Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > CNS NTs > Flashcards

CNS NTs Flashcards

1
Q

Anatomy for Glutamate:

A

Relay neurons all levels and some inter neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the receptors for Glutamate?

A

NMDA
AMPA
Kainate
Metabotropic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the mechanism for NMDA (glutamate)?

A

Excitatory: increase cation conductance (Ca)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the mechanism for AMPA (glutamate)?

A

Excitatory: increase cation conductance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the mechanism for Kainate (glutamate)?

A

Excitatory: increase cation conductance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the mechanism for metabotropic (glutamate)?

A

Inhibitory of presynaptic: decrease Ca and cAMP

Excitatory: decrease K and increase IP3 and DAG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the anatomy for glycine?

A

Spinal interneurons and some brainstem interneurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the receptor for glycine?

A

Glycine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the mechanism for glycine?

A

Inhibitory: increase Cl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the anatomy for GABA?

A

Supraspinal and spinal interneurons pre and post synaptic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the receptors for GABA?

A

GABAa

GABAb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the mechanism for GABAa?

A

Inhibitory: increase Cl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the mechanism for GABAb?

A

Inhibitory in presynaptic: decrease Ca

Inhibitory in postsynaptic: increase K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What anesthetics use the receptor GABAa?

A 
Barbiturates (enhance)
Propofol (enhance)
Etomidate (enhance)
Benzodiazepine (enhance)
Inhaled agents (enhance)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What anesthetics use the receptor glycine?

A

Barbiturates (enhance)
Propofol (enhance)
Etomidate (enhance)
Benzodiazepine (enhance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What anesthetics use the receptor NMDA?

A 
Ketamine (inhibit)
Inhaled agents (N20) (inhibit)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What anesthetics use the receptor nACh?

A

Barbiturates (inhibit)

Ketamine (inhibit)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What anesthetics use the receptor K+ channels?

A

Inhaled agents (enhance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Calming and drowsiness, decreases activity, moderates excitement, calms patient

A

Sedation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Produces drowsiness and facilitates the onset and maintenance of a state of sleep

A

Hypnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Global but reversible CNS depression resulting in loss of response to and perception of external stimuli “deafferentation”
Not all agents produce identical state
Collection of changes in behavior and perception – anesthetic state is:
•Amnesia
•Immobility to noxious stimuli
•Attenuation of autonomic response to noxious stimuli
•Analgesia
•Unconsciousness

A

Anesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Potential other effects of drugs?

A 
Amnesia 
Analgesia 
Anticonvulsant 
Muscle Relaxation 
Respiratory 
Depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the different drug classes (6)?

A 
Benzodiazepines 
Non-bz sedative hypnotic drugs (z drugs)
Barbiturates 
Melatonin Congeners 
IV Anesthetics 
Inhaled Anesthetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the triad of GA?

A

Unconsciousness
Analgesia
Muscle Relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What can IV agents be used for (5)?

A

Sedation-based anesthesia
Monitored anesthesia care (regional or local + sedation)
Conscious sedation (small doses used to alleviate anxiety)
Deep sedation
Light state of GA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What comes with light state of GA?

A

Loss of protective reflexes
Inability to maintain patent airway
Lack responsiveness to surgical stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

IV Anesthetics characteristics of each agent (7)

A 
Induction 
Analgesia 
Sedation/antianxiety 
Hypnosis 
Amnesia 
Muscle Relaxation 
Anesthesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Non-anesthesia drugs side effects of induction (5)

A 
Apnea 
CV
Hiccups 
Movement 
Pain - site of injection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Non-anesthesia drugs side effects of recovery (3)

A

Nausea
Vomiting
Restlessness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is GABA?

A

Inhibitory CNS NTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What kind of structure is GABAa receptor?

A

Pentameric with subunits alpha, beta, and gamma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What subunits of GABA is major isoform?

A

2 alpha1
2 beta2
1 gamma2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Where is the binding site for GABA?

A

Between alpha1 and beta2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Where is the binding site for BZ?

A

Between alpha1 and gamma2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What else is barbiturates known as?

A

Methohexital (brevital)

Thiopental (pentothal) and Thiamylal are no longer in US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Mechanism of action for barbiturates?

A 
Enhance GABA (Cl)
Increase duration of GABA
-High doses activate Cl and depress glutamate binding to AMPa receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What do barbiturates substitutions affect?

