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NMSP > Drugs for Pain > Flashcards

Drugs for Pain Flashcards

1
Q

What is an analgesic?

A

Drug that relieves pain without causing loss of consciousness

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2
Q

What causes signs and symptoms of inflammation?

A

excess of prostaglandins in inflamed tissue

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3
Q

-OA and other arthritis
-bursitis
-gout flare
-ankylosing spondylitis
-dysmenorrhea
-headache
are indications for what?

A

NSAIDS

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4
Q

Which COX is expressed in all tissues all the time and have a prominent role in responding to physiological stimuli and pathologic reponse that releases AA from cells

A

COX-1

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5
Q

What COX is induced in some tissues and has a physiologic role in the kidney and a prominent role in path?

A

COX 2

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6
Q

What drug irreversibly inhibits COX 2 and COX1 via acetylation?

A

Aspirin

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7
Q

What are toxicities of aspirin?

A
  • ulcer
  • increased risk for bleeding
  • multiple drug interactions
  • Reye syndrome
  • Increased serum creatine because kidneys lose PG eff
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8
Q

What level of aspirin is toxic?

A

> 400-500 mcg/mL

-respiratory alkalosis

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9
Q

What drug reversible inhibits COX1 and COX2 to decrease prostaglandin synthesis?

A

Ibuprofen

  • has antipyretic, analgesic, and anti-inflammatory properties
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10
Q

What are the effects of ibuprofen?

A
  • antipyretic
  • analgesic
  • anti inflammatory
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11
Q

What are ibuprofen toxicities?

A

NSAID use around 20 weeks or later can cause fetal renal dysfunction leading to oligohydramnios

  • at greater than 30 weeks it can cause closure of the ductus arteriosus
  • increase risk of MI and stroke–contraindicatd in CABG
  • can increase GI bleeding
  • may compromise existing renal function
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12
Q

Ibuprofen is contraindicated in what patients?

A

CABG because of increased risk of MI and stroke

pregnant

renal issues

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13
Q

What NSAID inhibits COX2 but not COX1 at therapeutic concentrations?

A

Celecoxib

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14
Q

What are BBW of celecoxib?

A
  1. Pregnancy–> fetal renal dysfunction leading to oligohydramnios and closure of ductus arteriosis at 30 wks
  2. severe risk of thrombotic event (MI and stroke) contraindicate celecoxib in CABG
  3. serious GI risk (bleeding, ulcer, perforation)- less concerning with COX-2 selective
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15
Q

How can risk of aspirin induced ulcers be minimized?

A

test for/eliminate H. pylori and give PPI

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16
Q

Ibuprofen, naproxen, and non aspirin NSAIDs antagonize what aspirin effect?

A

Antic platelet actions–> decrease aspirin protection against MI and stroke

  • minimize this adverse effect by takin aspirin 2hrs before other NSAIDs
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17
Q

Aspirin can increase bleeding risk in which patient?

A

Those on warfarin, heparin, or other anticoagulants

  • high dose aspirin should be discontinued 1 week before elective surgery but low dose can continue
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18
Q

What NSAID is recommended when NSAID therapy is required but the patient is at risk for CV complications?

A

NAPROXEN

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19
Q

What are contraindications of NSAID use?

A
  • CKD with creatinine clearance of less than 60 mL/min
  • Active duodenal or gastric ulcer
  • CV disease–> heart failure or uncontrolled HTN
  • Anticoagulat tx (warfarin)
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20
Q

What analgesic is believed to be a TRPV1 and TRPA activator or central PG synthhase inhibitor due to the activation of descending serotonergic inhibitory pathways in the CNS?

A

acetaminophen

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21
Q

What are the toxicities of acetaminophen?

A

-risk of medication errors and overdosage–> hepatotoxicity with acute liver failure and possible death

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22
Q

What is antidote for acetaminophen toxicity?

A

Acetaminophen becomes a toxic metabolic when glutathione is depleted

N-ACETYLCYSTINE IS ANTIDOTE

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23
Q

Acetaminophen inhibits prostaglandin synthesis in the CNS but not the periphery, what does this mean?

A

acetaminophen suppresses pain and fever but NOT INFLAMMATION

  • lacks anti-inflammatory actions
    -does NOT cause GI ulceration
    -does NOT suppress platelet aggregation
    does NOT impair renal function

used for temporary relied of minor aches, pains, and headache

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24
Q

Hepatic necrosis from glutathione depletion and increased bleeding risk can be caused by what?

A

Acetaminophen

25
Q

What is morphine MOA?

A

binds to opioid receptors in the CNS
-inhibits ascending pain pathways

  • alters perception of pain and response to pain
  • generalized CNS depressant
26
Q

What drug has BBW for respiratory depression with to without combining other drugs

A

Morphine

27
Q

What can create a physical dependence on opiods?

A

administration of opioids at high doses for > 20 days

28
Q

What is Amitriptyline MOA?

A
  • tricyclic antidepressant
  • inhibition of NE and 5-HT reuptake by the presynaptic neuronal membrane pump

effect ins to increase concentration of NE and 5HT in the synaptic cleft

29
Q

What are clinical applications of amitriptyline?

A
  • unipolar major depressive disorder
  • Chronic fatigue syndrome from sleep disturbances and pain
  • fibromyalgia
  • functional dyspepsia
  • neuropathic pain (including diabetic neuropathy
30
Q

What drugs have BBW of increased risk of suicidal thinking and behavior in children, adolescents, and young adults?

