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Pharmacology > Analgesics: Opioids And Nsaids > Flashcards

Analgesics: Opioids And Nsaids Flashcards

1
Q

3 sites of action of opioids

A

Brain (supraspinal)
Spinal cord (spinal)
Periphery

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2
Q

Action of opioids in brain

A

Pre and post synaptically to activate descending inhibitory pathways

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3
Q

Where opioids work in spinal cord

A

Dorsal horn directly

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4
Q

Where opioids work in periphery

A

Peripheral terminals of nociceptive neurons

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5
Q

Opioids used in anesthesia for 4

A
  1. Attenuate sns response to pain
  2. Adjust to inhaled agents
  3. Sole anesthetic (Fent/sufent/morphine-cv Anes/crit ill)
  4. Peri op and post op pain control
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6
Q

How opioids diff from other analgesics

A

Mod to severe pain
No max dose/ceiling effect
Tolerance can develop, assoc w phys dep but not nec psych dep
Cross tolerance
Analgesia w/o loss of: touch, proprioception, consciousness (smaller doses)

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7
Q

Opioids classifications

A

Naturally occurring (morphine and codeine)
Semisynthetic (analogs of morphine- heroin and dihydromorphone)
Synthetic (exogenous, 4 groups)

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8
Q

Opioid mechanism of action overall

A

Activate sterospecific G protein coupled receptors

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9
Q

Opioid MOA post synaptic

A

Decreased neurotransmission. Inc K conduc (hyperpolarization), ca channel inactiv (dec NT release), modulation of phosphoinositide- signaling cascade, inhib Adenylate cyclase (dec cAMP)

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10
Q

Opioid pre synaptic MOA

A

Inhibits release of excitatory NTs (acetylcholine, dopamine, norepi, substance p)

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11
Q

Opioid receptors
3
Theory

A

Mu, kappa, delta

Synthetic opioids mimic action of endogenous opioids by binding to opioid receptors

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12
Q

Opioid receptors
What they do
W drugs

A

Activate endogenous pain modulating systems

Variable affinity and efficacy at the diff receptor types among diff drugs in this class

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13
Q

Mu receptor
Subtypes
What acts on them
Where they are

A

Mu-1, mu-2, mu-3 (3-immune process)
Endogenous & exogenous agonists
Brain, periphery, spinal cord

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14
Q

Mu 1 receptor
Where effects are
What effects are
What acts on them

A

Supraspinal*, spinal, and peripheral
Euphoria, miosis, bradycardia, urinary retention, hypothermia
Endogenous and synthetic opioid agonists

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15
Q

Mu 2 receptor
Effects
Analgesia type
What acts on them

A

Hypoventilation, phys dependence, constipation
Spinal (some supraspinal)
Endogenous and exogenous agonists

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16
Q

Kappa receptor
Where
Effects
What acts on them

A

Supraspinal, spinal, peripheral
Dysphasia, sedation, miosis, dieresis
Dynorphins and opioid agonist-antagonists

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17
Q

Delta receptor
Where
Effects
What works on them

A

Peripheral*, supraspinal, spinal
Hypoventilation, constipation, urinary retention
Enkephalins

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18
Q

Mu 1 effects

A

Euhpohoria, miosis, bradycardia, hypothermia, urinary retention

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19
Q

Mu 2 effects

A

Ventilation depression, constipation

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20
Q

CYP2D6
What mutations alter metabolism of
Effects

A

Codeine, oxycodone, hydrocodone, methadone

Unpredictable pharmacokinetics and 1/2 lives

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21
Q

Which drug metab least likely to be impacted by genetic variability

A

Fentanyl

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22
Q

Rate of metabolism may influence what

A

Side effect rate

Ultra fast metabolizes at inc risk for PONV

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23
Q

Periop opioid CV effects

A

Minimal impairment alone (additive cv effects w anesthetics), bradycardia (vagal stim, sa and av depression), vasodilation/dec SVR. Impairs SNS responses and pronounced effect w hypovolemia

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24
Q

Morphine and Demerol CV effects

A

Dose dependent and infusion rate dep histamine release. Bronchospasm, drop in SVR and BP, variable responses in pts

