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NSAIDs > Traditional NSAIDs > Flashcards

Traditional NSAIDs Flashcards

1
Q

Salicylates that are important to know

A

sodium salicylate

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2
Q

Pyrazolone derivatives that are important to know (and brand names)

A

phenylbutazone, serious toxicity w/ misuse

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3
Q

What is the normal therapeutic use of Traditional NSAIDs

A

treat pain (anelgasic), fever (antipyretic), inflammation (anti-inflammatory)

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4
Q

Acetic/Carboxylic acid drug examples that are important to know

A

indomethicin (Indocin), ketorolac (toradol), nabumetone (relefen)

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5
Q

Main use for Acetic/Carboxylic acids at HIGH doses

A

Treatment of RA (rheumatoid arthritis)

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6
Q

Oxicam derivative examples that are important to know

A

meloxicam (Mobic), piroxicam (Feldene)

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7
Q

Propionic Acid derivatives that are commonly used

A

ibuprofen (motrin), naproxen (Naprosyn), Ketoprofen (Orudis), oxaprozin (Daypro)

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8
Q

longest half life, greatest potency class of traditional NSAIDs

A

Oxicam derivatives (15-50 hour 1/2 lives)

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9
Q

Class of NSAID generally used to treat Rheumatoid Arthritis

A

Acetic/Carboxylic Acid NSAIDs

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10
Q

Selective COX-2 inhibitor drug example

A

celecoxib (celebrex), reversible inhibition of COX-2. use for less GI side effects. analgesic, antipyretic, anti-inflammatory

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11
Q

Aspirin’s effects and why

A

analgesic, antipyretic, anti-inflammatory, ANTITHROMBOTIC; selective for COX1 in low doses and is IRREVERSIBLE inhibitor. The selectivity for COX1 makes it cardioprotective in patients at high risk for CVD.

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12
Q

ASA

A

acetylsalicylic acid = ASA = aspirin

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13
Q

Brand names Ibuprofen

A

Advil, Motrin

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14
Q

brand names Naproxen

A

Aleve, Naprosyn

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15
Q

Brand names Ketoprofen

A

Orudis-R1

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16
Q

Traditional NSAIDs given OTC

A

Ibuprofen, Naproxen, Ketoprofen

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17
Q

What do all traditional NSAIDs have as actions?

A

Anti-inflammatory, antipyretic, analgesic effects

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18
Q

Traditional NSAID absorption?

A

Rapid and complete, 90% protein bound

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19
Q

Traditional NSAID elimination?

A

• Renal excretion or liver metabolism

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20
Q

Compare Traditional NSAID to ASA or acetominophen for mild to moderate pain

A

• As effective or superior; headache, postextraction dental pain, postsurgical episiotomy pain, soft tissue athletic pain)

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21
Q

Are there parenteral options for traditional NSAIDs?

A

• Yes, IM/IV ketorolac (Toradol) - post surgical pain

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22
Q

What is useful in treating dysmenorrhea and why?

A

• Ibuprofen or naproxen; they inhibit endometrial prostaglandin synthesis

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23
Q

Is ibuprofen or ASA or acetominophen best for treating fever?

A

• All have equal anti-pyretic effects

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24
Q

What are the normal side effects of traditional NSAIDs?

A

• While safer in overdose than aspirin - mild nausea/vomiting, GI pain, RENAL FAILURE IS BIGGEST SCARE - adverse effects minimal for short duration pain management

25
Q

What is the worst worry in NSAID overdose?

A

• Renal failure

26
Q

GI tract Traditional NSAID side effects?

A
  • Interfere with gastric cytoprotection (COX1-PGE syntheis) - leads to dyspepsia and gastric ulceration
    • Lowest risk = ibuprofen, highest risk=naproxen
27
Q

What if a patient has a high risk for PUD (peptic ulcer disease)?

A

• Traditional NSAIDs are contraindicated (advanced age, history of PUD or NSAID gastropathy, concurrent glucocorticoid anti-inflammatory use)

28
Q

What other drug class can be used to protect against gastroduodenal toxicity in chronic Traditional NSAID use?

A

• PPI’s (proton pump inhibitors) - omeprazole

29
Q

Platelet side effects in traditional NSAID use?

A
  • COX1 - thromboxane A2 (TXA2) synthesis is INHIBITED - promotes bleeding
    • Asprin effects last lifetime of platelet (4-7 days)
    • NSAID effects last 2 days (agent dependent)
30
Q

What if patient is receiving antiplatelet or anticoagulant agents?

A

• Don’t use NSAIDs, you could make bleeding too easy in the patient

31
Q

What if patient is taking low dose ASA for cardioprotective effects?

A

• That’s fine, just use NSAID for pain one hour later

32
Q

Traditional NSAID side effects in kidney?

A

• Renal vasoconstriction by inhibition of COX1-COX2 PGE synthesis - leads to loss of vasodilator actions - leads to renal insufficiency

33
Q

IF NSAIDs can cause fluid retention, what kind of patient should you then be careful with?

