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PO Pain Flashcards

1
Q

What are the 3 majors sites of action of opioids?

A
  • Brain (supraspinal)- opioids work prea nd post synaptically to activate descending inhibitory pathways
  • Spinal cord (spinal)- directly on the dorsal horn of the SC
  • Periphery- peripheral terminals of nociceptive neurons
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2
Q

What are opioids are used for in anesthesia?

A
  • Attenuate the SNS response to noxious stimuli
  • Adjunct to inhaled agents during anesthesia
  • Sole anesthetic (fentanyl/sufent/morphine- cardiac anesthesia only high doses, critically ill pateints
  • perioperative and post op control of pain
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3
Q

What are opioid characteristics that set them apart from other analgesics?

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- tolerant to one opioid, will be tolerant to others
  • produce analgesia wihtout loss of
    • touch
    • proprioception
    • consciousness (in smaller doses)
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4
Q

What are some opioid classifications by class?

A
  • Naturally occuring
    • morphine and codein
  • Semisynthetic: analogs of morphine
    • heroin and dihydromorphone
  • Synthetic
    • exogenous 4 groups
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5
Q

What are opioid classifications by action at receptor?

A
  • Agonist- full activation
  • Partial agonist
  • Mixed agonist/antagonis- less activation
  • Antagonist- prevents activation
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6
Q

What is mechanism of action of opioid?

A

Activate sterospeicfic G protein coupled receptors

  • post synaptic- directly decrease neurotransmission
    • increased K conductance (hyperpolarization)
    • Ca channel inactivation (decreased NT release)
    • Modulation of phosphoinositide- signaling cascade and phospholipase C
    • Inhibition of adneylate cyclase (decreased cAMP)
  • pre synaptic- inhibits release of excitatory NT
    • decrease acetylcholine, dopamine, norepinephrine, substance P release
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7
Q

What are the main opioid receptors?

A
  • Mu, kappa, 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 the different drugs in this class
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8
Q

What are the Mu receptos?

A
  • Subtypes mu-1 and mu-2 (all opioids interact with these 2 receptors)
  • 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

What does Mu-1 cause?

A
  • Supraspinal (most), spinal and peripheral analgesia
  • euphoria
  • miosis
  • bradycardia
  • urinary retention
  • hypothermia
  • all endogenous and synthetic opioid agonists work on these receptors
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10
Q

What does Mu-2 cause?

A
  • Hypoventilation
  • Physical depedence
  • spinal analgesia (also some supraspinal)
  • constipation
  • all endogenous and exogenous agonists act on these receptors
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11
Q

What does Kappa receptor cause?

A
  • Suprasinal, spinal and peripheral analgesia
  • dysphoria
  • sedation
  • miosis
  • diuresis
  • dynorphins act on these receptors
  • opioid agonist-antagonists often have principle actions at the kappa receptor
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12
Q

What does delta receptor cause?

A
  • Peripheral, supraspinal and spinal analgesia
  • Hypoventilation
  • Constipation
  • Urinary retention
  • Physical dependence (on chart)
  • Enkephalins work on these receptors
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13
Q

What are some genetic influencings on cyp 450 system and influence on opioids?

A
  • CYP2D6 has 5 common mutations that can alter metabolism of
    • codeine, oxycodone, hydrocodone and methadone
    • can have unpredicatable pharmacokinetics and 1/2 lives
  • Fentanyl metabolism least likely to be impaced by genetic variability in surgical population= has predictable pharmacokinetics (most immune to variances in metabolism
  • Rate of metabolism may influence side effect rate
    • studies indicate ultra rapid metabolizers at increased r/f PONV
      • Believe someone if they say morphine makes them really nausous and avoid morphone analogs (fentanyl ok)
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14
Q

What are some systemic effects of opioids?

A
  • Many systemic effects similar among opioids
  • althought diff opioids are active at diff receptors to diff degress
  • variable s/e and efficacy profiles
  • makes sense if you consider the variance in chemical structures
  • morphine as prototype
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15
Q

What are some CNS effects of opioids?

