ↓ TPR via dilation of arterioles & venules --> via NO SE: Cyanide toxicity (only in long-term infusions) |
|
|
Minoxidil
|
MOA: Opens K channels, causing repolarization of smooth muscle --> arteriolar vasodilation
Use: Severe HTN - Baldness (topical) SE: hypertrichosis, edema, reflex tachycardia |
|
|
Diazoxide
|
MOA: Opens K channels, causing repolarization of smooth muscle --> arteriolar vasodilation
Use: Hypertensive emergencies - insulinoma Tx SE: Hyperglycemia (from ↓ insulin release), edema, reflex tachycardia |
|
|
nifedipine
and other "-dipines" |
Dihydropyridine CCBs
MOA: Block L-type Ca channels --> ↓ IC Ca --> ↓ TPR Use: HTN; Vasospastic angina (esp. Nifedipine) Nifedipine = DOC for Raynaud's Dz SE: Reflex tachycardia; Gingival hyperplasia |
|
|
Bosentan
|
Use: Pulmonary HTN
MOA: ETA receptor antagonist - Endothelin (ET-1) is a powerful vasoconstrictor through ET-A and -B receptors SE: associated w/ vasodilation -CI in pregnancy |
|
|
Epoprostenol
|
Prostacyclin (PGI2)
Admin: Infusion pump |
|
|
Sildenafil
(in pulmonary HTN) |
MOA: Inhibits type V PDE --> increases cGMP --> pulm artery relaxation
|
|
|
Nitroglycerin
|
Nitrate for angina
MOA: prodrug of NO --> venodilation --> ↓ preload --> ↓ cardiac work --> ↓ O2 requirement --> infarct size and post-MI mortality Admin: sublingual, transdermal, IV SE: flushing,headache, O. hypoTN Reflex tachycardia, fluid retention - Tachyphylaxis w/ repeated use (wear patch only 1/2 day) DDI: sildenafil (PDE-5) --> too much venodilation |
|
|
Isosorbide
|
Nitrate used in angina
Same as nitroglycerin, except in oral extended release form for chronic use |
|
|
Mannitol
|
Osmotic diuretic
MOA: Inhibits water resorption throughout the tubule --> increases urine volume Use: ↓ IOP in glaucoma, ↓ intracerebral pressure, oliguric states (rhabdomyolysis) SE: acute hypovolemia |
|
|
Acetazolamide
Dorzolamide ("-zolamide") |
Carbonic Anhydrase Inhibitors
MOA: Block CA --> ↑ Na and HCO3 in tubule lumen --> ↑ diuresis Use: Glaucoma (↓ production of fluid), Acute mountain sickness, Metabolic alkalosis SE: Bicarbonaturia & met. acidosis -Hypokalemia -Hyperchloremia -Renal stones (d/t ↑ urine pH) -Sulfa drug --> allergy |
|
|
Ethacrynic acid
|
Loop Diuretic
MOA, SE, Use, DDI same as furosemide except: - NOT a sulfa drug!!! Use for pts with sulfa allergies |
|
|
Furosemide
Torsemide |
Loop diuretic
MOA: Block Na/K/2Cl transporter in Thick Ascending Loops --> ↓ resorption of Ca and Mg --> diuresis **Loops lose Ca!** Use: Acute pulmonary edema, CHF, Refractory edemas, hypercalcemia - NOT a sulfa drug!!! SE: Hypokalemia and met. alkalosis, hypocalcemia, hyperuricemia (d/t competition) -Ototoxicity DDI: Aminoglycosides (enhance ototox) Lithium (↓ clearance) Digoxin (↑ tox d/t electrolyte disturbances) |
|
|
Bumetinide
|
Loop diuretic
Same as furosemide |
|
|
Hydrochlorothiazide
|
Thiazide diuretic
MOA: Inhibits Na/Cl transporter in DCT Use: HTN, CHF; nephrolithiasis; Nephrogenic diabetes insipidus SE: ↓ K & alkalosis --> ↑ glycemia, ↑ Ca, ↑ uricemia, ↑ lipidemia DDI: Digoxin - ↑ tox d/t electrolyte disturbance CI in pts w/ diabetes mellitus |
|
|
Indapamide
|
Thiazide diuretic
Same as HCTZ, except: -Doesn't raise blood lipids! |
|
|
Metolozone
|
Thiazide diuretic
Same is HCTZ, except: -Works at low GFR (< 30) |
|
|
Spironolactone
|
K-sparing diuretic (Aldosterone receptor blocker)
Use: hyperaldosteronism; adjunct to K-wasting diuretics; antiandrogenic uses (hirsutism); CHF SE: Hyperkalemia and acidosis Antiandrogen (gynecomastia) |
|
|
Amiloride
|
Na-channel blocker
Use: adjunct to K-wasting diuretics or lithium-induced diabetes insipidus SE: hyperkalemia and acidosis |
|
|
Eplerenone
|
Aldosterone receptor blocker (selective)
Diuretic w/o anti-androgenic activity |
|
|
Lovastatin and other "-statins"
|
HMG-CoA reductase inhibitor
MOA: ↓ liver cholesterol, ↑ LDL receptor expression --> ↓ plasma LDL --> VLDL --> ↓ triglycerides SE: Myalgia, myopathy (check creatine kinase) Rhabdomyolisis Hepatotoxicity (check LFTs) DD: Gemfibrozil (↑ rhabdo); P450 inhibitors ↑ statin toxicity |
|
|
Cholestyramine
|
Bile Acid Sequestrant
MOA: compelxes bile salts in the gut - ↓ enterohepatic recirculation of bile salts -↑ synthesis of new bile salts - ↓ liver cholesterol --> ↓ blood LDL - ↑ LDL-receptor expression SE: ↑ VLDL and triglycerides --> CI in hypertriglyceridemia! - GI disturbance - Malabsorption of lipid-soluble vitamins DDI: any orally administered drug |
|
|
Colestipol
|
Bile Acid Sequestrant
MOA: compelxes bile salts in the gut - ↓ enterohepatic recirculation of bile salts -↑ synthesis of new bile salts - ↓ liver cholesterol --> ↓ blood LDL - ↑ LDL-receptor expression SE: ↑ VLDL and triglycerides --> CI in hypertriglyceridemia! - GI disturbance - Malabsorption of lipid-soluble vitamins DDI: any orally administered drug |
|
|
Niacin
(Vit B3, Nicotinic acid) |
MOA: inhibition of VLDL synthesis
- ↓ plasma VLDL and LDL - ↑ plasma HDL SE: flushing, pruritis, rashes (use aspirin 30 min prior to prevent) - Hepatotoxicity |
|
|
Gemfibrozil
|
MOA: activation of lipoprotein lipases
- ↓ VLDL and IDL; modest ↓ in LDL - ↑ HDL in most pts - can ↑ LDL Use: Hypertriglyceridemia SE: Gallstones, myostitis |
|
|
Fenofibrate
|
MOA: activation of lipoprotein lipases (Binds PPAR-gamma to regulate transcription)
- ↓ VLDL and IDL; modest ↓ in LDL - ↑ HDL in most pts - can ↑ LDL Use: Hypertriglyceridemia SE: Gallstones, myostitis |
|
|
Ezetimibe
|
Use: ↓ LDL
MOA: prevents intestinal absorption of cholesterol SE: GI distress |
|
|
Orlistat
|
Use: Weight loss
MOA: inhibits pancreatic lipase --> ↓ triglyceride breakdown in intestine SE: steatorrhea, diarrhea; ↓ absorption of lipid-soluble vitamins (always take w/ a MV) |
