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ARCHIVED: Pharmacology for Nurse Anesthesia > Exam 2: NSAIDs and Opioids > Flashcards

Exam 2: NSAIDs and Opioids Flashcards

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1
Q

Receptor most responsible for transmission of pain signals:

A

TRPV1

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2
Q

Function of B2 receptor:

A

Enhances TRPV1 activity

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3
Q

Function of prostanoid receptor:

A

Aids in depolarization of pain fiber via enhancement of voltage-gated Na+ channel

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4
Q

Function of opioid, cannabinoid, and norepi receptors:

A

Hyperpolarization of pain fibers via ↑ K+ retention

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5
Q

B2 receptors activated by:

A

Bradykinin

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6
Q

Laminae of Αδ fibers:

A

I, II, III, V

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7
Q

Laminae of C fibers:

A

I, II

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8
Q

Laminae of substantia gelatinosa:

A

II, III

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9
Q

Substantia gelatinosa is important because:

A

Richly populated with opioid peptides, receptors

Inhibitory interneurons

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10
Q

Area of the brain that descends neurons into substantia gelatinosa:

A

Nucleus raphe magnus

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11
Q

Opioid action in the brain:

A

Pre- and postsynaptically activate descending inhibitory pathways

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12
Q

Opioid action in the SC:

A

Directly on the dorsal horn

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13
Q

Opioid action in the periphery:

A

Peripheral terminals of nociceptive neurons

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14
Q

Opioid effect on pain perception:

A

Changes tolerance of pain without necessarily changing ability to perceive pain

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15
Q

Opioid effect on physiological response to pain:

A

Reduces neuroendocrine response:
SNS activation
Cortisol
Norepi release

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16
Q

Opioid use in anesthesia:

A

Attenuate SNS response to stimuli
Adjunct to IAs
Can be sole anesthetic (cardiac/trauma)
Periop/postop pain mgmt

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17
Q

Unique characteristics of opioids vs. other analgesics:

A

No max dose or ceiling effect
Tolerance develops with chronic use
Produces analgesia without loss of touch/proprioception/consciousness

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18
Q

Ex. of naturally occuring opioids:

A

Morphine, codeine

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19
Q

Ex. of semisynthetic analogs of morphine:

A

Heroin, dihydromorphone

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20
Q

Classifications of opioids:

A

Full agonist
Partial agonist
Mixed agonist/antagonist
Antagonist

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21
Q

MoA (presynaptic) of opioids:

A

Inhibits release of excitatory NTs (ACh, dopamine, norepi, substance P)

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22
Q

MoA (postsynaptic) of opioids:

A

Directly decreases neurotransmission

↑ K+ conductance: hyperpolarization
↓ Ca2+ channel activity: ↓ NT release
Modulation of phospholipase C
↓ cAMP

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23
Q

Opioid receptors:

A

Mu
Kappa
Delta

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24
Q

Mu-1 receptor locations:

A

Supraspinal*
Spinal
Peripheral

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25
Q

Effects of mu-1 receptor activation:

A 
Euphoria
Miosis
Bradycardia (good in adults, not in peds)
Urinary retention
Hypothermia
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26
Q

Effects of mu-2 receptor activation:

A

Hypoventilation
Physical dependence
Constipation

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27
Q

Mu-2 receptor locations:

A

Spinal*

Some supraspinal

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28
Q

Kappa receptor locations:

A

Supraspinal*
Spinal*
Peripheral

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29
Q

Effects of kappa receptor activation:

A

Dysphoria
Sedation
Miosis
Diuresis

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30
Q

Drugs that work on kappa receptors:

A

Dynorphins

Opioid agonist-antagonists

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31
Q

Delta receptor locations:

A

Peripheral*
Supraspinal
Spinal

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32
Q

Effects of delta receptor activation:

A

Hypoventilation
Constipation
Urinary retention

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33
Q

Drugs that work on delta receptors:

A

Enkephalins

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34
Q

Two mutations to 6q24-q25 that can affect response to opioids:

A 
Nucleotide 118 (10-20%)
Nucleotide 17 (1-10%)
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35
Q

CYP450 mutation that alters metabolism of some opioids:

A

CYP2D6

Unpredictable PK and t1/2 of codeine, oxycodone, hydrocodone, and methadone

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36
Q

Drug least likely to be impacted by genetic variability:

A

Fentanyl

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37
Q

Ultra-rapid metabolizers at increased risk of:

A

PONV

and other side effects

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38
Q

CV effects of opioids:

A

Minimal impairment when used alone

Dose dependent bradycardia (vagal stimulation, direct SA/AV node depression)

Vasodilation/↓SVR (impairment of SNS tone, leading to ↓CO, ↓BP esp. with hypovolemia)

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39
Q

CV effects of morphine and meperidine:

