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Spring 2020 - Pharmacology 1 > Induction + Pain Management - Quiz 3 > Flashcards

Induction + Pain Management - Quiz 3 Flashcards

1
Q

Etomidate

A

Causes Hypnosis

No Pain Properties

Minimal CV Effects

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2
Q

Etomidate’s Chemical Structure

A

Carboxylated Imidazole

2 Isomers: R+ is active

PG Solvent

pH: 8.1

Only induction med that is NOT racemic mixture

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3
Q

Etomidate MOA

A

Potentiates GABAA mediated Chloride Shift

Act like Barbs at Higher Doses

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4
Q

Etomidate Pharmacokinetics

A
  • Rapid half-life, Rapid Total Clearance
  • Single Dose - extremely short duration (3-5 min)
  • Peak: 1 min
  • Protein Bound
  • 3 Compartment Model
  • Hepatic extraction
  • Minimal Buildup - can redose
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5
Q

What limits use of Etomidate

A

Transient Depression of Adrenocortical Function

  • Lasts 4-8 hrs.
  • Reversible
  • increased mortality in Septic/Hemorrhaging Pts.
  • Advantage: stress free anesthetic
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6
Q

Etomidate CNS Effects

A

Decreased CBF

Decreased CMRO2

Decreased ICP while maintaining CPP

Maintains cerebral vessel response to CO2

Decrease IOP

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7
Q

Etomidate CV Effects

A

CV stability - minimal changes

except

Pts. w/ aortic stenosis or mitral valve disease - significant drop in BP, PAP, PCWP

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8
Q

Etomidate Respiratory Effects

A

Decrease Minute Volume

Compensatory increase RR

Decrease ventilatory response to CO2

Apnea followed by Hyperventilation

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9
Q

Etomidate’s other effects

A

PONV

Does NOT effect duration of seizure

Myoclonic Jerks (decreased w/ prior opioid med)

No Histamine Release

Low Allergy Risk

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10
Q

Precedex

A

Highly Selective Alpha 2 Agonist

1600 : 1 - alpha2 : alpha 1

(220 : 1 for Clonidine)

Water Soluble

D-isomer is the Active Part

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11
Q

Precedex MOA

A

Negative Feedback on a2 receptors and makes a2 agonist effects

Sleep mimics Normal sleep

Pain Properties

Tolerance happens

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12
Q

Why is Clonidine sometimes used on kids?

A

Adjunct therapy for ADHD

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13
Q

Precedex Pharmacokinetics

A

Protein Bound

Rapid Hepatic Metabolization

Excreted in Urine & Bile

Rapidly Cleared

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14
Q

Precedex CNS Effects

A

Decrease CBF

No ICP Change

No CMRO2 Change

Decrease Plasma Catecholamine

Decrease MAC Requirement

Decrease need for Opioid

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15
Q

Precedex CV Effects

A

Moderate ↓HR & ↓SVR

Bolus may cause brief increase in BP & Bradycardia

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16
Q

Precedex Respiratory Effects

A

Small ↓Tidal Volume

No signifcant change in RR

No change to CO2 Response

Mild Airway Obstruction

Synergistic w/ other Sedatives

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17
Q

What is the max infusion time for Precedex per the package insert?

A

24 Hours

Still safe after 24hrs, but you might see lack of effect and changes in blood pressure.

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18
Q

Precedex Withdrawal

A

Upregulation of Receptors

An abrupt stop = accelerated HTN

Higher risk of HTN for pts who are already at risk.

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19
Q

General Anesthetics and Preggos

A
  • Black Box Warning: causes poor cognitive and school performance for the kid
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20
Q

General Anesthetics and Preggos:

American College of Ob/Gyn

A

Disagrees w/ Black Box Warning - Can’t generalize based on animal testing

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21
Q

General Anesthetics and Preggos

JAMA

A

Sibling Study: No adverse effects in child development

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22
Q

General Anesthetics and Preggos

MASK Trial

A

Single Exposure: No deficits

Secondary Exposure: Possible deficits in processing speeds and fine motor skills

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23
Q

Nociceptive Pain

A

Has obvious site of pain

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24
Q

Nociceptive Stimulation

A

Noxious Stimuli release neural chemicals that stimulate other nociceptors

  • Bradykinin, Substance P, Potassium, Histamine, Prostaglandin, Luekotriens
  • Transmits signal to Spinal Cord
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25
Q

Nociceptive Transmission

A

Action potential moves from stimuli site to dorsal horn of spinal cord, then CNS

  • Many pathways
  • A Fibers: large diameter, myelinated - sharp pain
  • C Fibers; small diameter, unmyelinated - dull, aching pain
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26
Q

What are released from the dorsal horn during nociceptive transmission?

