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Fall Pharm Block 3 > NSAIDs - Medications > Flashcards

NSAIDs - Medications Flashcards

1
Q

What are the indications for aspirin use (three A’s)?

A

Analgesic, antipyretic, anti-inflammatory

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2
Q

List three specific conditions mentioned in class for which aspirin is used as prophylaxis.

A

MI, colon cancer, uricosuria (uric acid in urine) against gout (high dose, > 5 g/day)

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3
Q

List 3 contraindications and 3 cautions for use of aspirin.

A

Contra: known bleeding, tartazine dye allergy, ASA syndrome (asthma, angioedema, nasal polyps)
Cautions: Peptic ulcer, elderly, renal disease

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4
Q

Why is aspirin not used in children?

A

Can cause Reyes Syndrome

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5
Q

What is an adverse effect of aspirin and how is it manged?

A

GI upset –> take with food

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6
Q

What is the primary sign of ASA overdose and why?

A

Tinnitus - NSAIDs increase the level of arachadonic acid which irritates the auditory nerve.

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7
Q

Describe buffered aspirin and why is it used?

A

Aspirin with HCO3 added to it to make it less harsh on the stomach

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8
Q

What is enteric coated aspirin?

A

ASA that is coated so that absorption is delayed until the duodenum or jejunum - less harsh on stomach

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9
Q

What are patients instructed to monitor for if they take aspirin regularly?

A

gum bleeding and bruising

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10
Q

What is the least acidic NSAID?

A

Nabumetone

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11
Q

What is Oxaprozin’s claim to fame?

A

QD dosing

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12
Q

What is arthrotec and how is it used?

A

Arthrotect is a combination of Diclofenac (NSAID) and Misoprostil (PG that stimulates mucus production in the gut). Used inc mucus production to protect patients on NSAIDs at risk for GI ulcers.

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13
Q

What are two problems with Misoprostil?

A
  1. Causes diarrhea

2. Causes uterine contraction (Pregnancy category X)

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14
Q

Is naproxen available OTC or by prescription?

A

Both –> OTC in lower doses, higher doses require Px

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15
Q

What is the primary use of naproxen?

A

Sports medicine –> preferred for soft tissue inflammation

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16
Q

What is the indication for IV indomethacin and by what mechanism?

A

Indication for ductus arteriosis –> PGs keep things open, indomethacin inhibits PGs.

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17
Q

What is an adverse effect of PO indomethacin?

A

Frontal lobe headache (mechanism unknown)

18
Q

For what types of patients is sulindac preferred and why?

A

Renal patients bc it is the NSAID least likely to decrease PGs at the afferent arteriole, thus it doesn’t constrict the afferent arteriole.

19
Q

What is unique about piroxicam and what is the clinical effect of this characteristic?

A

It has a very long half life - should be used very cautiously in elderly patients.

20
Q

What is unique about meloxicam and what is the clinical effect of this characteristic?

A

The most Cox-2 selective of all non-selective NSAIDs. It stays in the periphery and has less GI AEs.

21
Q

Is ibuprofen available OTC or by prescription?

A

Both –> OTC in lower doses, higher doses require Px

22
Q

What is the max daily dose of ibuprofen in the treatment of analgesia?

A

1200 mg/day –> higher dose only increases AEs, does not produce more analgesia.

23
Q

What are the two IV formulationss of ibuprofen?

A

Ibuprofen Lysine and Caldolor

24
Q

What is ibuprofen lysine used for?

A

IV infusion for patent ductus arteriosis

25
Q

What is Caldolor primarily used for?

A

IV infusion used as an adjunct for analgesia so you may use less of a narcotic. Also a strong anti-pyretic.

26
Q

What is the most potent NSAID?

A

Ketorolac

27
Q

By what routes is ketorolac administered and what is the maximum time it can be used and why?

A

PO and IM (only IM NSAID) –> max PO use is 5 days because it causes renal toxicity after 5 days.

28
Q

What is the most common use of ketorolac?

A

Emergency analgesia as an alternative to narcotics.

29
Q

What is the only Cox-2 selective NSAID still on the market and why is it rarely used?

A

Celecoxib –> rarely used bc of cost and worry for increased cardiovascular morbidity and mortality.

30
Q

What is the benefit of using a Cox-2 selective NSAID?

A

Stays in the periphery and causes less GI irritation and ulcers (bc it doesn’t inhibit Cox-1)

31
Q

Why have Cox-2 selective NSAIDs been associated with increased cardiovascular M&M?

A

They inhibit PGs that would stimulate angiogenesis (limits formation of collateral circulation)

32
Q

What is the theoretical benefit of Cox-2 selective NSAIDs in cancer/chemotherapy?

A

Inhibiting angiogeneis slows growth of neoplasm.

33
Q

What other drug does celecoxib have cross reactivity with and why?

A

Celecoxib has a sulfa-moiety and should be used cautiously in patients with sulfa allergies.

34
Q

What are the effects of acetaminophen?

A

Antipyretic and analgesic (poor antiinflammatory)

35
Q

What is the abbreviation for acetaminophen?

A

APAP

36
Q

What is true about the distribution of acetaminophen and how is this clinically relevant?

A

Highly lipophilic meaning it will enter the CNS with few effects on the periphery.

37
Q

What are the indications for acetaminophen use?

A

Fever (primarily), pain, headache

38
Q

T/F: Acetaminophen acts as an anti-platelet

A

False –> no effect on platelets

39
Q

What differentiates APAP from the NSAIDs in terms of its metabolism and what is the clinical relevance?

A

It is metabolized by the liver where most NSAIDs are metabolized renally. APAP toxicity causes hepatotoxicity.

40
Q

What substance interacts with APAP when ingested and how is this interaction described?

A

Alcohol interacts synergistically with APAP

41
Q

What is the antidote for APAP overdose?

A

N-acetylcysteine (NAC)

Fall Pharm Block 3 (8 decks)

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