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Quiz

ON7 Pain Management - Opioid Drugs

Gelöschter Nutzer 13 Fragen

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  1. 1Pain types:
    1. Nociceptive Pain. Acute, [blank_start]protective[blank_end] and physiological. Somatic (skin, bone, joint, muscle.) pain = [blank_start]throbbing[blank_end], localised. Visceral (large intestine, pancreas.) referred or [blank_start]localised[blank_end].

    2. Neuropathic (pathologic) pain. [blank_start]Disengaged[blank_end] from noxious stimuli. Chronic, [blank_start]neuronal[blank_end] damage.
    • Related pain syndromes: [blank_start]diabetic[blank_end] neuropathy, post-herpetic, IBS
    • Reported pain is [blank_start]greater[blank_end] than physical exam findings.

    3. Inflammatory. More acute. [blank_start]Repairing[blank_end], pathological.

    4. [blank_start]Dysfunctional[blank_end] pain. Chronic. No neuronal damage, noxious stimuli, or inflammation.
    1. Aprotective
    2. Bthrobbing
    3. Clocalised
    4. DDisengaged
    5. Eneuronal
    6. Fdiabetic
    7. Ggreater
    8. HRepairing
    9. IDysfunctional
  2. 2Molecular mechanisms of pain:

    1. Transduction
    Stimulation of [blank_start]nociceptors[blank_end]. Uses afferent fibres. [blank_start]High[blank_end] activation threshold eg >45C or <5C. Sensitisation by bradykinin, [blank_start]prostaglandins, interleukins, TNFa,[blank_end] serotonin, can [blank_start]lower[blank_end] threshold.

    2. Transmission
    Conduction of impulse from periphery to [blank_start]CNS[blank_end] across [blank_start]dorsal[blank_end] horn of spinal cord. Neurotransmitters: [blank_start]Glutamate, Substance P, CGRP.[blank_end] Associated with thalamus and sensorimotor cortex.

    3. Perception
    Afferent impulse goes to [blank_start]ascending[blank_end] pathways; also associated with thalamus and cortex. [blank_start]Conscious[blank_end] experience: cognition, behaviour

    4. Modulation
    [blank_start]Suppress[blank_end] transduction, conduction, transmission. Local inhibitory neurons: [blank_start]GABA[blank_end]. Descending pathway is [blank_start]locus coeruleus[blank_end], also affected by the inhibitory substances: [blank_start]Opioids[blank_end], 5HT, NA, endogenous cannabinoids.
    1. Anociceptors
    2. BHigh
    3. Cprostaglandins, interleukins, TNFa,
    4. Dlower
    5. ECNS
    6. Fdorsal
    7. GGlutamate, Substance P, CGRP.
    8. Hascending
    9. IConscious
    10. JSuppress
    11. KGABA
    12. Llocus coeruleus
    13. MOpioids
  3. 3The analgesic ladder (WHO)"
    STEP 1 [blank_start]Non-opioid analgesics[blank_end] e.g. paracetamol, NSAIDs
    STEP 2 [blank_start]Opioids[blank_end] suitable for moderate pain (or [blank_start]tramadol[blank_end]) ± simple analgesics e.g. codeine, dihydrocodeine
    STEP 3 Opioid suitable for [blank_start]severe[blank_end] pain ± simple analgesics e.g. morphine
    1. ANon-opioid analgesics
    2. BOpioids
    3. Ctramadol
    4. Dsevere
  4. 4Endogenous opioids: [blank_start]Agonists[blank_end] at opioid receptors, eg Beta endorphin, Enkephalin
    • Receptors: pre/post [blank_start]synaptic[blank_end] terminals in the [blank_start]apinal[blank_end] cord, limbic system, PNS
    • Inhibit [blank_start]transmission[blank_end] - stimulate inhibitory pathways
    • Euphoria

    All opioid Rs are coupled to [blank_start]inhibitory G proteins[blank_end]. R activation has many [blank_start]intracellular[blank_end] consequences.
    1. AAgonists
    2. Bsynaptic
    3. Cspinal
    4. Dtransmission
    5. Einhibitory G proteins
    6. Fintracellular
  5. 5Opioid Analgesics: Buprenorphine, codeine, fentanyl, morphine, diamorphine (heroin), oxycodone, tramadol.
    • Agonists at [blank_start]specific[blank_end] opioid Rs.

