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MSK-Derm by Minnie AH Version > SM 236a, 240a, 244a - Pharmacology, Opioids, and Pain I, II, III > Flashcards

SM 236a, 240a, 244a - Pharmacology, Opioids, and Pain I, II, III Flashcards

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1
Q

Describe the action of buprenorphine on the mu opioid receptor

A
  • Partial mu agonist = ceiling on agonism
  • Binds the mu opioid receptor with high affinity
  • Prevents other opioids from binding
    • Makes naloxone reversal difficult in OD
  • Use for opioid maintenance to treat addiction
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2
Q

What are the neurologic effects of opioid use?

A
  • Analgesia
  • Miosis
    • Even in patients who are tolerant
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3
Q

What factors might increase a patient’s risk of UGI bleed when taking NSAIDs?

A
  • Daily, long term use
  • High doses of NSAIDs
  • Combining NSAIDs with ASA
    • ASA = aspirin
  • Age
  • Prior PUD or UGI bleed
  • Anticoagulant use
  • Alcohol or steroid use
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4
Q

Which NSAID is okay to use in patients with CV disease?

A

ASA (aspirin)

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5
Q

Butorphanol is classified as a mu opioid receptor…

A. Agonist

B. Antagonist

C. Agonist/Antagonist

D. Partial agonist

A

C. Agonist/Antagonist

  • Analgesia is kappa mediated
    • Does not have as much pain relieve as mu agonists, but fewer GI effects
  • Can trigger withdrawl
    • Do not use in opioid tolerant patients
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6
Q

What is Misoprostol?

A
  • An agent that helps to protect the stomach lining from damage from NSAIDs
  • Note – also causes diarrhea
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7
Q

​A patient with oropharyngeal cancer is requiring management of pain due to tumor erosion into his mandible. A long duration opioid is desired in order to avoid his having to take medication frequently. Due to difficulty in swallowing, however, he can only consume liquids or tablets that are crushed and placed in applesauce. The best option is

  1. Sustained release morphine pills
  2. Sustained release oxycodone pills
  3. Hydromorphone pills
  4. Methadone
  5. Fentanyl lollipop
A

d. Methadone

Sustained release pills lose their duration when you crush them

Fentanyl lollipop is for acute pain; fast acting, short duration

Methadone is inherently long-acting; it has a long half life

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8
Q

Which opioids inhibit serotonin reuptake, leading to intense euphoria?

A

Merperidine

Tramadol

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9
Q

What is the difference between drug dependence and drug addiction?

A
  • Dependence
    • The patient will have physical withdrawal if the drug is stopped
  • Addiction
    • A psychological diagnosis involving misuse/abuse of the drug
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10
Q

What is the relevant metabolite of merperidine?

What are its effects?

A

Normeperidine

  • 10 hour half life
  • Causes CNS hyperactivity and seizures
  • Cleared by the kidney
    • Do NOT use in pts with renal failure
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11
Q

What is tolerance?

A

When prolonged use of a drug requires higher doses to achieve the same effect

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12
Q

How do opioid receptors vary person to person?

A
  • Different density of mu, kappa, and delta receptors
    • Due to different DNA
  • Different variants of mu, kappa, and delta subgroups
    • Due to splice variation
    • These splice variants have different affinities

Result: Different opioids work differently for different people!

If a patient is having side effects but no analgesia, change the opioid

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13
Q

Increasing glycine and GABA in the CNS would have what effect on pain perception?

A

Glycine and GABA work through the descending pain pathway to intercept ascending nociceptive signals

More glycine and GABA = More descending action = decreased pain perception

Note: Prostaglandins inhibit the release of glycine and GABA

NSAIDs inhibit prostaglandins, and therefore increase glycine and GABA in the CNS

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14
Q

What is the role of COX-1 in protecting our stomach lining?

A
  • Increase Mucous layer thickness
  • Decrease pH gradient
  • Increase Bicarbonate secretion
  • Increase Mucosal blood flow
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15
Q

Naloxone is classified as a mu opioid receptor…

A. Agonist

B. Antagonist

C. Agonist/Antagonist

D. Partial agonist

A

B. Antagonist

Used for heroine/opioid overdose

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16
Q

Nonsteroidal antiinflammatory drugs exert their analgesic effect by

  1. Binding to prostaglandin receptors in peripheral inflamed tissue
  2. Inhibiting the action of prostaglandins on peripheral nerves
  3. Inhibiting the formation of prostaglandins
  4. Inhibiting the formation of arachidonic acid
  5. Inhibiting lipooxygenase
A

c. Inhibiting the formation of prostaglandins

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17
Q

Where does the sensory neuron (pain fiber) synapse with the secondary (central) neuron)?

