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Spring 2020 - Pharmacology 1 > Induction Agents - Quiz 2 > Flashcards

Induction Agents - Quiz 2 Flashcards

1
Q

What helps moves neurotransmitters to the endplate to release itself to the synapse then to the receptor?

A

Calciuim

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2
Q

What is broken down to form GABA

A

Glutamate

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3
Q

What kind of an effect does the GABA Agonist have?

A

Inhibitory Neurotransmitter

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4
Q

How does Glutamate work?

A

Released by calcium –> binds with NMDA –> Influx of Positively charged ions

Excitatory Effect

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5
Q

How can the effects of Glutamate be blocked?

A

Ketamine - Noncompetitive Antagonist

(also rapid antidepressant)

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6
Q

How does the Alpha2 Receptor Negative Feedback Loop Work?

A

Excess Norepi binds to presynaptic alpha2 receptor and inhibits release of Norepi

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7
Q

How does Precedex work?

A

Binds to presynaptic alpha2 receptors, blocking release of Norepi = sedation

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8
Q

Location of Baroreceptors

A

Aortic Arch, Carotid Body - signals travel to medulla and regulate heart rate, arterial, and venous tone according MAP

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9
Q

What nerves do baroreceptor impules travel through?

A

Vagus, Glossopharyngeal, and Hering’s

Action: Inhibits/Stimulates sympathetic/parasympathetic system

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10
Q

Central Chemoreceptors

A

Respond to pH and CO2 changes

(Peripheral Chemoreceptors responds to O2)

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11
Q

Advantages of IV Anesthesia

A

Rapid onset of General Anesthesia (30 sec - 1 min)

Can be used for maintenance of General Anesthesia

Provides sedation for MAC

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12
Q

How long does it normally take for a patient to wake back up from induction meds?

A

9 Minutes

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13
Q

Disadvantages of IV Anesthesia

A

There is no ONE med that provides hypnosis, amnesia, analgesia, and immobility.

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14
Q

What is Balanced Anesthesia

A

Use of Multiple drugs

  • Inhalation agents
  • IV induction agents
  • Sedative/Hypnotic
  • Opioids
  • Neuromuscular Blockade
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15
Q

Are IV Induction Agents hydrophilic or lipophilic?

A

All are Lipophilic - for rapid onset in brain and spinal cord

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16
Q

Body Mass % of Normal Adult

A
  • Vessel Rich: 10%
  • Vessel Poor: 20%
  • Fat: 20%
  • Muscle: 50%
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17
Q

Blood Flow % of Cardiac Output

A
  • Vessel Rich: 75%
  • Vessel Poor: <1%
  • Fat: 6%
  • Muscle: 19%
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18
Q

How is the effect of a Single Dose of IV Induction agent stopped?

A

Distribution, Not Metabolism

Drug redistributed to less perfused tissues: vessel rich & poor

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19
Q

When does metabolism of IV Induction medications come into play?

A

When multiple doses are given and when there’s a buildup of the drug

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20
Q

IV Bolus Three Compartment Model

A

Med goes to general circulation –> distributes to vessel rich organs –> rapid redistribution to vessel poor (shallow) –> slow distribution to peripheral compartments (deep) –> metabolism

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21
Q

What are the vessel rich organs?

A

Brain

Liver

Kidneys

Gut

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22
Q

What are the Vessel Poor Organs

A

Shallow Compartment

Muscles

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23
Q

What is part of the Deep Compartment?

A

Fat

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24
Q

In what phase does distrbution last for 2-4 minutes?

A

Rapid distribution phase to vessel poor group

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25
Q

List classes of IV Induction Agents

A

Barbiturates
Benzos
Propofol
Ketamine
Etomidate
Precedex

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26
Q

Barbiturates

A

1930’s - Oldest Class

Sedative, Hypnotic, Anticonvulsant

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27
Q

Chemical Structure of Barbiturates

A

Barbituric Acid - lacks CNS Activity

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28
Q

How do hypnotic, sedative, and anticonvulsive effects occur regarding barbituric acid?

A

Subbing on N1, C2, C5 sites

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29
Q

Why do myoclonic jerks occur when bolus dose of induction agent is given?

A

Body’s natural response to bolus of inhibition = Sympathetic outflow

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30
Q

Barbiturate MOA

A

Acts with GABA to enhance profound hyperpolarization

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31
Q

What are GABA-mimetic effects?

A

Barbiturates dont need GABA with higher doses as opposed to Benzos

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32
Q

How does plasma albumin effect barbiturate binding?

A

Decreased albumin causes higher unbound barbs

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33
Q

What causes higher unbound fraction of barbiturate?

A

Decreased plasma protein concentration

  • Uremia
  • Liver disease
  • 3rd Trimester
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34
Q

What drugs compete with Barbiturates?

