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Fall 2024 > Therapeutics Exam 4 (Rheumatoid Arthritis) > Flashcards

Therapeutics Exam 4 (Rheumatoid Arthritis) Flashcards

1
Q

Does rheumatoid arthritis have symmetrical join involvement?

A

Yes

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2
Q

What kind of disease is rheumatoid arthritis?

A

chronic, inflammatory

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3
Q

At what age does onset of rheumatoid arthritis typically occur?

A

30-50

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4
Q

What are the 2 genetic tests that can be conducted for RA?

A

Major Histocompatibility Complex (MHC) Typing

Human Lymphocyte Antigen (HLA)

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5
Q

How does joint destruction occur in RA?

A

The synovial membrane is infiltrated with inflammatory cells that release cytokines
-this leads to cell proliferation and death

A Pannus forms (inflamed proliferating synovia) and invades into healthy cartilage and bone which destroys the joint

*This is a systemic inflammatory disease with an inflammatory response

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6
Q

What does the progression of RA over time look like?

A

-Inflammation declines over the course of the disease
-Disability increases over the course of the disease as the bone erodes

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7
Q

A score of what regarding the diagnostic criteria is used to diagnose RA?

A

6 or more

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8
Q

What are the most commonly affected joints in RA?

A

*Hands (MCP and PIP joints)
Wrists
*Feet

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9
Q

How does the location of RA differentiate it from OA?

A

RA is more common in the hands and feet

OA is more common in the hips, knees, and hands

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10
Q

What are the extra-articular manifestations of RA?

A

-Rheumatoid nodules
-Vasculitis
-Pulmonary
-Ocular
-Cardiac
-Felty’s

*note that these cover about every system we have because this is a systemic inflammatory disease

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11
Q

Where are rheumatoid nodules most likely to appear?

A

Hands
Elbows
Forearms

pressure points

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12
Q

When do we want to intervene with rheumatoid nodules?

A

Only if the patient is symptomatic!

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13
Q

What is vasculitis?

A

Inflammation of small, superficial blood vessels

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14
Q

What is the biggest concern with vasculitis in RA?

A

Infarction could lead to Necrosis!

-also associated with stasis ulcers

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15
Q

What pulmonary effects can the inflammation from RA have?

A

-Pleural effusions
-Pulmonary fibrosis
-Nodules

Rare: interstitial pneumonitis or arteritis (inflammation of arteries and lungs)

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16
Q

What ocular effects can RA have?

A

Keratoconjunctivitis sicca
-itchy, dry eyes, + inflammation

-when these symptoms are present it is called “Sjogren’s syndrome”

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17
Q

What cardiac effects can RA have?

A

-Increased risk of CV mortality
-Pericarditis
-Conduction abnormalities

Rare: myocarditis

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18
Q

What is Felty’s syndrome?

A

Combination of 3 conditions:
-Splenomegaly
-Neutropenia
-RA

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19
Q

The lab value Erythrocyte Sedimentation Rate (ESR) can be used to diagnose RA, what level is used to diagnose?

A

Normal: 0-20

Elevated Diagnostic: >20

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20
Q

The lab value C-Reactive Protein (CRP) can be used to diagnose RA, what level is used to diagnose?

A

Normal: 0-0.5

Elevated Diagnostic: >0.05

*note that >10 can indicate bacterial infection

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21
Q

What is the hallmark diagnostic criteria for RA?

A

Rheumatoid Factor (RF)

-antibody specific for IgM
*not all patients with RA are RF+ but majority are

-reported as a titer and the higher the titer, the poorer the prognosis

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22
Q

What is a hallmark way to diagnose RA?

A

Radiographic changes
-joint space narrowing
-bone erosion

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23
Q

What are the adjunct treatments used in RA (never used alone)?

A

NSAIDs
Corticosteroids

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24
Q

What are the disease modifying agents in RA?

A

DMARDs
Biologic Agents (Anti-TNF)
Biologic Agents (Non-TNF)

*these cannot cure the disease but can prevent further progression

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25
Q

What is the role of NSAIDs in RA?

A

Reduce pain, swelling, and stiffness

*Do not alter disease progression (use in combo with disease modifying agents)

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26
Q

Which NSAIDs cannot be used in sulfa allergy?

A

Celebrex
Sulfasalazine

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27
Q

What is the role of corticosteroids in RA?