A

Glutamate

Substance P

Calcitonin Peptide

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27
Q

Nociceptive Perceception

A

Conscious Pain Experience

Impulse relayed thru thalamus

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28
Q

Nociceptive Modulation

A

Impulse Inhibition via Brain Stem

  • Body’s opioid
  • Serotonin
  • Norepi
  • GABA
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29
Q

Neuropathic Pain

A

Does NOT follow pain cascade

Nerve Misfire

Never damage, Persistance Stimulation, Autonomic Dysfunction

Burning, tingling, shocks, hyperalgesia, headache

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30
Q

What is Chronic Pain

A

> 3 months or past the time of normal healing

20% of non cancer pts. receive opiods

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31
Q

Pain Monitoring

A
  • Provocative factors
  • Quality
  • Radiation
  • Severity
  • Temporal relations
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32
Q

Opiate Addiction

A

> 5 days = addiction risk

6% s/p minor surgery kept using opiates for at least 90 days

Increased addiction risk for middle age (45-64 yo)

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33
Q

Who are at risk for Inadequate Pain Control

A

Minorities

Women

Elderly

Cognitively Impaired

Cancer/EOL

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34
Q

Optimal Length of Opioid Scripts

A
  • General Surgery: 4-9 days
  • Women’s Health Procedures: 4-13 days
  • Musculoskeletal Procedures: 6-15 days
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35
Q

How does Esmolol work for pain?

A

Blunts cardiovascular effects of massive sympathetic outflow

Short half-life

36
Q

Location of Opioid Receptors

A

Brain

Spinal Cord

GI Tract

37
Q

What are the subtypes of Opioid Receptors

A

Delta

Kappa

Mu - primary

Nociceptive

38
Q

Delta Opioid Receptors

A

Brain & Peripheral Nerves

Analgesia, Antidepressant, Dependence

39
Q

Kappa Opioid Receptors

A

Brain, Spinal Cord, Periphery

Analgesia, Sedation, Miosis, Dysphoria, ADH Inhibition

Urinary Hesitance

40
Q

Mu Opioid Receptors

A

Brain, Spinal Cord, Periphery, Intestine

  • Mu1: Analgesia, Dependence
  • Mu2: Resp. depression, euphoria, reduced GI motility, dependence
  • Mu3: Unknown
41
Q

Nociceptive Opioid Receptors

A

Brain, Spinal Cord

Anxiety, Depression, Appetite, Tolerance to Mu Agonist

42
Q

How do Opiates Work

A

Presynaptic:

Binds to G-Coupled Proteins (2nd msgr) - Amplifies signal –> Inhibits Adenylate Cyclase –> lowers cAMP –> less Ca++ –> stops neurotransmitter release (stopping some pain signal)

Postsynaptic:

Glutamate can still bind, but opiate also binds here –> opens K+ channel for K+ release –> creates negative field –> glutmate unable to cause action d/t hyperpolarization

43
Q

NMDA Receptors & Opioids

A

Can reduce opioid effectiveness

Glutamate overstimulation = neuropathic pain

Methadone blocks NMDA

44
Q

Which structure form of Opioids have agonist action?

A

Levo Rotary Forms

45
Q

Are Opioids Ionized?

A

Yea, they gotta be to form a strong bond with the opioid receptor

(Lipophilic with an Ionized branch)

46
Q

How does codeine work?

A

Its a prodrug needing to be metabolized to turn into morphine.

47
Q

Morphine and Pain

A
  • Increases pain threshold and modifies pain perception
  • Works better for continuous dull pain vs sharp pain
  • Effective for visceral, skeletal, and skin pain
  • Most effective if given before surgical stimulus
  • Cause dysphoria if there is not pain
48
Q

Does morphine need to enter CNS to work?

A

No

49
Q

Morphine Metabolism

A

85%: M3G (Inactive)

10%: M6G (Active) & 100x more potent

Renal failure can cause M6G buildup

50
Q

Morphine CV Effects

A

Bradycardia

Reduced SNS Response

Histamine Release - itching, vasodilation

Orthostatic Hypotension

51
Q

Morphine Respiratory Effects

A

Dose dependent ventilatory depression

via

Mu2 Receptors

↓CO2 Response

↑Resting PaCO2

Asynchronous breathing + Cough Suppression

52
Q

Morphine CNS Effects

A

Careful with Head Injuries

Effects Wakefulness

Pupil Constriction

↑ICP

Broken Blood Brain Barrier increases morphine sensitivity

53
Q

How does pt’s EEG look on Morphine?