A
  • Analgesia
  • Euphoria
  • Drowsiness/sleep
  • miosis (pupillary constriction)
  • nausea- chemoreceptor trigger zone
  • does NOT produce amnesia
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16
Q

Pulmonary effects of opioids?

A
  • Decreased RR and increased TV
  • at higher doses, decreased RR and TV, leading to apnea
  • decreased response to CO2/hypoxia
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17
Q

What are some GI effects of opioids?

A
  • Decreased gastric emptying
  • direct stimulation of chemoreceptor trigger zone on the floor of 4th ventricle
    • partial dopamine agonist?
    • balanced by depression of the medullary vomiting center
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18
Q

What causes pruritis by opioids?

A
  • Cause unknown
  • occurs primarily on face, particularly nose
  • “fenatnyl nose itch”
  • histamine release most probably cause with some i.e. MSO4 (also demerol)
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19
Q

What is morphine?

A
  • Naturally occuring opioid
  • Severe acute pain almost always IM or IV admin
  • PO used for chronic pain and cancer pain
    • slow release formulations available- delayed onset 3-5 hours (not used preop/intraop much)
    • considerable first pass effect
    • 1/2 life 3-4 hours converted to active metabolite (morphine 6 glucuronide)

LAST SEMESTER STUFF (JUST IN CASE):

  • Poor lipid solubility, PB= 35% (dr e syas this is high…) hightly ionized
  • histamine release
  • IM peak effect 45 min; IV 15-30 MIN
  • DOA 4 hours
  • BRADYCARDIA VIA DIRECT STIMULATION OF VAGUS NERVE
    • ​Inhibition of SA node as well
  • metabolized by liver
    • active metabolite M6G > potency than MSO4
  • Kidneys play role in extrahepatic metabolism
    • renal failure will have prolonged effects d/t M6G- AVOID!!
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20
Q

What is codeine?

A
  • Mild pain relief
  • PO
  • e1/2 t= 3 hours
  • 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 effect remains even without conversion
  • better for cough (lower dose) than pain relief
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21
Q

What is hydrocodone?

A
  • Vicodan
  • PO
  • Always combinesd with either ASA, ibuprofen, antihistamine, acetaminophen
  • analgesic and antitussive
  • used for chronic pain
  • high abuse potential
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22
Q

What is oxycodone?

A
  • PO
  • AKA oxycontin, percocet, percodan
  • available in sustained release preparation (oxycontin)
  • mod to severe pain; useful for chronic pain, postop pain
  • also in combo with ASA or tynelol
  • no active metabolites- safer in patients with renal dysfunction
  • high abuse potential
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23
Q

What is methadone?

A
  • PO, IV, Sub q
  • synthetic
  • long plasma half life 8-59 hours or 13-100 hours (sources vary with range)
  • opioid addiciton treatment (maintenance) dosed QD
  • No active metabolites- safer in patients with renal dysfunciton
  • chronic pain syndrome treatment: doses BID or TID q 4-8 hours
    • neuropathic pain
    • at risk for severe respriatory depression secondary to prolonged and unpredictable e1/2t
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24
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 surmounted by increasing the dose
  • cross tolerance exists amojng all full agonists but is not complte
  • when switching to another opioid, start with half or less of the customary equianalgesic dose
  • switching opioid tolerant patients to methadone may improve pain relief
  • tolerance ot sedative and emetic effects develop rapidly but not constipation
    • a stimulant laxative with or without a stool softener should be started early in tx
    • senna/docusate
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25
Q

What is dependence?

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 an deven more rarely develop psychologicla dependence or addiction
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26
Q

Dosage of opioids?

A
  • Dose vary widely from one pt to another
  • no minimum or max dose except limitation by the dose of acetaminophen or aspirin
  • dose required to maintain optiumum pain relief with tolerable side effects must be used
  • after intiial titration with short-acting opioid in first 12-24 hours, dose determination by around the clock dosing is recommneded
  • a sustained release forumlation should be used in chronic pain
  • immediate release doses that are 10-15% 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
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27
Q

Equianalgesic doses for control of of chronic pain?