A

Dose dependent histamine release

Bronchospasm

↓SVR, ↓BP

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40
Q

Exception to bradycardia effect of opioids:

A

Meperidine; causes tachycardia with direct myocardial depression

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41
Q

CNS effects of opioids:

A 
Analgesia
Euphoria
Drowsiness
Miosis
Nausea
No amnesia
Decrease ICP and CBF - only if no hypoventilation though
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42
Q

Renal, GI, liver effects of opioids:

A

↑ tone of ureter and detrusor tone leads to urgency without ability to void

↓ catecholamine and cortisol release

Sphincter of Oddi spasm, ↑ biliary pressure

GI smooth muscle spasm
Constipation
N/V

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43
Q

How can opioids cause angina-mimicking pain?

A

Sphincter of Oddi/gallbladder spasms

44
Q

Means by which opioids cause N/V:

A

↓ gastric emptying

Stimulation of CTZ on floor of 4th ventricle

45
Q

Describe pruritis from opioids:

A

Unknown cause, likely histamine release

Primarily on face, esp. nose

46
Q

Skeletal muscle effects of opioids:

A

Rigidity in chest, abdomen, jaw, extremities (esp. large, rapid doses)

Difficult/impossible ventilation, ↑ airway pressure

Glottic rigidity/closure

47
Q

Opioids particularly prone to causing rigidity:

A

Fentanyl
Sufentanil
Hydromorphone

48
Q

Ventilatory effects of opioids:

A

Dose dependent respiratory depression (small doses: ↑ Vt, ↓ RR with overall ↓ MV; large doses: ↓ Vt and RR)
↓ chest wall compliance
Cough suppression
Constriction of laryngeal/pharyngeal muscles
↓ response to hypercarbia, hypoxia
Morphine/meperidine: histamine-related bronchospasm

49
Q

Opioid-induced changes in ventilatory response curve:

A

Reduced slope and shifted to right

50
Q

Indications for PO morphine:

A

Severe acute pain: IM/IV

Chronic/cancer pain: PO

51
Q

PK of PO morphine:

A

Considerable first pass effect
Et1/2: 3-4 hrs
Active metabolite

52
Q

Indications for PO codeine:

A

Mild pain

Cough (lower dose)

53
Q

PK of PO codeine:

A

Et1/2: 3hrs

Prodrug; 10% converted by CYP2D6 to active form, morphine

54
Q

Racial groups prone to missing CYP2D6:

A

Caucasian (10%)

Asian (30%)

55
Q

Indications for PO hydrocodone:

A

Chronic pain

Post-op pain relief

56
Q

Formulation of PO hydrocodone:

A

Always combined with APAP, ASA, ibuprofen, or antihistamine

57
Q

Indications for PO oxycodone:

A

Moderate to severe pain
Chronic pain
Post-op pain

58
Q

Formulation of PO oxycodone:

A

Alone
Sustained-release
Combined with APAP or ASA

59
Q

Patient population for which oxycodone and methadone are safer:

A

Renal - no active metabolites

60
Q

Indications for PO methadone:

A

Chronic pain syndrome

Opioid addiction

61
Q

PK of PO methadone:

A

Et1/2: 8-59 or 13-100 hrs

No active metabolites

62
Q

Dosing schedule for methadone:

A

QD for addiction

BID/TID for pain

63
Q

Order of events when tolerance develops to opioids:

A

↓ adverse effects
↓ duration of analgesia
↓ effectiveness of each dose

64
Q

When switching from one opioid to another:

A

Start with half or less of equianalgesic dose

65
Q

Side effect of opioids that pts do not develop tolerance to:

A

Constipation

66
Q

Breakthrough pain dose for opioids:

A

10-15% of total daily dose in immediate release form

67
Q

Receptors that provide neuraxial analgesia from opioids:

A

Mu receptors in substantia gelatinosa

68
Q

Cephalad movement of opioid in CSF limited by:

A

Lipid solubility

Fentanyl (highly lipid soluble) limited in migration

Morphine (less lipid soluble) will remain in CSF and migrate to cephalic region

69
Q

Epidural vs. spinal opioid dose:

A

Epidural is 5-10x higher dose

70
Q

Indications for non-opioid analgesics:

A

Mild to moderate pain

71
Q

Ceiling effect dose of ASA and APAP:

A

650-1300mg

72
Q

MoA of acetaminophen:

A

Central anti-prostaglandin effect

Blockade of NMDA receptor in CNS

Blockade of substance P in spinal cord

Weak anti-inflammatory behavior; no peripheral activity

73
Q

Dosage of acetaminophen:

A

PO: 325-650mg q4-6hr
IV: 1gm over 15 min infusion q4-6hr

74
Q

PK of acetaminophen:

