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msk-derm > Opiods/Pain > Flashcards

Opiods/Pain Flashcards

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1
Q

What receptor do opioids primarily act on?

A

Mu opioid receptor

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2
Q

What are the three known opioid receptors?

A

Mu, kappa, delta

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3
Q

How do opioids work generally?

A

They bind opioid receptors and inhibit ionic currents of nerve fibers in the CNS responsible for transmitting nociception and also indirectly activate the descending inhibitory system in the periaqueductal grey by inhibiting inhibitors of the periaqueductal grey.

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4
Q

How do opioid antagonists work?

A

They reversibly bind to opioid receptors without agonist activity, which prevents actions of exogenous and endogenous opioids (no clinical effect without opioid agonists)

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5
Q

How do agonist-antagonist opioids work?

A

Agonist actions on kappa receptors, antagonist actions on mu receptors

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6
Q

How do partial opioid agonists work?

A

They act as agonists on mu opioid receptors but cannot fully activate the receptor

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7
Q

What are the dose-dependent effects of opioids?

A

Analgesia, sedation/euphoria, respiratory depression, nausea, constipation, pruritis, and miosis.

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8
Q

Which opioid has the most histamine release?

A

Morphine

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9
Q

Which opioid has many notable active metabolites that can become problematic in renal failure?

A

Morphine

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10
Q

Which opioid is largely banned due to a toxic metabolite that can accumulate in renal failure and cause seizures?

A

Meperidine

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11
Q

Which opioid is a prodrug that does not convert to an active drug in some patients with genetic variants?

A

Codeine

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12
Q

Which opioid is commonly used for acute pain but does not often lead to histamine release or have many active metabolites?

A

Dilaudid

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13
Q

What is the active substance in drugs like oxycodone?

A

Oxycontin

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14
Q

Which opioid has a long half-life, lack of active metabolites, but can cause long QT syndrome at high doses?

A

Methadone

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15
Q

Which potentially fatal side effect is associated with methadone?

A

Methadone

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16
Q

What are commonly used agonist/antagonist drugs?

A

Butorphanol, nalbuphine

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17
Q

What is buprenorphine?

A

The only clinically available partial agonist available in the united states

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18
Q

What is naloxone?

A

A opioid antagonist

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19
Q

What does the term opiate refer to?

A

Drugs derived directly from opium

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20
Q

What does opioids refer to?

A

All opiate receptor agonists

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21
Q

What two drugs are considered weak opioids?

A

Codeine and propoxyphene

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22
Q

What are the two alkaloid types of opium?

A

Phenanthrene series and benzylisoquinoline series

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23
Q

How do opioid receptors work?

A

They work via G proteins to inhibit cellular adenylyl cyclase activity, activate potassium currents, and suppress calcium currents mostly in the pain transmitting fibers of the CNS

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24
Q

Why is their interpersonal variation in opioid response?

A

Splice variants in the three opioid receptors

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25
Q

What causes respiratory depression from opioids?

A

Activation of mu2 receptors in the brainstem, which leads to decreased ventillatory rate and reduced tidal volume

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26
Q

What is miosis?

A

Excessive constriction of pupils of eye

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27
Q

What causes miosis in opioid use?

A

Direct mu and kappa activation of the parasympathetic outflow to the eye. Classic finding of opioid usage.

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28
Q

What causes the GI effects of opioids?

A

Decreased gastrointestinal transit via action on mu2 receptors within the CNS and peripheral nerve plexus

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29
Q

Can opioids be used in pregnancy?

A

They cross the placental barrier, but have low risk of teratogenicity so they are safe to use for acute administrations.

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30
Q

What are symptomsof opioid withdrawal?

A

Sympathetic nervous system hyperactivity (sweating, cramping, diarrhea, elevated HR and BP, hyperventilation, pupil dilation)

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31
Q

What are possible drug interactions with opioids?

A

Anything that causes sedation on its own can cause severe and dangerous levels of sedation with opioids

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32
Q

What causes overdoses in opioid use?

A

Excessive ventilatory depression

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33
Q

What morphine metabolite causes excessive sedation in patients with renal failure?

A

Morphine-6-glucuronide

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34
Q

What is the bioavailability of morphine?

A

Low because it is poorly absorbed in oral formulations (higher in IM or subcutaneous injections)

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35
Q

How is fentanyl used?

