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MSKII Exam I + Gene decks > Pharm: NSAIDs and Non-Narcotic Analgesics > Flashcards

Pharm: NSAIDs and Non-Narcotic Analgesics Flashcards

1
Q

Explain the relationship between inflammation and AA, COX-1, and PGE2?

A
  • Inflammation stimulates AA release
  • COX-1 converts AA –> PGE2
  • PGE2 causes sx’s –> erythema, edema, and pain
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2
Q

What is the role of COX-2 in relation to the inflammatory resposne?

A
  • Inflammation also induces COX-2 expression
  • COX-2 also converts AA –> PGE2 which amplifies sx’s of COX-1 activation
  • Worse erythema, edema, and pain
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3
Q

How does the location and action of COX-1 vs. COX-2 differ?

A
  • COX-1 expressed in ‘all’ tissues, ‘all’ the time –> prominent role = responding to physiological stimuli
  • COX-2 induced in ‘some’ tissues, ‘some’ times: has physiologic role in kidney, complements COX-1 and prominent role in response to any pathologic stimuli that release AA from cells (i.e., inflammation)
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4
Q

What are the 4 major beneficial actions of Aspirin?

A
  • Suppression of inflammation (due to COX-1 and COX-2 inhibition)
  • Relief of mild to moderate pain (due to COX-1 and COX-2 inhibition)
  • Reduction of fever (due to COX-1 and COX-2 inhibition)
  • Prevention of MI and stroke due to inhibition of COX-1 in platelets, suppresses platelet aggregation
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5
Q

Because Aspirin inhibits COX-1 and COX-2, it may lead to what 3 complications?

A
  • Gastric ulceration
  • Bleeding
  • Renal impairment
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6
Q

What is the nature of the interaction between cyclooxygenase and aspirin, but not other NSAIDs?

A

Irreversible

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7
Q

What is the effect of aspirin on cyclooxygenase and why is this significant?

A
  • Irreversible inhibition of cyclooxygenase –> effects persist until cells make more COX because platelets cannot synthesize new COX
  • Anti-platelets effects last for life of platelet (~8 days)
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8
Q

What are 2 ways to minimize risk of aspirin-induced ulcers?

A
  • Test for/eliminate H. pylori before starting therapy
  • Give a proton pump inhibitor
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9
Q

What are the effects of ibuprofen, naproxen, and other non-aspirin NSAIDs on the antiplatelet actions of aspirin?

A

Antagonize the antiplatelet actions

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10
Q

Pt’s on which drugs are at a higher risk of bleeding when taking aspirin?

A

Those on warfarin, heparin, and other anti-coagulants

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11
Q

Long-term aspirin use may lead to what serious kidney dysfunction?

A

Renal papillary necrosis

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12
Q

Aspirin can impair renal function, causing Na+ and H2O retention, edema and HTN, adverse outcomes are more likely in people with what conditions?

A
  • Advanced age
  • Pre-existing renal dysf.
  • HYPOvolemia
  • HTN
  • Hepatic cirrhosis
  • Heart failure
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13
Q

Aspirin can cause hypersensitivity rxns, especially in those with what underlying conditions; treated how?

A
  • Asthma, rhinitis, and nasal polpys
  • Tx w/ epinephrine
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14
Q

Explain the 5 stages of progression in aspirin/salicylate toxicity?

A
  • Salicylates uncouple mitochondrial OxPhos in the CNS
  • Respiratory center senses ↓ ATP as hypoxemia, responds w/ hyperventilation
  • ↓ CO2 –> respiratory alkalosis - eventually prompts kidney to deplete HCO3
  • Organic acids accumulate because ATP is no longer generated via Krebs cycle
  • Metabolic acidosis becomes life-threatening
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15
Q

Although the MOA is similar to aspirin, what are some important difference with non-aspirin NSAIDs?

A
  • Are reversible, so effects decline as blood levels decline
  • Suppress platelet aggregation, but use acutally ↑ risk of MI and stroke
  • Therefore, should use lowest effective dosage for shortest possible time
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16
Q

Which NSAID causes less gastric ulceration and is indicated for patients with chronic pain/inflammation whom suffer from GI problems (i.e., ulcers)?

A

Celecoxib –> selectively blocks COX-2

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17
Q

What are the AE’s of the 2nd gen. NSAID, Celecoxib?

A
  • Does NOT inhibit platelet aggregation –> risk of bleeding
  • ↑ risk of MI and stroke
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18
Q

Where NSAID therapy is required for pt’s at risk of cardiovascular complications, what is the recommended NSAID of choice?

A

Naproxen

19
Q

What is the general consensus from the American Heart Association for the use of all NSAIDs (especially COX-2 selective agents)?

A
  • Should be used at their lowest effective dose
  • Avoided where possible in pt’s w/ CV risk factors ie HTN, hypercholesterolemia, angina, edema, recent bypass surgery or hx of MI
  • Be used only when sufficient pain relief is not achieved with other therapies and the benefit outweighs the ↑ CV risk
20
Q

What are 5 contraindiction for NSAID use?

