Rheumatoid Arthritis Flashcards

1
Q

A 37 y/o day care attendant is seen by a nurse practitioner after 4 weeks of polyarthritis of the wrists MCPs and knees. RA latex is positive. She is diagnosed with RA and started on low dose MTX. Which is true?

  1. A positive anti- CCP will confirm the diagnosis.
  2. X-ray or ultrasound may confirm the diagnosis.
  3. Treatment should always start with NSAIDs.
  4. CRP should be done before starting MTX.
  5. She probably has an alternative diagnosis.
A

She probably has an alternate Dx - parvovirus B19

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes carpal tunnel?

A

“MEDIAN TRAP”

Myxedema

Edema

Diabetes

Infiltration (sarcoid, leukemia, fibrosis)

Amyloid

Neoplasms

Trauma

RA

Acromegaly

Pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What infections should be expected for a gardner with septic joint?

A

Sporotrichosis

Nocardiosis

Blastomycosis* - decomposed wood in north central or southern US

Pantoea (Enterobacter) agglomerans - Opportunistic infection from plants and animal feces.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the ocular manifestations of RA?

A

Scleritis and potential scleromalacia perforans as isolated complication of RA or part of the Sicca Syndrome with keratoconjunctivitis sicca.

Dry eye

Sicca syndrome includes dry mouth with potential caries, test with Shermer test

scleromalacia perforans is when eye is flat, humor has run out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the cervical manifestations of RA?

A

A-A Subluxation

Erosion of odontoid process

C-spine ankylosis

With subluxation, patients tend to have C2 radiculitis and myelopathic symptoms, including extremity weakness, gait and balance problems.

+ Romberg test, with numbness in extremities

Important to measure displacement and amt of cord compression

  • anesthesia and hyperflexion of the neck indicates complete cord compression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the pulmonary manifestations of RA?

A

Cough

Dyspnea

“Cellophane crackles” – close to the ear crackles

Pulmonary fibrosis

Caplan’s syndrome (RA nodules in lungs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is Caplan’s syndrome?

A

rheumatoid pneumoconiosis, also known as Caplan’s syndrome, can occur in workers exposed to silica, as well as in patients with silicosis, coal workers’ pneumoconiosis or asbestosis.

It was originally described in coal workers with pneumoconiosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where can rheumatoid nodules present? What do they mean, and are more likely to have?

A

Rheumatoid nodules

  • in skin, sclera, lungs

Often mean RF seropositivity

  • more likely to have vasculitis and anti-CCP Ab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In addition to rheumatoid nodules, what skin changes are often present in RA?

A

Neutrophilic dermatosis/Sweet’s Syndrome

(Type IV/IL-8 &GM-CSF neutrophilia, overproduction of IL-8 in Th1 pathway inducing neutrophilia)

Pyoderma gangrenosum (all WBCs infiltrating skin, part of RA but also seen in CML, Crohn’s, UC, IgA myeloma)

Livedo reticularis - rheumatoid med vessel vasculitis, also seen in polyarteritis nodosa of anti-phospholipid Ab syndrome)

Small vessel vasculitis - circular purpura, RA vasculitis is most often small vessel vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What will many people with RA have on abdominal exam?

A

Felty’s Syndrome, complication of long-standing RA

SANTA:

Splenomegaly

Anemia (pale, hypochromic red cells)

Neutropenia Nodules

Thrombocytopenia

Arthritis - RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Explain the classification criteria for Dx of RA.

A

2010 Classification criteria for RA diagnosis:

6 out of 10 = RA

  1. Number and site of involved joints: 1-5 points

2 to 10 large joints = 1 point

1 to 3 small joints = 2 points

4-10 small joints = 3 points

> 10 joints (including at least one small joint) = 5 points

  1. Serological abnormality (RF or Anti-CCP): 2-3 points

Low positive (above the upper limit of normal, ULN) = 2 points

High positive (greater than 3 times the ULN) = 3 points

  1. Elevated acute phase response (ESR, C-RP): 1 point (above the ULN = 1 point)
  2. Symptom duration: 1 point

(at least six weeks = 1 point)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the newer biomarkers in RA?