A

• Risk of CVD (cardiovascular disease) - can make heart failure worse, can elevate blood pressure, can interfere with cardioprotective ASA effects

34
Q

What causes the side effect: GI ulceration and bleeding

A

NSAID inhibition of COX1 in gastric cells (they normally constitutively secrete protective things in response to prostaglandin presence)

35
Q

What causes the side effect: Increased bleeding risk

A

NSAID inhibition of COX1 in platelets (normally a constitutive production of TXA2 to help platelet aggregation). This is why you need to be careful if patients are already under pharmacological intervention for platelet aggregation

36
Q

What causes the side effect: Renal dysfunction/insufficiency

A

NSAID inhibition of COX1 and COX2 in kidney cells (normally there is vasodilator presence in the prostaglandins both constitutively and induced. when you inhibit the kidney’s ability to vasodilate you get reduced blood flow and reduced renal function)

37
Q

What causes the side effect: Delay labor (birthing)

A

COX2 inhibition in uterine smooth muscle cells

38
Q

What causes the side effect: Increased Thromboses (clotting and MI and stroke)

A

COX2 inhibition in endothelial cells

39
Q

platelets will, by nature, make what kind of prostaglandin?

A

Thromboxane A2 (TXA2), a product of constitutive COX1 action and used to promote clotting

40
Q

Endothelial cells will, by nature, make what kind of prostaglandin?

A

Prostacyclin (PGI2), a product of inducible COX2 and a signal to bust up clots

41
Q

What does N-acetylcysteine treatment do and what is it used for?

A

It repleneshes the appropriate level of GSH to de-toxify the hepatotoxic metabolite of acetaminophen. Used in Acetaminophen overdose situations

42
Q

Is Aspirin use effective for visceral pain?

A

NO

43
Q

Celebrex specifically inhibits what enzyme?

A

COX2 (as opposed to both COX1 and COX2). this is why it is better for GI problems, but it is more expensive (just reaching first generic phase)

44
Q

A low dose of Aspirin taken chronically is designed to do what?

A

antiplatelet effect, protect from clotting disorders, use in high risk CVD patients

45
Q

Aspirin’s effect on COX1 and COX2

A

irreversibly inhibits BOTH, but at low doses is selective for COX1 (that’s why it’s used for anti-platelet activity at low doses chronically)

46
Q

Aspirin’s effect on COX2 in the periphery

A

at high enough doses Aspirin can irreversibly inhibit COX2 so it is an analgesic

47
Q

Does Aspirin have antipyretic activity (work on COX2 in CNS)

A

Yes

48
Q

Does aspirin have an anti-inflammatory role and why?

A

Yes, it inhibits COX2 at the site of injury

49
Q

The other NSAIDs are as good as or better than aspirin at all therapeutic uses EXCEPT

A

anti-platelet activity at low doses. Selective for COX1 inhibition at low doses

50
Q

tNSAIDs have what effect on COX1 and COX2?

A

They all are reversible inhibitors of both enzymes, though depending on the agent they prefer one or the other (ibuprofen has a little more COX1 than 2, Naproxen has much more COX1 than 2, etc.

51
Q

do tNSAIDs have COX1 anti-platelet activity at low doses?

A

…yes…but NOT REALLY. ASA has the best selectivity for COX1 at low doses and is the best at fighting platelet aggregation

52
Q

Does Acetominophen have anti-inflammatory activity?

A

NOPE. It reversibly inhibits COX2 in the CNS, and does NOT work in the periphery

53
Q

You want to fight fever and pain without having ANY periphery side effects. What do you use?

A

Acetominophen. Has no periphery activity but fights fever and pain by reversibly inhibiting COX2 in CNS

54
Q

What are the important adverse effects of aspirin

A

GI upset, increased bleeding, decreased renal function, decreased labor contractions (JUST DOESN’T INCREASE CLOTTING RISK)

55
Q

what are the important adverse effects of tNSAIDs?

A

GI upset, increased bleeding, decreased kidney function, decreased labor contration (doesn’t really increase clotting risk)

56
Q

what are the important adverse effects of Acetaminophen

A

mostly hepatoxicity due to overdose. It doesn’t have the effects in the periphery that tNSAIDs do

57
Q

What are some important contraindications for Celebrex (or any COX2 specific drug) use?

A

Chronic Renal insufficiency, high risk of CVD, severe heart disease, volume depletion, hepatic failure (drug is metabolizyed by CYP enzyme)

58
Q

At what does does Acetominophen hit it’s ceiling of efficacy?

A

1000mg. Above that you just get risks with no additional benefit. If it doesn’t work at this dose you need another pain med

59
Q

what do you worry about in an alcoholic that’s been taking tylenol for pain?

A

Alchohol induces CYP2E1 to make the hepatotoxic metabolite of Acetominophen (strike one), it also reduces GSH levels (strike two), and there is another strike I don’t know about. BUT YOU WORRY HEPATOXICITY, METABOLIC ACIDOSIS, COMA

NSAIDs (2 decks)

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