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Pharmacology test 2 > Pain relief > Flashcards

Pain relief Flashcards

1
Q

Unique Opioid characteristics

A
  • Moderate to severe pain
  • No max dose or ceiling effect
  • Tolerance can develop with chronic use
  • Tolerance associated with physical dependence but not necessarily with psychological dependence
  • Cross-tolerance
  • Produce analgesia without loss of: Touch, Proprioception, Consciousness (in smaller doses)
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2
Q

Naturally occurring opioids

A

morphine, codeine

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3
Q

Semisynthetic

A

Analogs of morphine

-Heroin and dihydromorphone

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4
Q

Synthetics

A

exogenous, 4 groups

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5
Q

Opioid MOA

A

Activate stereospecific G-protein coupled receptor

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6
Q

Opioid MOA post-synaptic

A

directly decreased neurotransmission:
-Increased K conductance (hyper polarization)– main way
Ca channel inactivation (decreased NT release)
-Modulation of phosphoinositide – signaling cascade and phospholipase C
-Inhibition of adenylate cyclase (decreased cAMP )

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7
Q

Opioid MOA pre-synaptic

A

inhibits the release of excitatory neurotransmitters:

-decrease: ACh dopamine, NE, subs P release

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8
Q

Opioid Receptors

which ones, theory

A

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 the different receptors types among the different drugs in this class

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9
Q

Mu receptors

A

subtypes: Mu-1 and Mu-2
- Mu-3: thought to be involved in immune process
- All endogenous and exogenous agonist act on mu receptors
- Mu located in Brain, Periphery and SC

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10
Q

Mu-1

A

Supraspinal, spinal, and peripheral analgesia

  • Euphoria
  • Miosis
  • Bradycardia (bad in kids, in adults can blanace O2 consumption/demand)
  • Urinary retention
  • Hypothermia
  • All endogenous and synthetic opioid agonists act on these receptors
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11
Q

Mu-2

A
  • Hypoventilation
  • Physical dependence
  • Spinal analgesia (also some supra spinal)
  • Constipation
  • all endogenous and exogenous agonist act on these receptors
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12
Q

Kappa receptor

A

Supraspinal, Spinal and peripheral analgesia

  • Dysphoria
  • Sedation
  • Miosis
  • Diuresis (different from others)
  • Dynorphins act on these receptors
  • Opioid agonist-antagonists often have principle actions at the kappa receptor
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13
Q

Delta receptor

A

Peripheral, Supraspinal and spinal analgesia

  • Hypoventilation
  • Constipation
  • Urinary retention
  • Enkephalins work on these receptors
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14
Q

Genetic Code and the mu opioid receptor

A

opioid agonist binding can be influenced by mutation to the amino acid sequence

  • Nucleotide 118= aspartate in place of asparagine
  • Nucleotide 17= valine in place of alanie
  • Incidence varies with racial/ethic group
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15
Q

CYP2D6= 5 common mutations can alter the metabolism of:

-and least impacted

A

codeine, oxycodone, hydrocodone, and methadone

  • Unpredictable pharmacokinetics and 1⁄2 lives
  • Metabolism least impacted by genetic variability: Fentanyl
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16
Q

Rate of metabolism

A

may influence side effect rate

-ultra-rapid metabolizers at increased risk for PostOp N/V

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17
Q

Systemic Effects of opioids

A
  • many systemic effects are similar among the opioids
  • Varialbe SE and efficiency profiles (consider the carnage in chemical structures)
  • *morphine as prototype
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18
Q

Perioperative Cardiovascular effects

opioids

A
  • Minimal impairment in CV function when used alone
  • though: Additive CV effects with other anesthetics
  • considered Cardiac Stable
  • Dose dependent bradycardia
  • -Central vagal stimulation (nuclei in medulla), direct SA, VA nodal depression
  • Vasodilation/Decreased SVR (all pt dehydrated, bc we keep them NPO)
  • -impairment of SNS responses and baseline tone
  • -decreased CO and BP with venous pooling-orthostatic hypotension
  • pronounced effect with hypovolemia
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19
Q