A

Hypnotic potency and anticonvulsant activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What activity does phenobarbital affect?

A

Anti-convulsive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is thiopental, thiamylal activity?

A

Greater potency
More rapid onset
Shorter duration fo action compared to pentobarbital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How are barbiturates absorbed?

A

IV

Rectally in peds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What kind of distribution are barbiturates?

A

High lipid solubility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How fast does plasma:brain equilibrium occur in barbiturates?

A

Rapidly, onset within 30 sec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How is barbiturates diffusion to other tissues limits duration of induction?

A

Waken in about 20min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How do you dose elders with barbiturates?

A

Reduce induction does due to slower redistribution and longer duration of action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How is repeated doses (or continuous infusion) affected with barbiturate?

A

Saturate peripheral compartments and minimize the redistribution effect (increasing duration of action)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Does continuous infusion prolong the half life?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How should barbiturates be mixed with other solutions?

A

Alkaline solution to make soluble

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What happens with barbiturates when mixed with drugs that are weak bases (rocuronium, lidocaine, labetalol, morphine)?

A

Precipitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Barbiturate Pharmacodynamics to CNS (5)?

A

Onset 10-20sec; bolus lasts about 8-20min (half life 3-12hr)
Constrict cerebral vasculature (decrease CBF and ICP)
Decrease cerebral oxygen
Potent antibonvulsant (phenobarbital)
Lower pain threshold (hyperalgesic effect)
Involuntary muscle movements (excitatory with induction (methohexital))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Barbiturate Pharmacodynamics to CV (5)?

A

Peripheral vasodilation (small decrease in BP)
Negative inotropic effects
Venous vasodilation (peripheral pooling, decrease preload (CO&BP))
Vagolytic compensatory responses (HR&contractility)
Caution in patients without adequate baroreceptor responses (decrease BP&CO) (hypovolemia, beta blocker, CHF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Barbiturate Pharmacodynamics to respiratory (3)?

A

Depression (medullary center, decrease response to CO2&O2)
Don’t completely suppress airway reflexes (muscarinic nerve stimulation-atropine and thiopental to avoid bronchospasm
Apnea, bronchospasm (asthma), hiccup, laryngospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Barbiturate Pharmacodynamics to histamine release?

A

May cause hypotension, tachycardia
Caution in asthma patient
Rare allergic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Does barbiturates have muscle relaxation?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Additional info about Barbiturate Pharmacodynamics?

A

Pain on injection
No analgesia
Renal/hepatic - no short term toxicities
Contraindicated in acute intermittent porphyria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is porphyria?

A

Neurological disease cause by inadequate porphyria metabolism
-rate limiting step in haem synthesis (ALA synthetase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is porphyrins?

A

Highly reactive oxidants

Cause toxic neurological sequelae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What drug is barbiturates being replaced by?

A

Propofol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Thiopental (4)

A

Primary use was in induction
Used alone for short procedure with no pain
Promote sleep for local anesthesia
Critical care uses: ICU sedation, increased ICP, epileptic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

When is methohexital used?

A

For ECT or epilepsy-related surgical procedures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What interactions should be considered for dose reduction in barbiturate?

A

Combo with opioid
alpha2 adrenergic agonist
Benzodiazepine
Acute ethanol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What patients should be considered for dose reductions with barbiturate?

A 
Anemia 
Low protein 
Decreased CO 
Shock 
Elderly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What drugs are under benzodiazepines (BZ)?

A

Diazepam
Lorazepam
Midazolam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

BZ mechanism of action (5):

A

Interaction with GABA (inhibitory, Cl)
GABA inhibition at all levels (spinal cord to cerebral cortex)
Increase efficiency of GABA by increasing frequency of Cl challenge openings
Do NOT substitute for GABA, must be present
Do NOT directly activate GABA receptor (bind to BZ receptor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is BZ’s receptor competitive antagonist?

A

Flumazenil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What structure is BZ?

A

Heterocyclic ring with varied substituents that impact potency and metabolism (diazepine ring)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What does BZ water solubility affect?

A

Parent earl preparations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What does BZ lipid solubility impact?

A

CNS onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the kinds of formulations for BZ?

A

P.O., IM, IV administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How long is diazepam and lorazepam P0 onset?

A

1-2 hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is midazolam for PO administration?

