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3rd Quarter > Pharm2Final > Flashcards

Pharm2Final Flashcards

1
Q

What are the three naturally occurring catecholamines?

A
  1. epinephrine
  2. norepinephrine
  3. dopamine
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2
Q

What are the two synthetic catecholamines?

A
  1. isoproterenol

2. dobutamine

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3
Q

What are the six steps of cholinergic transmission?

A
  1. synthesis
  2. storage
  3. release via Ca++ mediated exocytosis
  4. binding
  5. degradation
  6. recycling
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4
Q

Sympathomimetic drugs have their effect on adrenergic receptors located in the _____ and _____.

A

CNS and the ANS

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5
Q

What is the nuerotransmitter for pre-ganglionic adrenergic neurons in the SNS?

A

Ach

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6
Q

What are the required neurotransmitters for sympathomimetic receptor types alpha and beta?

A

epi or norepi

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7
Q

What is the effects of alpha 1 stimulation and where are the receptors found at?

A

POST SYNAPTIC

vasoconstriction, mydriasis, relaxation of GI, contraction of GI sphincters, contraction of bladder sphincters

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8
Q

What is the effects of alpha2 stimulating and where are the receptors found?

A

PRESYNAPTIC-inhibition of NE

POSTSYNAPTIC-platelet aggregation, hyper polarization of cells in the CNS, sedation

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9
Q

Adrenergic receptors specifically bind to what two neurotransmitters?

A

epi and NE and they are activated by them

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10
Q

What is the selected agonist action of Beta 1?

A

increased myocardial contractility

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11
Q

What are 4 agents with beta 1 properties?

A
  1. isoproterenol
  2. dobutamine
  3. epi
  4. NE
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12
Q

What are 2 beta 1 antagonist?

A
  1. metoprolol

2. atenolol

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13
Q

What is the selected Beta 3 agonist action?

A

lipolysis—>”burn fat”

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14
Q

How is the action of catecholamines terminated?

A

by repute into the postganglionic sympathetic nerve endings

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15
Q

Sympathomimetics mimic actions of…..?

A

endogenous neurotransmitters, epi, NE and dopamine

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16
Q

Direct acting sympathomimetic agonist act on what receptors?

A

post-synaptic

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17
Q

Synthetic non-catecholamines activate adrenergic receptor how?

A

by evoking release of NE from POST GANGLIONIC sympathetic nerve endings

elicit mostly a and b-1 as NE is a weak b-2 agonist

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18
Q

Indirect acting sympathomimetics require _____ _____ to produce effect.

A

endogenous catecholamines; little activity if catecholamines are depleted

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19
Q

Do direct acting sympathomimetics require endogenous catecholamines to produce effect?

A

no; they activate even if catecholamines are depleted

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20
Q

Where is the location of the adrenergic receptors that direct acting sympathomimetics act upon?

A

post-synaptically on adrenergic receptors

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21
Q

Direct acting sympathomimetics include catecholamines and synthetic non-catecholamines(T/F)?

A

true

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22
Q

What are three uses of alpha 1 agonist?

A
  1. hypotension-to increase BP during anesthesia
  2. ophthalmic preparations-to induce mydrasis
  3. cough and cold preparations-induces constriction of nasal mucosa, decreases resistance to air flow
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23
Q

T/F-Direct acting alph agents-synthetic agents that directly activate alpha-1 adrenergic receptors?

A

true

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24
Q

What is the dose of Precedex?

A

1 mcg/kg bolus for 10 minutes

0.2 - 1 mcg/kg/hour maintenance

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25
Q

What are four examples of direct acting beta-1 agonist?

A
  1. dopamine
  2. dobutamine
  3. epinephrine
  4. isoproterenol
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26
Q

Stimulation of beta-1 receptors induces positive(3) effects?

A
  1. chronotropic
    2, dromotropic
  2. inotropic
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27
Q

How is epinephrine synthesized?

A

tryosine—>DOPA—>dopamine—>NE—>epi

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28
Q

How is epi released?

A
  • SNS acting vai splanchnic nerves to the adrenal medulla stimulate the release of epi
  • calcium triggers exocytosis of chromatin granules and realize of epi and NI into the bloodstream
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29
Q

Do indirect sympathomimetics act upon beta-2?

A

nope

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30
Q

What is THE adrenergic neurotransmitter?

A

norepinephrine

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31
Q

Where is NE released from?

A

released from presynaptic vesicles of postganglionic sympathetic nerve endings

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32
Q

What is the effects of NE release?

A
  • equal to epi at beta-1 with very little beta-2 action
  • potent alpha-1 producing intense vasoconstriction in arterial and venous vascular beds
  • causes >SBP, >DBP, >MAP
  • has no bronchodilating effects
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33
Q

By what action does NE increase BP?

A

primarily by increasing the SVR

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34
Q

What can be a reflex triggered by NE induced increase in SVR?

A

reflex bradycardia

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35
Q

What types of receptors does NE bind to causing stimulation of alpha and beta?

A

adrenergic receptors

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36
Q

What structure is the origin of most NE pathways in the brain?

A

Locus ceruleus

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37
Q

Is norepi released from pre-ganglionic SNS neurons or post-ganglionic?

A

post-ganglionic

Ach is released pre-ganglionic

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38
Q

What is the steroisomer of NE?

A

Levophed

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39
Q

How is NE synthesized?

A

synthesized in te adrenal medulla from the amino acid tyrosine

tyrosine—>L-dopa—>dopamine—>NE

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40
Q

How is the action of NE terminated?

A

either by degradation of NE or by NE UPTAKE BY SURROUNDING CELLS

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41
Q

After being released into the synaptic cleft, NE acts upon what type of receptors?

