Sympatholytics Flashcards

1
Q

A ______ alpha blockade that has been established cannot be reversed by sympathomimetics. The effects are terminated by _____.

A

Phenoxybenzamine; metabolism

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2
Q

Induced alpha receptor blockade permits enhanced neural release of _____ causing an ______ HR & CO

A

NorEpi; increased

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3
Q

Phentolamine

A

Nonselective alpha antagonist
Peripheral vasodilation and decreased BP w/in 2 min lasting 10-15 min
Used for hypertensive emergencies like w/ pheochromocytoma
30-70 mcg/kg (1-5 mg); continuous inf 0.1-2mg/min
Can be used for extravasation of sympathomimetic

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4
Q

Onset of blockade of Phenoxybenzamine

A

Slow up to 60 min to peak

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5
Q

Phenoxybenzamine produces little changes in systemic BP in the ____ patient in the absence of _____

A

Normovolemic; increased SNS activity

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6
Q

If given during maternal treatment can cause neonatal hypotension and resp distress in first 72 hrs of life

A

Phenoxybenzamine

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7
Q

Withdrawal of alpha 2 agonists even after short term use can result in rebound effect causing dramatic increase in sympathetic outflow causing?

A

Elevated HR and HTN to dangerous levels

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8
Q

Dexmedetomidine

A

Selective alpha 2 agonist 1,600:1
IV 0.1- 1.5 mcg/kg/min
H/l: 2 hrs
Extensive bio transformation in liver, E in urine
Potent binding & short half life can induce physiologic dependence resulting in withdrawal phenomenon (tachy, HTN, anxiety)

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9
Q

What determines if a beta drug acts as an agonist or an antagonist?

A

Substitutions on the benzene ring

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10
Q

Beta 1 receptor blockade:

A

Slows sinus rate

Slows conduction of cardiac impulses through AV node

Decreases inotropy

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11
Q

Among the beta adrenergic receptor antagonists, what is the only drug that is highly plasma protein bound?

A

Propranolol (90-95%)

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12
Q

Volume of distribution of beta adrenergic receptor antagonists is ____ and are _____ distributed following IV admin.

A

High; rapid

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13
Q

Why is Nadolol unique?

A

It’s long duration of action permits once daily administration
(H/t: 20-40 hrs)

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14
Q

How is timolol effective in treatment of glaucoma?

A

Its ability to decrease IOP presumably by decreasing production of aqueous humor

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15
Q

Protein binding of timolol

A

Not extensive

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16
Q

What is the systemic issue with timolol?

A

Administered as eye drops but systemic absorption may be sufficient to cause resting bradycardia and increased airway resistance

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17
Q

Prominent pharmacologic effect of Bisoprolol

A

Negative chronotropic effect

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18
Q

How does betaxolol compare with timolol in bronchoconstriction

A

Risk of bronchoconstriction in pts with airway hyper reactivity is less than with timolol

19
Q

Typical initial dose of ___ IV of Esmolol over about 60 sec with a full therapeutic effect evident within ____ min

Action ceases in approximately _____ min after adm stopped

A

0.5mg/kg; 5 min

10-30 min

20
Q

Although ____ & ____ may be used to blunt increase in SBP associated with laryngoscopes and tracheal intubation, neither influences ___

A

Fentanyl, lidocaine, HR

21
Q

what drug in the presence of inhaled anesthetics may cause profound bradycardia?

A

Timolol

22
Q

Additive CV effects with inhaled anesthetics and B-blockers:

A

Greater with Enflurane

Least with Isoflurane (Sevo & Des do not seem to be associated with sig additive effects either)

23
Q

Goal HR of preop B-blocker therapy

A

65-80

24
Q

Max SBP lower effect of an IV dose of Labetalol ____ is present in _____ min

A

0.1-0.5mg/kg; 5-10 min

25
Q

Safe to use in hypertensive emergencies and to control severe HTN associated with epinephrine overdose
Can be used for rebound HTN after withdrawal of clonidine

A

Labetalol

26
Q

Selectively interferes with inward Ca ion movement across myocardial and vascular smooth muscle cells

A

CCB

27
Q

CCB selective for atrioventricular node

A

Phenylalkylamines & Benzothiazepines

28
Q

CCB selective for arteriolar beds

A

Dihydropyridines

29
Q

CCB produce:

A

Decreased HR, myocardial contractility, activity of SA node, rate of conduction of cardiac impulses through AV node
Vascular smooth muscle relaxation w/ associated vasodilation
Decreased systemic BP

30
Q

All ______ are effective for treatment of coronary artery spasms

A

CCBs

31
Q

All CCB exert negative inotropic effects which are most significant with:

A

Verapamil

Diltiazem

32
Q

Verapamil primary site of action

A

AV node

33
Q

While Verapamil is 90% protein bound, what drugs can increase the unbound portion?

A

Lidocaine
Diazepam
Propranolol

34
Q

Lacks effects on SA and AV nodes but has the greatest vasodilating effects of all CCB

A

Nicardipene (Dihydropyridines)

35
Q

Of all antianginal drugs, what group of CCB profuse the greatest dilation of the peripheral arterioles?

A

Dihydropyridines

36
Q

NIcardipine

A

Long h/t
M: Liver
95% protein bound
Can be used as a tocolytic

37
Q

Blocks predominantly Ca channels of AV node and is a first line med for tx of SVT

A

Diltiazem

38
Q

Pharmacokinetics of Diltiazem

A

PO: excellent absorption O 15 min P 30 min

70-80% protein bound

Excreted in bile 60% urine 35%
H/t: 4-6 hrs

39
Q

Pt with preexisting cardiac conduction abnormalities may experience greater degrees of AV HB with CCB and?

A

Beta blockers or digoxin

40
Q

Myocardial depression and peripheral vasodilation produced by volatile anesthetics could be exaggerated by?

A

CCB

41
Q

How do you treat toxicity of CCB?

A

May be partially reversed with IV calcium or dopamine

42
Q

CCB potentiate the effects of ____ & _____

A

Depolarizing and nondepolarizing NMBD

43
Q

Antagonism of NMBD may be impaired b/c of diminished what in the presence of a CCB?

A

Presynaptic release of ACh