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NEUROPHARMACOLOGY > DRUGS USED IN THE MANAGEMENT OF PAIN > Flashcards

DRUGS USED IN THE MANAGEMENT OF PAIN Flashcards

1
Q

What is pain?

A

Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.

Its a perception and a sensation!

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2
Q

Drugs that have analgesic actions act by modulating the pain neural pathways in various ways that include:

A

 Inhibition of activity at nociceptors
 Inhibition of synthesis of mediators of nociception and pain transmission
 Inhibition of transmission of pain signals
 Potentiation of mediators that inhibit transmission of pain signals

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3
Q

Classification
of Pain

A

Acute Pain: occurs over a brief
period and usually associated with
a temporary disorder

Chronic Pain: continuous and
recurrent and sustained by
different mechanisms.

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4
Q

Pain syndromes may also be classified into:

A
  • Nociceptive pain: may be “referred” – e.g.
    injury to the hip referred to the knee
  • Neuropathic pain
  • Psychogenic pain
  • Idiopathic pain
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5
Q

Pharmacological Methods of Pain Management

A
  1. NSAIDs
  2. Opioids
  3. Adjunctive agents
  4. Local anesthetics
  5. General anesthetics
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6
Q

Non-Pharmacological Methods of Pain Management

A
  1. Counseling
  2. Acupuncture
  3. TENS
  4. Massage
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7
Q

Analgesic Ladder: Stepwise management of pain

A

Step 1. Start with non-opioid
(e.g. NSAID or paracetamol)

Step 2. Use an opioid for mild or
moderate pain if pain persists
e.g. codeine

Step 3. Use opioid for moderate
to severe pain if pain persists
e.g. morphine, fentanyl

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8
Q

Gate Control Theory Melzack and Wall 1965.

A

Pain stimulus is transmitted from
pain receptors, through peripheral nerves to the spinal cord to the brain. Through two different types of nerves fibres:
*A-delta “fast pain” and C-fibers “slow pain” nerve fibers.

Physiological and psychological
interactions suggests spinal gates
in the dorsal horn at each
segment of the spinal cord
*Competition at each gate for
heat, touch or pain to be
transmitted at each point

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9
Q

How does nociceptive pain occur?

A

①Transduction: Mediators, PG, HT, Histamine Sub P released, Generator Potentials (NSAIDS)
②Transmission via nerve fibers
③Modulation by PG, amines, neurokinins, GABA, neurotensin, cannabinoids (OPIODS)
④Perception (OPIODS)

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10
Q

NSAIDS: Nonselective Cox Inhibitors:

A

 Aspirin
 Ibuprofen
 Piroxicam
 Meclofenamate
 Diclofenac
 Indomethacin

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11
Q

NSAIDS: Selective Cox Inhibitors:

A

➢ Celecoxib
➢ Rofecoxib
➢ Meloxicam

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12
Q

NSAID common pharmacological effects

A

 Analgesic (CNS and peripheral
effect)
 Antipyretic (CNS effect)
 Anti-inflammatory (except
acetaminophen)
 Some are Antiplatelete: inhibit
activation, adhesion and
aggregation of platelets &
release of lysosomal enzymes
 Some are Uricosuric

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13
Q

Opioids: Nomenclature

A

 Opium: is the dried powdered mixture of alkaloids obtained from poppy

 Opiate: Any agent derived from opium

 Opioid: All substances (exogenous or endogenous) with morphine -like properties

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14
Q

Opiods: Classification

A

①Alkaloid: derived from poppy plant
*Morphine
*Codeine

②Semisynthetic: modification of morphine
functional groups:
* Diacetylmorphine (heroin)
*Hydrocodone
*Hydromorphone
* Oxycodone
* Oxymorphone

③Synthetic: progressive reduction in the number of fused rings in phenanthrene moiety:
*Meperidine
*Fentanyl
*Sufentanil
*Alfentanil

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15
Q

Opioid Receptor Classification

A

①mu receptor 1 (MOR1): most endogenous, natural or synthetic for SUPRASPINAL ANALGESIA

②)mu receptor 2 (MOR2): morphine, RESPIRATORY DEPRESSIONS, CVS

③kappa receptor (KOR): Ketocyclazocine and dynorphin for SPINAL ANALGESIA, SEDATION AND MIOSIS

④delta receptor (DOR): Enkephalins for SPINAL ANALGESIA

⑤sigma receptor: N-allylnormetazocine for PSYCOTOMIMETIC EFFECTS

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16
Q

Opioid Intrinsic Activity

A

 Agonists produce a maximum
biologic effect.