A

adrenergic

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42
Q

What is two ways uptake is done with NE?

A
  1. pre-synaptically

2. by non-neuronal cells in the vicinity

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43
Q

What is NE mechanism of action?

A

acts on target cells by binding to and activating adrenergic receptors.

unlike ep, NE does not activate beta-2 receptors—>just alpha-1, alpha-2 and beta-1

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44
Q

T or F: NE has different actions based on different cell types?

A

true

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45
Q

What types of patients is NE useful with?

A

NI is used to treat patients in vasodilatory shock states such as septic shock and neurogenic shock

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46
Q

Dopamine is a CNS neurotransmitter that is a _____ derivative.

A

phenethylamine

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47
Q

There are five types of dopamine receptors, how many of them have clinical significance?

A

only 2, D1,D2

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48
Q

Does dopamine have direct or indirect adrenergic action?

A

both

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49
Q

At what part of the NMJ does dopamine1 act and what is the affect?

A

POST-SYNAPTIC: vasodilation of renal, mesenteric, coronary and cerebral blood vessels

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50
Q

At what part of the NMJ does dopamine2 act and what is the affect?

A

PRE-SYNAPTIC: inhibits the release of NE

POST-SYNAPTIC: weak vasoconstricton

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51
Q

Dopamine actions include?

A

> CO
HR
SBP

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52
Q

Can dopamine cross the BBB?

A

nope

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53
Q

To increase dopamine in brains of patients with diseases such as Parkinson’s and dopa-responsive dystonia, _____ can be given because it crosses the BBB.

A

L-DOPA(levo-dopa)

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54
Q

Describe dopamine synthesis

A

synthesized by adrenal medulla —>tyrosine—>L-DOPA—>dopamine

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55
Q

How is dopamine stored and released?

A

In neurons, dopamine is packaged after synthesis into vesicles, released into synapses in response to pre-synaptic action potentials

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56
Q

How is dopamine inactivated?

A

by repute via dopamine transporter DAT

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57
Q

How is dopamine broken down?

A

by catechol-o-methyl transferase(COMT) and monoamine oxidase(MAO)

dopamine not broken down is repackaged into vesicles for reuse

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58
Q

Dopamine dosing?

A

-2-5 mcg/kg/min:
binds D1 receptors, dilating blood vessels, increasing blood flow to renal, mesenteric, coronary and cerebral arteries
-5-10 mcg/kg/min:
postitive inotropic and chronotropic effects via increased beta-1 receptor activation. Used in patients with shock or heart failure to increase CO and BP.
-10-20 mcg/kg/min:
dopamine causes vasoconstriction, increases SVR and increases BP through alpha-1 receptor activation.

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59
Q

By what effect does “renal dose” dopamine prob work?

A

by increasing the CO

McCarver not a believer in renal dose dopamine

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60
Q

What is the most potent activator of beta adrenergic receptors?

A

Isoproterenol

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61
Q

Does Isoproterenol directly affect the BP?

A

NO-has no alpha affect!

increased SBP is indirectly from greater CO, will see lower MAP and decreased DBP due to reduced SVR

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62
Q

What is Isoproterenol used for?

A
  • greater HR
  • increased myocardial contractility
  • cardiac automaticity
  • bronchodilation
  • reduction in PVR

use with post heart transplant patients due to deinnervation of the orthotropic heart transplant

mostly seen in heart blocks now

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63
Q

What particular caution should be observed when using Isoproterenol?

A

caution with low DBP and reduced coronary perfusion since increased HR causes increased myocardial oxygen consumption

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64
Q

What is the primary use of Isoproterenol?

A

bradycardia and heart blocks

  • resistant bradyarrhythmias when pacing is not available
  • pharmacologic pacing for torsade de pointes(polymorphic ventricular tach)

can also be used as a bronchodilator(very rare)

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65
Q

Isoproterenol caused what three effects?

A
  1. chrontropic
  2. dromotropic
  3. inotropic
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66
Q

What are some contraindication for use of Isoproterenol?

A

angina, pre-existing arrhythmias, tachycardia or AV block caused by cardiac glycoside intoxication. Ventricular arrhythmias due to AV nodal block

*significantly increased myocardial oxygen demand—>can cause vasodilation(beta-2 effect)

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67
Q

What is the dose for Isoproterenol?

A

usual effective dose 0.-2 mcg/kg/min

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68
Q

What type of catecholamine is Dobutamine?

A

synthetic

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69
Q

What is Dobutamine used to treat?

A

Sympathomimetic used to treat CHG and cariogenic shock.

-Used to treat acute and chronic heart failure as with heart surgery, sepsis and cardiogenic shock

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70
Q

What is the primary action of Dobutamine?

A

direct stimulation of beta-1 receptors

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71
Q

In what specific scenario is dobutamine not useful and why?

A

not useful in ischemic heart disease because it may increase HR, potentially increasing myocardial oxygen demand

also: +dromotrope so be careful with atrial fibrillation as HR may markedly increase—>so prob is contraindicated in patients with A-fib

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72
Q

Dobutamine best used in combo with other drugs like _____ in the presence of _____.

A

vasodilators; increased afterload

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73
Q

What are the results of using dobutamine?

A

increased CO
decreased atrial filling pressure
increased HR
increased SBP

allegedly a coronary artery vasodilator with no endogenous catecholamine release like dopamine

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74
Q

Describe the racemic mixture of dobutamine.

A

Dobutamine is given as a racemic mixture for both + and - isomers.

-The + isomer is a potent beta-1 agonist
-the - isomer is an alpha-1 agonist
Dobutamine also has mild beta-2 agonist activity

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75
Q

What are the specifics on Dobutamine dosing?

