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Pharm-Spring > PO Opioids/NSAIDs > Flashcards

PO Opioids/NSAIDs Flashcards

1
Q

3 Major Sites of Action of Opioids

A

Brain, Spinal Cord and Periphery:

  1. Brain (supraspinal): Opioids work pre- and post- synaptically to activate descending inhibitory pathways
  2. Spinal cord (spinal): Directly on dorsal horn of spinal cord
  3. Periphery: Peripheral terminals of nociceptive neurons
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2
Q

Opioids are used in Anesthesia for:

A
  1. Attenuate SNS response to noxious stimuli
  2. Adjunct to inhaled agents during anesthesia
  3. Sole anesthetic (fentanyl/sufent/morphine- cardiac anesthesia, critically ill pts)
  4. Peri-op and post-op control of pain
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3
Q

Unique Opioid Characteristics set them apart from other Analgesics

A
  • Moderate to severe pain
  • No max dose or ceiling effect
  • Tolerance can develop w/ chronic use
    • Tolerance associated w/ physical dependence but not necessarily w/ psychological dependence
  • Cross-tolerance
  • Produce analgesia w/out loss of
    • Touch
    • Proprioception
    • Consciousness (in smaller doses)
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4
Q

Opioid Classification

A
  • Naturally occurring
    • Morphine and codeine
  • Semisynthetic: Analogs of morphine
    • Heroin and Dihydromorphone
  • Synthetic
    • Exogenous, 4 groups
  • Further classified into:
    • Agonist, Partial agonist, Mixed agonist/antagonis, Antagonist
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5
Q

Opioids: Mechanism of Action:

Post-synaptic

A
  • Activate stereospecific G-protein coupled receptors
    • Post-synaptic - directly decreases neurotransmission
      • Increased K+ conductance (hyperpolarization)
      • Ca++ channel inactivation (decreased NT release)
      • Modulation of phosphoinositide – signaling cascade and phospholipase C
      • Inhibit adenylate cyclase (decreased cAMP)
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6
Q

Opioids: Mechanism of Action:

Pre-synaptic

A
  • Activate stereospecific G-protein coupled receptors
    • Pre-synaptic- inhibits release of excitatory NT’s
      • ↓ release of Ach, DA, norepi, substance P
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7
Q

Opioid Receptors

A
  • Receptors: mu, kappa, and delta
  • Theory: synthetic opioids mimic action of endogenous opioids by binding to opioid receptors
  • Activate endogenous pain modulating systems
  • Variable affinity and efficacy at different receptors types among different drugs in this class
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8
Q

Mu receptor

A
  • Subtypes mu-1 and mu-2
  • Mu-3 receptors thought to be involved in immune process
  • All endogenous and exogenous agonists act on mu receptors
  • Mu receptors in brain, periphery and spinal cord
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9
Q

Mu-1 receptor

A
  • Mu-1 receptor
    • Supraspinal, spinal, and peripheral analgesia
    • Low abuse potential
    1. Euphoria
    2. Miosis
    3. Bradycardia
    4. Hypothermia
    5. Urinary retention
  • All endogenous and synthetic opioid agonists act on these receptors
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10
Q

Mu-2 Receptor

A
  • Mu-2 Receptor
    • Spinal analgesia (also some supraspinal)
    • Physical dependence
    1. Hypoventilation
    2. Constipation
  • All endogenous and exogenous agonists act on these receptor
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11
Q

Kappa Receptor

A
  • Kappa Receptor
    • Supraspinal, spinal and peripheral analgesia
    • Low abuse potential
    1. Dysphoria
    2. Sedation
    3. Miosis
    4. Diuresis
  • Dynorphins act on these receptors
  • Opioid agonist-antagonists often have principle actions at kappa receptor
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12
Q

Delta Receptor

A
  • Delta Receptor
    • Supraspinal, spinal, and peripheral analgesia
    • Physical dependence
    1. Hypoventilation
    2. Constipation
    3. Urinary retention
  • Enkephalins work on these receptor
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13
Q