Morphine and Meperidine CV effects

A

dose depended and infusion rate dependent histamine release

  • Bronchospasm and dramatic drops in SVR and BP
  • Variable response among individual patients
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20
Q

Meperidine CV effects

A

the exception: Tachycardia with more prominent direct myocardial depression

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21
Q

Opioid CNS effects

A

Analgesia

  • Euphoria
  • Drowsiness/sleep
  • Miosis
  • Nausea- chemoreceptor trigger zone (at medulla)
  • Does not produce amnesia
  • ??If hypoventilation prevented: -Modest decrease in ICP -Decrease CBF
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22
Q

Opioid Perioperative: Renal/GI/Liver Effects

A

↑ tone and peristaltic activity of ureter and increased detrusor muscle tone = ↑ urgency with ↓ ability to void
-↓ catecholamine release and cortisol
-Spasm of sphincter of Oddi and gallbladder
contraction with ↑ in biliary pressure
-Spasm of GI smooth muscle
-Constipation-decrease GI motility
-Prolonged gastric emptying (aspiration risk)

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23
Q

Opioid N/V bc:

A

Decreased gastric emptying

  • Direct stimulation of the chemoreceptor trigger zone on the floor of the 4th ventricle
  • Partial dopamine agonist?
  • Balanced by depression of the medullary vomiting center (over time will get better ex: CA pt)
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24
Q

Opioid pruritus bc:

A

Cause unknown

  • Histamine release most probable cause with some
  • Occurs primarily on face particularly nose
  • “fentanyl nose itch
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25
Q

Opioid skeleteal muscle effects periop

A

Skeletal muscle rigidity in chest(wooden chest), abdomen, jaw and extremities
-Especially with large rapidly administered opioid doses
-Common with fentanyl, sufentanil, and hydromorphone
-Can make ventilation difficult or impossible (Wooden Chest)
-High airway pressures from increase intrathorcic
pressures/decrease venous return
-Glottic rigidity and glottic closure have been reported

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26
Q

opioid Ventilatory effects periop

A

Dose dependent respiratory depression

  • Smaller doses: Usually increased Vt with decreased RR; overall decrease in minute ventilation (↑CO2, ↓O2)
  • Larger doses decreased Vt
  • Decrease compliance in chest wall
  • Constriction of pharyngeal and laryngeal muscles
  • Cough suppression
  • Decreased response to hypercarbia and hypoxia
  • Morphine and Meperidine = histamine related bronchoconstriction
  • Ventilatory depression #1 reason people die from OD
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27
Q

Vent curve with opioids

A

Shift to the right and slope is decreased

  • wont clear CO2 very well
  • be careful with pt with increased ICP
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28
Q

Factors ↑ Magnitude/Duration of Opioid Induced Respiratory Depression

A 
Depends on context: amount of
pain/surgical stimulation, natural sleep
-Intermittent bolus vs. cont. infusion (less spiking, less meds)
-Speed of injection
-Concurrent admin with other anesthetics
-Decreased clearance
-Age
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29
Q

Morphine route and usage

A

-almost always IM or IV
-For severe acute pain
-PO for chronic pain and cancer pain
–slow release–delayed onset 3-5hrs (not used in preop or intraop)
*Considerable first pass effect
-1/2 life 3-4hrs
converted to active metabolite (morphine-6-glucuronide)

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30
Q

Codeine use, route, 1/2life, metabolized

A
  • Mild Pain Relief
  • PO
  • E1/2t = 3 hour
  • PO combined with APAP, guaifenesin, promethazine
  • *Prodrug: 10% is metabolized by CYP2D6 to its active form
  • Remaining drug is demethylated to inactive metabolite
  • *Active form = morphine
  • 10% Caucasians, 30% Asians lack 2D6 – no analgesic effect
  • Antitussive (cough) effect remains even without conversion(enzyme)–Better for cough (lower dose) than pain relief
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31
Q