A
  • Infusion should be started at low rates, 0.5-1.0 mcg/kg/min and titrated by patients response including SBP, HR and invasive monitoring
  • Optimal infusion rates typically 2-10 mcg/kg/min
  • use the lowest rate you can get away with*
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76
Q

What are some results are usually seen with dobutamine?

A
  • a 10-20 mm increase in SBP and increase in HR of 5-15 beats/min
  • 5% of patients experience PVC’s-dose related
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77
Q

What is the drug classification of phenylephrine?

A

Synthetic non-catecholamine

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78
Q

What is the principal effect of phenylephrine?

A
  • direct alpha-1 effect with only a small part via indirect release of NE
  • minimal if any beta effect

venoconstriction > arterial constriction

mimics NE but is less potent and longer lasting

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79
Q

What cardohemodynamic effects are seen with the use of phenylephrine?

A
  • increases SBP
  • decreases CO
  • lowers HR(reflex)
  • raises PAP
  • reduced CO most likely from baroreceptor-mediated reflex bradycardia rather than increases in after load*
  • may impair LV global function when given rapidly to anesthetized patients(1mcg/kg)*
  • can be used to treat SVT(500 mcg bolus)
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80
Q

Describe phenylephrine dosing

A
  • IV infusion(usual initial rate): 100-180 mcg/min
  • Usual maintenance rate: 20-60 mcg/min
  • Max rate: infusion rates as high as 10 mcg/kg,min may be required in shock
  • Adult IV bolus therapy: usual dose is 100 mcg and repeat as needed
  • SVT(PSVT): 0.5 mg(500 mcg) rapid IV push, subsequent doses may be increased in increments of 0.1-0.2 mg

wean as soon as possible as will hurt end organ perfusion

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81
Q

What is the novelty of Precedex?

A

unusual in its ability to provide sedation without causing respiratory depression

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82
Q

What type of agonist is Precedex?

A

like clonidine it is an alpha-2 adrenergic agonist

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83
Q

By what mechanism does Precedex decrease BP?

A

decreases sympathetic tone, with attenuation of neuroendocrine and hemodynamic responses to surgery

reduces anesthetic and opioid requirements

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84
Q

What type of compound is Precedex?

A

imidazole compound

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85
Q

What type of pharmacological active isomer is Precedex?

A

pharmacologically active dextroisomer of medetomidine

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86
Q

The pharmacological isomer of Precedex causes?(4)

A
  • hypotension
  • bradycardia
  • sedation
  • analgesia
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87
Q

Other responses to the activation of alpha-2 receptors by Precedex include….

A
  • decreased salivation, decreased secretion and decreased bowel motility
  • contraction of vascular and other smooth muscle
  • inhibition of renin release
  • increased glomerular filtration and increased secretion of sodium and water in the kidney
  • decreased intraocular pressure
  • decreased insulin release from the pancreas
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88
Q

What are the indications for Precedex?

A
  • indicated for sedation of critically ill and nonintubayted patients requiring sedation for surgery or procedures short-term.
  • useful as an adjunct for sedation and general anesthesia
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89
Q

What are the contraindications of the use of Dexmedetomidine?

A
  • no absolute contraindications
  • Very expensive
  • caution with boluses due to peripheral alpha-2 receptor stimulation with resulting hypertension and bradycardia(may see hypotension with loss of sympathetic tone)
  • high cost relative to generic medications

Individual variablity in HR and BP effects, as well as the sedative effects of the drug

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90
Q

Describe the drug Methoxamine, its classification, what receptors it stimulations and why its used

A
  • direct acting synthetic non-catecholalmine
  • alpha agonist
  • used in cath lab and tx for SVT
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91
Q

Describe the drug Clonidine, its classification, what receptors it stimulations and why its used

A
  • direct acting
  • selective alpha-2 agonist
  • used for the treatment of HTN and opioid withdrawal
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92
Q

Describe the drug Terbutaline, its classification, what receptors it stimulations and why its used

A
  • direct acting
  • beta-2 agonist
  • treatment of asthma and to slow uterine contractions
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93
Q

Describe the drug Albuterol, its classification, what receptors it stimulations and why its used

A
  • direct acting
  • beta-2 agonist
  • acute bronchospasm
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94
Q

Describe the indirect adrenergic agonist Amphetamines

A
  • resemble ephedrine in their alpha and beta receptor stimulation, however differ in their intense CNS activity
  • reflects the release of NI stores in the CNS
  • clinical uses include ADD, anoretics, troops in combat
  • Tyramine found in fermented foods(cheese) metabolized by MAO and may cause hypertensive crisis in patients with MaOI
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95
Q

Is Ephedrine a direct acting synthetic non-catecholamine, or an indirect acting synthetic non-catecholamine and why?

A

Ephedrine is a mixed acting synthetic non-catecholamine.

  • endogenous release of NE(indirect)
  • Direct stimulation of adrenergic receptors

**stimulates alpha and beta receptors

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96
Q

What are the two affects responsible for prolonged duration of Ephedrine?

A
  1. slow inactivation

2. slow excretion

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97
Q

Where on the NMJ is Ephedrine active?

A

presynaptically causing the release of NE—>primary beta effects

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98
Q

What are two things that Ephedrine may cause besides the intended affects?

A
  1. mydriasis

2. CNS stimulation

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99
Q

Can Ephedrine be given IM?

A

yes

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100
Q

Does Ephedrine have good absorption from the stomach?

A

yes

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101
Q

The ____ of Ephedrine will be the best due to ______.

