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Derm Rheum > NSAIDs and DMARDs - Sweatman > Flashcards

NSAIDs and DMARDs - Sweatman Flashcards

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1
Q

How do NSAIDs exert their analgesic effect?

A

Prevent release of inflammatory cytokines that act on nociceptors to cause pain

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2
Q

How do NSAIDs cause gastric ulcers?

A

Blocking PGE2 synthesis causes decreased mucous production and bicarbonate release and increases proton secretion
Decreases the protective effect of PGE2 on mucosal lining

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3
Q

What are some of the risk factors of adverse GI events with NSAID use?

A

1) Older age
2) Male
3) Use of maximum dose
4) Excessive alcohol use
5) Heavy smoking
6) Prolonged NSAID use

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4
Q

Which NSAID has the highest and lowest relative risk of adverse GI events?

A

Diclofenac has lowest, ibuprofen and naproxen have highest

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5
Q

Why are older patients at risk for increased CV risk with NSAID use?

A

Old people take low-dose prophylactic aspirin which irreversibly inhibits platelets –> giving NSAIDs will block the action of aspirin, this increasing risk for MI

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6
Q

All NSAIDs fuck up your liver. Which one is the worst?

A

Sulindac

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7
Q

Why is renal toxicity a concern with NSAID use?

A

Blocks PGI2 & PGE2, which are needed to control renal perfusion during abnormal conditions

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8
Q

What should you monitor in patients chronically on NSAIDs?

A

LFTs and CBCs –> hepatotoxicity and blood dyscrasias may occur

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9
Q

Why is salicylate poisoning a big concern with aspirin use?

A

Cerebral and pulmonary edema can kill the patient –> must decontaminate/provide support

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10
Q

What is the biggest concern in giving NSAIDs to old ass people?

A

GI bleeds and peptic ulcers

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11
Q

Why is acetaminophen the “special kid” of the NSAIDs?

A

Doesn’t have anti-inflammatory effects, only analgesia

GI problems are very rare, but overdose is a bigger problem

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12
Q

What are the bullshit NSAIDs we’re expected to memorize, not learn?

A

1) Acetaminophen
2) Aspirin
3) Diclofenac
4) Ibuprofen
5) Indomethacin
6) Ketoprofen
7) Ketorolac
8) Naproxen
9) Piroxicam
10) Sulindac
11) Celecoxib

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13
Q

What is the first line treatment of rheumatoid arthritis?

A

Methotrexate + NSAID + corticosteroids

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14
Q

What DMARD is used in milder cases of rheumatoid arthritis other than methotrexate?

A

Hydroxychloroquine –> fewer side effects

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15
Q

By what mechanism does methotrexate induce immunosuppression?

A

Increased adenosine inhibits lymphocyte proliferation –> suppresses secretion of IL-1, INF-gamma, and TNF

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16
Q

What unique metabolism does methotrexate undergo?

A

Polyglutamation keeps the drug intracellularly

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17
Q

What is the biggest adverse effect/concern with methotrexate administration?

A

Bone marrow suppression

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18
Q

What does methotrexate do to the lungs?

A

Interstitial pneumonitis and pulmonary fibrosis –> must monitor pt lung function

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19
Q

What is the mechanism of action of sulfasalazine?

A

Metabolized to sulfapyridine and mesalamine by bacteria in colon –> mesalamine inhibits prostaglandin and leukotriene production

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20
Q

What major allergy should you be careful of with sulfasalazine?

A

Sulfa allergy –> previous bad reaction to salicylate or sulfonamide drugs

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21
Q

What is the mechanism of action of leflunomide?

A

Inhibits dihydroorotate dehydrogenase –> blocks de novo pyrimidine synthesis in T and B cells

Also produces a uricosuric effect from metabolite

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22
Q

What are some of the cautions associated with leflunomide use?

A

Elevated LFT’s –> don’t drink booze with it
Category X drug
Can’t be used in patients with immune suppression or infections

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23
Q

What is the mechanism of action of hydroxychloroquine?

A

Increases intracellular vacuole pH –> antigenic peptides aren’t digested and MHC II proteins aren’t properly assembled –> CD4+ cells not stimulated

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24
Q

What are the major toxicities associated with hydroxychloroquine?

A

1) Concentrates in liver –> hepatotoxicity
2) Blood dyscrasia and CNS toxicity
3) Can cause corneal opacities, keratopathy, or retinopathy –> DO NOT USE IN OCULAR DISEASES

25
Q

What are the monitoring parameters for methotrexate?

A

1) CBCs with differential
2) LFTs
3) Serum creatinine/BUN
4) Serum uric acid
5) Pregnancy testing (category X)

26
Q

What are the monitoring parameters for sulfasalazine?

A

1) CBCs with differential
2) LFTs
3) Serum creatinine/BUN
4) Urinalysis –> assess renal function regularly

27
Q

What are the monitoring parameters for leflunomide?

A

1) CBCs with differential
2) LFTs
3) Pregnancy test (category X)
4) Serum electrolytes - causes diarrhea, hypokalemia, hypocalcemia

28
Q

What are the monitoring parameters for hydroxychloroquine?

