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Anesthesia Pharm > Week 7 - Pain Physiology & Opioids > Flashcards

Week 7 - Pain Physiology & Opioids Flashcards

1
Q

What is the definition of acute pain?

A

The direct result of tissue damage or potential damage and is a symptom

  • Well defined onset and clear pathology
  • Protect from tissue damage and allow time for healing
  • Frequently observable tissue damage
  • Usually adequately treated by pharmacological and treatment methods
  • It is useful and protective
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2
Q

What are the four components of nociception?

A

Transduction
Transmission
Modulation
Perception

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3
Q

What are nociceptors?

A

Specialized class of primary afferents that respond to intense, noxious stimuli in skin, muscles, joints, viscera, and vasculature

  • respond to multiple energy forms (thermal, mechanical, and chemical) that produce injury
  • provide info to CNS regarding location and intensity of noxious stimuli
  • are inactive until they are stimulated by sufficient energy to reach the threshold
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4
Q

What are the types of nociceptors?

A

C Fibers: unmyelinated, burning pain from heat stimuli and pain from sustained pressure

A Fibers Type 1 (Beta and some delta): myelinated, responsive to heat, mechanical, and chemical stimuli (polymodal), fast pain (>2m/sec)

A Fibers Type II (Delta): first pain sensation from heat (15m/sec)

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5
Q

What is the sensitization of nociceptors?

A

Increased responsiveness of peripheral neurons responsible for pain transmission to heat, cold, mechanical, or chemical stimuli

*frequently occurs and is attributed to the release of inflammatory mediators

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6
Q

What functions as a relay center for nociceptive and other sensory activity?

A

The spinal dorsal horn

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7
Q

Where does the perception of sensory-discriminative of peripheral painful stimuli occur (i.e. location and intensity of pain)?

A

Forebrain Somatosensory Cortex

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8
Q

Where does the perception of motivation-affective components of pain occur?

A

Limbic Cortex (Amygdala) and Thalamus

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9
Q

What modulates (either depress or facilitate) the integration of painful information in the spinal dorsal horn?

A

Descending projections originating from Periaqueductal Gray-Rostral Ventromedial Medulla system

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10
Q

What are the ascending pathways for pain transmission?

A

From spinal cord to sites in the brainstem and thalamus – important for perception and integration of nociceptive information

  • Spinothalamic Tract (direct projections to thalamus)
  • Spinomedullary and Spinobulbar Projections (direct projections to homeostatic control regions in medulla/brainstem)
  • Spinohypothalamic Tract (direct projections to the hypothalamus and ventral forebrain)
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11
Q

What are the descending pathways of pain modulation?

A

Originate from supraspinal regions and promote or supress nociceptive transmission through the dorsal horn

  • Descending Inhibition Pathway
  • Descending Facilitation Pathway
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12
Q

What are the inhibitory neurotransmitter effects on pain?

A
  • GABA (cerebral cortex, basal ganglia, cerebellum, spinal cord): increases Cl- which hyperpolarizes
  • ACh: increases K+ conductance in peripheral PNS
  • Dopamine: most likely inhibitory by acting on adenylate cyclase
  • Norepi: RAS & hypothalamus (inhibitory)
  • Epi: RAS (inhibitory)
  • Glycine (spinal cord): increases Cl-
  • Endorphins: excitatory for descending inhibitory pathway that inhibits pain transmission
  • Serotonin: inhibitory in the brain
  • Histamine: hypothalamus and RAS (inhibitory)
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13
Q

What are the excitatory neurotransmitters effects on pain?

A
  • Glutamate (hippocampus, outer layer of cerebral cortex, substantia gelatinosa): learning and memory (recall), central pain transduction, and excitotoxic neuronal injury
  • Inotropic Glutamate Receptors (NMDA receptors): ligand operated channel opens - influx of Na+, membrane depolarization
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14
Q

What is the mechanism of action of opioids?

A

Act as agonists at specific opioid receptors at presynaptic and postsynaptic sites in the CNS (brainstem and spinal cord) and the periphery

  • Mimic the actions of the endogenous ligands (Enkephalins, Endorphins, and Dynorphins) by binding to opioid receptors, resulting in the activation of the antinociceptive system
  • do not alter responsiveness of peripheral nerves to noxious stimuli nor impair impulse transmission
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15
Q

What state do opioids need to be in order to bind to the receptor?

A

Needs to be in the ionized state for strong binding to occur

Only levorotatory forms of the opioids exhibit agonist activity

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16
Q

What is the principal effect of opioid receptor activation?

