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Board Review CRNA (Sweat Book) > Drugs (s/e, dosing, MOA, onset, peak, etc) & some cardiac > Flashcards

Drugs (s/e, dosing, MOA, onset, peak, etc) & some cardiac Flashcards

1
Q

Trade name for Succinylcholine?

A

Anectine

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2
Q

Trade name for Mivacurium?

A

Mivacron

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3
Q

Trade name for Atracurium?

A

Tracurium

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4
Q

Trade name for Cisatracurium?

A

Nimbex

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5
Q

Trade name for Vecuronium?

A

Norcuron

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6
Q

Trade name for Rocuronium?

A

Zemuron

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7
Q

Trade name for d-Tubocurarine?

A

Tubarine

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8
Q

Trade name for Pancuronium?

A

Pavulon

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9
Q

Name the following (ultrashort, short, intermediate, or long):

1) Succinylcholine
2) Pancuronium
3) Mivacurium
4) Cisatracurium
5) d-Tubocurarine
6) Rocuronium
7) Atracurium
8) Vecuronium

A

1) Succinylcholine: ultra short
2) Pancuronium: long
3) Mivacurium: short
4) Cisatracurium: intermediate
5) d-Tubocurarine: long
6) Rocuronium: intermediate
7) Atracurium: intermediate
8) Vecuronium: intermediate

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10
Q

Name the onset time for the following:

1) Succinylcholine: ultra short
2) Pancuronium: long
3) Mivacurium: short
4) Cisatracurium: intermediate
5) d-Tubocurarine: long
6) Rocuronium: intermediate
7) Atracurium: intermediate
8) Vecuronium: intermediate

A

1) Succinylcholine: 0.5-1.5 min
2) Pancuronium: 2-4 min
3) Mivacurium: 3-4 min
4) Cisatracurium: 5-7 min
5) d-Tubocurarine: 2-4 min
6) Rocuronium: 1-1.5 min
7) Atracurium: 3-4 min
8) Vecuronium: 3-4 min

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11
Q

Name the duration to 25 % recovery for the following:

1) Succinylcholine: ultra short
2) Pancuronium: long
3) Mivacurium: short
4) Cisatracurium: intermediate
5) d-Tubocurarine: long
6) Rocuronium: intermediate
7) Atracurium: intermediate
8) Vecuronium: intermediate

A

1) Succinylcholine: 6-8 min
2) Pancuronium: 60-120 min
3) Mivacurium: 15-20 min
4) Cisatracurium: 35-45 min
5) d-Tubocurarine: 60-120 min
6) Rocuronium: 30-40 min
7) Atracurium: 35-45 min
8) Vecuronium: 35-45 min

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12
Q

Name the ED95 for the following:

1) Succinylcholine: ultra short
2) Pancuronium: long
3) Mivacurium: short
4) Cisatracurium: intermediate
5) d-Tubocurarine: long
6) Rocuronium: intermediate
7) Atracurium: intermediate
8) Vecuronium: intermediate

A

1) Succinylcholine: 0.30 mg/kg
2) Pancuronium: 0.06 mg/kg
3) Mivacurium: 0.08 mg/kg
4) Cisatracurium: 0.05 mg/kg
5) d-Tubocurarine: 0.50 mg/kg
6) Rocuronium: 0.30 mg/kg
7) Atracurium: 0.20 mg/kg
8) Vecuronium: 0.05 mg/kg

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13
Q

Name the primary route of elimination of the following:

1) Succinylcholine
2) Pancuronium
3) Mivacurium
4) Cisatracurium
5) d-Tubocurarine
6) Rocuronium
7) Atracurium
8) Vecuronium

A

1) Succinylcholine: metabolism (plasma cholinesterases)
2) Pancuronium: 85% RENAL/ 15% BILIARY
3) Mivacurium: metabolism
4) Cisatracurium: metabolism (HOFFMAN ONLY)–> nonspecific esterases are NOT involved
5) d-Tubocurarine: primary renal, secondary biliary
6) Rocuronium: 80% Biliary/ 20% renal
7) Atracurium: metabolism (2/3 by hydrolysis–> nonspecific esrterases, 1/3 by Hoffman elimination)
8) Vecuronium: 60% BILIARY/ 40% RENAL/ some metabolism
* *the termination of atracurium, cisatricurium, vec, and roc is by redistribution

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14
Q

Place the following NMB’s into the appropriate category:
vec, roc, pancuronium, atracurium, cisatracurium
1) monoquaternary aminosteroids
2) bisquaternary aminosteroids
3) bisquaternary benzylisoquinolines

