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Advanced Pharmacology ANE 8433 (Spring 2023) > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What is transduction?

A

Nerve/electrical impulses/signals start at the nerve endings. Damaged or not

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2
Q

What is transmission?

A

Travel of nerve/electrical impulses to the nerve body connecting to the dorsal horn of the spinal cord.

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3
Q

Where do peripheral nerve blocks work?

A

At the dorsal horn

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4
Q

What is modulation?

A

Process of altering (inhibitory/excitatory) pain transmission mechanisms at the dorsal horn to the PNS and CNS.

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5
Q

What are the locations of nociceptors?

A

Skin, muscles, joint, viscera, vascular

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6
Q

Describe unmyelinated & myelinated fibers?

A
  • Unmyelinated; C-fibers, burning pain from heat & pressure, travel at <2m/s.
  • Myelinated: Aβ & Aδ fibers, conduct heat, mechanical, chemical pain signals. Aδ fibers conduct fast heat pain. Travels >2m/s
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7
Q

What are the first chemical pain mediators?

A

Peptides: (Substance P, Calcitonin, Bradykinin, CGRP)

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8
Q

List chemical mediator groups?

A

Peptides, Eicosanoids, Lipids, Neutrophins, Cytokines, Chemokines, Extracellular proteases & protons

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9
Q

List all Lipid chemical mediators?

A
  • Prostaglandins
  • Thromboxanes
  • Leukotrienes
  • Endocannabinoids
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10
Q

List all receptors & Ion channels?

A

Dorsal Root Ganglion & Peripheral Terminals, Purinergic, Metabotropic, Glutamatergic, Tachykinin, TRPV I, Neurotrophic, Ion channels

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11
Q

Describe Hyperalgesia & Allodynia?

A
  • Hyperalgesia: Increased pain sensations to normally painful stimuli.
  • Allodynia: Perception of pain sensations in response to normally non-painful stimuli.
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12
Q

What is primary hyperalgesia & its 4 categories?

A
  • Pain at the original site of injury from heat and mechanical injury.
  • Decreased pain threshold, Increased response to suprathreshold stimuli, Spontaneous pain, Expansion of receptive field
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13
Q

What is Secondary Hyperalgesia?

A

Uninjured skin surrounding the injury (only from mechanical stimuli like pressure, inflammation). Sensitization of central neuronal circuits

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14
Q

Which Lamina do opioids work on?

A

Lamina II (substantia gelatinosa), on the afferent C-fibers

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15
Q

Which Laminae send innervating muscles & visceral pain?

A

Laminae I, IV, VII, & ventral horn

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16
Q

Which Lamia send substance P?

A

Laminae III & IV

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17
Q

Which Laminae are targeted for spinals & epidurals?

A

Laminae III & IV

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18
Q

Which laminae contains NKI receptors?

A

Laminae III & IV

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19
Q

Explain the Gate control theory of pain?

A

The gate is open & Aδ (small diameter, myelinated) & C fibers (unmyelinated) send pain signals. Then Aβ fibers (large diameter, myelinated: faster) deliver information about pressure and touch (rubbing) overriding Aδ signals.

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20
Q

What do the Periaqueductal gray -rostral ventromedial medulla (PAG-RVM) system do?

A

Depress or facilitate the integration of pain info in the spinal dorsal horn towards limbic cortex & thalamus.

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21
Q

List all Neuromodulators & which one is used by ketamine?

A
  • Substance P,
  • Glutamate
  • CGRP
  • NMDA (ketamine)
  • AMPA
  • BDNF
  • Cytokines
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22
Q

Injured tissues release what?

A

Nociceptors (Substance P & Glutamate)

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23
Q

Damaged cells, mast cells, and platelets release what mediators?

A

Bradykinin, Histamine, Prostaglandins, Serotonin, Hydrogen ion, Lactic acid

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24
Q

List all excitatory & inhibitory spinal modulators?

A
  • Excitatory: Glutamate, Calcitonin, Neuropeptide Y, Aspartate, Substance P.
  • Inhibitory: GABA, Glycine, Enkephalins, Norepinephrine, Dopamine
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25
Q

List the 4 ascending pathways of nociceptive information?