A

Substantia gelatinosa (in the dorsal horn)

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18
Q

Morphine is classified as a mu opioid receptor…

A. Agonist

B. Antagonist

C. Agonist/Antagonist

D. Partial agonist

A

A. Agonist

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19
Q

What are the metabolites of oxycodone?

What provides analgesia – the parent drug or the metabolites?

A

Relevant metabolite = oxymorphone

14x more potent than oxycodone

Both the parent drug and the metabolie provide analgesia

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20
Q

Which somatosensory pathway is involved with pain, temperature, and crude touch?

A

Anterolateral pathway (including spinothalamic tract)

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21
Q

Describe the pain pathway from the site of tissue injury to the brain

A
  • Injured tisssue
    • Prostaglandin, bradykinin, leukotriene
  • Sensitized nociceptor detects pain, fires an action potential
  • Pain travels up a sensory neuron to the dorsal horn
  • Sensory neuron synapses with the secondary neuron in the dorsal horn
  • Secondary neuron carries the pain signal to the brain
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22
Q

What protects our stomach lining from the acidic lumen?

A

Mucous layer containing HCO3

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23
Q

Which NSAIDs will not interfere with clotting?

A

COX2 selective NSAID

Ex: Celecoxib

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24
Q

Naltrexone is classified as a mu opioid receptor…

A. Agonist

B. Antagonist

C. Agonist/Antagonist

D. Partial agonist

A

B. Antagonist

Used to treat addiction

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25
Q

Why do NSAIDs work even when there is no inflammation?

A

NSAIDs prevent prostaglandin synthesis

  • Prostaglandins are relesed in peripherl tissues due to inflammation, but they are also contituitively present in the CNS
    • ​They normally work to amplify pain in the ascending pathway.
      • Sensitize the second degree neurons to substance P and glutamate
      • Inhibit the descending pathway by preventing glycine and GABA release
  • NSAIDs will prevent prostaglandins from having these effects on the CNS
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26
Q

Which NSAID will not increase a patient’s bleeding risk during surgery?

A

Celecoxib

COX2 selective inhibitor => will not interfere with platelet function

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27
Q

A patient comes to you suffering from pain following knee surgery 3 days ago. He reports that the opioid pain medication that he received from the orthopedic surgeon causes nausea and dysphoria but does nothing for his pain. He notes that a different opioid medication that he had from a prior surgery works well, and he requests you prescribe this for him instead.

What would the scientific justification be for prescribing this different opioid?

A

Different patients have splice variation in their mu, kappa, and delta receptrs

Different opioids have different affinities for these splice variants

Therefore, some opioids work better for some patients than others

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28
Q

What is the most common IV NSAID?

A

Ketorolac (no oral potency)

Same as ibuprofen, but ibuprofen is oral

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29
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

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30
Q

What is an opioid?

A

All drugs, both natural and synthetic, that bind to opioid receptors

  • All opiates are opioids, but not all opioids are opiates
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31
Q

A transplant recipient is in the recovery room following a renal transplant surgery. The attending surgeon cancels the resident’s order to give a single dose of ketorolac for pain. The best reason for canceling the order is

  1. Ketorolac can cause microemboli in the new kidney
  2. Ketorolac can reduce blood flow to the new kidney
  3. Ketorolac can reduce sodium reabsorption in the new kidney
  4. Ketorolac can prolong postoperative ileus (cessation of peristalsis that occurs postop)
  5. Ketorolac can cause respiratory depression
A

b. Ketorolac can reduce blood flow to the new kidney

Ketorolac is an NSAID

NSAIDs inhibit prostaglandin synthesis, and will therefore prevent vasodilation in the afferent arteriole of the kidney

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32
Q

What sensations utilize the anteriolateral somatosensory pathways?

A

Pain, temperature, crude touch

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33
Q

Which NSAID may cause tinnitus (ringing in the ears)?

