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APEX > Pharmacology IV anesthetics > Flashcards

Pharmacology IV anesthetics Flashcards

1
Q

What is the pKa of Propofol?

A

11

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2
Q

What is the preservative in brand name Propofol?

A

Diprivan has the preservative disodium edetate

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3
Q

What is the preservative in generic Propofol?

A

sodium metabisulfite

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4
Q

1% solution in an emulsion of egg lecithin, soybean oil, and glycerol describes what drug?

A

Propofol

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5
Q

What is the MOA of propofol?

A

Direct GABA - A agonist which increases Cl conductance and leads to neuronal hyperpolarization

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6
Q

What is the induction dose for propofol?

What is the infusion range?

A

induction - 1.5-2.5 mg/kg IV

infusion - 25-200 mcg/kg/min

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7
Q

duration for propofol?

A

5-10 min.

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8
Q

How is Propofol cleared?

A

Liver (P450 enzymes) + extrahepatic metabolism

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9
Q

Where does extrahepatic clearance of propofol occur?

A

in the lungs mainly

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10
Q

True or false:

clearance of Propofol exceeds liver blood flow?

A

True

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11
Q

What does the chemical structure of Propofol look like?

A

6 sided
CH(CH3)2 side chains (2)
and an OH side chain

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12
Q

After an IV bolus of Propofol the brain concentration peaks at what time period?

A

after 1 min.

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13
Q

Awakening from Propofol is due to what?

A

redistribution out of the brain

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14
Q 
Explain the cardio vascular effects of propofol in relation to:
BP
SVR
venous tone
myocardial contractility
A

decreased BP (due to decreased SNS tone and vasodilation)

decreased SVR

decreased venous tone (leads to decreased preload)

decreased myocardial contractility

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15
Q

Respiratory effects of Propofol?

A

Shifts the CO2 response curve down and to the right ( less sensitive to CO2).
Resp. depression and / or apnea inhibits hypoxic ventilatory drive.

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16
Q 
What are the CNS effects of Propofol?
CMRO2
CBF
ICP
IOP
A

decreased CMRO2
decreased CBF
decreased ICP
decreased IOP

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17
Q

Does Propofol have analgesic properties?

A

No

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18
Q

Does Propofol have anticonvulsant properties?

A

Yes

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19
Q

Can Propofol cause seizures?

A

There are a few reported cases of Propofol inducing seizures, but these are very rare exceptions.

It can cause myoclonus

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20
Q

If a Propofol infusion changes the urine color to green or cloudy, what does it mean?

A

green urine = phenol excretion

cloudy urine = increased uric acid excretion (does not suggest renal impairment or infection)

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21
Q

Explain Propofol infusion syndrome on the molecular level?

A

Propofol contains long chain triglycerides, and an increased LCT load impairs oxidative phosphorylation and fatty acid metabolism. This starves cells of oxygen, particularly in the cardiac and skeletal muscle.

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22
Q

What are they symptoms of Propofol infusion syndrome?

A

It presents with acute refractory bradycardia leading asystole and at least one of the following:

Metabolic acidosis ( base deficit > 10 mmol/L)

rhabdomyolysis

enlarged or fatty liver

renal failure

hyperlipidemia

lipemia (cloudy plasma or blood ) early sign

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23
Q

Are people who are allergic to eggs allergic to Propofol? Explain…

A

Most people with egg allergy are allergic to the albumin in the egg whites. Egg lecithin is derived from the yolk.

There is NO good evidence to support cross - sensitivity in egg allergic patients.

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24
Q

Is it safe to give people with egg allergies Propofol?

A

It is PROBABLY safe to administer to patients with egg allergies

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25
Q

Can patients who have a Soy allergy be given Propofol?

A

Any soy proteins that are capable of producing an immune response are removed during the refining process, thus propofol is safe to use in patients with soy allergies.

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26
Q

Can patients who have a peanut allergy be given Propofol?

A

Propofol is safe to administer to people with a Peanut allergy

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27
Q

What are the risk factors for developing Propofol infusion syndrome?

