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Clinical Medicine > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What is Rheumatoid arthritis?

A
  1. Systemic disease
  2. Autoimmune (unknown trigger)
  3. Inflammatory polyarthritis (multiple joints)
  4. Can erode and destroy the articular cartilage
  5. Effects are not limited to joints
    *can effect almost any organ system and range from mild to serious
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2
Q

What is the demographic of RA?

A
  1. More common in women (3:1)
  2. Prevalence increases with age (onset in late 40s and early 50s women, common between 20-40yoa
  3. Human leukocyte antigen (HLA)-DR4
    *genetic risk factor
    *more serious, seropositive disease
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3
Q

What is the patho physiology of RA?

A
  1. Synovial pannus (extra growth in your joints)
    *Proliferative synovial with mononuclear cells (monocytes and T lymphocytes)
  2. Pannus invades at bone-cartilage-synovial interface
    *will be destruction of bone and cartilage
    *marginal bony erosions on radiographs
  3. RA nodules
    *active inflammation
    *granulomas with central necrosis
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4
Q

What are the clinical symptoms of RA?

A
  1. Symptoms must be present for at least 6 weeks
  2. Pain, morning stiffness (> 30 mins, sometimes hours), swelling, systemic symptoms are common
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5
Q

When is anti-CCP (anti-cyclic citrullinated peptide) antibodies used?

A

Testing for RA
*More specific for RA than RF, but less sensitive

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6
Q

What could RA cause?

A

Felty’s syndrome
1. Splenomegaly
2. Neutropenia (leukopenia, low WBC)
3. Recurrent (pulmonary) infections common
*Common with RA with severe destructive arthritis

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7
Q

What are some clinic symptoms of RA?

A
  1. Joint symptoms predominate
    *vague periarticular pain and/or stiffness is common initially
  2. With increasing severity, multiple joints affected in the UE and LE
  3. May have spinal (cervical involvement)
    *Neck pain, stiffness
    *c1-c2 subluxation and spinal cord compression
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8
Q

What are some common physical exam findings for RA?

A
  1. Joint contractures (Decreases ROM cannot push passed the point)
  2. Joint effusions
  3. Joint deformity
  4. Painful motion
  5. Hand stiffness and swelling (PIP most common)
  6. Carpal tunnel syndrome
  7. RA nodules (extensor area of arm most common)
  8. Evidence of tendon rupture
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9
Q

What ways could the hand be positioned with RA?

A
  1. Ulnar drift
  2. Knuckle subluxation
  3. Wrist subluxation
  4. Finger swan neck
  5. Finger boutonnière
  6. Z-shaped thumb
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10
Q

What are RA nodules?

A

Happen over bony prominences, bursae, and tendon sheaths
*correlate with seropositivity (presence of Rf in serum)

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11
Q

What is the diagnosis criteria for RA?

A
  1. Periarticular morning stiffness lasts at least an hour
  2. Arthritis of 3 or more joints
  3. Symmetric arthritis
  4. RA nodules (Over extensor surfaces or bony prominences)
  5. Positive serum rheumatoid factor
  6. Radiographic changes
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12
Q

What is the likelihood of a positive Rf in a patient with RA?

A

Rf is elevated in over 3/4 of patients with RA
*But is NOT specific for RA
*Higher titer=more likely RA
*Rf negativity does not rule out RA

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13
Q

What other diagnostic testing is used for RA?

A

Erythrocyte sedimentation rate (ESR)
-usually elevated (proportional to disease severity)
C-reactive protein (CrP)
- Usually elevated (proportional to disease severity
CBC
- assess for anemia of chronic disease
Anti-CCP antibodies (ACPA)
- Most specific blood test for RA
- May be detected in healthy individuals years before onset of clinical RA
-Marker of erosive disease

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14
Q

If ANA (antinuclear antibodies) is negative what can that help rule out?

A

Helps exclude systemic lupus erythematosus (SLE) and other rheumatic diseases, may be + in up to 1/3 20% of RA patients

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15
Q

What will be shown on a radiograph of a patient with RA?

A
  1. Periarticular osteopenia
  2. Bony erosion at joint margin
    * at insertion of synovium
    *unequal bony decalcification (loss of calcium from the bones)
  3. Soft tissue swelling
  4. C1-C2 subluxation
  5. Joint space narrowing (wearing away of the cartilage)
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16
Q

What will happen to the platelet count and WBC count in patients with RA?

A

P: may be elevated
WBC: may be normal or minimally elevated

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17
Q

Why should you use aspiration when a patient has RA?

