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Musculoskeletal & Rheumatology > Rheumatoid and other inflammatory arthritis > Flashcards

Rheumatoid and other inflammatory arthritis Flashcards

1
Q

What are the components of a synovial joint?

A
  • Bone
  • Articular cartilage (type II collagen, proteoglycan)
  • Joint cavity containing synovial fluid (synovium= contain macrophage-like phagocytic cells and fibroblat-like cells that produce hyaluronic acid & type 1 collagen)
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2
Q

What is arthritis?

A

Disease of the joints
many different types

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3
Q

What are the 2 main divisions/ types of arthritis? what is the difference between both?

A
  1. Osteoarthritis:
    - worsens with activity
  2. Inflammatory arthritis:
    - improves with movement
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4
Q

What are the causes of joint inflammation?

A

SECONDARY INFLAMMATION IN RESPONSE TO A NOXIOUS INSULT=
1) Infection:
- Septic arthritis
- Tuberculosis
2) Crystal arthritis
- Gout (uric acid/ uric crystals)
- Pseudogout
PRIMARY INFLAMMATION=
3) Immune-mediated (“autoimmune”)

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5
Q

What are some causes of sterile vs non-sterile joint inflammation

A

NON-STERILE=
1) Infection:
- Septic arthritis
- Tuberculosis
STERILE=
2) Crystal arthritis
- Gout (uric acid/ uric crystals)
- Pseudogout
3) Immune-mediated (“autoimmune”)

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6
Q

What is septic arthritis?

A
  • Bacterial infection of a joint (usually caused by spread from the blood from another part of the body)
  • Septic arthritis is a medical emergency
    -> Untreated, septic arthritis can rapidly destroy a joint
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7
Q

What are the risk factors for septic arthritis?

A
  • immunosuppressed
  • pre-existing joint damage
  • intravenous drug use (IVDU)
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8
Q

What are the clinical presentations of septic arthritis?

A

-Acute red, hot, painful swollen joint
-Usually only 1 joint is affected* (monoarthritis)
-Typically fever. Patient often systemically unwell

Consider septic arthritis in any patient with an acute painful, red, hot, swelling of a joint, especially if there is fever

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9
Q

How is septic arthritis diagnosed?

A

by joint aspiration. Send sample for urgent Gram stain and culture

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10
Q

What are the common organisms in septic arthritis?

A

Staphylococcus aureus, Streptococci, Gonococcus

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11
Q

How is septic arthritis treated?

A

Treatment is with surgical wash-out (‘lavage’) and intravenous antibiotics

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12
Q

True or false, septic arthritis is monoarthritis?

A

false: this is usually the case:
*gonococcal septic arthritis is an exception:
-It often affects multiple joints (polyarthritis)
-It is less likely to cause joint destruction

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13
Q

what are the 2 types of crystal arthritis?

A
  1. GOUT:
    Caused by deposition of monosodium urate (MSU) (aka uric acid) crystals in/around joints
    -> inflammation
  2. PSEUDOPGOUT:
    Caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystals
    -> inflammation
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14
Q

What are the causes/ risk factors of gout?

A
  1. High uric acid levels (hyperuricaemia) = risk factor for gout
  2. Causes of hyperuricaemia:
    - Genetic tendency
    - Increased intake of purine rich foods, like beer (breakdown of purine -> uric acid)
    - Increased cell turn over eg chemotherapy
    - Reduced excretion (kidney failure)- can’t clear uric acid
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15
Q

What are the risk factors for pseudogout?

A

background osteoarthritis, elderly patients, intercurrent infection

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16
Q

What are the clinical presentations of gout (crystal arthritis)?

A
  • Tophi “white spots” (aggregated deposits of monosodium urate in tissue): often develop around hands, feet, elbows, and ears)
  • Big toe 1st MTPJ (metatarsophalangeal joint) most commonly affected (podagra)
  • Abrupt onset
  • Usually monoarthritis
  • Can also affects other joints: most frequently joints in the foot, ankle, knee, wrist, finger, and elbow
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17
Q

How do you diagnose crystal arthritis?

A

JOINT ASPIRATION
(Key investigation for any acute monoarthritis – NB SEPTIC joint)
1. Needle inserted into joint and fluid aspirated
2. Send to lab for:
- Microbiology (gram stain, culture and sensivities)
- Polarising light microscopy to detect crystals

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18
Q

How do you distinguish between gout and pseudogout?

A

GOUT:
- urate (MSU) crystals
- needle shaped crystals under microscope
- Birefringence (polarizing light microscopy)= negative

PSEUDOGOUT:
- Calcium crystals pyrophosphate dihydrate (‘CPPD’)
- brick shaped crystals under microscope
- Birefringence (polarizing light microscopy)= positive

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19
Q

What are the different diseases of/ types of autoimmune arthritis?

A
  • Rheumatoid arthritis
  • Seronegative arthritis (psoriatic arthritis, reactive arthritis, ankylosing spondylitis)
  • Lupus and related disorders
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20
Q

What is rheumatoid arthritis?