Genetics of CYP450 System and Influence on Opioids

A
  • CYP2D6 = 5 common mutations can alter metabolism of:
    • Codeine, oxycodone, hydrocodone, and methadone
    • Unpredictable pharmacokinetics and ½ lives
  • Fentanyl’s metabolism least likely to be impacted by genetic variability in surgical population = predictable pharmacokinetics
  • Rate of metabolism may influence side effect rate
    • Studies indicate ultra-rapid metabolizers at ↑ r/f PONV
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14
Q

Systemic Effects of Opioids

A
  • Many systemic effects similar among opioids
    • Although different opioids are active at different receptors to different degrees
    • Variable SE and efficacy profiles
      • Variance in chemical structures
  • Morphine = prototype
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15
Q

CNS Effects

A
  • Analgesia
  • Euphoria
  • Drowsiness/sleep
  • Miosis
  • Nausea- chemoreceptor trigger zone
  • Does not produce amnesia
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16
Q

Pulmonary Effects

A
  • ↓RR and ↑TV
  • At higher doses = ↓ RR & TV → leading to apnea
  • ↓ response to CO2 and hypoxia
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17
Q

GI Effects

A
  • N/V
  • Decreased gastric emptying
  • Direct stimulation of chemoreceptor trigger zone on floor of 4th ventricle
    • Partial dopamine agonist?
    • Balanced by depression of medullary vomiting center
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18
Q

Pruritis

A
  • Cause unknown
  • Occurs primarily on face particularly nose
  • “fentanyl nose itch”
  • Histamine release most probable cause w/ some (MSO4)
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19
Q

Morphine

A
  • Severe acute pain almost always IM or IV admin
  • PO used for chronic pain and CA pain
    • Slow release formulations available – delayed onset 3-5 hrs (not used pre-op/intra-op much)
    • Considerable first pass effect
    • E½t 3-4 hrs converted to active metabolite (morphine -6-glucuronide)
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20
Q

Codeine (3-methylmorphine)

A
  • Mild Pain Relief
    • ​Better for cough (lower dose) than pain relief
  • PO
  • E½t = 3 hrs
  • Prodrug: 10% is metabolized by CYP2D6 to its active form
    • Active form = morphine
    • Remaining drug demethylated to inactive metabolite
  • 10% Caucasians, 30% Asians lack 2D6 = no analgesic effect
  • Antitussive effect remains even w/out conversion
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21
Q

Hydrocodone

A
  • AKA – Vicodan
  • PO
  • Always combined w/ either ASA, antihistamine, acetaminophen, ibuprofen
  • Used for chronic pain
  • Analgesic and antitussive
  • High abuse potential
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22
Q

Oxycodone

A
  • AKA Oxycontin, Percocet, Percodan
    • ​oxycontin -sustained release preparation
  • PO
  • Moderate to severe pain; useful for chronic and post-op pain
  • Also in combo w/ ASA or acetaminophen
  • No active metabolites - safer in renal dysfunction
  • High abuse potential
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23
Q

Methadone

A
  • PO, IV, SubQ
  • Synthetic
  • Long E½t- 8-59 hrs or 13-100 hrs (sources vary)!
  • No active metabolites - safer w/ renal dysfunction
  • Opioid addiction treatment (maintenance) dosed QD
  • Chronic pain syndrome treatment: doses BID or TID (q4-8 hr)
    • Neuropathic pain
    • At r/f severe resp depression 2° to prolonged & unpredictable E½t
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24
Q

Tolerance to Opioids

A
  • Tolerance common w/ chronic use (after 2-3 wks of use)
  • Cross-tolerance exists among all full agonists but not complete
  • When switching to another opioid, start w/ ½ or less of customary equianalgesic dose
  • Switching opioid-tolerant pts to methadone may improve pain relief
  • Tolerance to sedative and emetic effects develop rapidly, but not constipation
    • A stimulant laxative +/- a stool softener should be started early (senna/docusate)
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25
Q