A

To help rule out a septic joint
*septic joint is common complication with RA

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18
Q

What is the “Joint Distribution” classification criteria for RA?

A

Large joint=0
2-10 large joints=1
1-3 small joints=2
4-10 small joints=3
>10 joints (at least one small)=5

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19
Q

What is the “Serology” classification criteria for RA?

A

Negative RF AND negative ACPA=0
Low positive Rf OR low positive ACPA=2
High positive Rf OR high positive ACPA=3

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20
Q

What is the “symptom duration” classification criteria for RA?

A

<6 weeks=0
>or equal 6 weeks=1

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21
Q

What is the “acute phase reactants” classification criteria for RA?

A

Normal CRP AND normal ESR=0
Abnormal CRP OR abnormal ESR=1

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22
Q

For the classification criteria for RA, what number is definite for RA?

A

> or equal to 6

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23
Q

What happens if the classification criteria is less than 6?

A

The patient might fulfill the criteria
1. Prospectively over time
2. Retrospectively

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24
Q

What are some adverse outcomes of RA?

A
  1. Joint contractures
  2. Pain
  3. Loss of function
  4. Loss of Ambulation
  5. Osteoporosis
  6. Multi system disorders
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25
Q

What general treatment for RA?

A
  1. Disease-modifying agents (DMARDs) (all patients will be on)
  2. Salicylates
  3. NSAIDs (not as mono therapy, use with DMARDs)
  4. Splinting (helps with pain, and deformities)
  5. Corticosteroids (use minimally)
  6. PT
  7. Custom shoes
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26
Q

If a patient has RA will bed rest be helpful?

A

No, bed rest is harmful to the patient
*moving decreases stiffness

27
Q

What was used as the original treatment for RA but is not used as much now?

A

ASA
1. Increased the dosage to the point of tinnitus, then decrease the dose
2. Increased the risk of bleeding

28
Q

How do ASA and NSAID work for RA?

A
  1. They only alleviate symptoms only
  2. They do NOT prevent erosions or alter disease progression
  3. May need a proton-pump inhibitor if GI Sxs
29
Q

What should NSAID been used with?

A

They should be used with DMARDs and not alone since they are for symptomatic relief only

30
Q

What are the side effects of NSAIDs?

A

GI side effects
*use COx-2 inhibitors and/or PPI if needed
Renal side effects
*low risk; monitor w/labs
Platelet effects
*NSAID prolong bleeding and block platelet function except COX2-inhibitors

31
Q

What is the dosage for corticosteroids?

A
  1. Prednisone 5-20mg po (try not to use daily)
    *fast acting
    *slow rate of articular erosion
    * SE often make them undesirable
    * Tapered when discontinued
    * Intra-articular helpful, should not be given >4x/yr
32
Q

What are the toxicity with corticosteroids?

A
  1. Osteoporosis
  2. Pathologic fractures (bone got so thin that it broke bc of the thinness)
  3. Avascular necrosis
  4. Skin thinning, bruising, vision changes
33
Q

What supplements should be used with corticosteroids?

A
  1. Ca++
  2. Vitamin D (w/o this can’t absorb Ca++)
  3. bisphosphonates should be added if long term therapy
    *Made for osteoporosis
34
Q

When is high dose corticosteroids used for RA?

A

For serious extra-articular manifestations

35
Q

When are intra-articular corticosteroids used?

A

Not for widespread use
*if 1-2 joints are primary complaints

36
Q

What are DMARDs/

A

“Slow acting anti rheumatic drugs” (SAARDs)

37
Q

When should DMARDs be used for RA?

A
  1. Start as soon as diagnosis of RA is made (used earlier now due to)
    *extent of disability if untreated
    *Effectiveness of the agents
    *Satisfactory safety profile
38
Q

What is Methotrexate? (DMARDs, first line for RA)

A

Immunosuppressive (shuts down inflammatory response), cytotoxic (can injure cells)

39
Q

What are the benefits of Methotrexate?

A
  1. High efficacy
  2. Relatively low toxicity/SEs compared to other medications
  3. Ease of administration- 7.5 mg orally once a week, increase to 15mg if no response after one month
  4. Most rapid onset of action of the DMARDs
40
Q

What are the toxicities of Methotrexate?

A
  1. Hematologic (cytopenia due to bone marrow suppression)
  2. Pulmonary
  3. Hepatic (small risk of cirrhosis); increased with alcohol use
  4. High potential for teratogenicity
  5. Gastric irritation and stomatitis
41
Q

What should be avoided and monitored with Methotrexate?

