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MSK II Exam I > NSAIDs & Non-Narcotic Analgesics > Flashcards

NSAIDs & Non-Narcotic Analgesics Flashcards

1
Q

Which COX enzyme is considered constitutive, as it is expressed in all tissues at all times and plays a prominent role in responding to physiologic and pathologic stimuli

A

COX-1

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2
Q

Which COX enzyme is inducible in some tissues, plays a physiologic role in the kidney where it complements COX-1, and plays a prominent role in response to any pathologic stimuli?

A

COX-2

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3
Q

MOA of aspirin

A

Irreversible inhibition of COX1 and COX2

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4
Q

AEs of aspirin

A

Gastric ulceration

Bleeding

Renal impairment possibly leading to papillary necrosis (more common in advanced age, pre-existing renal function, hypovolemia, HTN, hepatic cirrhosis, and heart failure pts)

Aspirin-induced asthma

Reye syndrome if given during viral illness

Hypersensitivity reactions

[to minimize risk of ASA-induced ulcers, test for Hpylori before starting therapy and give a PPI. Stop high-dose ASA before surgery to prevent bleeding complications.]

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5
Q

Indications for aspirin use

A

Suppression of inflammation, relief of mild to moderate pain, reduction of fever, prevention of MI and stroke

Commonly used for RA and other chronic inflammatory conditions

Also used to control post-op pain

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6
Q

What effect do ibuprofen, naproxen, and other non-aspirin NSAIDs have on antiplatelet actions of aspirin?

A

They antagonize the antiplatelet actions of aspirin, thus decreasing protection against MI and stroke

[minimize this risk by taking ASA 2 hrs before other NSAIDs]

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7
Q

5 basic events in progression of aspirin/salicylate toxicity

A
  1. Salicylates uncouple mitochondrial oxphos in CNS
  2. Respiratory center registers decreased ATP as hypoxemia and responds with hyperventilation
  3. Hyperventilation leads to drop in pCO2 and respiratory alkalosis — eventually prompting kidney to deplete bicarbonate
  4. Organic acids accumulate because ATP is no longer generated through Krebs cycle
  5. Metabolic acidosis becomes life-threatening
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8
Q

Like aspirin, non-aspirin NSAIDs (e.g., acetaminophen) may inhibit COX-1 and/or COX-2, suppress inflammation, pain, and fever, and may increase risk of gastric ulceration, renal impairment, and bleeding.

What are some important differences in non-aspirin NSAIDs when compared to aspirin?

A

Reversible

Suppress platelet aggregation, but use actually increases risk of MI and stroke

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9
Q

Acetaminophen suppresses pain and fever, but not _________. Its mechanism of action involves inhibition of ______ synthesis in the CNS but not in the periphery, consequently: it does not cause GI ulceration, suppression of platelet aggregation, or impairment of renal function

A

Inflammation; prostaglandin

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10
Q

Toxicities of acetaminophen

A

Hepatic necrosis from acetaminophen overdose results from accumulation of toxic metabolites when glutathione is depleted; risk is increased by undernourishment, alcohol, and pre-existing liver dz; Tx with acetylcysteine

Acetaminophen also inhibits metabolism of warfarin, and can increase risk of bleeding

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11
Q

Common anti-inflammatory indications frfom NSAIDs

A

Osteoarthritis and other arthritides

Bursitis

Gout “flare”

Ankylosing spondylitis

Dysmenorrhea

Headache

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12
Q

When taken for primary prevention, low-dose aspirin reduces the risk of first ____ in men, and first _______ in women

A

MI; ischemic stroke

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13
Q

Contraindications to NSAIDs

A

CKD with creatinine clearance <60 mL/min per 1.73 m^2

Active duodenal or gastric ulcer

Cardiovascular disease, particularly heart failure or uncontrollable HTN

NSAID allergy

Ongoing tx with anticoagulants - warfarin

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14
Q

Second generation NSAID that suppresses inflammation, pain, and fever, but does not inhibit platelet aggregation, so does NOT pose a risk of bleeding, and may cause less gastric ulceration than nonselective inhibitors

A

Celecoxib

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15
Q

Celecoxib selectively blocks _____

A

COX-2

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16
Q

Celecoxib ______ risk of MI and stroke

A

Increases

[thought to be due to blockade of prostacyclin synthesis in blood vessels]

17
Q

Diclofenac, ketorolac, and nabumetone are in what drug class?