A

If pain is well controlled and switching opioids, calculate equivalent dose and reduce by 25% for dose of new drug

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28
Q

What is equianalgesic dose of meperidine (PO and SQ/IV?)

A

PO= 150 mg

SQ/IV= 50 mg

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29
Q

What is equianalgesic dose for codeine (po and sq/iv?)

A

PO= 100 mg

sq/iv= 60 mg

30
Q

PO equianalgesic dose for hydryocodone?

31
Q

Morphine equianalgesic dose (PO and SQ/IV?)

A

PO= 15 mg

SQ/IV= 5 mg

32
Q

Equianalgesic dose of oxycodone (PO)

33
Q

Equianalgesic dose methadone? PO and SQ/IV?

A

10 mg PO

5 mg SQ/IV

34
Q

Hydromorphone equianalgesic dose (PO, SQ/IV?)

A

PO= 4 mg

SQ/IV= 1.5 mg

35
Q

What are some consideratiosn for non-opioid analgesics?

A
  • First line agents for mild to moderate pain
  • ceiling effect of ASA and acetaminophen b/w 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
36
Q

What is acetaminophen?

A
  • Central antiprostaglandin effect (unsure how)
    • antipyretic
    • pain reduced via blockade of:
      • NMDA receptor activation in CNS
      • Substance P in spinal cord
      • may also be cannabinoid
  • Lacks peripheral activity- weak antiinflammatory action (not a true NSAID)
    • good choice in:
      • peptic ulcer disease
      • ped patients
      • patients who need well functioning platelets
      • also good for pt with asthma because increase risk for NSAID reaction
37
Q

Dosing for acetaminophen?

A
  • PO similar potency as ASA (in single analgesic doses, has same time-effect curve)
  • PO dose= 325 mg-650 mg q 4-6 hours
  • IV formulation just FDA approved in US in 2010
    • IV dose 1 gram over 15 minutes infusion only q 4-6 hoursnot to exceed 4000 mg in 24 hours
38
Q

How is tylenol metabolized?

A

conjugated and hydroxylated to inactive metabolites; very little excreted unchanged in kidneys

39
Q

Issues with acetaminophen?

A
  • Overdose can cause serious or fatal hepatic injury
    • liver can only metabolize a limited amount of hepato-toxic metabolite N-acetyl-p-benzoquinone with glutathione
    • when glutathione outnumbered by OD of acetaminophen, hepatic injury occurs
    • max safe dose 4 grams/day
    • safe dose even lower in ETOH abuse (use caution) (also in pancreatitis)
    • also increased risk of toxicity in patients taking isoniazid
    • acetylcysteine can substitute for glutathione and prevent hepatic injury if given within 8 hours fo OD
40
Q

Renal toxicity with acetaminophen?

A
  • Renal papillary accumulation of metabolites can cause renal cell necrosis
  • may be responsible for devleopment of some cases of ESRD
    • Even though liver saved, can end up with ESRD from toxicity damag
    • however, NSAIDS higher risk of renal toxicity than acetaminophen
41
Q

What is the metabolism of arachidonic acid?

A
  • Arachidonic acid is released from phospholipids by enzyme phospholipase A2
  • Arachidonic acid is immediately metablized by either
    • cyclooxygenase lead to formation of
      • prostaglandin
      • prostacyclin
      • thromboxane
    • lipoxygenase leads to formation of
      • leukotrienes
      • lipoxins
    • Epoxygenase leads to formation of
      • epoxyeicosatetraenoic acoid (4 types)
        • regulated inflammation further researhc necessary to determine precise role
42
Q

How do NSAIDS work?

A

Inhibit cyclooxygenase

43
Q

How are phospholipase’s generated?

A

by inflammatory process, released from cell membrane

44
Q

What is Cox-1 and Cox 2?