A

Propofol dose > 4mg/kg/hr ( 67mcg/kg/min)

Propofol infusion duration > 48 hours

Sepsis (inadequate oxygen delivery)

Continues catecholamine infusions

high-dose steroids

Significant cerebral injury

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28
Q

What is the treatment for Propofol infusion syndrome?

A

D/C propofol, maximize gas exchange, cardiac pacing, PDE inhibitors, glucagon, ECMO, and or renal replacement therapy

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29
Q

What patient population did PIS used to be the most common in?

A

PIS used to be most common in children but the FDA released a warning about prolonged infusions in children (ICU use not anesthesia) and now PIS is most common in adult and elderly critically ill patients.

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30
Q

Which formulations of Propofol are completely safe for asthmatic patients, can precipitate bronchospasm in asthmatic patients, and/ or should be avoided in infants?

A

Diprivan which contains EDTA is completely safe for asthmatic patients.

Generic propofol which contains metabisulfite can precipitate bronchospasm in asthmatic patients.
Also, generic propofol has benzyl alcohol which should be avoided in infants.

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31
Q

Is Propofol antipruritic?

A

10 mg IV can reduce itching caused by spinal opioids and cholestasis

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32
Q

Is Propofol antiemetic?

A

10-20 mg IV can be used to treat PONV,.

An infusion of 10mcg/kg/min can also be used.

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33
Q

induction agent most commonly (highest percentage) associated with PONV?

A

Etomidate

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34
Q

In patients with a history of acute intermittent porphyria, what medications should be avoided?

A 
Ketamine
Etomidate 
Barbiturates
Ketorolac
Amiodarone
CCB (many but not all)
Birth control pills
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35
Q

Clearance of Etomidate is by what?

A

Hepatic P450 enzymes and plasma esterase’s

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36
Q

Which induction agent is a known inhibitor of adrenocortical, and specifically what does it inhibit?

A

Etomidate - known inhibitor of 11-beta-hydroxylase and 17-alpha hydroxylase

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37
Q

Which induction agent is known to supress the baroreceptor reflex? (part of the reason for it’s drop in BP)

A

Propofol

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38
Q

Explain the chemical structure of Thiobarbiturates and give examples of this drug?

A

Sulfur molecule in the 2nd position (increases lipid solubility and potency)

examples = Thiopental, Thiamylal

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39
Q

Explain the ring / chemistry of all barbiturates in general?

A

The ring is six sided (six pointed). Position 1 starts in the lower right corner of the ring and position two is directly in the middle right side of the ring and position 3,4,5,6, proceed counter clockwise

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40
Q

If you add a methyl group onto the nitrogen of a barbiturate ring what does it do, what drug does it become?

A

lowers the seizure threshold and increases potency

Methohexital

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41
Q

If you add a phenyl group at the five carbon of a barbiturate ring what does it do, what drug does it become?

A

increases the anticonvulsant effect

Phenobarbital

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42
Q

How would you create an oxybarbiturate?

examples of oxybarbiturates?

A

There is an oxygen molecule in the 2nd position

example = methohexital, pentobarbital

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43
Q

Thiopental, what is its solubility medium? What is it’s pH?

A

water soluble

pH= 9 (highly alkaline)

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44
Q

What happens when you mix thiopental with an acidic solution?

A

precipitate forms

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45
Q

Does Thiopental have any active metabolites?

A

not at low doses but at higher doses it will have the active metabolite pentobarbital

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46
Q

GABA A agonist - depresses the reticular activating system in the brainstem describes?

A

Thiopental

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47
Q

Cardiovascular effects of Thiopental?

A

Hypotension is primarily the result of venodilation and decreased preload, myocardial depression is a 2ndary cause.

non-immunogenic histamine release is short lived (may contribute some to hypotension)

baroreceptor reflex stays intact thus reflex tachycardia helps restore cardiac output.

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48
Q

Neuroprotection of Thiopental?

A

Focal ischemia: yes, helpful with CEA, temporal occlusion of cerebral arteries.