Tolerance to Opioids:

Patient notices…

A
  • Pt notices:
    1. Reduction in adverse effects
    2. Shorter duration of analgesia
    3. Decreased effectiveness of each dose
    4. Tolerance to most adverse effects include:
      • Respiratory and CNS depression
      • Can be surmounted by increasing dose
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26
Q

Dependence

A
  • Physical dependence causes abstinence symptoms w/ sudden d/c
  • Clinically significant dependence develops only after several wks of chronic tx
  • Addiction involves psychological dependence and biologic and social factors
  • CA pain and acute pain pts rarely experience euphoria; even more rarely develop psychological dependence or addiction
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27
Q

Dosage (PO)

A
  • Dose varies widely from pt to pt
  • No min or max dose except limitation by dose of acetaminophen or aspirin
  • Use dose required to maintain optimum pain relief w/ tolerable SE’s
  • After initial titration w/ short-acting opioid in first 12-24 hrs, dose determination by around-clock dosing recommended
  • Use sustained release formulas in chronic pain
  • Immediate release doses that are 10 to 15% of total daily dose should be used for breakthrough pain
  • PCA, given IV, SQ or other routes now widely used when PO route not feasible
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28
Q

Non-opioid Analgesics

A
  • Acetaminophen (Tylenol)
  • Cyclooxygenase-2 Specific Inhibitors
    • Celecoxib (Celebrex)
  • Acetylated Salicylate
    • Aspirin (ASA)
  • NSAIDS
  • (1) Ibuprofen (Motrin), (2)Naproxen (Naprosyn)
  • (3) Oxaprozin (Daypro)
  • (4) Sulindac (Clinoril), (5) Etodolac (Lodine)
  • (6) Ketorolac (Toradol), (7) Diclofenac (Voltaren)
  • (8) Indomethacin (Indocin)
  • (9) Nabumetone (Relafen), (10) Tolmetin (Tolectin)
  • (11) Piroxicam (Feldene), (12) Meloxicam (Mobic)
29
Q

Non-opioid Analgesics:

Factors to be considered

A
  • First line agents for mild to moderate pain
  • Ceiling effect of ASA and acetaminophen b/t 650-1300 mg
    • NSAIDs other than ASA may have higher analgesic ceiling
    • Exceeding ceiling dose of any of these drugs = increased adverse effects w/ no added efficacy
  • Tolerance does not develop to analgesic effects of these drugs
30
Q

Acetaminophen

effect/activity

A
  • Central anti-prostaglandin effect
    • Antipyretic
    • Pain reduced via blockade of:
      • NMDA receptor activation in CNS
      • Substance P in spinal cord
  • Lacks peripheral activity – weak anti-inflammatory action (not true NSAID)
    • Good choice in: PUD, Peds pts, Pts who need well functioning platelets
31
Q

Acetaminophen:

metabolism/excretion

A

​​Conjugated and hydroxylated to inactive metabolites; very little excreted unchanged by kidneys

32
Q

Acetaminophen

Dosing

A
  • PO similar potency as ASA (in single analgesic doses, has same time-effect curve)
    • PO Dose = 325-650 mg Q4-6 hrs
    • IV dose = 1 g over 15 min Q4-6 hrs
      • no > 4000 mg in 24 hrs (check to make sure no other sources of acetaminophen)
33
Q

Acetaminophen

Dosing/Toxicity

A
  • Overdose can cause serious or fatal hepatic injury
    • Liver can only metabolize limited amount of hepatotoxic metabolite N-acetyl-p-benzoquinone w/ glutathione
    • When glutathione outnumbered by OD of acetaminophen, hepatic injury occurs
    • Max safe dose 4 g/day
      • Safe dose lower in ETOH abuse (use caution)
    • Also ↑ r/f toxicity in pts taking isoniazid
    • Acetylcysteine can substitute for glutathione and prevent hepatic injury if given w/in 8 hrs of OD
  • Renal toxicity
    • Renal papillary accumulation of metabolites can cause renal cell necrosis
    • May be responsible for development of some cases of ESRD
    • However, NSAIDS higher risk of renal toxicity than acetaminophen
34
Q