A

Cyclooxygenase 1 and 2

  • Cox 1 - (constitutive= always working)
    • makes prostaglandins which:
      • protect gastric mucosa
      • endothelial function
      • (production of proaggregatory thromboxane A2 IN PLT– from book)
  • Cox 2- inducible (by cytokines IL-1 and TNF which are all inflammatory mediators)
    • makes prostaglandins which:
      • involved in pain, inflammation and fever
      • endothelial function

Non selective COX inhibits attack COX1 and 2 and can lead to severe GI bleeding and pt demise. Now have drugs that are more selective to COX2 and are more helpful

45
Q

What is aspirin?

A

salicylate class

  • aspirin effect in most mild to moderate pain
    • HA, muscle pain, arthritis
    • antipyretic
    • MI/storke prevention; protection during MI (antiplt)
  • Unlike other NSAIDs irreversible inhibition of cox
    • single dose inhibits PLT function for lifetime of platelet 8-10 days
46
Q

Effect of ASA on pt with ESRD?

A
  • ESRD not induced by chronic ASA (in contrast with other NSAIDS)
  • Prolonged bleeding (up to 15 minutes) in these patients with ASA
    • concern with ESRD pt taking ASA, falling, hitting head, can have huge risk for hematoma
  • usually don’t recommend ESRD to take ASA- because of bleeding, not necessarily an increase risk for ESRD issues
47
Q

ASA and Asthma?

A
  • Single dose can precipitate asthma in aspirin-sensitive patients
    • cross-sensitivity with other NSAIDS
      • if allerge to ASA, avoid other NSAIDS
48
Q

How can ASA affect LFT? GI? CNS?

A
  • asa can increaes LFT (usually reversible
  • like other NSAIDs, can cause GI bleeding and PUD
  • CNS stimulation
    • perhaps via NMDA receptor, not well described and not clinically relevant
49
Q

Dosing of ASA?

A
  • Analgesic vs anti-inflammatory dosing
    • analgesic/antipyretic 325-600 mg
    • anti inflammatory 1000 mg (3-5 g/day)
      • such a high dose and it can cause severe GI side effects
      • tend to avoid using ASA as antiinflammatory
      • increase dose gradually
      • follow serum salicylate levels
      • rarely used d/t GI side effects
50
Q

How is ASA cleared?

A
  • Hepatic clearance
    • E1/2 t is 15-20 minutes for ASA and 2-3 hours for active metabolite salicylic acid
  • Salicylate overdose: metabolic acidosis, tinnitus
51
Q

Can ASA be used in kids?

What type of salicylate acid has more favorable toxicity profile?

A
  • Should not be used during viral syndromes in children and teenagers because of risk of reye’s syndrome- (which causes encephalopathy)
  • Non acetylated salicylates have more favorable toxicity profile
    • do not interfere with PLT aggregation
    • rarely associated with GI bleeding
    • well tolerated by asthmatic patients
52
Q

What are nsaids?

A

non-steroidal anti-inflammatory drugs

  • Analgesic efficiacy
    • helpful for arthritis related pain, MS pain, HA and dysmenorrhea–> ceiling effect wiht post op pain
      • will decrease pain a litte, but not as much as opioids
    • ​more effective than full doses of ASA or acetaminophen
    • equal or greater than usual doses of an opioid combined with acetaminophen
  • Different NSAIDS have:
    • similar efficacy at equipotent doses
    • patient- to patient differences (depends how pt metabolizes drug and genetic profile)
    • toxicity difference
  • Anti-inflammatory
53
Q

MOA of NSAIDS?

A
  • Cyclooxygenase (COX) inhibiotr
  • Blocks conversion of arachidonic acid to prostaglandins (PGs)
  • decreases production and release of PGs
  • analgesic, anti-inflammatory, antipyretic activity
54
Q

Pharmacokinetics of NSAIDS?

A
  • Weak acids- well absorbed
  • Highly protein bound >95%
    • longer DOA
  • small Vd (non-speicifc NSAIDS)
  • extensively metabolized and excreted in urine
    • most of the drug is metabolized and never reaches patient
    • ​metabolized by cyp450 in liver
  • Half-life varies from <6 hours to >12 hours
55
Q

S/E NSAIDS?

