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Drugs for hyperlipid?
- 1. statin (avartostatin)
- 2. ezetimibe
- 3. acid binding
- a) nicotinic (Niacin)
- b) bile sequestrants (cholestyramine)
- c) fibric (gemfibrozil)
SE of statin?
- 1. liver toxic
- 2. myopathy
- 3. rabdomyolysis
- 4. pregnancy X
- 5. increase warfarin, digoxin
SE of nicotinic acid?
- 1.liver toxic
- 2. flushing
- 3. hyperglycemia
- 4. gout
SE of cholestyramine?
- just do not absorb into circulation.
- mixed with fluid
- do not take with other drugs
SE of gemfibrozil?
same as statin + gallstone
3 classes of lipids?
- 1. triglycerides = most
- 2. steroids => atherosclerosis
- 3. phospholipid = build membrane
Meds for antidysrhythmias?
- 1. Sodium channel blocker (quinindine)
- 2. Beta blocker (propranolol)
- 3. potassium blocker (aminodarone)
- 4. cacium channel blocker (verapamil)
- 5. Others (digoxin & adenosine)
what is dysrhythmias?
- -abnormalities of conduction or rhythm
- -harmless or deadly
sx of dysrhythmias?
dz, weakness, fainting, decreased exercise tolerance, sob. Skipped beat
where Na & Ca? where K?
- Na & Ca outside cell
- -Na rush inside cell => depolarization
- -Ca rush inside cell => depolarization/contraction
- K inside cell
- -K rush outside cell => back to polarized
Action of Sodium channel blocker?
- -block Na channel => slow rate of conduction
- (similar to local anesthetics = lidocaine)
Drugs of sodium blocker?
- quinidine (protype)
- phenytoin (dilantin)
SE of sodium channel blocker?
- -as slow conduction (rate) => H/B, dz, fainting.
- -new dysrythmias or worsening
- -anticholinergic (dry mouth, urine retention)
- -double digoxin
- -increase risk of heartblock with aminodarone
Lidocaine (Na blocker)
- -rapid control of Ventricular dysrthymias
- -local anesthetic
- SE = H/B, worsened dysrhythmias, heart block, respiratory (asthmaticus), confusion/sz/lightheadedness, lethargy, blurred vision.
- -toxic if prolong => check level, mus be on cardiac monitor
Action of beta blocker in dysrhythmias?
- 1) reduce automaticity & conduction velocity => reduce heart rate
- 3) reduce contractility =>reduce CO => reduce bp
SE of beta blocker in dysrhy?
- -H/B, dz, fainting (same as Na blocker)
- -as also beta 2 (lung) => bronchospasm => asthma and COPD
- -metoprolol = heart block, HF, alter insulin (diabetes), + digoxin => bradycardia
- -propanolol = also tx migraine/ha. Do not give with MAO inhibitor
Action of K channel blocker?
slow conduction + prolong refractory period (resting) => stablizing dysrhythmias
what meds used as CODE for dysrhythmias?
- aminodarone (K channel blocker)
- => V-tach, A-tach/fib (# v-fib = CPR, defri)
- *also long half life
SE of K channel blocker?
- - H/B, dz, heart block, HF
- -pulmonary toxic, pneumonia-like synd
- - hepatic
- -increase digoxin/anticoagulant/herbal
- ***IV=continuous EKG
Action of CCC in dysrhyth?
- -to treat supraventricular dysrhyth only
- same as BAB
- 1) reduce automaticity
- 2) reduce conduction
- 3) reduce contractility
- => prolong refractory period
- * verapamil = slow conduction, dilate coronary arteries (tx angina)
- *Diltiazem = tx vasospastic angina = help coronary arteries relax, HTN, A-fib/flutter
SE of CCC?