Review Physiology of Arachidonic Acid Metabolism

A
  • Arachadonic acid is released from phospholipids by enzyme phospholipase A2
  • Arachadonic acid is immediately metabolized by either:
    • Cyclooxygenase leads to formation of:
      • Prostaglandins
      • Prostacylcin
      • Thromboxanes
    • Lipoxygenase leads to formation of:
      • Leukotrienes
      • Lipoxins
    • Epoxygenase leads to formation of:
      • Epoxyeicosatetraenoic acid (4 types) – regulates inflammation further research necessary to determine precise role
35
Q

Salicylates: Aspirin

Effects

A
  • Unlike other NSAIDs, irreversible inhibition of COX
    • Single dose inhibits plt function for lifetime of plt (8-10 days)
    • Large doses can also decrease prothrombin
  • ESRD
    • Not induced by chronic ASA (in contrast to other NSAIDS)
    • Prolonged bleeding (up to 15 min) in these pts w/ ASA
  • Can increase LFTs (usually reversible)
  • Single dose can ppt asthma in aspirin-sensitive patients
  • Cross-sensitivity w/ other NSAIDS
  • Like other NSAIDs, can cause GI bleeding, PUD
  • CNS stimulation
36
Q

Aspirin Uses

A
  • Aspirin effective in most mild-mod. pain: Headache, muscle pain, arthritis
  • Antipyretic
  • MI/stroke prevention; protection during MI (anti-plt)
37
Q

Aspirin Clearance

A
  • Hepatic clearance:
    • E½t = 15-20 min for aspirin and 2-3 hrs for active metabolite salicylic acid
38
Q

Salicylates: Aspirin

Analgesic vs Anti-inflammatory dosing

A
  • Analgesic/antipyretic: 325-650 mg
  • Anti-inflammatory: 1000 mg (3-5 g/day)
    • Increase dose gradually
    • Follow serum salicylate levels
    • Rarely used d/t GI side effects
39
Q

Salicylate overdose

A

metabolic acidosis,

tinnitus

40
Q

When should aspirin not be used?

A

Aspirin should not be used during viral syndromes in children and teenagers because of risk of Reye’s syndrome-encephalopathy

41
Q

Nonacetylated salicylates

A
  • Nonacetylated salicylates have more favorable toxicity profile
    • Do not interfere w/ plt aggregation
    • Rarely associated w/ GI bleeding
    • Well tolerated by asthmatic pts
42
Q

NSAIDs

Mechanism

A
  • Mechanism
    • Cyclooxygenase (COX) inhibition –> Blocks conversion of arachidonic acid to prostaglandins (PGs) –> Decreases production & release of PGs
    • ​Reversible inhibition of plt aggregation
      • Inhibition of COX-1 blocks synthesis of thromboxane A2 which inhibits plt aggreg
  • ​Analgesic, anti-inflammatory, antipyretic activity
43
Q

NSAIDs

A
  • Analgesic efficacy
    • Helpful for arthritis-related pain, musculoskeletal pain, headaches and dysmenorrhea → ceiling effect w/ post-op pain!
    • More effective than full doses of ASA or acetaminophen
    • Equal or greater than usual doses of an opioid combined w/ acetaminophen
  • Different NSAIDs: Similar efficacy at equipotent doses. Pt-to-pt differences…Toxicity differences
  • Anti-inflammatory
  • Asthma and anaphylactoid reaction in aspirin-sensitive pts
44
Q

T or F: NSAIDS can cause physical dependence

A

FALSE.