A

Aspirin (ASA)

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34
Q

Describe the mechanism of tramadol

A
  • 2 mechanisms
    • M1 metabolite is a mu opioid receptor agonist
    • Parent drug blocks reuptake of 5-HT (serotonin) and norepinephrine
      • Use caution if the patient is on other SSRIs
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35
Q

A patient in the ICU is recovering from a surgical resection of dead bowel. The patient is septic and requires hemodialysis three times a week. He is being given meperidine every 3 hours for control of his pain and to supplement his sedation. After two days on this regimen, you are called to his bedside because of seizures. The most appropriate therapy would be

  1. Naloxone to treat the meperidine induced seizure
  2. Benzodiazepines to treat the meperidine metabolite induced seizure
  3. Naloxone to control effects of delayed meperidine clearance
  4. Nalbuphine to antagonize the effect of the opioid while providing some analgesia
  5. Urgent dialysis to remove the accumulated meperidine
A

b. Benzodiazepines to treat the meperidine metabolite induced seizure

Normeperidine is a seizure-inducing metabolite of meperidine, normally cleared by the kidney

The seizures have nothing to do with the opioid recepotors, and should be treated as you would treat any seizure (with benzos)

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36
Q

What are the mechanisms of NSAID GI toxicity?

A
  • Direct gastric irritation
    • Most NSAIDs are weak acids
  • Decreased cytoprotection via inhibition of COX1
    • Decreased mucous layer thickness
    • Increased pH gradient
    • Decreased bicarb secretion
    • Decreased mucosal blood flow
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37
Q

Describe the inflammatory prostaglandin synthesis pathway. Include the relevant enzymes and intermediates.

NSAIDS inhibit the synthesis of which of these intermediates?

A
  • Cell injuory or other trigger causes phospholipid release
  • Phospholipid -> Arachadonic acid
    • Phospholipase A2
  • Arachadonic acid -> Prostaglandin H2
    • Cyclooxygenase (COX)
    • NSAIDs act here to inhibit COX
  • Prostaglandin H2 -> Tissue-specific prostaglandin
    • ​Tissue specific PG synthase
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38
Q

How do prostaglandins enhance pain in the CNS?

Describe the mechanism

A

Prostaglandins act at the synapse between the nociceptor and the second-degree neuron in the dorsal horn

  • Enhance substance P and glutamate release
  • Sensitize the second degree neuron to substance P and glutamate
  • Decrease glycine and GABA release from the descending pathway
    • Descending pathway cannot effectively modulate the ascending pathway

These three mechanisms result in hyperalgesia

(Prevented by NSAIDs)

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39
Q

What do all NSAIDs have in common?

A

They inhibit cyclooxygenase (COX), the enzyme that makes prostaglandins

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40
Q

Which opioids might cause seizures?

A
  • Morphine
    • M-3-G metabolite produced by the liver may produce hyperalgesia, allodyina, myclonus, and seizure
  • Merperidine
    • Normeperidine metabolite has a 10 hour half life
      • Cleared by the kidney - do not use in pts with renal failure
    • Causes CNS hyperreactivity and seizures
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41
Q

What are the differences between high lipohilicity opioids adn low lipophilicity opioids?

A
  • High lipophilicity
    • Fast onset, short duration
    • Fentanyl, meperidine
  • Low lipophilicity
    • Slow onset, long duration
    • Morphinne, hydromorphone
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42
Q

Hydromorphone is classified as a mu opioid receptor…

A. Agonist

B. Antagonist

C. Agonist/Antagonist

D. Partial agonist

A

A. Agonist

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43
Q

How do opioids affect the ascending pain pathway?

How do opioids affect the descending pain pathway?

A
  • Ascending
    • Opioids inhibit cellular adenylyl cyclase, which increases K+ currents and decreases Ca2+ currents
    • This causes hyperpolarization of the neuron, and therefore decreased pain transmission
      • Acts on the pre-synaptic and post-synaptic neurons in the dorsal horn
  • Descending
    • Opioids inhibit the inhibitors of the descending pathway
    • Normally, inhibitory neurons prevent the descending pathway from affecting ascending pain transmission
    • Opioids inhibit the GABA releasing inhibitory neurons in the periaqueductal grey and elsewhere
    • This allows the descending pathway to block the ascending pain signals
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44
Q

Arachidonic acid is the precursor for which two substances?

Which enzymes are involved?

A
  • Arachidonic acid -> Prostaglandin H2
    • Cyclooxygenase (COX)
    • This is the pathway relevant to the pain pathway
  • Arachidonic acid -> Leukotriene
    • Lipooxygense
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45
Q

Which COX enzyme is involved in inflammation?