A
  • Spinothalamic
  • Spinomedullary
  • Spinobulbar
  • Spinohypothalamic
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26
Q

What is send thru the Spinothalamic pathway & which laminae are used?

A

Pain, temperature, and itch (Laminae I, VII, & VIII: All afferent fibers)

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27
Q

What is send thru the Spinobulbar pathway & which laminae are used?

A

Behavior toward pain (Laminae I, V, VII)

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28
Q

What is send thru the Spinohypothalamic pathway & which laminae are used?

A

Autonomic, neuroendocrine, and emotional aspects of pain (Laminae I, V, VII, & X)

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29
Q

What are the 6 Supra-spinal modulation of nociception areas?

A

Forebrain S1 & S2, Anterior cingulate cortex (ACC), Insular cortex (IC), ACC and IC, Prefrontal cortex, Thalamus, Cerebellum

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30
Q

What does the forebrain process?

A

Location & intensity of pain

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31
Q

What does the Insular cortex (IC) process?

A

Emotional & motivational aspects

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32
Q

Where do descending inhibitory tracts originate & its pathway?

A

Periaqueductal gray through the rostal ventromedial medulla (RVM) –> dorsolateral funiculus –> synapse in dorsal horn

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33
Q

What are the descending inhibitory neurotransmitters?

A

Endorphins, enkephalins, serotonin

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34
Q

What fibers & how are they affected during descending inhibition?

A

Hyperpolarize Aδ & C fibers, Decrease release of substance P. Opening of K+ channels/inhibition of Ca2+ channels.

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35
Q

What are the 2 Descending pathways of pain modulation?

A

Descending Inhibition Pathway (DI) & Descending Facilitation Pathway (DF)

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36
Q

What receptors are used by the PAG-RVM systems?

A

µ, κ, δ opioid receptors

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37
Q

Where does the pain impulse originate if it is pertaining to the descending inhibitory tract?

A

PAG-RVM

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38
Q

What is the Primary Objective for pain?

A

Tissue healing without repeated injury.

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39
Q

What are the time frames for Acute & Chronic pain?

A
  • Acute: days to weeks after injury.
  • Chronic: >3-6 months, persists beyond tissue healing
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40
Q

What is Neuropathic pain, who is at increased risk & what is the treatment?

A

Persists after the tissue has healed ➔ allodynia and hyperalgesia Increased risk: Cancer patients d/t chemo and radiation therapy Treatment: symptomatic (opioids gabapentin, amitryptiline, cannabis)

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41
Q

Describe Visceral pain & its causes?

A

Diffuse & poorly localized (referred to somatic sites: muscle & skin) –> CT scan. Causes: ischemia, stretching of ligamentous attachments, spasms, distention.

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42
Q

What is Complex Regional Pain Syndrome & examples?

A
  • A variety of painful conditions following injury in a region with impairment of sensory, motor, and autonomic systems.
  • Examples: Spontaneous pain, allodynia, hyperalgesia, edema, autonomic abnormalities, active and passive movement disorders, and trophic changes of skin & SQ tissues.
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43
Q

Describe pain in Neonate and Infant?

A

Pain perception starts at 23 weeks of gestation. Lower pain threshold & exaggerated pain responses.

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44
Q

Describe the cardiovascular response to pain?

A

Prominent: Hypertension, Tachycardia, Myocardial irritability, ↑ SVR, Compromised LV –> decreased CO, Myocardial ischemia

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45
Q

Describe the Pulmonary Response to pain?

A

↑ total body O2 consumption/CO2 production, ↑ Vm and work of breathing, Splinting, Decreased movement of chest wall, Atelectasis, Intrapulmonary shunting (VQ mismatch). Impaired coughing

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46
Q

Describe the GI/GU response to pain?

A

Enhanced sympathetic tone:↑ sphincter tone, and ↓ motility –> Ileus & Urinary retention. Hypersecretion of stomach acid –> Stress ulceration, Aspiration & Increased gastric contents. N/V & Abdominal distention

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47
Q

Describe the endocrine response to pain?

A

↑ catabolic hormones: Catecholamines, Cortisol & Glucagon.
↓ anabolic hormones: Insulin & Testosterone.
Effects: Negative nitrogen balance, Carbohydrate intolerance & Increases renin, aldosterone, angiotensin

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48
Q

Describe the Hematologic response to pain?

