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Spring '20/ L. Pharm Exam 3 - sympatholytics/mimetics, LAs, antiarrhythmics, vaso > Vasodilators PPT part 1 through clonidine > Flashcards

Vasodilators PPT part 1 through clonidine Flashcards

1
Q

Systemic HTN is defined as

A

Stage 1: 150-159/90-99 mmHg
or > = to
Stage 2: 160/100 mmHg

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2
Q

The most common type of HTN is

A

“essential” or “primary”

-for which there is no clear unifying pathophysiology despite DECADES of research.

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3
Q

HTN is a major risk factor for: (5)

A
  • atherosclerosis
  • cardiovascular disease
  • HF
  • Renal disease
  • Stroke
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4
Q

“Secondary” htn is much less common and can be d/t (5)

A

a variety of causes:

  • Aortic coarctation
  • Endocrine Disease
  • Medications
  • OSA
  • Renal Disease
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5
Q

Name associated disorders of RENAL Disease in Systemic HTN (tbl 20.1) (2)

A
  • Renal parenchymal disease

- Renal artery stenosis

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6
Q

Name associated disorders of ENDOCRINE Disease in Systemic HTN (tbl 20.1)

A
  • Cushings’s disease
  • Hyperparathyroidism
  • Hyper-and hypothyroidism
  • Pheochromocytoma
  • Primary aldosteronism
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7
Q

Name specific MEDICATIONS associated with Systemic HTN (tbl 20.1) (4)

A
  • Alcohol
  • Antidepressants
  • Chronic NSAID use
  • Oral Contraceptives
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8
Q

Calcium Ch Blockade offers direct:

A

vasodilator effects

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9
Q

Calcium Ch Blockade offers direct vasodilator effects without the requirement of:

A

salt restriction

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10
Q

Are calcium ch blockers associated with side effects?

A

relatively few

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11
Q

ACE inhibitors or ARB target the:

A

renin-angiotensin system

*a major contributor to BP control

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12
Q

This system is a major contributor to BP control

A

renin-angiotensin system

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13
Q

Decreased renal perfusion and increased sympathetic nervous system activity cause the release of

A

Renin

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14
Q

Renin acts on:

A

“renin substrate” or angiotensin I

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15
Q

Renin acts on “renin substrate”/angiotensin I at variousu sites in the body to release

A

angiotensin II

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16
Q

Angiotensin II is a potent

A

Vasoconstrictor

Promotes Na and water retention

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17
Q

What type of medication inhibits Angiotensin II production?

A

ACE Inhibitor

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18
Q

Inhibition of angiotensin II production or blockade of receptor causes what:

A

a reliable and potent antihypertensive effect

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19
Q

What class of medication blocks the angiotensin II receptor?

A

ARB

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20
Q

In most types of cardiac patients, what drugs have a well known survival benefit?

A

ACE inhibitors

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21
Q

Another agent that may be associated with inferior stroke protection in pts >60yrs are:

A

Beta adrenergic blockers

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22
Q

Beta blockers may be associated with stroke protection however, they have a greater potential for

A

systemic side effects

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23
Q

Metoprolol

(moa/dose/onset/duration) Table 20.2

A

Beta 1 blocker
1-5mg
1-5min
1-4h

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24
Q

Labetalol

(moa/dose/onset/duration) Table 20.2

A

Alpha 1, Beta 1 and 2 blocker
5-20mg or 0.5-2mg/min
1-5min
1-4h

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25
Q

*Esmolol

(moa/dose/onset/duration) Table 20.2

A

beta 1 blocker
50-300 mcg/kg/min
1-2 min
Half life: 9 min (no clinical duration given)

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26
Q

Nicardipine

(moa/dose/onset/duration) Table 20.2

A

Dihydropyridine Ca Blocker
100 mcg or 5-15mg/h
2-10 min
2-4h

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27
Q

*Hydralazine

(moa/dose/onset/duration) Table 20.2

A

Arteriolar dilator
5-20mg
5-20 min
1-8h

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28
Q

Fenoldopam

(moa/dose/onset/duration) Table 20.2

A

dopamine type 1 agonist
0.05-1.6 mcg/kg/min
5-10 min
30-60 min

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29
Q

Nitroprusside

(moa/dose/onset/duration) Table 20.2

A

No donor
0.25-4 mcg/kg/min
1-2 min
1-10 min

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30
Q

Nitroglycerin

(moa/dose/onset/duration) Table 20.2

A

No Donor
5-300 mcg/kg/min
1-2 min
5-10 min

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31
Q

Beta blockers are less commonly used as ______ agents in HTN

A

first line agents

*as other agents may have a better safety profile for this indication in those > 60 yrs

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32
Q

Beta- adrenergic blockers are:

A

sympatholytics

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33
Q

What are the potential SE’s of Beta Blockers that limit their use in many patients?