A

COX2

  • Appears when inflammation/injury occurs - it is responsible for pain
    • Most tissues
  • Constitutitively active in some tissues
    • CNS, kidney, uterus
    • This means that selective COX2 inhibitors are not protective against kidney injury
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46
Q

What is dependence?

How is it different from tolerance?

A
  • Dependence
    • Patient will have withdrawal if the drug is stopped
    • The patient is physically dependent on the drug
  • Tolerance
    • Increased dose required for the same effect
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47
Q

What are the effects of opioid use on the heart?

A

Not many! – considered a hemodynamically stable class of drugs

48
Q

Which COX enzyme is constitutively present in the GI tract, platelets, and kidneys?

A

COX1

A selective COX2 inhibitor will have fewer GI effects, and will not affect coagultion

However, the kidneys also have COX2 - will be affected (and potentially injured) by a selective COX2 inhibitor

49
Q

Which NSAID is contraindicated in a child with a viral syndrome?

Why?

A

Aspirin (ASA)

Risk of Reye’s syndrome: Hepatic injury and encephalopathy

50
Q

Meperidine is classified as a mu opioid receptor…

A. Agonist

B. Antagonist

C. Agonist/Antagonist

D. Partial agonist

A

A. Agonist

51
Q

Why are NSAIDs contraindicated in severe asthmatics?

A

Blocking COX leads to increased lipoxygenase activity, resulting in increased leukotriene synthesis

Leukotrienes are involved in allergic/asthmatic inflammation

52
Q

What neurotransmitters are released from the 1st degree neuron in the dorsal horn in order to synapse with the second degree neuron?

A

Substance P and Glutamate

Note: Their release is enhanced by prostaglandins

(And therefore inhibited by NSAIDs)

53
Q

Which NSAID can be given topically?

When is this most useful?

A

Diclofenac

Used on superficial joints, fewer systemic side effects

54
Q

What are the hematologic effects of ASA?

A

ASA irreversibly acetylates COX in platelets (and elsewhere)

  • The platelets will never be able to make more COX – in order to have normal platelets again, the patient needs to make more platelets
    • Platelets do not have nuclei, and therefore cannot make new COX
  • It will take 7-10 days for clotting to return to normal
  • This means that even low doses of aspirin are cardioprotective (will prevent thrombosis)

Note: other NSAIDs irreversibly bind COX, so the anti-coagulative effect does not last as long

55
Q

Which part of the body has the most opioid receptors outside of the CNS?

A

GI tract - enteric nervous system

56
Q

How do prostaglandins affect nociceptive nerve endings?

Describe the mechanism

A

Prostaglandin E binds to the nociceptive nerve endings

  • -> Increased Na+ influx into the neuron
  • -> Increase resting membrane potential (closer to threshold)
    • > Nociceptor is more likely to fire an action potential and transmit a pain signal to the brain
57
Q

The brainstem ventilation nuclei contains opioid receptors.

What is the implication of this?

A

Opioids will act on the ventilation system of the brain to decrease respiratory drive

58
Q

What are the therapeutic effects of opioids on the respiratory system?

A

Anti-tussive action

Prevent hyperventilation from pain and anxiety

Helps to avoid increased in bronchomotor tone in asthma

59
Q

What are the GI effects of opioid use?

A

Slowed peristalsis -> constipation

Nausea/vomiting

60
Q

What is the half life of Naloxone?

Why is this relevant?

A

Naloxone has a short half life - 1 hour

  • Naloxone is used as a rescue drug for opioid use, but the rescue may not last as long as the drug that was overdosed
61
Q

What are the major side effects of NSAIDs?

A
  • Stomach/duodenal ulcer
  • Decreased clotting
  • Decreased blood flow to kidneys
  • Edema and hypertension
    • In at-risk patients only (CV risks)
  • Reports of hepatic dysfunction
62
Q

Which area of the brain is considered our “emotional” center?

A

Amygdala

Note - contains opioid receptors

63
Q

List the relevant mu opioid receptor antagonists

A
  • Naloxone
    • Use if overdose
  • Naltrexone
    • Use to treat addiction
64
Q

Which drug is put in opioid pills to prevent IV abuse?

How does this work?