A

Syrup

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What kind of absorption do you get from IM diazepam?

A

Painful and erratic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What kind of absorption do you get with IM lorazepam and midazolam?

A

Well absorbed and peak in 90min (lorazepam) and 30min (midazolam)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is the only IV BZ for induction and how is its onset?

A

Midazolam and among BZ shortest onset (but still longer compared to other classes of agents)
-diazepam and others can be given IV but not used for induction due to delayed onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

BZ lipid solubility distribution from highest to lowest:

A

M > D > L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Distribution of BZ to brain - time to onset highest to lowest:

A

L > D > M

  • L slowest CNS uptake and onset
  • BZ have slower onset for induction vs propofol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the redistribution time and what kind of bound is BZ?

A 
Rapid redistribution (3-10min), but short duration of effect 
Highly protein bound (>90%)
77
Q

Hepatic metabolism for BZ in mostly phase I or II?

A

Most phase I oxidation

Phase II conjugation of metabolites for renal elimination

78
Q

Which of BZ are active metabolites?

A

D and M

79
Q

Which of BZ has the highest to lowest half life?

A

D > L > M

80
Q

Which of BZ deals with enterohepatic recirc?

A

D

81
Q

What happens if you high does midazolam?

A

Accumulation of active metabolite in patients with kidney failure

82
Q

CNS effects of BZ (8)

A 
Sedation 
Hypnosis 
Anesthesia 
Amnesia 
Anticonvulsant 
Muscle relaxation (not paralysis) 
Tolerance - physiologic and psychologic (patient history and/or cross tolerance)
Dependence
83
Q

What kind of CNS effects do BZ have compared to barbiturates?

A

Decrease CBF, O2 consumption, ICP but at a lesser degree than barbiurates

84
Q

What kind of amnesia does BZ have at CNS level?

A

Anterograde amnesia

85
Q

Does BZ have analgesic effects?

A

NO

86
Q

BZ affects on CV?

A

Minimal effects and may be used to balance effects of other agents
Large doses through IV or combo with opioids maybe reduce BP (vasodilation)
Possible increase in HR with midazolam

87
Q

BZ affect with respiratory?

A

Minimal depression alone but additive with other agents
Decrease ventilatory response to CO2
Induction apnea

88
Q

Which BZ has the most to least common thrombophlebitis?

A

D > M&raquo_space; L

89
Q

Drug interaction will induce or inhibit what enzyme?

A

CYP P450

90
Q

What does opioids + BZ get?

A 
Decrease SVR (hypotension)
Caution with patients with ischemic heart disease, valvular heart disease
91
Q

Does BZ increase or decrease potency of inhaled agents?

A

Increase potency (decrease MAC)

92
Q

What are the 5 status that BZ’s are used?

A 
Perioperative 
Sedation-hypnosis with local anesthesia 
Alone for procedures not requiring analgesia or full anesthesia 
Control seizures 
ICU sedation
93
Q

What does Flumazenil do?

A

Reverse symptoms of OD or therapeutic effects of BZ

Does not affect BZ elimination or concentration

94
Q

What is the half life for flumazenil?

A

54min (duration of action about 20min)
Shorter compared to BZ
May cause withdrawal in dependent patients, seizures in those at risk

95
Q

Ketamine’s mechanism of action

A

Inhibit NMDA receptor complex (glutamate receptor)

96
Q

What kind of anesthesia is ketamine?

A

Dissociative anesthesia - dissociated thalamus (relays sensory) to limbic (awareness)

97
Q

How do you appear with Ketamine?

A

Awake, eyes open, swallow, muscle contracture, but unable to respond to sensory input
-NOT global CNS depression, in fact some stimulation

98
Q

What are some special properties to ketamine?

A

May limit use or make desirable in certain patient situations

99
Q

What drug is ketamine most similar to?

A

Phencyclidine (vet anesthetic)

100
Q

What kind of potency is ketamine?

A

0.1 potency, but has some psychotomimetic effects

May cause some hallucinations at sub-anesthetic doses (midazolam or other sedative will minimize)

101
Q

What is a potent anesthetic without psychotomimetic effects?

A

S+ isomer

-greater affinity for NMDA receptor (greater potency)

102
Q

Normal absorption for ketamine?

A

IV or IM

103
Q

Distribution for ketamine?