A

Aspirin

Naproxen

Indomethacin

Warfarin

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35
Q

Pharmacokinetics of Barbiturates

A

3 Compartment Model

Redistribution has major effect on duration

Metabolism

Inactive metabolites excreted in urine

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36
Q

CNS Effects of Barbiturates

A
  • Rapid Loss of Consciousness
  • Significant post anesthesia drowsiness
  • No pain management properties
  • Decrease in O2 Consumption (CMRO2)
  • Decrease Cerebral Blood FLow
  • Decrease ICP & IOP
  • Anticonsulvant Properties
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37
Q

Barbiturates CV Effects

A
  • Decrease Medullary vasomotor center
  • Decrease Sympathetic system
  • Decrease BP d/t vasodilation (transient)
  • Compensatory Increase in HR
  • Decreased venous return
38
Q

When are exaggerated hypotensive responses seen with Barbiturates?

A

Hypovolemia

Cardiac Tamponade

Cardiomyopathy

CAD

Valvular Disease

Large Induction Dose

Rapid Drug Injection

39
Q

Barbiturate Respiratory Effects

A
  • Dose related respiratory depression
  • Laryngo/Bronchospasm
  • Transient apnea
  • Decrease stimulation by CO2 to breath
  • Laryngeal reflex/cough reflex suppression
40
Q

Barbiturate Anaphylaxis

A
  • Cause histamine release -> vasodilation
  • 1 in 30,000
  • Tissue necrosis if injected not in vein
  • Immunosuppression
41
Q

What happens if you inject barbiturates in the artery?

A

Immediate Vasospasm and Constriction

Intense Pain

Entire Extremity Blanching

Ischemic Gangrene

42
Q

How to treat arterial injection of Barbiturates

A
  • Dilute with injection of NS through same site
  • Treat vasospam with Papaverine 40-80mcg
  • Stellate or Brachial Plexus block to increase flow to extremity
  • Systemic Heparin
43
Q

Absolute Contraindications to Barbiturates

A
  • History of Allergic Reaction
  • History of Porphyria - Less than 20,000/yr
    • Autonomic System Disturbance
    • Abd Pain
    • Skin Lesions
    • HTN
    • Tachycardia
    • Seizures
44
Q

Benzo Drugs

A

Librium

Diazepam

Serax

Ativan

Versed

45
Q

Benzo MOA

A

Activates GABA Receptor

Big Influx of Chloride Ions - Hyperpolarizes

Versed has greater potency & affinity for GABA

2-3x more than diazepam

46
Q

Why are Benzos used more in clinical Situations

A

Broad scope of properties with low side effect profile

  • Anxiolitic - amygdala, hippocampus, limbic
  • Sedation - brainstem & cortical receptors
  • Muscle relaxation - spine
  • Amnesia - Forebrain & hippocampus
47
Q

Benzo Vs. Bariburates

A

Less abuse potential

Bigger margin of safety

Less significant drug interactions

Dont induce liver enzymes

48
Q

Imidazole Ring of Versed

A
  • Open at pH:4
  • Closed > pH 4 = lipophilic = rapid onset
49
Q

Versed Pharmacokinetics

A

Highly protein bound

Rapid onset, but slow effect site equilibrium

CYP substrate

Urinary excretion

50
Q

Benzo CNS Effects

A

Decreased CMRO2

Decreased CBF

CANNOT make isoelectric EEG

No ICP change

Anticonvulsant

Paradoxical excitement in < 1%

51
Q

Benzo CV Effects

A

Decreased BP (Versed > Diazepam)

Cardiac Output unchanged

Does NOT prevent sympathetic response to intubation

52
Q

Benzo Respiratory Effects

A

Same as Barbiturates

53
Q

Benzo Side Effects

A
  • Allergic rxns rare
  • Pain on injection - ativan, diazepam
  • NonRestorative sleep
  • Anterograde Amnesia
54
Q

Benzo and Barb Withdrawal

A

Lasts weeks to months

Anxiety, insomnia, seizures, coma, agitation, psychosis, mania, suicide

HTN, Tachycardia, Postural Hypotension

55
Q

Benzo & Barb Overdose

A

Resp. depression, hypotension, coma, confusion

Use supportive therapy first before reversing

56
Q

What is the reversal for only Benzo Overdose

A

Flumazenil - competitive antagonist

200 mcg q1-2 min, max 3mg/hr

May cause immediate withdrawal

57
Q

Remimazolam

A

Metabolism via Esterases

Rapid Clearance - may only stay in 1st or 2nd compartment

Less Buildup

58
Q

Propofol

A

Most frequently used for induction

Needs lipid vehicle so it doesnt separate out

Supports bacterial growth

59
Q

Propofol Reformulations

A

Swtched from EDTA to Sodium Metabisulfite

Anaphylaxis and Asthmatic Episodes

60
Q

Propofol MOA

A

Acts on GABA receptors

61
Q

Propofol Pharmacokinetics

A

Rapid Onset

Rapid Return of Consciousness (3-10 Min)

