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Adv. Pharm > Quiz 4 - CNS > Flashcards

Quiz 4 - CNS Flashcards

1
Q

Describe the breakdown of the nervous system

A
  • peripheral nervous system
  • central nervous system
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2
Q

Describe the 2 divisions of the peripheral nervous system

A
  • autonomic nervous system
  • somatic nervous system
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3
Q

Describe the 2 divisions of the autonomic nervous system

A
  • parasympathetic nervous system
  • sympathetic nervous system
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4
Q

Acetylcholine contains a (tertiary/quaternary) amine which means it (can/cannot) cross the BBB

A
  • quaternary
  • cannot
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5
Q

What 2 main functional groups are found on ACh?

A
  • 4* amine
  • ester
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6
Q

The products of ester hydrolysis include:

A
  • acid
  • alcohol
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7
Q

Where does AChE exist in the myoneural junction?

A

at the motor endplate

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8
Q

List the depolarizing NMBAs:

A

succinylcholine

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9
Q

List the steroid derivative NMBAs:

A
  • rocuronium
  • vecuronium
  • pancuronium
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10
Q

List the benzylisoquinoline derivative NMBAs:

A
  • atracurium
  • cisatracurium
  • mivacurium
  • d-tubocurarine
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11
Q

What structure is typical of steroid derivative NMBAs?

A

4-ring structure and 4* amine

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12
Q

Succinylcholine is 2 of which molecule linked together?

A

ACh

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13
Q

Describe ester hydrolysis:

A

ester –> enzyme + H20 –> acid + alcohol

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14
Q

Atracurium and cisatracurium produce which metabolite? Through which process?

A

Laudanosine through Hoffman elimination

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15
Q

Which 2 processes do Atracurium and Cisatracurium undergo?

A
  • ester hydrolysis
  • Hoffman elimination
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16
Q

Hoffman elimination depends on…

A

pH and temperature

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17
Q

NMBAs have a (small/large) Vd. Why?

A
  • small
  • presence of a charge makes them hydrophilic
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18
Q

List the NMBAs eliminated in the plasma:

A
  • Atracurium (ester hydrolysis and HE)
  • Cisatracurium (ester hydrolysis and HE)
  • Mivacurium (plasma ChE)
  • Succinylcholine (plasma ChE)
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19
Q

List the NMBAs eliminated primarily in the kidney:
- What implication does this have on DOA?

A
  • d-Tubocurarine
  • Pancuronium
  • Pipecuronium

kidney = slow clearance = longer DOA

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20
Q

List the NMBAs eliminated primarily in the liver:

A
  • Rocuronium
  • Vecuronium
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21
Q

5 things that affect onset of paralysis:

A

1) dose
2) potency (# of molecules)
3) Keo (chemistry/blood flow)
4) clearance
5) age

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22
Q

Describe which has a quicker onset, Roc or Vec? Why?

A

Roc - you have to give more molecules to get it to work (0.6mg/kg = 6x as much as the dose of Vec) which makes the onset faster

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23
Q

What effect does a nondepolarizing NMBA have on the ion channel?

A

closes and blocks the channel

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24
Q

What effect does a depolarizing NMBA have on the ion channel?

A

opens and blocks the channel

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25
Q

List ways to assess postop NM function:

A
  • sustained 5sec head lift
  • ability to clench teeth
  • negative inspiratory force >-40cmH2O
  • ability to open eyes x5 sec
  • hand grip strength
  • sustained arm/leg lift
  • quality of speaking voice
  • tongue protrusion
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26
Q

A TOF ration of >___% indicates patient is ready for reversal

A

<90%

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27
Q

What TOF ratio was previously the gold standard for reversal?

A

70%

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28
Q

NMBAs that can cause histamine release:

What effect can this have?

A
  • Atracurium
  • Mivacurium
  • d-tubocurarine +++
  • succinylcholine

decreased SVR

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29
Q

Which NMBA produces a moderate block on cardiac muscarinic receptors? What effect can this have?