A

Lipophilic with rapid brain uptake

-fast onset with short duration (10-15min duration of action)

104
Q

Metabolism for ketamine?

A

Induction of hepatic enzymes (repeated doses and they develop tolerance)
Active metabolite Norketamine (less potent)
Extensive hepatic extraction

105
Q

Excretion for ketamine?

A

Renal elimination of metabolites

106
Q

Dosing for ketamine?

A

Excellent analgesic at sub anesthetic doses

Can be ‘complete’ anesthetic (analgesic, amnesia, unconsciousness)

107
Q

CNS with ketamine (5)?

A

Cerebral vasodilator (increased CBF and ICP)
Onset 15-30sec and lasts 10-15min
Analgesia/amnesia is instant and last 40min
Does NOT lower seizure threshold
Emergence reactions (10%-30% of adults)

108
Q

What kind of emergence reactions do you get with ketamine?

A

Delirium, excitement, confusion, euphoria, fear, vivid dreaming, hallucinations
First hour of emergence
Lower rate in children
Minimize with BZ

109
Q

CV with ketamine?

A

Central sympathetic stimulation, inhibits NorE reuptake

Increases HR, BP, CO

110
Q

When should you use caution or avoid with ketamine?

A

Patients with CAD, uncontrolled HTN, CHF, or arterial aneurysms

111
Q

What is the exception with ketamine in some patients?

A

Depleted catecholamines or spinal cord transaction

May see direct myocardial depression (Ca channel blocker) with very large doses (no longer mask sympathetic effects)

112
Q

Respiratory with ketamine?

A

Minimal effect on ventilatory drive (CO2)
Bronchodilator (racemic) which is useful in asthma and peds
Increased salivary and trachiobronchial secretions (can premed to reduce)

113
Q

Muscle effect with ketamine?

A

Myoclonic activity (no change in EEG)
No MH
Stimulated uterine muscle contraction

114
Q

Which drug interactions block the ketamine sympathetic effects?

A

Alpha and beta adrenergic receptor antagonists which leads to direct myocardial depressant effects

115
Q

What other drug interactions is ketamine additive with?

A

Inhaled anesthetics

Propofol, BZ, and other GABA acting agents

116
Q

When is ketamine used?

A

Used with BZ in emergent and trauma situations, procedures for analgesia and amnesia
Now used for severe depression to treat resistant and suicidal

117
Q

Is ketamine an excellent analgesic at sub anesthetic doses?

A

YES

118
Q

When is ketamine used in anesthesia?

A

Induction and maintenance

119
Q

Mechanism of action for propofol?

A

Interacts with GABAa receptor complex (binds to beta subunit)
Allosterically increases binding affinity for GABA (hyperpolarization of nerve membrane)
Binds to multi ion channels (glutamate related)

120
Q

What is propofol formulation?

A

NOT water soluble
1% (10mg/ml) solution available as oil in water (O/W) emulsion
Lipophilic in 10% fat emulsion

121
Q

What is in propofol?

A

Soybean oil
Glycerol
Egg lecithin (egg yolk)
Preservatives to prevent bacterial growth (metabisulfite and edetate)

122
Q

What is the problem with lipophilic?

A 
Once opened use within 6-8hours 
Linked to sepsis, mortality, other infectious complications with ICU long term sedation
Periodic shortages (problems with particulate matter and microbial contaminations)
123
Q

What is the absorption for propofol?

A

IV only

124
Q

What is the distribution for propofol?

A

Rapid onset
Rapid awakening from single bolus dose (half life 2-8min)
Vd reduced in elders (lower dose)

125
Q

Metabolism for propofol?

A

Hepatic and extra renal clearance

  • hepatic conjugation to inactive metabolites then really cleared
  • no dose change for cirrhosis or renal failure
126
Q

Cerebral affect on propofol?

A

Decrease CBF, blood volume and ICP

Use caution for patients with elevated ICP (can cause critical reduction)

127
Q

Does propofol have analgesic effect?

A

NO

128
Q

CNS effect from propofol?

A

Dystonic movements (NOT seizure activity)
Has some anticonvulsant properties
Tolerance dos not occur in repeated doses
Uncommon cause of dependence or addiction

129
Q

CV for propofol?

A

Reduced BP by 15%-40% (greater than thiopental)

  • decreased SVR and preload
  • inhibit baroreceptor response to change in BP (HR unchanged)
130
Q

Who has a greater impact on with propofol?