A

Depression
Fatigue
Impotence

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34
Q

Why is impotence a SE that is important to know about?

A

compliance

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35
Q

Beta blockers are indicated for Long term tx of patients with:

A

CAD
HF

(and for their antihypertensive action in these pts)

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36
Q

Beta Blockers can be classed according to whether they exhibit /or possess (3 things):

A
  1. Beta 1 selective [versus]
  2. nonselective properties
  3. possess intrinsic sympathomimetic activity
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37
Q

Beta blockers with selective properties bind primarily to

A

Beta 1 (cardiac) Receptors

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38
Q

nonselective beta blocker properties bind to which receptors?

A

equal affinity for B1 and B2 receptors

vascular, bronchial SM, and metabolic

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39
Q

B Blockers with intrinsic sympathomimetic activity tend produce less

A

bradycardia

—-> thus, less likely to unmask left ventricular dysfunction

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40
Q

The antihypertensive effect of Beta Blockers and other vasodilators may be attenuated by

A

NSAIDS

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41
Q

NSAIDs may attenuate what?

A

The antihypertensive effect of Beta Blockers and other vasodilators

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42
Q

What type of B Blocker is likely to exacerbate symptoms of peripheral vascular disease?

A

B blockers w/ intrinsic sympathomimetic activity

*less likely to produce vasospasm / thus to exacerbate s/s of pvd

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43
Q

Name some cardioselective B1 blockers

A

acebutolol
atenolol
bisoprolol
metoprolol

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44
Q

Compared to Propranolol (NS B blocker), Cardioselective B1 blockers in low-moderate doses are unlikely to produce:

A

bronchospasm
mask hypoglycemia
decrease peripheral blood flow

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45
Q

Cardioselective B1 Blockers are the preferred drugs for patients with

A

pulmonary disease
Insulin-dept DM
or
Symptomatic PVD

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46
Q

This drug has been shown to improve survival in pts with systolic HF

A

Carvedilol (NS Beta; which has Alph 1 blocking action as well)

*metoprolol and bisoprolol also provide a survival benefit in this population; not as great as Carvedilol

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47
Q

Labetalol is a

A

nonselective B blocker

also has significant Alpha 1 blocking action

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48
Q

The presence of alpha-adrenergic blocking properties in NS BB’s results in

A

less bradycardia
negative inotropic effects

*compared to “pure”BB’s

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49
Q

The Alpha properties in some BB’s may lead to

A

orthostatic hypotension

*labetalol

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50
Q

Dose labetalol have an incidence of bronchospasm?

A

yes

similar to that seen w/atenolol or metoprolol

51
Q

IV Labetalol is used in

A
  • HTN emergencies
  • managing pts w/Type B aortic dissections
  • facilitating conversion from IV to oral medications
52
Q

The risks associated with treat HTN with BB’s

A
  • Bradycardia
  • Heart Block
  • HF
  • Bronchospasm
  • claudication
  • masked hypoglycemia
  • sedation
  • impotence
  • angia pectoris or even MI–> precipitated if abruptly d/c’d
53
Q

what patient type generally cannot tolerate more than moderate doses of BB’s?

A

any degree of HF

54
Q

Despite the low tolerance of BB’s in pts with CHF, what is clear about dosage and use?

A
  • that when dosage is slowly increased
  • given chronically
  • the anti-adrenergic effect provides a significant benefit in chronic SYSTOLIC HF
55
Q

B Blockers should be avoided in patients with:

A

symptomatic Asthma

56
Q

B Blockers potentially increase the R/O serious

A

hypoglycemia in diabetics

57
Q

Why do B B’s increase r/o hypoglycemia in pts w/DM?

A

they blunt autonomic Nervous System responses that would warn of hypoglycemia

58
Q

Nevertheless, the incidence of hypoglycemia has not been shown to be ______ in diabetic pts being tx w/ B-adrenergic antagonists to control HTN

A

increased

59
Q

Name the Alpha-1 receptor blockers:

A
  • Doxazocin
  • Prazosin
  • Terazosin
60
Q

Selective postsynaptic Alpha 1-adrenergic receptor antagonist result in:

A

vasodilating effects on both arterial and venous vasculature

61
Q

Alpha-1 receptor blockers have vasodilating effects on arterial, venous, or both arterial/venous vasculatures?

