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Anesthesia Pharm Oral Exam > Core Anesthesia Drugs 1: benzos, barbs, antimuscarinics > Flashcards

Core Anesthesia Drugs 1: benzos, barbs, antimuscarinics Flashcards

1
Q

Diazepam: class

A

Benzodiazepine

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2
Q

Diazepam: MoA

A

Increases the affinity for GABA at GABA receptors.

The binding of GABA to the receptor causes the opening of the Cl- channel allowing influx into the cell. Because the channel remains open, this hyperpolarizes the post synaptic membrane.

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3
Q

Diazepam: PK

A 
Onset: rapid
DoA: 6-8hrs
98% PB (albumin)
Vd 1L/kg
Highly lipid soluble
E1/2t = 20-50hrs
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4
Q

Diazepam: metabolism

A

CYP450 metabolism in the liver.

3 metabolites. 1 active metabolite: desmethydiazepam = half life of 48-96hrs. Leads to hangover effect.

Metabolites excreted in the urine.

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5
Q

Diazepam: AE

A 
ALL BENZOS:
Decreased CBF, CMRO2 Decreased EEG
Does not attenuate response to DVL
Paradoxical excitement (rare) 
*Dose dependent resp depression
Minimal decrease in SVR and increase in HR

Diazepam-specific:
Pain on injection
Fatigue, dry mouth, nausea

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6
Q

Diazepam: CI

A 
Hypersensitivity
Pregnancy
Glaucoma
Reduce dose in elderly
Caution when hypoalbuminemia from hepatic or renal disease
Severe hypotension
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7
Q

Diazepam: drug interactions

A

Most highly protein bound benzo

Reversal: flumazenil

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8
Q

Diazepam: dosing

A
  1. 3 - 0.6 mg/kg IV induction

2. 5 - 10 mg IV in 0.5-2mg increments

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9
Q

Midazolam: structure

A

Imidazole ring

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10
Q

Midazolam: class

A

Benzodiazepine

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11
Q

Midazolam: MoA

A

Increases the affinity for GABA at GABA receptors.

The binding of GABA to the receptor causes the opening of the Cl- channel allowing influx into the cell. Because the channel remains open, this hyperpolarizes the post synaptic membrane.

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12
Q

Midazolam: PK

A 
Onset: 30 - 60 sec 
Peak: 3 - 5 min
DoA: 30 - 90 mins
E1/2t: 1 - 4 hrs
94% protein bound
Vd: 1.5 L/kg
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13
Q

Midazolam: metabolism

A

CYP450 metabolism

Renal excretion

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14
Q

Midazolam: AE

A 
ALL BENZOS:
Decreased CBF, CMRO2 Decreased EEG
Does not attenuate response to DVL
Paradoxical excitement (rare) 
*Dose dependent resp depression
Minimal decrease in SVR and increase in HR

Midazolam specific:
Depresses gag reflex (good for endo)

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15
Q

Midazolam: CI

A 
Hypersensitivity
Pregnancy
glaucoma
Reduce dose in elderly
Caution with hypoalbuminemia in hepatic or renal pts
Severe hypotension
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16
Q

Midazolam: drug interactions

A

Additive effect with opioids
Reversed with flumazenil
No hangover effect
Great for beir blocks – if local anesthetic toxicity – already have benzo on board

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17
Q

Midazolam: dosing

A

0.5 - 5mg IV

or 0.04-0.08mg/kg IV

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18
Q

Lorazepam: class

A

Benzodiazepine

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19
Q

Lorazepam: MoA

A

Increases the affinity for GABA at GABA receptors.

The binding of GABA to the receptor causes the opening of the Cl- channel allowing influx into the cell. Because the channel remains open, this hyperpolarizes the post synaptic membrane.

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20
Q

Lorazepam: PK

A 
Onset: rapid 1 - 2mins
DoA: 10 - 20 hrs
E1/2t: 10 - 20hr
80% PB (albumin)
Highly lipid soluble
Vd: 1L/kg
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21
Q

Lorazepam: metabolism

A

CYP450 metabolism

Renal excretion

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22
Q

Lorazepam: AE

A 
ALL BENZOS:
Decreased CBF, CMRO2 Decreased EEG
Does not attenuate response to DVL
Paradoxical excitement (rare) 
*Dose dependent resp depression
Minimal decrease in SVR and increase in HR

Lorazepam-specific:
Pain on injection/thrombophlebitis
Platelet aggregating inhibition (long term)

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23
Q

Lorazepam: CI

A 
Hypersensitivity
Pregnancy
Glaucoma
Reduce dose in elderly
Caution with hypoalbuminemai in hepatic or renal pts
Severe hypotension
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24
Q

Lorazepam: drug interactions

A

Additive effect with opioid
Reversed with FLUMAZENIL
NO hangover

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25
Q

Lorazepam: dosing

A

50 mcg/kg or 1 - 4 mg

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26
Q

Methohexital: class

A

Barbiturate

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27
Q

Methohexital: structure

A

Has a methyl radical, which contributes to convulsant activity

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28
Q

Methohexital: MoA

A

Decreases the rate of dissociation from GABA receptor. Increases duration of chloride channel remaining open and allowing Cl- to flow into the cell. This hyperpolarizes the cell and makes it more difficult to create a neuronal transmission.

Suppresses RAS and enhances sleep
↓ transmission in sympathetic ganglion
↓ post synaptic membrane sensitivity to ACh

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29
Q

Methohexital: PK

A 
Onset: rapid
DoA: 5-10 minutes
E1/2t: 4 hrs
Vd: 2L/kg
Highly lipid soluble
70% PB
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30
Q

Methohexital: metabolism

A

Hepatic metabolism

Renal/fecal elimination

31
Q

Methohexital: AE

A

*Induces seizures
*Myoclonus
*Hiccups/cough/laryngospasm
Reflex tachycardia
Decreased CBF, ICP and CMRO2
Histamine release
Dose dependent resp depression
Pain on injection
Decreased threshold for pain
CYP450 inducer

32
Q

Methohexital: CI

A

Seizure history
Pregnancy
Porphyria!
Asthma

33
Q

Methohexital: drug interactions

A

CYP450 inducer; may need frequent NMB redosing

Will precipitate in LR

34
Q

Methohexital: dosing

A

1 - 2 mg/kg IV

35
Q

Thiopental: class

A

Barbiturate

36
Q

Thiopental: structure

A

Sulfur at carbon #2

37
Q

Thiopental: MoA

A

Decreases the rate of dissociation from GABA receptor. Increases duration of chloride channel remaining open and allowing Cl- to flow into the cell. This hyperpolarizes the cell and makes it more difficult to create a neuronal transmission.

Suppresses RAS and enhances Sleep
↓transmission in sympathetic ganglion
↓post synaptic membrane sensitivity to ACh

38
Q

Thiopental: PK

A 
Onset: rapid
E1/2t: 12 hrs
Vd: 2.5 L/kg
Highly lipid soluble
80% PB (albumin)
39
Q

Thiopental: metabolism

A

CYP450 to hydroxythipental (10-20%).

Metabolites excreted in urine.

40
Q

Thiopental: AE

A 
Reflex tachycardia
Decreased CBF, ICP and CMRO2
Isoelectric EEG
Histamine release
Dose dependent resp depression
Pain on injection
Decreased threshold for pain
N/V
41
Q

Thiopental: CI

A

Pregnancy
Porphyria
Asthma

42
Q

Thiopental: drug interactions

A

CYP450 inducer; expect increased NMB redosing

Decrease dose 30% in 1st trimester, elderly

43
Q

Thiopental: dosing

A

3 - 5mg/kg IV

44
Q

Phenobarbital: class

A

Barbiturate

45
Q

Phenobarbital: structure

A

Phenyl group at carbon #5

46
Q

Phenobarbital: MoA

A

Decreases the rate of dissociation from GABA receptor. Increases duration of chloride channel remaining open and allowing Cl- to flow into the cell. This hyperpolarizes the cell and makes it more difficult to create a neuronal transmission.

Suppresses RAS and enhances sleep
Causes drowsiness and decreases motor activity

47
Q

Phenobarbital: PK

A

*Onset: 5 mins
*Peak: 30 mins
*DoA: 4 - 10 hrs
*E1/2t: 54 - 170 hrs
40% PB

48
Q

Phenobarbital: metabolism

A

CYP450 metabolism with 60% unchanged in urine

49
Q

Phenobarbital: AE

A 
Reflex tachycardia
Decreased CBF, ICP and CMRO2, isoelectric EEG
Dose dependent resp depression
Pain on injection
Decreased threshold for pain
N/V

Specific to phenobarb:
Bone marrow suppression
Agranulocytosis, thrombocytopenia, megaloblastic anemia
Hepatotoxicity
Stevens Johnson syndrome
Ataxia
**Intra arterial injection can cause loss of limb.

50
Q

Phenobarbital: CI

A

Severe liver disease
Porphyria
Pregnancy

51
Q

Phenobarbital: drug interactions

A

STRONG CYP450 inducer!!

Will precipitate in LR

52
Q

Phenobarbital: dosing

A

10-20 mg/kg

Then 5 mg/kg q 15-30mins until seizure controlled

Max of 30 mg/kg

53
Q

Atropine: class

A

Tertiary amine muscarinic receptor antagonist

54
Q

Atropine: MoA

A

Competitively and reversibly bind to muscarinic receptors to inhibit binding of Ach allowing sympathetic response to dominate

Antagonizes histamine and serotonin

55
Q

Atropine: PK

A 
Onset: 1 min
DOA: 30 - 60 mins
E1/2t: 2-3 hrs
Vd: 1.5L/kg
Highly lipid soluble
40% PB
56
Q

Atropine: metabolism

A

Hepatic metabolism

18% unchanged in the urine

57
Q

Atropine: AE

A 
Blurry vision
Pupillary dilation
↑ IOP
Delirium
Sedation/hallucinations/disorientation
Dry mouth
Increased HR and CO
Urinary retention and constipation
58
Q

Atropine: CI

A 
Glaucoma
CAD
Pheochromocytoma
Thyrotoxicosis
Hyperpyrexia
Mobitz II
GI obstruction
AchE therapy
59
Q

Atropine: dosing

A

Bradycardia: 0.4 - 1 mg IV

Reversal for edrophonium: 0.01 mg/kg IV

Resuscitation: 1 mg IV up to 3 mg

60
Q

Scopolamine: class

A

Tertiary amine muscarinic receptor antagonist

61
Q

Scopolamine: MoA

A

Competitively and reversibly bind to muscarinic receptors to inhibit binding of Ach, preventing the action on parasympathetic systems and allowing sympathetic response to dominate

62
Q

Scopolamine: PK

A 
Onset: 10 mins
DOA: 2 hrs
E1/2t: 4.8 hrs (3-7 days for full recovery)
Vd: crosses BBB, placenta
PB: reversibly binds, % unknown
63
Q

Scopolamine: metabolism

A

Hepatic metabolism

Renal excretion

64
Q

Scopolamine: AE

A 
*Sedation and weakness
V-fib
Increased HR
Orthostatic hypotension
Delayed awakening
Increased IOP
Blurry vision
Dry mouth and constipation
65
Q

Scopolamine: CI

A 
Hypersensitivity
Liver disease
AMS
Glaucoma
CAD
Pheochromocytoma
Thryotoxicosis
Myasthenia gravis
66
Q

Scopolamine: dosing

A

0.3-0.6mg IV Q4-6 hours

67
Q

Glycopyrrolate: class

A

Quaternary amine muscarinic receptor antagonist

68
Q

Glycopyrrolate: MoA

A

Reversible competitive blockade of Ach at muscarinic receptors. Allows sympathetic response to dominate.

69
Q

Glycopyrrolate: PK

A

Onset = 3-5mins
DOA = 2-4 hrs
E1/2 t = 1.5hrs
Vd = 0.4L/kg

70
Q

Glycopyrrolate: metabolism

A

Hepatic metabolism with 85% unchanged in the urine

71
Q

Glycopyrrolate: AE

A 
Blurred vision
Dry mouth
PVC and tachycardia
Dysrhythmias
N/V
Ileus and constipation
**Malignant hyperthermia
Headache
72
Q

Glycopyrrolate: CI

A 
Hypersensitivity
Infants
CAD
Renal disease!
Hyperthyroid
Hx of MH
Pheochromocytoma
73
Q

Glycopyrrolate: dosing

A

Antisialagogue or bradycardia: 0.1 - 0.2 mg IV

Reversal with neostigmine: 0.01 mg/kg IV

Anesthesia Pharm Oral Exam (5 decks)

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