A

first, endogenous catecholamine depletion

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102
Q

What hemodynamic affects will be seen with Ephedrine administration?

A
  • CV effects are similar to Epi except milder
  • SBP increased are less intense but last 10 times longer, takes 250X an ephedrine dose to equal an epi dose
  • increased SBP, DBP, HR & CO
  • Renal and splanchnic blood flows are decreased(due to alpha effect), coronary and skeletal muscle blood flows are increased
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103
Q

What is the principle mechanism for the CV effects of Ephedrine?

A
  • principle mechanism of CV effects is increased myocardial contractility due to activation of beta-1 receptors
  • in the presence of beta blockage, predominant CV effect may be a receptor stimulation
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104
Q

In the beta blocked patient what effect will you primarily see when administering Ephedrine?

A

alpha cause they are beta blocked

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105
Q

Is Vasopressin an adrenergic agent? Does it bind to alpha or beta receptors?

A

No it is a:

  • peptide hormone derived from pre-prohormones synthesized in the hypothalamus
  • stored in the posterior pituitary for the release into the bloodstream or directly into the brain
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106
Q

What is the dose of Vasopressin and why give it?

A
  • given as single IV dose of 40 units
  • Given as an alternative to epi for treatment of shock-resistant v-fib or pulseless v-tach

used to increase SVR

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107
Q

What are the three arginine Vasopressin receptor types?

A
  1. AVPR1A-vasoconstriction, gluconeogenesis, platelet aggregation, coagulation
  2. AVPR1B-ACTH secretion in response to stress
  3. AVPR2-anti diuretic effect
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108
Q

Where are Vasopressin receptors present in the body?

A

brain, liver, kidney and vascular

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109
Q

What effect does Vasopressin have on the body?

A
  • Vasopressin is released when the body is dehydrated, causing kidneys to conserve water by decreasing UOP
  • In higher {}, vasopressin raises BP by increasing SVR
  • Vasopressin increases permeability to water of distal convoluted tubules and collecting tubules in nephrons allowing water reabsorption and excretion of small volumes of more {} urine
  • ANTI-DIURETIC drug
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110
Q

What are the hemodynamic reasons to use Vasopressin?

A

for hemodynamic support in septic shock

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111
Q

What is the dose for vasopressin?

A
  • For shock, bolus of 0.5-20 units followed by an IV infusion rate of 0.01-0.4 units/minute
  • doses above 0.04 units/minute do not consistently improve hemodynamics and may contribute to adverse events
  • adding vasopressin to NE may allow reduction of NI doses
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112
Q

What is the blood-gas partition coefficient of Isoflurane?

A

1.46

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113
Q

What is the blood-gas partition coefficient of Nitrous Oxide?

A

0.46

114
Q

What is the blood-gas partition coefficient of Desflurane?

A

0.42

115
Q

What is the blood-gas partition coefficient of Sevoflurane?

A

0.69

116
Q

What is the MAC value of Isoflurane?

A

1.17%

117
Q

What is the MAC value of Desflurane?

A

6.6 %

118
Q

What is the MAC value of Sevoflurane?

A

1.8%

119
Q

What is the MAC value of Nitrous Oxide?

A

104%

120
Q

What is the action of anticholinergic drugs at the NMJ?

A

Anticholinergic drugs COMPETITIVELY ANTAGONIZE effects of acetylcholine at cholinergic POST-GANGLIONIC sites known as muscarinic receptors

121
Q

What three terms describe belladonna compounds?

A
  1. anticholinergic
  2. antimuscarinic
  3. parasympatholytic
122
Q

Where are muscarinic cholinergic receptors found and what is the MOA in each place?

A
  1. heart(increase HR)
  2. salivary glands(decrease secretion)
  3. GI/GU smooth muscle(decrease)
123
Q

What is acetylcholine?

A

neurotransmitter at post-ganglionic nicotinic receptors of the NM junction and the autonomic ganglia

124
Q

Anticholinergics in usual doses have no effect on post-ganglionic NICOTINIC receptors(t/f)

A

true

125
Q

Anticholinergics are specific to which receptors?

A

muscarinic

126
Q

Describe the classification of atropine and scopolamine.

A

naturally occurring tertiary amine anticholinergic drugs

they will cross BBB

127
Q

What is the classification of glycopyrrolate.

A

semi-snthetic quaternary ammonium compound

*will NOT CROSS BBB

128
Q

Natural occurring anticholinergics are _____ _____, Synthetic anticholinergics are _____ _____ _____.

A

tertiary amines

quaternary ammonium compounds

129
Q

If an anticholinergic is described as alkaloid what does that mean?

A

it is a tertiary amine…it has CNS effects meaning it can cross the BBB….contains tropic acid and it is a racemic mixture

**atropine/scopolamine

130
Q

If an anticholinergic is not an alkaloid what does that mean?

A

it is a quaternary ammonium compound…has no CNS effects…will not cross the BBB…contains mandolin acid and is not a racemic mixture

glycopyrrolate

131
Q

What is the name of the racemic mixtures of atropine and scopolamine? Of the two racemic mixtures which exerts anticholinergic effects?

A
  1. dextro
  2. levorotary

Levorotary form exerts anticholinergic effects

132
Q

What type of acid dos glycopyrrolate contain?

A

madelic acid

133
Q

What type of acid does atropine and scopolamine contain?

A

tropic acid

134
Q

What is the mechanism of action of anticholinergics?

A
  • Anticholinergics combine reversibly with muscarinic cholinergic receptors and prevent acetylcholine from binding
  • Anticholinergic drugs bind to muscarinic receptors without eliciting a muscarinic response
135
Q

How many types of muscarine cholinergic receptors are there…what are their names?