A

Both - arterial and venous vasculature

62
Q

The absence of [THIS] leaves intact the normal inhibitory effect on Norepi release from nerve endings

A

Presynaptic Alpha 2 receptor antagonism

63
Q

These drugs are unlikely to elicit reflex increases in cardiac output and renin release:

A

Alpha 1 Receptor blockers

64
Q

Oral phenoxybenzamine and IV phentolamine are

A

NonSelective Alpha Blockers that also block Alpha 2 receptors

65
Q

What durgs are NonSelective Alpha Blockers that also block Alpha 2 receptors?

A

Oral phenoxybenzamine

IV phentolamine

66
Q

Name two drugs used almost exclusively in the mgmt of pheochromocytoma

A 
Oral phenoxybenzamine ([pre-op) 
and IV phentolamine (periop)
67
Q

catecholamine-secreting tumor formed by chromaffin cells inside the adrenal medulla is known as

A

pheochromocytoma

68
Q

Another pre-op drug for pheochromocytoma is

A

Prazosin

69
Q

This drug may be of value for decreasing afterload in pts with CHF, as well as treating essential HTN

A

Prazosin

alpha 1 receptor blocker

70
Q

This drug has been used to relieve the vasospasm of Raynaud’s phenomenon:

A

Prazosin

71
Q

Prazosin is used for treatment of:

A
  • essential HTN
  • pheocromocytoma
  • decreasing afterload in CHF
  • raynaud’s
  • shrinking the prostate gland (BPH)
72
Q

A useful indication for Prazosin in addition to tx of essential HTN in the presence of BPH

A

this drug decreases the size of the gland

73
Q

SE’s of Prazosin

A
  • fluid retention
  • orthostatic hypotension
  • vertigo
74
Q

What drugs may interfere with the antihypertensive effect of Prazosin?

A

NSAIDS

75
Q

Prazosin is nearly completely metabolized after PO administration. This and the bioavailabilty <60% suggest

A

-substantial first pass hepatic metabolism

76
Q

Because Prazosin is metabolized in the ____ permits its use in pts with ____ w/o altering the dose.

A

metabolized: LIVER

pts with: RF

77
Q

The elimination half-time of Prazosin is about 3hrs.

It’s prolonged by ___, but not by ____.

A

Prolonged by HF

but not renal dysfunction

78
Q

These symptoms may accompany tx with Prazosin (not SE’s):

A
  • Dry mouth
  • Lethargy
  • Nasal congestion
  • nightmares
  • Sexual dysfunction
  • Urinary frequency
79
Q

In the presence of Prazosin, what may be exaggerated?

Why?

A

hypotension during epidural anesthesia

-reflecting drug-induced Alpha 1 blockade that prevents compensatory vasoconstriction in the unblocked portions of the body.

80
Q

In epidural anesthesia and prazosin, what may occur?

A

hypotension

-reflecting drug-induced Alpha 1 blockade that prevents compensatory vasoconstriction in the unblocked portions of the body.

81
Q

In epidural hypotension in the presence of prazosin, what medication should be administered? What would the pt likely be unresponsive to?

A

May not be responsive to phenylephrine
—-> d/t the resulting decrease of SVR results in hypotension.

Epi may be necessary to increase SVR and SBP.

82
Q

The combination of prazosin and B Blocker could result in:

A

refractory hypotension during regional anesthesia.

83
Q

Why does particularly refractory hypotension result in the combination of prazosin and a BB during regional anesthesia?

A

D/T potentially blunted responses to B1 and A1 agonists

84
Q

Clonidine is a centrally acting

A

selective partial Alpha 2 - agonist

85
Q

Clonidine acts as an antihypertensive drug by virtue of its ability to decrease:

A

sympathetic output from the CNS

86
Q

Clonidine adult dose:

A

0.2-0.3 mg/daily

87
Q

Clonidine is particularly effective in the tx of:

A

patients with:

  • severe HTN
  • renin-dependent disease
88
Q

Clonidine MOA

A

Alpha 2 agonists

-binds to A2 receptor (3 subtypes)

89
Q

Name the Alpha2 receptor subtypes:

A

Alpha-2A
Alpha -2B
Alpha-2C

  • they’re distributed ubiquitously
  • each may be uniquely responsible for some of the actions of Alpha 2 agonists
90
Q

Alpha 2 receptors mediate:

A
  • analgesia
  • sedation
  • sympatholysis
91
Q

Alpha 2B receptors mediate:

A

-vasoconstriction
and possibly
-anti-shivering effects

92
Q

Clonidine stimulates Alpha 2 adrenergic inhibitory neurons in the

A

medullary vasomotor center

93
Q

Stimulation from the medullary vasomotor center results in a:

