Pain Flashcards
Describe the 3 main types of pain
Types: Nociceptive, neuropathic & centralized pain
Which medications/interventions are most effective to manage 3 main pain types
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
How is acetaminophen different from NSAIDs in terms of its mechanism of action?
-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
How is acetaminophen different from NSAIDs in terms of its mechanism of action and adverse effects?
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
What is the maximum daily dose of acetaminophen for an adult patient?
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)
Describe the difference between COX-1 and COX-2 selectivity.
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
Arrange the following NSAIDs from most COX-2 selective to least COX-2 selective: Meloxicam, ibuprofen, naproxen, celecoxib
MOST celecoxib, meloxicam, ibuprofen, naproxen LEAST (PPT)
What is the reason valdecoxib was removed from the market?
Increased risk for CV events (822)
Which NSAID cannot be used for more than 5 days? What is the reason for this?
ketorolac-increased risk of cardiac thrombotic events, renal failure, peptic ulcers, and increased risk of bleeding beyond this point
List the NSAID that is available as a topical formulation.
Diclofenac
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?
-Yes pt is at risk (PPT) -PPIs for GI prophylaxis: omeprazole 20 mg/d, lansoprazole 30 mg/d or esomeprazole 20 mg BID
DOA & mineralocorticoid activity: Methylprednisolone
DOA intermediate, mineralocorticoid activity 0
DOA & mineralocorticoid activity: Hydrocortisone
DOA short, mineralocorticoid activity ++
DOA & mineralocorticoid activity: Dexamethasone
DOA long, mineralocorticoid activity 0
DOA & mineralocorticoid activity: Prednisone
DOA intermediate, mineralocorticoid activity +
Naturally occurring full mu-agonist
morphine
describe what “hypothalamic-pitutitary-adrenal axis suppression” means
adrenal fatigue. a condition that occurs when the body’s stress response is impaired due to reduced cortisol production
Weak mu-agonist also known to increase serotonin and norepinephrine
Tramadol
Synthetic opioid that should only be initiated in patients on at least 60 mg of morphine or equivalent per day
Fentanyl patch
Partial mu-agonist also used in the treatment of opioid use disorder
Buprenorphine
Describe the clinical effects of opioids at mu receptors.
Mu (classic morphine receptor) Mu 1 - supraspinal analgesia -Mu 2 - spinal analgesia, resp depression, dependence, tolerance, constipation, euphoria
Describe the clinical effects of opioids at kappa receptors.
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)
Describe the clinical effects of opioids at delta receptors
Delta (spinal analgesia) -No CV events -Almost insensitive to classic opiates
List the metabolites you would expect to find in a urine drug test for a patient taking hydrocodone/acetaminophen.
-Hydrocodone - norhydrocodone (inactive), hydromorphone (active) (PPT) -Acetaminophen - N/A
In 10 words or less, how would you describe the role of naloxone to a patient?
Reverses the effects of opioid OD (opioid antagonists) (PPT)
What medications are approved to treat opioid use disorder? What is the mechanism of action of these medications?
-Methadone- full mu agonist
-Bupenorphine- partial opioid agonist
-Naltrexone- opiate antagonist
What are two reasons naloxone can’t be given orally?
Victims of OD are usually unconscious, First Pass Effect
What are 3 adverse effects associated with triptans?
-Common: paresthesias, dizziness, warm sensations, somnolence, chest pressure/tightness
-Rare: cardiac events (e.g., MI, angina) (PPT)
Describe the neurotransmitters involved in neuropathic pain.
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)
What is the “clinically effective” dose of gabapentin?
300 mg to 3600 mg/d (target about 1800 mg/d) (PPT)
Lidocaine patches are only FDA approved for which indication?
Chronic pain d/t postherpetic neuralgia (PPT)
What class of medications are first line for fibromyalgia? When should they be dosed? -
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)
___________ is a serotonin-norepinephrine reuptake inhibitor that is ONLY indicated for fibromyalgia.
Milnacipran (Savella) (PPT)
Longest-acting triptan
Frovatriptan
Describe the mechanism of action of “triptans”.
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
May be effective for patients who have not responded to other triptans
Eletriptan
Available in a nasal spray
Sumatriptan
Associated with fewer side effects compared to other triptans
Almotriptan
Describe the mechanism of action of CGRP antagonists.
CGRP antagonists “-gepant” -CGRP = calcintonin gene-related peptide; Vasoactive peptide released from sensory nerves believed to be assoc w/onset of migraine (PPT)
Agents for acute migraine
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)
Agents for migraine prophylaxis
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)
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.
-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)
If the patient fails your initial treatment for OA, what other options would be available?
-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)