A

There are 5 muscarinic cholinergic receptors

m1,m2,m3,m4,m5

136
Q

What is the function of the M1 muscarinic cholinergic receptor?

A

CNS, stomach, inhibits NE release

137
Q

What is the function of the M2 muscarinic cholinergic receptor?

A

SA, AV nods, Purkinje fibers, reduces myocardial oxygen demands and relaxes bronchial smooth muscles

138
Q

What is the function of the M3 muscarinic cholinergic receptor?

A

CNS, bronchial smooth muscle, glands, vascular beds, iris, ciliary body, GI

anti-sialogoge and drying of bronchial secretions elicited with lower doses of anticholinergic than M2 receptor effects of increased HR and CNS changes

for example—>0.1 - 0.2 mg glycopyrrolate before an awake intubation without significantly increasing HR

139
Q

What is the function of the M4 and M5 muscarinic cholinergic receptor?

A

CNS

140
Q

It takes a _____ dose to inhibit M1 receptor mediated H+ secretion in gastric secretions

A

huge

141
Q

In what type of patient should scopolamine by avoided in?

A

Mydriatic effects of scopolamine are greater than atropine-scopolamine avoided in glaucoma patients

Glycopyrrolate safest has least effect on pupil size

142
Q

Which of the anticholinergic agents has the greatest antisialagogue and ocular effects?

A

scopolamine

143
Q

What is the primary reason to give scopolamine to preop open heart patients?

A

decreased metabolic oxygen requirements…..atropine causes no change and glycopyrrolate increases oxygen demand.

144
Q

Which anticholinergic is most potent in decreasing reticular activity?

A

scopolamine is 100X more potent than atropine in decreasing reticular activity

145
Q

Does glycopyrrolate have any sedative effects?

A

no it does not cross the BBB

146
Q

What reverses restlessness/somnolence due to tertiary amine anticholinergic drugs?

A

Physostigmine

147
Q

Which anticholinergic is a good choice when sedation and potent antisialagogue actions is desired?

A

Scopolamine

Scopolamine>glycopyrrolate>atropine(antisialagogue action)

148
Q

By what action does atropine treat intraoperative bradycardia resulting form vagal activity?

A

Atropine 15-70 mcg/kg increased HR by blocking ACh effects on the SA node.

149
Q

Will anticholinergics alter HR in the de-innervated(transplanted) heart?

A

no

150
Q

Antagonism of non-depolarizer NMB with antichozlinesterases requires co-administration of atropine or glycopyrrolate to…….

A

counteract parasympathomimetic effects of antichlinesterase drugs

scopolamine not used to reverse**

151
Q

High doses of anticholinergics needed to decrease H+ secretions are associated with?

A

unpleasant to dangerous side effects

152
Q

What is the drug of choice for treatment of central cholinergic syndrome?

A

physostigmine

153
Q

What is the definition of postoperative residual NMB?

A
  • TOF ratio < 0.9 after reversal

- clinical weakness

154
Q

Smaller dose of neostigmine prudent if…..?

A

time since relaxant is less than hours

155
Q

Cholinesterase inhibitors Hydrolyze how many molecules of ACh per minute?

A

300,000

156
Q

What is the three mechanisms of actions of cholinesterase inhibitors?

A
  1. weak agonist action
  2. formation of desensitized receptor complex intermediates
  3. alteration of conductance properties of active channels
157
Q

Edrophonium, neostigmine and pyridostigmine are quaternary ammonium compounds which means?

A
  • they are poorly lipid soluble

- minimal penetration through lipid barriers(GI tract, placenta, BBB)

158
Q

If edrophonium, neostigmine or pyridostigmine administered how is the mechanism of action impacted?

A

inhibition achieved via different mechanisms

159
Q

Neostigmine and Pyridostigmine form ____ ____ at ___ sites of cholinesterase.

A

carbamyl-ester complexes at esteratic sites of cholinesterase

160
Q

Neostigmine and Pyridostigmine increase {} of _____ around _____.

A

endogenous ACh around cholinoreceptors

161
Q

What are two NMB reversal mechanisms?

A
  1. increasing ACh in junctional cleft changing agonist-antagonist ratio
  2. longer ACh life within cleft due to increased ACh
162
Q

Both Neostigmine and Pyridostigmine increase ACh inactivation by forming?

A

covalent bonds

163
Q

Of Neostigmine and Pyridostigmine which is most potent and which has the more rapid onset of action?

A

Neostigmine

164
Q

What describes the activity of the metabolites of Neostigmine?

A

metabolies 1/10 activity of neostigmine(very weak)

165
Q

What is the Vd of Neostigmine?

A

0.7 L/kg in healthy patient(poor lipid soluble), increases to 0.8 L/kg with renal failure

166
Q

Pyridostigmine is the cholinesterase inhibitor with the?

A

longest onset and duration

167
Q

What type of bond does Edrophonium form?

A
  • does not form covalent bonding

- binds reversibly with negatively charged enzyme sites by ELECTROSTATIC ATTRACTION of positively charged nitrogen

168
Q

What are some pharmacologic causes of prolonged paralysis?

A
  • Aminoglycoside toxicity
  • penicillin toxicity
  • steroid myopathy
  • antihypertensives(Ca+ channel blockers, B-blockers, Lasix)
  • antidysrhythmics(quinidine/procainamide/LA)
  • Aminoglycosides abx(Polymyxin B/Clindamycin/Tetracycline)
169
Q

What is the dose, speed of action, duration of action and most common SE of Neostigmine?

A

25-75 mcg/kg
5-15 minutes
45-90 minutes
+PONV

170
Q

What is the dose, speed of action, duration of action and most common SE of Pyridostigmine?