Hydrocodone use, route, precautions

A

AKA – Vicodan (hydrocodone + APAP)

  • PO
  • Always combined with either APAP, ASA, ibuprofen, antihistamine
  • Analgesic and antitussive
  • Used for chronic pain
  • High abuse potential (dangerous bc of APAP)
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32
Q

Oxycodone route ,use, metabolites SE

A

PO
-AKA Oxycontin, Percocet, Percodan
-Available in sustained release preparation (oxycontin)
-Moderate to severe pain; useful for chronic pain, post- op pain
-Also in combination with APAP and ASA
-No active metabolites - safer in patients with renal
dysfunction
-High abuse potential

33
Q

Methadone route, 1/2life, use, metabolize,

A

PO, IV, SubQ

  • Synthetic
  • Long plasma half-life- 8-59 hours or 13-100 hrs
  • Opioid addiction treatment (maintenance) dosed QD
  • No active metabolites - safer in patients with renal dysfunction
  • Chronic pain syndrome treatment: doses BID or TID (q4-8 hr)
  • Tx: Neuropathic pain, chronic pain, opioid addiction tx
  • At risk for severe respiratory depression secondary to prolonged and unpredictable E1/2t
34
Q

Naloxone with opioid agonist

A

Competitive antagonist

35
Q

Tolerance to opioids

A

Tolerance is common with chronic use of opioids (after 2-3 weeks of use)

  • Pt first notices a reduction in adverse effects
  • Shorter duration of analgesia
  • Followed by decrease in effectiveness of each dose
  • Tolerance to most adverse effects include:
  • Respiratory and CNS depression
  • Can be overcome by increasing the dose
  • -Switching opioid-tolerant patients to methadone may improve pain relief
  • Tolerance to sedative and emetic effects develop rapidly but not constipation
  • A stimulant laxative with or without a stool softener should be started early in tx
  • ex: senna/docusate
36
Q

Cross-tolerance to opioids

A

Cross-tolerance exists among all full agonists but is not complete (not 1:1)
-When switching to another opioid, start with half or less of the equianalgesic dose

37
Q

Dependence of opioid

A
  • Physical dependence causes abstinence symptoms upon sudden D/C
  • Clinically significant dependence develops only after several weeks of chronic tx
  • Addiction involves psychological dependence and biologic and social factors
  • Cancer pain and acute pain patients rarely experience euphoria and even more rarely develop psychological dependence or addiction
38
Q

PO dosage of opioids

A

-Dose vary widely from one pt to another
-No minimum or maximum dose except limitation by the dose of
APAP or aspirin
-“Weak” vs “strong” terminology usually inappropriate (codeine exception) - can dose different drugs so that they are equivalent
-Dose required to maintain optimum pain relief with tolerable side effects must be used
-After initial titration with short-acting opioid in the first 12 to 24 hrs, dose determination by around-the-clock dosing is recommended

39
Q

Dosage PO sustained vs immediate

A
  • A sustained release formulation should be used in chronic pain
  • Immediate release doses that are 10 to 15% of the total daily dose should be used for breakthrough pain
  • PCA, given IV, SQ or other routes are now widely used when the oral route are not feasible
40
Q

Opioids: Neuraxial effects spinal and systemic effects

A

Analgesia a result of diffusion of the drug
-Across the dura to mu receptors in substantia
gelatinosa
-Into the vasculature – systemic effect
-Opioids given epidural or spinal have different onset, duration, and side effects as same drug given IV
-Opioids placed in epidural space may undergo uptake into fat, systemic absorption or diffusion into CSF: get both spinal and systemic
–Lipid soluble get resp depression sooner
–Water soluble (morphine) stays in CSF then hits the brain stem get resp depression 24 hrs later