A

NSAIDs

18
Q

Where NSAID therapy is required for pts at risk of cardiovascular complications, ______is recommended as the NSAID of choice

A

Naproxen

19
Q

In pts with renal disease, administration of NSAIDs rapidly reduces renal function. This is largely due to _____ inhibition

NSAID-mediated suppression of _____ in the gastric mucosa increases acid secretion and compromises integrity of gastric mucosa

_______-selective inhibitors are associated with increased risk of MI, stroke, and/or heart failure

A

COX-1

COX-1

COX-2

20
Q

Tricyclic antidepressants have independent analgesic effects as well as an ability to relieve the depressive symptoms associated with chronic pain. ______ has been the most widely studied TCA in chronic pain

A

Amitriptyline

[others include doxepin, imipramine, nortriptyline, desipramine]

21
Q

AEs of TCAs used to tx chronic pain

A 
Dry mouth
Constipation
Tachycardia
Palpitations
Nausea
Vomiting
Sedation
Mental clouding

[AEs may diminish over time]

22
Q

______ and ______ are SNRIs used to treat chronic pain and are especially beneficial in pts with concurrent depression

A

Venlafaxine

Duloxetine

23
Q

AEs of SNRIs like venlafaxine and duloxetine used to tx pain

A 
Nausea
Dizziness
Diaphoresis
Sexual dysfunction
Insomnia/agitation
Increased BP
24
Q

GABA analog used for pain that exerts its effects by binding to alpha2-delta subunit of voltage-gated calcium channels within the CNS — modulates calcium influx at nerve terminals, thereby inhibiting excitatory NT release; has few interactions with other drugs, but AEs are common (e.g., dizziness, sleepiness, etc)

A

Pregabalin

25
Q

4 approved indications for pregabalin (Lyrica)

A

Neuropathic pain associated with diabetic neuropathy

Postherpetic neuralgia

Adjunct therapy for partial seizures

Fibromyalgia [first drug approved for this, but benefits are modest and fade]

26
Q

GABA analog that exerts its effects by binding to alpha2-delta subunit of voltage-gated calcium channels within CNS — modulates calcium influx at nerve terminals thereby inhibiting excitatory NT release; has broad-spectrum anti-seizure activity and is approved as an adjunctive therapy for partial seizures. However, 80% of Rxs are written for off-label use in postherpetic neuralgia, DM neuropathy, prophylaxis for migraine, tx of fibromyalgia, RLS

A

Gabapentin

27
Q

Codeine analog and weak mu agonist but works primarily by blocking NE and 5-HT reuptake, results in activation of monoaminergic spinal inhibition of pain

A

Tramadol

28
Q

AEs of tramadol

A 
Sedation
Dizziness
Headache
Dry mouth
Constipation

Rare serious side effects: seizures in epileptics, hypertensive crisis if combined with MAOI, serotonin syndrome if combined with SSRI, TCA, triptans, MAOI, etc

29
Q

Moderate to strong opioid agonist similar to oxycodone at mu receptors that also blocks reuptake of NE and is reserved for pts who are not effectively treated with other non-opioids and opioids

A

Tapentadol

30
Q

NMDA antagonist used for anesthesia and post-op pain

A

Ketamine

31
Q

AEs of ketamine

A

Psychological reactions — agitation, confusion, hallucinations

Tendency to elevate BP

32
Q

Alpha2-adrenergic agonist used for analgesia and sedation; approved for short-term sedation in critically ill pts who were intubated and are undergoing mechanical ventilation, as well as during surgical procedures

A

Dexmedetomidine

33
Q

AEs of dexmedetomidine

A 
Hypotension
Bradycardia
Nausea
Dry mouth
Transient HTN
Agitation
Constipation
Respiratory depression
34
Q

Alpha2-adrenergic agonist used for HTN and relief of severe pain; administered by continuous infusion through epidural catheter where it blocks transmission of pain signals from periphery to brain

A

Clonidine

35
Q

AEs of clonidine

A

Hypotension
Confusion
Dry mouth

36
Q

Selective antagonist at N-type voltage sensitive calcium channels on nociceptive afferent neurons in dorsal horn of spinal cord — prevents transmission of pain signals from periphery to brain and indicated ONLY for chronic severe pain in those for whom intrathecal administration is warranted and when refractory to other treatments

A

Ziconotide

37
Q

AEs of ziconotide

A

Adverse CNS effects with cognitive impairment and psychiatric symptoms common

Muscle injury (elevated serum creatine kinase)

38
Q

2 Topical analgesics that are counterirritants via stimulation of TRPV1 receptors, desensitizes and/or depletes substance P; moderate to poor efficacy for both nociceptive and neuropathic pain

A

Capsaicin

Camphor

39
Q

Topical analgesic that stimulates TRPM8 “cold” receptors to cause cool sensation

A

Menthol

MSK II Exam I (8 decks)

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