A
  • Asthma and anaphylactoid rection in aspirin-sensitive patients
    • always double chekc hx
    • ask what precipitates asthma
      • ​exercise induced- if asked on exam, don’t give toradol, but clinically, would give it
  • reversible inhibiton of PLT aggregation
    • inhibition of COX-1 blocks synthesis of thromboxane A2 which inhibits PLT aggregation
  • Unlike opioids, no physicla dependence
  • rare adverse effects
    • hepatic injury
    • aseptic meningitis
56
Q

Pregnancy and use of NSAIDS?

A
  • best avoided but cat B if necessary
  • avoid in 3rd trimester, CAT D, due to premature closure of DA
57
Q

Overview of common side effects of NSAIDs?

A
  • Aseptic meningitis
  • antipyretic effect
  • impaired bone fusion (controversial)
  • hepatotoxicity (certian nsaids RARE)
  • decrease renal perfusion
  • decrease GFR
  • Decrease sodium transport
  • angioedema (rare)
  • HTN/increased CV risk
  • bronchoconstriction
  • rash/urticaria
  • anti-plt effect (cox 1 and asa only)
  • gastric ulceration (cox 1> cox2)
  • antiinflammatory effect
58
Q

GI adverse effects of NSAIDS? Risk factors for GI s/e?

A
  • Dyspepsia, GI bleeding PUD
    • Can see red dots on colonoscopy, not necessarily bad
  • Inhibiton of PGs that maintain normal gastric and duodenal mucosa
    • increases acid production
    • decreases mucus produciton, gastric blood flow
  • Local irritaiton
    • 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
59
Q

What are specific GI risks for various NSAIDs? (low, med, high risk)

A

Low risk

  • Ibuprofen and naproxen at low doses
  • etodolac, sulindac
  • celecoxib

medium risk

  • ibuprofen and naproxen at mod-high doses
  • diclofenac, oxaprozin, meloxicam, nabumetone

High risk

  • tolmetin, piroxicam, ASA, indomethacin, ketorolac (only get toradol 3-4 days in a row)
60
Q

NSAID 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 HTN
    • Intersitital nephritis (rare)
    • in healthy people, rarely of clinical significance
  • risk factors (people who require prostaglandins for renal perfusion)
    • old age (even if older pt is otherwise healthy, still have decline in GFR)
    • CHF
    • HTN
    • DM
    • Renal insufficiency
    • ascites
    • volume depletion
    • duiretic therapy
61
Q

Renal risk of speicifc nsaids?

A
  • Can occur with all NSAIDs
  • Increased risk
    • longer half life
    • highly potent COX inhibitors
      • ketorolac, indomethacin
    • higher doses
  • “renal sparing”- lower risk, but not devoid
    • sulindac, nabumetone
    • celecoxib
62
Q

Drug interactions of NSAIDS?

A
  • Displaces other highly protein bound agents
    • increases levels of warfarin, phenytoin, sulfonylureas, sulfonamids, digoxin
  • Reduces effect of diuretics, beta blocker,s ACEIs, via suppression of renal PGs
  • Increases lithium levels- competing for protein binding sites
  • increased risk of GI bleed when combined with anti-coagulants
  • probencid increases levels of most NSAIDS
    • avoid with ketorolac
63
Q

What is ketorolac?

A
  • Non-selective cox inhibitor
  • Only IV NSAID available in US
  • IM or IV comparable to mild opioids
  • double blind single dose study suggested similar time to pain relief with ketorolac or morphine
    • comparable to mild opioids
    • advantage: no vnetialtory or cardiac depression
  • adverse effects similar ot typical NSAID
    • increased bleeding time and periop blood loss
    • serious GI bleeding, ulceration, perforation and/or renal toxicity can occur (especially in elderly or hypovolemic)
    • potential for life-threatening bronchospasm
64
Q

Ketorolac pharmacokinetics?