A

Inflammation of the synovial membrane:
RA = chronic autoimmune disease
Primary site of pathology is in the synovium

21
Q

What are the possible sites of rheumatoid arthritis?

A

Synovium found at:
1. Synovial (diarthrodial) joints:
- proximal inter-phalangeal joint synovitis
2. Lining of tendons:
Extensor tenosynovitis
– note swelling is not above either the wrist or MCP joints
- Note also that the patient has incomplete extension of the little and ring fingers (cannot stick the fingers out straight) – this is consistent with extensor tendon damage by the tenosynovitis
3. Bursa (fluid filled sacs)
- olecranon bursa

22
Q

What are the key features of rheumatoid arthritis?

A
  1. Chronic arthritis
    - Polyarthritis
    - Pain, swelling and early morning stiffness in and around joints
    - May lead to joint damage and destruction - ‘joint erosions’ on radiographs
  2. Systemic disease with extra-articular manifestations (e.g. lungs, eyes)
  3. Auto-antibodies usually detected in blood
23
Q

What causes rheumatoid arthritis?

A

mixture of genetics & environment:
1. Strongest genetic risk factor = HLA-DR
HLA-DRb chain amino acids 70-74 (‘shared epitope’). Smoking & shared epitope synergistically increase risk
2. Genome-wide association studies (GWAS):
>100 other genetic loci that contribute to RA risk (polygenic)
E.g. PTPN22, IL6R
environment:
1. Smoking
2. Microbiome
3. Porphyromonas gingivalis
4. Poor oral health

24
Q

What is the pattern of joint involvement for rheumatoid arthritis?

A
  1. Symmetrical
  2. Affects multiple joints (polyarthritis)
  3. Affects small and large joints, but particularly hands, wrists and feet
  4. Commonest affected joints:
    - Metacarpophalangeal joints (MCP)
    - Proximal interphalangeal joints (PIP)
    - Wrists
    - Knees
    - Ankles
    - Metatarsophalangeal joints (MTP)
25
Q

What are the extra-articular features of rheumatoid arthritis?

A
  1. Common
    - Fever, weight loss
    - Subcutaneous nodules
  2. Uncommon
    - Lung disease – nodules, fibrosis, pleuritis
    - Ocular inflammation e.g. episcleritis
    - Vasculitis
    - Neuropathies
    - Felty’s syndrome – triad of splenomegaly, leukopenia and rheumatoid arthritis
    - Amyloidosis
26
Q

What are subcutaneous nodules?

A
  1. Central area of fibrinoid necrosis surrounded by histiocytes (macrophage-like cells) and peripheral layer of connective tissue
  2. Occur in ~30% of patients
  3. Associated with:
    - Severe disease
    - Extra-articular manifestations
    - Rheumatoid factor
  4. common in hands, and ulnar border of forearm
27
Q

Describe the pathogenesis of rheumatoid arthritis

A

Synovial membrane is abnormal in rheumatoid arthritis:
1. The synovium becomes a proliferated mass of tissue (pannus- looks malignant but is not) due to:
- Neovascularisation
- Lymphangiogenesis
- inflammatory cells:
* activated B and T cells
* plasma cells
* mast cells
* activated macrophages
2. Recruitment, activation and effector functions of these cells is controlled by a cytokine network
3. There is an excess of pro-inflammatory vs. anti-inflammatory cytokines (‘cytokine imbalance’)
4. The cytokine tumour necrosis factor-alpha (TNFα) is the dominant pro-inflammatory cytokine in the rheumatoid synovium
5. Its pleotropic actions are deterimental (leads to lose of cartilage/ bone

28
Q

How is rheumatoid arthritis monitored/ investigated?

A

a) BLOOD TESTS:
1. Haemoglobin (decreased or normal)
2. Mean cell volume (normal)
3. white cell count (usually normal)
4. platelet count (normal or increased)
5. ESR (usually increased)
6. CRP (increased)
b) Rheumatoid factor:
- Antibodies that recognize the Fc portion of IgG as their target antigen
- typically IgM antibodies i.e. IgM anti-IgG antibody
c) (Anti-citrullinated protein antibodies: ACPA)
d) X-rays
e) Ultrasound
f) MRI

29
Q

What blood test readings would you expect to see in osteoarthritis?

A
  1. Haemoglobin (normal)
  2. Mean cell volume (normal)
  3. white cell count (normal)
  4. platelet count (normal)
  5. ESR (normal)
  6. CRP (normal)
30
Q

What blood test readings would you expect to see in septic arthritis?

A
  1. Haemoglobin (usually normal)
  2. Mean cell volume (normal)
  3. white cell count (increased leucocytosis)
  4. platelet count (normal or increased)
  5. ESR (usually increased or normal)
  6. CRP (increased)
31
Q

What are radiographic features of RA are seen on X-Ray?

A
  • Soft tissue swelling
  • Peri-articular osteopenia
  • Bony erosions
    (NB erosions occur only in established disease. The aim of modern therapy is to treat EARLY before erosions (permanent damage) has occurred)
32
Q

What ultrasound changes are seen in RA?