A

decease in SNS outflow from the CNS to peripheral tissues

94
Q

Decreased sympathetic nervous system activity is manifested as

A

peripheral vasodilation and decreases

  • Systemic BP
  • HR
  • CO
95
Q

α2 receptors on blood vessels mediate

A

vasoconstriction

96
Q

Alpha receptors on peripheral sympathetic nervous system nerve endings inhibit release of

A

norepinephrine

97
Q

The ability of clonidine to do [this] may be the mechanism for profound decreases in anesthetic requirements

A

The ability of clonidine to modify the function of potassium channels in the CNS
*cell membranes become HYPERpolarized

98
Q

Neuraxial placement of clonidine inhibits

A

spinal substance P release

and nociceptive neuron firing produced by noxious stimulation.

99
Q

Clonidine is rapidly absorbed (PO) and reaches peak plasma concentrations with

A

60-90mins

100
Q

Elimination half-time of clonidine is

A

b/w 9-12hrs

101
Q

Clonidine is metabolized in

A
  • 50% in the liver

- the rest is unchanged in urine

102
Q

Clonidine duration (of hypotensive effect) after a singe PO dose is

A

about 8 hrs

103
Q

How long does the TD route of Clonidine need to produce a steady-state, therapeutic plasma concentration?

A

48hrs

104
Q

The decrease in systolic blood pressure produced by clonidine is more prominent than the decrease

A

in diastolic blood pressure.

105
Q

patients treated chronically with Clonidine, SVR is little affected, how does CO change with chronic treatment

A

returns toward pre-drug levels

106
Q

With clonidine homeostatic cardiovascular reflexes are maintained. This means

A

pts avoid orthostatic hypotension or hypotension during exercise

107
Q

The most common SE of clonidine:

A
  • sedation

- xerostomia (dry mouth)

108
Q

Clonidine’s agonist effect on postsynaptic A2 receptors in the CNS do what for GA?

A

nearly 50% reduction :

  • in MAC/anesthetic requirements for inhaled anesthetics
  • injected, preanesthetic drugs
109
Q

Pt’s pretreated with clonidine often manifest less ____ in response to surgical stimulation.

A

catecholamines

*occasionally require tx of bradycardia

110
Q

Why is a combination of clonidine w/a diuretic often necessary?

A

retention of sodium and water

111
Q

Additional SE’s of clonidine:

A
  • skin rashes are frequent
  • impotence occurs occas.
  • orthostatic hypotension is rare
112
Q

What drug prevents opioid-induced skeletal muscle rigidity and produces skeletal muscle flaccidity?

A

clonidine

113
Q

Do A2 agonists have an effect on the responses evoked by NMBDs?

A

No

114
Q

rebound htn from abrupt d/c of clonidine can result how many hours after the last dose?

A

8hrs and as late as 36hrs

115
Q

Clonidine rebound htn is most likely to occur in daily dosages greater than

A

1.2mg /daily

116
Q

what s/s typically precede the actual increase in SBP with clonidine rebound htn?

A
  • abd pain
  • diaphoresis
  • H/A
  • Nervousness
  • tachycardia
117
Q

β-Adrenergic blockade may exaggerate the magnitude of (clonidine) rebound hypertension by blocking the

A
  • β2 vasodilating effects of catecholamines and

- leaving their Alpha vasoconstricting actions unopposed

118
Q

TX of clonidine induced rebound htn:

A
  • re-instituting clonidine

- administering vasodilators such as hydralazine or nitroprusside

119
Q

What (other) drug may be useful in the management of patients experiencing rebound hypertension (from clonidine)

A

labetalol with α and β antagonist effects

120
Q

How long can TD clonidine provide sustained, therapeutic levels should PO therapy need to be interrupted for surgery?

A

as long as 7 days

121
Q

how should planned withdrawl of clonidine be done?

A

clonidine dosage should be gradually decreased over 7 days or longer

122
Q

clinical evidence of excessive SNS activity has been associated with abrupt d/c of :

A

Beta Blocker therapy

123
Q

Antihypertensive drugs that act independently on central and peripheral SNS mechanisms do not seem to be associated with:

A

rebound htn after sudden d/c of therapy

*these are Direct vasodilators, ACE inhibitors

124
Q

Hydralazine administration in OR (supplied, dose)

A

supplied: 20mg/ml
Dose: 5-10mg – start low

Spring '20/ L. Pharm Exam 3 - sympatholytics/mimetics, LAs, antiarrhythmics, vaso (17 decks)

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