Card Set Information
Drugs for hyperlipid?
1. statin (avartostatin)
3. acid binding
a) nicotinic (Niacin)
b) bile sequestrants (cholestyramine)
c) fibric (gemfibrozil)
SE of statin?
1. liver toxic
4. pregnancy X
5. increase warfarin, digoxin
SE of ezetimibe?
SE of nicotinic acid?
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?
SE of sodium channel blocker?
-as slow conduction (rate) => H/B, dz, fainting.
-new dysrythmias or worsening
-anticholinergic (dry mouth, urine retention)
-increase risk of heartblock with aminodarone
Lidocaine (Na blocker)
-rapid control of
H/B, worsened dysrhythmias, heart block, respiratory (asthmaticus
-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
toxic, pneumonia-like synd
2 meds of CCC?
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
angina = help coronary arteries relax, HTN, A-fib/flutter
SE of CCC?
- 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)
SS of angina pectoris?
sharp pain in heart region, moving to
side of neck, lower jaw, left arm
Common cause of angina/MI?
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
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)
-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
-NO = consumption of food high K food (interfere with clotting time) eg. leafy green veg,
Meds for HF?
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)
3) digoxin (watch serious SE)
2nd choice = severe & when 1st not effective =
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
-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
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 =>
traction force (same as digoxin = positive inotropic)
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?
2) BAB (metoprolol)
3) ACE (captopril, lisinopril)
4) CCC (diltiazem)
6) direct-acting vasodilator (hydralazine, nitroprusside)