A 
Hypovolemia 
Elderly 
LV dysfunction
Receiving beta blockers 
-reduce dose or combo with IV opioid or BZ
131
Q

Respiratory with propofol?

A 
Profound depression (reduce CO2)
Apneic for 30-60sec
Inhibits airway reflexes (less cough, layrngospasm)
Minimal histamine release 
Fewer problems with asthmatic patients
132
Q

Does propofol have muscle relaxation?

A

NO

133
Q

Is there pain with injection of propofol and how to fix?

A

Yes, use lidocaine before or with propofol

134
Q

Other effects of propofol?

A

Sedative & antianxiety
Antiemetic at sub anesthetic doses
Antipruritic
Safe in OB/GYN (may cause neonatal depressed after prolong infusion)

135
Q

Is there a chance with porphyrinogenic with propofol?

A

Yes, increases ALA reductive activity

136
Q

When is hypertriglyceridemai possible with propofol?

A

Critical care and peds

Continuous infusions

137
Q

What is propofol infusion syndrome?

A

Metabolic acidosis

Lipemic plasma, myocardial failure, hepatomegaly, rhabdomyolysis

138
Q

When is propofol used?

A

Induction
Maintenance
ICU

139
Q

What is the rapid onset and awakening for propofol?

A

10-20sec onset

2-8min awakening

140
Q

What is TIVA?

A

Total IV anesthesia

-combo with other short acting agents (remifentanil, alfentanil, sufentanil)

141
Q

What other drug is propofol used with during induction?

A

Midazolam (additive effects so reduce propofol by 10%)

142
Q

What other drug is propofol used with during TIVA?

A

Combo with remifentanil and ketamine

143
Q

What do you do to propofol with high concentrations of fentanyl and alfentanil?

A

May be able to reduce dose

144
Q

Do you change dose of propofol for obesity, cirrhosis, or renal failure?

A

NO

145
Q

When do you use smaller induction doses of propofol?

A

Elderly

TIVA

146
Q

What is formulation of fospropofol?

A

Sterile aqueous clear solution to avoid pain on injection and lipid emulsion
Water soluble prodrug
Onset and recovery are prolonged compared to propofol
Use for moderate IV sedation (MAC) with O2

147
Q

Mechanism of action for etomidate?

A 
Enhance GABA (GABAa receptor)
-may have dis-inhibitory effect in extrapryramidal area (basal ganglia) that lead to EPS like movement (increased myoclonus compared to other agents)
148
Q

What is the absorption for etomidate?

A

IV

149
Q

What is the distribution for etomidate?

A

High protein binding, but rapid onset due to high lipid solubility and large non-ionized fraction
Recovery depends on redistribution to inactive tissue sites

150
Q

Metabolism for etomidate?

A

Plasma ester ashes and hepatic CYP enzymes -inactive metabolites

151
Q

How is renal clearance for etomidate?

A

Of metabolites

152
Q

CNS of etomidate?

A

Potent short acting hypnotic
Onset 20-30sec and lasts 5min
Decreases cerebral metabolic rate, CBF, ICP
Maintained cerebral perfusion
Involuntary muscle movements- dis-inhibitory on EP motor control high rate excitatory phenomena (more than 50% of patients)

153
Q

How can etomidate cause EEG changes?

A

Enhance some to sensory evoked potentials
Useful in intraoperative; epileptic ablation procedures
Not evoke seizure undergoing ECT

154
Q

How do you reduce involuntary movement with etomidate?

A

Pretreat with opioid or BZ

155
Q

CV of etomidate?

A

Reduce sympathetic NS and baroreceptor responses
Mild decline in SVR
Not elicit histamine release
Low rate of hypersensitivity

156
Q

When is etomidate especially useful?

A

Impaired LV function
Cardiac tamponade
Hypovolemia
Emergent Rachael intubation

157
Q

Respiratory for etomidate?

A

Less depression compared to barbiturates and BZ

Does not result in apnea unless with opioids

158
Q

Endocrine of etomidate?

A

Inhibit adrenal steriodogenesis; interferes with stress response
NOT used for ICU sedation
Linked to increased mortality after surgery

159
Q

Does etomidate have analgesia?

A

NO

160
Q

When is etomidate used?

A

With BZ for induction

In case of CV risk or neurosurgical case

161
Q

What is dexmedetomidine?

