Drugs for the treatment of CHF, HTN, angina and HLD Flashcards
Digoxin MOA
Inhibits the Na/K ATPase at the potassium binding site (less Na so more Ca) to increase contractility. Reduces HR (decreases SNS tone which prevails in CHF). Increases CO in the failing heart.
Digoxin Main Effect
Positive Inotrope for CHF.
Digoxin Side Effects
Narrow margin of safety. Earliest sign of toxicity is GI upset. CNS effects. Cardiac arrhythmias are the most common and most dangerous: Bigeminy.
Treatment of Digoxin toxicity
Discontinue or reduce amount of digoxin. Moderate toxicity: oral/IV potassium. Severe: Digitalis immune Fab with potassium.
increased Digoxin toxicity
Hypokalemia (loops/thiazides and diarrhea)
Phosphodiesterase Inhibitors MOA
Inhibit cAMP phosphodiesterase to increase cAMP leading to more calcium influx and stronger contraction with significant vasodilation.
Inamrinone
Phosphodiesterase Inhibitor
Milrinone
Phosphodiesterase Inhibitor
Phosphodiesterase Inhibitors Indication
Acute heart failure. Increases CO as a last ditch effeort
Drugs that Reduce CHF mortality
Aldosterone antagonists, beta blockers, ACE-I and ARBs
Dopamine Indications
Severe refractory CHF. At a moderate dose will bind beta 1 receptors in the heart. IV only.
Dobutamine (Dobutrex)
Beta-1 agonist that is a positive inotrope (less tachycardia). Decreases filling pressure and increases oxygen consumption. IV only.
Diuretics Used for CHF
Spironolactone and Eplerenone (aldosterone antagonists). Reduces mortality rate in CHF. Decreases venous pressure to decrease edema and cardiac size.
DOC for CHF
ACE inhibitors (-prils). Reduces mortality.
ACE inhibitors MOA
“-prils” Inhibits ACE to stop conversion of angiotensin I to angiotensin II. Decreases afterload (Less angio II induced vasoconstriction) and decreases preload (less aldosterone) decreases cardiac remodeling.
ACE inhibitor Side Effects
Dry cough and angioedema due to increases in bradykinin.
Angiotensin II receptor blockers (ARB) MOA
“-sartans” Block the binding of angiotensin II to the AT1 receptor.
Beta-Blockers and CHF
Decreases renin secretion, attenuates catecholamine effects, decreases HR, stops cardiac remodeling. Decreases mortality. Only use in the early stages due to negative inotropic effect. Carvedilol and metoprolol.
Vasodilators used for CHF
Sodium nitroprusside (nitropress), Isosorbide dinitrate, hydralazine (SLE causing). Decrease preload, afterload and cardiac remodeling.
DOC for HTN
Thiazides
Adverse effects of thiazides
Reduced glucose tolerance
Thiazide contraindication
Diabetes
Clonidine
Centrally acting sympatholytic.
Methyldopa
Centrally acting sympatholytic
Centrally acting sympatholytic MOA
Bind alpha 2 adrenergic receptors to decrease neurotransmitter release and decrease peripheral SNS activity.
Centrally acting sympatholytic Effects
Decrease SNS outflow
DOC for HTN in pregnancy
Methyldopa
Methyldopa Side effects
Hemolytic anemia
Prazosin
Alpha-adrenergic Antagonist
Terazosin
Alpha-adrenergic Antagonist
Doxazosin
Alpha-adrenergic Antagonist
Alpha-adrenergic Antagonist Indications
Useful for treating HTN in men with BPH
Alpha-adrenergic Antagonist Side Effects
First dose phenomenon
Timolol
Non-selective Beta Blocker
Propanolol
Non-selective Beta Blocker
Nadolol
Non-selective Beta Blocker
Metoprolol
Beta 1 blocker
Atenolol
Beta 1 blocker
Nebivolol
Beta 1 blocker
Acebutolol
Beta 1 blocker
Beta Blocker effects
Decrease CO, renin secretion and SNS tone.
Beta Blocker Indications
Reduces mortality in CHF. Angina, Post-MI, Migraines.
Beta Blocker side effects
Blocks insulin release and inhibits recovery from hypoglycemia.
Beta Blocker contraindications
DM, asthma, heart block and end stage CHF
Carvedilol
Alpha and Beta Blocker
Labetalol
Alpha and Beta Blocker
Alpha and Beta Blocker MOA
Vasodilation without the reflex tachycardia or renin release
Labetalol Indications
HTN emergencies. Acute and maintenance use in pregnancy.
