MSS Inflammatory Arthropathies Flashcards

1
Q

Describe the epidemiology of RA

? are ? to have arthritis than ?
?, such as the ?, have higher rates of arthritis compared to ?.
The annual incidence of RA is around ? people in US and Europe.
RA is most common in people aged ?

A

Women are 2-3 times more likely to have arthritis than men
Native Americans, such as the Pima, have higher rates of arthritis compared to native Japanese.
The annual incidence of RA is around 40 per 100,000 people in US and Europe.
RA is most common in people aged 65 to 80 years old.

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2
Q

5 Risk factors for RA?

family history
succeptibiltiy genes
demograpghic risk factors
lifestyle factors
infections

A
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3
Q

Describe the pathogenesis of RA

A

Dendritic cells get exposed to cell gene +activated
Present to & activate T then B cells
In RA, T & B cells travel to the lining of synovium and start activating Fibroblasts, macrophages, chondrocytes, osteoblasts etc
These produce cytokines which activate enzymes which destroy cartilage = inflammatory response

B cells -> plasma cells -> Abs = RF (one of the Abs)

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4
Q

What is a consequence of cartiliage damage due to enzymes?

A

As inflammation continues, the synovium becomes hypertrophic and tumour like
hypertrophic synovium can invade the surrounding cartilage= “pannus.”

The pannus releases metalloproteinases, which break down proteins, inc collagen–> lead to secondary cartilage erosion and bone damage.

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5
Q

Explain why RA is a systemic infalmmatoy disease

A

Vasculitis - inflammation in the lining of the blood vessels -> BF disturbed - Eventually lead to blockage !
Lead to ulcers, ischaemic
Scleritis - thinning and eventually perforated

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6
Q

Describe the patterns of joint involvement in RA

A
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7
Q

Which joints are more commonly vs less affected in RA?

A
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8
Q

What are the 5 common joint deformities in RA?

A
  • Boutonniere deformity
  • Swan neck deformity
  • Ulnar deviation of the fingers
  • Z-shaped deformity of the thumb (Hitchhiker’s thumb)
  • Claw toe deformity
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9
Q

75% of patients develop one or more extra-articular manifestations within 5 years of the onset of RA, for example fatigue and weight loss (early on), or rheumatoid nodules.

Describe rheumatoid nodules and where they develop

A

.

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10
Q

Describe Haematological features of RA

A

Normochromic, normocytic anaemia (Iron utilisation is impaired)

Thrombocytosis

Felty’s: rare RA complication, splenomegaly, neutropenia, increased risk of infection

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11
Q

Describe 3 Pulmonary and 2
cardiac features of RA

A
  • Pleural effusion: common, usually subclinical
  • Interstitial lung disease, may lead to irreversible scarring if left untreated
  • Pulmonary nodules: rare
  • Pericarditis is most common cardiac manifestation
  • Cardiovascular disease
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12
Q

Describe ocular features of RA

A

Keratoconjunctivitis Sicca= conjunctiva + cornea inflammation. Caused by dryness resulting from a deficiency or disorder of the tear film.

Episcleritis–> red eye, due to inflammation of the episcleral tissues. This condition can be nodular or simple. Nodular= discrete, elevated area of inflamed episcleral tissue.

Scleromalacia perforans= autoimmune anterior scleritis, potentially blinding. Appears as a black area of scleral thinning surrounded by inflammatory tissue

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13
Q

Describe neuro features of RA
- CEP

A

Subluxation= dislocation

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14
Q

Describe vasculitis features of RA

A
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15
Q

What would you look for upon clinical examination of someone with RA?

A
  • joint warmth, swelling and tenderness
  • joint range of movement and deformities
  • anaemia
  • nodules
  • eyes
  • vasculitis
  • other symptoms: resp, cardiovascular and neurological.
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16
Q

What would you look for in blood tests for suspected RA?

A

RF: positive in 75% of patients with RA. High titre in extra-articular disease, nodules and in severe disease. Higher titre suggests more aggressive treatment needed

Anti-CCP= Specific for RA. Patients with positive anti-CCP Ab = aggressive disease more likely
Certain meds work better for pts who have this kind of Ab

ESR/CRP: Elevated in most RA pts. After treatment, CRP will drop quickly but ESR will lag behind

FBC: Normocytic, normochromic anemia. Thrombocytosis. Leukopenia U+Es, LFTs

17
Q

What imaging investigations would you undertake for suspected RA?

A

X-rays of affected joints: Early changes: soft tissue swelling. Later changes inc erosions, joint space narrowing

US shows synovial hypertrophy, synovial fluid effusions, and power Doppler signal indicating increased blood flow. + can detect synovitis

MRI can shows early changes: synovitis, bone edema, & bone erosions

18
Q

Describe the classification criteria for RA

A
19
Q

Describe the differential diagnoses of RA

A

Osteo can affect large joints like knees
Morning stiffness more likely in inflammatory rather than osteoarthritis
Arthralgia=pain w no swelling → this is why imaging can be helpful
Viral is acute so watch out for that

20
Q

Describe the difference between RA and PA

A

Seropositive RA refers to the presence of RF and/or anti-CCP antibodies in a person diagnosed with RA. Seronegative RA refers to the situation where both antibodies are not elevated. 

21
Q

Crystalline arthritis can cause gout and psedo gout.
Describe gout associated w Crystalline arthritis vs pseudo-gout

A

Crystalline arthritis- psedo-gout
* Calcium pyrophosphate crystals in synovial fluids
* Chondrocalcinosis on radiographs
* Usually acute monoarthritis

Old person comes in w UTI, suddenly they have swollen wrist or knee = likely to be pseudo-gout. Need to exclude psoriatic arthritis

22
Q

psedo gout.

A
23
Q

RA management involves early diagnosis, early intervention and tight control. compare 3 pharmacological therapies.

A

Corticosteroids: Start w this then move straightaway to the next step - medications to modify the course of the disease (immunosuppressive therapies)

Conventional synthetic disease-modifying antirheumatic drugs (sDMARD): methotrexate, sulfasalazine, hydroxychloroquine, leflunomide. These are 1st line, can use individually or juntos

Biologic therapies (bDMARD): TNF inhibitors, IL6 inhibitors, B-cell depletion therapy, T-cell costimulation blocker, JAK inhibitors