cardio pharm Flashcards
diabetic nephropathy
ACE inhibitors and ARBS are protective
calcium channel blockers
block voltage dependant L-type calcium channels of cardiac and smooth muscle –> reduce muscle contractility
Vascular smooth muscle: amolidipine = nifedioine > diltiazem> verapamil
Heart: verapamil> diltiazem > amlodipine = nifedipine
dihydropyridines (amlodipine and nifedipine) are used for?
HTN, angina (including prinzmetal), raynaud
non-dihydropyridines (diltiazem, verapamil) are used for?
HTN, angina, atrial fibb/flutter
Nimodipine a calcium channel blocker is used for?
subarachnoid hemorrhage (prevents cerebral vasospasm)
Calcium channel blockers side effects
cardiac depression, AV block, peripheral edema, flushing, dizzyness, hyperprolactinemia and constipation
Class IV antiarryhthmics - Ca2+ channel blockers:
Verapamil and diltiazem
-slow the rise of the action potential on nodal cells (Ica phase 0)
-prolongue the repolarization at the AV node
… decrease in conduction velocity, increase in ERP and an increase in PR interval
used:
prevention of nodal arrhthmias (SVT), rate control in a fibb
side effects: constipation, flushing, edema, CHF, AV block, sinus node depression
Hydralazine
increases cGMP–smooth muscle relaxation. Vasodilates arterioles> veins; decreases after load
use: HTN, CHF, first line with pregnancy with methyldopa, frequently coadministered with a beta blocker to prevent reflex tachycardia
tox: compensatory tach (contraindicated in angina/CAD), fluid retension, nausea, headache, angina can cause lupus like syndrome
hypertensive emergency
nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam
nitroprusside
short active increases cGMP –> NO–> vasodilation, can cause cyanide toxicity as it release CN
Fenoldopam
Dopamine D1 receptor agonist - coronary, peripheral, renal, splanchnic vasodilation –> decrease BP and increase naturesis
Nitrogylcerin, isosorbide dinitrate
-vasodilate increase NO via cGMP increase
dilate veins» arteries decrease preload
use: angina, acute soronary syndrome and pulmonary edema
toxicity: reflex tach (treat with a beta blocker), hypotension, flushing, headahce
Monday disease in industrial exposure:
development of tolerance for the vasodilating action during the work week, loss of tolerance over the weeknd. on monday exposure–> tach, dizzy, headache
Mg
effective in torsades de pointes and digoxin toxicity
Cadiac gycoside: digoxin
75% bioavailabilty
20-40% protein bound
t1/2 = 40 hours
urinary excreted
mech: inhibits na/k/atpase leads to less Na out of cell and a build up of Na in the cell, so less Na wants to enter the cell to kick out the Ca in the Na/Ca exchanger
increase in the intracellular Ca –> positive inotropy.
It also stimulates the vagus nerve –> decrease the HR
treat: CHF, increase contractility; a fibb (decreases conduction at the AV node and depression of the SA node)
digoxin antidote
slowly normalize K, cardiac pacer, anti digoxin Fab fragments, Mg
Digoxin toxicity
cholinergic (stimulates vagus) - nausea, vomiting, diarrhea, blurry yellow vision
ECG- increase PR, decreases QT, ST scooping, T-wave inversion, arrhythmia, AV block
Can lead to hyperkalemia
factors predisposing to toxicity:
renal failure, hypokalemia (permits digoxin to bind at the K+ binding site on ?Na/k/atpase since less competition), verapamil and miodarone, quinidine (decreases digoxin clearance; diplaces digoxin from tissue binding sites)
HMG CoA reductase inhibitors: lovastatin pravastatin simvastatin atorvastatin rosuvastatin
decrease LDL
Increase HDL
Decrease TG’s
-inhibit hmgcoa conversion to mevalonate a cholesterol precurser
side effects: hepatotoxicity (increase LFTS)
rhabdomyolysis, espeically when used with vibrates and niacin
Niacin (vitamin B3)
decrease LDL
Increase HDL
Decrease TG
Inhibit lipolysis in adipose tissue (decrease VLDL to IDL and LDL); reduces hepatic VLDL synthesis
side effects:
red flushed face, which is decreased with aspirin
cause:
hypergycemia, may see acanthosis nigricans
hyperuricemia (exacerbate gout)
Bile acid resins :
cholestyramine, colestipol, colesevelam
decrease LDL
Slightly increase HDL
Slightly increase TG
Prevent intestinal reabsorption of bile acids; so the liver must use cholesterol to make more!