A

Pancuronium

increase HR

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30
Q

Pancuronium effect on HR

A

increases HR (vagolytic)

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31
Q

Onset / duration / reversal of Pancuronium

A
  • onset slower
  • DOA intermediate
  • not reversed
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32
Q

Vecuronium effect on HR, BP

A

no effects on HR, BP; no histamine release

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33
Q

NMBA that requires reconstitution

A

Vec

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34
Q

Rocuronium effect on HR, BP

A

no effects on HR, BP; no histamine release

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35
Q

Ropacuronium effects on HR, BP

A

minimal effects on HR, BP; no histamine release

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36
Q

Ropacuronium was removed from the market due to…

A

potential for bronchospasm

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37
Q

4 problems with depolarizing NMBAs:

A

1) hyperkalemia
2) increased IOP
3) intragastric pressure
4) muscle pain

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38
Q

Drugs that interact with NMBAs:

A
  • inhaled anesthetics
  • antibiotics
  • Mg
  • other NMBA
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39
Q

Group of antibiotics that interact with NMBAs

A

Aminoglycosides (Gentamycin, Tobramycin)

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40
Q

Effect that Mg can have on neuromuscular blockade

A

prolongs it

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41
Q

How do acetylcholinesterase inhibitors interact with NMBAs?

A

increase ACh so it can compete with the NMBA

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42
Q

Why might early reversal with neo/glyco not work?

A

There is a ceiling effect (AChE is an enzyme) and it will take much longer for the patient to recover if it is used up before complete reversal can occur

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43
Q

Adverse effects of Neostigmine

A
  • muscarinic effects
    –bradycardia
    –increased secretions
    –N/V
    –abdominal cramping
  • nicotinic effects
    –muscle fasciculations
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44
Q

Adverse effects of Glycopyrrolate

A
  • tachycardia
  • xerostomia
    *less CNS anticholinergic effects than Atropine
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45
Q

Sugammadex falls under which class of drugs?

A

selective relaxant binding agent (SRBA)

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46
Q

Sugammadex is a _______. Specifically, Sugar ___-____

A

cyclodextrin

Sugar gamma-cyclodextrin

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47
Q

The core of Sugammadex is (lipophilic/hydrophilic) and the surrounding functional groups are (basic/acidic)

A

core = lipophilic
functional groups = acidic

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48
Q

Sugammadex reverses which NMBAs?

A

steroidals

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49
Q

The functional groups on Sugammadex interact with:

A

N+ on the steroidal NMBAs

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50
Q

The core of Sugammadex interacts with…

A

the 4 lipophilic rings of steroidal NMBAs

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51
Q

Sugammadex effectiveness with NMBAs

A

Roc > Vec > Pan

NO effect on benzyls or succs

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52
Q

Sugammadex (does/not) interact with the cholinergic system

A

does not

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53
Q

The Sugammadex-NMBA complex is excreted through the

A

kidneys

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54
Q

Roc must be in the (central/peripheral compartment) to bind to Sugammadex

A

central

the equilibrium shifts rapidly to pull Roc from tissues and back into plasma

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55
Q

Sugammadex should be dosed based on (IBW, LBW, TBW)

A

TBW

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56
Q

Sugammadex is incompatible with which drug commonle given at the end of surgery?

A

Ondansetron

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57
Q

Sugammadex notably interacts with which drugs?

A

hormonal contraceptives

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58
Q

ACh is made from which 2 substances?

A

Acetyl CoA and choline

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59
Q

ACh is hydrolyzed into which 2 substances?

A

Acetate and choline

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60
Q

ACh is an (inhibitory/excitatory) NT

A

both

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61
Q

There are ___ subtypes of muscarinic receptors

A

5

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62
Q

Stimulation of nicotinic receptors leads to opening of which channels and what effect in the cell?

A

opens Na+ and K+ channels resulting in depolarization

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63
Q

The 2 muscarinic receptors most relevant to anesthesia

A

M2 and M3

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64
Q

Where are M2 receptors located?

A
  • CNS
  • heart
  • smooth muscle
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65
Q

Where are M3 receptors located?

A
  • smooth muscle
  • exocrine glands
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66
Q

Describe what happens when M2 receptors are stimulated

A
  • Gi protein
  • inhibits adenylyl cyclase
  • negative inotropic effect –> decreased relaxation of smooth muscle
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67
Q

Describe what happens when M2 receptors are stimulated

A
  • Gq protein
  • effector = phospholipase C
  • results in mobilization of Ca++
  • smooth muscle contraction
  • exocrine secretion
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68
Q

List the direct acting cholinergic agonists

A
  • ACh
  • Nicotine
  • Muscarine
  • Bethanechol
  • Pilocarpine
69
Q

ACh and Carbachol are unique in that they are cholinergic agonists that…

A

act on both muscarinic and nicotinic receptors

70
Q

Succinylcholine is rapidly hydrolyzed by what enzyme?

A

Plasma/butyryl cholinesterase

71
Q

Which substance does plasma cholinesterase NOT hydrolyze?

A

acetyl-B-methylcholine

72
Q

Which substance does acetylcholinesterase NOT hydrolyze?