A

A decrease in neurotransmission

  • this occurs largely by presynaptic inhibition of neurotransmitter release (ACh, Dopamine, Norepi, Substance P)
  • postsynaptic inhibition of evoked activity may also occur
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17
Q

What are the intracellular biochemical events initiated by occupation of opioid receptors with an opioid agonist?

A

Increased K+ conductance (hyperpolarization) and/or Ca++ channel inactivation

Leads to immediate decrease in neurotransmitter

*opioid receptor-mediated inhibition of adenylate cyclase is not responsible for immediate effect but may have a delayed effect (via reduction in cAMP)

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18
Q

Opioid cross the blood brain barrier based on what? (4)

A
  1. Molecular size (smaller is better)
  2. Lipid solubility (lipid soluble is better)
  3. Non-ionized is better
  4. Protein binding (greater protein bound = less drug available to cross)
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19
Q

What are the types of opioid receptors? What endogenous opioid bind to each type?

A

Mu – Endorphins and Endomorphins

Delta – Endorphins and Enkephalins

Kappa – Dynorphins

*the opioid-receptor-like 1 (ORL1) is involved in pain response and opioid tolerance

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20
Q

Where are opioid mu receptors located?

A

Brain: cortex, thalamus, striatum, periaqueductal gray, and rostra ventromedial medulla

Spinal cord: substantia gelatinosa

Peripheral sensory neurons

Intestinal tract

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21
Q

What are the actions of opioid mu receptors?

A
  • Sedation
  • Analgesia
  • Physical Dependence
  • Respiratory Depression (Mu2)
  • Miosis
  • Euphoria
  • Reduced GI motility
  • Vasodilation
  • Mu1 = low abuse potential
  • Mu2 = physical dependence
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22
Q

What are agonists at the mu receptors?

A

Endorphins
Morphine
Synthetic opioids

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23
Q

Where are opioid kappa receptors located?

A

Brain: hypothalamus, periaqueductal gray, and claustrum

Spinal Cord: substantia gelatinosa

Peripheral sensory neurons

*high intensity painful stimulation may be resistant to kappa receptor effects (as compared to mu)

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24
Q

What are the actions of opioid kappa receptors?

A
  • Analgesia
  • Anticonvulsant effects
  • Dissociative and delirium
  • Diuresis
  • Dysphoria
  • Miosis
  • Sedation
  • Reduces shivering

*low abuse potential

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25
Q

What are agonists at the kappa receptor?

A

Dynorphins

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26
Q

Where are opioid delta receptors located?

A

Brain: pontine nuclei, amygdala, olfactory bulbs, cortex

*NO spinal cord or peripheral sensory

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27
Q

What are the actions of opioid delta receptors?

A
  • Analgesia
  • Antidepressant effects
  • Convulsant effects
  • Physical dependence
  • Respiratory depression
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28
Q

What are agonists at the delta receptor?

A

Enkephalins

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29
Q

What are the general side effects of opioids?

A
  • Sedation (precursor to respiratory depression)
  • Respiratory depression (usually prevented by intense pain)
  • N/V (treat with antiemetics)
  • Decreased GI motility (leads to constipation)
  • Euphoria
  • Anti-tussive (codeine)
  • Miosis (pupillary constriction)
  • Pruritis
  • Biliary spams (mostly morphine - cautious use in gallbladder surgeries)
  • Myoclonus/Seizure (high dose)
  • Chest wall rigidity (high doses, given quickly IV)
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30
Q

What are the cardiovascular effects of opioids?

A
  • Orthostatic hypotension
  • Bradycardia due to increased activity of vagal nerves (may directly stimulate SA node as well - decreased vulnerability to VF)
  • Peripheral vasodilation due to histamine release
  • Protect myocardium from ischemia (kappa receptors mostly – enhance resistance to oxidative stress)
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31
Q

What is the onset, duration, and T1/2 of Morphine?

A 
Onset = 15-30 min
Duration = ~4-6 hours
T1/2 = 2-3 hours
  • Only 23% unionized so only a small amount gets into CNS
  • Minimal cross to BBB due to poor lipid solubility, highly ionized at pH 7.4, high protein binding, and quick glucuronidation
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32
Q

What are the effects of morphine?

A
  • Analgesia
  • Euphoria
  • Sedation
  • Diminished ability to concentrate
  • Nausea
  • Feeling of body warmth
  • Heaviness of extremities
  • Mouth dryness
  • Pruritus (especially nose) (mu receptor effect – not histamine related)
  • Influences the motivation-effective aspect of pain
  • Biliary spasm (increases phasic wave frequency of sphincter of Oddi)
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33
Q

How does morphine produce analgesia?