 Antagonists have no intrinsic
activity and prevent the access of
agonists to the receptors .

 Partial agonists have a submaximal
response

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17
Q

Opioid Partial agonism:

A

interaction at a single receptor type
e.g. buprenorphine on mu receptors

18
Q

Opioid Mixed Agonist-antagonists:

A

have divergent activities at different receptors, acting simultaneously as an
agonist at one receptor and an antagonist at another;
e.g. ①pentazocine: antagonist on mu, agonist on sigma and kappa
➁butorphanol: antagonist on mu, agonist on sigma and kappa
③nalbuphine: antagonist on mu, partial agonist on sigma and agonist on kappa

19
Q

MoA of Opioid agonists= analgesia

A
  • Activate the descending pathways
    from the midbrain and brain stem
    and exert a strong inhibitory effect
    on dorsal horn transmission
  • Inhibit excitation of sensory nerve
    terminals in the periphery (increase
    pain threshold)
20
Q

Primary Effect of Opioid Receptor
Activation

A

 Release of pain-signaling
neurotransmitters is regulated by
endogenous opioid peptides or by
exogenous opioid agonists.
 Through presynaptic inhibition of substance P release, thereby producing analgesia
 Involves changes in transmembrane ion conductance
 Increase potassium conductance
(hyperpolarization)
 Inactivation of calcium channels

21
Q

Pharmacological Effects of Opioids

A

①Sedation and anxiolysis
* Drowsiness and lethargy
* Apathy
* Cognitive impairment
* Sense of tranquility
➁Depression of respiration
* Main cause of death from opioid overdose.
* Combination of opioids and alcohol is
especially dangerous.
③Cough suppression
* Opioids suppress the “cough center” in the
brain.
④Pupillary constriction
* pupillary constriction in the presence of
analgesics is characteristic of opioid use.
⑤Nausea and vomiting
 Stimulation of receptors in an area of the medulla called the chemoreceptor trigger zone causes nausea and vomiting
 Unpleasant side effect, but not life threatening
⑥Gastrointestinal symptoms
 Opioids relieve diarrhea as a result of their direct actions on the intestines
 Billiary tract spasm, especially of the sphincter of Oddi
 Reversible by naloxone, nitroglycerin

⑦Other effects
 Opioids can release histamines causing itching or more severe allergic reactions including bronchoconstriction
 Opioids can affect white blood cell function and immune function

22
Q

Morphine: Prototype of
the group

A

Routes: PO, IM, IV, SQ,
nebulized & rectal

Morphine: conjugated
in the liver

Has several active
metabolites

23
Q

Diamorphine (Heroin)

A

 Derived from morphine
 Higher potency than morphine
 More lipid soluble than morphine, so
enters the CNS more readily
 Causes more euphoria than morphine
and has higher abuse potential

24
Q

Pethidine (meperidine)

A

*Less potent than morphine

*Less respiratory depression compared to morphine and has no effect on the cough reflex

*Causes tremors, muscle twitches
and rarely convulsions (due to a
toxic metabolite – norpethidine)

*Unlike other opioids, large doses cause pupil dilatation, tachycardia (has anti-muscarinic effects) and hyper-active reflexes (due to norpethidine)

*Pethidine is preferred to morphine in the relief of labour pain because it has a shorter duration of action and causes less respiratory depression in the newborn (the newborn does not have glucuronidation enzyme for morphine and therefore cannot metabolise morphine)

*Pethidine is also the preferred opioid analgesic in biliary and ureteric colic since it causes less smooth muscle spasm.

25
Q

Methadone

A
  • Equal analgesic potency with morphine
  • Has a longer duration of action, is more orally active, induces less euphoria and has less sedative
    effects compared to morphine
  • Used in the management of opioid dependence
26
Q

Fentanyl, alfentanil and sufentanil

A
  • More lipid soluble and more potent than morphine
  • Used in general anaesthesia
27
Q

Codeine

A

Much less potent analgesic than
morphine and produces less euphoria

Good anti-tussive activity at doses
that do not cause analgesia

Has lower abuse potential
than morphine

Used for mild to moderate pain and
for cough suppression

28
Q

Propoxyphene and dextropropoxyphene (weak opioids)

