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Pharmacology II > antihypertensives - SNS (exam 2) > Flashcards

antihypertensives - SNS (exam 2) Flashcards

1
Q

alpha 1 affinity for NE and E

A

NE > E

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2
Q

alpha 2 affinity for NE and E

A

E > NE

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3
Q

beta 1 affinity for NE and E

A

E = NE

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4
Q

beta 2 affinity for NE and E

A

E&raquo_space; NE

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5
Q

central alpha 2 agonists target

A

alpha 2 autoreceptors

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6
Q

what is the dominant SNS drug used to treat hypertension?

A

alpha 1 antagonists

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7
Q

central alpha 2 agonists

A

methyldopa (Aldomet)
Clonidine (catapres)

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8
Q

alpha 1 receptor antagonists

A

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

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9
Q

cardioselective beta blockers

A

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

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10
Q

nonselective beta blockers

A

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

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11
Q

mixed alpha/beta blockers

A

carvedilol
labetalol (trandate)

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12
Q

beta blockers with ISA

A

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

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13
Q

use of central alpha 2 agonists leads to

A

a decrease in cardiac output and increase in vasodilation

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14
Q

central alpha 2 agonists MOA

A

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

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15
Q

methyldopa conversion to active metabolite

A

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

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16
Q

methyldopa is a

A

prodrug that needs to be converted to methylnorepinephrine

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17
Q

uptake of methyldopas active metabolite relies on

A

amino acid transporter

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18
Q

clonidine is ___________ and can cross the __________

A

lipophilic

BBB

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19
Q

methyldopa vs clonidine onset of action

A

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

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20
Q

ADRs of central alpha 2 agonists

A

sedation
dry mouth
orthostatic hypotension

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21
Q

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

A

rebound hypertension

tapering

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22
Q

PK considerations for methyldopa

A

extensively metabolized in liver

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23
Q

PK considerations for clonidine

A

excreted unchanged in the urine
metabolized in the liver

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24
Q

methyldopa is used for

A

gestational HTN since it is safe in pregnancy

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25
Q

are central alpha 2 agonists considered first line?

A

no

they have low efficacy

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26
Q

clonidine has many other uses including

A

decrease in opioid withdrawal symptoms
treatment for ADHD

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27
Q

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

A

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

28
Q

how does rebound hypertension occur for beta blockers

A

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

29
Q

how does rebound hypertension occur for central alpha 2 agonists?

A

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

30
Q

how is rebound hypertension prevented?

A

tapering the dose slowly to discontinuation

31
Q

MOA of alpha 1 receptor blockers

A

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

32
Q

ADRs of alpha 1 antagonists

A

orthostatic hypotension
dizziness
possible syncope

33
Q

first dose effect of alpha 1 receptors

A

50% of patients have
symptomatic orthostatic hypotension

34
Q

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

A

start with low dose at bedtime and titrate up

35
Q

PK of prazosin

A

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

36
Q

PK of terazosin and doxasozin

A

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

37
Q

are alpha 1 antagonists first line agents for HTN?

A

NO, lower efficacy

38
Q

alpha 1 antagonists are more commonly used in the treatment of

39
Q

primary target of beta blockers

A

beta 1 receptors

40
Q

MOA of beta blockers

A

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

41
Q

beta blockers also have

A

vasodilatory effects

42
Q

cardioselective beta blockers are antagonists at

A

beta 1 receptors

43
Q

nebivolol also causes

A

nitric oxide mediated vasodilation

44
Q

nonselective beta blockers are antagonists at

A

all beta receptors

45
Q

mixed alpha/beta blockers are antagonists at

A

all beta receptors and alpha 1 receptors

46
Q

intrinsic sympathomimetic activity is a

A

partial agonist at beta receptors

47
Q

acebutolol is _____________ while penbutolol and pindolol are _________________

A

cardioselective

nonselective

48
Q

can binding to beta 2 still occur with cardioselective agents?

A

yes, especially at higher doses

49
Q

relative affinity for beta 1 over beta 2 for cardioselective agents

A

nebivolol > bisoprolol > metoprolol = atenolol

50
Q

beta blockers with ISA

A

low intrinsic activity
low risk of bradycardia

51
Q

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

A

net antagonist

net agonist

52
Q

clinical considerations for effects of beta 1 blockers on the heart

A

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

53
Q

clinical considerations for effects of beta 1 blockers on the kidneys

A

additional factor for reduction in BP

54
Q

clinical considerations for effects of beta 1 blockers on the brain

A

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

55
Q

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

A

hypoglycemia

diabetes

blood sugar

56
Q

clinical considerations for effects of beta 2 blockers on the lungs

A

causes bronchoconstriction which can worsen asthma or COPD

57
Q

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

A

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

58
Q

clinical considerations for effects of beta 2 blockers on the muscle

A

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

59
Q

clinical considerations for effects of beta 2 blockers on the vasculature

A

causes vasoconstriction which may worsen PVD or Raynaud syndrome

60
Q

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

A

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

61
Q

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

A

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

62
Q

ADRs of beta blockers

A

dry mouth
weight gain

63
Q

clinical considerations for effects of alpha 1 blockers on the vasculature

A

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

64
Q

alpha 1 blockers effects what types of tissue?

A

vasculature
prostate and bladder neck
liver

65
Q

labetolol is often used in the treatment of

A

gestational HTN

66
Q

beta blockers PK

A

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

Pharmacology II (11 decks)

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