Pharm: NSAIDs and Non-Narcotic Analgesics Flashcards
Aspirin can impair renal function, causing Na+ and H2O retention, edema and HTN, adverse outcomes are more likely in people with what conditions?
- Advanced age
- Pre-existing renal dysf.
- HYPOvolemia
- HTN
- Hepatic cirrhosis
- Heart failure
What is the effect of acetaminophen on warfarin?
Inhibits the metabolism of Warfarin and therefore can ↑ risk of bleeding
What are 2 ways to minimize risk of aspirin-induced ulcers?
- Test for/eliminate H. pylori before starting therapy
- Give a proton pump inhibitor
Explain the 5 stages of progression in aspirin/salicylate toxicity?
- 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
What is the MOA of Dexmedetomidine and what is it used for?
- 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
Pt’s on which drugs are at a higher risk of bleeding when taking aspirin?
Those on warfarin, heparin, and other anti-coagulants
What are the 4 major beneficial actions of Aspirin?
- 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
Gabapentin has broad-spectrum anti-seizure activity, but what are 5 common off label uses it is prescribed for?
- Post-herpetic neuralgia
- Diabetic neuropathy
- Prophylaxis for migraine
- Tx of fibromyalgia
- Restless leg syndrome
How does the location and action of COX-1 vs. COX-2 differ?
- 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)
What are two dual reuptake inhibitors of serotonin and norepinephrine (SNRIs) that may be used in patients as analgesics with concurrent depression?
Venlafaxine & Duloxetine
What is Ziconotide indicated for; how is it administered?
Only for chronic severe pain in those for whom intrathecal administration is warranted and when refractory to other tx’s
What is the nature of the interaction between cyclooxygenase and aspirin, but not other NSAIDs?
Irreversible
What is the effect of aspirin on cyclooxygenase and why is this significant?
- 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)
Aspirin can cause hypersensitivity rxns, especially in those with what underlying conditions; treated how?
- Asthma, rhinitis, and nasal polpys
- Tx w/ epinephrine
Acetaminophen overdose results in what; how is it treated?
- 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
Explain the relationship between inflammation and AA, COX-1, and PGE2?
- Inflammation stimulates AA release
- COX-1 converts AA –> PGE2
- PGE2 causes sx’s –> erythema, edema, and pain
What are the AE’s of the 2nd gen. NSAID, Celecoxib?
- Does NOT inhibit platelet aggregation –> risk of bleeding
- ↑ risk of MI and stroke