A
  • Weaker analgesics than codeine
  • Used in the treatment of mild to
    moderate pain
  • Often used in combination with aspirin and paracetamol
29
Q

Buprenorphine (weak opioids)

A
  • High efficacy opioid analgesic
  • A partial agonist on mu receptors,
    and antagonist on delta and kappa
    receptors
  • Can antagonize morphine
30
Q

Pentazocine

A

Is a mixed opioid receptor agonist-
antagonist (agonist on kappa receptors and antagonist on mu receptors)

Causes dysphoria rather than euphoria

Promotes analgesia by activating opioid receptors in the spinal cord

High doses increase blood pressure and can cause hallucinations, nightmares,tachycardia and dizziness

31
Q

Tramadol

A

Moderate to moderately severe pain
*Binds to μ-opioid receptors.
*Inhibits reuptake of serotonin and norepinephrine in the CNS.
Crosses the placenta; enters breast milk.

Metabolised by CYP2D6 enzyme system
which exhibits genetic polymorphism;
*~7% of population may be poor metabolizers and small
proportion are ultra–rapid metabolizers of CYP2D6 and
have significantly ↑ concentrations of M1 metabolite.
30% eliminated unchanged in the urine.
Half-life: Tramadol– 6–8 hr, ER– 7.9 hr; active

metabolite– 7–9 hr;
*both are ↑ in renal or hepatic impairment.

32
Q

Naltrexone

A

Antagonist
* Onset (oral tablet 15-30 min.)
Duration of action 24-72 hours
* Peak effect (6-12 hours)
EFFECTS
* Reverses the psychotomimetic effects of opiate agonists.
* Reverses hypotension and cardiovascular instability
* potent vasodilators
* Inhibits Mu, Delta, and Kappa receptors.

33
Q

CLINICAL USES OF OPIOIDS

A

 Mild to moderate pain: codeine, dihydrocodeine, propoxyphene, dextropropoxyphene and buprenorphine
 Severe pain: morphine, diamorphine, pethidine and other high efficacy opioid analgesics
 Post-operative pain: morphine, pethidine
 General anaesthesia: fentanyl, alfentanil and sufentanil
 Acute myocardial infarction: morphine and diamorphine
 Pain of advanced malignant disease: fentanyl, morphine
 Treatment of opioid dependence: methadone.

34
Q

Combination Analgesics

A

 Hydrocodone with acetaminophen
 Vicoprofen (ibuprofen 200/7.5 mg
hydrocodone)
 Note:
“ All opioids can be made equipotent or
equianalgesic by adjusting for physicochemical and pharmacokinetic
differences among individual opioids by
correcting for dose and route of
administration.”

35
Q

Treatment of Breakthrough Pain

A

Intermittent flares of pain that can
occur despite fixed schedule
analgesic medication for pain
control.

Ideal medication for this should

  • Be easy to administer
  • Have rapid onset of action
  • Be eliminated within a short time
  • ORAL TRANSMUCOSAL FENTANYL CITRATE (ACTIQ)
    recommended by FDA
  • OXYCODONE and HYDROMORPHONE may also
    be used
36
Q

Symptoms of opioid
withdrawal:

A
  • Diaphoresis (ex sweating)
  • Lacrimation
  • Coryza
  • Tachycardia
  • Hypertension
  • Abdominal cramps
  • Nausea
  • Vomiting
37
Q

NEUROPATHIC
PAIN

A

Usually associated with
damage to nerves centrally
or peripherally

Several classes of
pharmacological agents are
available for its treatment

Many guidelines, but
significant consistency

38
Q

Consideration for Management(Mx) of
Neuropathic Pain

A

 Comorbidities
 Medication efficacy
 Side effect profile of the drugs

39
Q

Tricyclic Antidepressants

A

E.g. nortriptyline, desipramine,
amitriptyline, imipramine.

MOA: Blockade of 5HT, NA reuptake;
block cholinergic, adrenergic,
histaminergic transmissions; Block
Na+ channels.

Useful for distal peripheral
neuropathy, painful polyneuropathy,
postherpetic neuralgia, postmastectomy pain.

40
Q

Serotonin-norepinephrine Reuptake Inhibitors (SNRIS)

A

 E.g., Duloxetine, venlafaxine
 Useful for diabetic neuropathic pain
 Recommended 1st line treatment for neuropathic pain by the International Association for the Study of Pain (IASP)

NEUROPHARMACOLOGY (5 decks)

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