A

100-300 mcg/kg
10-20 minutes
60-120 minutes
slow onset, long duration

171
Q

What is the dose, speed of action, duration of action and most common SE of Edrophonium?

A

50-1000 mcg/kg
5-10 minutes
30-60 minutes
not for deep block, rapid

172
Q

The number of twitches (TOF count) correlates with degree of NMB. T4 disappears at ___ depression of T1.
T3 disappears at ___ depression of T1.
T2 disappears at ___ depression

A

75%
80-85%
90%

reversal of residual NMB safety achieved when TOF count is 3 or greater

173
Q

Traditionally, it had been accepted that a TOF ratio of _______ was an indication of adequate reversal. However it has been challenged recently and it is now thought that a TOF ratio of ___ should be achieved before extubation.

A
  1. 7 or greater

0. 9

174
Q

The use of tetanic stimulation is limited due to?

A

pain

175
Q

During partial depolarizing block, is fade observed with tetanic stimulation?

A

no

176
Q

What is the NMJ neurotransmitter?

A

Acetylcholine

177
Q

ACh is released in the synaptic cleft as packets or?

A

quanta

178
Q

How many molecules are in a quanta?

A

1000

179
Q

What are the 5 post junctional nicotinic cholinergic receptors?

A
  • alpha1
  • alpha2
  • beta
  • gamma
  • delta
180
Q

How many receptors are opened by the burst of ACh at the nmj?

A
  • at least 400K

- the current flows through open receptors, depolarizes end-plates, starts action potentials

181
Q

What is the basis for NM transmission?

A

the flow of ions

182
Q

NDNB show preference for?

A

1 of 2 alpha subunits

183
Q

What receptors of the nicotinic receptors are the sites of action for NMB agents in addition to binding ACh?

A

the 2 alpha units

184
Q

If 2 alpha subunits are occupied simultaneously, ion channel opens and?

A

fasciculations occur

185
Q

NDNB act on ?

A
  • NDNB act by combining with nicotinic cholinergic receptors without any activation of ion receptor channels
  • Act on POST-JUNCTIONAL alpha subunits
186
Q

Occupation of less than 70% of nicotinic cholinergic receptors……..?

A

no evidence of block by single twitch test

187
Q

Neurotransmission fails when _______% of alpha subunit post-junctional nicotinic cholinergic receptors are blocked.

A

80-90%

188
Q

Non-depolarizing NMB characteristics

A
  • decreased response to single twitch
  • fade during tetanus
  • TOF ratio < 0.7
  • post tetanic potentiation
  • potentiation of other NDNB
  • antagonism by anticholinesterase drugs
  • NO FASCICULATIONS
189
Q

There is no detectable block until _____% of receptors are occupied?

A

75 - 85 %

190
Q

Paralysis is complete at _____% receptor occupancy?

A

90 - 95%

191
Q

During non-depolarizing block response to single twitch stimulation is not reduced until at least ____% of receptors are occupied?

A

75 - 80%

192
Q

Single twitch does not detect block of < than ___, limiting clinical applicability of single twitch stimulation?

A

<70%

193
Q

With nerve stimulation monitoring, first twitch is accurate only if how many seconds have elapsed since previous stimulation?

A

10 seconds

194
Q

With nerve stimulation monitoring, disappearance of the fourth response after TOF stimulation corresponds to?

A

70 - 75% single twitch depression

195
Q

With the use of NDNB, post-tetanic facilitation can be repeated every?

A

10 - 12 seconds

196
Q

With tetanus fade is first noted at __% receptor occupancy?

A

70%

197
Q

How does Hemiplegia affect the use of NDNB?

A

resistance to non-depolarizers develops within 2-3 days, central inhibition

always monitor the unaffected side

198
Q

What kind of response do NDNB agents have on those suffering from Parkinsons or multiple sclerosis?

A

normal

199
Q

What affect does NDNB agents have on burn patients?

A

> than 30% body surface burns acquire NDNB resistance

  • begins 10 after injury
  • peaks @ 40 days
  • declines after 60 days
200
Q

What are the three metabolites of Vecuronium?

A
  1. 3-desacetyl vecuronium(1/2 as potent as vecuronium)
  2. 17-desacetyl vecuronium(1/10 as potent)
  3. 3,17-desacetyl vecuronium(1/10 as potent)
201
Q

Can vec be used in OB patients?

A

yes, insufficient vec {} cross placental barrier to produce significant effects on newborn

202
Q

Does vec alter intraocular pressures?

A

no

203
Q

Does vec trigger MH?

A

no

204
Q

Duration of action of vec may be _____ in patients over 130% of ideal weight?

A

130%

205
Q

What makes rocuronium special of the NDNB?

A

the only ND that serves as an alternative to succinylcholine for rapid sequence.

206
Q

Which nerve response should be monitored for best intubating conditions?

A

obicularis oculi

207
Q

Which nerve response should be monitored for the best return of breathing?

A

adducter pollicis

208
Q

What classification of ND is cisatracurium?

A

Benzylisoquinolinium

209
Q

What is responsible for principle degradation with cisatracurium?

A

Hoffman elimination

210
Q

With cisatracurium, NMB is easily maintained by

A

constant rate infusion without diminishing over time

211
Q

Hoffman eliminaton accounts for _____ of clearance, renal clearance accounts for ____?

A

77%, 16%

in ESRD, no alteration in neuromuscular blocking profile

212
Q

What is the mechanism of action of Succinylcholine?

