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2-Pharm Exam 3 > Sympatholytic Drugs > Flashcards

Sympatholytic Drugs Flashcards

1
Q

Define Sympatholytic Drugs.

A

Drugs that block activation of adrenergic receptors

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2
Q

What are some examples of sympatholytic drugs?

A
  • •Alpha-adrenergic receptor antagonists & α-2 agonists
  • Beta-adrenergic receptor antagonists
  • Combined alpha & beta-adrenergic receptor antagonists

Calcium channel blockers

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3
Q

Review predominent phsyiologic effects of alpha 1 adrenergic and dopamine receptors.

A
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4
Q

What do Alpha-Adrenergic Receptor Antagonists block?

A

Block the effects of catecholamines/sympathomimetics

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5
Q

What is the side effects of Alpha-Adrenergic Receptor Antagonists?

A
  • orthostatic hypotension
  • baroreceptor-mediated reflex tachycardia
  • impotence
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6
Q

What does Absence of beta-adrenergic blockade results in?

A

maximum expression of cardiac stimulation from NE which leads to tachycardia

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7
Q

Review tissue location and actions of Alpha 1 and 2 receptors.

A
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8
Q

What is the MOA of Phentolamine?

A

Nonselective (reversible) α antagonist acting on postsynaptic α1 and presynaptic α2 receptors

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9
Q

What is the clinical effects of Phentolamine (4)?

A
  • Peripheral vasodilation & decreased systemic BP resulting from α1 blockade; reflects direct action on vascular smooth muscle
  • Reflex baroreceptor-mediated increase in sympathetic cardiac activity
  • α2 blockade permits enhanced neural release of NE resulting in increased CO, HR
  • Cardiac dysrhythmias and angina may result
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10
Q

What is the onset of Phentolamine?

A

Onset within 2 min, lasting 10-15 (transient effects)

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11
Q

What is the most common clinical indications of Phentolamine?

A

Treatment of acute HTN emergencies (ex: pheochromocytoma)

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12
Q

What is the infusion of Phentolamine?

A

Infusion: 0.1-2 mg/min

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13
Q

What is the dose for local inflitration?

A

5-15 mg/10 ml normal saline to treat extravasation of vasoconstricting sympathomimetic drug

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14
Q

What is the MOA of Phenoxybenzamie?

A

Nonselective α-adrenergic antagonist (combines covalently w/A-adrenergic receptor

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15
Q

Which alpha block associated with Phenoxybenzamie has the more intense response?

A

α 1 blockade more intense than α 2 blockade

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16
Q

What is the onset of Phenoxybenzamie?

A

Slow onset (up to 60 min with IV)

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17
Q

What is the elimination half-time of Phenoxybenzamie?

A

half-time 24 hrs

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18
Q

What is the side effects of Phenoxybenzamie?

A

Orthostatic hypotension, pronounced in preexisting HTN or hypovolemia

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19
Q

What drug interaction can occur with Phenoxybenzamie?

A

Exaggerated BP decreases: blood loss and volatile anesthetics (vasodilation)

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20
Q

What are the clinical uses of Phenoxybenzamie?

A
  • Main use: control BP with pheochromocytoma
  • Works best in cutaneous vasoconstriction as seen with Raynaud disease
  • Miosis, nasal stuffiness, sedation (chronic therapy)
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21
Q

What are some αlpha-Adrenergic Receptor Antagonists?

A
  • Phentolamine
  • Phenoxybenzamie
  • Yohimbine
  • Doxazosin
  • Prazosin (Minipress)
  • Terazosin
  • Tamsulosin
    *
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22
Q

What is the MOA of Yohimbine?

A

Selective presynaptic α-2 antagonist

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23
Q

What does Yohimbine promote release of?

A

enhanced NE release from nerve endings

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24
Q

What Yohimbine associated with?

A

Associated w/increased skeletal muscle activity & tremors

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25
Q

What is Yohimbine used to treat?

A

idiopathic orthostatic hypotension; impotence

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26
Q

What can excessive doses of Yohimbine produce?

A
  • tachycardia
  • HTN
  • rhinorrhea
  • paresthesias
  • dissociative states
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27
Q

What is the MOA of Doxazosin?

A

Selective postsynaptic α-1 antagonist

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28
Q

What is the clinical use of Doxazosin?

A

HTN, BPH

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29
Q

What is the MOA of Prazosin (Minipress)?

A

Selective postsynaptic α-1 antagonist; maintains α-2 effects to inhibit NE release from nerve endings

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30
Q

What are the effects of Prazosin (Minipress)?

A
  • less likely to get reflex tachycardia
  • dilates arterioles & veins
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31
Q

What is the clinical use of Prazosin (Minipress)?

A

HTN

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32
Q

What is the MOA of Terazosin?

A

α-1 antagonist targeted for BPH

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33
Q

What is the MOA of Tamsulosin?

A

α-1 antagonist targeted for BPH

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34
Q

What effect do BPH drugs have with anesthesia?