A

Transdermal patch, IV (forsurgery)

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36
Q

What is tramadol?

A

A partial opioid agonist, partial SSRI that is used for pain relief, particularly for back pain

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37
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

a) naloxone to treat the meperidine induced seizure
b) benzodiazepines to treat meperidine metabolite induced seizure
c) naloxone tocontrol effects of delayed meperidine clearance
d) nalbuphine to antagonize the effect of the opioid while providing some analgesia
e) 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. It has nothing to do with opioid receptors and seizures from it should be treated like any seizure.

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38
Q

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

a) sustained release morphine pills
b) sustained release oxycodone pills
c) hydromorphone pills
d) methadone
e) fentanyl lollipop

A

d) methadone

Sustained release pills lose their long duration when you crush them, and the fentanyl lollipop is for acute pain. Only methadone is inherently long acting by virtue of its long half life.

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39
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 a different opioid?

A

Different people have different splice variants in opioid subreceptors that have a variety of affinities for different drugs

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40
Q

Which opioid has the longest half life?

A

Methadone

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41
Q

What does cyclooxygenase do?

A

It is an enzyme that forms prostaglandins

42
Q

What is the pathway of arachidonic acid formation?

A

Phospholipids are released by cells and acted on by phospholipase A2 to form arachidonic acid

43
Q

What are two possible products derived from arachidonic acid?

A

Leukotrienes and prostaglandin H2

44
Q

What enzyme converts arachidonic acid to prostaglandin H2?

A

Cyclooxygenase

45
Q

What is the proposed mechanism of prostaglandin-mediated pain?

A

PGEs bind to nociceptive nerve endings, which lowers their firing threshold so that even light touch can cause pain. They also form changes in pain transmission in the CNS

46
Q

What is the general type of pain-reduction caused by NSAIDs?

A

Anti-hyperalgesia (not analgesia) because they reduce the body’s ability to amplify pain signals without actually reducing pain (in the way that opioids do)

47
Q

What is unique about a selective COX2 inhibitor?

A

It relieves pain like all other NSAIDs, but it does not affect coagulation because coagulation is only mediated by COX1

48
Q

What is the normal role of prostaglandins in the stomach?

A

Form mucus, improve blood flow, prevent autodigestion

49
Q

What is the normal role of prostaglandins in the kidney?

A

Maintain blood flow in low-flow states, involved in sodium/water balance

50
Q

What is the normal role of prostaglandins in the uterus?

A

Contraction of uterine muscles

51
Q

What is the normal role of prostaglandins in platelets?

A

Thromboxane (a prostaglandin) enables platelets to clump and form clots

52
Q

What is the normal role of prostaglandins in the endothelium?

A

Prostacyclin causes vasodilation and inhibits platelet adherence

53
Q

What is the normal role of prostaglandins in the CNS and periphery?

A

Enhanced pain transmission

54
Q

What is unique about ASA?

A

It irreversibly binds COX, which is cardioprotective because platelets can’t produce more thromboxane and are rendered permenantly non-functional (until new platelets are formed)

55
Q

What is the toxic effect of NSAIDs on GI?

A

Ulcer formation

56
Q

What is the toxic effect of NSAIDs on the kidneys?

A

Reduced blood flow in low flow states

57
Q

What is the toxic effect of NSAIDs on the blood?

A

Reduced coagulation

58
Q

What is the toxic effect of NSAIDs on bone?

A

Reduced bone healing

59
Q

What toxicity can be triggered by NSAIDs in asthma patients?

A

Arachadonic acid will disproportionally form leukotrienes, which can trigger severe asthma symptoms

60
Q

What does acetaminophen do?

A

Nobody is really sure how it works, but it is NOT an NSAID

61
Q

What are important side effects to consider for acetaminophen?