A

Naloxone - competitive antagonist at the mu opioid receptor

  • Naloxone has very poor oral availability
    • It won’t interfere with whatever is in the pill, if taken orally
  • However, if a person tries to crush up a pill and inject it, there will be no mu agonist effect
65
Q

What are the relevant metabolites of hydrocodone?

What provides analgesia?

A

Hydrocodone metabolized to hydromorphone

Ongoing debate as to which one provides analgesia

66
Q

What is the role of the periaqueductal grey in the central modulation of pain?

A

Periaqueductal gray inhibits pain transmission in the dorsal horn via a relay in the rostral ventral medulla

67
Q

NSAIDs prevent the synthesis of what substance?

A

Prostaglandin H2

Prostaglanins sensitize peripheral pain nerve endings (allodynia) and enhance pain transmission in the CNS (hyperalgesia)

68
Q

How is naloxone administered?

A

IV only

Basically zero oral availability

69
Q

A 25 year old patient with no significant past medical history presents to your office for a routine introductory checkup. During your history, you learn that as an athlete, he uses 200mg of OTC (over the counter) ibuprofen three times per day every day for various muscle aches, and has done so for the past year. Further evaluation at this visit should include (select the best answer):

  1. Drug screening for opioids
  2. Drug screening for other NSAIDs
  3. Thyroid stimulating hormone levels
  4. Examination for hearing loss
  5. Stool guiac for blood
A

e. Stool guiac for blood

70
Q

List the relevant mu opioid receptor agonists

A

My OH My, Can He Feel Me Toot?

  • Morphine
  • Oxycodone
  • Hydrocodone
  • Merperidine
  • Codeine
  • Hydromorphone
  • Fentanyl
  • Methadone
  • Tramadol

Note: If it starts with an N or a B, it is not a pure agonist

  • Antagonists: Naloxone, Naltrexone*
  • Agonist/Antagonist: Nalbuphine*
  • Partial agonist: Buprenorphine*
71
Q

How do NSAIDs affect blood pressure?

A

NSAIDs increases blood pressure over time in people who have been treated for hypertension

People with normal blood pressure to begin with are unaffected

72
Q

List the relevant mu opioid receptor partial agonist

A

Buprenorphine

73
Q

What is the action of naloxone on the mu opioid receptor?

A

Competitive antagonist

74
Q

How does the inhibition of prostaglandin synthesis affect our perception of pain peripherally?

Centrally?

Which drug does this?

A

NSAIDs inhibit prostaglandin syntehsis

  • Peripheral effect
    • Prostaglandins sensitize pain nerve endings by increasing Na+ influx, thus bringing the resting membrane potential closer to threshold -> more AP firing -> more pain signals
    • NSAIDS inhibit the synthesis of prostaglandins, which prevents sensitization of these nociceptive nerve endings
      • ​They do not become excitable, and therefore do not transmit excessive pain signals
  • Central effect
    • At the synapse of the nociceptive neuron in the dorsal horn, prostaglandins increase substance P and glutamate from the 1st degree neuron and sensitize the 2nd degree neuron
    • They also inhibit the descending pathway by decreasing glycine and GABA release
    • Inhibiting the synthesis of protaglandins prevents the enhanced substance P and glutamate release from the 1st degree neuron, prevents senitization of the 2nd degree neuron, and allows the descending pathway to block the ascending pain signal
75
Q

Which somatosensory pathway is involved with proprioception, vibration, and fine touch?

A

Posterior column-medial lemniscal pathway

76
Q

What are the signs of opioid overdose?

How is it treated?

A
  • Respiratory depression or arrest
    • Perform CPR, support ventilation
  • Sedation
  • Unresponsive
  • Miosis

Administer Naloxone

77
Q

How does the descending pathway modulate pain?

A

Activation of the descending pathway results in the release of pain inhibitors

  • Serotonin, norepinephrine
  • Endorphins
  • Enkephalins
  • Dynorphin

Opiois help activate the descending pathway by removing the inhibition that normally acts on the descending pathway

78
Q

NSAID or Opioid?

Blocks transmission of pain

A

Opioid

79
Q

What is the mechanism of action of NSAIDs?

A

COX inhibition

  • Without COX, arachidonic acid is not converted to prostaglandin H2
  • This prevents the synthesis of tissue-specific prostaglandins, which normally work to sensitize peripheral pain nerve endings and enhance pain transmission in the CNS
80
Q

What opioid would be best for patients with pre-existing GI problems?