Unlike opioids, no physical dependence

45
Q

NSAIDS

Adverse Effects

A

Rare adverse effects:

Hepatic injury

Aseptic meningitis

46
Q

NSAIDS and Pregnancy

A
  • Pregnancy
    • Best avoided but Category B if necessary
    • Avoid in 3rd trimester, Category D, due to premature closure of DA
47
Q

NSAIDS

Pk

A
  • Weak acids - well-absorbed
  • Highly protein-bound >95%
  • Small Vd (non-specific NSAIDS)
  • Extensively metabolized and excreted in urine
  • Half-life varies from <6 hrs to >12 hrs
48
Q

NSAIDs: GI Adverse Effects

A
  • Dyspepsia, GI bleeding, PUD
  • Inhibition of PGs that maintain normal gastric and duodenal mucosa
    • Increases acid production
    • Decreases mucus production, gastric blood flow
  • Local irritation
    • ​Lipid soluble at low pH - enter gastric mucosal cells - lose lipid solubility - become trapped in cell
49
Q

NSAIDS GI Adverse Effects:

Risk Factors

A
  1. High doses
  2. Prolonged use
  3. Previous GI ulcer or bleeding
  4. Excessive ETOH
  5. Elderly
  6. Corticosteroid use
50
Q

GI Risk of Specific NSAIDs

A
  • Low Risk
    • Ibuprofen and naproxen at low doses
    • Etodolac, sulindac
    • Celecoxib
  • Moderate Risk
    • Ibuprofen and naproxen at mod-high doses
    • Diclofenac, oxaprozin, meloxicam, nabumetone
  • High Risk
    • Ketorolac
    • Piroxicam, indomethacin, tolmetin, aspirin
51
Q

NSAIDs:

Renal Adverse Effects

A
  • Decreased synthesis of renal vasodilator PGs (PGE2)
    • Leads to decreased renal blood flow
    • Fluid and Na+ retention
    • May cause renal failure or HTN
    • Interstitial nephritis (rare)
    • Rarely clinically significant in healthy people
52
Q

NSAIDS Renal Adverse Effects:

Risk Factors

A
  • Risk factors (i.e. people who require prostaglandins for renal perfusion)
    1. Old age
    2. CHF
    3. HTN
    4. DM
    5. renal insufficiency
    6. ascites
    7. volume depletion
    8. diuretic therapy
53
Q

Renal Risk of Specific NSAIDs

A
  • Can occur w/ all NSAIDs
  • Increased risk
    • Higher dose
    • Longer E1/2t
    • Highly potent COX inhibitors
      • Ketorolac, indomethacin
  • “Renal sparing” (lower risk, not devoid)
    • Sulindac, celecoxib
    • Nabumetone
54
Q

NSAIDs: Drug Interactions

A
  • Displaces other highly protein-bound agents
    • Increases levels of warfarin, phenytoin, sulfonylureas, sulfonamides, digoxin
  • Increases lithium levels
  • Probencid increases levels of most NSAIDs
    • Avoid w/ ketorolac
  • ​Increased r/f GI bleed when combined w/ anticoags
  • Reduces effect of:
    • diuretics, b-blockers, ACEIs via suppression of renal PGs
55
Q

Ketorolac

A
  • Only IV NSAID available in US
  • IM or IV comparable to mild opioids
    • Similar time to pain relief w/ ketorolac or morphine
      • Advantage: No ventilatory or CV depression
  • Adverse effects similar to typical NSAID:
    • Increased bleeding time, peri-op blood loss, GI bleeding, ulceration, perforation and/or renal toxicity (esp in elderly or hypovolemic), potential life-threatening bronchospasm
  • Do not exceed 5 days of use
56
Q

Ketorolac

Pharmacokinetics

A
  • IV onset: ~ 10 min
  • DOA: 6-8 hrs
  • E½t: 5 hrs (prolonged in elderly 30-50%)
  • Highly protein bound (99%)
  • Conjugated in liver
57
Q

Ketorolac

Dose

A
  • Dose IV:
    • 30 mg IV X 1 or q 6 hrs
    • Daily max dose 120 mg
    • Elderly: (if you use at all) cut dose in ½
58
Q

