Med neuro > Pain > Flashcards

Pain Flashcards

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0
Q

High efficacy pain relief: trt

A
  • act on central aspect of pain
  • phenylcyclidine and ketamine: inhibit ion transmission through NMDA
  • ketamine prevents CNS sensitization to pain after trauma
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1
Q

Peripheral sites of action

A

Moderated by PGE via COX

  • substance P and NK-1
  • serotonin, bradykinin
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2
Q

Opioid receptors: location and modification

A
  • receptors concentrated in the spinal cord, released by interneurons, but can be found any where were pain transmission synapses occur
  • inhibit the release of substance P and other excretory neurotransmitters
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3
Q

PAG

A
  • 5-HT, NE form a negative feed back loop
  • 5-HT: stimulates endogenous opioids
  • NE: stimulates inhibitory interneurons and activates inhibitory a-2 adrenoreceptors
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4
Q

Duloxetine, milnacipran, venlefaxine

A
  • for treatment of chronic NOT acute pain
  • block reuptake of 5-HT, NE (increasing activity in PAG)
  • antidepressant effect takes longer
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5
Q

Neuropathic pain: etiology, trt, sensation

A
  • burning/tingling
  • anticonvulsants (gabapentin, pregamblin)
    ~ prolonged inactivated state of number of Na (injury prolongs
    activations)
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6
Q

Treating neuropathic pain

A

TCA, venlefaxine, duloxetine

- gabapentin, pregamblin

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7
Q

Gabapentin and pregablin

A

Inactive Na channels

  • also blocks a2D subunit of the N-type voltage sensitive calcium channel
  • cannabinoids has shown efficacy within the cord
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8
Q

C fiber activation

A

Both sensory and affective response

  • receptors in hypothalamus, and limpid system as well as CNS
  • opioids decrease both affective moreso
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9
Q

Enkephalins

A
  • MET and LEU have different receptor subtypes

- rapidly degraded

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10
Q

Beta endorphins and dynorphins

A
  • from proopiomelanocortin: also produces MSH and ACTH
  • B: 31 AA peptide, both hormone and NTSMTr
  • from long axoned neurons in hypothalamus
  • Dynorohan: 8-9 AA (peptidase susceptible), 13-17 (peptidase resistant)
    ~ both hormone and ntsmtr activity
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11
Q

Endogenous opioids and intractable pain

A

Low levels observed

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12
Q

Reinforcement process

A
  • Opioid system one component
  • they inhibit GABA neurons -> increasing DA cells
  • also have circuits to the reward system
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13
Q

Chronic opioid effect mechanism

A

Decrease coupling of the mu receptor to G proteins
- Degree of craving primarily dependent on long-lasting decrease in mesolimbic dopamine function (rather than amount of uncoupling)

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14
Q

Opioid subtypes: (4)

A
  • mu (mop) - morphine B- endorphins
  • kappa (kop) - selected drugs and dynorphins
  • delta (dop) - no selective drugs, beta endorphins and enkephalins
  • sigma: non-opioid, involved in cough suppression
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15
Q

Mu activation

A
  • morphine and B-endorphins
  • classic effects of opioids: miosis, respiratory depression, hypothermia, indifference to pain, euphoria, GI and physical dependance
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16
Q

Kappa activation

A
  • selected drugs and dynorphins

- slight miosis, spinal/supraspinal analgesia, sedation, diuresis, CV side effects

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17
Q

Morphine

A
  • mu: agonist
  • kappa: weak agonist
  • delta: weak agonist
  • convers to active M-6-glucuronide
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18
Q

Delta activation

A
  • Spinal analgesia, respiratory depression, supraspinal analgesia, physical dependence, euphoria
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19
Q

Buprenorphin

A
  • more potent than morphine
  • Mu partial agonist (only)
  • highly lipophilic
  • between mu and kappa resp depression
  • binds to extensively to protein
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20
Q

Naxalone (narcan)

A
  • mu and delta antagonist
  • weak kappa antagonist
  • push with caution -> immediate withdrawal
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21
Q

Pentazocine

A
  • kappa agonist
  • partial mu agonist (can antagonize morphine and precipitate withdrawal)
  • ceiling on respiratory depression
  • high dose stimulatory
  • lower abuse potential
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22
Q

