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Medicine Phase 2a MSK and Rheumatology > Rheumatoid arthritis > Flashcards

Rheumatoid arthritis Flashcards

1
Q

Describe

A

Chronic, Autoimmune type III Hypersensitivity reaction
Principally affects the joints (synovial especially) but may also affect other organs
Symmetrical deformation of joints
Pain is worse in the morning

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2
Q

Clinical presentation

A 
Insidious onset of pain in the Distal Small joints
Morning stiffness (>30 mins) / Pain is worse in mornings
Hand Deformities e.g. Ulnar deviation, swan neck and boutonniere
Symmetrical deformation of joints
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3
Q

Pathophysiology

A

Infiltration of the synovium by inflammatory cells

  • > Angiogenic cytokines
  • > Formation of new synovial blood vessels
  • > Synovium proliferates and grows out over the surface of cartilage producing a pannus
  • > Pannus damages the cartilage and subchondral bone below, by blocking its normal route for nutrition and by effects of cytokines on the chondrocytes
  • > Bony erosions
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4
Q

Aetiology

A

HLA DR4 and HLA DR1 confer susceptibility

Triggering antigen not known, but thought to be a type III hypersensitivity reaction

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5
Q

Epidemiology

A

1% of population will experience
More common in women
Peak incidence in 40s

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6
Q

Diagnostic tests

A

Anti-CCP (marker of disease but not pathogenic itself)
Rheumatoid factor - also AntiNuclear antibody
X-ray

Normochromic normocytic anaemia on bloods

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7
Q

Describe X-ray of Rheumatoid arthritis

A 
(Peri-articular erosions)
Juxta-articular osteopenia
Soft tissue swelling
Joint deformity
Loss of joint space
(Also osteopenia - soft bones)
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8
Q

Treatment

A

DMARDs e.g. Methotrexate (oral)
NSAIDs and COX inhibitors (relieve joint pain and stiffness) and paracetamol +/-opioid (for pain management)
TNF- alpha inhibitor (slows/halts erosion formation)
Physiotherapy
Interarticular corticosteroid injection (semicrystalline steroid)

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9
Q

Complications of rheumatoid arthritis

A 
Carpal tunnel syndrome
Cervical myopathy
Pericarditis
Tendon rupture
Sjogren's syndrome
Social impact and depression
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10
Q

How can you tell the difference between rheumatoid and osteo-arthritis

A

OA is defined as joint stiffness caused by loss of cartilage between joints due to wear and tear, while RA stems from an autoimmune attack on joints.
RA - get more generalised symptoms (not present in OA); frequent fatigue; morning stiffness >1 hour; relatively rapid (wks to months)
OA - morning stiffness <1 hour; slow (years); more later in life

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11
Q

Examples of TNF-alpha inhibitor

A

Infliximab (IV monoclonal antibody)

Adalimumab (SC monoclonal antibody)

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12
Q

Examples of DMARDs (oral)

A

Sulfasalazine (for mild/moderate disease) used in young and women
Methotrexate (gold standard for more active disease, CI in pregnancy)

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13
Q

What does DMARD stand for

A

Disease-modifying antirheumatic drugs

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14
Q

Side effects of Methotrexate DMARD

A

Nausea, mouth ulcers, diarrhoea, abnormal LFTs, neutropenia, thrombocytopenia, renal impairment

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15
Q

RA (inflammatory) vs OA (degenerative)

Age at which condition starts

A 
RA = any time in life
OA = usually begins later in life
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16
Q

RA (inflammatory) vs OA (degenerative)

Speed of onset

A 
RA = relatively rapid, over wks to months
OA = slow, over years
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17
Q

RA (inflammatory) vs OA (degenerative)

Joint symptoms

A 
RA = joints are painful, swollen and stiff
OA = joints ache and may be tender but have little or no swelling
18
Q

RA (inflammatory) vs OA (degenerative)

Pattern of joints affected

A 
RA = often affects small and large joints on both sides of the body (symmetrical), such as both hands, both wrists or elbows or balls of both feet
OA = symptoms usually begin on one side of the body and may spread to the other side; symptoms begin gradually and are often limited to one set of joints - usually finger joints closest to the fingernails or the thumbs, large weight-bearing joints (hips and knees) or the spine
19
Q