Selective NSAIDs

A
  • Celecoxib (Celebrex) only agent available today
    • Rofecoxib (Vioxx), Valdecoxib (Bextra) withdrawn from market d/t ↑ MI risk
  • Selectively inhibit COX-2 (nonselective NSAIDs inhibit COX-1 and COX-2)
  • No more effective at reducing pain and inflammation
  • COX-1: gastric protection and production of TxA2 (vasoconstrictor, plt aggregator)
  • COX-2: production of prostacyclin (vasodilator, plt inhibitor)
  • Same risk of renal adverse effects
59
Q

Celecoxib

A
  • Use lowest effective dose
    • < 200 mg/day
    • 200 mg/day = naproxen 500 mg BID
  • Consider pt’s r/f: CV and GI events
    • Weigh risk vs. benefit
  • PO
    • Taken w/ food
  • Avoid in pts w/ sulfonamide allergy
60
Q

Black Box Warnings

Selective and non-selective NSAIDs

A
  • CV Risk
    • ↑ r/f serious CV thrombotic events, MI, stroke, which can be fatal
  • GI Risk
    • ↑ r/f bleeding, ulceration, perforation of stomach or intestines → can be fatal
61
Q

Adjuvant Analgesics

A
  • Antidepressants and anticonvulsants - drugs of choice for neuropathic pain syndromes
    • TCAs (amitriptyline, nortriptyline, etc.)
      • Diabetic neuropathy, postherpetic neuralgia, polyneuropathy, and nerve injury or infiltration with cancer
      • May also improve underlying depression and insomnia
    • Venlafaxine (Effexor)-SSNRI
      • Neuropathic pain, headache, fibromyalgia, postmastectomy pain
    • Duloxetine (Cymbalta)-SSNRI
62
Q

Other Agents

A
  • Hydroxyzine
    • Low-dose IV/IM add analgesic effect to opioids in CA and post op pain while ↓ incidence of N/V
  • Corticosteroids
    • Can produce analgesia in some pts w/ inflammatory dz or tumor infiltration of nerves
  • Topical analgesics
    • 5% Lidocaine (lidoderm) approved for post herpetic neuralgia
    • Topical EMLA useful for cutaneous anesthesia
    • Capsaicin cream (Zostrix) for neuropathic and osteoarthritic pain
    • Transdermal clonidine patch may improve pain and hyperalgesia in sympathetically maintained pain
    • THC/CBD
    • Ketamine
    • Magnesium
63
Q

Adjuvant Analgesics: Anticonvulsants (List them)

A
  1. Gabapentin (Neurontin) –mechanism not well understood
  2. Pregabalin (Lyrica) –gabanergic, analogue of GABA
  3. Carbamazepine (Tegretol)-Na channel blocker, and GABAnergic
  4. Phenytoin (Dilantin), Sodium Valproate (Depakote), Clonazepam (Klonopin), and Topiramate (Topamax)
  5. Lamitrogen (Lamictal)-Gabanergic
64
Q

Gabapentin (Neurontin)

A

Gabapentin (Neurontin)

  • Mechanism not well understood
  • Diabetic neuropathy, postherpetic neuralgia
65
Q

Pregabalin (Lyrica)

A
  • Gabanergic, analogue of GABA
  • Diabetic neuropathy, postherpetic neuralgia, fibromyalgia
  • Analgesic effects may be related to Ca++ influx inhibition as well as inhibition of release of excitatory NT’s in spinal and supraspinal pathways via binding to α 2 δ-1 subunit of presynaptic voltage-gated Ca++ channels in CNS.
66
Q

Carbamazepine (Tegretol)

A
  • Na channel blocker and GABAnergic
  • FDA approved for trigeminal neuralgia
67
Q

Phenytoin (Dilantin), Sodium Valproate (Depakote), Clonazepam (Klonopin), and Topiramate (Topamax)

A

May relieve neuropathic pain

68
Q

Lamitrogen (Lamictal)

A
  • Gabanergic
  • Effective for central post-stroke pain and HIV-associated painful sensory neuropathies

Pharm-Spring (7 decks)

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