    [blank_start]Muse-R[blank_end] stimulation (raphe magnus)
    • Less activity in [blank_start]GABA[blank_end] neurons = descending 5-HT neurons (brainstem)
    • Presynaptic connection = [blank_start]afferent[blank_end] nociceptive neurons (spinal cord)

    Inhibition of GABA permits [blank_start]increased[blank_end] firing in [blank_start]descending[blank_end] pathway.
    Analgesia: inhibition of release of [blank_start]pain mediators[blank_end] (substance P, NO, glutamate.)
    1. Aspecific
    2. BMuse-R
    3. CGABA
    4. Dafferent
    5. Edescending
    6. Fincreased
    7. Gpain mediators
  6. 6Opioid analgesia:
    Muse R activation = increased pain [blank_start]modulation[blank_end]
    Kappa R activation = [blank_start]antagonizes[blank_end] m-mediated analgesia + has unopposed [blank_start]spinal[blank_end] analgesia

    Also present on peripheral nerves:
    Muse agonists: decrease [blank_start]sensitivity[blank_end] of nociceptive neurons (inflamed tissue)
    Kappa receptors: endothelial cells, T lymphocytes, macrophages. Modulate [blank_start]immune[blank_end] response.
    1. Amodulation
    2. Bantagonizes
    3. Cspinal
    4. Dsensitivity
    5. Eimmune
  7. 7All opioids have maximum potency for [blank_start]muse[blank_end] receptors.
    Morphine, diamorphine, pethidine, oxycodone, codeine have specificity for [blank_start]kappa and delta[blank_end].
    Methadone has [blank_start]NO[blank_end] kappa or delta specificity, [blank_start]only[blank_end] muse.
    Fentanyl has no [blank_start]kappa[blank_end] sensitivity, just muse and [blank_start]delta[blank_end].
    Naloxone has specificity for muse, less for kappa(but [blank_start]more[blank_end] than most opiods), and some for delta.
    1. Amuse
    2. Bkappa and delta
    3. CNO
    4. Donly
    5. Ekappa
    6. Fdelta
    7. Gmore
  8. 8Other CNS effects:
    - Euphoria - Mediated by [blank_start]muse[blank_end], contributes to analgesia
    - Dysphorial ([blank_start]kappa[blank_end])
    - Respiratory Depression - primary cause of [blank_start]morbidity[blank_end]; depress rhythm generation in [blank_start]medulla[blank_end], desensitize brainstem [blank_start]chemoreceptors[blank_end] (increasing [blank_start]pCO2[blank_end])
    - Cough suppression - Antitussive, direct effect on [blank_start]cough center[blank_end] in medulla - [blank_start]codeine, dextromethorphan[blank_end]
    1. Akappa
    2. Bmuse
    3. Cmorbidity
    4. Dmedulla
    5. Echemoreceptors
    6. FpCO2
    7. Gcough center
    8. Hcodeine, dextromethorphan
  9. 9Peripheral effects:
    GI Tract
    • increased [blank_start]resting[blank_end] tone (m, k)
    • [blank_start]constipation[blank_end] (80%)
    • affecst [blank_start]absorption[blank_end] of other drugs
    • less stomach [blank_start]motility[blank_end] – anorexia, N&V

    Cardiovascular system
    • Few effects on heart or circulation
    • High dose – depress [blank_start]medullary vasomotor[blank_end] center
    • Hypotension (parenteral use of [blank_start]morphine[blank_end])

    SEs are dose dependent.
    1. Aresting
    2. Bconstipation
    3. Cabsorption
    4. Dmotility
    5. Emedullary vasomotor
    6. Fmorphine
  10. 10Tolerance and dependence:
    [blank_start]Continuous[blank_end] use causes adaptive changes in R function.
    • More drug for same effects = [blank_start]tolerance[blank_end]
    • [blank_start]Withdrawal[blank_end]= adverse physiological effects (dependence)

    Tolerance
    • Learned ([blank_start]psychological[blank_end])
    • (Adaptive) [blank_start]R downregulation/desensitization[blank_end]
    • Most pharmacological effects ([blank_start]not[blank_end] constipation, pupil constriction)

    Dependence (withdrawal syndrome, m)
    • Anxiety, sweating, craving (12h)
    • Rhinorrhea, [blank_start]dilated[blank_end] pupils, yawning, chills, pilo[blank_start]erection[blank_end], [blank_start]hyper[blank_end]ventilation, diarrhoea
    • Duration of action varies
    1. AContinuous
    2. Btolerance
    3. CWithdrawal
    4. Dpsychological
    5. ER downregulation/desensitization
    6. Fnot
    7. Gdilated
    8. Herection
    9. Ihyper

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Beschreibung
Der Nutzer hat seine Fachbereichs-Information gelöscht. Quiz am ON7 Pain Management - Opioid Drugs, erstellt von Gelöschter Nutzer am 09/10/2019.
Autor
Gelöschter Nutzer
Sprache
English
Aufrufe
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