41
Q

Neuraxial effect opioids

-lipid solubility

A

Cephalad movement of opioid in the CSF depends on lipid solubility
-Highly lipid soluble will be limited in migration by
uptake into the spinal cord ie. fentanyl
**Whereas less soluble opioid will remain in CSF for transfer to cephalic location ie. Morphine
-Penetration into CSF/vasculature depends upon lipid solubility
-More lipid soluble, quicker peak CSF/systemic concentration

42
Q

Neuraxial effects dose spinal vs epidural

A

Dose for epidural is 5-10X higher than spinal dose

-May reduce local anesthesia dose in epidural/spinal as reducing overall anesthetic requirements

43
Q

Non-opioids

A

Acetaminophen
Acetylated Salicylate
NSAIDS
Cyclooxygenase-2 Specific Inhibitors

44
Q

NSAIDS

names 12

A
  • Ibuprofen (Motrin)
  • Naproxen (Naprosyn)
  • Oxaprozin (Daypro)
  • Diclofenac (Voltaren)
  • Etodolac (Lodine)
  • Indomethacin (Indocin)
  • Ketorolac (Toradol)
  • Nabumetone (Relafen)
  • Sulindac (Clinoril)
  • Tolmetin (Tolectin)
  • Piroxicam (Feldene)
  • Meloxicam (Mobic)
45
Q

Non-opioid analgesics factors to consider 5

A
  • First line agents for mild to moderate pain
  • Ceiling effect of ASA and APAP between 650 and 1300 mg
  • NSAIDs other than aspirin - analgesic ceiling may be higher
  • Exceeding the ceiling dose of any of these drugs will result in increased adverse effects with no added efficacy
  • Tolerance does not develop to the analgesic effects of these drugs
46
Q

Acetaminophen: MOA, lacks, uses

A

Central anti-prostaglandin effect

  • Antipyretic
  • Pain reduced via blockade of: NMDA receptor activation in CNS and Substance P in spinal cord
  • weak anti-inflammatory action (not a true NSAID)
  • Good choice in:
  • -Peptic ulcer disease
  • -Pediatric patients (safe)
  • Patients who need well functioning platelet
47
Q

Acetaminophen dose

A

PO similar potency as ASA (in single analgesic doses, has same time-effect curve)

  • PO Dose = 325-650 mg Q4-6 hrs
  • IV formulation just FDA approved in US in 2010.
  • IV dose 1 gram over 15 minutes infusion only q4-6 hours not to exceed ***4000mg in 24 hours (check to make sure no other sources of acetaminophen)
48
Q

Acetaminophen metabolism

A
  • IV give at end of case because of plasma concentration

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

49
Q

Acetaminophen overdose

A

Overdose can cause serious or fatal hepatic injury

  • Liver can only metabolize a limited amount of the hepato- toxic metabolite N-acetyl-p-benzoquinone with glutathione
  • When glutathione outnumbered by OD of acetaminophen hepatic injury occurs
  • Maximum safe dose 4 grams per day
  • Safe dose even lower in ETOH abuse (use caution)
  • Also increased risk of toxicity in patients taking **isoniazid
  • Acetylcysteine can substitute for glutathione and prevent hepatic injury if given within 8 hours of OD
50
Q

Acetaminophen renal toxicity

A
  • 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
51
Q

Arachidonic Acid Metabolism

A
  • NSAIDS and ASA:
  • Arachadonic acid is released from phospholipids by the enzyme phospholipase A2
  • Arachadonic acid is immediately metabolized by either:
  • -Cyclooxygenase
  • -Lipoxygenase
  • -Epoxygenase
52
Q

Cyclooxygenase lead to formation of:

A
  • Prostaglandins
  • Prostacylcin
  • Thromboxanes
53
Q

Lipoxygenase leads to the formation of:

A

Leukotrienes

lipoxins

54
Q

Epoxygenase leads to the formation of

A

Epoxyeicosatetraenoic acid ( 4 types ) – regulates inflammation further research necessary to determine precise role