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25
Q

Periop cv effects

Demerol unique effects

A

Tachycardia, direct myocardial depression

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26
Q

Opioid CNS effects

A

Analgesia, euphoria, drowsy, miosis, nausea, doesnt produce amnesia*

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27
Q

How do opioids produce nausea

A

Direct activity at chemoreceptor trigger zone

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28
Q

Opioid CNS effects if hypoventilation prevented

A

Modest decrease ICP, decrease CBF

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29
Q

Periop renal effects of opioids

A

Inc tone and peristaltic activity of ureter. Inc detrusor muscle tone. Inc urgency with decreased ability to void

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30
Q

GI effects opioids

A

Spasm of GI smooth muscle. Constipation (decreased gi motility), prolonged gastric emptying

Decreased catecholamine release and cortisol prevents SNS activity

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31
Q

Gallbladder effects from opioids

A

Spasm of sphincter of oddi and gallbladder contraction, inc in biliary pressure

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32
Q

How opioids cause NV

A

Decreased gastric emptying, direct stim of chemoreceptor trigger zone in 4th ventricle. Partial dopamine agonist. Balanced by depression of medullary vomiting center.

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33
Q

How opioids cause pruritis

A

Unknown. Primarily on face/nose (esp fentanyl). Histamine most probably cause, esp morphine.

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34
Q

Skeletal muscle SF opioids

Rigidity where
Which drugs

A

Rigidity in chest, abdomen, jaw, and extremities. Esp if large/fast dose. Common w fentanyl, sufentanil, and hydromorphone.

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35
Q

Skeletal muscle SF opioids

A/w changes

A

High a/w p from inc intrathoracic p/dec venous return

Glottic rigidity and closure reported

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36
Q

Periop vent effects opioids

Resp depression

A

Dose dependent
Small dose: inc vt, dec rr, overall decrease in minute vent (inc co2 dec o2)
Large: dec rr and vt

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37
Q

Periop vent effects opioids

Overall 4

A

Decrease chest wall compliance, cough suppression, constriction of pharyngeal/laryngeal muscles, decreased response hypercarbia/hypoxia

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38
Q

Periop vent effects opioids

Which 2 in particular have AE

A

Morphine and meperidine have histamine related bronchoconstriction

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39
Q

Factors that inc magnitude and duration of opioid resp depression

A

Amt of pain, surgical stim, natural sleep, cont vs intermittent gtt, speed of injec, admin of other anesthetics, age, decreased clearance

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40
Q

Morphine

Indication/routes

A

Severe acute pain IM or IV

PO for chronic and cancer pain

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41
Q

Morphine

Metabolism, 1/2 life, duration

A

Slow release- 3-5 hrs
Large 1st pass effect
1/2 life 3-4 hrs, converted to active metabolite

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42
Q

Active metabolite of morphine

A

Morphine 6 glucuronide

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43
Q

Chemical name codeine

A

3 methylmorphine

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44
Q

Codeine
Indication, route
Half time

A

Mild pain relief, PO, 3 hrs

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45
Q

Codeine
Metabolism
Active form

A

Prodrug: 10% metab by CYP2D6 to its active form (morphine). Leftover drug demethylated to inactive metabolite

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46
Q

Codeine

Analgesic variation
Better for what

A

10% whites 30% asians lack 2D6, no analgesic effect

Antitussive effect remains without conversion (better for cough than pain relief)

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47
Q

Hydrocodone
Other name
Route
Given with

A

Vicodan
PO
Asa, ibuprofen, antihistamine, acetaminophen

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48
Q

Hydrocodone
Uses
Risk

A

Analgesic, antitussive, chronic pain

High abuse potential

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49
Q

Oxycodone
Route
Other names
Sustained release name

A

Po
Oxycontin, Percocet, percodan
OxyContin

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50
Q 
Oxycodone 
Use 
Combo w 
Safe in who, why 
Risk
A

Moderate to severe pain, chronic pain, post op pain
Asa and acetaminophen
No active metabolites so safe if renal dysfunction
High abuse potential

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51
Q

Methadone
Routes
Composition
1/2 life

A

Po, iv, sq
Synthetic
Long. 8-59 hrs or 13-100 hrs

52
Q

Methadone
Tx for what
Safe for who

A

Opioid addiction QD
Chronic pain syndrome BID or TID (neuropathic pain, resp dep risk)

