Lec 38 CVS Pharma HPN and HF Flashcards
Alpha blockers that are more sensitive to alpha1 than alpha 2
Prazosin, Terazosin, Doxazosin (BASICALLY MGA SIN)
Facilitates urinary outflow
Alpha1 blockers (mga sin)
Toxicities of Alpha blockers
Orthostatic hypotension (alpha-1 is responsible in maintaining BP in postural changes)
Manifests with the first dose phenomenon
Alpha1 blockers (mga sin)
NERVE TERMINAL BLOCKERS
Reserpine and Guanethedine
Inhibits the Ca2+-dependent release of norepinephrine
Guanethedine
Toxicities of Guanethedine
Severe orthostatic hypotension and sexual dysfunction
Blocks vesicular amine transporter
Reserpine
Toxicities of Reserpine
Psychiatric depression and GI disturbances (Lowering the levels of NE, DA, 5-HTwill impair brain and gut functions)
Competitively block nicotinic cholinoceptors in both sympathetic and parasympathetic ganglia
Hexamethonium
Centrally acting sympathoplegic drugsthat reduce sympathetic flow and inhibit NE
Alpha2 agonists
Best for refractory hypertension as a last resort
Alpha2 agonists
Examples of Alpha 2 agonists
Clonidine, Methyldopa
Withdrawal of Methyldopa causes____.
Rebound hypertension
Examples of Beta 1 blockers
Acebutolol (partial agonist), Betaxolol, Esmolol,Atenolol, Metoprolol (A BEAM of beta1 blockers)
Examples of nonselective Alpha and Beta antagonists
Labetalol, Carvedilol (Curb Love)
Drugs with intrinsic sympathomimetic properties
Partial agonists (Pindolol, Acetabulol)
Toxicity of beta blockers
Increased triglycerides, hyperglycemia (can cause new onset DM)
Nonselective ? blocker
propanolol
Oral vasodilator that cause NO release and can be used by women since it does not cross placenta
Hydralazine
Vasodilator that dilates Arterioles NOT veins
Hydralazine and Minoxidil
Toxicities of Hydralazine
Angina, tachycardia, Lupus-like syndrome
Oral vasodilator that cause opens K channels in vascular smooth muscle
Minoxidil
Toxicities of Minoxidil
Angina, tachycardia, headache, sweating, hirsutism (now used as topical for baldness)
Examples of parenteral vasodilators
NITROPRUSSIDE, FENOLDOPAM, DIAZOXIDE
Parenteral vasodilators that release NO
Nitroprusside
Parenteral vasodilators that activates D1 receptors
Fenoldopam
Parenteral vasodilators that open K channels
Diazoxide
Toxicities of nitroprusside
excessive BP lowering and accumulation of cyanide
What type of calcium channels do CCBs inhibit?
L-type
CCBs with more affinity to heart particularly the SA node
non-DHPs VERAPAMIL, DILTIAZEM
greatest depressant effect on the heart; may cause supraventricular arrhythmia
Verapamil
CCBs that reduce vascular resistance and have more affinity to smooth muscles
DHPs (NIFEDIPINE, AMLODIPINE)
Examples of ACE inhibitors
Captopril, Enalapril, Lysinopril (mga pril)
Mode of action of ACE inhibitors
blocks bradykinin breakdown
ACE inhibitor that is a prodrug and thus NOT the active drug
Enalapril
Toxicities of ACE inhibitors
ARF with bilateral renal artery stenosis, Contraindicated during second and third trimester of pregnancy
Example of ARBs
LOSARTAN, VALSARTAN
No effect in bradykinin metabolism and hence don’t cause cough
ARBs
inhibits renin action
Aliskiren (“Alis ka renin”)
Contraindications of Aliskiren
Pregnancy (because of the toxicity of ACE inhibitors and ARBs)
First line drug in chronic heart falure
HYDROCHLOROTHIAZIDES
What is the mode of action of Thiazides?
Inhibit NaCl transport predominantly in the distal convoluted tubule
Toxicities of Thiazides
hyperGLUC (Glycemia, Lipidemia, Uricemia, Calcemia)
Most potent diuretics available
Loop diuretics
Inhibit NaCl reabsorption in thick ascending loop of Henle (Na+/K+/2Cl- transporter)
Loop diuretics
Example of loop diuretics
IV Furosemide
Toxicities of loop diuretics
Hypokalemic metabolic alkalosis, Allergy, Nephritis, Dehydration, Ototoxicity, Gout (HANDOG)
Example of potassium sparing diuretics
Spironolactone
Mode of action of Spironolactone
Competitive antagonist of aldosterone
Treatment goals of HF drugs
Enhance oxygen delivery, Temper compensatory mechanisms, Prevent progressive cell death and structural deterioration to decrease morbidity and mortality
What is the mechanism of action of digoxin
Direct inhibition of Na+/K+ ATPase; Stimulates vagus nerve
What are the clinical applications of digoxin?
CHF (inc contractility), Atrial fibrillation
What is the mode of excretion of digoxin?
Urinary excretion
Toxicities of digoxin
Bigeminal rhythm, hypokalemia, tachycardia, fibrillation
Mechanism of action of digoxin
vasodilator, inotropic, chronotropic
Major excretion products of dobutamine in the urine
conjugates of dobutamine and 3-O-methyl dobutamine
most widely used selective beta1-agonist in heart failure
dobutamine
Where is dopamine metabolized?
liver, kidney, and plasma by MAO and catechol-O-methyltransferase
The drug choice for patients with congestive heart failure, hypotension and oliguria.
Dopamine
Mode of action of Milrinone
Inhiibt phosphodiesterase (PDE3) which inactivates camP and thus leads to increased cAMP
T or F Milrinone has a greater cardiac than vascular effect
F. Milrinone has a greater vascular than cardiac effect so that arterial pressure is lowered in the presence of augmented cardiac output.
Most common side effect of Milrinone
Ventricular arrhythmias
Example of a Vasopressin antagonist
Conivaptan
What is the mode of action of Nesiritide?
Increases cGMP in smooth muscles
Adverse effects of Nesiritide
excessive hypotension; reports of significant renal damage and deaths