A
  1. amitriptyline

2. duloxetine

31
Q

What is MOA of duloxetine?

A
  • potent inhibitor of neuronal 5 HT and NE reuptake
  • weak inhibitor of DA uptake
  • anxiety benefits are observed within 2 weeks of tx and continue to improve through 4-6 weeks
32
Q

What drugs are dual reuptake inhibitors of serotonin and NE making them beneficial in patients with concurrent depression?

A
  • duloxetine

- venlafaxine

33
Q

What is pregabalin MOA?

A

-Binds alpha-2-delta subunit of voltage gated calcium channels to modulate calcium influx at nerve terminals

34
Q

What are clinical applications of pregabalin (Lyrica)?

A
  • Neuropathic pain (diabetic peripheral neuropathy and spinal cord injury)
  • seizures (focal and partial)
  • postherpetic neuralgia
  • fibromyalgia (modest benefits)
35
Q

What is gabapentin MOA?

A

-binds to the alpha2-delta subunit of calcium gated channels to inhibit excitatory NT release (glutamate)

36
Q

What drug has broad spectrum antiseizure effects?

A

gabapentin

37
Q

What is MOA of Tramadol?

A
  • partial agonist at mu opiate receptors in the CNS (weak action)
  • schedule IV controlled substance
  • inhibits reuptake of NE and 5-HT (primary mode of action )
38
Q

What drug has BBW of
-risk of medication error

  • addiction, abuse, and misuse
  • interactions with drugs affecting cytochrome P450 isoenzymes withdrawal syndroms
  • increased risk of respiratory depression from concomitant use with other benzodiazepine or other CNS depressants
A

Tramadol

also causes sedation, dizziness, headache, dry mouth, and constipation

39
Q

What is MOA of tapentadol?

A
  • moderate-strong opioid agonist similar to oxycodone at mu receptors
  • blocks reuptake of NE
  • causes less constipation than traditional opioids
40
Q

Why would someone use tapentadol over other opioids?

A
  • less constipation

- reserved for patients not effectively treated with other non-opioids and opioids

41
Q

What is the MOA of ketamine?

A

Non-competitive NMDA receptor antagonist that blocks glutamate

KetAMiNe –> only missing the D and it tells you what it does

42
Q

What is dexmedetomidine MOA?

A
  • selective alpha2 adrenoceptor agonist
  • anesthetic and sedative properties thought to be due to activation of G-proteins by alpha2a adrenoceptors in the brainstem
43
Q

does ketamine elevate or lower BP?

A

Elevate! differs from many other anesthetics that lower it

44
Q

How is dexmedetomidine administered? What is it used for?

A
  • IV administered (unlike clonidine)

- alpha 2 adrenergic agonist used for analgesia and sedation

45
Q

What is clonidine MOA? Use?

A
  • alpha 2 adrenergic agonist for
  • HTN
  • relief of severe pain
46
Q

What is ziconotide MOA?

A
  • selectively binds to N-type voltage sensitive calcium channels
  • located on the nociceptive afferent nerves of the dorsal horns in the spinal cord
47
Q

What is BBW of ziconotide?

A
  • severe psychiatric sx and neuro impairment
  • significant pt harm if used in error
  • n type voltage sensitive ca2+ channel inhibitor
48
Q

What is BBW of ziconotide?

A
  • severe psychiatric sx and neuro impairment

- significant pt harm if used in error

49
Q

What is only indicated for sever pain when intrathecal (into spinal cord) administration is warranted when refractory to other treatments?

A

Ziconotide

50
Q

What topical anti pain agent stimulate TRPV1

A

Camphor- in ICY hot
Capsaicin from red pepper desensitizes and depletes substance P
- moderate to poor efficiency on nociceptive and neuropathic pain

51
Q

How does aspercreme work?

A

ir is a topical Na+ channel blocker

52
Q

how does sumatriptan work?

A
  • selective 5HT1B and 5HT1D agonist
  • activates receptors on intracranial blood vessels and sensory nerves of the trigeminal
  • used for migranes of moderate to severe intensities
  • cluster headaches
53
Q

What are clinical applications of sumatriptan and how?

A

Sumatriptan is used for migraines of moderate to severe intensity

  • causes vasoconstriction and reduces neurogenic inflammaiton
54
Q

Risk of sumatriptan?

A
  • prolonged QT–> torsades
  • MI
  • stroke
  • transient / permanent blindness
  • serotonin syndrome
55
Q

What is lasmiditan MOA?

A

high affinity, high selectivity 5HT1F receptor agonist

  • decrease stimulation of the trigeminal system
  • treat migraine pain without causing vasoconstriction
56
Q

What are the effects of lasmiditan?

A

-decreased stimulation of the trigeminal system

–treat migraine pain without vasoconstriction

57
Q

What is MOA of ubrogepant?

A

Calcitonin gene-related peptide receptor antagonist

  • tx of migraine with or without aura
58
Q

What is MOA of dihydroergotamine?

A
  • ergot alkaloid
  • binds serotonin, dopamine, and adrenergic receptors
  • late tx option for migra
  • cluster headahces

off label: orthostatic hypotension, pelvic congestion with pain

NMSP (14 decks)

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