A

Liver toxicity from buildup of a metabolite (NAPQI) if the daily dose is exceeded or if there are combinations of medications taken

62
Q

Nonsteroidal antiinflammatory drugs exert their analgesic effect by:

a) binding to prostaglandin receptors in peripheral inflamed tissue
b) inhibiting the action of prostaglandins on peripheral nerves
c) inhibiting the formation of prostaglandins
d) inhibiting the formation of arachidonic acid
e) inhibiting lipooxygenase

A

c) inhibiting the formation of prostaglandins

63
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:

a) ketorolac can cause microemboli in the new kidney
b) ketorolac can reduce blood flow to the new kidney
c) ketorolac can reduce sodium reabsorption in the new kidney
d) ketorolac can prolong postoperative ileus (cessation of peristalsis that occurs postop)
e) ketorolac can cause respiratory depression

A

b) ketorolac can reduce blood flow to the new kidney

64
Q

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

a) risk of salicylate poisoning in a dehydrated patient
b) risk of NSAID induced renal injury in a dehydrated patient
c) risk of hepatic injury and encephalopathy from the aspirin
d) risk of gastric bleeding
e) risk of hematuria

A

c) risk of hepatic injury and encephalopathy from the aspirin

This describes Reye’s syndrome, which is a risk in children with a viral syndrome who are given aspirin

65
Q

What is Reye’s syndrome?

A

A syndrome that can present with liver damage and encephalopathy in children after a viral infection, particularly if the infection symptoms are treated with aspirin. The mechanism is unknown.

66
Q

A 25 y.o. patient with no significant PMH presents to your office for a routine checkup. During your history, you learn that as an athlete, he uses 200 mg of OTC ibuprofen three times per day for various muscle aches and has done so for the past year. Further evaluation at this visit should include which of the following:

a) drug screening for opioids
b) drug screening for other NSAIDs
c) thyroid stimulating hormone levels
d) examinationfor hearing loss
e) stool guiac for blood

A

e) stool guiac for blood

NSAIDs do not affect thyroid function, only aspirin affects ears (tinnitus), but all NSAIDs pose a risk for GI bleeds

67
Q

A patient with knee osteoarthritis asks if acetaminophen can be as helpful for his pain as NSAIDs, which treat inflammations. You explain that it can be as effective because acetaminophen:

a) blocks formation of prostaglandins like NSAIDs
b) unlike NSAIDs, works by blocking binding of prostaglandins to cells

c) blocks COX-2 in the CNS
d) activates opioid receptors

e) is a nonspecific medication for pain with no known mechanism

A

e) is a nonspecific medication for pain with no known mechanism

we don’t know how they work, they just do

68
Q

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

a) reassure the patient that this is a side effect of the diclofenac
b) reassure the patient that this is a side effect of the misoprostal
c) advise the patient that he needs to go to the ED to evaluate for an ulcer
d) advise the patient that this is an allergic response and to stop the medication
e) 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 misoprostal

diclofenac does not cause diarrhea, but misoprostol promotes mucus formation in the GI tract (which can cause diarrhea)

69
Q

What is indomethacin used for?

A

Gout by rheumatologists

70
Q

What is the only nonacidic NSAID?

A

Nabumetone

71
Q

What is the only COX-2 selective inhibitor in the US?

A

Celecoxib

72
Q

What does misoprostol do?

A

It provides GI protection from NSAIDs by stimulating GI mucus protection

73
Q

What is allodynia?

A

Increased sensitization to pain (ex. a touch causes pain)

74
Q

What is hyperalgesia?

A

Pain is amplified (ex. a slap hurts more than it would ordinarily if you are sunburned)

75
Q

Do prostaglandins cause hyperalgesia or allodynia? How?

A

They cause both. Hyperalgesia is through enhanced pain in the CNS and allodynia is through sensitized nerve endings.

76
Q

What can be done to prevent GI toxicity of NSAIDs?

A
  • enteric coating on pills
  • PPI prophylaxis to prevent NSAID UGI ulcer
  • Misoprostol combination drug that increases mucus formation (and also diarrhea)
77
Q

What is the temporal definition of chronic pain?

A

Pain lasting longer than three months

78
Q

What is plasticity in the context of pain?

A

Changes in pain processing that lead to prolonged and exaggerated painful signs and symptoms

79
Q

What kinds of fibers generally transmit nociceptive pain messages?

A

myelinated A delta fibers and unmyelinated C fibers

80
Q

What fibers are active with low intensity mechanical stimuli?

A

A beta fibers

81
Q

What neurotransmitter is released during low intensity noxious stimulation?

A

Glutamate

82
Q

What is transduction in pain processing?

A

The process of converting pain or noxious stimuli into electrical activity by chemicals released from nociceptors

83
Q

What is conduction in pain processing?

A

The electrical signals (action potentials) are the result of transduction and are conducted via primary afferent nociceptive neurons to the dorsal horn of the spinal cord

84
Q

What are the two ascending pathways for pain to the brain?

