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NMSP Exam 1 > Drugs for Pain > Flashcards

Drugs for Pain Flashcards

1
Q

What are some nonpharmacologic therapy for pain?

A
  • Exercise
  • Physical therapy
  • Heat, ice, massage
  • Sleep hygiene techniques
  • Behavioral/psychological therapies
  • Healthy lifestyle
  • Acupuncture
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2
Q

What are some common non-inflammatory indications for NSAIDs?

A
  • Osteoarthritis and other arthritides
  • Bursitis
  • Gout ‘flare’
  • Ankylosing spondylitis
  • Dysmenorrhea
  • Headache
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3
Q

Where is COX-1 expressed and what is its role?

A
  • Expressed in “all” tissues
  • Prominent role in responding to physiological stimuli
  • Also contributes to response to any pathological stimuli that release AA from cells
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4
Q

How does COX-1 and COX-2 contribute to inflammation?

A
  • Inflammation stimulates AA release –> COX-1 and COX-2 convert AA into PGE2 which causes symptoms
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5
Q

What is the MOA of aspirin?

A
  • Irreversibly inhibits COX-1 and COX-2 enzymes
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6
Q

What are the clinical applications of immediate release aspirin?

A
  • Analgesic, antipyretic, and anti-inflammatory
  • Revascularization procedures
  • Ischemic stroke, TIA
  • STEMI or NSTEMI
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7
Q

What are the clinical applications of extended release aspirin?

A
  • Ischemic stroke or TIA

- Stable ischemic heart disease

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8
Q

What are the toxicities seen in aspirin use?

A
  • Ulcer
  • Increased risk of bleeding
  • Multiple drug interactions
  • Reye syndrome in children <18
  • Increased NSAIDs causes increased serum creatinine due to loss of PG effects in kidneys
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9
Q

What is the progression of aspirin toxicity?

A
  1. Salicylates uncouple mitochondrial oxidative phosphorylation in the CNS
  2. Respiratory center registers decreased ATP as hypoxemia and responds with hyperventilation
  3. Hyperventilation blows off CO2, drop in PCO2 causes respiratory alkalosis –> eventually prompting kidney to deplete bicarbonate
  4. Organic acids accumulate because ATP is no longer generated through the Krebs cycle
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10
Q

What are some differences between aspirin and nonaspirin NSAIDs?

A
  • They are reversible unlike aspirin
  • Suppress platelet aggregations, but use actually increases risk of MI and stroke
  • Therefore use the lowest effective dosage for shortest time possible
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11
Q

What is the MOA of IBU? What about naproxen?

A
  • Reversibly inhibits COX-1 and COX-2

- Naproxen has similar MOA but half life is 12-17 hours

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12
Q

What are some toxicities of IBU?

A
  • NSAIDs around 20 weeks gestation or later may cause fetal renal dysfunction leading to oligohydramnios, > 30 weeks closure of ductus arteriosus
  • Increased risk of MI and stroke –> contraindicated in CABG
  • Increased risk of GI bleeding
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13
Q

What is the MOA of celecoxib?

A
  • Inhibits PG synthesis via COX-2 but not COX-1 at therapeutic concentrations
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14
Q

What are the clinical applications of celecoxib?

A
  • Acute pain
  • Ankylosing spondylitis
  • Juvenile idiopathic arthritis
  • Osteoarthritis
  • Primary dysmenorrhea
  • RA
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15
Q

What are some toxicities of celecoxib?

A
  • NSAIDs around 20 weeks gestation or later may cause fetal renal dysfunction leading to oligohydramnios, > 30 weeks closure of ductus arteriosus
  • Serious risk of thrombotic events, including MI and stroke
  • Serious GI risk but less due to being only COX-2 selective
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16
Q

What are some commonly used NSAIDs?

A
  • Aspirin
  • Celecoxib
  • Diclofenac
  • IBU
  • Indomethacin
  • Ketorolac
  • Naproxen
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17
Q

When should COX-2 selective agents by avoided?

A
  • Patients with CV risk factors
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18
Q

What NSAID should be used in those with CV complications?

A
  • Naproxen
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19
Q

What are some contraindications for NSAID use?

A
  • Chronic kidney disease
  • Active duodenal or gastric ulcer
  • Cardiovascular disease
  • NSAID allergy
  • Ongoing treatment with anticoagulants –> warfarin
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20
Q

What is the MOA of acetaminophen?

A
  • Not fully elucidated
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21
Q

What are the clinical applications of acetaminophen?

A
  • Temporary reduction of fever

- Pain, oral –> temporary relief of minor aches, pains, and headache

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22
Q

What are some toxicities of acetaminophen?

A
  • Risk of medications errors –> confusing mL and mg

- Overdose –> hepatotoxicity with acute liver failure and death possible

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23
Q

Why does acetaminophen not suppress inflammation?

A
  • Inhibits PG synthesis in the CNS but not periphery
24
Q

What are some drug interactions of acetaminophen?

A
  • Inhibits metabolism of warfarin and therefore can increase risk of bleeding associated with its use
25
Q

What are the first line agents for neuropathic pain?

A
  • Calcium channel alpha 2 delta ligands –> gabapentin
  • SNRIs –> duloxetine
  • TCAs –> amytriptyline
26
Q

What is the MOA of amitriptyline?