RA (inflammatory) vs OA (degenerative)

duration of morning stiffness

A 
RA = morning stiffness lasts >30 mins
OA = morning stiffness lasts <30 mins, stiffness returns at the end of the day or after periods of activity
20
Q

RA (inflammatory) vs OA (degenerative)

presence of symptoms affecting the whole body (systemic)

A 
RA = frequent fatigue and a general feeling of being ill are present
OA = whole-body symptoms are NOT present
21
Q

What is anti-ccp

A

Anti-Cyclic Citrullinated Peptide

22
Q

Give examples of hand deformities seen in rheumatoid arthritis

A

Ulnar deviation
Swan neck/Z thumb
Boutonniere deformity

23
Q

Pathophysiology again but more detail

A
  • RA is primarily a synovial disease and synovitis (inflammation of the synovial lining) occurs when chemoattractants produced in the joint, recruit circulating inflammatory cells
  • Over-production of TNF-alpha leads to synovitis and joint destruction, driven by the interaction of macrophages, T and B lymphocytes
  • Synovium becomes greatly thickened and becomes infiltrated by inflammatory cells
  • Angiogenic cytokines induce generation of new synovial blood vessels and activates endothelial cells to produce adhesion molecules that FORCE Leucocytes into the synovium, where they can trigger inflammation
  • The synovium proliferates and grows out over the surface of the cartilage (past the joint margins), producing a tumour-like mass called ‘pannus’
  • This pannus of inflamed synovium DAMAGES the underlying cartilage by blocking its normal route for nutrition and by direct effects of cytokines on the chondrocytes
  • The cartilage becomes thin and the underlying bone exposed
  • The pannus DESTROYS the articular cartilage and subchondral bone resulting in bony erosions
24
Q

What is the name of the tumour-like mass formed by the proliferation of the (inflamed) synovium over the surface of the cartilage

A

Pannus

25
Q

How does the pannus damage underlying cartilage

A

By blocking its normal route of nutrition and by direct effects of cytokines on the chondrocytes

26
Q

How does the pannus cause bony erosions

A

Pannus damages underlying cartilage
Cartilage becomes thin and the underlying bone is exposed
Pannus destroys the articular cartilage and subchondral bone, resulting in bony erosions

27
Q

Conservative treatment

A

Patient education
Encourage exercise
Refer to physiotherapy
Assess activities of daily living

28
Q

Medical treatment

A

Glucocorticoids
*Disease modifying antirheumatic drugs (DMARDs are 1st line) e.g. gold salts, methotrexate, sulfasalazine
Anticytokine therapies may be considered in patients intolerant of methotrexate

29
Q

Surgical treatment

A

Excision arthroplasty or replacement may be considered in severely affected joints

30
Q

Where are signs and symptoms in RA

A 
Hands
Wrist
Feet 
Skin
Cardiovascular
Respiratory
Bones
Pain and stiffness!!
31
Q

Signs and symptoms in hands

A 
Z deformity
Boutonniere deformity
Swan neck deformity
Ulnar deviation
Subluxation (partial dislocation) of the fingers
Raynauds phenomenon
32
Q

Signs and symptoms in wrist

A

Carpal tunnel syndrome

33
Q

Signs and symptoms in feet

A

Subluxation (partial dislocation) of the toes

Hammer toe deformity

34
Q

Signs and symptoms in skin

A

Rheumatoid nodule

Vasculitis

35
Q

Signs and symptoms in cardiovascular system

A

Atherosclerosis is increased in RA

36
Q

Signs and symptoms in respiratory system

A

Pulmonary fibrosis

37
Q

Signs and symptoms in bones

A

Osteoporosis

38
Q

Investigations

A

Bloods

Radiology

39
Q

Blood investigations

A

80% test positive for rheumatoid factor
ESR and CRP raised
Cyclic citrullinated peptide (CCP) antibodies - if positive this is suggestive of erosive disease

40
Q

Radiology investigations and signs

A

Radiological signs are visualised on a plain film:
Bony erosion
Subluxation
Carpal instability
Periarticular osteoporosis
Joint involvement of metacarpophalangeal joint (MCPJ) and Metatarsophalangeal joint (MTPJ)

41
Q

Examples of DMARDs

A

Methotrexate

Sulfasalazine (also used in Crohns and UC)

Medicine Phase 2a MSK and Rheumatology (18 decks)

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