A

14-3-3η (eta)

Multibiomarker Disease Acticity (MBDA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is 14-3-3η? What is the usefulness when Dx’ing RA?

A

14-3-3η involved in the regulation of protein phosphorylation and mitogen-activated protein kinase pathways. It can help to diagnose early RA when CRP is negative, most specific test.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the MBDA biomarker in RA Dx? What is it helpful with?

A

Multibiomarker Disease Acticity (MBDA). Includes IL-6, TNKr type 1, VCAM 1, EGF, VEGF-A, etc*.

ie.YKL-40, matrix metalloproteinase-1, MMP-3, CRP, SAA, leptin, resistin

High MBDA > 44 is associated with rapid radiologic progression, and response to TNFi ove triple therapy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the rheumatic diseases with a positive RF?

A

Rheumatic diseases with positive (> 50%) RF:

Cryoglobulinemia*

Sjogrens

RA

MCTD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the non-rheumatic diseases with positve RF?

A

Non-rheumatic diseases with positive RF:

Infections – parasites, leprosy, SBE*, virus (Hep C)

Lung diseases – silicosis, IPF

Miscellaneous - PBC

*High titer RF without rheumatic disease, Subacute Bacterial Endocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is RF?

A

Rheumatoid Factor:

anti-IgG IgG

or

anti-IgG IgM

IgM is more troublesome b/c its larger

18
Q

What is anti-CCP Ab from?

A

anti-cyclic citrullinated protein

  • inflamed joints produce cyclic citrullinated proteins from breakdown of arginine

anti-CCP Ab are initially produced against bacterial by-products

  • Porphyromonas gingivalis from oral plaque, Proteus from GU, Prevotella and Leptotrichia from GI tract
19
Q

Which individuals develop anti-CCP Ab?

A

APCs pick up CCP Ag

presented to T-cells

T-cells in HLA-DRB1 SE carriers activate B-cells and create anti-CCP Ab

epitope spreading causes Ab to attack CCPs in human joints

20
Q

What is the use of X-ray in dx of RA?

A

show erosions on lateral/marginal signs

  • difference between gouty (lateral extension of the spur) and OA signs/erosions
  • shows early erosion at tip of ulnar styloid
21
Q

What does US show in RA?

A

joint synovitis, with erosions and joint spaces

22
Q

What does MRI show in RA?

A

MRI is gold standard

early signs picked up as edema of the bone

Erosions

23
Q

What is the pathology of RA?

A
  • Synovial cell hyperplasia and endothelial cell activation are seen in early RA.
  • CD4 T cells, mononuclear phagocytes, fibroblasts, osteoclasts, and neutrophils, and B cells (RF) play major roles. Cytokines, chemokines, and other inflammatory mediators (eg, TNF-a, interleukin IL-1, IL-6, IL-8, TGF-ß, FGF, PDGF) are all active.
  • Ultimately, inflammation and exuberant proliferation of the synovium (ie, pannus) leads to destruction of cartilage, bone, tendons, ligaments, and blood vessels.
  • Destruction of the cartilage and erosion of the underlying bone with pannus from a patient with rheumatoid arthritis.
24
Q

What are some other forms of arthritis that are DDXs for RA?

A

Osteoarthritis

Gout

Spondyloarthropathies

Lyme arthritis

FMF

25
Q

What infections are DDXs for RA?

A

Infections

Parvo B 19

Hepatitis C

26
Q

What collagen vascular diseases are DDXs for RA?

A

SLE

Polymyalgia rheumatica

Wegeners granulomatosis

RF

27
Q

What are some cancers that are part of the DDX for RA?

A

Hypertrophic pulmonary osteoarthropathies – lung and GI cancers

Palmar fasciitis – ovarian carcinoma

28
Q

What are the SSXs of FMF? What causes it, and how is it treated?

