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Hypertension > Sympatholytics > Flashcards

Sympatholytics Flashcards

1
Q

What are the 3 classes of sympatholytics?

A

peripheral adrenergic receptor blocker
central α2 agonists
neurotransmitter depleters

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2
Q

What are the subclasses of the peripheral adrenergic receptor blockers?

A

α1 blockers
β blockers
mixed α + β blockers (vasodilating β blockers)

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3
Q

What are the α1 blocker agents?

A

Prazosin
Terazosin
Doxazosin

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4
Q

α1 receptor antagonists block what?

A

post-synaptic α1 receptor

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5
Q

α1 receptors naturally cause vaso________ on vascular smooth muscle.

A

vasoconstriction

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6
Q

Blocking the α1 receptor causes what?

A

vasodilation

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7
Q

The decrease in BP from α1 blockers initially causes ________ _________.

A

sympathetic stimulation or baroreceptor reflex

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8
Q

What are some results of sympathetic stimulation?

A

Increased HR and CO

Increase in plasma renin activity/release

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9
Q

In the use of α1 blockers renal blood flow is _______.

A

unchanged

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10
Q

α1 blockers can cause ______ _______, or what is known as the “first dose effect”.

A

postural hypotension

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11
Q

Inhibition of smooth muscle contraction with the use of α1 blockers occurs in what other areas of the body?

A

urinary bladder sphincter
prostate
seminal vesicles
uterus

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12
Q

What other conditions are α1 blockers indicated?

A

BPH

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13
Q

What are the adverse effects of α1 blockers?

A

Peripheral vasodilation: dizziness, postural hypotension, edema, palpitations, fatigue, nasal congestion
Anaphylaxis
Priapism

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14
Q

What are some drug interactions with α1 blockers?

A

combining with other antihypertensives can cause hypotension

Verampamil causes increased Terazosin levels

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15
Q

What is the ending for α1 blockers?

A

-zosin

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16
Q

What groups are α1 blockers contraindicated?

A

pregnancy

those with pheochromocytoma (adrenal tumor)

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17
Q

α1 blockers are/are not recommended for monotherapy?

A

are not

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18
Q

What populations may benefit from α1 blockers over other agents?

A

HTN diabetics
gout
BPH

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19
Q

What are the β blocker agents?

A

Propranolol
Metoprolol
Atenolol

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20
Q

What is the ending for β blockers?

A

-olol

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21
Q

What is the MOA for β blockers?

A

Blocking the β receptors reduces cardiac contractility and HR to reduce CO. β blockers also reduce the secretion of renin and lower plasma Ang II levels.

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22
Q

What is the most effective β blocker in treating HTN?

A

They are all equally effective.

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23
Q

How do β blockers effect the BP in normotensive patients?

A

no change

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24
Q

Pure β receptor antagonists _____ CO and cause and immediate reflex _______ in TPR.

A

reduce

increase

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25
Q

Partial β receptor antagonists produce a ______ in CO but BP falls due to a _______ in TPR.

A

lesser decrease than pure β receptor antagonists

decrease

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26
Q

What are the vasodilating β blockers?

A

Labetolol
Carvedilol
Nebivolol

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27
Q

Vasodilating β blockers provide effective therapy in what stages of HTN?

A

all stages of HTN

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28
Q

In what cases are β blockers an appropriate first choice therapy?

A

post MI
heart failure
arrhythmias
angina

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29
Q

Can you combine β blockers with ACEIs or ARBs?

A

no - its redundant

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30
Q

Are diuretics needed in combination with β blockers?

A

no

31
Q

What are the adverse effects of β blockers?

A

bronchoconstriction
bradycardia
masks symptoms of hypoglycemia
fatigue/dizziness/depression

32
Q

Which subclass of sympatholytics are preferred in diabetics?

A

Vasodilating β blockers

33
Q

What are the dosing considerations for β blockers?

A

start low, titrate up, titrate down

34
Q

What drug interaction blunts the hypotensive effect of β blockers?

A

NSAIDS

35
Q

What drug interaction can cause a hypertensive crisis?