A

Classic Mu opioid receptor agonist

  • Brain (Central) – mu1 – periaqueductal gray, locus coeruleus, medullary nuclei
  • Sends descending inhibitory signals
  • Spinal Level – mu2
  • presynaptic inhibition of primary afferents (decrease in substance P)
  • postsynaptic hyperpolarization of interneurons (substantia gelatinosa) – decreases afferent transmission of nociception

Central and spinal synergy

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34
Q

How does gender affect morphine?

A

Morphine exhibits greater analgesic potency and slower speed of offset in women than men

*higher post-op opioid consumption in men compared to women

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35
Q

What are the respiratory effects of morphine?

A
  • Causes respiratory depression (onset of resp depression parallels onset of analgesia)
  • Shifts the CO2 response curve to the right to resting PaCO2 and to apnea (protects pt from receiving too much morphine)
  • Slower RR and normal tidal volume
  • Decreased ventilatory response to hypoxia/hypoxemia

*hypercarbia will enhance CNS effect (decreases ionization)

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36
Q

How does morphine induce N/V?

A

By direct stimulation of the chemoreceptor trigger zone (CTZ)

37
Q

What occurs with prolonged use of morphine?

A

Tolerance develops with continued exposure
Hyperalgesia may develop

*Patients show signs and symptoms of withdrawal with it is discontinued

38
Q

How is morphine metabolized?

A

70% in liver via glucuronidation

  • M-3-glucuronide (75-85%): inactive metabolite
  • M-6-glucuronide (5-10%): active metabolite – 10x more potent than morphine

*liver disease has minimal effect on metabolism of morphine (reduced hepatic blood flow reduces clearance)

39
Q

How is morphine eliminated?

A

Excretion of metabolites via the kidneys

  • M6G is secreted by organic ion transporters in kidneys and is impaired in renal disease – M3G also accumulates
  • Patients with renal insufficiency may develop prolonged sedation or coma due to M6G accumulation
40
Q

What are the pharmacokinetics of Hydromorphone (Dilaudid)?

A

Morphine Derivative – ~5x more potent than morphine
1-2mg IV Hydromorphone = 10-20mg IV Morphine

IV: onset in 5 minutes and peaks in 10-20 minutes
PO: 2-4mg Q4-6H – onset 20-40 min and peaks in 1.5 hours

Metabolized via glucuronidation in the liver

41
Q

What is Codeine?

A

Morphine Derivative – prodrug that is converted to morphine via CYP2D6

  • low affinity for opioid receptors
  • Analgesic effect due to ~10% conversion to morphine
  • Less 1st pass metabolism when taken orally

Commonly mixed with acetaminophen:

  • Tylenol #3 (30mg codeine + 300mg Tylenol)
  • Tylenol #4 (60mg codeine + 300mg Tylenol)
42
Q

What is Hydrocodone?

A

Derivative of codeine

  • Similar in potency to oral morphine and similar duration of analgesic action
  • Commonly combined with acetaminophen
  • Used to treat acute pain associated with illness or injury
  • Metabolized via CYP2D6 to hydromorphone
43
Q

What is oxycodone? What are the dosages?

A

Morphine Derivative – 2x as potent as oral morphine with similar duration of analgesia

  • Less 1st pass metabolism than morphine
  • Metabolized via CYP2D6/CYP3A4

Percocet (Oxycodone + 325mg acetaminophen)

  • Adults 5-15mg (1-3 tabs) Q6H
  • Peds 0.05-0.15mg/kg Q4-6H

Oxycotin (sustained release tablets) – taken whole, get bolus “high” when crushed

  • 10-20mg Q12H
  • 80-120mg for opioid tolerant pts (cancer)
44
Q

What are the opioid antagonists?

A

Naloxone (Narcan) – use for opioid OD

Naltrexone (Antabuse) – long acting, not used for an OD but rather for maintenance treatment of opioid dependence

Nalmefene – equipotent to naloxone, 15-25mcg every 5 min IV – longer duration than naloxone

45
Q

Where does Naloxone act and how is it administered?

A

Competitive antagonist at mu, kappa, and delta opioid receptors

Admin IV, intranasal, or SQ
*Peak effect in 1-2 minutes

46
Q

What is the dose of Naloxone for a slow/partial reversal and for “code blue”?

