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Medicine Year 2 > Week 224 - Rheumatoid Arthritis > Flashcards

Week 224 - Rheumatoid Arthritis Flashcards

0
Q

Define rheumatoid arthritis

A

Chronic Systemic Inflammatory Disorder of unknown trigger

Uncontrolled inflammation resulting in joint destruction.

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1
Q

What is the primary site of pathology in RA?

A

The synovium

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2
Q

What is Pannus formation?

A

Thickened, inflammed synovium. Causes damage to bone, cartilage and sometimes ligaments in and around the joint

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3
Q

What are the key details in the epidemiology of RA?

A

Race - worldwide
Female:Male > 3:1
Age - any - peak = 35-45
Smoking - clear link to incidence and increased severity
Genetics - certain influence (HLA-DR4 and PTPN22)

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4
Q

How can RA present?

A

Many different possible clinical manifestations:

  • gradual onset - small peripheral joints, usually symmetrical
  • acute, abrupt onset polyarthritis
  • slow or acute monarticular presentation
  • palindromic rheumatism
  • local or systemic extra-articular features
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5
Q

What will typical RA histories contain to make it different to OA?

A

Usually small joints (MCP, proximal IP - NOT usually distal IP joint)
Worst in the morning
Improves with activity over a few hours

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6
Q

What is the most common progression pattern in RA patients?

A

75% experience ongoing joint pain with flare ups

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7
Q

Describe a “Swan-neck deformity”

A

Hyperextension of PIP joint with

Fixed flexion at DIP

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8
Q

Describe “Boutonnaire” deformity

A

Fixed flexion at PIP joint with

Hyperextension at DIP joint

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9
Q

What 3 signs are you likely to see on a hand x-ray in the presence of RA?

A

Periarticular osteopenia - areas of bone appear darker
Periarticular erosions - distal heads of metacarpals often
Reduced joint spaces

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10
Q

According to the ACR Classification criteria 1989 how many of the 7 criteria must be present to diagnose RA?

A

=/> 4

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11
Q

What causes the ulnar deviation seen in more severe progressions of RA?

A

Reduced integrity of the MCP joints - due to erosion for example - subluxation occurs

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12
Q

What combination of methods are usually required to diagnose RA?

A

History and examination
Bloods: ESR, CRP, Rheumatoid Factor, anti-CCP (cyclic citrullinated peptide)
Imaging: x-ray, USS/MRI - synovitis

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13
Q

Which of the various blood tests is more useful in the diagnosis and why?

A

Useful: CRP (more so than ESR) and Anti-CCP (more specific to RA than rheumatoid factor)
Arguably rheumatoid factor - present in ~80% with but also ~5% general population

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14
Q

What exactly is rheumatoid factor a measure of?

A

It detects the level of IgM antibody

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15
Q

Why is ESR not a very useful blood test result in the diagnosis of RA (and many other conditions!)?

A

Too many other factors effect levels of ESR including:
Age
Renal function
Anaemia

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16
Q

There are many extra-articular manifestations of RA. What are the constitutional manifestations alone?

A

Fever, fatigue and weight loss

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17
Q

What percentage of Rheumatoid Factor +ve patients are thought to experience rheumatoid nodules?

A

~20% (rare in RF -ve pts)

Can remove but often return and have little effect besides being an irritation

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18
Q

What pulmonary manifestations can occur with RA?

A

Pulmonary manifestations are frequent but often subtle

  • pleural effusions
  • interstitial fibrosis
  • primary nodules from RF
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19
Q

What cardiac / CVS manifestations can occur with RA?

A

Vasculitis - severe RA; venous HTN and ulcers

  • increased risk of IHD
  • pericarditis / pericardial effusions
  • coronary vasculitis
  • non-specific myocarditis
  • valvular disease *similar CVS disease risk to diabetics
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20
Q

What ocular manifestations can occur with RA?

A
  • Episcleritis

- Scleritis - usually effects vision, painful > treat aggressively or perforation can occur

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21
Q

What neurological manifestations can occur with RA?

A
  • Entrapment e.g. Carpal Tunnel
  • Atlanto-axial subluxation > cervical myelopathy
  • Mononeuritus multiplex
  • Central NS vasculitis
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22
Q

What haematological manifestations can occur with RA?

A
  • Anaemia (chronic disease - bone marrow suppression - NSAIDs and DMARDs)
  • Thrombocytosis (hence increased risk of IHD)
  • Rarely lymphadenopathy and Felty’s syndrome
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23
Q

What is Amyloidosis?

A

A RARE condition but one to be aware of!

Result of chronic inflammation: increased serum amyloid-A protein (SAP) - every organ may be involved

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24
Q

What causes splinter haemorrhages and nail-fold infarcts and what condition are they most often linked with?

A

Caused by blocked vessels

Commonly linked to endocarditis

25
Q

What occurs in pericardial tamponade?

A

Pericardial effusion becomes so large that the pressure squashes the ventricles to the point at which they stop functioning

26
Q

What pathological manifestations do the various multi-system autoimmune connective tissue disorders tend to have in common?

A
  • arthritis
  • myositis
  • nephritis
  • alveolitis
  • serositis
  • lung and renal fibrosis sometimes
27
Q

There is often overlap in clinical presentation / symptoms of connective tissue disease. What do these include?

A

Fatigue; arthralgia/myalgia; depression; malaise; fever; weight loss; (lymphadenopathy)

28
Q

What do the various common -itis (pathological) manifestations of autoimmune connective tissue disorders contribute to largely?

A

Increased thrombotic risk

29
Q

What is Raynaud’s Phenomenon?