A

epinephrine

36
Q

What is the most concerning ADR with β blockers?

A

New onset diabetes

37
Q

What conditions are the use of β blockers most supported in?

A

heart failure

post MI

38
Q

What are the central α2 agonist agents?

A

α-methyldopa
clonidine
guanabenz
guanfacine

39
Q

What is the MOA of central α2 agonists?

A

By acting on the presynaptic α2 receptor, central NT release is decreased. Sympathetic outflow is reduced and BP is decreased.

40
Q

Why are central α2 agonists not 1st line?

A

ADRs

41
Q

Methyldopa is an analog of what?

A

DOPA

42
Q

What is the MOA of methyldopa?

A

Acts in the brainstem to reduce sympathetic outflow

43
Q

Is methyldopa degraded by monoamine oxidase?

A

no

44
Q

Methyldopa has _____ effect on CO and HR except in _____.

A

little

elderly

45
Q

In the use of α2 agonists the baroreceptor reflex is ____ ______.

A

turned down

46
Q

In the use of α2 agonists, renal blood flow and function is ________.

A

unaffected

47
Q

In the use of α2 agonists plasma renin levels ______.

A

decrease

48
Q

α2 agonists should be combined with _______ to maintain efficacy.

A

diuretic

49
Q

What medication is preferred for HTN in pregnant women?

A

Methyldopa

50
Q

What are the adverse effects of Methyldopa?

A

CNS: sedation, depression, dry mouth, ↓ libido, Parkinsonian signs, hyperprolactinemia, bradycardia
Hepatotoxicity
Hemolytic anemia

51
Q

α2 agonists _____ CO and ______ TPR.

A

decrease

decrease

52
Q

Guanfacine is _____ selective for α2 receptors than clonidine and guanabenz.

A

more

53
Q

Which α2 agonist is available in a patch?

A

clonidine

54
Q

What are the adverse effects of α2 agonists?

A

CNS: sedation, dry mouth, sleep disturbances, bradycardia, sexual dysfunction

55
Q

What is a main concern about discontinuing α2 agonists?

A

withdrawal syndrome

56
Q

What does α2 agonist overdose look like?

A

opioid overdose

57
Q

What are the minor sympatholytic agents?

A

Guanadrel

Reserpine

58
Q

Guanadrel specifically targets what?

A

postganglionic adrenergic neurons

59
Q

Guanadrel is taken up into ________ via the ___ _____.

A

presynaptic terminal

NE transporter

60
Q

Guanadrel ______ NE in NT granuals.

A

replaces

61
Q

Guanadrel has ______ agonist activity.

A

no

62
Q

What drug interaction will blunt effectiveness of Guanadrel?

A

TCAs
cocaine
chlorpormazine

63
Q

What population is Guanadrel contraindicated?

A

pheochromocytoma

CHF

64
Q

Guanadrel causes vaso_____, __ TPR, minor __ in renal blood flow and GFR.

A

vasodilation
decrease
decrease

65
Q

What are the adverse effects of Guanadrel?

A

orthostatic hypotension
exercise intolerance
volume expansion
weakness, lassitude, sexual dysfunction, diarrhea

66
Q

Guanadrel is not used as monotherapy due to what?

A

orthostatic hypotension

67
Q

Reserpine binds to ___ ______ _____.

A

NT storage vesicles

68
Q

Reserpine impairs ______, ________, ________ neurotransmission.

A

adrenergic
dopaminergic
serotonergic

69
Q

Reserpine depletes NTs peripherally, centrally, or both?

A

both

70
Q

Reserpine ___ TPR ___CO ___HR

A

decreases
decreases
decreases

71
Q

In the use of Reserpine, orthostatic hypotension is/isn’t a problem.

A

is not

72
Q

In the use of Reserpine, plasma renin levels ______.

A

decrease

73
Q

What are the adverse effects of Reserpine?

A

sedation, inattention, nasal congestion, sexual dysfunction, suicidal depression

74
Q

Reserpine should/shouldn’t be combined with a diuretic?

A

should

Hypertension (8 decks)

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