No active metabolites- safe if renal dysfunction

53
Q

How naloxone works

A

Competitive agonist at opioid receptor. Binds to same site but doesnt activate it

54
Q

Tolerance to opioids

Common when
What happens

A

2-3 weeks of use

Reduction in adverse fx, shorter duration of relief, decrease in effectiveness, tolerance of: resp and cns dep

55
Q

Tolerance to opioids

Cross tolerance in what
When switching to another opioid do what

A

Full agonists

Start w 1/2 or less of equianalgesic dose

56
Q

Tolerance to opioid

Do what to improve pain relief
Tolerance to what effect isn’t as rapid, what is

A

Switch to methadone
Constipation
Sedative and emetic effects

57
Q

Opioid dependence
How long it takes
Factors
Who doesnt experience it

A

Several weeks of chronic tx
Psychological dep, biological, and social factors
Cancer and acute pain pts, rarely experience euphoria

58
Q

Dosage
Limits
Dose determination

A

No min/max except limit by dose of aspirin or Tylenol

After short acting opioid 1st 12-24h need around the clock dose determination

59
Q

Dosage (PO)
What for chronic pain
What for breakthrough pain

A

Sustained release formula

Immeadiate release doses that are 10-15% of total daily dose

60
Q

Titration of opioids in general anesthesia

A

Titration to BP, HR (if NM blocker and controlled vent), and RR (mainly)

61
Q

If pain is well controlled and switching opioids do what

A

Calculate equivalent dose and reduce by 25% for dose of new drug

62
Q

Neuraxial effects opioids

Where they go/effect

A

Diffuse across the dura to mu receptors in substantia gelatinosa. Into vasculature for systemic effect

63
Q

Opioids given epidural/spinal differences from IV

A

Diff onset, duration, and side effects are different than same drug given IV

64
Q

Opioids in epidural space may undergo what

A

Uptake into fat, systemic absorption, or diffusion into CSF

65
Q

Cephalad movement of opioid in CSF depends on

A

Lipid solubility

66
Q

What has limited migration by uptake in spinal cord

A

Highly lipid soluble meds, fentanyl

67
Q

Which meds remain in CSF for transfer to cephalic locations

A

Less soluble opioids, morphine

68
Q

How lipid solubility relates to uptake and concentration of opioid in neuraxial anesthesia

A

More lipid soluble means quicker peak and systemic concentration

69
Q

Dose of opioid in epidural vs spinal

How these affect local anesthesia dose

A

Epidural dose 5-10x higher than spinal

Can reduce LA dose and overall anesthetic reqs

70
Q

Non opioid analgesics

Indication
Ceiling effect of what

A

1st line mild - moderate pain
ASA and acetaminophen of 650-1300 my
NSAIDs other than aspirin, analgesic ceiling may be higher

71
Q

Acetaminophen

MOA

A

Central anti prostaglandin effect. Antipyretic. Pain reduced by block of NMDA receptor activation in CNS. Substance P in spinal cord

72
Q

Acetaminophen
Lacks what
Good in who

A

Peripheral activity, weak anti-inflammatory action

PUD, peds, pts who need well functioning platelets

73
Q

Acetaminophen
Potency
Po dose

A

Similar potency as ASA, same time-effect curve

325-650 mg q4-6h

74
Q

Acetaminophen

IV dose/timing

A

1g over 15 min infusion only** q4-6 hours. Max 4000mg in 24h.

75
Q

Acetaminophen

Metabolism

A

Conjugated and hydroxylated to inactive metabolites. Very little excreted unchanged by kidneys.