A

Adult Dose = 0.5-1.5mcg/kg (40-100mcg) for slow/partial reversal of unwanted opioid side effects
Standard ampule = 0.4mg (400mcg) – give full ampule (400mcg) in a “code blue” respiratory depression or narcotic overdose

-Will reverse excessive opioid induced respiratory depression

**Duration of action = 30-40 min and T1/2 = 65 min (adults) and 3hr (neonates) — what is the T1/2 of opioid - may need to redose

47
Q

What is Meperidine and its properties?

A

Synthetic Opioid – 1/10th potency of morphine but has faster onset (more lipid soluble)

  • Acts on mu and kappa opioid receptors
  • Less bradycardia and respiratory depression than equianalgesic dose of morphine
  • Some LA activity (sensory/motor block – block Na+ channel)
  • Dysphoric/Psychomimetic effects from kappa receptor
  • Less biliary pressure effect
  • Greater histamine release than morphine
  • Metabolized in liver (CYP2D6/CYP3A4)– active metabolite Normeperidine T1/2 14-21 hours (can lead to seizures/delirium)
48
Q

What is the primary clinical use of Meperidine?

A

Very useful for post-op shivering – kappa receptor stimulation and alpha2 activation

  • does cause N/V
  • Clonidine and Burophanol better at decreasing shivering
49
Q

What may occur with the administration of meperidine to patients receiving antidepressant drugs? What are the symptoms of it?

A

Serotonin Syndrome – meperidine inhibits reuptake of serotonin

Manifests as:

  1. Delirium - altered mental status, agitation, excitement and confusion
  2. Fever - tachycardia, tachypnea, autonomic hyperactivity, diaphoresis
  3. Convulsions - neuromuscular hyperactivity, tremor, clonus, myoclonus, hyper-reflexia, and pyramidal rigidity
50
Q

Where does fentanyl act and how does it compare to morphine?

A

It is almost completely mu receptor agonist

50-100x more potent than morphine
*100 mcg Fentanyl = 10 mg Morphine

Effects and side effects are similar at equianalgesic doses

  • no direct reduction in myocardial contractility (BP will drop if pain relieved and SNS slows down, acts on baroreceptors to slow HR)
  • no histamine release
51
Q

What is the onset of fentanyl?

A

Onset of effects in 3-5 minutes IV

  • more rapid brain equilibration than morphine (highly lipid soluble)
  • Lipid solubility 816 = 80% to Vascular Rich Group

*Rapid onset of analgesia = rapid respiratory depression

52
Q

Explain fentanyl’s context-sensitive half-time

A

During prolonged infusions inactive tissue sites become saturated with fentanyl – This tissue reservoir replaces fentanyl eliminated by hepatic metabolism – leads to slow decrease in plasma concentrations when infusion is discontinued

Depends on length of administration:
1 min infusion = T1/2 5 min
1 hour infusion = T1/2 20 min
8 hour infusion = T1/2 250 min (4hr)

53
Q

What effects do opioids have on inhaled anesthetics?

A
  • Increased opioid allows reduced Iso concentration (MAC)
  • MAC reduction may be greater than 75%
  • MAC reduction occurs at moderate plasma levels of opioid concentration
  • Iso can NOT be eliminated

*Fentanyl upon induction will reduce MAC requirements for inhaled anesthetic

54
Q

What are the infusion doses of fentanyl?

A

Loading Dose = 8-12 mcg/kg (500-850 mcg in 70kg pt)

Maintenance Dose = 1-2 mcg/kg/hr

55
Q

Where does alfentanil act and how does it compare to morphine and fentanyl?

A

Almost completely mu receptor agonist

10x as potent as morphine
1/10 - 1/4 as potent as fentanyl

1000mcg Alfentanil = 100mcg Fentanyl = 10mg Morphine

*effects/side effects similar at equianalgesic dose

56
Q

How is fentanyl metabolized?

A

100% hepatic extraction – CYP3A4

inactive metabolites

  • clearance directly correlated to liver blood flow
  • decreased with P450 inhibitors
57
Q

What is the onset of Alfentanil?

A

Extremely rapid onset ~1-2 minutes

  • 90% unbound is unionized at pH 7.4
  • Rapidly crosses B:B barrier

*rapid onset = rapid onset of respiratory depression

58
Q

How is alfentanil metabolized?

A

~30-50% in the liver

  • Inactive metabolites
  • Clearance is directly proportional to liver blood flow
  • Reduced with P450 inhibitors
  • Metabolism is lower in elderly and CHF – decreased blood flow to liver
59
Q

What is the context-sensitive T1/2 for alfentanil?