Carvedilol Inditations
HTN and CHF especially post-MI
Alpha and Beta Blocker Side effects
Hepatotoxicity (especially labetalol)
Vasodilator side effects
Reflex tachycardia, HA, fluching, palpitations. Long term lead to fluid retention.
Hydralazine
Vasodilator that acts through NO.
Hydralazine side effects
Lupus is slow acetylators
Sodium Nitroprusside
Vasodialtor that acts through NO. Emergency HTN, IV only.
Sodium Nitroprusside adverse effects
Metabolized by thiocyanate and causes cyandide accumulation
Minoxidil MOA
Vasodilator that opens potassium channels to cause hyperpolarization and smooth muscle relaxation.
Fenoldopam
D1 receptor agonist. Mainly effects the renal vasculature.
Nifedipine
CCB dihydropine. Strongest vasodilatory effects so increases HR
Verapamil
CCB with the strongest cardiac effects leading to a decreased HR
Diltiazem
CCB with vasodilatory and cardiac effects.
CCB contraindications
CHF. don’t use along with a nitrate.
DOC for HTN in DM
ACE-I
-prils
ACE-I
DOC for HTN in CKD
ACE-I
DOC for HTN in CHF
ACE-I
ACE-I adverse effects
Increased bradykinin leading to dry cough and angioedema
-sartans
ARBs
ARBs MOA
Block the effects of angiotensin II without effecting Bradykinin (no cough or angioedema). Similar to ACE-I
DOC For Acute Anginal Attack
Nitrates
Nitrate indications
Acute use in classic and vasospastic. Long term maintenance in classic angina.
Nitrate Side effects
Throbbing head aches
Nitrate contraindications
Don’t use with sildenafil
Monday’s disease
Frequent exposure to nitrates builds up tolerance. Not effective for long term treatment
CCB indications
Treatment of HTN and angina
Beta blockers and Angina
Decrease cardiac workload to decrease oxygen demand. Only useful in classic angina
Ranolazine Indications
Refractory angina
Sildenafil (viagra)
Phosphodiesterase type 5 inhibitor
Sildenafil (viagra) Adverse effects
Blue visual disturbances
Sildenafil (viagra) Contraindications
Use with an alpha blocker, nitrate or grapefruit juice
Vardenafil (levitra)
Phosphodiesterase type 5 inhibitor. More selective for PD5 and faster onset of action.
Tadalafil (cialis)
Phosphodiesterase type 5 inhibitor. More selective for PD5. Longer duration of action.
Statin MOA
Structural analog for HMG-CoA reductase. Blocks de novo synthesis of cholesterorl in the liver causing and increase in high affinity LDL receptors which will decrease plasma levels.
DOC for Decreasing LDL
Statins
Statin effects
Decreases LDL and triglycerides while increasing HDL. Decreases CRP, lipoprotein oxidation and platelet aggregation. Increases NO production and plaque stability.
Statin adverse effects
Increased LFTs (caution in patients will existing liver problems). Muscle pain that can lead to rhabdomyolysis.
Statin Contraindications
pregnancy, Grapefruit juice.
Statin drug interactions
gemfibrozil will inhibit their metabolism
Chlestyramine
Bile acid binding resin
Colestipol
Bile acid binding resin
Colesevelam
Bile acid binding resin
Bile acid binding resin MOA
inhibits bile acid reabsorption. Decrease LDL. No effect on familial hypercholesteremia
Bile acid binding resin Side effects
Constipation and bloating. Impairs the absorption of fat soluble vitamins and other drugs.
Niacin MOA
Inhibits VLDL secretion and increases HDL
Niacin adverse effects
Cutaneous vasodilation due to prostaglandins (aspirin first)
Gemfibrozil
Fibric Acid Derivative
Fenofibrate
Fibric Acid Derivative
Fenofibric acid
Fibric Acid Derivative
Fibric Acid Derivative MOA
PPAR-alpha ligand receptor to upregulate LPL genes. Decrases Triglycerides.
Fibric Acid Derivative Side effects
Gall stones
Ezetimibe MOA
Blocks intestinal absorption of cholesteral. Synergistic with statins.
Alirocumab
PCSK9
Evolocumab
PCSK9
PCSK9 MOA
Antibodies that inhibit LDL receptor breakdown. Given as a subcutaneous injection.
Treatment of HTN with Angina
Beta-blocker
Treatment of HTN post-MI
Beta blocker
Treatment of HTN with asthma
CCB
Treatment of HTN with DM
ACEI
Treatment of HTN with CKD
ACEI
Treatment of HTN with BPH
Alpha blocker
Treatment of HTN with migraines
Beta blocker