Butorphanol

A
  • kappa agonist
  • weak mu antagonist
  • increases cardiac workload
  • ceiling on resp depression
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23
Q

Nalbuphine

A
  • mu antagonist
  • kappa agonist
  • ceiling of resp depression
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24
Chemical structure: substitution of allyl group
Turns an agonist into an antagonist
25
General effect of opioids
Excitation and depression: excitation predominating - opioid prototype: morphine ~ miosis, constipation, constriction of ciliary and bladder sphincters
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Major effects of morphine
- analgesia - drowsiness/mental clouding, lethargy - mood alteration: generally euphoria, some have opposite effect (more common in pain free administration), pupillary constriction (slow tolerance), reduced respiratory drive via CO2 sensitivity, nausea vomiting, antiemetic (following penetration of CNS)
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Ambulatory patients and opioids
Ambulatory patients more likely to vomit
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Cardio respiratory effects of opioids
- mild suppression of baroreceptor reflex - release of histamine: vasodilation and bronchoconstriction - decreased systemic adrenergic tone - INCREASED CO2 DILATES CEREBRAL BLOOD VESSELS -> increased ICP - decreased GI secretion and increased long tone: constipation
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Urinary/GI effects of opioids
- Decreased secretion, increased long tone: constipation - constriction of sphincter of oddi -> increase biliary colic - increased urinary sphincter tone, and decreased detrusor activity: urinary urgency
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Methadone
- similar to morphine: longer lasting better oral absorption - low plasma concentrations decrease "high" - cyp3a4 metabolism: lots of drug interactions - renal failure - can also be useful for neuropathic pain
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Codeine
- cough, mild pain, diarrhea - converted to morphine - CYP2D6: wide variability in metabolism ~ maybe ineffective or toxic
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Propoxyphene
- Conjugate of methadone - less effective than codine, (NO SUPERIORITY) - potential for toxic psychosis
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Fentanyl
- extremely potent - neuroleptic anesthesia, patches for severe chronic - lozenges for kids - nasal spray
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Oxycodone (oxycontin: extended release)
- better oral availability than morphine | - sometimes combined with naxalone so it can't be injected (naxalone doesn't survive first pass)
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Hydrocodone
- available with APAP (a partial mu agonist) - similar to morphine - commonly used
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Tramadol
- weak mu agonist blocks reuptake 5-HT, NE - SE: Nausea, constipation, and drowsiness; No cardiopulmonary effect (hence why dad got it after his MI) - requires bioactivation
37
Meperidine
- less biliary spasm, ANS effects during withdrawal - fast onset, short duration - drug interactions - renally cleared - diphenoxylate useful diarrhea - loperamide (immodium)
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Pure agonist: morphine
Alone: usual picture Acute morphine addition: additive Chronic morphine addition: substitute
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Partial agonist: buprenophine
Alone: similar to morphine Acute morphine addition: additive Chronic morphine addition: low doses substitute; high doses precipitate withdrawal
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Mixed agonist/antagonist: nalbuphine
Alone: analgesia, resp dep, some dysphoria Acute morphine addition: reverses mu and substitutes kappa Chronic morphine addition: precipitates withdrawal
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Pure antagonist: naxalone
Alone: no effect Acute morphine addition: reverses Chronic morphine addition: precipitates withdrawal
42
Opioid antagonists
``` Naxalone: short acting - orally ineffective (high first pass) Naltrexone: long acting - orally effective - opioid and alcohol abuse Methylnaltrexone: for opioid constipation (doesn't cross BBB) ```
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Opioid absorption
- better perenterally (some orally) - IV with caution (resp distress, gut spasms) - entrance into the CNS related to how quickly it crosses BBB - *heroine is deacetylated to morphine* which accounts for most of its effects
44
Excretion of opioids
Converted to M-6-glucuronide - higher concentrations of that than morphine - longer lied and more potent analgesic
45
Withdrawal
Rebound effects: | - Nausea, vomiting, diarrhea, cramps, yawning, twitching, NE over reaction
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Tolerance to opioids
- tolerance noted for its depressant effects - will show miosis and constipation - increase in lethal dose