Global ischemia: No (cardiac arrest)

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49
Q

What is Acute Intermittent Porphyria?

A

It is a defect in heme synthases that promotes the accumulation of heme precursors.

Heme is a key component of hemoglobin, myoglobin, and the cytochrome P450 enzymes.

AIP is made worse by stimulating the ALA synthase, emotional stress, prolonged NPO status, and CYP450 induction.

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50
Q

Phenobarbital is excreted unchanged in the urine, how is this different from other barbiturates?

A

all other barbiturates are metabolized by the P450 hepatic enzymes

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51
Q

What is the gold standard drug for ECT?

A

Methohexital, it decreases the seizure threshold and produces a better quality seizure

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52
Q

Tell me about ketamine and Cardiovascular effects?

A

increases SNS tone thus it is helpful in a hemodynamically unstable patient but would be harmful if they have severe CAD.

Increases all cardiovascular measures (SNS tone, CO, HR, SVR, PVR) but is actually a myocardial depressant. The increases in all the cardiovascular markers require an intact SNS. The myocardial depressant effects will be unmasked in patients with depleted catecholamine stores such as sepsis or sympathectomy.

Increased PVR would not be good for someone with severe RV failure

53
Q

What is the pKa of dexmedetomidine and its solubility?

A

pKa = 7.1

water soluble

54
Q

Dexmedetomidine MOA?

A

Alpha 2 agonist which decreases cAMP and leads to inhibition of the locus coeruleus in the pons (sedation)

55
Q

What is the loading dose and maintenance infusion for dexmedetomidine?

A

loading dose: 1mcg/kg over 10 min.

maintenance infusion: 0.4-0.7 mcg/kg/min

56
Q

Onset of action of Precedex?

A

(with loading dose) 10-20 min.

57
Q

after Precedex infusion is stopped what is the duration?

A

10-30 min.

58
Q

How is Precedex cleared?

A

Liver (P450 enzyme)

59
Q

Most common side effects of Precedex?

A

Bradycardia and hypotension

60
Q

What might happen if you rapidly administer dexmedetomidine?

A

rapid administration can cause hypertension (alpha-2 stimulation in the vasculature leading to vasoconstriction). This direct effect occurs before the centrally mediated reduction in SNS tone. Once the CNS effect kicks in, the central alpha 2 effect will over power the peripheral alpha 2 effects. This explains why hypertension, if it occurs at all is short lived.

61
Q

Precedex and how it affects the respiratory system?

A

Does NOT cause resp. depression, no changes in respiratory anything.

62
Q

Produces sedation that resembles natural sleep describes?

A

Precedex

63
Q

Patient’s who should shiver don’t describes an effect of what drug?

A

Precedex

64
Q

Does Precedex have analgesic properties?

A

Yes, produced by alpha 2 stimulation on the dorsal horn of the spinal cord (decreased substance P and decreased glutamate release)

65
Q

In the formulation of a imidazole ring, if it is in an acidic pH what happens vs if it is in physiologic pH?

A

Acidic pH opens the imidazole ring and increases water solubility.

Physiologic pH closes the imidazole ring and increases lipid solubility

66
Q

MOA of benzodiazepines?

A

GABA A agonist which increases the FREQUENCY of channel opening causing neuronal hyperpolarization.

*most GABA -A agonists increase the channel open time BUT benzos increase open frequency.

67
Q

What is the IV induction dose of Versed vs the IV sedation dose of Versed?

A

induction: 0.1-0.4 mg/kg
sedation: 0.01-0.1 mg/kg

68
Q

What is the duration of Versed?

A

20-60 min.

69
Q

How is Versed cleared?

A

Liver (P450 enzymes)

Intestines (P450 enzymes)

70
Q

Does Versed have any active metabolites?

A

1-hydroxymidazelam

0.5x potency of midazolam

rapidly conjugated to an inactive compound

renal failure prolongs the effect of 1-hydroxymidazolam

71
Q

Midazolam effects on the CV, Resp. and CNS?