A
  • attaches to alpha subunit of nicotinic cholinergic receptors
  • mimics action of acetylcholine
  • depolarizes the post-junctional membrane
213
Q

With Succinylcholine, sustained receptor ion channel opening and depolarization of post-junctional membranes caused K+ leakage from cell interiors…..how much increase in serum K+ is seen?

A

0.5 mEq/L

214
Q

Succinylcholine dosing: > than 2 mg/kg, repeated doses and succinylcholine infusions may cause?

A

Phase II block

215
Q

With Succinylcholine, what are four characteristics of a Phase I block?

A
  1. reduced response to single twitch
  2. reduced but sustained response to tetanus
  3. TOF ratio > than 0.7
  4. no post-tetanic facilitation
216
Q

When Succinylcholine is metabolized, what are its two metabolites?

A
  1. succinic acid

2. choline

217
Q

Succinylcholine is contraindicated in what four types of patients? Succinylcholine administration to such individuals may result in what?

A
  • major burns
  • multiple trauma
  • extensive denervation of skeletal muscle
  • upper motor neuron injury

SEVERE HYPERKALEMIA which may result in cardiac arrest

218
Q

Of the many possible adverse reactions to Succinylcholine, most will be minimized by pretreatment by a NDMB….which will not?

A

HYPERKALEMIA

219
Q

Although Succinylcholine has no direct effect on the myocardium, what does it stimulate which can lead to what?

A
  • Succinylcholine stimulates autonomic ganglia and muscarinic receptors which cause changes in cardiac rhythm including cardiac arrest.
  • Changes in rhythm may result from vagal stimulation or from hyperkalemia, particularly in children.
220
Q

When is Succinylcholine dysrhythmias most likely to occur?

A
  • most likely to occur when a second succinylcholine dose follows 5 minutes after the first dose
  • due to succinylcholine actions at cardiac muscarinic cholinergic receptors where succinylcholine mimics acetylcholine effects
  • atropine will not treat this bradycardia
  • pretreatment with a NDNB may prevent the occurrence of cardiac dysrhythmias
221
Q

If a healthy appearing kid develops cardiac arrest after succinylcholine not due to inadequate ventilation, oxygenation, or anesthesia OD, immediate treatment for hyperkalemia should be instituted. What are the 4 steps to immediately take?

A
  1. IV calcium
  2. bicarbonate
  3. glucose with insulin
  4. hyperventilation
222
Q

Tetanic response is fully sustained with the TOF ratio was_____. When the ratio is _____, variable degrees of fade of tetanus were evident.

A

above 0.7, less then 0.7

223
Q

Describe the significance of having no twitches on TOF.

A

100% blocked, suitable for intubation

224
Q

Describe the significance of having 1 twitch with TOF

A

90% blocked, mechanical ventilation

225
Q

Describe the significance of having 2 twitches with TOF

A

80-90% blocked, short term relaxation

226
Q

Describe the significance of having 3 twitches with TOF

A

75-80% blocked, maintenance doses needed

227
Q

Describe the significance of having 4 twitches with TOF

A

0-75% blocked, rapid cholinesterase inhibitors reversal

228
Q

A TOF ratio of ____ or _____ reliably indicates the recovery of thesinale twitch to control height and a sustained response to tetanic stimulation

A
  1. 7 or higher
    * reliance on the recovery of thesinale twitch to control height as a criterion of spontaneous return to normal clinical neuromuscular function may be misleading*
229
Q

What are the characteristics of a phase II block(5)?

A
  • decreased single twitch response
  • fade on tetanus
  • TOF ratio < 0.7
  • post-tetanic facilitation
  • fade on TOF
230
Q

What is the initial sign of phase II block?

A

tachyphylaxis

231
Q

With plasma cholinesterase, a Dibucaine # of 80 means what?

A

80% inhibition of plasma cholinesterase activity—>NORMAL

232
Q

With plasma cholinesterase, a Dibucaine # of 20 means what?

A

20% inhibition of plasma cholinesterase activity-found 1 out of 3200 patients—>means they are homozygous for an atypical plasma cholinesterase variant.
in these patients, succinylcholine last up to 3 hours in normal doses

233
Q

With plasma cholinesterase, a Dibucaine # of 40-60 means what?

A

40-60% inhibition of plasma cholinesterase activity-found in 1 of 480 patients—>means they are heterozygous for atypical plasma cholinesterase.
These patients may have prolonged succinylcholine blocks lasting up to 30 minutes.

234
Q

The dubucaine # is an indicator of _____ of plasma cholinesterase, not _____.

A

quality not quantity

235
Q

What is the pharmacologic effects of a neuromuscular blocking agent?

A

-interrupts nerve impulse transmission at the neuromuscular junction.

236
Q

What are two classifications of NMB?

A
  • depolarizers

- non depolarizers

237
Q

What are the two classifications of non-depolarizering NMB and what drugs belong to each class?

A
  • benzylisoquinolinium(nimbex/atracurium(nimbex’s daddy)

- aminosteroid compounds(pancuronium/rocuronium/vecuronium)

238
Q

How is the equal potency between NMB drugs measured ?

A

by dose required to suppress 95% of single twitch responses

239
Q

What are the principle sites we measure NMB and what types of twitch at each site?

A
  • adductor pollicis(slow twitch)

- obicularis oculi(fast twitch)

240
Q

Where is NMB affect seen first and last?

A
  • small rapidly moving skeletal muscles first(loss of eye lid reflex)
  • diaphragm last(first muscle that returns)

Non-depolarizing NMB onset more rapid yet less intense at laryngeal muscles than diaphragm

241
Q

Laryngeal muscles(fast twitch) equilibrate _____ with plasma NMB {} than slow twitch muscles(adductor pollicis)

A

more rapidly

  • laryngeal muscle relaxation is brief
  • laryngeal relaxation declining by time of maximal diaphragmatic relaxation with short and intermediate action NDNB*
  • Dose required to produce a degree of NMB at diaphragm is 2 X that required for an equal block at adductor pollicis or obicularis oculi*
242
Q

Adductor pollicis monitoring is best for monitoring what?