Rapid Clearance - less hangover

3 Compartments

CYP Substrate & Inhibitor

62
Q

Propofol CNS Effects

A

Same as Benzos and Barbz

63
Q

Propofol CV Effects

A

Profound dereased BP - afterload & preload

Dramatic Inhibition of Baroreceptor Reflex

Profound Bradycardia

64
Q

How does Propofol supress apoptosis and inflammation

A

Structurally looks like Vitamin E

65
Q

Propofol Respiratory Effects

A
  • Potent respiratory depressant
  • Apnea after induction dose
  • Decreased response to CO2 and O2
  • Big reduction in airway reflexes
  • Less risk of laryngo and bronchospasms than barbs
66
Q

Other Propofol Effects

A
  • Anti-emetic (10mcg/kg/min)
  • Does not potentiate muscle relaxants
  • Injection Pain - stay way from hand
  • Elevated triglycerides
  • Risk for PE
  • Antipyretic
  • Antioxidant
67
Q

Propofol Infusion Syndrome

A

Lactic Acidosis for use > 48 hrs or 67mcg/kg/min

Unexpected Tachycardia

Hepatomegaly

68
Q

How do you treat Propofol Infusion Syndrome

A

Stop infusion

Treat acidosis

Support multi-system failure

69
Q

How does propofol infusion syndrome present in kids?

A

Anion Gap Acidosis

Bradyarrhythmia

Rhabdo

Liver Dysfunction

MODS

Hyperkalemia

AKI

70
Q

How does Propofol work in kids’ bodies

A
  • Enters mitochondria easily, stops ATP production, and stops fatty acid metabolism = fatty acid buildup
  • Carb deficiency makes kids more prone to these problems
71
Q

Fospropofol (Lusedra)

A

Water Soluble Produg of Propofol

no need for lipid vehicle

72
Q

Fospropofol vs. Propofol

A

Slower Onset

Stronger & Longer Duration

More Itching & Paresthesia

Less Pain on Injection

Doesnt enter CNS until metabolized

73
Q

Ketamine

A

Dissociative Anesthesia

EEG Dissociation b/t thalamocortical & limbic

Pt. Non Communcative

Blank stare

Limited skeletal movement

74
Q

What does ketamine do well and dont do well?

A

Great pain control

but

No complete amnesia, needs a benzo

Emergence Delerium - reduced by benzo

75
Q

Ketamin’s chemical structure is similiar to what?

A

PCP

Partially water soluble

S-enantiomer (Ketanest) is more potent, but cost $$$$$$$

76
Q

Ketamine MOA

A

NMDA Noncompetitive Receptor Antagonist

Inhibits C++ Influx

Weak action on GABA

May effect opioid, muscuranic, and monoaminergic receptors

77
Q

How does Ketamine produce its analgesic effects?

A

Inhibits Nitric Oxide Synthase

78
Q

How does Ketamine stimulate Sympathetic system?

A

Inhibits Catecholamine Reuptake

79
Q

How does Ketamine produce Beta-2 agonism and respiratory relaxation?

A

Induces Catecholamine Release

80
Q

Ketamine Pharmcokinetics

A

Not really bound to plasma proteins

Leaves blood fast to be distributed to tissues

Extremely lipophilic

3 Compartment Model

81
Q

Metabolism of Ketamine

A

Really metabolized by liver enzymes

Demethylation of ketamine to norketamine

82
Q

What is Norketamine

A

Active Metabolite of Ketamine

  • 1/3 - 1/5 as potent
  • contributes to prolonged effects of ketamine
  • Hydroxylated then conjugated into water soluble inactive metabolites
83
Q

Ketamine CNS Effects

A

Increases CBF

Increases CMRO2

Used for seizures if other meds fail

May cause myoclonic jerks

84
Q

Ketamine CV Effects

A

Direct Myocardia Depressant

Produces significant transient Increases in BP, HR, CO

Increased Cardiac Metabolic Requirment for Oxygen

85
Q

Ketamine Respiratory Effects

A

No Respiratory Depression

Respiratory response to CO2 present

Transient hypoventilation

Relaxes bronchial smooth muscle

Increased Salivation

86
Q

Ketamine Side Effects

A

Emergence Reactions: 10-30%

Vivid Dreams, Out of Body Experience, Hallucinations

Can last hours

Nystagmus

87
Q

What is the half-life of Flumazenil

A

1 Hour

88
Q

Where do barbs bind on the GABA receptor?

A

Between GABAB and GABAY

89
Q

Where do Benzos Bind on the GABA Receptor

A

Between GABAa and GABAY

90
Q

Where do GABA Neurotransmitters bind on the GABA Receptor

A

Between GABAa and GABAB

Spring 2020 - Pharmacology 1 (11 decks)

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