A

at sedation doses on average no effects are seen (unless you add opioids then you might see some respiratory depression at a sedation dose)

At induction doses you can see a decrease in BP, SVR, respiratory depression, decreased CMRO2 and decreased CBF

72
Q

Does Versed produce retrograde or anterograde amnesia?

A

anterograde amnesia (only amnesia after the drug is given)

73
Q

Does Versed have analgesic effects?

A

No

74
Q

Can versed produce isoelectric EEG?

A

No, but propofol and barbiturates can

75
Q

Name this drug: anticonvulsant
anxiolysis
spinally mediated skeletal muscle relaxation (antispasmodic - useful in patients with CP)

A

Versed (benzo)

76
Q

Drug that undergoes enterohepatic recirculation which explains why it stays in the body with a t 1/2 of 43 hours?

A

Diazepam

77
Q

How long does Lorazepam’s amnestic effects last?

A

up to 6 hours

78
Q

What limits lorazepam’s use as an anticonvulsant?

A

slow onset

fine if you are keeping seizures that may occur in time at bay such as DT’s

79
Q

rank from greatest to least the relative potency of the three major benzos?

A

lorazepam > midazolam > diazepam

80
Q

which benzos have propylene glycol added to them to increase water solubility?

A

diazepam and lorazepam which increases venous irritation

81
Q

Why does Midazolam ( versed ) not require propylene glycol added?

A

Versed contains an imidazole ring which makes it water soluble inside the vial and lipid soluble in the bloodstream

82
Q

What kind of drug is Flumazenil?

A

competitive antagonist of the GABA-A receptor

83
Q

What is the initial dose of flumazenil and how is it titrated?

A

Initial dose is 0.2 mg IV and it is titrated in 0.1 mg increments q 1 min.

84
Q

Why might you have to re-dose Flumazenil?

A

short duration of action (30-60 min)

85
Q

How is Flumazenil different from Narcan?

A

Narcan reverses opioids and flumazenil reverses benzos

Also, reversal of opioids can cause profound increase in SNS tone but post operative benzo reversal with flumazenil dose NOT increase SNS tone, anxiety or neuroendocrine evidence of stress.

86
Q

Why would you be cautious to use Flumazenil in a chronic benzo user?

A

chronic benzo users who are reversed with Flumazenil can have signs of withdrawal including seizures

87
Q

When you use Flumazenil to reverse a benzo, what effects of that benzo does flumazenil reverse more so than “other” effects?

A

tends to reverse the sedative effects more than the amnestic effects of a benzo

88
Q 
IV dosing of Ketamine:
Induction
Maintenance
Low dose infusion
Analgesia

IM
PO

A

Induction: 1-2mg/kg

Maintenance: 1-3 mg/kg

Low dose infusion: 1-3 mcg/kg/min (opioid sparing effect)

Analgesia: 0.1-0.5 mg/kg

IM: 4-8 mg/kg

PO: 10 mg/kg

89
Q

Is ketamine a lipid soluble solution or aqueous solution?

A

water soluble solution

90
Q

What is the pKa of ketamine?

A

7.5

91
Q

MOA of Ketamine?

A

NMDA receptor antagonist (antagonizes glutamate)

Secondary receptor targets: opioids, MAO, serotonin, NE, M, sodium channels

dissociates the thalamus (sensory) from the limbic system (awareness)

92
Q

What is the duration of Ketamine dose?

A

10-20 min but it may take 60-90 min. to return to full orientation

93
Q

How is Ketamine cleared?

A

Liver (P450 enzymes)

94
Q

What occurs in chronic ketamine use?

A

Chronic ketamine use induces the enzymes that metabolize it, this manifests as rapid escalation in tolerance.

95
Q

Does ketamine have any active metabolites?

A

Norketamine which is 1/3 to 1/5 the potency of ketamine and it is renally excreted

96
Q

If you give a sub hypnotic dose of ketamine will it activate the SNS?

A

usually it will not activate the SNS, this is doses less than 0.5 mg/kg

97
Q

Which induction agent can prevent opioid induced hyperalgesia after remifentanil infusion?

