Pharm: antiHTN CCBs and BBs

What are the non-DHP L-type calcium channel blockers?

verapamil and diltiazem

what are the DHP oral L-type calcium channel blockers?

nifedipine and amlodipine

what are the DHP I.V. L-type calcium channel blockers?

nicardipine and clevidipine

Why would we choose an IV DHP CCB over an oral one?

the IV forms have a short onset of action (within minutes) so they are used for crisis

Which calcium channel blocker has slow absorption, minimal peaks and troughs and a prolonged effect so it causes less reflex tachycardia?

amlodipine

explain the advantage of extended-release forms of the calcium channel blockers

these forms reduce the number of daily doses needed to maintain therapeutic levels

____ extended-release appears to cause less reflex tachycardia than the immediate relase formulation

nifedipine

immediate release of DHP CCBs with ____ is not recommended

why?

short half-lives

becuase each time they are given you get peaks and troughs of BP and less control/stability

What is the significance of calcium during smooth muscle contraction?

calcium bind to calmodulin and activates the myosin light chain kinase that phosphorylates the myosin head and allows for myosin-actin interaction that leads to smooth muscle contraction

CCBs bind more effectively to _____ and ____ channels

open channels and inactivated channels

Which drug(s) effects:

decrease the channels rate of recovery, channel block is enhanced as the frequency of stimulation increases, depress the rate of the sinus node pacemaker, and slows AV conduction

the non-DHP CCBs; verapamil and diltiazem

Which drug’s effects:

potent vasodilators (reflex tachycardia), do not affect the channel’s rate of recovery, do not affect conduction through the AV node

the DHP CCBs; amlodipine, nifedipine, nicardipine, and clevidipine

Which CCBs slow heart rate, slow AV conductance, and reduce myocardial contractility?

non-DHP CCBs; verapamil and diltiazem

How do CCBs work to treat HTN?

they relax smooth muscle arterioles → decreased systemic vascular resistance → decreased BP

How do CCBs treat angina?

decreased peripheral vascular resistance → decreased afterload → increased coronary blood flow → increased oxygen delivery to myocardium

What can we use to treat supraventricular tachyarrhythmias, and raynaud phenomenon

CCBs

What drug(s) are used to treat a subarachnoid hemorrhage?

nimodipine

What drug(s) are used to treat migraines

verapamil

What drug(s) are used as a tocolytic to supress premature contractions in preterm labor?

nifedipine

What drugs AE include GERD aggravation?

both non-DHP and DHP

What drugs AE include peripheral edema and with immediate-release: HA, flushing, dizziness, and hypotention with reflex tachycardia

DHP CCBs

What drugs AE include bradycardia and worsening CO and constipation?

non-DHP (constipation heavily associated with verapamil)

an IV beta-blocker plus ____ is contraindicated becuase it can lead to a heart block

IV verapamil

What drug(s) are contraindicated in patients with: ventricular sysfunction, SA or AV nodal conduction disturbances, or systolic BPs below 90 mmHG

verapamil or diltiazem (non-DHP CCBs)

_____ is not for use in pts with acute or unstable angina or STEMI

nifedipine immediate-release

_____ is not appropriate in the long-term treatment of angina or HTN

nifedipine short-acting formulations (want slow release formulation)

quinidine plus ___ can cause excessive hypotension

verapamil

What are the beta-blockers?

propranolol, labetalol, carvedilol, metoprolol, and esmolol

beta blockers reduce BP in hypertensive pts by ___

reducing CO and renin secretion

What is/are the classical non-selective beta blocker(s)

propranolol

What is/are the beta-1 selective beta blockers?

esmolol and metoprolol

Which beta-blocker has a short duration of action an is used for the management of HTN crisis/emergency

esmolol

What is/are the non-selective beta-blockers (not the prototype) with additional actions

carvedilol and labetalol

Which beta-blocker also has alpha-1 receptor antagonism, Ca2+ entry blockade, and antioxidant activity?

carvedilol

Which beta-blocker also has alpha-1 receptor antagonism?

labetalol (carvedilol does too but it has additional actions too)

What is the recommende agent for the tx of hypertensive emergency in pregnant pts?

labetolol

What drug(s) can be used to tx HTN, intraoperative tachycardia, ischemic heart disease (angina), CHF, certain arrhythmias, hyperthyroidism, performance anxiety, and glaucoma

beta blockers

What is the MOA for the use of beta blockers to treat HTN?

they reduce CO and lower BP and supress renin release

Explain beta blockers action on a heart at rest vs a heart during exercise or stress

they have little effect on the normal heart of an individual at rest but profound effects when sympathetic control of the heart is dominant (like during exercise or stress)

____ should not be abruptly d/c after prolonged regular use

beta blockers

withdrawal syndrome may involve upregulation or supersensitivity of the beta adrenoceptors

What are some things we would see with BB withdrawal syndrome?

nervousness, tachycardia, increased BP, increased intensity of angina, increased risk of sudden death

What drug(s) AE include decreased insulin sensitivity, increased plasma VLDL and decreased HDL, decreased release of free fatty acids from adipose tissue, CNS effects like fatigue, insomnia, and nightmares, and decreased libido

beta blockers

What drugs(s) can cause asthma or COPD exacerbation, delyed recovery from insulin-induced hypoglycemia, peripheral vascular insufficiency, and excessive bradycardia

beta blockers

What drug(s) may be less prone to inhibit recovery from hypoglycemia?

beta-1 selective agents; esmolol and metoprolol

When in doubt, the MOA for the AEs caused by the beta-blockers most likely has to do with what?

blocking the beta-2 actions

What drug is used to treat performance anxiety?

propranolol