A

Stress related –> Plt adhesiveness, reduced fibrinolysis & hypercoagulability

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49
Q

Describe the emotional & immune responses to pain?

A
  • Emotional: Anxiety, sleep disturbances, depression.
  • Immune: Stress related Leukocytosis & depressed Reticuloendothelial system –> increased infection
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50
Q

What medication classes work @ perception & what is the MOA?

A
  • Meds: Opioids, alpha 2-agonists, general anesthetics.
  • MOA: activate descending inhibitory pain pathways & memory.
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51
Q

What medication classes work @ Modulation & what is the MOA?

A
  • Meds: Local anesthetics, opioids, ketamine, & alpha 2-agonists.
  • MOA: modulation of afferent signals in the dorsal horn of spinal cord & production of reflex reaction.
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52
Q

What medication classes work @ Transmission & what is the MOA?

A

Local anesthetics & transmission of action potentials via Aδ & C fibers

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53
Q

What medication classes work @ Transduction & what is the MOA?

A
  • Meds: Local anesthetics, NSAIDs.
  • MOA: transduction of mechanical, chemical & thermal stimuli into an action potential.
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54
Q

Delineate the pathway of pain signals?

A

Stimuli –> dorsal horn –> afferent thru medulla –> thru midbrain –> thalmic nuclei –> forebrain.

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55
Q

What two populations have a higher fat component?

A

Geriatric & older women

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56
Q

What is myoclonus & what drug has a high incidence of it?

A

Involuntary movements, be careful before giving more meds. & Etomidate

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57
Q

When is Etomidate water soluble & lipid soluble?

A

Water soluble at acidic pH & lipid soluble at physiologic pH.

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58
Q

What structure does only Etomidate have?

A

Carboxylated imidazole

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59
Q

What is the MOA of Etomidate?

A

Selective modulator of GABA-a receptors

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60
Q

What are the pharmacokinetics of Etomidate (Onset, clearance, metabolism, elimination, excretion)?

A
  • Onset= within 1min IV. 76% Albumin bound, Large Vd.
  • Clearance is 5x faster than Thiopental= prompt awakening.
  • Metabolism: Hydrolysis by hepatic microsomal enzynmes & plasma esterases.
  • Elimination: 85% urine & 10-13% in bile.
  • E ½ time: 2-5hrs
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61
Q

How long should someone not drive after Etomidate?

A

24hrs

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62
Q

What is the IV dose for Etomidate?

A

0.3mg/kg

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63
Q

When is Etomidate especially useful?

A

In Pt’s with unstable CV systems & little to no cardiac reserve

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64
Q

What type of med must/should be given in conjunction with Etomidate for induction?

A

Opioids as Etomidate does not have analgesic effects

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65
Q

What are the CV side effects of Etomidate?

A
  • Minimal changes to HR, SV, CO & contractility.
  • Mild decrease in MAP d/t decreased SVR.
  • Sudden hypotension with hypovolemia especially with high 0.45mg/kg induction doses.
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66
Q

What are Etomidate’s ventilation side effects?

A
  • Less depressant than barbs. Apnea with rapid injection.
  • Transient 3-5mins decreased Vt, offset by increased RR.
  • Stimulates CO2 medullary centers.
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67
Q

What is the MOA of Gabapentin?

A

Binds to V-G calcium channels —> enhances descending inhibition & inhibits excitatory neurotransmitter release

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68
Q

Gabapentin is lipid soluble/nonsoluble & binds/does not bind to protein?

A

Soluble & does not bind

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69
Q

What are the drug interactions with gabapentin?

A

None

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70
Q

What is the Pre-op dose for gabapentin?

A

300-1200 mg PO 1-2hrs prior to Sx

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71
Q

What are Gabapentin’s contraindications?

A

MG, myoclonus

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72
Q

What are the side effects of Gabapentin?

A

Somnolence,
fatigue
ataxia
vertigo
constipation
abrupt withdrawal in seizure Pts
weight gain

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73
Q

What are the MOA, dose, peak, duration & C/I of ofirmev?