A

Alpha 2 adrenergic receptor agonist used for anxiolytics, sedation, and analgesia

162
Q

When does FDA indication to use dexmedetomidine?

A

Sedation of intubation and ventilated patient in ICU

Sedation prior to and/or during surgical or other procedures of non-intubate patients

163
Q

What does alpha 2a subtype do?

A

Mediating sedation
Hypnosis
Analgesia
Sympatholytic

164
Q

What does alpha 2b subtype do?

A

Vasoconstriction
Antishiver
Analgesia

165
Q

Mechanism of action for dexmedetomidine?

A

Selective alpha 2 adrenergic agonist

166
Q

What is the sedation time for dexmedetomidine?

A

Less than 24 hours; prolong may cause withdrawal, rebound hypertension

167
Q

dexmedetomidine uses (7)?

A 
Presedation (nasal or oral in peds)
Procedural sedation 
Supplement to GA (reduce opioid and emergence delirium)
ICU sedation (continuous infusion)
Treatment/prevention of withdrawal 
No amnesia 
Epidural regional analgesia/anesthesia
168
Q

CV effects of dexmedetomidine?

A

Hypotension (25-50%)
Bradycardia (5-15%)
Withdrawal effects when used >24hrs

169
Q

Respiratory for dexmedetomidine?

A

Little effect on ventilation vs opiates

170
Q

Does dexmedetomidine cause nausea?

A

YES

171
Q

Dose for dexmedetomidine?

A

1mcg/kg IV over 10min with maintenance infusion rate of .2-.7mcg/kg/hr

172
Q

Onset and half life of dexmedetomidine?

A

Rapid onset

Half life about 2 hours

173
Q

Do you reduce dose in renal and hepatic insufficiency?

A

YES

174
Q

When do you use caution in dexmedetomidine when in combo with:

A

Vasodilators
Cardiac depressant
Drugs that decrease HR

175
Q

What do you do to dexmedetomidine when in combo with other hypnotics and anesthetic agents?

A

Reduce dose to offset excessive hypotensive effects

176
Q

What other uses are for dexmedetomidine?

A

Treatment of postoperative shivering (central thermoregulatory inhibition and peripheral effect)
Premed to attenuate cardiostimulatory effects of ketamine and intubation

177
Q

When is best to use dexmedetomidine (7)?

A 
Drug or alcohol withdrawal 
Chronic pain 
Unable/unwilling to take opioids 
Hypertension 
Hypotension surgical procedure
Ophthalmic surgery 
Ketamine anesthesia
178
Q

How does doxapram affect respiratory and CNS?

A

Respiratory depression secondary to anesthesia

179
Q

What does doxapram active with low doses?

A

Carotid chemoreceptors:

Hypoxic drive, COPD, drug induced respiratory depression

180
Q

CNS affect of doxapram?

A

Seizures, muscle fasciculation, HA, dizzy, agitation, confusion

181
Q

Cardiac affects with doxapram?

A

Tachycardia, arrhythmia

182
Q

Does doxapram cause nausea?

A

YES

183
Q

When should you avoid doxapram?

A 
Epilepsy
Cerebrovascular and CAD 
Acute head injury 
HT
Asthma
184
Q

Dosing for bolus and continuous infusion for doxapram?

A

IV bolus .5-1mg/kg (increase minute vent)
-onset 1min and duration of 5-10min
Continuous infusion 1-3mg/min (max dose of 4mg/kg)

185
Q

When does MH normally occur?

A

Upon anesthesia induction

186
Q

Pathophysiology effect of MH?

A

Uncontrolled release of intracellular Ca in skeletal muscle (intense muscle contraction and enhanced and sustained ATP activity)

187
Q

How to manage MH (7)?

A 
DC inhaled agent and Sux 
Hyperventilate 
Administer NaHCO3
Mix dantrolene and give 2.5mg/kg 
Cooling measures 
Inotrope, press or, anti arrhythmic 
Treat hyperkalemia
188
Q

How does dantrolene work?

A

Binds to RyR1 receptor of Ca channel and inhibits Ca release from SR

189
Q

Dosing of dantrolene?

A

Use sterile water; 20mg/60ml of water
2.5mg/kg every 5min (max 10mg/kg)
Half life about 6hrs
If symptoms return 1mg/kg every 6hr next 24-48hrs

Pharmacology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions