Core Anesthesia Drugs 1: benzos, barbs, antimuscarinics Flashcards Preview

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

Flashcards in Core Anesthesia Drugs 1: benzos, barbs, antimuscarinics Deck (73):
1

Diazepam: class

Benzodiazepine

2

Diazepam: MoA

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.

3

Diazepam: PK

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

4

Diazepam: metabolism

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.

5

Diazepam: AE

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

6

Diazepam: CI

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

7

Diazepam: drug interactions

Most highly protein bound benzo
Reversal: flumazenil

8

Diazepam: dosing

0.3 - 0.6 mg/kg IV induction

2.5 - 10 mg IV in 0.5-2mg increments

9

Midazolam: structure

Imidazole ring

10

Midazolam: class

Benzodiazepine

11

Midazolam: MoA

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.

12

Midazolam: PK

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

13

Midazolam: metabolism

CYP450 metabolism
Renal excretion

14

Midazolam: AE

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)

15

Midazolam: CI

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

16

Midazolam: drug interactions

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

17

Midazolam: dosing

0.5 - 5mg IV

(or 0.04-0.08mg/kg IV)

18

Lorazepam: class

Benzodiazepine

19

Lorazepam: MoA

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.

20

Lorazepam: PK

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

21

Lorazepam: metabolism

CYP450 metabolism
Renal excretion

22

Lorazepam: AE

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)

23

Lorazepam: CI

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

24

Lorazepam: drug interactions

Additive effect with opioid
Reversed with FLUMAZENIL
NO hangover

25

Lorazepam: dosing

50 mcg/kg or 1 - 4 mg

26

Methohexital: class

Barbiturate

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Methohexital: structure

Has a methyl radical, which contributes to convulsant activity

28

Methohexital: MoA

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

29

Methohexital: PK

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

30

Methohexital: metabolism

Hepatic metabolism
Renal/fecal elimination

31

Methohexital: AE

*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

Methohexital: CI

Seizure history
Pregnancy
Porphyria!
Asthma

33

Methohexital: drug interactions

CYP450 inducer; may need frequent NMB redosing
Will precipitate in LR

34

Methohexital: dosing

1 - 2 mg/kg IV

35

Thiopental: class

Barbiturate

36

Thiopental: structure

Sulfur at carbon #2

37

Thiopental: MoA

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

Thiopental: PK

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

39

Thiopental: metabolism

CYP450 to hydroxythipental (10-20%).
Metabolites excreted in urine.

40

Thiopental: AE

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

Thiopental: CI

Pregnancy
Porphyria
Asthma

42

Thiopental: drug interactions

CYP450 inducer; expect increased NMB redosing
Decrease dose 30% in 1st trimester, elderly

43

Thiopental: dosing

3 - 5mg/kg IV

44

Phenobarbital: class

Barbiturate

45

Phenobarbital: structure

Phenyl group at carbon #5

46

Phenobarbital: MoA

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

Phenobarbital: PK

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

48

Phenobarbital: metabolism

CYP450 metabolism with 60% unchanged in urine

49

Phenobarbital: AE

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

Phenobarbital: CI

Severe liver disease
Porphyria
Pregnancy

51

Phenobarbital: drug interactions

STRONG CYP450 inducer!!
Will precipitate in LR

52

Phenobarbital: dosing

10-20 mg/kg

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

Max of 30 mg/kg

53

Atropine: class

Tertiary amine muscarinic receptor antagonist

54

Atropine: MoA

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

Antagonizes histamine and serotonin

55

Atropine: PK

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

56

Atropine: metabolism

Hepatic metabolism
18% unchanged in the urine

57

Atropine: AE

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

58

Atropine: CI

Glaucoma
CAD
Pheochromocytoma
Thyrotoxicosis
Hyperpyrexia
Mobitz II
GI obstruction
AchE therapy

59

Atropine: dosing

Bradycardia: 0.4 - 1 mg IV

Reversal for edrophonium: 0.01 mg/kg IV

Resuscitation: 1 mg IV up to 3 mg

60

Scopolamine: class

Tertiary amine muscarinic receptor antagonist

61

Scopolamine: MoA

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

Scopolamine: PK

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

Scopolamine: metabolism

Hepatic metabolism
Renal excretion

64

Scopolamine: AE

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

65

Scopolamine: CI

Hypersensitivity
Liver disease
AMS
Glaucoma
CAD
Pheochromocytoma
Thryotoxicosis
Myasthenia gravis

66

Scopolamine: dosing

0.3-0.6mg IV Q4-6 hours

67

Glycopyrrolate: class

Quaternary amine muscarinic receptor antagonist

68

Glycopyrrolate: MoA

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

69

Glycopyrrolate: PK

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

70

Glycopyrrolate: metabolism

Hepatic metabolism with 85% unchanged in the urine

71

Glycopyrrolate: AE

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

72

Glycopyrrolate: CI

Hypersensitivity
Infants
CAD
Renal disease!
Hyperthyroid
Hx of MH
Pheochromocytoma

73

Glycopyrrolate: dosing

Antisialagogue or bradycardia: 0.1 - 0.2 mg IV

Reversal with neostigmine: 0.01 mg/kg IV