A
  1. Monitor with liver function tests and CBC Q 12 weeks
  2. Avoid alcohol use (liver)
  3. Consider giving folate
  4. Avoid with any form of chronic hepatitis
42
Q

What is the RA treatment algorithm?

A
  1. Initially Methotrexate mono therapy unless contraindication
  2. No response to MTX, and a (low) second DMARD
  3. Residual disease activity is
    *mild, add non-biological
    *moderate, add non-biological or biological
    *severe, add targeted therapy
43
Q

What is Sulfasalazine?

A

Initiated second-line after attempt with methotrexate
1. DO not use if ASA sensitivity
2. Glucose 6-phosphate dehydrogenase (G6PD) level check before tx

44
Q

What can sulfasalazine cause if there is a G6PD deficiency?

A

Can cause hemolysis (breakdown of blood cells)

45
Q

What is the dosage of sulfasalzine?

A

0.5g orally BID, increase weekly until improvement or reach 3g

46
Q

What are the side effects of sulfasalazine?

A
  1. Neutropenia
  2. Thrombocytopenia
    *Monitor with CBC Q 3 months (2-4 weeks for first 3 months)
47
Q

What is Leflunomide?

A
  1. Primitive synthesis inhibitor
  2. Carcinogenic and teratogenic
  3. Half-life of 2 weeks
  4. Contraindicated in premenopausal women and in men who wish to father children
48
Q

What is the wash-out method for Leflunomide?

A

Use cholestyramine for 11 days, may need contraception for up to two years if opted not to have wash-out tx

49
Q

What are the SE of Leflunomide?

A
  1. Diarrhea
  2. Rash
  3. Reversible alopecia
  4. Hepatotoxicity
  5. Weight loss
50
Q

What is plaquenil/ hydroxychloroquine?

A

An anti-malarial drug
1. Lowest in toxicity of the DMARDs
2. Less effective for severe disease (used for mild RA)
3. May cause macular damage
*retina exam annually is necessary

51
Q

What is Tofacitinib? (least common)

A

Inhibit Janus Kinase (JAK) 3
1. Oral, quick onset
2. Effective as mono therapy or in combination with MTX or another DMARD
3. Used for severe RA

52
Q

What is the dosage for Tofacitinib?

A

5-10mg twice daily

53
Q

If someone is prescribe for Tofacitinib what should they be screened for?

A

Latent TB prior to tx

54
Q

What are the biologic DMARDs

A

Usually added to or started with methotrexate
1. Etanercept (Enbrel)
2. Infliximab (Remicade)
3. Adalimumab (Humira)
4. Abatacept (Orencia)
5. Rituximab (Rituxan)
6. Tocilizumab (Actemra)

55
Q

How does Etanercept (Enbrel) work?

A
  1. Inhibit the action of TNF-A
  2. Increases the risk for serious infections (especially TB)
56
Q

How does Infliximab (Remicade) work?

A
  1. Anti-TNF antibody
57
Q

How does Adalimumab (Humira) work?

A
  1. Recombinant monoclonal antibody that binds to TNF receptor site
58
Q

When is Abatacept (Orencia), Rituximab (Rituxan), Tocilizumab (Actemra) used?

A

A: helps with 1/2 of patients still symptomatic with methotrexate and TNFi (tissue necrosis face inhibitor)
R: used with methotrexate if no response to TNFi
T: used with methotrexate if no response to TNFi

59
Q

When should combinations of DMARDs be used?

A
  1. Used after failure of single agents
  2. Methotrexate and a TNF inhibitor is the most common combination
60
Q

Is it okay to combine two biologics DMARDs

A

No, it can increase the risk of cancer and immunosuppressant

61
Q

What is the prognosis of RA?

A

Around 50% of individuals are disabled within 5 years of diagnosis becoming longer with increased treatment
*due to joint deformities

62
Q

What are the 2 most important factors leading to a poor RA prognosis?

A
  1. Delay in diagnosis
  2. Delay in initiating treatment with DMARDs
63
Q

When should you refer to a specialist?

A
  1. Persistent symptoms greater than 3 months
  2. Uncontrollable pain at rest
  3. Joint deformity
  4. Foot deformities not responding to custom shoes
  5. Extra-articular findings
    *Do not delay in referring to a rheumatologist
64
Q

What is the RADx5?

A

Usually ordered at large centers
Have two 2 traditional treatments and 3 new treatments
*the more positive increases the likelihood of RA

Clinical Medicine (164 decks)

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