A

1) monoquaternary aminosteroids: vec, roc
2) bisquaternary aminosteroids: panc
3) bisquaternary benzylisoquinolines: atrac, cisatra
* *aminosteroids= “curonium”
* *benzylisoquinolines= “curium”
* *ALL are quaternary ammonium compounds

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15
Q

Which NMB’s produce autonomic ganglionic blockade? (2)

A

d-tubocurarine and metocurine block nicotinic receptors at the autonomic ganglia

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16
Q

Which NMB’s elicit the release of histamine? (5)

A

sux, mivacurium, atracurium, d-tubocurarine, and metocurarine

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17
Q

Which NMB’s produce bradycardia and why? (1)

A

succinylcholine mimics the action of acetylcholine and directly stimulates muscarinic receptors of the sinoatrial node

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18
Q

Which NMB’s produce tachycardia and why? (5)

A
  • atracurium, d-tubocurarine, metocurine produce reflex tachycardia
  • pancuronium and gallamine competitively antagonize acetylcholine, which are referred to as direct vagolytic, or more specifically antimuscarinic, actions
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19
Q

Which NMB’s produce significant hypotension? (3)

A

succinylcholine, d-tubocurarine, metocurarine

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20
Q

Which NMB’s produce significant hypertension? (2)

A

pancuronium and gallamine

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21
Q

The acronym “M-SAC” is my way to remember NMB’s that are primarily eliminated by METABOLISM. What does it stand for?

A 
M- mivacurium
S- succinylcholine
** BOTH of the above are by plasma cholinesterase
A- atracurium
2/3 hydrolysis, 1/3 Hoffman
C- cisatricurium
ALL by Hoffman
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22
Q

I am a long acting non-selective alpha adrenergic antagonist used to control blood pressure in patients with pheochromocytoma.

A

phenoxybenzamine

* another non-selective alpha adrenergic antagonist is phentolamine

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23
Q

I am a selective alpha 2 adrenergic antagonist used to treat impotence.

A

yohimbine

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24
Q

How is prazosin different from other alpha adrenergic antagonists?

A

unlike non-selective alpha blockers, prazosin (a selective alpha 1 adrenergic antagonist) lowers BP without increasing release of NE from postganglionic sympathetic nerve terminals b/c it doesn’t block alpha 2

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25
Q

Name one of the primary non-selective beta antagonists, and why it isn’t usually used for with irritable airways.

A

propanolol–> beta 2 adrenergic receptor blockade can induce bronchoconstriction

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26
Q

I am a competitive antagonist of beta 1 adrenergic receptors. I am also very short acting and am metabolized in the _______ by __________ of the red blood cell.

A

Esmolol. in the plasma by non-selective esterases of the red blood cells

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27
Q

What are some uses of esmolol?

A

1) treat intraop SVT
2) treat intraop HTN
3) blunt reflex cardiovascular responses to DL and produce controlled hypotension

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28
Q

What receptors does labetalol competitively antagonize?

A

alpha 1, beta 1, beta 2

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29
Q

Name 2 uses of labetalol?

A

1) treat HTN emergencies
2) produce controlled hypotension
* decreases HR, myocardial contractility, and SVR

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30
Q

What is the alpha to beta ratio of the block produced by labetalol?

A

7:1 beta to alpha (so stronger beta than alpha)

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31
Q

What drugs can be used to treat excess myocardial depression induced by beta antagonists?

A

1) Atropine (incremental doses of 7mcg/kg)
2) Dobutamine (selective beta 1)
3) Calcium Chloride (250 to 1000mg IV)
4) Glucagon (1-10 mg IV, followed by 5 mg/hr IV)
5) transvenous artificial cardiac pacer
* Isoproterenol not good d\t its beta 1 and beta 2 effects, could cause vasodilation
* Dopamine NOT recommended

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32
Q

Why is Ketamine not normally recommended for use with beta blockers?

A

b\c it promotes SNS stimulation and with beta blockade it promotes increased SVR–> not able to be compensated by increased myocardial contractility (b\c the heart is beta blocked)–> heart failure may ensue
*same thing can happen with pheochromocytoma if beta blockade is produced prior to alpha blockade

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33
Q

What alpha adrenergic blocker could you use to control HTN during a pheo case?

A

phentolamine (regitine)

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34
Q

What drugs should you avoid in the asthmatic patient?

A

1) beta 2 blockers like propanolol and labetalol

2) drugs that stimulate histamine release (trimethaphan, d-tubocurarine, atracurium, and mivacurium)

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35
Q

Order MOST to LEAST on sedation: atropine, scopolamine, robinul.