A

Conjugated/hydroxylated to inactive metabolites

Very little excreted unchanged by kidneys

75
Q

Overdose of acetaminophen:

A

Serious or fatal hepatic injury when glutathione overwhelmed by acetaminophen

↑ risk of toxicity in ETOH, isoniazid use

Tx with acetylcysteine to sub for glutathione

76
Q

Renal toxicity from acetaminophen:

A

Metabolites accumulate in renal papillae and cause renal cell necrosis

Relatively low risk

77
Q

Three pathways of arachadonic acid metabolism:

A

Cyclooxygenase
Lipoxygenase
Epoxygenase

78
Q

Cyclooxygenase metabolism of arachadonic acid leads to formation of:

A

Prostaglandins
Prostacylcin
Thromboxanes

79
Q

Lipoxygenase metabolism of arachadonic acid leads to formation of:

A

Leukotrienes

Lipoxins

80
Q

COX-1 prostaglandins serve in:

A

Gastric protection
Hemostasis
Renal function

81
Q

COX-2 prostaglandins serve in:

A

Pain
Inflammation
Fever

82
Q

Indications for aspirin:

A

Mild to moderate pain
Fever
MI/stroke prevention

83
Q

Duration of action of aspirin:

A

Life of platelet; 8-10 days

Irreversible!

84
Q

System side effects of aspirin:

A 
Prolonged bleeding but no renal disease
Can ↑ LFTs (reversible)
Can potentiate asthma
GI bleeding/PUD
CNS stimulation
85
Q

Dosage of aspirin:

A

Analgesic: 325-650mg

Anti-inflammatory: 1000mg (3-5g/day)

86
Q

PK of aspirin:

A

Hepatic clearance
Active metabolite
Et1/2: 15-20 min for ASA, 2-3 hrs for salicylic acid

87
Q

S/s of ASA overdose:

A

Metabolic acidosis

Tinnitis

88
Q

Efficacy of NSAIDs:

A

More effective than ASA/APAP

Equal or greater than usual doses of opioid+APAP

Anti-inflammatory

89
Q

MoA of NSAIDs:

A

Blocks conversion of arachidonic acid to prostaglandins –> analgesic, anti-inflammatory, antipyretic

90
Q

PK of NSAIDs:

A 
Weak acids, well absorbed
Highly protein bound (>95%)
Small Vd
Extensively metabolized
Excreted in urine
Et1/2 varies: < 6 to > 12 hrs
91
Q

Side effects of NSAIDs:

A

Asthma/anaphyalctoid rxns
Plt inhibition (reversible)
Hepatic injury, aseptic meningitis (rare)

92
Q

Pregnancy and NSAIDs:

A

Avoid in third trimester d/t premature closure of DA

93
Q

COX inhibition in the peri-op period can cause:

A

Renal injury
Gastric ulcers
Bleeding
Impaired bone healing

94
Q

GI adverse effects of NSAIDs:

A 
Dyspepsia
GI bleeding
PUD
↑ acid production
↓ mucus production, gastric blood flow
Irritation due to trapping in mucosal cells
95
Q

Risk factors for GI effects with NSAIDs:

A 
High dose
Long-term use
Hx of ulcer/GIB
ETOH
Elderly
*Corticosteroids
96
Q

Low-risk NSAIDs:

A

Low-dose ibuprofen, naproxen
Etodolac
Sulindac
Celecoxib

97
Q

High-risk NSAIDs:

A 
Tolmetin
Piroxicam
Aspirin
Indomethacin
Ketorolac
98
Q

Renal side effects of NSAIDs:

A

↓ synthesis of renal vasodilator PGE2

↓ renal blood flow –> fluid/Na+ retention –> renal failure/hypertension (this is only in susceptible populations)

99
Q

Drug interactions with NSAIDs:

A

Displaces other protein-bound drugs (warfarin, phenytoin, sulfonamides, digoxin)

↓ effect of diuretics, β blockers, ACEIs

↑ lithium levels

Probencid ↑ levels of NSAIDs

100
Q

Only IV NSAID in US:

A

Ketorolac

101
Q

PK of ketorolac:

A 
Onset 10 min (IV)
Et1/2: 5 hrs
Duration: 6-8 hrs
99% protein-bound
Conjugated in liver
102
Q

Dosing of ketorolac:

A

30mg IV q6hr
Daily max 120mg

1/2 dose for elderly

103
Q

Only selective NSAID:

A

Celecoxib

104
Q

Dosing of celecoxib:

A

< 200mg/day

105
Q

Adjuvant analgesics:

A

Antidepressants/anticonvulsants for neuropathic pain

Hydroxyzine for cancer and post-op pain (plus ↓ PONV)

Corticosteroids for inflammatory disease of tumor infiltration of nerves

Topical analgesics

ARCHIVED: Pharmacology for Nurse Anesthesia (20 decks)

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