A

Familial Mediterranean Fever

caused by lack of “pyrin”, a neutrophil protein that keeps them from mobbing body spaces

eventually causes a deadly secondary amyloidosis

Treated with colchicine

episodic fever

arthritis

pleuritis

peritonitis

hot ankle rash

29
Q

What are the SSXs and complications of vasculitis throughout the body?

A

CNS - stroke

Eye - reduced visual acuity

Nose- epistaxis

Heart - MI, HTN

Lungs - bloody cough, lung infiltrates

GI - bloody stools, abdominal pain

Kidneys - glomerular nephritis

MM pain

Joints - pain, arthritis

Skin - palpable purpura, livedo reticularis

General SSXs: fever, HA, weight loss

30
Q

What is the DSA-28?

A

Disease Activity Score 28 (used for staging and prognosis, determines Tx)

  • count the number of tender joints
  • count the number of swollen joints
  • measure the ESR
  • Ask the patient to rate global activity of arthritis during the past week from 0 (no symptoms) to 100 (very severe)
  • enter data into calculator or work out
31
Q

What is the Vectra test?

A

Some rheumatologist use the Vectra test (12 biomarkers with emphasis on CRP, Il6, and SAA) to evaluate disease activity

32
Q

What are the major structures/features of a joint affected by RA? What are the major cell types involved?

A

Inflamed synovial membrane

Pannus:

mostly T-cells and macrophages

also has fibroblasts, plasma cells, endothelium, dendritic cells

Synovial fluid (mostly neutrophils)

33
Q

What are the major classes of drugs to Tx RA?

A

NSAIDs

Steroids

DMARDs (nonspecific)

Biologic DMARDs (specific)

34
Q

What are the DMARDs for RA?

A

MTX

Sulfasalazine

Hydroxychloroquine

Leflunamide - pyrimidine synthesis inhibitor

Minocycline

35
Q

What are the biological DMARDs for RA, and what do they do?

A

Biologic DMARDs (specific)

TNFi - adalimumab, etanercept, infliximab, certolizumab, golimumab

Abatacept – blocks T cell costimulation

Rituximab – depletes B cells

Tocilizumab - blocks IL6 receptor

Tofacitinib – inhibits Janus Kinase 3

36
Q

Which biologics do what in RA and disease progression?

A

Abatacept - downregulates APC presentation to T-cells, downregulates T-cells stimulating B-cells to make RF/ACPA

Rituximab - downregulates B cells making RF/ACPA

Anti-TNFs - works on APCs; stops synovial inflammation, destructive joint changes, systemic inflammation

Anakinra - works on APCs, anti-IL-1 that reduces destructive changes and systemic inflammation

Tocilizumab - works on APCs, reduces IL-6 and reduces synovial inflammation, destructive changes, systemic inflammation

37
Q

32 y/o female with 3 year of RA. AM stiffness > 30 minutes. Slight wrist, with some MCP and PIP swelling (synovitis). X-rays normal.

Treatment:

A

NSAIDs and prednisone?

MTX + folic acid– reevaluate in 2-3 months

38
Q

36 y/o female with 1 year RA. AM stiffness > 90 minutes. Prominent synovitis. US shows early erosions.

Treatment:

A

1.MTX sulfasalazine, hydroxychloroquine (or MTX/lefluonamide)

39
Q

30 year old female with 2 years of RA. Marked synovitis. Some joint deformity. Bilateral erosions. On MTX, HCQ, Sulfa.

Treatment:

A

MTX with etanercept – advantage to totally arrest joint damage

Consider other biologics if TNFs fail

40
Q

What are the long term complications of RA?

A

MI – decreased with response to anti- TNF therapy*!

Osteoporosis

NSAID bleeds and perforations

Lymphoma and GU malignancies

41
Q

A 52 y/o female with RA has been on MTX and etanercept for 4 months with little response. What is the next step?

A.Continue the program.

B.Change to tofacitinib

C.Add tofacitinib

D.Change to rituximab

E.Switch to MTX with adalimumab

A

Continue the program as it may take 6 – 12 months for a response.