A
  • MOA: reduces prostaglandin metabolites
  • Dose: 1000mg Q4-6hr Max 3000-4000mg QD.
  • Peak: IV 30-60mins & 1-3hrs PO
  • Duration: 6-8hrs C/I: hepatic dysfunction
74
Q

What are the MOA, dose, peak of ketorolac?

A
  • MOA: inhibits PG synthesis by inhibiting COX1 & 2
  • Dose: 15-30mg Q6h Max 60-120mg QD
  • Peak: 45-60mins
75
Q

What are the contraindications of ketorolac?

A

Severe renal impairment
bleeding
CAD
CABG
pregnancy
NSAID allergy

76
Q

What are the MOA, dose, peak & excretion of ibuprofen?

A
  • MOA: anti-inflammatory, analgesic, antipyretic (inhibits COX1 & 2)
  • Dose: 200-800mg IV over 30mins Q6H Max 3200mg QD.
  • Peak: 1-2hrs.
  • Excretion: urine & bile
77
Q

What are the contraindications of ibuprofen?

A

NSAID allergy
CABG
bleeding ulcers

78
Q

What is the MOA of Magnesium?

A
  • Anti-nociceptive effects
  • NMDA receptor antagonist
  • Regulates calcium access into cell, neurotransmission, cell signaling & enzyme function.
79
Q

What are the contraindications for magnesium?

A
  • MG
  • renal failure
80
Q

What is the dose for lidocaine & when is it stopped?

A
  • 1-2mg/kg IV (initial bolus) over 2-4mins
  • Then 1-2 mg/kg/hr (Qtt)
  • Stopped in 12-72hrs
81
Q

What is monitored with lidocaine infusions?

A
  • Cardiac
  • hepatic
  • renal dysfunction
82
Q

What are the first signs of lidocaine toxicity?

A
  • Tinnitus
  • circum-oral numbness
  • muscle twitching
  • hypotension
  • myocardial depression
83
Q

What is the magnesium pre-op dose?

A

50mg/kg IV

84
Q

What is the magnesium intraop dose?

A

8 mg/kg/hr

85
Q

Magnesium significantly reduces the use of?

86
Q

What is the plasma ½ life of Zofran?

87
Q

What is the pediatrics dose for Zofran?

A

0.1 mg/kg IV

88
Q

What increases the effectiveness of Zofran?

A

Corticosteroids

89
Q

What is the MOA of decadron?

A
  • Anti-inflammatory
  • Inhibition of phospholipase
  • Cytokines
90
Q

What are the equilibration times for Fentanyl, Sufentanil, Alfentanil & remifentanil?

A

6.8mins
6.2mins
1.4mins
1.1mins

91
Q

Which opioid agonists have the lowest & highest clearance in ml/min?

A

Lowest= Alfentanil
Highest= Remifentanil

92
Q

Which opioid agonists have the lowest & highest % nonionized?

A

Lowest= Meperidine (7)
Highest= Alfentanil (89)

93
Q

What are the opioid effects on Mu1 receptors?

A

Analgesia
bradycardia
euphoria
hypothermia
miosis
urinary retention
low abuse potential

94
Q

What are the opioid effects on Mu2 receptors?

A
  • Dependence
  • ventilation depression
  • constipation
  • Analgesia
95
Q

What are the opioid effects on Kappa receptors?

A
  • Analgesia
  • dysphoria
  • diuresis
  • low abuse potential
  • miosis
  • sedation
96
Q

What are the opioid effects on Delta receptors?

A
  • Analgesia,
  • ventilation depression
  • dependence
  • constipation
  • urinary retention
97
Q

What are the Mu1 receptor agonists?

A

Endorphins, morphine, synthetic opioids

98
Q

What are the Mu2 receptor agonists?

A

Endorphins, morphine, synthetic opioids

99
Q

What are the Kappa receptor agonists?

A

Dynorphins

100
Q

What are the Delta receptor agonists?

A

Enkephalins

101
Q

What are the Mu1, Mu2, Kappa & Delta receptor antagonists?

A

Naloxone, naltrexone, nalmefene

102
Q

What are the uses for naloxone?

A
  • Opioid OD
  • dependence
  • hypovolemic/septic shock,
  • can reverse general anesthesia with high doses.
103
Q

What are the Naloxone doses for Intraop & post op?