A

Fentanyl transermal patch

Does note need to be absorbed by the GI tract

81
Q

How do NSAIDs affect the kidney?

A

NSAIDs inhibit prostaglandin synthesis, and therefore will interefere with afferent arteriole dilation during low-flow states

This can lead to kidney injury

  • Decreased perfusion -> ischemia
  • Especially bad when a patient has low blood volume, low blood pressure, or low cardiac output
  • Both COX1 and COX2 are active in the kidney, so a COX2 selective inhibitor will not protect the kidney from decreased perfusion
82
Q

Nalbuphine is classified as a mu opioid receptor…

A. Agonist

B. Antagonist

C. Agonist/Antagonist

D. Partial agonist

A

C. Agonist/Antagonist

  • Analgesia is kappa mediated
    • Does not have as much pain relieve as mu agonists, but fewer GI effects
  • Can trigger withdrawl
    • Do not use in opioid tolerant patients
83
Q

A patient with knee osteoarthritis asks you if acetaminophen can be as helpful for his pain as NSAIDs, which treat inflammation. You explain that it can be as effective because acetaminophen (select the best answer):

  1. Blocks the formation of prostaglandins similarly to NSAIDs
  2. Unlike NSAIDs, works by blocking the binding of prostaglandins to cells
  3. Blocks COX-2 in the central nervous system
  4. Activates opioid receptors
  5. Is a nonspecific medication pain with no known mechanism
A

e. Is a nonspecific medication pain with no known mechanism

But can be aseffective as NSAIDs in mild osteoarthritis pain

84
Q

Meperidine is classified as a mu opioid receptor…

A. Agonist

B. Antagonist

C. Agonist/Antagonist

D. Partial agonist

A

A. Agonist

85
Q

Which nerve fibers are affected by opioids?

A

Pain fibers - not touch or motor fibers

86
Q

What are the symptoms of opioid withdrawal?

A

Sympathetic overdrive + diarrhea and abdominal crampin

  • Anxiety
  • Insomnia
  • Diaphoresis
  • Yawning
  • Rhinnorhea
  • Lacrimation
  • HTN
  • Tachycardia
  • Hyperventilation
87
Q

What is vicoden?

A

Hydrocodone + acetaminophen

88
Q

Which opioid is most likely to cause histamine release?

What is the result?

A

Morphine

Itching, rash, hypotension

89
Q

Describe the metabolism of codeine

A

10% metabolized to morhine via CYP2D6

  • Codeine does not provide analgesia - the morphine metabolite does
    • Codeine does not have a high affinity for the mu opioid receptor
    • It is considered a weak opioid
  • People with CYP2D6 mutations will not get pain relief from codeine
90
Q

What effects are modulated by the kappa opioid receptor?

A
  • Mild analgesia
    • Less than Mu
  • Some respiratory depression
    • Less than Mu
  • Psychomimetic effects
    • Not euphoria
91
Q

What are the effects of prostaglandins on our perception of pain?

A

Prostaglandins…

  • Sensitize pain nerve endings
    • -> Allodynia
  • Enhance pain transmission in the CNS
    • -> Hyperlgesia
92
Q

What is the #1 cause of death related to opioid use?

A

Respiratory depression

93
Q

What is allodynia?

A

When touch causes pain

94
Q

Which drug blocks prostaglandin in the brain?

A

Acetaminophen

95
Q

What are the adverse effects of opioids on the respiratory system?

A

Respiratory depression

  • Activation of the mu opioid receptor inhibits the ventrilatory response to hypercapnia
    • The patient will breathe if prompted, but the natural ventilatory response is not there
    • Risk of death because patient may forget to breathe
96
Q

When pain transmission reaches the brain, which part of the brain does it go to?

A

Thalmus

Note - the thalmus contains opioid receptors

97
Q

What is a narcotic?

A
  • Any substance that induces sleep
  • Any substance which acts on opioid receptors
  • Any illicit substance

Not descriptive! Has a connotation of misuse, abuse, and addiction

98
Q

NSAID or Opioid?

Prevents amplification of pain signal

A

NSAIDs

Note - NSAIDs do not block transmission; signals can still get through, but they are not amplified; no hyperalgesia

99
Q

What are the hematologic effects of non-ASA NSAIDs?