A

Succinylcholine

73
Q

List the types of drugs that inhibit cholinergic transmission:

A
  • inhibitors of vesicular storage
  • inhibitors of release
  • nicotinic antagonists
  • muscarinic antagonists
  • inhibitors of high-affinity choline transport
  • inhibitors of pyruvate dehydrogenase
74
Q

List the drugs that enhance or mimic cholinergic transmission:

A
  • nicotinic agonists
  • muscarinic agonists
  • cholinesterase inhibitors
75
Q

Describe the effects that muscarinic agonists have on the following systems:
- eye
- GI
- bladder
- vascular smooth muscle

A
  • pupil constriction
  • increased GI motility
  • increased urination
  • vascular smooth muscle dilation
76
Q

Describe the effects that muscarinic agonists have on the following systems:
- bronchial smooth muscle
- exocrine glands
- heart
- brain

A
  • bronchoconstriction
  • exocrine gland secretion
  • negative inotropic, chronotropic, and dromotropic effects on heart
  • brain excitation, tremor, hypothermia
77
Q

Describe the effects that AChE inhibitors have on the following systems:
- eye
- GI
- urinary bladder
- bronchial smooth muscle

A
  • pupil constriction
  • increased GI motility
  • increased urination
  • bronchoconstriction
78
Q

Describe the effects that AChE inhibitors have on the following systems:
- exocrine glands
- heart
- skeletal muscle
- brain

A
  • increased exocrine secretion
  • negative inotropic, chronotropic, and dromotropic effects on heart
  • increased skeletal muscle strength
  • brain excitation, tremor, hypothermia
79
Q

List the 5 nerve gases

A

1) GA (Tabun)
2) GB (Sarin)
3) GD (Soman)
4) VX
5) GF

80
Q

Describe the MOA of nerve gases

A

potent organophosphate compounds that bind to and inhibit AChE and cause a cholinergic crisis

81
Q

DUMBELLS stands for

A

diarrhea
urination
miosis
bradycardia
emesis
lacrimation
lethargy
salivation

82
Q

Cholinergic crisis/muscarinic stimulation = what acronym?

A

DUMBELLS

83
Q

Nicotinic receptor simulation produces which syndrome?

A

MTWHF syndrome:
muscle pain
tremors
weakness
HTN
fasciculation

84
Q

Describe the 2 steps of nerve gas binding to AChE

A

1st stage: reversible with pralidoxime
2nd stage: “aging” is irreversible

85
Q

Symptoms of nerve agent poisoning

A
  • confusion
  • altered LOC
  • seizures
  • coma
86
Q

How do organophosphates occupy enzymes?

A

covalently bonded

87
Q

What is the treatment for nerve gas poisoning?

A

1) Atropine - counteracts muscarinic effects
2) Pralidoxime (2-PAM) - counteracts nicotinic effects
2) Benzos - counteracts CNS effects

88
Q

MOA of Pralidoxime

A

reactivates AChE at the NMJ - if the aging process has not occurred within 5 min to 24 hours, depending on the nerve agent

89
Q

Patient monitoring after nerve gas poisoning

A
  • minor symptoms = 6-8 hrs
  • 2-PAM administration = ICU
90
Q

Muscarinic agonists are used to treat:

A
  • glaucoma
  • postop ileus
  • urinary retention
  • xerostomia
91
Q

Cholinesterase inhibitors are used to treat:

A
  • glaucoma
  • postop ileus
  • urinary retention
  • myasthenia gravis
  • reverse NM blockade
  • SVT
  • Alzheimer’s dz
92
Q

SE of cholinergic agonists:

A
  • hypotension
  • bronchoconstriction
  • salivation
  • miosis
  • sweating
  • GI discomfort
93
Q

Cholinergic agonists are contraindicated for which patients?

A
  • asthma
  • COPD
  • peptic ulcer
  • urinary obstruction
  • GI obstruction
94
Q

List 5 tertiary amines that are anticholinergics:

A
  • Atropine
  • Scopolamine
  • Pirenzepine
  • Dicyclomine
  • Tropicamide
95
Q

Ipratroprium is a (4/3) amine used to treat _____

A

4* amine used to treat COPD (prevents bronchoconstriction) as it does not need to cross the BBB

96
Q

Benztropine is a (4/3) amine used to treat _____

A

3* amine used to treat EPS/Parkinson’s; is able to cross the BBB

97
Q

List 2 quaternary amines that are anticholinergics:

A
  • Propantheline
  • Glycopyrrolate
98
Q

Describe the effects of muscarinic antagonists/anticholinergics on the following body systems:
- eye
- GI smooth muscle
- bladder
- bronchial smooth muscle

A
  • pupil dilation
  • decreased GI motility
  • decreased urination
  • bronchodilation
99
Q

Describe the effects of muscarinic antagonists/anticholinergics on the following body systems:
- exocrine glands
- heart
- brain

A
  • blockade of secretion/gastric acid secretion
  • tachycardia, increased dromotrophic effect
  • impaired memory, increased excitement
100
Q

What effects does Atropine cause at lower doses (0.5mg)? Higher doses (1.0mg)?

