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Rheum/Musculoskeletal/Derm Week 1 > NSAIDs > Flashcards

NSAIDs Flashcards

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Dermatology Board Prep flashcards
1
Q

What are the drug classes for treatment for RA?

A
  • NSAIDs
  • DMARDs
  • Biological Agents

Note that both classical and biological DMARDs possess the ability to slow progression of the disease process, an attribute that is not evident with NSAIDs.

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2
Q

Is acetaminophen (tylenol) used for RA?

A

No, even though it is an NSAID, it provides no anti-inflammatory
action (only relief of pain and fever)

Doesn’t change course of disease

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3
Q

What NSAIDs can be used for RA?

A
  • Aspirin (acetyl-salicyclic acid)
  • Ibuprofen (Motrin, Advil)
  • Celecoxib (Celebrex)
  • Naproxen, Ketoprofen, Piroxicam
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4
Q

What is unique about Celecoxib?

A

Cox-2 specific drug

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5
Q

T or F. NSAID action on COX is reversible

A

T, except in aspirin

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6
Q

What is different between expression of COX-1 and COX-2?

A

COX-1 is constitutive and COX-2 is inducible

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7
Q

How are most NSAIDs metabolized?

A

extensive hepatic metabolism with predominant elimination in the urine and some in feces

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8
Q

What NSAID is noticably metabolized differently?

A

Ketorolac (58% unchanged in urine) and little in feces

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9
Q

What prostaglandin in particular is involved in activation of inflammatory cells?

A

PGE2.

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10
Q

What happens following tissue damage?

A

mast cells and macrophages are activated and some blood-borne immune cells, including neutrophils may be recruited. Various immune mediators, such as TNF-a, IL-1B, IL-6, and others are released which exert their allegoric effects by a ting directly on nociceptors or indirectly through the release of prostanoids

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11
Q

What are the effects of COX-2 inhibition?

A
  • anti-inflammatory
  • analgesic
  • antipyretic
  • increased BP
  • reduced urinary PGI2 metabolites

thus, these effects are seen in ALL NSAIDs

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12
Q

What are the effects of COX-1 inhibition?

A
  • reduce urinary TXA2

- inhibit platelet activity and increase bleeding time

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13
Q

GI toxicity is related to inhibition of which COX enzyme?

A

possibly both

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14
Q

What ‘traditional’ NSAIDs have a propensity for COX-2 over COX-1?

A

etodolac

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15
Q

What ‘traditional’ NSAIDs have a propensity for COX-1 over COX-2?

A

ketorolac

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16
Q

How does chronic NSAID consumption lead to gastric damage and bleeding?

A

Not only is there direct chemical irritation of the mucosal tissue but the inhibition of PGE2 interrupts essential cytoprotective mechanisms in the stomach involving mucus secretion, bicarbonate release and the initiation of essential repair processes in underlying tissue.

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17
Q

What are some risk factors for GI bleeding with NSAIDs?

A
  • older age (risk doubles ever decade over 55)
  • male sex
  • CV disease, HTN, diabetes, hepatic or renal impairment
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18
Q

Other risk factors for GI bleeding with NSAIDs?

A
  • helicobacter pylori infection
  • excessive alcohol use
  • heavy smoking
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19
Q

What concurrent meds can increase risk of GI bleed with NSAIDs?

A
  • aspirin
  • warfarin
  • oral corticosteroids
  • SSRIs
  • venlafaxine or duloxetine
20
Q

What are some ways to reduce GI bleed risk with NSAIDs?

A
  • enteric coating (doesn’t eliminate)
  • MAYBE advocate taking NSAIDs on an empty stomach to achieve faster onset of action and avoid ‘extra’ doses because relief isn’t met fast enough by the patient
21
Q

Other ways to reduce GI bleed risk with NSAIDs?

A

-COX-2
-co-administer prostaglandin analogue misoprostol, or more usually these days an H2 receptor antagonist or proton pump inhibitor.
-

22
Q

What is the benefit of PPIs with NSAIDs?

