Sympatholytics Flashcards

1
Q

Types of cholinergic receptors and sites of action

A

1) Nicotinic: ganglia and skeletal muscle
2) Muscarinic: glands (lacrimal, salivary, gastric), smooth muscle (bronchial, GI, bladder, and vessels), and heart (SA and AV node)

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2
Q

All preganglionic neurons release what neurotransmitters? Is it excitatory or inhibitory?

A

Acetylcholine. Excitatory.

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3
Q

What is the rate-limiting step in the synthesis of epi and norepi in the adrenal medulla?

A

tyrosine hydoxylase

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4
Q

Ratio of Epi/norepi synthesis in the adrenal medulla

A

80/20

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5
Q

What neurotransmitter precedes the synthesis of norepinephrine?

A

dopamine

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6
Q

Metabolism of norepi and epi

A

Metabolic degradation by MOA and COMT. However, 80% is reuptake.

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7
Q

Beta-1 selective antagonists

A

atenolol, esmolol, and metoprolol

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8
Q

Beta-blockers with alpha effects

A

labetalol and carvedilol

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9
Q

Phentolamine MOA and SE

A

nonselective reversible IV alpha-blocker. Produces vasodilation. Produces baroceptor-mediated increases in CO and HR. May cause dysrhythmias and angina, as well as hyperperistalsis, abdominal pain, and diarrhea due to the predominance of parasympathetic activity.

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10
Q

Clinical uses for phentolamine

A

Intraop management of pheochromocytoma, autonomic dysreflexia (SCI), and extravasation of IV sympathomimetic.

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11
Q

Phenoxybenzamine MOA and SE

A

nonselective IRREVERSIBLE alpha-blocker. Profound hypotension in the presence of hypovolemia, blood loss, vasodilators, and inhalation agents. Noncardiac effects include miosis, nasal stuffiness, and sedation.

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12
Q

Phenoxybenzamine clinical uses

A

Preoperative management of pheochromocytoma, inoperable adrenal tumors, Raynaud’s diseases (more effective in cutaneous vasoconstriction rather than skeletal muscle flow)

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13
Q

Preoperative management of pheochromocytoma with phenoxybenzamine

A

0.5-1 mg/kg PO beginning two weeks prior to surgery. Make sure intravascular volume is adequate. Prazosin as an alternative.

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14
Q

Yohimbine MOA

A

Selective presynaptic alpha-2 antagonist. Enhances the release of norepinephrine.

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15
Q

Yohimbine clinical uses

A

idiopathic orthostatic hypotension, former treatment for impotence.

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16
Q

Prazosin MOA

A

selective post-synaptic alpha-1 antagonist. Dilates both arterioles and veins. Reflex tachycardia less common because drug has no inhibitory effect on alpha-2 receptors.

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17
Q

Prazosin clinical uses

A

HTN, Raynaud’s, BPH

18
Q

Vasodilators are often combined with which drug and why?

A

beta-blockers to minimize baroreceptor mediated increases in heart rate and cardiac output.

19
Q

beta-blockers for the management of CHF

A

metoprolol, carvedilol, and bisoprolol

20
Q

Which beta-blocker increases the risk of amide local anesthetic toxicity and why?

A

Propranolol. Propranolol induced decreases in hepatic metabolism decrease the clearance of amide LA.

21
Q

Most selective beta-blocker

A

Atenolol

22
Q

Which type of beta-blocker is preferred in diabetics? Why?

A

Selective beta-blockers, because they do not potentiate insulin-induced hypoglycemia seen with nonselective beta-blockers (think beta-2 effects).

23
Q

How is esmolol metabolized?

A

rapid hydrolysis by plasma esterases. Ultra-short acting. Elimination half-life 9 minutes. Return of HR to predrug levels within 10-30 minutes.

24
Q

DOC for treating massive beta-adrenergic antagonist overdose

A

glucagon

25
Q

Percentage of B1 and B2 receptors in the heart

A

75% beta-1 and 20% beta-2

26
Q

Which beta-blocker is highly protein-bound?

A

Propranolol

27
Q

What drug decreases the pulmonary first-pass uptake of fentanyl?

A

Chronic administration of propranolol results in 2-4 times as much fentanyl being injected into the systemic circulation. Both are basic lipophilic amines.

28
Q

Nonselective beta-blockers should not be used in what type of patients?

A

Patients with reactive airway disease, peripheral vascular disease, and those who are prone to hypoglycemia.

29
Q

Useful in the management of perioperative thyrotoxicosis, pregnancy-induced HTN, and epinephrine or cocaine-induced cardiotoxicity.

A

Esmolol because of its rapid onset and it is short-acting.

30
Q

Beta-blockers can affect the serum concentration of what electrolyte?

A

Potassium, serum concentrations are increased due to the inhibition of insulin release.

31
Q

What receptors does labetalol work on?

A

alpha 1, beta 1, beta 2. Decreases SVR (alpha 1 blockade) with attenuation of reflex tachycardia by simultaneous beta-blockade.

32
Q

Which common beta-blocker depends on the kidneys as its primary route of elimination?

A

Atenolol

33
Q

Common beta-blocker with intrinsic sympathomimetic activity

A

Labetalol

34
Q

alpha 1 receptor stimulation effects

A

mydriasis, bronchoconstriction, vasoconstriction, uterine contracture, contraction of sphincters of GI/GU tract

35
Q

alpha 2 receptor stimulation effects

A

Decreased NE release, decreased sympathetic outflow resulting in peripheral vasodilation and decreased BP, sedation, inhibition of insulin release, platelet aggregation

36
Q

Beta 1 receptor stimulation

A

positive chronotropic, dromotropic, and inotropic effects

37
Q

Beta 2 receptor stimulation

A

Smooth muscle relaxation (bronchodilation, vasodilation, uterus/bladder/gut), glycogenolysis, lipolysis, gluconeogenesis, insulin secretion, activation of Na/K pump (K goes intracellular, can produce hypokalemia and dysrhythmia)

38
Q

contraindications to beta-blockade

A

sinus or AV node dysfunction, heart block, hypotension, decompensated heart failure, severe reactive airway disease.

39
Q

Clinical uses for esmolol

A

HTN & tachycardia in response to intraop noxious stimulation & intubation, ECT, pheo, thyrotoxicosis, PIH, epi or cocaine-induced cardiac toxicity.

40
Q

Which beta-blocker does not cross the BBB/placenta?

A

esmolol due to its poor lipid solubility

41
Q

Most common SE of labetalol

A

orthostatic hypotension