A

non-ASA NSAIDs reversibly bind COX

  • COX is necessry for the synthesis of TXA2, which is necessary for platelet aggregation and vasoconstriction
  • NSAIDs will therefore interfere with coagulation
  • Coagulation will return to normal after a few half lives

Note: ASA irreversibly acetylates COX; that platelet will never work again. Effect lasts 7-10 days after mediation is stopped

100
Q

What are the most common uses for fentanyl?

A
  • IV
    • During operations and ICU anesthesia
    • Usually only in patients that are closely monitored
  • Transdermal
    • Sustained release for chronic pain
    • Given as a patch or lollipop
101
Q

What is hyperalgesia?

A

Amplification of pain

102
Q

A patient you prescribed a combination drug of diclofenac/misoprostol calls you noting excellent pain relief but also the onset of marked diarrhea shortly after taking their first dose of the medication. Your next best step would be to

  1. Reassure the patient that is is a side effect of the diclofenac
  2. Reassure the patient that this is a side effect of the misoprostol
  3. Advise the patient that he needs to go to the ED to evaluate for an ulcer
  4. Advise the patient that this is an allergic response and to stop the medication
  5. Advise the patient that this can be managed by taking the medication with food
A

b. Reassure the patient that this is a side effect of the misoprostol

103
Q

What is the precursor for prostaglandin in human tissue?

A

Arachidonic acid

104
Q

What causes “double pain?”

A

Sharp, initial pain due to A-delta (fast) fibers

Subsequent thobbing pain due to C (slow) fibers

105
Q

What is an opiate?

A

A drug derived from opium

Does not include synthetic drugs that act by the same mechanism

  • All opiates are opioids, but not all opioids are opiates
106
Q

What are the indications or buprenorphine?

A

Opioid maintenance for drug addiction (an alternative to methodone)

  • Has some indications for chronic pain, but most often use other agents for this
107
Q

People taking opioids for a long time can become tolerant to…

But they will not become tolerant to…

A
  • Tolerant to
    • Euphoria
    • Sedation
    • Analgesia
    • Respiratory depression
  • Will not become tolerant to
    • Miosis
    • Constipation
108
Q

Which opioid receptor is most strongly involved in analgesia?

A

Mu

109
Q

A mother brings in her 4-year-old child who is suffering from flu type symptoms (malaise, vomiting, diarrhea) and who has a temperature of 103o F. The resident in the Emergency Department writes for aspirin to control the fever, but the attending changes the order to acetaminophen. The best reason for this change is

  1. Risk of salicylate poisoning in a dehydrated patient
  2. Risk of NSAID induced renal injury in a dehydrated patient
  3. Risk of hepatic injury and encephalopathy from the aspirin
  4. Risk of gastric bleeding
  5. Risk of hematuria
A

c. Risk of hepatic injury and encephalopathy from the aspirin

Aspirin is contraindicated in a child with viral syndrome; risk of Reye’s syndrome

110
Q

What effects are modulated by the mu opioid receptor?

A
  • Analgesia
  • Euphoria
  • Respiratory depression
  • Miosis
  • GI effects
  • Dependence
111
Q

Which areas of the brain contain opioid receptors?

What are the functions of these areas?

A

TAP - BASS

  • Thalmus - pain
  • Amygdala - emotions
  • Periaqueductal grey - descending pain pathway
  • Brainstem ventilation nuclei - respiratory drive
  • Area postrema - vomiting
  • Spinal trigeminal nucleus - deep/crude touch, pain, and temperature
  • Substantia gelatinosa - synapse between sensory neuron and secondary neuron

Note: GI tract also contains opioid receptors

112
Q

Which area of the brain modulates the descending pain pathway?

A

Periaqueductal grey

113
Q

What is the role of COX1 in platelet activation?

A

COX1 aids the formation of TXA2, which is necessary for platelet aggregation and vasoconstriction

Note - non-selective NSAIDs inhibit COX1, and therefore will inhibit coagulation

114
Q

What is a nociceptor?

A

The receptive portion of a peripheral neuron that senses pain

115
Q

List the relevant mu opioid receptor agonist/antagonist

A

Nalbuphine

116
Q

What are the advantages of hydromorphone over morphine?

A
  • Hydromorphone has a better side effect profile
    • Less likely to cause seizure
      • H3G isn’t as dangerous as M3G
    • Less pruitis, sedation, nausea, and vomiting
  • More potent

MSK-Derm by Minnie AH Version (47 decks)

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