A

possesses superior effectiveness due to the more complete suppression of acid
secretion, a mechanism-based issue (just as good as a COX-2)

23
Q

What should be considered when giving a PPI with an NSAID?

A

-PPIs can alter the efficacy of concurrent drugs that rely on stomach acidity for absorption

24
Q

Contraindications of PPIs?

A

concurrent with cloidogrel

25
Q

What NSAID will not change the balance between TXA2 and PGI2, and thus lower CV exacerbation risk?

A

ibuprofen because it doesn’t have an increased affinity for COX-1 or COX-2

26
Q

What is another potential thing to consider with a COX-2 inhibitor?

A

promotes shift toward TXA2 production from COX-1 and thus a pro-thrombotic state

27
Q

T or F. High doses of ibuprofen is associated with increased risk of vascular events

A

T. Even though it is COX neutral.

28
Q

High dose of what NSAID is not associated with increased CV related (thrombo-forming) risk?

A

Naproxen

29
Q

What is the major difference between NSAIDs and aspirin?

A

aspirin irreversibly inhibits the COX enzyme by acetylating it.

30
Q

DD interaction of aspirin?

A

There is a real potential for concurrent administration of NSAIDs to inhibit the ability of low-dose aspirin to reach its binding site in the platelet and to provide irreversible enzyme inhibition in prophylaxis of MI.

Since the traditional NSAID action is reversible, there is a potential for antiplatelet activity to be lost and increased cardiovascular risk to occur.

31
Q

Which NSAID has the highest risk of hepatotoxicity?

A

Sulindac (via hypersensitivity mechanism)

32
Q

What is the role of PGE2 and PGI2 at the kidneys?

A

Prostaglandin I2 and E2 play an important role in micro-regulation of perfusion in renal tissue, most especially in abnormal “stress” situations where they help to maintain GFR.

and NSAIDS can block this!!*

33
Q

What is the effect of chronic NSAID use by blocking PGE2 and PGI2?

A

reversible renal ischemia, reduced glomerular hydraulic pressure and reduced GFR

34
Q

NSAIDs decrease the clearance of what drugs?

A

lithium and methotrexate

35
Q

T or F. NSAIDs can
antagonize the effects of
uricosuric agents.

A

T.

36
Q

Recommended patient monitoring with chronic NSAID use

A
  • LFTs
  • Serum creatinine/BUN
  • Stool guaiac
  • CBC
37
Q

Why get CBC with chronic NSAID use?

A

NSAIDs can rarely cause various blood dyscrasia

38
Q

Chronic aspirin therapy may warrant monitoring of _______

A

serum salicylate

39
Q

What does overdose of salicylate cause?

A

capable of passing across the BBB where it stimulates the respiratory centre, resulting in respiratory alkalosis.

The metabolite also disrupts intermediary metabolism contributing to metabolic acidosis.

The picture is thus one of a mixed alkalosis/acidosis phenomenon;

40
Q

How does salicylate overdose cause metabolic acidosis?

A

it causes uncoupling of oxidative phosphorylation and interruption of glucose and fatty acid metabolism

41
Q

Death in salicylate overdose is most commonly due to what?

A

cerebral and pulmonary edema (via increased capillary permeability) lead to ultimate demise if the patient is not decontaminated.

42
Q

Which NSAIDs should be avoided in elderly?

A
  • Indomethacin (worst bleed risk)
  • Ketorolac

all others should consider giving a PPI or misoprostol too

43
Q

T or F. Acetaminophen (tylenol) has no peripheral action

A

T. Not anti-inflammatory (not an NSAID)

44
Q

Acetaminophen (Tylenol) is most often associated with what AE?

A

acute hepatic failure

45
Q

Why not add a prostaglandin antagonist with chronic NSAID use?

A

not as effective (short duration of action)- PPIs are irreversible which is why they are so effective

46
Q

Which NSAID has the lowest CV risk?

A

Naproxen

47
Q

T or F. GCs can cause hyperlipidemia

A

T. As well as hyperglycemia

Rheum/Musculoskeletal/Derm Week 1 (25 decks)

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