A

Intraop & Postop= 40-80mcg

104
Q

What are the onset & duration of action of naloxone?

A
  • Onset= 1-5mins
  • Duration= 30-45mins
105
Q

What are the side effects of naloxone?

A
  • N/V
  • crosses placenta
  • increased SNS
  • pulmonary edema
  • dysrhythmias (V-fib)
106
Q

What is the use & duration of Naltrexone?

A

Used for alcoholism & duration is 24hrs PO

107
Q

What is the dose & E1/2 time of Nalmefene?

A
  • Dose: 15-25mcg IV
  • E 1/2: 10.8hrs
108
Q

What is methylnaltrexone used for?

A

Gastric emptying, antagonizes N/V, & in peripheral

109
Q

Which opioid antagonist does not reverse centrally mediated analgesia?

A

Methylnaltrexone

110
Q

What receptors does Alvimopan affect?

111
Q

What is Alvimopan used for?

A

Post-op ileus

112
Q

Where is Alvimopan metabolized?

113
Q

What are Alvimopan’s limitations?

A

Longterm use can lead to CV events

114
Q

What is Suboxone?

A
  • Buprenorphine plus naloxone
  • Su(b)o(xone)= b=buprenorphine; xone= naloxone
115
Q

What is Embeda?

A
  • Extended release morphine plus naltrexone
  • (E)(m)beda= E=xtended & m=morphine
116
Q

What is OxyNal?

A

Oxycodone plus naltrexone

117
Q

Sufentanil, Alfentanil, & Remifentanil decrease MAC by how much?

A

Sufentanil= 70-90%, Alfentanil= 70%, Remifentanil= 50-91%

118
Q

Butorphanol, Nalbuphine, & Pentazocine reduce MAC by how much?

A
  • Butorphanol= 11%
  • Nalbuphine= 8%
  • Pentazocine= 20%
119
Q

What is the main receptor for opioids in the spinal cord?

A

Substantia gelatinosa (laminae 2)

120
Q

Why is epinephrine used in epidurals?

A

To avoid systemic absorption through the venous plexi

121
Q

What are the epidural CSF peak times for fentanyl & sufentanil & morphine?

A
  • Fentanyl= 20mins
  • Sufentanil= 6mins
  • morphine= 1-4hrs
122
Q

What are the epidural plasma peak times for morphine, fentanyl & sufentanil?

A
  • Morphine= 10-15mins
  • Fentanyl= 5-10mins
  • Sufentanil= <5mins
123
Q

What are the intraop & post op doses for morphine?

A
  • Intraop= 1-10mg
  • Postop= 5-20mg
124
Q

What are the onset, peak & duration of morphine?

A
  • Onset= 10-20mins
  • Peak= 15-30mins
  • Duration= 4-5hrs
125
Q

What is the intraop dose for fentanyl?

A

Intraop= 1.5-3 mcg/kg

126
Q

What are the onset & duration of fentanyl?

A
  • Onset= 30-60sec
  • Duration 1-1.5hrs
127
Q

What is the intraop dose for sufentanil?

A

0.3-1mcg/kg

128
Q

What are the onset & duration of sufentanil?

A
  • Onset= 30-60sec
  • Duration= 1-1.5hrs
129
Q

What are the intraop & postop dose for hydromorphone?

A
  • Intraop= 1-4mg
  • Postop= 1.5-4mg
130
Q

What are the onset & duration of hydromorphone?

A
  • Onset= 5-15mins
  • Duration= 2-4hrs
131
Q

What is the infusion rate for sufentanil?

A

0.5-1 mcg/kg/hr

132
Q

What is the infusion rate for Remifentanil?

A

0.125-1mcg/kg/hr

133
Q

What is the intraop dose for Remifentanil?

A

0.5-1mcg/kg/hr

134
Q

What are the onset & duration of Remifentanil?

A
  • Onset= 30-60sec
  • Duration=6-8mins
135
Q

What is the duration of meperidine?

136
Q

What are the effects of meperidine?

A
  • Sedation
  • euphoria
  • N/V
  • ventilation depression
137
Q

What is the E1/2 time for meperidine?

A

3-5hrs (35hrs with renal failure)

138
Q

What are the toxicities of meperidine?