A

1) CBCs

2) Opthalmologic exam

29
Q

Which non-biogical DMARDs do you have to check CBC on?

A

All of them: methotrexate, sulfasalazine, leflunomide, hydroxycholorquine

30
Q

Which non-biological DMARDs do you have to to check LFTs on?

A

Methotrexate, sulfasalazine, leflunomide –> all except hydroxycholoroquine

31
Q

Which non-biological DMARDs do you have to check serum creatinine/BUN?

A

Methotrexate and sulfasalazine?

32
Q

Why do you have to give an opthalmalogic exam with hydroxycholorquine?

A

Can cause corneal opacity, keratopathy, and retinopathy –> pts slowly lose vision

33
Q

What are the beneficial effects of giving corticosteroids?

A

NF-kb expression decreased –> decreased production of TNF-a, IL-1, IL-5

34
Q

What are the major bad effects of giving corticosteroids chronically?

A

Increased RANK-L and MCF expression –> glucocorticoid induced osteoporosis –> initial increase in respiration and then decreased formation

35
Q

What should be given with glucocorticoids to prevent osteoporosis?

A

Bisphosphonates, VitD, Ca2+

36
Q

RA patients are at 2x greater risk for CV events. Why?

A

Chronic inflammatory condition and drugs used to treat (especially glucocorticoids–>obesity, accelerated atherosclerosis)

37
Q

What steroids are best for intra-articular injection?

A

The less water soluble ones –> Triamcinolone, methylprednisone, betamethasone –> stay in joint space

38
Q

What should you monitor in a patient on chronic glucocorticoid therapy?

A

1) Blood sugar
2) Bone mass
3) Glaucoma
4) Edema

39
Q

What are the biological DMARDs (there are 9)?

A

1) Abatacept –> CTLA4/IgG1 Fc fusion protein
2) Adalimumab –> TNF-a antibody
3) Anakinra –>IL-1 receptor antagonist
4) Certolizumab –>TNF-a antibody Fab fragment
5) Etanercept –> TNF receptor linked to IgG
6) Golimumab –> TNF-a antibody
7) Infliximab –> IgG1k against TNF-a
8) Rituximab –> IgG1k against CD20
9) Toclizumab –> IL-6 receptor antibody

40
Q

What is the mechanism of action of abatacept?

A

Binds CD80 and CD86 –> prevents T cell co-stimulatory signal

41
Q

What is the mechanism of action of adalimumab?

A

Binds TNF-a preventing interaction with p55 and p75 cell receptors

42
Q

What is the mechanism of action of anakinra?

A

Competitively inhibits IL-1a and IL-1b binding to IL-1 type 1 receptor

43
Q

What is the mechanism of action of certolizumab?

A

TNF-a antibody that neutralizes membrane-bound and soluble TNF-a

44
Q

What is the mechanism of action of etanercept?

A

Soluble TNF-a receptor/antibody fusion protein

Binds to and inactivates circulating TNF –> does not affect production or serum levels

45
Q

What is the mechanism of action of golimumab?

A

Binds and neutralizes soluble and membrane-bound TNF-a

46
Q

What is the mechanism of action of infliximab?

A

Binds and neutralizes soluble and membrane-bound TNF-a

47
Q

What is the mechanism of action of rituximab?

A

Binds CD20 and recruit immune cells to induce B cell apoptosis

48
Q

What is the mechanism of action of toclizumab?

A

Binds soluble and membrane-bound IL-6 receptors to inhibit signaling

49
Q

What is the biggest side effect/problem associated with using the biological DMARDs?

A

Immunosuppression –> increased susceptibility to bacterial, fungal, and parasitic infection
May have increased likelihood of malignancy

50
Q

Which biological DMARDs are associated with CHF or hypotension/angina/dysrhythmia?

A

1) Rituximab
2) Adalimumab
3) Infliximab
4) Golimumab

51
Q

Which biological DMARDs are associated with causing a lupus-like syndrome (arthralgia, myalgia, fatigue, skin rash)?

A

1) Adalimumab
2) Certolizumab
3) Etanercept
4) Infliximab

52
Q

Which biological DMARD is associated with Steven-Johnson syndrome?

A

Rituximab

53
Q

Why must women taking rituximab be on contraception?

A

Can cross placenta and deplete B-cells in fetus

54
Q

Which biological DMARDs are associated with blood dycrasias?

A

1) Anakinra
2) Certolizumab
3) Rituximab
4) Tocilizumab

55
Q

Which biological DMARDs should you monitor LFT for?

A

1) Golimumab
2) Infliximab
3) Tocilizumab

56
Q

Which biological DMARD should you get a serum lipid profile for?

A

Toclizumab

57
Q

Which drugs should you counsel the patient to rotate the site of injection?

A

1) Abatacept
2) Adalimumab
3) Anakinra
4) Certolizumab
5) Etanercept
6) Golimumab

58
Q

Which biological DMARD is approved for use in psoriatic arthritis and plaque psoriasis?

A

Apremilast –> orally active PDE4 inhibitor that reduces pro-inflammatory mediators

59
Q

What are major adverse effects you should watch for in patients taking apremilast?

A

Weight loss and depression

Derm Rheum (39 decks)

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