A
  • lower doses = decreased salivation and micturition
  • higher doses = increased HR and decreased accommodation
101
Q

Anticholinergic with greatest effect on HR

A

Atropine (+)

102
Q

Anticholinergic with greatest effect on secretions

A

Scopolamine (-)

103
Q

Anticholinergic with greatest effect on CNS

A

Scopolamine (+)

104
Q

Treatment for anticholinesterase poisoning

A

Atropine

105
Q

6 emesis receptors

A
  • serotonin
  • opioid
  • CN VIII
  • dopamine
  • histamine
  • muscarinic
106
Q

Effects of anticholinergics on the eye

A
  • increase dilation
  • decrease accommodation
107
Q

Closed-angle glaucoma surgical treatment

A

surgically placed hole in the iris to allow aqueous humor to drain and reduce IOP

108
Q

Receptors involved in the eye

A
  • alpha
  • beta
  • muscarinic
109
Q

2 drugs used to treat open-angle glaucoma and their effects

A
  • Pilocarpine = cholinomimetic = ciliary muscle contraction
  • Timolol = beta blocker = decreased aqueous secretion from ciliary epithelium
110
Q

Side effects of anticholinergics

A
  • urinary retention
  • constipation
  • tachycardia
  • dry mouth
  • mydriasis
  • inhibition of sweating
  • toxic psychosis
111
Q

Structural characteristics of a catechol

A

OH on 3rd and 4th carbons

112
Q

Rate limiting step of NE synthesis

A

hydroxylation of tyrosine to DOPA by tyrosine hydroxylase

113
Q

Why doesn’t dopamine cross the BBB?

A

too polar

114
Q

Final step in NE synthesis

A

hydroxylation of dopamine by dopamine-B-hydroxylase

115
Q

COMT =

A

catechol-o-methyl transferase

116
Q

NE is an (excitatory/inhibitory) NT

A

both - depending on the receptor it hits

117
Q

Effect of stimulating A1 receptors

A

(excitatory)
formation of IP3 and DAG –> increased intracellular Ca2+

118
Q

Effect of stimulating A2 receptors

A

(inhibitory)
inhibition of adenylyl cyclase –> decreased cAMP

119
Q

Effect of simulating B1 receptors

A

(excitatory)
simulation of adenylyl cyclase –> increased cAMP

120
Q

Effect of stimulating B2 receptors

A

(excitatory)
simulation of adenylyl cyclase –> increased cAMP

121
Q

A1 receptor locations

A
  • smooth muscle
    (vascular, genitourinary, intestinal, cardiac, and hepatic)
122
Q

A2 receptor locations

A
  • CNS
  • platelets
  • lipocytes
  • smooth muscle
123
Q

B1 receptor locations

A
  • heart
  • kidneys
124
Q

B2 receptor locations

A
  • lungs
  • blood vessels
  • eyes
  • uterus
  • bladder
  • liver
  • GI
125
Q

B3 receptor locations

A

lipocytes (fat mobilization)

126
Q

Effect of making the N on a catecholamine more nonpolar

A

more B effects

127
Q

List the catecholamines

A
  • Epi
  • NE
  • Dopamine
  • Isoproterenol
128
Q

List the sympathomimetic amines

A
  • Phenylephrine
  • Ephedrine
  • Methoxamine
  • Amphetamine
129
Q

B1-selective agonists

A
  • DoButamine
  • Prenalterol
130
Q

B2-selective agonists

A
  • Rotidrine
  • Terbutaline
131
Q

Types of drugs that enhance of mimic noradrenergic transmission:

A
  • facilitate release
  • block reuptake
  • receptor agonists
132
Q

Types of drugs that reduce noradrenergic transmission:

A
  • inhibit synthesis
  • disrupt vesicular storage
  • inhibit release
  • receptor antagonists
133
Q

Phenylephrine acts on which receptors:

A

A1, maybe some B1

134
Q

Effect of phenylephrine

A

vasoconstriction

135
Q

NE acts on which receptors:

A

A1=A2>B1»»>B2

136
Q

Epinephrine works on which receptors:

A

A1»A2
B1»B2
dose dependent

137
Q

Ephedrine works on which receptors:

A

A1 (indirect)
B1»B2 (direct)

138
Q

How does Ephedrine indirectly stimulate the A1 receptor?