A
  • Do not exceed 5 days of use
  • IV onset ~10 min
  • E1/2 t 5 hours (prolonged in elderly 30-50%)
  • DOA 6-8 HOURS
  • 99% protein bound
  • conjugated in liver
  • Dose IV:
    • 30 mg IV x 1 or q 6 hours
    • Daily max 120 mg
    • elderly : if you use it at all, cut dose in 1/2
65
Q

What are some selective NSAIDs?

A
  • Celecoxib (celebrex) only agent available today
  • withdrawn from market d/t increased MI risk
    • rofecoxib (vioxx) valdecoxib (bextra)
      • removed d/t risk storke/MI
  • Selectively inhibit COX2 (nonselective NSAIDs inhibit COX 1 and 2)
    • cox 1: gastric protection and produciton of TxA2
      • vasoconstrictor, plt aggregation
    • cox 2: produciton of prostacyclin (vasodilator, plt inhibitor)
  • No more effective at reducing pain and inflammation
  • same risk fo renal adverse effects
66
Q

What is celecoxib?

A

celebrex

  • Use the lowest effective dose
    • <200 mg/day
    • 200 mg/day= naproxen 500 mg BID
  • BLACK BOX WARNING
    • Consider pt risk for CV events
    • consider pt risk for GI events
  • weight risk vs benefit
  • PO
  • Should be taken with food
  • avoid in pt with sulfonamide allergy
67
Q

Black box warning for NSAIDs?

A
  • CV risk
    • increased risk of serious CV thrombotic events, MI, stroke, which can be fatal
  • GI risk
    • increased r/f bleeding, ulceration, perforaiton of stomach or intestines, which can be fatal
  • selective and non-selective NSAIDs
68
Q

What are some adjuvant analgesics?

A

Antidepressants and anticonvulsants- drugs of choice for neuropathic pain

  • TCA (amitriptyline, nortiptyline)
    • diabetic neuropathy, postherpetic neuralgia, polyneuropathy, and nerve injury or infiltration with Ca
    • may also improve underlying depression and insomnia
  • Venlafaxin- (EFFEXOR) SSNRI
    • neuropathic pain, HA, fibromyalgia, postmastectomy pain
  • Duloxetine (cymbalta) SSNRI
69
Q

What are some anticonvulsants that are used as adjuvant analgesics?

A
  • Gabapentin (Neurontin) –mechanism not well understood
    • Diabetic neuropathy, postherpetic neuralgia
  • Pregabalin (Lyrica) –gabanergic, analogue of GABA
    • Diabetic neuropathy, postherpetic neuralgia, fibromyalgia
    • Analgesic effects may be related to calcium influx inhibition as well as inhibition of the release of excitatory neurotransmitters in spinal and supraspinal pathways via binding to α 2 δ-1 subunit of presynaptic voltage-gated calcium channels in the CNS.
  • Carbamazepine (Tegretol)-Na channel blocker, and GABAnergic
    • FDA approved for trigeminal neuralgia
  • Phenytoin (Dilantin), Sodium Valproate (Depakote), Clonazepam (Klonopin), and Topiramate (Topamax)
    • May relief neuropathic pain
  • Lamitrogen (Lamictal)-Gabanergic
    • Effective for central post-stroke pain and HIV-associated painful sensory neuropathies
70
Q

How can hydroxyzine help with pain?

A
  • Low dose IV/IM add analgesic effect to opioids in Ca and postop pain while reducing incidience of N/V
  • is a histamine blocker
71
Q

How can corticosteroids help with pain?

A

Can produces analgesia in some patients with inflammatory diseases or tumor infltration of nerves

72
Q

Other analgeisc agents and topical analgesics?

A
  • Topical
    • 5% lidocaine approved for post herpetic neuralgia
    • topical EMLA useful for cutaneous anesthesia
    • capsaicin cream (zostrix) for neuropathic and osteoarthetiic pain
    • transdermal clonidine patch may improve pain and hyperalgesia in sympathetically matained pain
  • THC/CBD
  • Ketamine
  • Magnesium

Adv. Pharm Test 2 (6 decks)

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