A

Anti-inflammatory + Immunosuppressive

*not monotherapy

*use in acute flares! and patients with extraarticular manifestations

-Bridge therapy: In combo with DMARD while waiting for onset of action

-Long term/Low dose: for advanced disease or difficult to treat cases

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28
Q

How do we dose corticosteroids in RA?

A

Physiological dose

Low Dose: <10mg/day prednisone
High Dose: 10mg/day - 60 mg/day
Short-Term: < 3 months of therapy

Injections:
Do not use > every 2-3 months

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29
Q

*What are the short-term adverse effects of corticosteroids?

A

Hyperglycemia
Gastritis
Mood Changes
Elevated BP

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30
Q

*What are the long-term adverse effects of corticosteroids?

A

Aseptic Necrosis
Cataracts
Obesity
Growth Failure
HPA suppression
Osteoporosis

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31
Q

What do we monitor with corticosteroids?

A

BP
Blood glucose (hyperglycemia)

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32
Q

What does DMARD stand for?

A

Disease Modifying Anti-Rheumatic Drug

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33
Q

What are the 3 main considerations with DMARDs?

A

-Will potentially decrease/prevent joint damage and preserve joint integrity

-Timing of initiation is critical (need to start immediately upon diagnosis)

-Onset of action is delayed (6 mo)

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34
Q

What are the 4 traditional DMARDs used?

A

Methotrexate**
Sulfasalazine
Leflunomide
Hydroxychloroquine

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35
Q

What is the DMARD of choice for RA treatment?

A

Methotrexate

36
Q

How do we dose methotrexate?

A

7.5 mg per WEEK po or IM

*up to 15-20mg weekly

-dose taken once weekly

37
Q

What are the adverse effects of methotrexate?

A

Bone marrow suppression*

-GI symptoms are what patients struggle with most-
N/V/D*
Stomatitis/Mucositis*

Hepatic (cirrhosis, hepatitis, fibrosis)

Pulmonary (pneumonitis, fibrosis)

Dermatitis (rash, urticaria, alopecia)

Teratogenic!

38
Q

What can be done to reduce symptoms with methotrexate?

A

Give 1mg/day of folic acid

*especially for GI symptoms

39
Q

When is methotrexate contraindicated?

A

-Pregnancy/ Nursing
-Chronic liver disease (EtOH abuse)
-Immunodeficiency
-Blood dyscrasias
-Pleural/Peritoneal effusions
-Leukopenia/Thrombocytopenia
-CrCl < 40

40
Q

What is an important consideration with the DMARD Leflunomide?

A

It is a prodrug

It has a long half life (14-16 days) -toxicity precaution

41
Q

How do we dose Leflunomide?

A

100 mg po x 3 days, the 20 mg daily

42
Q

What are the adverse effects of leflunomide?

A

Teratogenic
Alopecia
Increased LFTs
Diarrhea + Rash

43
Q

What do we monitor with leflunomide?

A

CBC
SCr
LFT

44
Q

What are important considerations for the DMARD sulfasalazine?

A

-Prodrug
-DO NOT USE IN SULFA ALLERGY

45
Q

How do we dose sulfasalazine?

A

500 mg po BID to TID
-can do 1 g 2-3 times daily

46
Q

What are the adverse effects of sulfasalazine?

A

N/V/D, anorexia

Photosensitivity

-more but photo is the main one

47
Q

What do we monitor with sulfasalazine?

A

CBC
SCr
LFT

48
Q

What is the role of hydroxychloroquine in DMARD therapy?

A

-Used in combination or early therapy
-Less efficacious than others

49
Q

What are the adverse effects of hydroxychloroquine?

A

Retinal Toxicity
-N/V/D
-Increase skin pigment, rash alopecia

50
Q

What is a potential advantage to using hydroxychloroquine?

A

-No myelosuppression
-No hepatic or renal toxicity

51
Q

What do we monitor with hydroxychloroquine?

A

Vision exam

52
Q

What are the Biologic DMARDs used?

A

TNF Antagonists (The Neutralizers):
-Etanercept
-Infliximab
-Adalimumab
-Golimumab
-Certolizumab

53
Q

What are the precautions for using TNF-antagonist DMARDs?

A

-Infection risk

-Do not use in combo with IL-1 inhibitors or t-cell co-stimulation modulators

BLACK BOX WARNING:
-Neurologic/Demyelinating disorders
-Malignancies
-Congestive heart failure
-Hepatitis B reactivation
*do not give live vaccines

54
Q

What are the adverse effects of the neutralizers (Anti-TNF)?