A
  • Delirium
  • myoclonus
  • seizures
139
Q

Which opioid receptor causes Diuresis?

140
Q

Which opioid receptors cause urinary retention?

A

Mu1 & Delta

141
Q

Which opioid receptors cause constipation?

A

Mu2 (marked) & Delta (minimal)

142
Q

Which opioid receptors have a low abuse potential?

A

Mu1 & Kappa

143
Q

What are the advantages of opioid agonist-antagonists?

A
  • Analgesia
  • low ventilation depression
  • low dependence
  • ceiling effect
144
Q

What are the intrathecal/CSF times of fentanyl, sufentanil & morphine?

A
  • Fentanyl & sufentanil are minimal &
  • morphine= 1-5hrs
145
Q

What is the most common side effect of neuraxial opioids & the cause?

A
  • Pruritus in the face, neck & upper thorax.
  • Caused by cephalad migration to trigeminal nucleus
146
Q

What are the treatments for neuraxial pruritus?

A
  • Naloxone
  • antihistamines
  • propofol
  • gabapentin
147
Q

What are the side effects of neuraxial opioids?

A
  • Ventilation depression (from 2 to 12hrs)
  • Depressed LOC from hypercarbia, sedation
  • CNS excitation (tonic skeletal muscle rigidity like seizures)
  • Herpes reactivation (2-5 days after epidural
  • Neonatal morbidity (negligible in breast milk)
148
Q

What is the onset, Vd, metabolism, elimination & E1/2 time for Etomidate?

A
  • Onset: 1min
  • Vd: Large w/ prompt awakening
  • Metabolism: Hydrolysis by hepatic enzymes & plasma esterases
  • Elimination: 85% urine, rest in bile
  • E1/2 time: 2-5hrs
149
Q

What is the dose for etomidate?

150
Q

When is it wise to use etomidate & what else must be given?

A
  • Has no or little CV effects
  • Must give opioid in conjunction
151
Q

What are the side effects of Etomidate?

A
  • Myoclonic movements
  • alteration of inhibitory & excitatory thalamocortical tract (balance)
  • attenuated by opioids or benzos
  • caution in seizure patients
  • adrenocortical suppression
152
Q

Who should not receive etomidate & why?

A
  • Septic or hemorrhaging Pt’s due to inhibition of cholesterol to cortisol conversion –> severe hypotension, longer ventilation.
  • Inhibition can last 4-8hrs.
153
Q

What are the CNS side effects of etomidate?

A
  • Decreased CBF & CMRO2 (direct cerebral vasoconstrictor, decreased ICP)
  • EEG changes (excitatory spikes) may activate foci seizure
154
Q

What are the CV effects of etomidate?

A
  • Minimal decrease in MAP d/t decreased SVR.
  • Sudden hypotension w/ hypovolemia w/ high >0.45mg/kg induction doses
155
Q

What are etomidate’s ventilation side effects?

A
  • Apnea with rapid injection, transient 3-5mins decrease in Vt, stimulates CO2 medullary center
156
Q

Ketamine is derived from?

A

Phencyclidine

157
Q

Ketamine causes amnesia & intense___?

158
Q

What does someone look like that received ketamine?

A
  • Noncommunicative but wakefulness
  • hypertonus & purposeful skeletal muscle movements
159
Q

What are ketamine’s advantages & disadvantages over propofol & etomidate?

A
  • Advantage: no injection pain, profound analgesia.
  • Disadvantage: frequency of emergence delirium, abuse potential
160
Q

What is ketamine’s preservative?

A

Benzethonium chloride

161
Q

What are the benefits of S-ketamine?

A
  • More analgesia (2x> racemic, 4x> R isomer)
  • more rapid metabolism & recovery
  • less salivation
  • lower incidence of emergence reactions.
162
Q

What are the benefits of racemic ketamine?

A
  • Less fatigue
  • less cognitive impairment
163
Q

Which receptors does ketamine bind to?

A
  • Noncompetitively to NMDA
  • All opioid receptors
  • muscarinic
  • V-G Na+ & L-type calcium channels
  • neuronal nACh
  • GABAa receptors.
164
Q

What are ketamine’s CNS side effects?

A
  • Potent cerebral vasodilator
  • no increase in ICP
  • Myoclonus
  • Does not alter seizure threshold
165
Q

What are ketamine’s CV side effects?