- -H/B, ha
- - increase digoxin (both have effect of slowing conduction)
- -increase level with grapefruit
* diltiazem = AV block, HF, insomnia, photosensitivity
Action of digoxin in antidysrhythmias?
same as BAB & CCC, except that instead of reduce contractility, it increase contractility => dysrhythmias if execess => take apical
SE of digoxin in antidysrhythmias?
- -dysrhythmias if excess
- -interact with many common drugs
- -hypotentsion, HF, anorexia
- -toxic if pt with hypoK
Action of adenosine?
- -bolus IV to terminate serious A-tach by slowing conduction thru AV and automaticity SA.
- -PSVT = paroxysmal supraventricular tachycardia
why do we need to notify dentist, surgeons and eye doctor when taking propranolol?
meds lower intraocular pressure
what e-lyte produce depolarization?
what meds in antidysrhythmias interact with digoxin?
- -quinidine => need to reduce digoxin
- -metoprolol, propanolol => + digoxin => increase digoxin=> bradycardia
- -CCC => elevate digoxin
what outcome to be expected when taking antidysrhythm?
2 CCC, besides treating dysrhythmias, what else are they used for?
- -verapamil = tx angina
- -diltiazem = HTN
what meds for angia & MI?
- 1) O2 & morphine
- 2) nitrates (nitroglycerin)
- 3) BAB (atenolol)
- 4) CCC (diltiazem?? verapamil)
- 5) thrombolytics (reteplase)
- 6) antiplatelet
SS of angina pectoris?
sharp pain in heart region, moving to left side of neck, lower jaw, left arm
Common cause of angina/MI?
- -mitral stenosis
- -peptic ulcer
what food rich in K and Mg
banana, kidney bean, spinach, tomatoes, apricot, peanut butter, sweat potato, leafy green
surgical procedures for angina/MI?
- PTCA (areaof narrowing is opened using either balloon cath or laser)
4 mechanisms to reduce cardiac workload by pharmacological goal in angina/MI?
- 1) slow heart rate
- 2) reduce contractility
- 3) dilate vein (so heart can receive less blood =reduced preload)
- 4) lower bp (heart can push blood out of chamber = reduced afterload)
Action and SE of morphine?
- -dilate coronary arteries
- -SE = H/B, cardiac/resp arrest, sedation, clouded sensorium, euphoria, sz, thrombocytopenia, urine retention
- -Naloxone (Narcan)
action of nitroglyceride?
- 1) dilate vein => reduce preload returning blood => afterload CO
- 2) dilate coronary artery => more O2 for myocardium, relax spasm
Types and Meds of nitrates?
- 1) short = SL, spray, cream = nitroglyeride
- 2) long = oral, patch = isosorbide
SE and contraindication of nitrates?
- -H/B (may), reflex tachycardia (palpitation or skipped beat) ha, dz, flushing
- -No = viagra, tidalafil (Cialis) => severe hypotension
in angina/MI, BAB used with CCB may cause?
excessive cardiac suppression
In angina/MI, BAB used with digoxin may cause?
slowed AV conduction => heartblock
- 1) nitroglycerides (short nitrate)
- 2) isosorbide (long nitrate)
- 3) hydralazine (direct)
- 4) nesiritide (IV in ICU only for HF)
* used for chest pain
cause of MI?
plaque builup narrowing arteries => a broken piece goes to smaller vessel to lodge => block O2 supply => ischemic
what meds for MI?
- 1) thrombolytic (reteplase) = dissolve clot by activating plasminogen to bind to fibrin = effective w/in 30 minutes and not later 12 hrs
- 2) antiplatelet = aspirin
- 3) anticoagulant = heparin; glycoprotein IIb/IIIa, ADP receptor blocker
- 4) BAB = effecitve w/in 24 hrs (reduce O2 demand by reduce rate/contractility/bp). H/r watch sx of dysrhyth b/c its ability to slow conduction
- 5) ACE = w/in 1-2 days
- 6) narcotic analgesic (morphine)
what to know when taking anticoagulant? (SE)
- SE = pt with active bleeding
- -NO = consumption of food high K food (interfere with clotting time) eg. leafy green veg, herbal
Meds for HF?