A

Depends on length of admin but less affected than fentanyl

1 min infusion = T1/2 1 min
1 hour infusion = T1/2 30 min
8 hour infusion = T1/2 50 min

60
Q

What is the dosing for alfentanil?

A

Loading dose = 35-70 mcg/kg
*2,500-5,000mcg in 70kg pt – comes in 500mcg/mL

Maintenance infusion = 0.25-0.5 mcg/kg/min

61
Q

Where does remifentanil act and how does it compare to fentanyl?

A

Almost completely mu receptor agonist

Equipotent to Fentanyl – 50 mcg Remifentanil = 50 mcg Fentanyl

62
Q

What is the onset of remifentanil?

A

very rapid onset ~1 minute

63
Q

What is the metabolism and clearance of remifentanil?

A

Metabolism is by non-specific plasma esterases (NOT pseudocholinesterase)

Clearance is CONSTANT and not affected by liver flow, renal failure, or length of infusion

*no residual analgesia – need long acting opioid before turning off

64
Q

What is the context-sensitive T1/2 of Remifentanil?

A

Independent of length of infusion

1 min infusion = T1/2 3 min
1 hour infusion = T1/2 3 min
8 hour infusion = T1/2 3 min

*Duration ~6-9 min after infusion turned off

65
Q

What is the dosing for remifentanil?

A

Infusion is the only way to use remifentanil

  • Loading dose = 1-2 mcg/kg (70-140mcg)
  • Infusion = 0.05-0.25 mcg/kg/min

*UIHC: mix 4 mcg/mL for non-intubated cases and 10 mcg/mL for intubated/GA cases

66
Q

What is the mechanism behind opioid tolerance and hyperalgesia?

A

Prolonged exposure to opioid activates NMDA glutamate receptors via second messenger mechanisms and also downregulates spinal glutamate transporters

-the resultant high synaptic concentrations of glutamate and NMDA receptor activation contributes to tolerance and hyperalgesia

**treat with small doses of ketamine (NMDA antagonist)

67
Q

What characteristics of opioids do you look at when choosing and dosing an opioid?

A

Onset – percent non-ionized

Control of effects – protein binding %

Duration – clearance/elimination T1/2

Potency – partition coefficient

68
Q

What opioids are used as spinal opioids?

A

Morphine or Fentanyl – must be preservative free!

  • Act on mu receptors in the dorsal horn to produce analgesia
  • Admin intrathecally (directly into cerebro-spinal fluid) for chronic pain
  • Admin intrathecally or epidurally for acute pain
  • morphine controls pain well and produces less sedation and resp depression for the same amount of analgesia
  • however, resp depression, N/V, sedation, and itching still frequently occur
69
Q

What is the result of opioid synergism?

A

Opioid + Benzo or Opioid + Propofol

Can cause significantly greater respiratory depression, obtundation, and respiratory arrest at much lower doses than those given when agents are admin alone

  • shown with ALL opioids
  • fast onset opioids are that much more dangerous secondary to lack of time for onset of side effects
70
Q

What opioids have active metabolites?

A 
Morphine (M6G)
Hydrocodone (hydromorphone)
Meperidine (normeperidine)
Oxycodone (oxymorphone)
Codeine (morphine)
Tramadol (o-desmethyl-tramadol (M1))
71
Q

What are the advantages and disadvantages of opioid mixed agonist/antagonist?

A

Partial agonists at all 3 receptors

Advantages:

  • Ability to produce analgesia with limited respiratory depression
  • Low potential for physical dependence

Disadvantages:

  • Have ceiling effect – increase dose doesn’t increase additional response
  • Once antagonized, difficult to then use opioid agonist
72
Q

What is Butrophanol?

A

Mixed opioid agonist-antagonist

  • low affinity for mu receptors to produce antagonism
  • moderate affinity for kappa receptors to produce analgesia and anti-shivering effects
  • minimal affinity for sigma receptor so incidence of dysphoria is low
73
Q

What is Buprenorphine?

A

Mixed opioid agonist-antagonist

  • affinity for mu receptors 50x greater than morphine with slow dissociation from these receptors – prolonged duration
    0. 3mg buprenorphine = 10mg morphine
  • Can be used post-op for moderate to severe pain
  • Can be placed in epidural space – high lipid solubility and affinity for opioid receptors limits cephalad spread thus likelihood of resp depression
  • Antagonist effects reflect ability to displace opioid agonists from mu receptors
74
Q

What is the mechanism of action of NSAIDs?

