OA and RA Flashcards

1
Q

What is rheumatoid arthritis?

A

A chronic systemic immune disease as a result of a cell mediated immune response that attacks soft tissue and bone.

It is not limited to synovial joints and follows a stereotypical pattern of joint involvement but manifests in almost every body system.

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2
Q

What is the typical presentation of fully developed RA?

A

Symmetrical inflammatory polyarthritis which is primary peripheral, with significant morning stiffness lasting well past 30 mins.

Progressive deformities and erosion with subcutaneous nodules. +ve RF and anti-CCP antibodies.

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3
Q

What is the genetic component of RA?

A

HLA human leukocyte antigen (associated with worse disease) and MHC major histocompatibility complex.

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4
Q

What is citrullination?

A

The conversion of the amino acid arginine into citrulline.

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5
Q

Explain how environmental trigger is involved in the initiation of RA

A

Environmental trigger leads to citrullination of a host protein meaning modified protein is immunogenic, and treated like an antigen triggering an immune response.

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6
Q

Explain the immune response process that occurs in RA.

A
  • Citrullinated immunogenic protein formed via environmental trigger is processed and presented to T cells by dendritic cells and B cells.
  • Protein presented to T cells via Human leukocyte antigen
  • T cells activate B cells by releasing cytokines
  • Activated B cells form plasma cells which release auto-antibodies such as RF and anti-CCP.
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7
Q

What is Pannus?

A

Latin for table cloth

Grossly thickened synovium as a result of inflammation:

  • autoimmune attack on synovium, synovial fibroblast proliferation causes hypertrophy and hypovascularity of synovial
  • causing synovium to enlarge and spread over and between joint surfaces like a tablecloth.
  • Releases damaging agents eroiding joint and infiltrating bone.
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8
Q

What is a typical presentation of underdeveloped RA?

A
  • Joint pain, swelling, stiffness which is polyarticular, symmetrical and small joint > large joints
  • Morning stiffness lasting longer than 30 mins
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9
Q

What is a swan neck deformity?

A

Hyperextension at PIP and flexion at DIP

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10
Q

What is a Z deformity?

A

Flexion at the MCP and hyperextension at the interphalangeal joint

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11
Q

What deformities are common in RA?

A

Swan neck deformity, Z deformity, ulnar deviation of finger due to subluxation or dislocation of joints.

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12
Q

What are some extra-articular MSK Presentations of RA? (3)

A
  • Bursitis
  • Subcutaneous nodules
  • Tendon inflammation or rupture
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13
Q

What are some systemic manifestations of RA? (4)

A
  • myocardial infarctions
  • Stroke
  • Infection
  • Non-hodgkin’s lymphoma
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14
Q

What are 4 red flags to look out for in RA?

A
  • Atlantoaxial subluxation/instability
  • Pericarditis
  • Monoarticular flare (septic arthritis)
  • Scleritis
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15
Q

What is the significance of Atlantoaxial subluxation/instability?

A

C1 sides forward on C2 which an cause spinal cord compression with pain at the back of the head and neck, and numbness down arms.

Can result in sudden death if spinal cord injured.

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16
Q

What is the significance of scleritis?

A

Sudden onset of eye pain and lacrimation which untreated sclera may become involved leading to thinning, perforation and blindness.

17
Q

What are the main key differences between RA and OA?

A

RA is symmetrical, with longer lasting morning stiffness and not affecting DIP-Js

OA is unsymmetrical with shorter lasting morning stiffness and longer stiffness after rest, affects DIP-Js

18
Q

What 3 investigations are required for an RA diagnosis?

A
  1. Measure CRP and ESR baseline
  2. Test for RF and anti-CCP antibodies
  3. X-ray hands and feet
19
Q

What are some imaging signs of RA?

A
  • erosive arthritis with joint space narrowing, subchondral erosions and ankylosis with gull wing appearance.
  • Subluxations or dislocations
  • Bowstringing.
20
Q

What are the principles of treatment for RA? (3)

A
  • maximise health related quality of life through symptoms control
  • Abrogation of inflammation
  • Treatment tailored to disease activity
21
Q

What is the management of RA?

A
  • Early initiation of DMARDS monotherapy with MTX and SSZ combined with short term use of glucocorticoids for flares
  • consider bDMARDs e.g. TNF inhibitors and rituximab
22
Q

How can you monitor RA?

A
  • Activity and drug efficacy with VAS, labs for esr and CRP and DAS 28 score
  • disease progression with radiographs and functional assessment of joints
  • Drugs safety with labs
23
Q

What is OA?

A

A disorder characterised by degeneration of articular cartilage, remodelling of subchondral bone, osteosclerosis and osteophytes.

24
Q

What conditions could result in secondary OA?

A

DETAMIN:

  • Developmental e.g. SUFE
  • Endocrine e.g. acromegaly
  • Traumatic e.g. interarticular fracture
  • Aseptic necrosis e.g. corticosteroids, sickle cell disease.
  • Metabolic e.g. paget’s
  • Inflammatory e.g. RA, gout
  • neuropathic e.g. diabetes
25
Q

What are the radiological features of osteoarthritis?

A

narrowing joint space, osteophytosis, altered bone contour, bone sclerosis and cysts, periarticular calcification.

26
Q

What are the modifiable local risks of OA? (5)

A
  • Muscle strength
  • Physical inactivity
  • Joint injury
  • Joint alignment
  • leg length inequality
27
Q

What are 3 age related physiological changes contributing to OA risk?

A
  • Decline in proprioception
  • Decrease in muscle strength (sarcopenia)
  • Changing shape of bones
28
Q
A