Time to reach concentration 30 min faster iv than oral

76
Q

Acetaminophen

Why OD happens

A

Liver can only metab ltd amt of hepato toxic metabolic n acetyl p benzoquinone w glutathione. When glutathione outnumbered by OD of tyelenol- liver injury

77
Q

Tyelenol

Max safe dose, considerations

How to prevent injury

A

4g/day. Even lower in ETOH use/abuse

Inc toxicity risk if taking isoniazid. Acetylcysteine can substitute for glutathione and prevent liver injury if given within 8h of OD

78
Q

Tyelenol

About renal toxicity

A

Renal papillary accum of metabolites can cause renal cell necrosis. Can develop ESRD. NSAIDs higher risk than tyelenol for renal toxicity

79
Q

Arachidonic acid released by what

Metabolized to what

A

Phospholipids by the enzyme phospholipase A2

Metab by cyclooxygenase, lipoxygenase, or epoxygenase

80
Q

Breakdown products of arachidonic acid

A

Cyclooxygenase: prostaglandins, prostacyclin, thromboxanes
Lipoxygenase: leukotrienes, lipoxins
Epoxygenase: epoxy. Acid

81
Q

Prostacyclin does what

Thromboxane does what

A

P- vasodilation and inhib plt activation

T- vasoconstriction and plt aggregation

82
Q

Epoxy. Acid role

A

Regulates inflammation

83
Q

Cox 1 does what

A

Breaks arachidonic acid into prostaglandins (gastric protection, hemostasis, renal function)

84
Q

Cox 2 does what

A

Inducible, breaks into prostaglandins that mediate pain, inflammation, and fever

85
Q

Aspirin

Uses

A

HA, muscle pain, arthritis, antipyretic
Mild to moderate pain
MI/stroke prevention
In MI for anti plt action

86
Q

Aspirin

How its unlike other nsaids

A

Irreversible inhibition of COX. Single dose lasts lifetime of plt 8-10 days. Large doses can decrease PT

87
Q

Aspirin

Adverse fx

A 
ESRD: not induced by chronic asa, prolonged bleeding (15 min)
Inc LFTs (reversible) 
Ppt athsma
Cross sensitive w other nsaids 
GI bleed, cns stim
88
Q

Aspirin

Dosing

A

Analgesic/antipyretic 325-650 mg

Anti-inflammatory 1000mg (3-5g/day)
Inc dose gradually, follow serum levels, rarely used d/t gi fx

89
Q

Aspirin clearance

OD leads to what

A

E 1/2t 15-20 min aspirin and 2-3h for active metabolite salicylic acid

Metabolic acidosis and tinnitus

90
Q

Aspirin

When it shouldn’t be used

A

Viral syndromes in kids and teens, risk Reye’s syndrome encephalopathy

91
Q

How non acetylated salicylates compare to aspirin

A

More favorable toxicity profile. Dont mess w plt aggregation, rarely assoc w gi bleed, tolerated by athsmatics

92
Q

NSAIDs

Use for

A

Arthritis, musculoskeletal pain, ha, dysmenorrhea
Ceiling effect in postop pain
More effective than aspirin or tyelenol

93
Q

NSAIDs

Mechanism

A

Cox inhibition. Blocks conversion of arachidonic acid to prostaglandins (upstream). Decreases release and production of PGs. Anti-inflammatory, antipyretic, analgesic

94
Q

NSAIDs

About drug and metabolism

A 
Weak acid, well absorbed 
Highly protein bound 
Small Vd
Extensively metabolized and excreted in urine 
1/2 life 6-12h, varies
95
Q

NSAIDs
Reaction/who

Interaction w platelets

A

Athsma and anaphylactic reaction in aspirin sensitive pts

Reversible inhibition of plt agg. Cox 1 blocks synthesis of thromboxane A2

96
Q

NSAIDs

Adverse effects
Pregnancy

A

Hepatic injury, aseptic meningitis

Category b, avoid in pregnancy. Esp 3rd trimester, category d d/t premature closure of DA

97
Q

NSAIDs peri-op

SE in surgery

A

Inhib of cox can lead to renal injury, gastric ulceration, excessive bleeding, and impaired bone healing

98
Q

NSAID effects on GI

Fx/how

A

Dyspepsia, GI bleed, PUD

Inhib of PGs that maintain normal gastric and duodenal mucosa- inc acid production and decreases mucus production/gastric bf

99
Q

NSAIDs

Local gastric irritation caused by what

A

Lipid soluble at low ph, enter gastric mucosal cells, lose lipid solubility, become trapped in cell

