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2-Pharm Exam 3 > Sympatholytic Drugs > Flashcards

Sympatholytic Drugs Flashcards

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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
What is Yohimbine used to treat?
idiopathic orthostatic hypotension; impotence
26
What can excessive doses of Yohimbine produce?
* tachycardia * HTN * rhinorrhea * paresthesias * dissociative states
27
What is the MOA of Doxazosin?
Selective postsynaptic α-1 antagonist
28
What is the clinical use of Doxazosin?
HTN, BPH
29
What is the MOA of Prazosin (Minipress)?
Selective postsynaptic α-1 antagonist; maintains α-2 effects to inhibit NE release from nerve endings
30
What are the effects of Prazosin (Minipress)?
* less likely to get reflex tachycardia * dilates arterioles & veins
31
What is the clinical use of Prazosin (Minipress)?
HTN
32
What is the MOA of Terazosin?
α-1 antagonist targeted for BPH
33
What is the MOA of Tamsulosin?
α-1 antagonist targeted for BPH
34
What effect do BPH drugs have with anesthesia?
BPH drugs (α-1 blockers) can result in sudden hypotension with anesthesia
35
What is the MOA of alpha 2-Adrenergic Receptor Agonists?
These drugs bind selectively to presynaptic alpha-2 adrenergic receptors and by negative feedback mechanism
36
What does αlpha 2-Adrenergic Receptor Agonists decrease?
decrease release of NE from presynaptic nerve terminals which reduce sympathetic outflow
37
Where is the location of most αlpha 2-Adrenergic Receptor Agonists?
found in CNS, esp brainstem & locus ceruleus
38
What does peripheral inhibition of αlpha 2-Adrenergic Receptor Agonists cause?
•result in inhibition of insulin release & induction of glucagon from pancreas
39
What are the clinical effects of αlpha 2-Adrenergic Receptor Agonists?
* hypotension * bradycardia * central sedation * mild analgesia
40
What can happen with abrupt withdrawal of αlpha 2-Adrenergic Receptor Agonists?
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
What are the common αlpha 2-Adrenergic Receptor Agonists?
Clonidine & Dexmedetomidine
42
What clinical effect can be seen with Clonidine?
Administration results in dose-dependent decrease in HR & BP
43
What is the clinical use for Clonidine?
Used in tx of resistant HTN, tremors from central stimulant medications, & opioid withdrawal
44
What is the formularies for Clonidine?
Available in IV, oral, and transdermal
45
What is a caution to be taken with clonidine?
rebound HTN with sudden withdrawal
46
What is the MOA of Dexmedetomidine?
Selective alpha-2 agonist w/ central sympatholytic effects
47
What is the dose of Dexmedetomidine?
Administered as IV infusion 0.1-1.5 mcg/kg/min
48
What is the elimination half life of Dexmedetomidine?
2 hours
49
What is the clinical use for Dexmedetomidine?
Used for sedation & analgesia
50
What is the metabolism for Dexmedetomidine?
liver impairment can increase plasma levels and duration of action
51
What is a property of Dexmedetomidine?
Physiologic dependence occurs after several days of administration
52
What is the signs of Dexmedetomidine withdrawal?
tachycardia, HTN , & anxiety
53
What is the effects of large doses of Dexmedetomidine? Why does this occur?
* 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
Review alpha 2 agonist receptor.
55
What is the MOA of βeta-Adrenergic Receptor Antagonists?
they bind to beta-receptors in competitive manner & prevent the actions of catecholamines and other beta-agonists on the beta receptor
56
What are βeta-Adrenergic Receptor Antagonists structurally related to?
Structurally related to isoproterenol
57
Describe the characteristics of the G-protein-coupled receptors βeta-Adrenergic Receptor Antagonists.
* Stimulation activates adenylate cyclase to produce cAMP * Phosphorylates proteins including L-type voltage dependent Ca++ channels and troponin C
58
What type of receptors are βeta-Adrenergic Receptor Antagonists?
G-protein-coupled receptors
59
What are the net effects in the heart?
positive inotropy, chronotropy, dromotropy
60
Review the stimulation of the PNS and SNS on the heart.
61
Review the receptor effects from muscarainic ACH receptors and beta adrenergic receptors.
62
What effect does binding to βeta-Adrenergic Receptor Antagonists cause?
prevent catecholamines or other sympathomimetics in provoking beta-adrenergic responses on the heart, airway/lung smooth muscle, or blood vessels
63
Why should βeta-Adrenergic Receptor Antagonists be continued throughout the perioperative period?
