Pain Flashcards

1
Q

Describe the 3 main types of pain

A

Types: Nociceptive, neuropathic & centralized pain

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2
Q

Which medications/interventions are most effective to manage 3 main pain types

A

Meds/interventions:
-Nociceptive - NSAIDs, injx, sx, opioids?
-Neuropathic - local tx (topical, sx, injx), or CNS-acting rx
-Centralized pain - CNS-acting rx, non-pharmacologic therapy

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3
Q

How is acetaminophen different from NSAIDs in terms of its mechanism of action?

A

-MOA (PPT) -acetaminophen - not clear, may inhibit COX-3 (centrally located) -NSAIDs - nonselective reversibly inhibit COX-1 & COX-2; selective reversibly inhibit COX-2 only

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4
Q

How is acetaminophen different from NSAIDs in terms of its mechanism of action and adverse effects?

A

ADEs: -Acetaminophen - relatively well tolerated; risk for liver toxicity, esp w/chronic/high doses &/or when combined w/ETOH; considered a safer pain reliever than NSAIDs in pts w/cirrhosis -NSAIDs - GI complications (ulcers); risk is greater w/NSAIDs that are more COX-1 selective & have a longer DOA; COX-1 is responsible for increasing GI mucosal bl flow, mucus & bicarbonate production & epithelial growth

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5
Q

What is the maximum daily dose of acetaminophen for an adult patient?

A

Recommended adult dose = 325-1000 mg q 4-6 hrs (max daily dose = 4 g; may consider limiting dose to no more than 3250 mg/d) (PPT)

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6
Q

Describe the difference between COX-1 and COX-2 selectivity.

A

COX enzyme (PPT) See 822 for more: –Required in rate limiting step for conversion of arachidonic acid to prostaglandins -COX-1 is responsible for increasing GI mucosal bl flow, mucus & bicarbonate production & epithelial growth COX-2: -Contribute to inflammation & malignancy -Expressed constitutively in CNS, trachea & kidneys

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7
Q

Arrange the following NSAIDs from most COX-2 selective to least COX-2 selective: Meloxicam, ibuprofen, naproxen, celecoxib

A

MOST celecoxib, meloxicam, ibuprofen, naproxen LEAST (PPT)

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8
Q

What is the reason valdecoxib was removed from the market?

A

Increased risk for CV events (822)

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9
Q

Which NSAID cannot be used for more than 5 days? What is the reason for this?

A

ketorolac-increased risk of cardiac thrombotic events, renal failure, peptic ulcers, and increased risk of bleeding beyond this point

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9
Q

List the NSAID that is available as a topical formulation.

A

Diclofenac

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10
Q

You decide to start a 68-year-old male on naproxen for osteoarthritis. Should GI prophylaxis also be initiated? Why or why not? If yes, what regimen would you initiate?

A

-Yes pt is at risk (PPT) -PPIs for GI prophylaxis: omeprazole 20 mg/d, lansoprazole 30 mg/d or esomeprazole 20 mg BID

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11
Q

DOA & mineralocorticoid activity: Methylprednisolone

A

DOA intermediate, mineralocorticoid activity 0

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12
Q

DOA & mineralocorticoid activity: Hydrocortisone

A

DOA short, mineralocorticoid activity ++

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13
Q

DOA & mineralocorticoid activity: Dexamethasone

A

DOA long, mineralocorticoid activity 0

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14
Q

DOA & mineralocorticoid activity: Prednisone

A

DOA intermediate, mineralocorticoid activity +

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15
Q

Naturally occurring full mu-agonist

A

morphine

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15
Q

describe what “hypothalamic-pitutitary-adrenal axis suppression” means

A

adrenal fatigue. a condition that occurs when the body’s stress response is impaired due to reduced cortisol production

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16
Q

Weak mu-agonist also known to increase serotonin and norepinephrine

A

Tramadol

17
Q

Synthetic opioid that should only be initiated in patients on at least 60 mg of morphine or equivalent per day

A

Fentanyl patch

18
Q

Partial mu-agonist also used in the treatment of opioid use disorder

A

Buprenorphine

19
Q

Describe the clinical effects of opioids at mu receptors.

A

Mu (classic morphine receptor) Mu 1 - supraspinal analgesia -Mu 2 - spinal analgesia, resp depression, dependence, tolerance, constipation, euphoria

20
Q

Describe the clinical effects of opioids at kappa receptors.

A

Kappa (spinal analgesia, only weakly reversed by naloxone) -No cross-tolerance w/morphine -Does not precipitate or prevent withdrawal -**Less euphoria, addiction, resp & CV depression (PPT)

21
Q

Describe the clinical effects of opioids at delta receptors

A

Delta (spinal analgesia) -No CV events -Almost insensitive to classic opiates

22
Q

List the metabolites you would expect to find in a urine drug test for a patient taking hydrocodone/acetaminophen.