A

BPH drugs (α-1 blockers) can result in sudden hypotension with anesthesia

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35
Q

What is the MOA of alpha 2-Adrenergic Receptor Agonists?

A

These drugs bind selectively to presynaptic alpha-2 adrenergic receptors and by negative feedback mechanism

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36
Q

What does αlpha 2-Adrenergic Receptor Agonists decrease?

A

decrease release of NE from presynaptic nerve terminals which reduce sympathetic outflow

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37
Q

Where is the location of most αlpha 2-Adrenergic Receptor Agonists?

A

found in CNS, esp brainstem & locus ceruleus

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38
Q

What does peripheral inhibition of αlpha 2-Adrenergic Receptor Agonists cause?

A

•result in inhibition of insulin release & induction of glucagon from pancreas

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39
Q

What are the clinical effects of αlpha 2-Adrenergic Receptor Agonists?

A
  • hypotension
  • bradycardia
  • central sedation
  • mild analgesia
40
Q

What can happen with abrupt withdrawal of αlpha 2-Adrenergic Receptor Agonists?

A

Withdrawal (even after short term use) can result in rebound effect w/dramatic increase in sympathetic outflow causing increased HR/BP (possibly to dangerous levels)

41
Q

What are the common αlpha 2-Adrenergic Receptor Agonists?

A

Clonidine & Dexmedetomidine

42
Q

What clinical effect can be seen with Clonidine?

A

Administration results in dose-dependent decrease in HR & BP

43
Q

What is the clinical use for Clonidine?

A

Used in tx of resistant HTN, tremors from central stimulant medications, & opioid withdrawal

44
Q

What is the formularies for Clonidine?

A

Available in IV, oral, and transdermal

45
Q

What is a caution to be taken with clonidine?

A

rebound HTN with sudden withdrawal

46
Q

What is the MOA of Dexmedetomidine?

A

Selective alpha-2 agonist w/ central sympatholytic effects

47
Q

What is the dose of Dexmedetomidine?

A

Administered as IV infusion 0.1-1.5 mcg/kg/min

48
Q

What is the elimination half life of Dexmedetomidine?

A

2 hours

49
Q

What is the clinical use for Dexmedetomidine?

A

Used for sedation & analgesia

50
Q

What is the metabolism for Dexmedetomidine?

A

liver impairment can increase plasma levels and duration of action

51
Q

What is a property of Dexmedetomidine?

A

Physiologic dependence occurs after several days of administration

52
Q

What is the signs of Dexmedetomidine withdrawal?

A

tachycardia, HTN , & anxiety

53
Q

What is the effects of large doses of Dexmedetomidine? Why does this occur?

A
  • Large IV boluses (0.25-1mcg/kg over 3-5 min) can result in paradoxical HTN w/decreased HR resembling phenylephrine d/t crossover alpha-1 stimulation
54
Q

Review alpha 2 agonist receptor.

A
55
Q

What is the MOA of βeta-Adrenergic Receptor Antagonists?

A

they bind to beta-receptors in competitive manner & prevent the actions of catecholamines and other beta-agonists on the beta receptor

56
Q

What are βeta-Adrenergic Receptor Antagonists structurally related to?

A

Structurally related to isoproterenol

57
Q

Describe the characteristics of the G-protein-coupled receptors βeta-Adrenergic Receptor Antagonists.

A
  • Stimulation activates adenylate cyclase to produce cAMP
  • Phosphorylates proteins including L-type voltage dependent Ca++ channels and troponin C
58
Q

What type of receptors are βeta-Adrenergic Receptor Antagonists?

A

G-protein-coupled receptors

59
Q

What are the net effects in the heart?

A

positive inotropy, chronotropy, dromotropy

60
Q

Review the stimulation of the PNS and SNS on the heart.

A
61
Q

Review the receptor effects from muscarainic ACH receptors and beta adrenergic receptors.

A
62
Q

What effect does binding to βeta-Adrenergic Receptor Antagonists cause?

A

prevent catecholamines or other sympathomimetics in provoking beta-adrenergic responses on the heart, airway/lung smooth muscle, or blood vessels

63
Q

Why should βeta-Adrenergic Receptor Antagonists be continued throughout the perioperative period?

A

avoid sympathetic nervous system hyperactivity (rebound) asso w/abrupt discontinuation of these drugs

64
Q

What occurs with chronic administration of βeta-Adrenergic Receptor Antagonists?

A

upregulation of β receptors

65
Q

Review βeta-Adrenergic Receptor Antagonists physiological effects.

A
66
Q

What are βeta-Adrenergic Receptor Antagonists classified by?

A

basis of their selectivity

67
Q

What are nonselective βeta-Adrenergic Receptor Antagonists?

A

Nonselective for beta-1 and beta-2 receptors (propranolol, nadolol, timolol)

68
Q

What are cardioselective βeta-Adrenergic Receptor Antagonists?

A

Cardioselective for beta-1 receptors (metoprolol, atenolol, esmolol, bisoprolol)

69
Q

What βeta-Adrenergic Receptor Antagonists is better for patients w/reactive airways (asthma, COPD)?