A

diaphragm relaxation

243
Q

Obicularis oculi monitoring is best for monitoring?

A

laryngeal relaxation

244
Q

Single-twitch response gives what type of data?

A

POST-junctional data

245
Q

Tetanus and TOF gives what type of data?

A

PRE- junctional data

246
Q

Do depolarizing NMB have fade with TOF?

A

no

fade will differentiate between depolarizer vs. non-depolarizer NMB

247
Q

The positive TOF fade with non-depolarizing NMB is known as ?

A

Wedensky inhibition

continous refractory state preventing repolarization…occurs when nerve is stimulated with high electrical frequencies and ends when application of current stops

248
Q

Neuromuscular blockers have quaternary ammonium groups which make them:?

A
  • highly ionized
  • water soluble at physiologic pH
  • poorly lipid soluble
  • small volume of distribution(due to lipid insolubility)
249
Q

What lipid membranes are not crossed by NMB(4)?

A
  • BBB
  • renal tubular epithelium
  • GI
  • placenta
250
Q

The rate of disappearance of long acting NMB is due to?

A

rapid initial decline is due to redistribution followed by slower decline from clearance

251
Q

How does hypovolemia affect NMB?

A

equal drug doses produce exaggerated effects due to greater plasma concentrations

252
Q

For laryngospasm, doses as small as ___ of succinylcholine are effective.

A

0.1 mg/kg

253
Q

TOF < than ____ reflects adequate return of skeletal muscle strength for spontaneous ventilation.

A

0.7

254
Q

What is the only NDNMB with an onset similar to succinylcholine?

A

rocuronium

255
Q

NMB selection is determined by

A
  • speed of onset needed
  • duration of action needed
  • drug effects at other than NMJ
256
Q

The last muscles(2) paralyzed are the?

A

intercostals and diaphragm

257
Q

NMB affect _____ before muscles of the _____?

A

small rapidly moving muscles(eyes and digits), trunk and abdomen.

258
Q

Skeletal muscle recovery occurs……

A

in reverse order with the diaphragm first

259
Q

What is the NMB structure of succinylcholine?

A

2 molecules of acetylcholine linked by acetate methyl group(most resembles ACh)

260
Q

Which NMB does this describe? Long, flexible, slender structure that binds to and activates cholinergic receptors?

A

Succinylcholine

261
Q

Which NMB does this describe? Bulky and rigid molecules that contain acetylcholine structure but can’t bind to and activate cholinergic receptors?

A

Non-depolarizering agents

262
Q

Which NMB are quaternary ammonium groups found?

A

all of them

263
Q

Acetylcholine has a + charged quaternary ammonium group(4 carbons attached to a nitrogen) that……

A

attaches to negative charged cholinergic receptors

264
Q

-90 mv resting membrane potential is painted by????

A

unequal distribution of K+ and Na+ ions across the cell membrane

265
Q

NMJ contains 3 types of cholinergic nicotinic receptors what are they?

A

2 -are post-synaptic on skeletal muscle surfaces
(1 junctional and 1 extra junctional)

1 - is pre-synaptic on the nerve endings

266
Q

What is the characteristic of TOF twitches in phase 1 NMB in a depolarizing block?

A

constant by diminished twitches

267
Q

What is the characteristic of TOF twitches in phase 2 NMB in a depolarizing block?

A

twitches with fade

268
Q

What is the characteristic of TOF twitches NMB using a non-depolarizing block?

A

fade

269
Q

What is the characteristic of tetanus twitches in phase 1 of NMB in a depolarizing block?

A

constant but diminished

270
Q

What is the characteristic of tetanus twitches in phase 2 of NMB in a depolarizing block?

A

fade

271
Q

What is the characteristic of tetanus twitches NMB using a non-depolarizing block?

A

fade

272
Q

What is the characteristic of post-tetanic potentiation twitches of a phase I depolarizing block?

A

NO TWITCHES(absent)

273
Q

What is the characteristic of post-tetanic potentiation twitches of a phase 2 depolarizing block?

A

present

274
Q

What is the characteristic of post-tetanic potentiation twitches of a non-depolarizer block?

A

present

275
Q

Acetylcholine in the motor nerve endings is made by what and controlled by what?

A

made by acetylation of choline;controlled by the enzyme choline acetylase

276
Q

Where is acetylcholine stored?

A

in the synaptic vesicles in motor nerve endings

277
Q

How is acetylcholine released?

A

Released in synaptic cleft as packets or quanta-1000 molecules

278
Q

What is the receptor acetylcholine binds to on the post-synaptic membrane

A

nicotinic receptors

279
Q

In addition to binding acetylcholine, the 2 alpha units(alpha, beta, gamma, delta) are the sites of what?

A

sites of action for NMB drugs

Non-depolarsing NMB show preference for 1 of 2 alpha subunits

280
Q

What is the result of occupation of the 1 of 2 alpha subunits by non-depolarizing NMB?

A

causes ion channel formed by receptors to remain closed
when we pretreat with a non-depolarizer(preventing fascinations)

-ion flow ends and depolarization can not occur

281
Q

If 2 alpha subunits are occupied simultaneously, what happens?

A

ion channels opens and fasciculations occur

282
Q

How much more is the epidural opioid dose more then the subarachnoid dose?

A

5-10 times more

3rd Quarter (22 decks)

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