A

Inhibit the biosynthesis of prostaglandins by preventing the substrate arachidonic acid from binding to the COX enzyme active site

  • COX 1: catalyzes production of prostaglandins that are involved in numerous physiologic functions and production of proaggregatory thromboxane A2
  • COX 2: expression induced by inflammatory mediators in many tissues and has a role in mediation of pain, inflammation, and fever

*in addition to peripheral blockade of prostaglandin synthesis, central inhibition of COX2 may play an important role in modulation nociception

75
Q

What are the general effects of NSAIDs on platelet function?

A

Inhibit the activity of COX1 thus the production of thromboxane A2 that is responsible for platelet aggregation

76
Q

What are the general effects of NSAIDs on GI tract?

A

Upper GI: endoscopic ulcers and sometimes serious ulcer complications including perforation and bleeding

Increased Risk Factors for GI complications:

  • High Dose
  • Older age
  • H-pylori infection
  • Concomitant use of low-dose ASA, anticoagulants, or corticosteroids
77
Q

What are the general effects of NSAIDs on CV system?

A

Increased risk of MI, HF, and HTN

  • COX inhibition disturbs balance between COX2 mediated production of proaggregatory thromboxane in platelets and antiaggregatory prostaglandin I2 in endothelial cells
  • Naproxen has safer profile
78
Q

What are the general renal effects of NSAIDs?

A

Changes in excretion of Na+
Changes in tubular function
Potential for interstitial nephritis
Reversible renal failure due to alterations in filtration rate and renal plasma flow

*all except ASA decrease GFR (occurs more frequently in pts with CHF or renal disease)

79
Q

What are the general pulmonary effects of NSAIDs?

A

Patients with allergic rhinitis, nasal polyposis, and/or history of asthma are at increased risk for anaphylaxis
*due to the inhibition of prostaglandin synthesis in local tissues

Highly selective COX2 inhibitors as an alternative to ASA/other NSAIDs suggested for pts with ASA-exacerbated respiratory disease

80
Q

What is the mechanism of action of Acetaminophen?

A

Antipyretic and analgesic but has no anti-inflammatory action

Central analgesic effect mediated through activation of descending serotonergic pathways – may inhibit prostaglandin synthesis via COX3
Spinal cord level - antagonize neurotransmission by NMDA, substance P, and nitric oxide pathways

81
Q

What is the dosing for Acetaminophen?

A

Excellent Bioavailability

PO: 325-650 mg Q4-6H (do not exceed 4,000mg)

IV provides around 4 hours of effective analgesia

*Combination of Acetaminophen and an NSAID may offer superior analgesia compared with either drug alone

82
Q

What is the oldest and most widely used medicinal compound around the world?

A

Aspirin

*derivative of salicylic acid – rapidly metabolized by plasma esterases

83
Q

What is aspirin predominantly used to treat?

A

Cardiovascular and cerebrovascular disease

84
Q

What is the mechanism of action of aspirin?

A

Irreversibly blocks the action of the COX enzymes preventing production of prostaglandins

*leads to prolonged inhibition of platelet aggregation

85
Q

How do steroids treat pain?

A

Its anti-inflammatory action results in decreased production of various inflammatory mediators that play a major role in amplifying and maintenance of pain perception
-Also possibly by inhibition of phospholipase A2 as well as changes in cell function induced by glucocorticoid receptor activation

Glucocorticoids>Corticosteroids in anti-inflammatory

86
Q

How does dexamethasone affect post-op pain management?

A

Patients treated with dexamethasone experience less post-op pain

  • Require less post-op opioid
  • Longer time to first analgesic dose
  • Need less rescue analgesia
  • Shorter PACU stays
87
Q

What is Capsaicin?

A

Transient receptor potential vanilloid (TRPV1) channel agonist

  • TRPV1 receptor is markedly reduced in inflammatory conditions and is present on unmyelinated C fibers in the periphery
  • Activation of TRPV receptors releases high-intensity impulses and releases substance P, which results in the initial phase of burning – continued release of substance P in presence of Capsaicin leads to depletion and subsequent decrease in C fiber activation
88
Q

What is Capsaicin used for?

A

Temporary relief of pain from arthritis, myalgias, arthralgias, and neuralgias

Treatment of postherpetic neuralgis (Shingles), intermetatarsal neuroma, erythromelalgia, and HIV associated neuropathy

Anesthesia Pharm (18 decks)

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