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Med neuro > Pain > Flashcards

Pain Flashcards

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
Q

Chemical structure: substitution of allyl group

A

Turns an agonist into an antagonist

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25
Q

General effect of opioids

A

Excitation and depression: excitation predominating
- opioid prototype: morphine
~ miosis, constipation, constriction of ciliary and bladder sphincters

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26
Q

Major effects of morphine

A
  • 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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27
Q

Ambulatory patients and opioids

A

Ambulatory patients more likely to vomit

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28
Q

Cardio respiratory effects of opioids

A
  • 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
29
Q

Urinary/GI effects of opioids

A
  • Decreased secretion, increased long tone: constipation
  • constriction of sphincter of oddi -> increase biliary colic
  • increased urinary sphincter tone, and decreased detrusor activity: urinary urgency
30
Q

Methadone

A
  • 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
31
Q

Codeine

A
  • cough, mild pain, diarrhea
  • converted to morphine
  • CYP2D6: wide variability in metabolism
    ~ maybe ineffective or toxic
32
Q

Propoxyphene

A
  • Conjugate of methadone
  • less effective than codine, (NO SUPERIORITY)
  • potential for toxic psychosis
33
Q

Fentanyl

A
  • extremely potent
  • neuroleptic anesthesia, patches for severe chronic
  • lozenges for kids
  • nasal spray
34
Q

Oxycodone (oxycontin: extended release)

A
  • better oral availability than morphine

- sometimes combined with naxalone so it can’t be injected (naxalone doesn’t survive first pass)

35
Q

Hydrocodone

A
  • available with APAP (a partial mu agonist)
  • similar to morphine
  • commonly used
36
Q

Tramadol

A
  • 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
Q

Meperidine

A
  • less biliary spasm, ANS effects during withdrawal
  • fast onset, short duration
  • drug interactions
  • renally cleared
  • diphenoxylate useful diarrhea
  • loperamide (immodium)
38
Q

Pure agonist: morphine

A

Alone: usual picture
Acute morphine addition: additive
Chronic morphine addition: substitute

39
Q

Partial agonist: buprenophine

A

Alone: similar to morphine
Acute morphine addition: additive
Chronic morphine addition: low doses substitute; high doses precipitate withdrawal

40
Q

Mixed agonist/antagonist: nalbuphine

A

Alone: analgesia, resp dep, some dysphoria
Acute morphine addition: reverses mu and substitutes kappa
Chronic morphine addition: precipitates withdrawal

41
Q

Pure antagonist: naxalone

A

Alone: no effect
Acute morphine addition: reverses
Chronic morphine addition: precipitates withdrawal

42
Q

Opioid antagonists

A 
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)
43
Q

Opioid absorption

A
  • 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
Q

Excretion of opioids

A

Converted to M-6-glucuronide

  • higher concentrations of that than morphine
  • longer lied and more potent analgesic
45
Q

Withdrawal

A

Rebound effects:

- Nausea, vomiting, diarrhea, cramps, yawning, twitching, NE over reaction

46
Q

Tolerance to opioids

A
  • tolerance noted for its depressant effects
  • will show miosis and constipation
  • increase in lethal dose
47
Q

Dependance: effects and treatment

A

Marked by withdrawal illustrating rebound effect opposite the drug
- Clonadine (a2 agonist) can alleviate these symptoms

48
Q

Cross tolerance and cross dependance

A
  • tolerance to drugs of same class

- dose adjustments must be made

49
Q

Abuse potential

A
  • drugs that rapidly cross BBB produce immediate high

- drugs which have a short active time and req frequent administration reduce abuse potential

50
Q

Overdose: signs and treatment

A
  • common “trifecta”: respiratory depression, pinpoint pupils, coma
  • ventilate/protect airway push naxalone (carefully)
  • Clonadine can elevate the NE related effects
51
Q

Considerations: cancer PTs. Obstetrical and pt. controlled analgesia

A
  • 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
Q

Opioids and cardiac emergencies

A
  • indicated in left ventricular heart failure

- alleviates stress on heart due to decrease oxygen consumption and work load

53
Q

Opioid drug interactions: +-

A
  • 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
54
Q

CSF path

A
  • choroid plexus (lateral and 4th primarily) -> Monroe -> third -> Sylvius -> 4th -> magendi -> subarachnoid
55
Q

CSF production

A

Blood -filtration through fenestrated capillary endothelium-> almost everything sans RBCs -> choroid plexus ependyma active transport-> brain ECS

56
Q

CSF ependymal proteins

A

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
57
Q

CSF composition

A
  • Same osmolarity and Na comp of blood plasma
  • lower concentration: K, Ca, glucose, AAs
  • higher concentration: h2o, Cl, Mg
  • No cells
58
Q

CSF volume

A
  • CSF formation/absorption

- flow can change ICP: decreased production -> decreased absorption

59
Q

Hydrocephalus

A
  • 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
Q

CSF volume maintenance

A

Blood space more labile, regulation of cerebral blood volume and osmolarity can help control ICP

61
Q

Hypercapnea

A
  • 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
62
Q

CSF in diagnosis

A

Decreased glucose can be an indicator of bacterial infection

Resultant from deactivation of Na/gluc transporters

63
Q

Factors increasing cerebral blood volume (5)

A 
Hypercapnea
Hypoxia (PaO2 < 50 mmHg) 
REM
Volatile anesthetics 
NO
64
Q

Decrease in cerebral blood volume

A

Hypocapnea
Hyperoxia
Hypothermia
Barbiturates

65
Q

Vasogenic edema

A

Damage/dysfunction in BBB
Edema but no cells
- malignant tumors, abscesses, postinfectious state, hematoma, cerebral contusion,

66
Q

Cytotoxic edema

A

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
67
Q

Cerebral profusion pressure and loss of function

A

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
Q

Treatment of increased ICP

A

Starting ICP determines prognosis

  • Hyperventilation (20-25 mmHg PCO2) and induction of hyperosmotic state (320 mOsmol/L)
  • High-dose barbiturates (cytoprotective)
69
Q

Phenylcyclidine and ketamine

A

NMDA ion channel inhibition: uncouples the affective aspect of pain

70
Q

3A4 and C2D metabolism

A

3A4: methadone and fentanyl
2D6: codeine and tramadol

Med neuro (17 decks)

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