- 2)diuretic (furosemide)
- 3) ACE (lisinopril - used when pt also has HTN)
- 4) phosphodiesterase (milrinone)
- 5) vasodilator (isosorbide)
- 6) BAB (carvedilol)
- 7) natriuretic peptides (nesiritide - new, IV in ICU, vasodilation => cause severe hypotension)
what and cause of HF?
- -inability of ventricle to pump enough blood for body's demand
- -cause = weakened muscle.
- - can be both, but normally left ventricle
- -decreased contractility => decreased CO =>
- 1) increased preload => lung congestion
- 2) decreased bp =>
- a- increased demand => increased rate => increased workload
- b-decreased flow to kidneys => ADH & renin pathway activated => Na/water retention => increased blood volume => increased bp => increased afterload => increased work
Drug of choice in HF?
- first choice = mild to moderate
- 1) ACE (esp with HTN which normally the case)
- 2) diuretic
- 3) digoxin (watch serious SE)
- 2nd choice = severe & when 1st not effective =
- 1) phosphodieterase
- 2) vasodilator
- 3) BAB
3 important factors of HF?
- 1) preload (stretch)
- 2) contractility (snap back)
- 3) afterload (force of LV to pump against)
action of digoxin?
1) inhibit Na& K tapse => release Ca => increase force of contraction = increased CO (positive inotropic effect # BAB = negative) => increased UOP => relieve lung congestion & peripheral edema
2)suppress SA & slow conduction AV (watch serious SE = excessive slow heart rate)
SE of digoxin?
- - most dangerous = create dysrhythmias (particularly pt w hypoK) even tho digoxin can also be used for dysrthythmias
- - toxic if overdose (hypo and hyper K). hypoK predispose pt to toxic
- -blurred vision, anorexia, sob, leg muscle cramp
Action of ACE?
- -inhibit ACE that cause conversion of angiotension I to II
- -diate arterioles & veins => reduce blood volume and bp, peripheral edema
- -prevent pathologic changes in cardiac structure
SE of lisinopril (ACE)?
- -caution in renal failure/insufficiency/DM
- -dry cough
- -angiodema (swelling of face/trachea/hand)
action of diuretic?
- inhibit transport of Na, K & Cl across loop of Henle = blocking NaCl (water) reabsorption => increase UOP => reduce blood volume => reduce bp, edema, congestion
- * K-sparing (spironolactone) = inhibit aldosterone in distal tubule (far from loop => spare K)
SE of furosemide?
- -hypoK (cause lethal dysrhythmias), hypo e-lytes
- -large dose => ototoxicity
- -leukopenia, thrombocytopenia
most prescribed diuretic for HTN/HF?
- -act on different part of kidney to incresase UOP => less hypoK
SE of K-sparing diuretics?
- -HyperK!!! (#furosemide and HCTZ (less)
action, use, SE of phosphodiesterase inhibitor?
- -blocking phosphodiesterase => increase Ca => increaes contraction force (same as digoxin = positive inotropic)
- - vasodilation
- **short term (2-3 days) control of acute HF, toxic => only for pt who not respond to ACE & digoxin
- -SE = ventricular dysrhythmias => EKG monitor
action, use, SE of vasodilator (isosorbide) in tx of HF?
- -act directly on vein to cause vedodilation => reduce venous return (preload) => reduce work for heart
- -dilate coronary arteries => mroe O2 for myocardial tissue
- -SE = hypotension, reflex tachycardia, ha
- -contraindication = viagra
pt with HF also experiencing angia, which meds?
isosorbide (b/c we have to take care of angia first)
Meds for HTN?
- 1) diuretic
- 2) BAB (metoprolol)
- 3) ACE (captopril, lisinopril)
- 4) CCC (diltiazem)
- 5) ARB(losartan)
- 6) direct-acting vasodilator (hydralazine, nitroprusside)