A

-Hydrocodone - norhydrocodone (inactive), hydromorphone (active) (PPT) -Acetaminophen - N/A

22
Q

In 10 words or less, how would you describe the role of naloxone to a patient?

A

Reverses the effects of opioid OD (opioid antagonists) (PPT)

23
Q

What medications are approved to treat opioid use disorder? What is the mechanism of action of these medications?

A

-Methadone- full mu agonist
-Bupenorphine- partial opioid agonist
-Naltrexone- opiate antagonist

23
Q

What are two reasons naloxone can’t be given orally?

A

Victims of OD are usually unconscious, First Pass Effect

24
Q

What are 3 adverse effects associated with triptans?

A

-Common: paresthesias, dizziness, warm sensations, somnolence, chest pressure/tightness
-Rare: cardiac events (e.g., MI, angina) (PPT)

24
Q

Describe the neurotransmitters involved in neuropathic pain.

A

Neurotransmitters such as substance P, GABA, cholecystokinin, somatostatin, Calcitonin gene-related peptide & excitatory amino acids (glutamate) bind to the neurons in the pathway of the spinal cord to transmit impulses to the brain (1242)

24
Q

What is the “clinically effective” dose of gabapentin?

A

300 mg to 3600 mg/d (target about 1800 mg/d) (PPT)

25
Q

Lidocaine patches are only FDA approved for which indication?

A

Chronic pain d/t postherpetic neuralgia (PPT)

25
Q

What class of medications are first line for fibromyalgia? When should they be dosed? -

A

NOTE: non-pharmacologic tx is considered first line (PPT) -Tricyclic compounds like amitriptyline; amitriptyline provides analgesic effect, aids in sleep, & tx concomitant mood & anx DOs; monotherapy preferred initially (vs combination)

26
Q

___________ is a serotonin-norepinephrine reuptake inhibitor that is ONLY indicated for fibromyalgia.

A

Milnacipran (Savella) (PPT)

26
Q

Longest-acting triptan

A

Frovatriptan

27
Q

Describe the mechanism of action of “triptans”.

A

MOA (PPT)
-Selective serotonin (5-HT-1B/1D) agonist (centrally acting)
-Cx vasoconstriction (vasodilation believed to be cx of migraines)
-Interrupts pain signal transmission
-NOTE: Generally considered DOC for acute migraine

28
Q

May be effective for patients who have not responded to other triptans

A

Eletriptan

28
Q

Available in a nasal spray

A

Sumatriptan

29
Q

Associated with fewer side effects compared to other triptans

A

Almotriptan

30
Q

Describe the mechanism of action of CGRP antagonists.

A

CGRP antagonists “-gepant” -CGRP = calcintonin gene-related peptide; Vasoactive peptide released from sensory nerves believed to be assoc w/onset of migraine (PPT)

31
Q

Agents for acute migraine

A

Acute migraine rx: -PO - rimegepant (Nurtec) & ubrogepant (Ubrelvy)

-NOTE: Some rx (e.g., rimegepant) in this class are approved for both acute & preventative tx of migraines (PPT)

32
Q

Agents for migraine prophylaxis

A

Migraine prophylaxis -CGRP antagonist-monoclonal antibody; Monthly or quarterly self-administered subQ injx; benefit may be seen as soon as 1 month; Ex: erenumab (Aimovig), fremanezumab (Ajovy) (PPT) -PO - atogepant (Qulipta) (WebMd) - -NOTE: Some rx (e.g., rimegepant) in this class are approved for both acute & preventative tx of migraines (PPT)

33
Q

Patient Case: You are seeing a 67 year-old male with a medical history significant for hypertension. He has been complaining of right hip pain that occurs at rest and decreases with motion. His current medications include benazepril and vitamin D 1000 units daily. An x-ray done in the office today is consistent with osteoarthritis. What medication would you use to manage this patient’s pain? Explain your rationale for selecting the medication.

A

-OA is nociceptive pain, tx includes NSAIDs, injx, sx & possibly opioids (PPT) -OA rx therapy includes acetaminophen, NSAIDs & COX-2-Is; initially acetaminophen in doses of 650 mg QID or 1 g TID (max 3 g/24 hr) are given to manage jt pain (827)

33
Q

If the patient fails your initial treatment for OA, what other options would be available?

A

-If this rx (acetaminophen) fails to control pain, NSAIDs are prescribed (827) -Pts who don’t have a good response to full-dose acetaminophen should try systemic NSAIDs or intra-articular corticosteroid injx; all NSAIDs except ketorolac & mefenamic acid have an indication for OA tx (831)