A

-Headache
-Rash
-Infection risk
-Injection site reaction risk
-CHF exacerbation
-Malignancy risk
-Risk of demyelinating disease

55
Q

True or False: If a patient fails one TNF-antagonist therapy they can still use another one

A

True, they inhibit TNF in different ways

56
Q

***What is the role of Etanercept in therapy?

A

Monotherapy or Combination with methotrexate

57
Q

***How do we dose Etanercept?

A

50mg SQ once weekly

*may be difficult for patients with joint issues to self inject

58
Q

***Whit is the role of Infliximab in therapy?

A

Only to be used in combination with methotrexate

59
Q

***How do we dose Infliximab?

A

IV at 0, 2, and 6 weeks

Then every 8 weeks

60
Q

***What is the role of Adalimumab in therapy?

A

-For patients with inadequate response to one or more DMARDs

-Monotherapy or Combination

61
Q

***How do we dose Adalimumab?

A

SC every other week

If monotherapy, can use weekly

62
Q

***What is the role of Golimumab in therapy?

A

Moderate-Severe RA

Combination with methotrexate only

63
Q

***What is the dosing of Golimumab?

A

SC once monthly

64
Q

***What is the role of Certolizumab in therapy?

A

Moderate-Severe RA

Monotherapy or Combination with non-BRM DMARDs

65
Q

***What is the dosing of Certolizumab?

A

SQ at 0, 2, 4 weeks

Then every 2 or 4 weeks

66
Q

What is the IL-1 Receptor Antagonist biologic used for RA? (BMR/bDMARD)

A

Anakinra

67
Q

***What is the role of Anakinra in therapy?

A

Moderate-Severe RA in patients who failed one or more DMARDs

Monotherapy or Combination

*not in combo with TNF agents or abatacept

68
Q

***How is Anakinra dosed?

A

SC daily

*Renal adjustment: if CrCl<30, do every other day

69
Q

What do we monitor with Anakinra?

A

neutrophil count

70
Q

What is the Selective T-cell Co-stimulation Modulator used for RA? (BMR/bDMARD)

A

Abatacept

71
Q

***What is the role of Abatacept in therapy?

A

Moderate-Severe RA

-Use if inadequate response to one or more other DMARDs

-Monotherapy or Combination with DMARD (not TNF-a inhibitors or IL-1 antagoists)

72
Q

***How is abatacept dosed?

A

Weight-based

IV over 30 minutes

Dose at 0, 2, and 4 weeks then every 4 weeks

73
Q

What are the warnings associated with Abatacept?

A

Do not use with TNF antagonists or IL-1 antagonists

Increased infection risk

No live vaccines

Caution in COPD

74
Q

What are the IL-6 receptor inhibitor biologics used in RA treatment?

A

Tocilizumab
Sarilumab

75
Q

What is the role of IL-6 receptor inhibitors in therapy?

A

Moderate-Severe RA after inadequate response to one or more DMARDs

Monotherapy or Combination with MTX or other DMARDs

76
Q

How is Tocilizumab dosed?

A

IV infusion over one hour monthly

77
Q

How is Sarilumab dosed?

A

SQ every 2 weeks

78
Q

What warning is associated with IL-6 inhibitors?

A

BLACK BOX WARNING:
Infections

79
Q

What adverse effect is unique to IL-6 inhibitors?

A

Lipid Abnormalities

80
Q

What is the anti-CD20 antibody used for RA treatment?

A

Rituximab

81
Q

What is the role of Rituximab in therapy?

A

Moderate-Severe RA

Pts with inadequate response to TNF antagonists

Combination with methotrexate

*last resort

82
Q

How is Rituximab dosed?

A

Two 1g infusions separated by 2 weeks

-Can retreat every 6 months

*Must give methylprednisolone 30mins before each infusion to reduce reaction

83
Q

For which drug must you give methylprednisolone 30 minutes before an infusion to reduce the infusion reaction?

A

Rituximab

84
Q

What class of drugs is considered targeted synthetic DMARDs?

A

JAK inhibitors

85
Q

What is the role of JAK inhibitors in therapy?

A

Moderate-Severe RA after inadequate response to TNF

Alone or Combination with methotrexate or another DMARD

*do not use in combo with biologic response modifiers, azathioprine, or cyclosporine

*Newest medications, not first-line but this may change

86
Q

What are the warnings for JAK inhibitors?

A

CYP P450 interactions

Cardiovascular events

87
Q

What are the benefits of combination therapy?

A

Leads to decreased dosages which minimizes adverse effects

Can produce dramatic disease slowing

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