A

(a much better test for detecting synovitis.)
US changes in RA:
- Synovial hypertrophy (thickening)
- Increased blood flow (seen as doppler signal)
- May detect erosions not seen on plain X-ray

US (usually of hands and wrists) can be performed alongside clinical assessment in a dedicated early arthritis clinic

33
Q

what are some disadvantages of using MRI to investigate RA?

A

Can be used but expensive and time-consuming

34
Q

What are the main requirements for RA treatment?

A

Treatment goal: prevent joint damage

Requires:
- Early recognition of symptoms, referral and diagnosis
- Prompt initiation of treatment: joint destruction = inflammation x time
- Aggressive pharmacological treatment to suppress inflammation

35
Q

What pharmacological treatment is available for rheumatoid arthritis?

A
  1. Glucocorticoid therapy (‘steroids’) useful acutely but avoid long-term use because of side-effects.
  2. NSAIDs (non-steroidal anti-inflammatory drugs e.g. ibuprofen): symptom relief but increasingly less important and unfavourable long-term safety profile
  3. ‘DMARDs’ (disease-modifying anti-rheumatic drugs) = drugs that control the disease process (usually immunosuppressive)

1st line treatment regime:
- IM or short course of oral steroids
Start combination DMARD therapy (usually Methotrexate + hydroxychloroquine &/or sulfasalazine)
2nd line regime:
- Biological therapies offer potent and targeted treatment strategies

36
Q

How does Methotrexate help RA?

A

it is a DMARDS (Immunosuppressive/anti-inflammatory)
- Inhibits dihydrofolate reductase (”folate antagonist”)

37
Q

What are the possible side effects of Methotrexate?

A

Nausea
Hair loss
Fall in WCC
Abnormal liver function
Pneumonitis (inflammation of the lung)
Infection risk

38
Q

What is meant by “biological therapies” in the treatment of RA?

A

Biological therapies are proteins (usually antibodies) that specifically target a protein such as an inflammatory cytokine

39
Q

What are some examples of biological therapies?

A
  1. Inhibition of tumour necrosis factor-alpha (‘anti-TNF’)
  2. B cell depletion
    - Rituximab – antibody against the B cell antigen, CD20
  3. Modulation of T cell co-stimulation
  4. Inhibition of interleukin-6 signalling
40
Q

What is Psoriatic arthritis?

A

(example of seronegative arthritis)
Psoriasis is an immune-mediated disease affecting the skin

41
Q

What are the signs/ clinical presentations of psoriatic arthritis?

A
  • Scaly red plaques on extensor surfaces (eg elbows and knees)
  • ~10% of psoriasis patients also have joint inflammation

Varied clinical presentations:
-Classically asymmetrical arthritis affecting IPJs

But also can manifest as:
-Symmetrical involvement of small joints (rheumatoid pattern)
-Oligoarthritis of large joints
-Arthritis mutilans
-Spinal and sacroiliac joint inflammation

42
Q

What is the pathogenic pathway of psoriatic arthritis?

A

Dominant pathogenic pathway is interleukin-17/interleukin-23
(IL17-IL23)

43
Q

How does psoriatic arthritis differ from RA?

A

Unlike RA, rheumatoid factors are not present (“seronegative”- no AB’s)

44
Q

What is reactive arthritis?

A

Sterile inflammation in joints following infection elsewhere in the body (Reactive arthritis NOT the same as infection in joints (septic arthritis))

Common infections:
- urogenital (e.g. Chlamydia trachomatis)
- gastrointestinal (e.g. Salmonella, Shigella, Campylobacter infections)

45
Q

What are some important extra-articular manifestations of reactive arthritis?

A
  • Enthesitis (tendon inflammation)
  • Skin inflammation
  • Eye inflammation
46
Q

What are possible causes of reactive arthritis?

A
  1. Reactive arthritis may be first manifestation of HIV or hepatitis C infection
  2. Commonly young adults with genetic predisposition (e.g. HLA-B27) and environmental trigger (e.g. Salmonella infection)
    - Symptoms follow 1-4 weeks after infection and this infection may be mild
47
Q

What are the differences between septic arthritis and reactive arthritis?

A

septic A:
positive synovial fluid culture
antibiotic therapy works
joint lavage is used for investigation (for large joints)

reactive arthritis:
sterile synovial fluid culture
antibiotic therapy does not work
joint lavage NOT USED for investigation

48
Q

What is Inflammatory Spondyloarthritis (SpA)?

A

[Classic example is Ankylosing spondylitis (AS), SpA can also occur as a manifestation of psoriatic arthritis and inflammatory bowel disease (IBD)]

  • Primarily inflammation of the spine (spondylitis) and sacro-iliac joints (sacro-iliitis)
  • Peripheral joints, esp. tendon insertions (entheses), can also be affected
49
Q

What are some possible extra-articular manifestations of Inflammatory Spondyloarthritis ?

A
  • Extra-articular manifestations including anterior uveitis (iritis)
  • Dactylitis (‘sausage finger’) due to enthesitis

Musculoskeletal & Rheumatology (6 decks)

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