A

Spinothalamic tract and spinoparabrachial tract that bothgo to the thalamus

85
Q

What is the path of the spinothalamic tract?

A

It relays signals through the thalamus to the somatosensory cortex

86
Q

What is modulation in pain processing?

A

Inhibitory spinal interneurons and projects from the brainstem to the dorsal horn of the spinal cord modulate pain signaling by limiting transfer of incoming sensory input to the brain

87
Q

How does perception of pain occur via the brain?

A

The spinothalamic tract relays pain information through the thalamus to the somatosensory cortex and associated areas, allowing for localization of pain, avoidance behavior, and cognitive processing of pain.

88
Q

What is the affective response in pain processing?

A

The spinoparabrachial tract relays the pain stimulus to the parabrachial nucleus of the brainstem, continuing on to the ventral medial nucleus of the hippocampus and the central nucleus of the amygdala, brain regions involved in the affective response to pain.

89
Q

How does chronic pain result from maladaptive processes in pain sensing?

A

The neural pathway of pain is sensitized by pain triggers that lead to higher levels of pain from minimally painful or benign stimuli as a protective mechanism to prevent injury (even though there is no risk of injury)

90
Q

What is wind up?

A

Repetitive C fiber stimulation that results in a nonlinear increase in output from the dorsal horn

91
Q

What is peripheral sensitization?

A

Reduction in the firing threshold for A delta and C fiber nociceptors in the skin that can cause allodynia or hyperalgesia

92
Q

What is central sensitization?

A

Rewiring of the synaptic connections centrally (structural plasticity) that can lead to allodynia, hyperalgesia, or increased dorsal horn excitability which increases the response from A beta and A delta fibers

93
Q

In normal pain processing, pain or noxious stimuli are transduced into electrical activity by various types of nociceptors. The electrical signals are the result of transduction and are conducted via primary afferent nociceptive neurons to the dorsal horn of the spinal cord. Signals are then transmitted to the brain via ascending pathways. The sensation of pain and the response to pain are affected not only by pain transmission, but also by the brain’s response to that transmission can be described as:

a) perception
b) sensation
c) modulation
d) transduction

A

c) modulation

modulation is the upregulation or downregulation of pain signals in sucha way that alters the way they are perceived by the brain

94
Q

A 79 y.o. woman with a 10 year history of severe diabetic peripheral neuropathy develops severe burning pain in her distal lower extremities. On examination, light stroking of her skin, in the dorsal and plantar part of the feet, causes significant pain and guarding. This physical exam finding could be described as:

a) paresthesia
b) allodynia
c) hyperalgesia
d) hyperesthesia

A

b) allodynia

painful response to non-noxious stimuli

95
Q

Which of the following areas of the brain is felt to be primarily a relay station for pain messages and not an end receptor area for perception of pain and emotional suffering?

a) prefrontal cortex
b) thalamus
c) anterior cingulate cortex
d) amygdala

A

b) thalamus

thalamus is the major relay station for pain signaling in the brain

96
Q

A patient with 10 years of low back pain that now encompasses all areas of the body and presents depression, anxiety, and fear avoidance is least likely to respond to which of the following treatments:

a) exercise with PT and OT
c) CBT and clinical psychology
c) biofeedback and other relaxation/mind body techniques
d) lumbar fusion from L1-S1 by spinal surgery service

A

d) lumbar fusion from L1-S1 by spinal surgery service

10 years of pain that has spread throughout the body and has associated mood disturbances is considered chronic and should be treated in a pain management program

97
Q

Which of the following statements is false?

a) regionalization of pain is characteristic of chronic pain
b) in chronic pain anxiety can cause deconditioning
c) depressed patients perceive less pain
d) acute pain signals tissue injury and is protective

A

c) depressed patients perceive less pain

98
Q

What are the goals of interdisciplinary pain programs?

A
  • increase physical activity
  • decrease pain intensity
  • improve pain medication regiment
  • improve psychosocial functioning
  • return to leisure pursuits and work
  • reduce utilization of health care services
99
Q

All of the following are goals of the treatment of chronic pain, EXCEPT:

a) maximization of function
b) improve psychosocial functioning
c) resolution of pain
d) improve coping

A

c) resolution of pain

100
Q
A

msk-derm (41 decks)

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