A
  • SNS like stimulation –> increases plasma Epi & Norepinephrine levels, which is blunted by benzos or inhaled anesthetics.
166
Q

What does it mean if someone has a sudden drop in SBP & CO after ketamine & what do you do?

A
  • Depleted catecholamine stores.
  • Give Neo
167
Q

Fentanyl decreases MAC by how much?

A

50% for Isoflurane & desflurane

168
Q

Who should NOT receive propofol (6)?

A
  • Hypovolemic Pt’s
  • Pt’s w/ compromised LV function
  • Pediatric strabismus Sx d/t increased incidence of oculocardiac reflex
  • Bradycardic Pt’s unless treating w/ direct beta agonist
  • Pt’s w/ Hx of allergies to soy, glycerin, yolk lecithin & Na+ edetate d/t bronchoconstriction
  • Parkinson’s Pt undergoing stereotactic neurosurgery d/t temporary abolition of tremors
169
Q

Who should/can receive propofol?
What does propofol not affect?

A
  • Renal dysfunction d/t no influence on clearance
  • Cirrhosis. Similar to alcoholics
  • Pregnant – crosses placenta but rapidly cleared
  • Malignant hyperthermia Pt’s
  • Asthmatics d/t bronchodilation effects
  • Pt’s with seizures
  • Pt’s w/ Hx of PONV
  • Pt’s with gastric emptying issues as it does not inhibit emptying but also not a prokinetic
  • Neuraxial pruritis
  • Pt’s w/ increased ICP d/t decrease in CMRO2 & CBF
  • Pt’s w/ abnormal rhythms d/t lack of effect on SA & AV nodes
  • Pt’s undergoing laparoscopic Sx d/t decreasing intraocular pressure
  • Acute lung injury d/t peroxynitrite-scavenging activity of propofol
  • CABG Pt’s d/t attenuation of lipid peroxidation
170
Q

Pt’s with what kind of diseases or disorders should NOT receive ketamine (5 should not & 4 are possible but need other interventions)?

A
  • Pulmonary HTN
  • Increased ICP, increases CBF & CRMO2
  • Eye exams or Sx d/t nystagmus effects
  • MG Pt’s d/t enhancement of NDMB & Scc
  • Pt’s w/ Hx of bleeding disorder if going for Sx d/t platelet aggregation inhibition
  • Not useful in neuraxial anesthesia unless combined with epinephrine
  • Pt’s with CAD due to increased MVO2. Unless preceded w/ 0.5mg/kg diazepam
  • Cardiac unstable Pt’s d/t increase in SNS activity unless blunted by pre-administration of benzos
  • Delirious Pt’s unless pre medicated with midazolam
171
Q

o Who should/can receive ketamine?

A

 Burn Pt’s for dressing changes, skin grafts, debridement
 Chronic pain Pt’s due to inhibition of spinal NMDA receptors
 Pregnant women
 Peds post cardiac Sx
 Asthmatics d/t its bronchodilation effects
 Malignant hyperthermia Pt’s
 Traumatic brain injury w/ mechanical ventilation  significant decrease in ICP
 Seizure Pt’s, does not alter seizure threshold
 Pt’s with bronchospasms
 Renal impaired Pt’s

172
Q

What is the MOA for propofol?

A

Acts on GABAa –> increase chloride into cell –> hyperpolarize

173
Q

Which induction drug can cause lactic acidosis?

A

Propofol infusion syndrome –> fatal bradycardia in children

174
Q

Which induction drug should not be used in septic or hemorrhaging Pt’s?

A

Etomidate: It causes Adrenocortical suppression (sepsis or hemorrhage= need cortisol response)

175
Q

Which induction drug is great for hypovolemic Pt’s?

176
Q

Which induction drug should not be used in Neuro or pulmonary HTN Pt’s?

177
Q

Which induction drug does not cause histamine release & does not cause intra-arterial damage?

178
Q

Which induction drug does not cause seizures or myoclonus?

179
Q

Which induction drug causes a decrease in SBP?

180
Q

Which induction drug causes decreased SNS & baroreceptor reflex?

Advanced Pharmacology ANE 8433 (Spring 2023) (16 decks)

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