A
  • Chronic kidney disease: with creatinine clearance of <60 mL/min
  • Active duodenal or gastric ulcer
  • CV disease, particularly heart failure or uncontrollable HTN
  • NSAID allergy
  • Ongoing tx with anticoagulants - Warfarin
21
Q

What is the effect of acetaminophen on pain, fever, and inflammation; where does it exert its MOA?

A
  • Inhibition of prostaglandin synthesis in the CNS, but not the periphery
  • Suppresses pain and fever
  • NOT inflammation
22
Q

Acetaminophen overdose results in what; how is it treated?

A
  • Hepatic necrosis; due to accumulation of a toxic metabolite that forms when glutathione is depleted
  • OD is treated w/ acetylcysteine, a drug that substitutes for depleted glutathione
23
Q

What is the effect of acetaminophen on warfarin?

A

Inhibits the metabolism of Warfarin and therefore can ↑ risk of bleeding

24
Q

What is the most widely studied TCA used for chronic pain?

A

Amitriptyline

25
Q

What are some of the AE’s associated with Amitriptyline used as anti-depressant and analgesic?

A
  • Anticholinergic: dry mouth & constipation
  • Cardiovascular: tachycardia & palpitations
  • GI: nausea & vomiting
  • Neurologic: sedation & mental clouding
26
Q

What are two dual reuptake inhibitors of serotonin and norepinephrine (SNRIs) that may be used in patients as analgesics with concurrent depression?

A

Venlafaxine & Duloxetine

27
Q

What is the MOA of Pregabalin and Gabapentin?

A
  • GABA analog, but exerts its effects by binding to α2δ subunit of voltage-gated Ca2+ channels within CNS
  • Modulates Ca2+ influx at the nerve terminals, thereby inhibiting excitatory NT release

*Don’t be tricked, it doesn’t bind GABA*

28
Q

What are the 4 approved indications for using Pregabalin?

A
  • Neuropathic pain assoc. w/ diabetic neuropathy**
  • Postherpetic neuralgia
  • Adjunctive therapy for partial seizures
  • Fibromyalgia
29
Q

Gabapentin has broad-spectrum anti-seizure activity, but what are 5 common off label uses it is prescribed for?

A
  • Post-herpetic neuralgia
  • Diabetic neuropathy
  • Prophylaxis for migraine
  • Tx of fibromyalgia
  • Restless leg syndrome
30
Q

What is the MOA of Tramadol as an analgesic?

A
  • Codeine analog, weak mu-opioid agonist, but works primarily by blocking NE and 5-HT reuptake
  • Activates monoaminergic spinal inhibition of pain
31
Q

What is Tramadol used for?

A

Moderate to moderately severe pain

32
Q

What are some of the AE’s associated with Tramadol?

A

Sedation + dizziness + HA + dry mouth + constipation

33
Q

What is the MOA of Tapentadol used as analgesic?

A
  • Moderate to severe opioid agonist at mu-receptors
  • Also blocks re-uptake of NE
34
Q

What are some of AE’s of ketamine and what effect makes it stand out from other anesthetics?

A
  • Psychological rxns: such as agitation, confusion, and hallucinations
  • Has a tendency to ↑ BP, unlike other anesthetics that lower it
35
Q

What is the MOA of Dexmedetomidine and what is it used for?

A
  • α2-adrenergic agonist used for analgesia and sedation
  • Approved for: short-term sedation in critically ill pt’s who were intubated and are undergoing mechanical ventilation
  • Sedation prior to/during surgeries
36
Q

What are some of the AE’s of the analgesic, Dexmedetomidine?

A

HYPOtension + bradycardia + nausea + dry mouth + transient HTN + agitation + constipation + respiratory depression

37
Q

What is the MOA and use for Clonidine?

A
  • α2-adrenergic agonist used for 1) HTN and 2) relief of severe pain
  • Blocks transmission of pain signals from periphery –> brain
38
Q

How is the α2-adrenergic agonist Dexmedetomidine administered vs. Clonidine?

A
  • Dexmedetomidine: administered IV for pain
  • Clonidine: administered by continous infusion through an epidural catheter
39
Q

What are some of the AE’s associated with Clonidine?

A

Highly lipid soluble, escapes blood to cause HYPOtension + confusion + dry mouth

40
Q

What is the MOA of the analgesic, Ziconotide?

A
  • Selective antagonist at N-type voltage sensitive Ca2+ channels on nociceptive afferent neurons in doral horn of spinal cord
  • Prevents transmission of pain signals from periphery –> brain
41
Q

What is Ziconotide indicated for; how is it administered?

A

Only for chronic severe pain in those for whom intrathecal administration is warranted and when refractory to other tx’s

42
Q

What are some AE’s associated with Ziconotide?

A
  • CNS effects w/ cognitive impairment and psychiatric sx’s = common
  • Also causes muscle injury (↑ serum creatine kinase levels)
43
Q

What are the MOA of Capsaicin and Camphor used as topical analgesics?

A
  • Capsaicin: “heat” from red peppers; counterirritant via stimulation of TRPV1 receptors, desensitizes and/or depletes substance P

- Camphor: “heat,” also desensitizes TRPV1 receptors

44
Q

What is the MOA of Menthol as a topical analgesic?

A

Stimulates the TRPM8“cold” receptors to cause cool sensation

MSKII Exam I + Gene decks (16 decks)

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