side effects: patients hate it tastes bad, GI discomfort, decreased absorption of fat soluble vitamins, you can also get cholesterol gallstones
Cholesterol absorption blockers:
Ezetimibe
decrease LDL
Prevent cholesterol absorption at small intestine brush border
side effects: rare increase in LFTS
diarrhea
Fibrates (gemfibrozil,clofibrate, bezafibrate, fenofibrate)
decrease LDL a bit
increase HDL a bit
Super decrease TG
Upregulate lipoprotein lipase, this will increase TG clearance. Activate PPAR-a to induce HDL synthesis
side effects: myositis (expeically with concurrent statins)
hepatotoxicity (increased LFTS)
cholesterol gallstones (esp with concurrent bile resins)
Name the Antiarrhthmic Na channel blockers
Class 1A
Quinidine, Procainamide, Disopyriamide
The Queen Proclaims Disco pyramid partayyyy
Name the Antiarrhthmic Na channel blockers
Class 1B
Lidocaine, Mexiletine
Name the Antiarrhthmic Na channel blockers
Class 1C
Flecainide, Propafenone
Name the Antiarrhthmic Beta blockers
Class II
Metoprolol, propanolol, esmolol, atenolol, timolol, carvediol
Name the Antiarrhthmic K+ channel blockers
Class III
Amiodarone, Ibutilide, Dofetilide, Sotalol
amiodarone toxicity
pulmonary fibrosis hepatotoxicity hypothyroidism/hyper 40% iodine by wt corneal deposits skin deposits (blue grey) resulting in photo dermatitis neurologic effects constipation bradycardia, heart block, CHF
it has Class i , ii,iii and iv effects!
remember check PFT, LFT and TFT
Antiarrhthmic Na channel blockers
Class 1A:
Quinidine, Procainamide, Disopyriamide
- decreases the slope of phase 0
- increased action potential
- increased the ERP
- Increase the QT interval (ventricle contraction)
clinical use: atiral and ventricular ayyhythmias, espeically re-entrant and ectopic SVT and VT
toxicity:
Cinchonism (headahce, tinnitus with quinidine)
reversible SLE syndrom with procainamide
heartfailure with disopyrimide
-thrombocytopenia
-torsades de points due to increased QT interval
Antiarrhthmic Na channel blockers
Class 1B: Lidocaine, Mexiletine, phenytoin
- decrease action potential duration, steeper slope of phase 3
- preferentially affect ischemic or depolarized purkinge and ventricular tissue.
use:
acute ventricle arrhthmia escially post MI, gigitalis induces arrhythmias
tox:
CNS stimulation/depression, cardiovascular depression
Antiarrhthmic Na channel blockers
Class 1C
Flecainide, Propafenone
- prolongs refractory period at AV node
- minimal affect on AP duration, slope at phase 3 is the same
use:
SVT, including AF, onyl as a last reost in VT
tox:
proarrhthmic, especially post-MI (contraindicated). Contraindicated in structural and ischemic heart disease
Antiarrhthmic Beta blockers
Class II
Metoprolol, propanolol, esmolol, atenolol, timolol, carvediol
- decrease SA and AV nodal activity
- decrease cAMP and thus PKA and thus less SR release of Ca
- decrease Ca inward currents
- decrease the slope of phase 4 depolarization in abnormal pacemaker cells
- AV node is particularily sesistive, increase the PR interval
note esmolol is very short acting
Antiarrhthmic K+ channel blockers
Class III:
Amiodarone, Ibutilide, Dofetilide, Sotalol
- increase action potential
- increase ERP
- prolong repolariation slope of phase 3 decreases
- increase QT interval
use:
a fibb, atrial flutter, v tach (amiodarone and sotolol)
note sotolol- cause torsades de pointes and excessive B blockade
ibutilide-torsades de points
Antiarrhthmic Na channel blockers
Class 1A general:
slow or block conduction especially in depolarized cells. they decrease the slope of phase 0 (depolarization) and increase the threshold for firing in abnormal pacemaker cells. they are state dependent, selectively depress tissue that is frequently depolarized hyperkalemia cause increased toxicity for all class I drugs
Antiarrhthmic Beta blockers
Class II toxicity
- impotence, exacerbation of COPD and asthma
- bradycardia, AV block, CHF
- sedation, sleep alterations
- may mask the signs of hypoglycemia
- metoprolol can cause dislipidemia
- propanolol can exacerbate vasospasm in prinzmetal angina
- contrain in cocaine users
Treat overdose with glucagon