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Dependance: effects and treatment
Marked by withdrawal illustrating rebound effect opposite the drug - Clonadine (a2 agonist) can alleviate these symptoms
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Cross tolerance and cross dependance
- tolerance to drugs of same class | - dose adjustments must be made
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Abuse potential
- drugs that rapidly cross BBB produce immediate high | - drugs which have a short active time and req frequent administration reduce abuse potential
50
Overdose: signs and treatment
- common "trifecta": respiratory depression, pinpoint pupils, coma - ventilate/protect airway push naxalone (carefully) - Clonadine can elevate the NE related effects
51
Considerations: cancer PTs. Obstetrical and pt. controlled analgesia
- Many terminal cancer patients are undertreated for pain - Should be used with great care in obstetrical work, Opioids cross the placenta - Post op, sickle cell crisis and cancer (better pain management, lower doses)
52
Opioids and cardiac emergencies
- indicated in left ventricular heart failure | - alleviates stress on heart due to decrease oxygen consumption and work load
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Opioid drug interactions: +\-
- meperidine: interactions with 5-HT - additive effect with ASA or NSIADS: better control with lower dose - euphoria enhanced with sympathomimetics (amphetamines) - CYP2D6: metabolizes prodrugs codeine and tramadol to active - CYP3A4: metabolizes methadone and fentanyl
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CSF path
- choroid plexus (lateral and 4th primarily) -> Monroe -> third -> Sylvius -> 4th -> magendi -> subarachnoid
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CSF production
Blood -filtration through fenestrated capillary endothelium-> almost everything sans RBCs -> choroid plexus ependyma active transport-> brain ECS
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CSF ependymal proteins
Carbonic anhydrase - H/Na transport: pump Na into cell - Cl/HCO3: pumps Cl into cell - Na/K, K leak and Cl leak maintains gradient -> CSF
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CSF composition
- Same osmolarity and Na comp of blood plasma - lower concentration: K, Ca, glucose, AAs - higher concentration: h2o, Cl, Mg - No cells
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CSF volume
- CSF formation/absorption | - flow can change ICP: decreased production -> decreased absorption
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Hydrocephalus
- Communicating: Blockage occurs within the ventricles before exit to the subarachnoid space - Noncommunicating: Obstruction occurs within the subarachnoid space impeding the subarachnoid villi resorption of CSF
60
CSF volume maintenance
Blood space more labile, regulation of cerebral blood volume and osmolarity can help control ICP
61
Hypercapnea
- leads to increased ICP -> cerebral blood vessel dilation - hyperventilation can be a short term adjunct treatment for increased ICP ~ each mm increase in mmHg above 40 ~ 2.5 % of resting value - in treatment hypocapnic state can cause vasoconstriction BUT increases systemic pressure causing decrease in absorption (increase enous pressure in arachnoid grans); compensate by elevating head
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CSF in diagnosis
Decreased glucose can be an indicator of bacterial infection | Resultant from deactivation of Na/gluc transporters
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Factors increasing cerebral blood volume (5)
``` Hypercapnea Hypoxia (PaO2 < 50 mmHg) REM Volatile anesthetics NO ```
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Decrease in cerebral blood volume
Hypocapnea Hyperoxia Hypothermia Barbiturates
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Vasogenic edema
Damage/dysfunction in BBB Edema but no cells - malignant tumors, abscesses, postinfectious state, hematoma, cerebral contusion,
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Cytotoxic edema
Accumulation of water mainly in astrocytes - usually metabolic dysfunction of parenchymal, neurons or glial cells - usually both cytotoxic and vasogenic edema co occur - ischemic infarct, hypoxia, hypertensive encephalopathy, Pb/Hg, liver failure
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Cerebral profusion pressure and loss of function
SAP-ICP=CPP - loss of higher function (confusion and combativeness) - drowsiness (compression in RAS) - sixth nerve palsy - papilledema - vomiting and cardio-resp impairment - grand mal seizure - when ICP > SAP brain is not being perfused
68
Treatment of increased ICP
Starting ICP determines prognosis - Hyperventilation (20-25 mmHg PCO2) and induction of hyperosmotic state (320 mOsmol/L) - High-dose barbiturates (cytoprotective)
69
Phenylcyclidine and ketamine
NMDA ion channel inhibition: uncouples the affective aspect of pain
70
3A4 and C2D metabolism
3A4: methadone and fentanyl 2D6: codeine and tramadol
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