A

simulates endogenous Epi release, Epi then acts on the A1 receptor

139
Q

Dopamine works on which receptors:

A

A1 + to +++++
B1»B2
DA1
dose dependent effects on A1

140
Q

Effects of low-dose Dopamine

A

increases renal and mesenteric blood flow

141
Q

Effects of high-dose dopamine

A

A1 agonist > B1 agonist

142
Q

Dobutamine works on which receptors:

A

A1 (little bit)
B1»B2
inotropism > chronotropism

143
Q

Isoproterenol works on which receptors:

A

B1=B2

144
Q

Which adrenergic agonist is most effective at augmenting BP? Why?

A

Norepi - equally affects A1 venous and A1 arterial receptors more than other agonists

145
Q

Effect that Isoproterenol has on BP and the subsequent effect on HR

A

decreases BP –> direct (B stim) and indirect (reflex) increase in HR

146
Q

Effect that NE has on BP and the subsequent effect on HR

A

increases BP –> direct increase and reflex decrease in HR

147
Q

Effect that Phenylephrine has on BP and the subsequent effect on HR

A

increases BP d/t A1 stimulation –> no direct effect but a reflex decrease in HR

148
Q

Effect that Dobutamine has on BP and the subsequent effect on HR

A

no effect on BP but a direct increase in HR d/t B1 stimulation

149
Q

Uses of adrenergic drugs

A
  • hypotension
  • reduction in regional blood flow
  • cardiac applications
  • respiratory
  • ophthalmic
  • uterine relaxation
  • decongestant
  • CNS uses
  • central A2
150
Q

Problems with adrenergic drugs

A
  • HTN
  • HoTN
  • tachycardia
  • ventricular arrhythmias
  • infiltration with A agents
  • CNS toxicity
151
Q

Metoprolol, Atenolol, and Esmolol work on which receptors:

A

B1»»B2
cardio-selective BUT increase dose = increase B2 effects

152
Q

Propranolol and Timolol work on which receptors

A

B1=B2

153
Q

Labetalol and Carvedilol work on which receptors

A

B2=B2>A1>A2
cause A1 receptor blockade

154
Q

Butoxamine works on which receptors

A

B2»>B1
no practical medical use for it

155
Q

BB with high lipid solubility:
Why is this relevant?

A

Propranolol
- can cross the BBB and is used to treat migraines

156
Q

MOA of BB for HTN

A

decrease HR and inhibit RAAS system leading to a reduction in HTN

157
Q

Uses of BB

A
  • HTN
  • ischemic heart disease
  • cardiac arrhythmias
  • glaucoma
  • hyperthyroidism
  • migraines
  • portal HTN
158
Q

First line treatment for chronic HF

A

ACE + BB

159
Q

3 alpha blocking agents:

A

1) Phentolamine
2) Phenoxybenzamine
3) Prazosin

160
Q

What happens to the receptor effects when NE and Epi are blocked by Phentolamine

A
  • Phentolamine blocks A receptors
  • see an increase in B1 and B2 effects
161
Q

Which drug is a nonselective A blocker?

A

Phentolamine
- blocks both A1 and A2 receptors
- leads to an increase in B effects (increased HR)

162
Q

Which drugs are selective A blockers?

A

Prazosin & Phenoxybenzamine
- selectively blocks A1 receptors
- A2 receptors maintain - feedback loop with NE
- normal NE acting on B receptors = less tachycardia

163
Q

Which drug is a noncompetitive A blocker?

A

Phenoxybenzamine

164
Q

Prazosin, Terazosin, and Doxazosin work in which receptors:

A

A1»»A2

165
Q

Phenoxybenzamine works on which receptors:

A

A1>A2

166
Q

Phentolamine works on which receptors:

A

A1=A2

167
Q

Uses of alpha blockers

A
  • pheochromocytoma
  • HTN
  • peripheral vascular dz
  • infiltration of A agents
168
Q

Uses of alpha blockers

A
  • pheochromocytoma
  • HTN
  • peripheral vascular dz
  • infiltration of A agents
  • BPH
  • make sexual dysfxn
169
Q

Problems with alpha blockers

A
  • Orthostatic hypotension
  • sedation
  • nasal stuffiness
  • HF in patients with cardiac dz

Adv. Pharm (5 decks)

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