HTN Drugs Flashcards
Diuretics specifics
Includes thiazides, loop diuretics and K+ sparing diuretics.
MOA is relatively unknown but decreases blood volume by eliminating sodium and water resorption.
- decreases CO
indapamide has direct vasodialation properties, but other diuretics dont
Moderate effective as a monotherapy (20/10) but increases efficacy of other antihypertensive effects.
- MUCH greater efficacy in African-American and elderly
PK = PO with onset of action in 2-4 was (DONT increase dose, since increasing doseage does not benefit, but increases chances of ADRs)
ADRs: hypokalemia and hyperuricemia
Populations to be wary of
-diabetic patients (increases glucose) -hyperlipidemia (elevate plasma LDL and TG) presentations
B-adrenergic (class 2 LOLs) - speciafically propranolol and a-methyldopa
MOA: blocks B1 and B2 receptors in heart, kidney, and vascular system
- decreases HR/contractility
- decreases blood pressure
- decreases renin release
- induces Angll formation
PK: PO/IV
- moderate efficacy in monotherapy and better in combination patients
ADRs:
- hyperlipidemia
- erectile dysfunction
- hyperlipidemia
- exacerbate CHF
- GI and CNS nausea
Populations to be wary of:
- smokers: lower efficacy of BBs
- diabetics: masked signs and symptoms of hypoglycemia (can lead to increased coma and SCD rates)
- asthma: exacerbate the effects of asthma
What two specific B-adrenergic antagonists are very good at lowering BP in heart failure
Labetalol and carvedilol
- block B1/B2/a1 receptors
PO is for long term management
IV is for hypertensive emergencies (labetalol only)
Centrally-acting sympatholytics
- specifically Clonidine
MOA 2 ways:
1) post-synaptic a2 agonist in CNS
- decrease HP/TPR
2) pre-synaptic a2 agonist in the periphery
- decreases NE release from post-ganglion is nerve terminals
Efficacy is 35/20 and monotherapy is recommended
- is the drug of choice for treatment of chronic HTN in women that are pregnant
- often combined with diuretics
ADRs:
- prominent erectile dysfunction
- dry mouth/ sedation
- can produce Frank hemolytic anemia (determined via positive Coombs test to the drug, make sure to test while on drug)
Peripherally-acting sympatholytics that are not in use
- specifically reserpine and trimethaphan
MOA: destroys both central and peripheral catecholamines storage granules in nerve terminals
- produces severe decreases in HR, MAP and CO
- also severe decrease in renal function (renin secretion)
PK: PO w/ high t1/2( 33hrs)
- low efficacy (5/5) as monotherapy (jumps to 15/10 w/ a diuretic on board)
ADRs:
- parkinson-like syndrome
- GI disorders (diarrhea)
- erectile dysfunction
- orthostatic hypotension
- NOT USED OFTEN due to dangerous permanent affects*
Peripherally acting sympatholytics that are still in use
- specifically “azosins”
MOA: selective antagonist for vascular smooth muscle a1 receptors
- induces vasodilation and decreases SVR
PK: PO
- efficacy is moderate as monotherapy (15/10), goes up (25/25) w/ diuretic
possesses added benefits by lowering LDL, Tryglycerides and total cholesterol
ADRs:
- erectile dysfunction
- reflex tachycardia!! (Monitor this)
Calcium channel antagonists
- specifically verapamil/diltiazem
MOA: direct vasodilator by inhibiting both Ca2+ entry into smooth muscle and Ca2+ release into Sarcoplasmic reticulum
- decreases SVR
PK: IV/PO
- efficacy varies
1) verapamil (30/20)
2) diltiazem (20/15)
ADRs:
- induce cardio depression (which can be used to counteract reflex tachycardia, but be careful).
Nifedipine
Specific class 4 calcium channel antagonist that is a dihydropyridine CCB
MOA: same as verapamil/diltiazem except DOES NOT affect cardio tissue (only systemic vasculation)
PK: PO
- good efficacy (30/20) as monotherapy
ADRs:
- almost always produces a reflex tachycardia (use BB to counter)
Direct-acting vasodilators
- specifically hydralazine
MOA: direct vasodilation via guanylate Cyclase stimulation
- causes increase in intracellular cGMP and prevent degradation
- increases Ca2+ sequestration = smooth muscle relaxation
PK: PO primarily effects arterioles (afterload) w/out affecting preload
- efficacy is (25/25) as monotherapy
- can develop tolerance (tachyphylaxis) this is due to prominent baroreflex*
- must use BBs and diuretics in connection if occurs
ADRs:
- SLE syndrome (if slow acetylator)
- palpaitations and tachycardia
- ONLY used in resistant fulminant hypertension and management hypertensive emergencies*
Direct-acting vasodilator minoxidil
MOA: direct arteriolar vasodilation via stimulation of vascular smooth muscle K+ channel opening/ agonists
- results in membrane hyperpoalrization (prolonged phase 3)
PK: topical (for alopecia) and oral (for HTN specifically)
- low efficacy by itself (5/5) with SLE-like ADRs
- must use BBs and diuretics in conjunction, never use monotherapy
Only used for severe, refractory hypertension due to increased chance of developing tachyphylaxis
Sodium nitroprusside
Very potential vasodilator that is direct acting
- decreases both afterload (arterial dilation) and preload (venodilation) which results in cardiac muscle relaxation
- sequesters Ca+
- increases cGMP and prevents degradation via Nitro oxide gas paraenterally infused agent.
ADRs: (all only if extended continuous use and because of these, this drug is only used in HTN emergencies)
- methemoglobinemia
- cyanide poisoning
- cellular hypoxia
PK: parenteral use only and only in HTN emergencies
ACE inhibtors (ACEIs) - specifically captopril, enalapril, linsinopril “Prils”
MOA: blockers angiotensin converting enzyme
- prevents angiotensin 1 -> angiotensin 2 conversions.
- also raises bradykinin levels and prevents degradation
- is sustained while on ACEI and produces vasodilation
PK: PO (w/out food)
- maximal effects take 4-8 weeks to develop (slow acting)
- efficacy is good (25/20)
ADRs:
- dry, persistent coughs (due to build up of bradykinin, must take off if asked to by patient)
- proteinuria
- angioedema
Populations to be careful of:
- African American: less efficacy due to genetics. (must use BBs w/ and cant be monotherapy)
- pregnant patients (CONTRAINDICATED)
Angiotensin receptor blockers
“Sartans”
MOA: specific antagonists of angiotensin 2 by binding to AT1 receptors on vascular smooth muscle in the adrenal cortex, brain, heart
- prevents angiotensin 1 -> angiotensin 2 without directly blocking the ACE anzyme
PK: PO administration (w/out food)
- efficacy is (25/20) and does not have decreased effects w/ African Americans
ADRs:
- N/A
- PREGNANCY IS CONTRAINDICATED
Why are ACEIs and angiotensin receptor blockers (AT1 blockers) contraindicated in pregnant patients
Renin-angiotensin system is very important in fetal development
- are teratogenic after 1st trimester and can produce visible malformations in the child.
What is angina?
Severe pressure or constricting pain in chest which may/may not radiate to the extremities and neck
- usually causes by the release of bradykinin and adenosine onto nociceptive afferents
can be counteracted by agents or procedures that improve myocardial perfusion or decrease its metabolic demands
- done via two ways: improve oxygen delivery or decrease work-load to the myocardium