A

Looks like sleep w/ no seizure activity

54
Q

With Morphine, sedation happens ________ pain relief and is not equivalent.

A

BEFORE

55
Q

How does morphine effect the biliary tract?

A

Cause biliary spasms and increased pressure

56
Q

What can be used to treat opioid induced biliary spasms?

A

Glucagon 2mg IV

(normally used for bradycardia from beta blocker overdose)

57
Q

Morphine and GI Tract

A

Constipation

Biliary Colic

Delayed Emptying

NV from Chemoreceptor Trigger Zone Stimlulation

58
Q

How to treat Opioid Induced Constipation

A
  1. Senna, NOT Docusate
  2. Add 2-3 OTC laxatives
  3. Consider New Mu Antagonist
59
Q

Morphine GU Effects

A

Have to pee but cant

60
Q

Morphine Other Effects

A

No affect on NMB drugs

Rapid injection = chest rigidity

Exaggerated CNS depression w/ MAO inhibitors

61
Q

Dilaudid Vs Morphine

A

Synthetic and has no active metabolites

More Stable for Renal Dysfunction

No significant Histamine Release

62
Q

Fentanyl vs Morphine

A

More Potent

Faster Onset (Not Instant)

Shorter Duration

Protein Bound

More Lipophilic

63
Q

Fentanyl Pharmacokinetics

A

Redistributes to Inactive Tissues

Lungs store 75% of single dose

Stay in blood for a while d/t reuptake from inactive tissues

64
Q

Fentanyl Metabolism

A

Liver Enzymes

Norfentanyl Metabolite (limited activity)

Excreted in urine

Can be detected in urine for 72 hrs.

65
Q

Fentanyl CNS Effects

A

Modest ↑ICP

No Seizure

Low-Mod doses don’t effect evoked potentials

66
Q

Fentanyl CV Effects

A

Bradycardia

↓BP

↓CO

No Histamines

67
Q

Fentanyl Respiratory Effects

A

Persistent Ventilation Depression

Recurrent ventilation depression from second Peak

68
Q

What kind of drug interactions do Opioids have with Benzos?

A

Synergism

1+1 = 3

69
Q

Why is there less opioid plasma concentration in cardiopulmonary bypass?

A

Fentanyl sticks to the machine

70
Q

Intrathecal Fentanyl

A

Rapid

Profound Labor Pain Relief

71
Q

Oral Fentanyl (Actiq)

A

Used to reduce Pre-op Anxiety

and

Help with Induction

72
Q

Fentanyl Patch

A

Last 3 Days

Takes much longer for it to work

73
Q

Sufentanil vs Fentanyl

A

5-10x more Potent

Shorter Half Life than Fentanyl

74
Q

Sufentanil Metabolism

A

Liver Enzymes

Renal Dysnfunction = prolonged ventilation depression

75
Q

Sufentanil CNS Effects

A

↓CMRO2

↓CBF

76
Q

Sufentanil CV Effects

A

Bradycardia

↓CO

77
Q

Sufentanil Respiratory Effects

A

Ventilation Depression

Chest rigidity

78
Q

Alfentanil

A

1/5 - 1/10 as potent as Fentanyl

Short half-life

Fast effect-site equilibrium

Useful for ICU intubation, cardioversion, retrobulbar block

79
Q

Afentanil Metabolism

A

Highly Dependent on Liver

80
Q

Remifentanil

A

Selective Mu Agonist

Similar Potency to Fentanyl

Fast site equilibrium similiar to Alfentanil

Moderatly Lipophilic

Structurally Unique - Ester Link

81
Q

Remifentanil Pharmacokinetics

A

Very rapid Clearance - 3L/min

Works the same in all shapes and sizes of people

82
Q

Remifentanil Metabolism

A

Excreted by kidneys

6 minute half life

No buildup

Precisely Titratable

83
Q

Remifentanyl CNS Effects

A

No ICP/IOP Change

High Dose = ↓CMRO2 & ↓CBF

84
Q

Remifentanil CV Effects

A

Mild ↓HR

Mild ↓BP

No Histamine release

85
Q

Remifentanil Respiratory Effects

A

Ventilation Depression

Nausea and Vomiting

86
Q

Remifentamnil Tolerance

A

High Post-Op Analgesia requirement

Spring 2020 - Pharmacology 1 (11 decks)

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