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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
Lorazepam: dosing
50 mcg/kg or 1 - 4 mg
26
Methohexital: class
Barbiturate
27
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

Anesthesia Pharm Oral Exam (5 decks)

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