A
  • Inhibition of NE and 5HT reuptake by the presynaptic neuronal membrane pump
27
Q

What are some toxicities of amytriptyline?

A
  • Increased risk of suicidal thinking and behavior in children, adolescents, and young adults
  • Anticholinergic effects
28
Q

What is the MOA of duloxetine?

A
  • Potent inhibitor of neuronal 5HT and NE reuptake
29
Q

What are some clinical applications of duloxetine?

A
  • Fibromyalgia
  • GAD
  • Major depressive disorder
  • MSK pain, chronic
  • Neuropathic pain associated with DM
30
Q

What are some toxicities of duloxetine?

A
  • Increased risk of suicidal thoughts and behaviors
  • Activation of mania or hypomania
  • Bleeding risk
  • Hepatotoxicity
  • Hyponatremia
  • Acute angle closure glaucoma
31
Q

What is the MOA of pregablin?

A
  • Binds to CNS alpha-2-delta subunit of VGKC –> modulates calcium influx at the nerve terminals
32
Q

What are some toxicities of pregabalin?

A
  • Depression, suicidal ideation
33
Q

What are the four indications of pregabalin?

A
  • Neuropathic pain associated with DM
  • Postherpetic neuralgia
  • Adjunctive therapy for partial seizures
  • Fibromyalgia
34
Q

What is the MOA of tramadol?

A
  • Partial agonist at mu-opiate receptors

- Also inhibits the reuptake of NE and 5HT

35
Q

What are some toxicities of tramdol?

A
  • Risk of medication errors/ingestion by children –> overdose and death
  • Addiction, abuse, and misuse
  • Interactions with drugs affecting cyp 450
  • Withdrawal syndrome
  • Increased risk of respiratory depression from concomitant use with benzos or other CNS depressants
36
Q

What are some side effects of tramadol?

A
  • Sedation
  • Dizziness
  • Headache
  • Dry mouth
  • Constipation
37
Q

What is tapentadol?

A
  • Moderate to strong opioid agonist similar to oxycodone at mu receptors
  • Also blocks reuptake of NE
  • Causes less constipation
38
Q

What is the MOA of ketamine?

A
  • Noncompetitive NMDA receptor antagonist
39
Q

What are the toxicities of ketamine?

A
  • Requires careful monitoring

- Could have prolonged, undesired effects

40
Q

What are some main uses for ketamine?

A
  • Complex regional pain syndrome

- Neuropathic pain

41
Q

What is the MOA of dexmedetomidine?

A
  • Selective alpha2-adrenoceptor agonist –> clonidine has similar MOA
42
Q

What is the use of dexmedetomidine?

A
  • Potent anxiolytic, part of multimodal approach to postoperative pain management
  • Short term sedation in critically ill patients who were intubated and are undergoing mechanical ventilation
  • Sedation prior to/during surgical procedures
43
Q

What are some toxicities of dexmedetomidine?

A
  • Bradycardia, hypotension, and sinus arrest

- Transient hypertension

44
Q

What is the MOA of ziconotide?

A
  • Selectively binds to N-type voltage sensitive calcium channels located on the nociceptive afferent nerves of the dorsal horn
45
Q

What is the clinical application of ziconotide?

A
  • Management of severe chronic pain in patients requiring intrathecal therapy
46
Q

What are some toxicities of ziconotide?

A
  • Severe psychiatric symptoms and neurological impairment may occur
  • This medication among those listed for heightened risk of causing significant patient harm when used in error
47
Q

What is the MOA of sumatriptan?

A
  • Selective 5HT1B and 5HT1D agonist
48
Q

What are the clinical applications of sumatriptan?

A
  • Migraine of moderate to severe intensity
49
Q

What are some toxicities of sumatriptan?

A
  • Prolonged QT interval on ECG –> torsades, V fib
  • Coronary artery vasospasm –> MI
  • Hypertension –> stroke
  • CNS depression –> dizziness, drowsiness
  • Transient/permanent blindness or partial vision loss
  • Serotonin syndrome
50
Q

What is the MOA of lasmiditan?

A
  • High affinity, highly selective 5HT1F receptor agonist
  • Decreased stimulation of the trigeminal system
  • Treat migraine pain without causing vasoconstriction
51
Q

What are some applications for lasmiditan?

A
  • Use if there are >3 consecutive attacks unresponsive to triptran
52
Q

What are some toxicities of lasmiditan?

A
  • Dizziness
  • CNS depression
  • Risk of serotonin syndrome
  • P-glycoprotein interactions can potentiate toxic effects of other drugs
53
Q

What is the MOA of ubrogepant?

A
  • Calcitonin gene-related peptide receptor antagonist
54
Q

What are some toxicities of ubrogepant?

A
  • Nausea
  • Somnolence
  • Dry mouth
  • Negligible by itself but potential for many via drug interactions
55
Q

What is the MOA of dihydroergotamine?

A
  • Ergot alkaloid
56
Q

What are some clinical applications of dihydroergotamine?

A
  • Late treatment for migraine

- Cluster headaches

57
Q

What are some toxicities of dihydroergotamine?

A
  • Ergot alkaloids are contraindicated with potent CYP3A4
  • Concomitant use associated with an increased risk of vasospasm leading to cerebral ischemia and/or ischemia of the extremities

NMSP Exam 1 (12 decks)

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