A

Ketamine

98
Q

What is the only induction medication that provides good analgesia and opioid sparing effect?

A

Ketamine

99
Q

Plasma binding of Ketamine?

A

12%

100
Q

Chronic ketamine use can not only induce the enzyme that breaks it down and cause tolerance, but it can also cause what GI issue?

A

Ulcerative colitis

101
Q

What is an off label use of Ketamine?

A

severe depression

102
Q

Would you want to use ketamine in chronic pain patients?

A

Yes, ketamine is good for chronic pain patients

103
Q

Relieves somatic pain greater than visceral pain describes which induction agent?

A

Ketamine

104
Q

Ketamine can increase EEG activity thus you would want to avoid ketamine use in patients who have a history of?

A

seizures

105
Q

Ketamine can cause emergence delirium, how would you try to avoid this side effect?

A

give a benzo with the ketamine (before/ during/ after) midazolam is better than diazepam.
The hallucinations and nightmares can last for up to 24 hours.

106
Q

What are the risk factors for ED with ketamine use?

A

age greater than 15, female gender, ketamine dose greater than 2 mg/kg, and hx of personality disorder

107
Q

What does ketamine do that would cause you to give glyco with it?

A

increases oral and pulmonary secretions

108
Q

If a patient is actively wheezing then what Induction medication can help with this?

A

Ketamine, it is a bronchodilator

109
Q

Etomidate has an imidazole ring, what does this mean?

A

that in acidic pH environment it is water soluble but in physiologic pH it is lipid soluble

110
Q

What is the key benefit of Etomidate?

A

hemodynamic stability, minimal changes in HR, SV, or CO.

SVR is decreased and this accounts for the SMALL reduction in BP.

111
Q

Does etomidate block the SNS response to laryngoscopy?

A

No, an opioid or esmolol will help

112
Q

Does etomidate provide analgesia?

A

No

113
Q

CPP =?

A

MAP -ICP

114
Q

Respiratory effects of Etomidate?

A

Mild resp. depression (less than propofol and barbiturates)

115
Q

What drugs belong to the class alkylphenol?

A

Propofol and fospropofol

116
Q

Ketamine belongs to what drug class?

A

Arylcyclohexylamine

117
Q

etomidate and dexmedetomidine have in common what?

A

both are imidazole compounds

118
Q

Which drugs cause pain on injection (that you would commonly give) and rank from most to least.

A

diazepam +++
Etomidate +++
Propofol ++
Lorazepam +

119
Q

Why do we not give diazepam or etomidate IM?

A

Irritating and can cause venous irritation and phlebitis (propylene glycol solvent does this)

120
Q

Egg Lecithin is found where?

A

It is in the egg yolk and NOT in the whites

121
Q

What is the primary pathway of etomidate metabolism?

A

Hydrolysis

122
Q

MOA of etomidate?

A

Etomidate enhances the ease of binding of GABA to the GABA A receptor in the Brian

123
Q

Anesthetic management for Acute Intermittent Porphyria?

A

liberal hydration
glucose supplementation
prevention of hypothermia

acute exacerbation is treated with glucose and heme arginate

124
Q

NMDA receptor agonist would be?

NMDA receptor antagonist would be?

A

agonist = glutamate

antagonist = ketamine, nitrous oxide, methadone

125
Q

Which receptor stimulates the “wind up” phenomenon?

A

NMDA and ketamine counteracts this process

126
Q

The NMDA receptor is an ion channel permeable to what electrolytes?

A

sodium
calcium
potassium

When the channel is open sodium and calcium enter and potassium leaves

127
Q

How does magnesium mediate pain transmission?

A

Magnesium acts as a plug inside the NMDA channel which explains how exogenous Mag. supplementation can mediate pain transmission

128
Q

Does Hypercarbia or Hypocarbia increase ICP?

A

Hypercarbia

129
Q

PO Ativan vs IV Ativan, what is the Cp therapeutic time frame?

A

PO = 24-48 hours

IV = 6-10 hours

APEX (18 decks)

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