avoid sympathetic nervous system hyperactivity (rebound) asso w/abrupt discontinuation of these drugs
64
What occurs with chronic administration of βeta-Adrenergic Receptor Antagonists?
upregulation of β receptors
65
Review βeta-Adrenergic Receptor Antagonists physiological effects.
66
What are βeta-Adrenergic Receptor Antagonists classified by?
basis of their selectivity
67
What are nonselective βeta-Adrenergic Receptor Antagonists?
Nonselective for beta-1 and beta-2 receptors (propranolol, nadolol, timolol)
68
What are cardioselective βeta-Adrenergic Receptor Antagonists?
Cardioselective for beta-1 receptors (metoprolol, atenolol, esmolol, bisoprolol)
69
What βeta-Adrenergic Receptor Antagonists is better for patients w/reactive airways (asthma, COPD)?
β-1 blocking drug that is cardioselective
70
What is true about Beta selectivity?
dose-dependent: beta selectivity diminishes when increased doses of a beta-selective drug is administered
71
What is the treatment for essential HTN?
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
What impact does nonselective agents have?
interfere with epinephrine-induced glycogenolysis in response to hypoglycemia
73
What does βeta-Adrenergic Receptor Antagonists blunt?
the signs of hypoglycemia such as tachycardia
74
What does βeta-Adrenergic Receptor Antagonists inhbit?
Inhibits skeletal muscle uptake of K+- can raise serum levels (mainly an issue with nonselective)
75
What is true about the properties of βeta-Adrenergic Receptor Antagonists?
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
What is true of abrupt DC of beta-adrenergic blocking drugs?
withdrawal syndrome
77
What is at increased risk with B-2 blockade? What patient population is this more of a concern with?
(nonselective drugs or large doses of selective drugs) increases risk of bronchospasm (asthma, COPD)
78
What patient populations can βeta-Adrenergic Receptor Antagonists worsen symptoms?
* 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
Why is caution taken in diabetic patients on βeta-Adrenergic Receptor Antagonists?
masks signs of hypoglycemia
80
What is the properties of acute withdrawal from βeta-Adrenergic Receptor Antagonists (Beta Blockers)?
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
How can profound, resistant hypotension occur with βeta-Adrenergic Receptor Antagonists?
Administering to hypovolemic patients w/compensatory tachycardia
82
What are the clinical uses of βeta-Adrenergic Receptor Antagonists?
* Tx of angina * HTN * postmyocardial infarctions * SVTs * atrial fibrillation * suppression of increased sympathetic activity (i.e., during endotracheal intubation)
83
What can βeta-Adrenergic Receptor Antagonists help manage?
* Management of hypertrophic obstructive cardiomyopathies * CHF * treatment of migraine Headaches * preoperative prep of hyperthyroid patient * digitalis-induced dysrhythmias * atrial & ventricular dysrhythmias
84
When is perioperative beta-blockade needed?
for high risk patients for high-risk surgery (goal HR 65-80 bpm)
85
When is continuing patients on βeta-blockers through perioperative period recommended?
for patients at high risk of coronary ischemia having major surgical procedure
86
What are the primary IV beta blocking drugs that are used in anesthesia?
Metoprolol, esmolol, & labetalol
87
What is another term for βeta-Adrenergic Receptor Antagonists?
Beta Blockers
88
When should βeta-Adrenergic Receptor Antagonists not be used?
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
What is the effect of beta blockade with cocaine or systemic absorption of topical or subcutaneous epinephrine?
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
What is beta blockade in conjunction with the use of cocaine or systemic absorption of topical or subcutaneous epinephrine?
* 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
What is the treatment for catecholamine-induced SNS stimulation?
resulting from acute increases in LV afterload that occurs with cocaine & excessive epinephrine absorption more safely treated with a peripheral vasodilator drug
92
What is some medications for the treatment of catecholamine-induced SNS stimulation?
sodium nitroprusside, nitroglycerin, hydralazine
93
Review characteristics of Beta adrenergic receptor antagonists.
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
Describe the components of the cardiac action potential.
95
Review drugs affecting the cardiac action potential.

2-Pharm Exam 3 (14 decks)

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