A

scopolamine, atropine, glyco

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36
Q

Order MOST to LEAST on antisialogogue: atropine, scopolamine, robinul.

A

scopolamine, glyco, atropine

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37
Q

Order MOST to LEAST on increased HR: atropine, scopolamine, robinul.

A

atropine, glyco, scop

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38
Q

Order MOST to LEAST on relax smooth muscle: atropine, scopolamine, robinul.

A

atropine and glyco, scop

39
Q

Order MOST to LEAST on mydriasis: atropine, scopolamine, robinul.

A

scop, atropine, glyco

40
Q

Order MOST to LEAST on motion sickness prevention: atropine, scopolamine, robinul.

A

scopolamine, atropine, glyco

41
Q

What antimuscarinic LEAST crosses the BBB?

A

glyco, b\c it has a charged quaternary ammonium group (ions DO NOT like to cross lipid membranes)

42
Q

What is the treatment for anticholinergic syndrome?

A

physostigmine (an acetylcholinesterase inhibitor) 15-60mcg/kg IV

43
Q

T/F? Decreased tone of the lower esophageal sphincter is a disadvantageous feature of antimuscarinics.

A

TRUE

44
Q

What is the action of milrinone?

A

well… cAMP is normally cleaned up by phosphodiesterase…… so, milrinone is a PDA blocker–> causing a buildup of cAMP

45
Q

When administering terbutaline… what receptor does it agonize? Is it metabotropic or ionotropic? Why?

A

works on beta 2–> terbutaline is a 1st messenger (Gs protein)–> the substrate ATP combines with enzyme adenylyl cyclase to activate 2nd messenger cAMP (the product)–> activates protein kinase–> bronchodilation

46
Q

When looking at bronchiole smooth muscle, the presence of Ca+ indicates _______.

A

constricition…. absence of Ca+ = dilation

47
Q

How does nitric oxide (NO) work?

A

it is a 1st messenger that crosses the lipid membrane (lipid soluble, so no receptor needed)–> acts with GTP–> cGMP (2nd messenger inside the cell)–> bronchodilation

48
Q

What is the 2nd messenger of terbutaline in bronchiole smooth muscle?

A

cAMP

49
Q

What is the 2nd messenger of nitric oxide in bronchiole smooth muscle?

A

cGMP

50
Q

What is the 2nd messenger of atropine and ipratroprium in bronchiole smooth muscle?

A

IP3 and Ca+; AcH binds to muscarinic receptor–> phospholipase C cuts the head off… that is IP3–> IP3 helps release Ca+–> both are second messengers–> bronchoconstriction

51
Q

cAMP and cGMP are “cleaned up” by _________.

A

phosphodiesterase; but different kind called isoform

52
Q

Name the phosphodiesterase isoform for: cAMP

A

PDE III

53
Q

Name the phosphodiesterase isoform for: cGMP

A

PDE V

54
Q

What is aminophylline?

A

a phosphodiesterase inhibitor–> so causes buildup of cAMP–> promote bronchodilation as cAMP accumulates

55
Q

How does nitroglycerin and nitroprusside (nitric oxide donors) promote bronchodilation?

A

by increasing the concentration of cGMP

56
Q

How do atropine and ipratropium (atrovent– an inhaled antimuscarinic) promote bronchodilation?

A

competitively inhibit muscarinic 3 receptors

57
Q

What 4 second messengers are at work in bronchial smooth muscle cells?

A

1) cAMP
2) cGMP
3) IP3
4) Ca+

58
Q

In bronchial smooth muscle, which first messenger does NOT bing to a cell membrane receptor?

A

nitric oxide (NO)

59
Q

Name two common xanthines.

A

aminophylline and theophylline–> competitively antagonize adenosine receptors
CNS: nervousness, anxiety, n/v
RESP: bronchodilation

60
Q

Does aminophylline readily cross the placenta?

A

YES

61
Q

How do antimuscarinics cause bronchodilation?

A

atropine & ipratropium (atrovent); they antagonize AcH–> cause bronchodilation because less inositol triphosphate IP3 is produced, so less calcium is available for contractile proteins

62
Q

What second messenger promotes bronchoconstriction?