100
Q

GI adverse effects of NSAIDs

Risk factors

A

High dose, prolonged use, prev ulcers, ETOH intak, elderly, corticosteroid use**

101
Q

Low GI risk nsaids

A

Low dose: ibuprofen and naproxen

Also: etodolac, sulindac, celecoxib

102
Q

Moderate risk nsaids gi

A

Ibuprofen and naproxen and med to high doses

Diclofenac, oxaprozin, meloxicam, nabumetone

103
Q

High risk nsaids to gi

A

Tolmetin, peroxicam, aspirin, indomethacin, ketorolac

104
Q

NSAIDs renal adverse effects

A

Dec synthesis of renal vasodilator PGs (pge2)
Decreased renal bf, na and fluid retention, can cause renal fail/htn.
Interstitial nephritis rare.

105
Q

NSAIDs renal AE

RFs

A

People who require prostaglandins for renal perfusion: elderly, CHF, htn, dm, renal insufficiency, ascites, volume depletion, diuretic therapy

106
Q

Renal risk of specific nsaids

A

Can occur with all

Inc risk: longer 1/2 life, potent cox inhibitors (toradol and indocin), higher dose

107
Q

Renal risk nsaids

Which ones are renal roaring

A

Lower risk but not devoid of risk

Sulindac, nabumetone, celecoxib

108
Q

NSAIDs drug interactions

Increases effects of what/how

A

Displaces highly protein bound agents: warfarin, phenytoin, sulfonylureas, sulfonamids, digoxin

109
Q

NSAIDs

Reduces effects of

A

Diuretics, b blockers, ACEIs via suppression of renal PGs

110
Q

NSAIDs

Inc __ levels
What increases levels of most nsaids

A

Lithium

Probenecid, avoid w ketorolac

111
Q

Ketorolac

Comparison

A

IM or IV compared to mild opioids. Similar timing of pain relief to morphine but no vent/cv depression

112
Q

Ketorolac

Adverse effects

A

Similar to typical nsaids

GI, bleeding time, renal toxicity, bronchospasm

113
Q

Ketorolac
Max use
Onset
E 1/2t

A

5 days max
10 min IV
5 hours, prolonged 30-50% in elderly

114
Q

Ketorolac

About drug
DOA
Metabolism

A

99% protein bound
6-8hrs
Conjugated in liver

115
Q

Ketorolac

IV dose

A

30 mg IV x 1 or q6 hrs

Max dose daily 120 mg

Cut dose in 1/2 for elderly

116
Q

Selective nsaids

Which/action

A

Celebrex. Inhibit cox 2. Not more effective at pain/inflam but less gastric effects, same renal AE

117
Q

Celebrex

Dosage
Consider what
Dont give to who

A

<200mg/day
Comparable to 500mg of naproxen bid

Risk for CV and GI events
Take w food and dont give to pts w sulfonamide allergy

118
Q

Selective and non selective nsaids

Black box warnings

A

Inc risk cv thrombotic events, mi, stroke

Inc gi bleed/ulcer/perf of stomach or intestines

119
Q

Adjuvant analgesics

A

Antidepressants and anticonvulsants for neuropathic pain

120
Q

Neurontin for what

A

Diabetic neuropathy and postherpetic neuralgia

121
Q

Lyrica
How it works
For what

A

Gabanergic

Diabetic neuropathy
Postherpetic neuralgia
Fibromyalgia

122
Q

Tegretol

How it works
For what

A

Na channel blocker and gabanergic

Trigeminal neuralgia

123
Q

Dilantin, depakote, klonopin, and topamax for what

A

Neuropathic pain

124
Q

Lamictal

How it acts
For what

A

Gabanergic

Central post stroke pain and HIV associated pain

125
Q

Hydroxyzine

Indication and action

A

Low dose iv/Im adds analgesic effect to opioids in cancer and post op pain, reduces ponv

Antihistamine and antiinflammatory

126
Q

Corticosteroids

Indication

A

Analgesia in pts w inflammatory diseases or tumor infiltration of nerves

127
Q

Topical analgesics

Which drugs

A

Lidoderm-post herpetic neuralgia
Topical Emla
Capsaicin- neuropathic/OA pain
Transdermal clonidine patch- pain/hyperalgesia in sympathetically maintained pain

Pharmacology (19 decks)

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