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NGR6462 Pharm & Chem Anesthesia I > Induction Drugs > Flashcards

Induction Drugs Flashcards

1
Q

Gold standard for IV anesthetics

A

Barbs

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2
Q

barbituric acid is composed of

A

urea + malonic acid

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3
Q

Barbs: sedative & hypnotic properties are determined by alterations in which carbon atoms?

A

2 & #5

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4
Q

Name the oxybarbiturates

A

Methohexital
Phenobarbital
Pentobarbital
Secobarbital

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5
Q

The characteristic effect of methohexital due to methyl group on the nitrogen

A

Increased risk of excitatory phenomenon, seizures, and hiccoughs

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6
Q

The phenyl group at the #5 position for Phenobarbital leads to what drug effect?

A

increased anticonvulsant properties

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7
Q

How do pentobarbital and secobarbital differ in chemical structure from the other oxybarbiturates?

A

O2 atom at the #2 carbon atom

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8
Q

Name the two Thiobarbiturates.

A

Thiopental
Thiamylal

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9
Q

How does the chemical structure of thiobarbiturates differ, and what does this mean for the drug characteristics?

A

There is sulfur at the #2 carbon atom. This leads to increased lipid solubility and hypnotic potency.

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10
Q

Barbs MOA

A

Increase affinity for GABA. Barbs can also mimic GABA and activate chloride channels even with no GABA present.

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11
Q

How does the metabolism of oxybarbs and thiobarbs differ?

A

Oxybarbs = Liver
Thiobarbs = Liver, Kidney, Brain

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12
Q

Intra-arterial injection of which barb can lead to cyanosis and gangrene?

A

Thiobarb

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13
Q

What effect does sustained delivery of barbs have on liver enzymes, and which medication is the biggest culprit?

A

Liver enzymes are induced leading to increased metabolism of drugs. Phenobartibal is the most potent liver enzyme inducer.

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14
Q

Liver enzyme induction accelerates the metabolism of which drugs?

A

oral anticoagulants
phenytoin
TCA
corticosteroids
bile salts
vitamin K

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15
Q

What is Porphyria, and what drug class is avoided by patients presenting with it?

A

The autosomal dominant disease leads to defective heme metabolism. This leads to neurological damage, peripheral and autonomic neuropathies, and psychiatric manifestations.
Barbiturates should be avoided.

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16
Q

Why are barbiturates bad for patients with AIP?

A

Barbiturates accelerate heme production. AIP presents as a defect in heme metabolism which leads to excessive accumulation of heme, eventually leading to acute attacks and death.

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17
Q

Categorize the BZ by their elimination half-life.

A

Short: Midazolam
Intermediate: Lorazepam
Long: diazepam

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18
Q

T 1/2 of Midazolam?

A

<6 hours

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19
Q

T 1/2 of Lorazepam?

A

6-24 hours

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20
Q

T 1/2 of Diazepam?

A

24-37 hours

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21
Q

BZ MOA

A

BZ bind to GABBA-A receptors and modulates their activity (enhances affinity). GABA is required as BZ are unable to open chloride channels without them.

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22
Q

The imidazole ring found in BZ requires what state to increase lipid solubility, and under what circumstances does this occur?

A

Closed state, and occurs at physiological pH.

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23
Q

Which BZ are preferred for increased age and liver disease, and why?

A

Lorazepam, oxazepam, temazepam.
These are metabolized by glucuronidation, which is not effected by age or liver disease.

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24
Q

A symptom of BZ withdrawal in the elderly presents as what?

A

Confusion

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25
Q

Long-term use of BZ leads to two significant things in the patient population.

A

Tolerance & cognitive decline

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26
Q

BZ produce more _____ than sedation.

A

amnesia

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27
Q

PO administration of which drug has a high first-pass hepatic extraction.

A

Midazolam

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28
Q

Drugs that inhibit CYP450 enzymes and prolong metabolism include (5).

A

Fentanyl
Erythromycin
CCB
Antifungals
Cimetidine

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29
Q

CNS effects include anterograde amnesia.

A

Midazolam

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30
Q

Respiratory effects of Midazolam

A

decreased TV
increased RR

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31
Q

May increase cardiac output in CHF patients.

A

Midazolam

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32
Q

Modest CV effects include decreased ABP and increased HR.

A

Midazolam

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33
Q

Most common preoperative sedative in adults and children.

A

Midazolam

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34
Q

Used prophylactically to raise seizure threshold when performing regional blocks

A

BZ

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35
Q

Avoid this bz medication in pregnant patients

A

Midazolam

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36
Q

Po administration results in 100% bioavailability.

A

Diazepam

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37
Q

Mixing with NS or water for dilution results in cloudiness.

A

Diazepam

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38
Q

This medication crosses the placenta, resulting in fetal concentrations equal to or greater than the mother

A

Diazepam

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39
Q

Which active metabolite of a BZ contributes to sustained drug effects and return of drowsiness 6-8 hours after administration?

A

Desmethyldiazepam

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40
Q

Which drug can decrease LVED pressure with small doses?

A

Diazepam

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41
Q

Minimal CV effects with this drug. They equate to natural sleep.

A

Diazepam

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42
Q

Used to produce skeletal muscle relaxation in lumbar disc disease.

A

Diazepam

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43
Q

This BZ is the most potent sedative and amnesic.

A

Lorazepam

44
Q

BZ with a slower onset due to lower lipid solubility.

A

Lorazepam

45
Q

This is the only BZ that has no active metabolites.

A

Lorazepam

46
Q

Contraindicated in patients on antiepileptic drugs.