55
Q

Arachidonic Acid

Cox 1 and 2

A 
Cox1: prostaglandins:
-Gastric Protection
-Hemostasis
-Renal Function
COX2: prostaglandins
-Pain
-Fever
-Inflam
*block Cox 2 then increased the other half of the pathway. Thats why selective COX2 blockers were dangerous  increased platelet aggregation and put puts at risk for Stroke and MI
*NSAIDS block both sides
56
Q

Salicylates: Aspirin use, MOA

A

Aspirin effective in most mild to moderate pain

  • HA muscle pain, arthritis
  • Antipyretic
  • MI/stroke prevention; protection during MI (anti-plt)
  • IRReversible inhibition of COX, if going to hold before sure have to hold for a least a week
  • Single dose inhibits platelet function for lifetime of platelet (8-10 days)
  • Large doses can also decrease prothrombin
57
Q

Salicylates: Aspirin Side effects

A

ESRD: NOT induced by chronic ASA

  • Prolonged bleeding (up to 15 minutes) in these patients with ASA
  • Can increase LFTs (usually reversible)
  • Single dose can potentiate asthma in aspirin-sensitive patients
  • Cross-sensitivity with other NSAIDS
  • can cause GI bleeding, PUD
  • CNS stimulation tinnitus
58
Q

Salicylates: ASA dosing, clearance, overdose

A

*Analgesic vs anti-inflammatory dosing
-Analgesic/antipyretic: 325-650mg
-Anti-inflammatory: 1000mg (3-5 g/day)
-Increase dose gradually
-Follow serum salicylate levels
-Rarely used due to GI side effects
*Hepatic clearance
-E1/2t is 15-20 minutes for aspirin and 2-3 hrs for the active
metabolite salicylic acid
*Salicylate overdose: metabolic acidosis, tinnitis

59
Q

Salicylates: ASA contraindications

A

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

60
Q

NSAIDS analgesic efficacy

A
  • Helpful for arthritis related pain, musculoskelatal pain, headaches and dysmenorrhea → **ceiling effect with post-op pain!
  • More effective than full doses of aspirin or APAP
  • Equal or greater than usual doses of an opioid combined with APAP
  • Anti-Inflamm
61
Q

Different NSAIDs

A
  • Similar efficacy at equipotent doses
  • Patient-to-patient differences
  • Toxicity differences
62
Q

NSAID: MOA, protein bound, VD, Metabolized, half life

A

Cyclooxygenase (COX) inhibition

  • Blocks conversion of arachidonic acid to prostaglandins (PGs)
  • Decreases production and release of PGs
  • Reversible inhibition of platelet aggregation
  • -Inhibition of COX-1 blocks synthesis of thromboxane A2 which inhibits platelet aggreg
  • Analgesic, anti-inflammatory, antipyretic activity (cox2 side)
  • Weak acids - well-absorbed
  • Highly protein-bound >95%
  • Small Vd (non-specific NSAIDS)
  • Extensively metabolized and excreted in urine
  • Half-life varies from 12 hrs
63
Q

NSAIDs contraindications

A

Asthma and anaphylactic reaction in aspirin-sensitive patients

  • no physical dependence
  • Rare adverse effects:
  • Hepatic injury
  • Aseptic meningitis
  • Pregnancy
  • Best avoided but Category B if necessary
  • Avoid in 3rd trimester, Category D, due to premature closure of DA
64
Q

NSAIDs in peri-op inhibition of COX enzyme may result in..

A
  • Renal injury
  • Gastric ulceration
  • Excessive bleeding
  • Impaired bone healing (consult with surgeon)
65
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
*Risk factors
-High doses, prolonged use, previous GI ulcer or bleeding, excessive ETOH intake, elderly, corticosteroid use

66
Q

GI risk of specific NSAIDs low, moderate, high

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
-Tolmetin, piroxicam, aspirin, indomethacin, keto

67
Q

NSAIDs renal adverse effects

A

Decreased synthesis of renal vasodilator PGs (PGE2):

