antihypertensives - SNS (exam 2) Flashcards by Emily Andrle

alpha 1 affinity for NE and E

NE > E

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alpha 2 affinity for NE and E

E > NE

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beta 1 affinity for NE and E

E = NE

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beta 2 affinity for NE and E

E&raquo_space; NE

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central alpha 2 agonists target

alpha 2 autoreceptors

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what is the dominant SNS drug used to treat hypertension?

alpha 1 antagonists

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central alpha 2 agonists

methyldopa (Aldomet)
Clonidine (catapres)

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alpha 1 receptor antagonists

prazosin (minipress)
terazosin (hytrin)
doxazosin (cardura)

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cardioselective beta blockers

atenolol
bisoprolol (zebeta)
metoprolol (lopressor)
esmolol (brevibloc)
nebivolol (Bystolic)

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nonselective beta blockers

nadolol (corgard)
propranolol (inderal)
timolol (blocadren)

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mixed alpha/beta blockers

carvedilol
labetalol (trandate)

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beta blockers with ISA

pindolol (visken)
penbutolol (levatol)
acebutolol (sectral)

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use of central alpha 2 agonists leads to

a decrease in cardiac output and increase in vasodilation

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central alpha 2 agonists MOA

activate presynaptic alpha 2 receptors
decrease NE and decreased activation of SNS

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methyldopa conversion to active metabolite

methyldopa converted to methyldopamine by aromatic amino acid decarboxylase
methyl dopamine converted to methylnorepinephrine by dopamine beta hydroxylase

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methyldopa is a

prodrug that needs to be converted to methylnorepinephrine

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uptake of methyldopas active metabolite relies on

amino acid transporter

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clonidine is ___________ and can cross the __________

lipophilic

BBB

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methyldopa vs clonidine onset of action

methyldopa - 4-5 hours
clonidine - 30-60 minutes

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ADRs of central alpha 2 agonists

sedation
dry mouth
orthostatic hypotension

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when central alpha 2 agonists are suddenly discontinued this can lead to ________________, which is why _____________ is required

rebound hypertension

tapering

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PK considerations for methyldopa

extensively metabolized in liver

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PK considerations for clonidine

excreted unchanged in the urine
metabolized in the liver

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methyldopa is used for

gestational HTN since it is safe in pregnancy

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are central alpha 2 agonists considered first line?

no they have low efficacy

clonidine has many other uses including

decrease in opioid withdrawal symptoms treatment for ADHD

when rebound hypertension occurs from sudden discontinuation of clonidine, what occurs?

large increase in NE increased HR (10-20 bpm) increase in SBP within 1 day with continued rise over 3 days

how does rebound hypertension occur for beta blockers

antagonism of beta 1 receptors on the heart leads to compensatory up regulation of beta1 receptors

how does rebound hypertension occur for central alpha 2 agonists?

agonism of presynaptic alpha 2 receptors in the brain leads to compensatory down regulation of alpha 2 receptors

how is rebound hypertension prevented?

tapering the dose slowly to discontinuation

MOA of alpha 1 receptor blockers

block alpha 1 receptors in the vasculature (arterial and venous) leading to vasodilation

ADRs of alpha 1 antagonists

orthostatic hypotension dizziness possible syncope

first dose effect of alpha 1 receptors

50% of patients have symptomatic orthostatic hypotension

since alpha 1 antagonists can cause syncope, what is recommended?

start with low dose at bedtime and titrate up

PK of prazosin

rapid onset of action shorter half life higher rate of ADRs 2-3 times a day

PK of terazosin and doxasozin

slower onset longer half life lower rate of ADRs once a day

are alpha 1 antagonists first line agents for HTN?

NO, lower efficacy

alpha 1 antagonists are more commonly used in the treatment of

BPH

primary target of beta blockers

beta 1 receptors

MOA of beta blockers

blocks beta 1 to reduce HR and contractility also blocks beta1 in kidneys which reduces renin secretion

beta blockers also have

vasodilatory effects

cardioselective beta blockers are antagonists at

beta 1 receptors

nebivolol also causes

nitric oxide mediated vasodilation

nonselective beta blockers are antagonists at

all beta receptors

mixed alpha/beta blockers are antagonists at

all beta receptors and alpha 1 receptors

intrinsic sympathomimetic activity is a

partial agonist at beta receptors

acebutolol is _____________ while penbutolol and pindolol are _________________

cardioselective nonselective

can binding to beta 2 still occur with cardioselective agents?

yes, especially at higher doses

relative affinity for beta 1 over beta 2 for cardioselective agents

nebivolol > bisoprolol > metoprolol = atenolol

beta blockers with ISA

low intrinsic activity low risk of bradycardia

beta blockers with ISA reduce cardiac output during exercise and are considered _____________ and they maintain cardiac output during rest and are considered ________________

net antagonist net agonist

clinical considerations for effects of beta 1 blockers on the heart

major factor for reduction in BP can cause bradycardia, fatigue, dizziness

clinical considerations for effects of beta 1 blockers on the kidneys

additional factor for reduction in BP

clinical considerations for effects of beta 1 blockers on the brain

highly lipophilic medications can cross the BBB and produce sedation, fatigue, nightmares or depression

beta 1 blockers can reduce some symptoms of _____________ which main mean patients with _____________ need to check ____________ more

hypoglycemia diabetes blood sugar

clinical considerations for effects of beta 2 blockers on the lungs

causes bronchoconstriction which can worsen asthma or COPD

clinical considerations for effects of beta 2 blockers on the pancreatic beta cells

decreases insulin release, can be a problem for patients with diabetes

clinical considerations for effects of beta 2 blockers on the muscle

decreases glucose uptake, can be a problem for patients with diabetes

clinical considerations for effects of beta 2 blockers on the vasculature

causes vasoconstriction which may worsen PVD or Raynaud syndrome

clinical considerations for effects of beta 2 blockers on the lipoprotein lipase enzyme

can increase TGs and decrease HDLs which can be a problem for patients with dyslipidemia

clinical considerations for effects of beta 2 blockers on the liver/muscle

inhibits gluconeogenesis and glycolysis which can be a problem for recovery from hypoglycemia in diabetic patients

ADRs of beta blockers

dry mouth weight gain

clinical considerations for effects of alpha 1 blockers on the vasculature

causes vasodilation which reduces BP; risk for orthostatic hypotension and dizziness

alpha 1 blockers effects what types of tissue?

vasculature prostate and bladder neck liver

labetolol is often used in the treatment of

gestational HTN

beta blockers PK

short half lives, dosed multiple times per day metabolized by CYP enzymes glucuronidation in liver

antihypertensives - SNS (exam 2) Flashcards

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