A

Ca+ and IP3

63
Q

Anti HTN: Name the trade name and action: hydralazine

A

Apresoline–> arterial vasodilator

64
Q

Anti HTN: Name the trade name and action: diazoxide

A

Hyperstat–> arterial dilator (can cause hypoglycemic coma)

65
Q

Anti HTN: Name the trade name and action: nitroglycerin

A

venodilator

66
Q

Anti HTN: Name the trade name and action: nitroprusside

A

Nipride–> arterial and venous dilator

67
Q

CCB: Name the trade name and action: verapamil

A

Calan, Isoptin–> arterial dilator and decreased HR

68
Q

CCB: Name the trade name and action: diltiazem

A

arterial dilator and decreased HR

69
Q

CCB: Name the trade name and action: nifedipine

A

Procardia–> arterial dilator (causes reflex increase in HR)

70
Q

ACE INH: Name the trade name and action: captopril

A

Capoten–> arterial dilator

71
Q

ACE INH: Name the trade name and action: enalapril

A

Vasotec–> arterial dilator

72
Q

PDE INH: Name the trade name and action: inamrinone

A

Inocor–> block breakdown of cAMP= inc. myocardial contractility= dec. SVR (relaxes vascular smooth muscle)

73
Q

PDE INH: Name the trade name and action: milrinone

A

Primacor–> block breakdown of cAMP= inc. myocardial contractility= dec. SVR (relaxes vascular smooth muscle)

74
Q

What is the action of Adenosine?

A

it is an endogenous nucleotide occurring in all cells of the body…. can be administered to:

1) slow conduction of impulses through the AV node
2) interrupt reentry pathways through AV node
3) restore NSR in pt’s with paroxysmal SVT, including the associated WPW syndrome

75
Q

What is the dose of Adenosine?

A

6-12 mg IV as rapid injection

76
Q

What is the elimination half time of Adenosine?

A

< 10 seconds owing to rapid metabolism

77
Q

“Fast, Full, and Forward” applies to ______.

A

regurgitation; you want a faster HR so you spend LESS time in systole

78
Q

What is the mneumonic to remember what will increase or decrease an outflow obstruction?

A

Old Cats Pee Alot
Obstruction: up down (increased or decreased)
——————————————-
Contractility: up down
Preload: down up
Afterload: down up

79
Q

Is ephedrine good to give a patient with a valve obstruction?

A

No! increases HR (you want to maintain)

80
Q

Is digitalis good to give a patient with a valve obstruction?

A

No! increases contractility and worsens obstruction

81
Q

Is increasing PEEP good for a patient with a valve obstruction?

A

No! decreases venous return= Not good, worsens obstruction

82
Q

Aortic regurgitation can either be congenital or from ______.

A

rheumatic fever–> causes valvular problems

83
Q

Aortic annulus dilation can cause regurgitation. What are causes of aortic annulus dilation?

A

syphilis, rheumatoid and psoriatic arthritis, ankylosing spondylitis, cystic medial necrosis, annuloaortic ectasia

84
Q

What happens when there is aortic regurgitation and eccentric LV hypertrophy?

A

ventricles experience a large increase in volume with a small increase in pressure… left ventricular compliance is large–> fluid backs up into LV and starts to dilate it

85
Q

Where is the coronary “take-off” located?

A

right after the aortic arch

86
Q

Patients with acute aortic regurgitation present with the sudden onset of _______ and _______.

A 
pulmonary edema and HTN
typically the 3 things seen are:
1) severe dyspnea
2) hypotension
3) weakness
87
Q

Chronic aortic regurgitation normally presents as _______. Symptoms are minimal when the regurgitant volume are < _____, and severe if > ______ of SV.

A

CHF; 60%
Can remembers rule of 1/2’s:
1/2 SV= severe

88
Q

Chronic aortic regurgitation can be heard as a ______ murmur, best heard at the _______.

A

diastolic murmur, best heard at the left sternal border (b\c blood is flowing anterograde
* other manifestations: widened pulse pressure, bounding peripheral pulses, mitral regurg

89
Q

Arterial waveform of a pt with IHSS may be ____.

A

bifid…. bisferiens pulse

90
Q

What is the pressor of choice with aortic and mitral regurgitation?

A

Ephedrine… keep it fast full and forward.. phenylephrine would increase the afterload

91
Q

Chronic mitral regurgitation is usually d\t _______. (3)

A

rheumatic fever, incompetent valve, or destruction of mitral valve annulus

92
Q

What is the rule to remember when comparing the symptomatic progression of mitral regurgitation?

A

rule of 1/3rds

60= severe

93
Q

Chronic mitral regurgitation is heard as a ________ murmur, best heard at the _____.

A

holosystolic murmur best heard at the apex

Board Review CRNA (Sweat Book) (38 decks)

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