  • Leads to decreased renal blood flow
  • Fluid and sodium retention
  • May cause renal failure or hypertension
  • Interstitial nephritis (rare)
  • In healthy people rarely of clinical significance
  • Risk factors (i.e. people who require prostaglandins for renal perfusion)
  • -Old age, CHF, HTN, DM, renal insufficiency, ascites, volume depletion, diuretic therapy
68
Q

NSAIDs renal risk

A

Can occur with all NSAIDs

  • Increased risk
  • Longer half-life
  • Highly potent COX inhibitors: Ketorolac, indomethacin
  • Higher dose
  • “Renal sparing” (lower risk, not devoid)
  • Sulindac, nabumetone
  • Celecoxib
69
Q

NSAIDS drug interactions

A

Displaces other highly protein-bound agents
-Increases levels of warfarin, phenytoin, sulfonylureas, sulfonamides, digoxin
-Reduces effect of diuretics, β-blockers, ACEIs via suppression of renal PGs (angiotensin 2)
-Increases lithium levels
-Increased risk of GI bleed when combined with anti-
coagulants
-Probencid (gout drug) increases levels of most NSAIDs: Avoid with ketorolac

70
Q

Ketoraolac general

A

-IM or IV comparable to mild opioids
-similar time
to pain relief with ketorolac or morphine
-Advantage: No ventilatory or cardiac depression
-Adverse effects similar to typical NSAID:
-Increased bleeding time and peri-op blood loss, Serious GI bleeding, ulceration, perforation and/or renal toxicity can occur (especially in the elderly or hypovolemic), potential for life-threatening bronchospasm

71
Q

Ketorolac 1/2life, duration of action, protein binding, metabolized, dose

A

Do not exceed 5 days of use

  • IV onset ~ 10 minutes
  • E1/2t: 5 hours (prolonged in elderly 30-50%)
  • DOA: 6-8 hours
  • 99% protein bound
  • Conjugated in the liver
  • Dose IV: 30mg IV X 1 or q 6 hours
  • Daily max dose 120mg
  • Elderly: if you use at all cut dose in 1/2
72
Q

Selective NSAIDs

name, problems

A
  • Celecoxib (Celebrex) only agent available
  • Withdrawn from the market due to increased MI risk: Rofecoxib (Vioxx), Valdecoxib (Bextra)
  • Selectively inhibit COX-2
  • No more effective at reducing pain and inflammation
  • COX-1: gastric protection and production of TxA2 (vasoconstrictor, platelet aggregator)
  • COX-2: production of prostacyclin (vasodilator, platelet inhibitor)
  • Same risk of renal adverse effects
73
Q

Celecoxib

A

Use the lowest effective dose: < 200 mg/day, 200 mg/day = naproxen 500 mg BID

  • Consider patient’s risk for cardiovascular events
  • Consider patient’s risk for GI events
  • PO
  • Should still be taken with food
  • Avoid in patients with a sulfonamide allergy
74
Q

Adjuvant analgesics: antidepressants and anticonvulsants

A 
ANTIdepressents:
-TCAs (amitriptyline, nortriptyline, etc.)
-Venlafaxine (Effexor)
-Duloxetine (Cymbalta)
ANTIconvulsants:
Gabapentin (Neurontin)
-Pregabalin (Lyrica)
-Carbamazepine (Tegretol)
-Phenytoin (Dilantin), Sodium Valproate (Depakote), Clonazepam (Klonopin), and Topiramate (Topamax)
-Lamitrogen (Lamictal)
75
Q

Hydroxyzine

A

1st generation antihistamine

Low-dose IV/IM add analgesic effect to opioids in cancer and post operative pain while reducing incidence of N&V

76
Q

Corticosteroids

A

Can produce analgesia in some patients with inflammatory diseases or tumor infiltration of nerves

77
Q

Topical analgesics

A

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 pa

78
Q

NONacetylated salicylates toxicity profile (vs ASA)

A
  • have a more favorable toxicity profile
  • -Do not interfere with platelet aggregation
  • -Rarely associated with GI bleeding
  • -Well tolerated by asthmatic patients

Pharmacology test 2 (6 decks)

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