A

Flumazenil

47
Q

Propofol induction dose

A

1.5-2.5mg/kg

48
Q

Propofol onset of action

A

30 seconds

49
Q

This drug promotes bacterial growth

A

Propofol

50
Q

This drug contains metabisulfate, known to exacerbate asthma and trigger sulfate allergies.

A

Generic propofol

51
Q

This drug is a low lipid emulsion that is preservative-free, however, there remains significant pain with injection

A

Ampofol

52
Q

This drug produces formaldehyde byproducts leading to perineum burning.

A

Fospropofol

53
Q

A propofol syringe needs discarding after how many hours?

A

6

54
Q

The mixing of what two drugs lead to fat emboli

A

Propofol + Lidocaine

55
Q

Propofol pKa

A

11

56
Q

Propofol EHL

A

0.5-1.5 hours

57
Q

Propofol Vd

A

1000-4000 L

58
Q

How is the induction dose of propofol adjusted for elderly patients, and why?

A

Decrease the dose by 25-50%. Elderly patients have experience increased drug effects and decreased clearance of the drug.

59
Q

Off-Label uses for Propofol

A

Antiemetic
Antipruritic
Anticonvulsant
diminish bronchoconstriction

60
Q

Which drug contains a preservative resulting in allergies and bronchoconstriction.

A

Propofol (Diprivan)

61
Q

Propofol: MAC v. GA dosages

A

MAC: 25-100mcg/kg/min
GA: 100-300mcg/kg/min

62
Q

Hypnosis with Propfol lasts how long?

A

5-10 minutes

63
Q

Propofol respiratory effects

A

decreased TV, RR, and response to hypoxia

64
Q

How does a propofol dose of 2-2.5mcg/kg impact CV.

A

40% drop in BP, CO, SVR, and reduced myocardial consumption.

65
Q

Propofol CV effects

A

decreased BP, HR unchanged, blunted baroreceptor reflex

66
Q

What is propofol infusion syndrome?

A

high doses of propofol + steroids = multi-organ failure, AKI (rhabdo)

67
Q

Etomidate pKa

A

4.24

68
Q

Etomidate induction dose

A

0.2-0.4mg/kg

69
Q

Etomidate has two isomeric forms. Which isomer has hypnotic/sedative properties?

A

S (+)

70
Q

Etomidate metabolism

A

Liver enzymes & plasma esterases

71
Q

Flumazenil has no effect on this non-barb drug.

A

Etomidate

72
Q

Etomidate EHL

A

2-5 hours

73
Q

Etomidate: special CNS considerations

A

It causes myoclonus and may activate seizures.

74
Q

Drug known for its hemodynamic stability

A

Etomidate

75
Q

Etomidate respiratory effects

A

decreased TV, increased RR, decreased response to CO2, hiccoughs, emergence excitement

76
Q

High incidence of PONV

A

Etomidate

77
Q

Good drug to use for patients with reactive airway disease.

A

Etomidate

78
Q

First choice drug category for alcohol detox.

A

BZ

79
Q

Ketamine induction dose

A

1-2mg/kg

80
Q

Only agent producing dissociate anesthesia

A

Ketamine

81
Q

Drug contains potent analgesic properties

A

Ketamine

82
Q

Ketamine pKa

A

7.5

83
Q

This drug is not extensively protein-bound, unlike other induction agents.

A

Ketamine

84
Q

Commercial preparations given as a racemic mixture

A

Ketamine

85
Q

Ketamine EHL

A

2-3 hours

86
Q

What are the effects of norketamine?

A

1/3-1/5 potency, which leads to prolonged drug effects

87
Q

Ketamine MOA

A

NMDA antagonist
minor GABA action

88
Q

Suppresses inflammatory mediators which improve blood flow

A

Ketamine

89
Q

Ketamine CNS effects

A

increase CBF, CMRO2, ICP
antidepressant, potentiates NDNMB, emergence delirium, nystagmus

90
Q

Emergence delirium with Ketamine is more prevelent in what patient population?

A

Women 15 years of age and older with a history of personality disorder or dreaming, and with doses of 2mg/kg or more.

91
Q

What can attenuate emergence delirium seen with Ketamine?

A

Midazolam

92
Q

Ketamine respiratory effects

A

Bronchodilation
increased secretions

93
Q

Ketamine CV effects

A

increased BP, HR, CO
release of NE, and inhibits uptake
increased PVR and RV workload

94
Q

It acts as a direct myocardial depressant and is not recommended for patients with CAD.

A

Ketamine

95
Q

Ketamine LOC

A

30-60 seconds

96
Q

Ketamine return of consciousness time v. return of awareness

A

consciousness 10-20minutes
awareness 60-90 minutes

97
Q

Ketamine chemical compound is a derivative of?

A

PCP

98
Q

Chronic Ketamine use causes what metabolic phenomenon to occur?

A

Enzyme induction which quickens the metabolism of ketamine leading to drug tolerance

99
Q

Dexmedetomidine MOA

A

Alpha 2 adrenergic agonist

100
Q

Decreased SNS activity seen with dexmedetomidine is caused by?

A

Decrease in NE levels

101
Q

Dexmedetomidine EHL

A

2-3 hours

102
Q

Dexmedetomidine dosing

A

Loading: 1mcg/kg (10min)
maintenance: 0.2-1mcg/kg/hr

103
Q

Dexmedetomidine adverse effects

A

hypotension
hypertension (loading phase)
Nausea
Bradycardia
Anemia
Hypothermia

104
Q

Exercise extreme cause in using this drug with patients diagnosed with severe heart block and/or severe ventricular dysfunction.

A

Dexmedetomidine

105
Q

Dexmedetomidine: CSHF of a 4 min infusion v. a 250 min infusion

A

4 min = 10 min
250 min = 8 hours

NGR6462 Pharm & Chem Anesthesia I (4 decks)

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