A

Spasm of the blood vessels in the fingers or toes resulting in a triphasic response +/- environmental stress
Pallor > Cyanosis > Erythema
(Pallor due to vasoconstriction; cyanosis due to prolonged spasm then erythema due reactive hyperaemia)

30
Q

Systemic Lupus Erythmatosis is associated with antibody formation. Which antibodies are associated with SLE?

A
  • ANA (“anti-nuclear antibody - 100% of all SLE pts)
  • ds DNA (50%, more specific than ANA)
  • anti-Ro / -La (20%)
  • anti-Sm (15%)
31
Q

Which of the antibodies associated with SLE has been linked with neonatal SLE ?

A

Anti-Ro

Therefore all female pts with CTD wanting to get pregnant should be tested for anti-Ro as it crosses the placenta

32
Q

List clinical manifestations of SLE

A

Malar/Butterfly Rash; Arthritis (non-erosive); mouth ulcers; alopecia; vasculitis > small infarcts on pads of fingers “nail fold infarcts”

Renal, neurological, haematological > serositis

33
Q

What combination of factors helps to diagnose SLE?

A
  • Clinical features
  • Urine (protein and blood) & bloods
  • Serology - ANA, ds DNA, anti-Ro/-La, anti-Sm
  • Complements - reduced C3 and C4 - lots of complement activation so become used up due to antibody binding to them
34
Q

What factors can affect the ANA antibody levels detected?

A

Infection; Age; Other autoimmune diseases; Malignancy; FHx

35
Q

What are the treatment options for SLE?

A

Arthralgia - NSAIDs
Myalgia/Lethargy - hydroxychloroquine (HCQ)
Arthritis/Pleuritis/Pericarditis - prednisolone +/- HCQ / MTX
Haemolytic anaemia - Azathioprine / ???

36
Q

Give 2 examples of Inflammatory Muscle Disease (a form of connective tissue disease)

A
  • Polymyositis

- Dermatomyositis

38
Q

What are some of the more common symptoms associated with Inflammatory Muscle Disease?

A
  • Proximal muscle weakness (which can progress to cause complications such as aspiration and restrictive pulmonary disease)
  • Heliotrope rash - on eyelids (dermato. specifically)
  • Guttrons papules - skin thickening on dorsum of hands
  • Cracking of skin on finger tips
38
Q

What is considered the best diagnostic investigation for IMD?

A

Muscle biopsy

39
Q

In blood tests and serology what might help diagnose Inflammatory Muscle Disease?

A
  • Elevated CK (also elevated in rhabdomyolitis)
  • Troponin T - odd since cardiac specific but believed to be released from muscles when they regenerate in IMD
  • Anti-Jo antibodies
40
Q

Systemic Sclerosis is divided into 2 categories, what are they?

A

Limited Scleroderma and Diffuse Scleroderma

41
Q

What is the principle common feature in both limited and diffuse scleroderma?

A

Skin tightening

42
Q

How is Diffuse Scleroderma diagnosed?

A
  • If disease progresses proximal to the elbow in the arms

- Anti-scl70 antibody

43
Q

How do you treat Diffuse Scleroderma?

A

Mycofentolate Mofeil (ltd benefit!) or Cyclophosphamides

44
Q

Why must you NEVER treat diffuse scleroderma with steroids?

A

Can induce “renal crisis”

45
Q

What was Limited Scleroderma originally known as and why?

A

CREST as this serves as a mnemonic for the symptoms it displays

46
Q

What does CREST stand for?

A

Calcinosis (calcification deposits on fingers)
Raynaud’s
E(o)sophageal dysmotility
Sclerodactyly
Telengectasia (dilation of blood vessels - blanching red spots)

47
Q

What other major impact can limited scleroderma have on the fingers?

A

Distal phalanx reabsorption can occur

48
Q

What antibody is associated with limited scleroderma?

A

Anti-centromere antibody

49
Q

How do you treat limited scleroderma?

A

There are no disease modifying medications available. Can only try to treat symptoms as they appear.

50
Q

List 3 risks associated with Systemic Sclerosis (both limited and diffuse scleroderma)

A
  • accelerated HTN
  • pulmonary fibrosis
  • renal crisis
52
Q

A patient presents with these symptoms:
Dry eyes, dry mouth, bilateral cheek swellings anterior to each earlobe and purpura.
What is the principle differential?

A

Sjogren’s Syndrome

53
Q

What antibodies in serology would help you diagnose Sjogren’s?

A

Anti-Ro or -La
ANA (98%)
Usually RF+ve also (90%)

53
Q

What are the 5 main pharmacological treatment types involved in Rheumatoid Arthritis?

A

1) Analgesia
2) NSAIDs
3) Corticosteroids
4) DMARDs
5) Biologics

54
Q

How do you manage Sjorgren’s Syndrome?

A

Supportive management:
Artificial tears and saliva, sugar free gum
Immunosuppressants rarely used

55
Q

Which of the 5 pharmacological treatment groups prevent RA progressing?

A

DMARDs and Biologic agents

56
Q

What are the 3 most commonly used DMARDS?

A

Methotrexate
Sulphasalazine
Leflunomide

57
Q

What is most important when diagnosis of RA is made with regard to treatment?

A

Put on more than one DMARD (combo better than 1)

“Disease Modifying Anti-Rheumatoid Drugs”

58
Q

What are the side effects of DMARDs?

A
  • bone marrow suppression
  • increase susceptibility to infection
  • renal and liver toxicity
59
Q

What is given with Methotrexate and why?

A

Folic Acid - MTX is a folate pathway inhibitor

60
Q

Give at least 3 examples of biologics that may be added to a DMARD in the treatment of RA

A

etanercept; infliximab; adalimumab;

rituximab; certolizumab; abatacept

Medicine Year 2 (28 decks)

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