A

β-1 blocking drug that is cardioselective

70
Q

What is true about Beta selectivity?

A

dose-dependent: beta selectivity diminishes when increased doses of a beta-selective drug is administered

71
Q

What is the treatment for essential HTN?

A

Cardioselective beta blocking drugs better suited as tx for essential HTN because these drugs lack inhibition of peripheral B-2 receptors that produce vasodilation

72
Q

What impact does nonselective agents have?

A

interfere with epinephrine-induced glycogenolysis in response to hypoglycemia

73
Q

What does βeta-Adrenergic Receptor Antagonists blunt?

A

the signs of hypoglycemia such as tachycardia

74
Q

What does βeta-Adrenergic Receptor Antagonists inhbit?

A

Inhibits skeletal muscle uptake of K+- can raise serum levels (mainly an issue with nonselective)

75
Q

What is true about the properties of βeta-Adrenergic Receptor Antagonists?

A

Beta receptors can be upregulated or downregulated: long-term tx w/ beta-blockers leads to up-regulation fo beta receptors or an increase in the absolute number and activity of receptors

76
Q

What is true of abrupt DC of beta-adrenergic blocking drugs?

A

withdrawal syndrome

77
Q

What is at increased risk with B-2 blockade? What patient population is this more of a concern with?

A

(nonselective drugs or large doses of selective drugs) increases risk of bronchospasm (asthma, COPD)

78
Q

What patient populations can βeta-Adrenergic Receptor Antagonists worsen symptoms?

A
  • Patients with peripheral vascular disease (may worsen sxs)
  • Patients w/ bradydysrhythmias
  • acute decompensated heart failure (not caused by tachycardia)
  • AV heart blocks (i.e., complete heart block)
79
Q

Why is caution taken in diabetic patients on βeta-Adrenergic Receptor Antagonists?

A

masks signs of hypoglycemia

80
Q

What is the properties of acute withdrawal from βeta-Adrenergic Receptor Antagonists (Beta Blockers)?

A

Acute withdrawal of beta-blocking drugs in patients chronically treated w/beta-blocking drugs can result in excess sympathetic activity within 24-48 hours (due upregulation of beta receptors)

81
Q

How can profound, resistant hypotension occur with βeta-Adrenergic Receptor Antagonists?

A

Administering to hypovolemic patients w/compensatory tachycardia

82
Q

What are the clinical uses of βeta-Adrenergic Receptor Antagonists?

A
  • Tx of angina
  • HTN
  • postmyocardial infarctions
  • SVTs
  • atrial fibrillation
  • suppression of increased sympathetic activity (i.e., during endotracheal intubation)
83
Q

What can βeta-Adrenergic Receptor Antagonists help manage?

A
  • Management of hypertrophic obstructive cardiomyopathies
  • CHF
  • treatment of migraine Headaches
  • preoperative prep of hyperthyroid patient
  • digitalis-induced dysrhythmias
  • atrial & ventricular dysrhythmias
84
Q

When is perioperative beta-blockade needed?

A

for high risk patients for high-risk surgery (goal HR 65-80 bpm)

85
Q

When is continuing patients on βeta-blockers through perioperative period recommended?

A

for patients at high risk of coronary ischemia having major surgical procedure

86
Q

What are the primary IV beta blocking drugs that are used in anesthesia?

A

Metoprolol, esmolol, & labetalol

87
Q

What is another term for βeta-Adrenergic Receptor Antagonists?

A

Beta Blockers

88
Q

When should βeta-Adrenergic Receptor Antagonists not be used?

A

Beta-adrenergic blocking drugs should NOT be used to treat excessive sympathetic nervous system activity produced by cocaine or systemic absorption of topical or subcutaneous epinephrine

89
Q

What is the effect of beta blockade with cocaine or systemic absorption of topical or subcutaneous epinephrine?

A

Beta-blockade of beta-2 receptor blocks vasodilating effect produced by beta-2 receptors and leaves unopposed alpha-adrenergic effects of cocaine/epinephrine leading to peripheral vasoconstriction

90
Q

What is beta blockade in conjunction with the use of cocaine or systemic absorption of topical or subcutaneous epinephrine?

A
  • Associated with paradoxical HTN, pulmonary edema, and cardiovascular collapse
  • Beta-adrenergic blocking drugs should NOT be used to treat excessive effects of these medications
91
Q

What is the treatment for catecholamine-induced SNS stimulation?

A

resulting from acute increases in LV afterload that occurs with cocaine & excessive epinephrine absorption more safely treated with a peripheral vasodilator drug

92
Q

What is some medications for the treatment of catecholamine-induced SNS stimulation?

A

sodium nitroprusside, nitroglycerin, hydralazine

93
Q

Review characteristics of Beta adrenergic receptor antagonists.

A

Flood, p. 479: Note the differences that separate the various agents and how these would dictate their use among various settings and patient populations.

94
Q

Describe the components of the cardiac action potential.

A
95
Q

Review drugs affecting the cardiac action potential.

A

2-Pharm Exam 3 (14 decks)

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