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Year 2 Clinical > Rheumatology Master Deck > Flashcards

Rheumatology Master Deck Flashcards

1
Q

Differences between arthropathy, arthritis and arthralgia?

A

Arthropathy - disease of a joint

Arthritis - inflammation of a joint

Arthralgia - pain in a joint

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2
Q

2 main categories of arthritis?

A
  • Non-inflammatory arthritis (commonly osteoarthritis)

* Inflammatory arthritis

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3
Q

Sub-divide inflammatory arthritis?

A

Seropositive arthritis - antibodies present in serum, inc. RA and connective tissue disease

Seronegative inflammatory arthropathy

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4
Q

Overall classifications of inflammatory arthritis?

A

PICTURE 1 IN UNI

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5
Q

Which antibodies are assoc. with which auto-immune condition?

A

PICTURE 2 IN UNI

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6
Q

Describe osteoarthritis (OA)

A

Most common form of arthritis; primarily, a degenerative disorder, where, over time, normal structure of the bone is subject to wear and tear

There may be assoc. inflammation, leading to periodic flares

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7
Q

Pathophysiology of osteoarthritis?

A

Imbalance between wear and repair of cartilage within joints

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8
Q

Types of OA?

A

Primary - no causative factor found

Secondary - causative factor is found, e.g: previous injury, crystal arthropathy, genu varum/valgum

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9
Q

4 signs of OA on X-ray?

A

LOSS:

  • Loss of joint space
  • Osteophytes
  • Subchondral sclerosis
  • Subchondral cysts

PICTURE 3 IN UNI

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10
Q

Management of OA?

A

Simple analgesia for pain control; mild opiates may be helpful

Physiotherapy to strengthen surrounding structures

Weight loss and exercise are also important

Sometimes, surgery is an option

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11
Q

4 groups of inflammatory arthropathies?

A
  1. Seropositive
  2. Seronegative
  3. Infectious
  4. Crystal deposition disorders
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12
Q 
Typical patterns of joint involvement in:
A - Rheumatoid arthritis
B - Psoriatic arthritis
C - Inflammatory spondylitis 
D - Osteoarthritis

?

A

PICTURE 4 IN UNI

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13
Q

Features suggestive of joint inflammation and inflammatory arthritis?

A 
Joint pain with associated swelling
• Morning stiffness
• Improvement in symptoms with exercise
• Synovitis on examination
• Raised inflammatory markers (CRP and PV)
• Extra-articular symptoms
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14
Q

Describe rheumatoid arthritis (RA)

A

Most common seropositive inflammatory arthropathy

It is an autoimmune inflammatory SYMMETRIC polyarthropathy that most commonly affects small joints of the hands and feet; as the disease progresses, large joints can become inv.

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15
Q

Occurrence of RA?

A

WOMEN are affected more than men

Peaks between the ages of 35 and 50 years

First-degree relatives are at higher risk

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16
Q

Pathogenesis of RA?

A

Immune response is initiated against synovium, leading to synovitis and tenosynovitis

Inflammatory pannus forms which then attacks and denudes articular cartilage, leading to joint destruction

Tendon ruptures and soft tissue damage can occur leading to joint instability and subluxation

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17
Q

Triggers of RA?

A

Smoking, infection, trauma, etc

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18
Q

Classification criteria for RA in newly presenting patients?

A

A score of 6/10 is required for diagnosis

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19
Q

Clinical features of RA?

A

Symmetrical synovitis (doughy swelling) with pain and morning stiffness

Hands and feet tend to be inv. early

MCP and PIPs joints are affected, as well as wrists, but DIP joints are NOT AFFECTED

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20
Q

What can aggressive/untreated RA lead to?

A

Deformities

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21
Q

Spine in RA?

A

With longstanding disease, atlanto-axial subluxation of the cervical spine can develop, leading to cervical spinal cord compression

PICTURE 6 IN UNI

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22
Q

Extra-articular manifestations of RA?

A
  • Rheumatoid nodule can occur in some RA patients; they are most commonly found on EXTENSOR surfaces or sites of frequent mechanical irritation
  • Lung inv. includes pleural effusion, interstitial fibrosis and pulmonary nodules
  • CV morbidity and mortality increased
  • Ocular inv. is common and inc. keratoconjunctivitis sicca, episcleritis, uveitis, nodular scleritis (may lead to scleromalacia)
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23
Q

Ix for RA?

A

Measure rheumatoid factor and anti-CCP antibody (more specific)

CRP, ESR and PV raised

X-ray

US may be helpful in detecting synovial inflammation, if uncertain

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24
Q

X-ray features of RA?

A

May show no joint abnormality in early disease; may show:
• Peri-articular osteopenia
• Soft tissue swelling

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25
Q

Aim of RA treatment?

A

Early and aggressive treatment can improve outcomes

Goal is to commence DMARD therapy within 3 months of symptoms onset

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26
Q

Treatment of RA?

A

Simple analgesia, NSAIDs and IM/intra-articular/oral ateroids; these are used short-term, for symptoms relief, as bridging therapy, until DMARDs begin working

DMARD:
1st line is methotrexate
Others - sulfasalazine, hydroxychloroquine, etc

If no response to DMARDs, biologic therapy (anti-TNF drugs)

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27
Q

Side effects of DMARDs?

A

Increased risk of infection

Bone marrow suppression

Reactivation of TB (with anti-TNF drugs)

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28
Q

How is disease activity measured?

A

DAS 28 score, which is a composite score of 4 domains:
• Tender joint count • Swollen joint count
• CRP/ESR
• Visual analogue score (patients own assessment of their disease activity)

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29
Q

Values of DAS 28 score and their meaning?

A

PICTURE 7 IN UNI

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30
Q

When are patients eligible for biologic therapy?

A

DAS 28 score > 5.1

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31
Q

Other therapies available for RA?

A

Physiotherapy and occupational therapy

Podiatrists and orthotists

Surgery for resistant disease (uncommon now)

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32
Q

4 types of seronegative arthritis?

A
  1. Ankylosing spondylitis
  2. Psoriatic arthritis
  3. Enteropathic arthritis
  4. Reactive arthritis
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33
Q

Characteristics of seronegative arthritis?

A

Inflammation and/or arthritic disease of the spine, known as spondylarthropathy, and an ASYMMETRIC oligoarthritis

Sacroiliitis, uveitis, dactylitis (inflammation of a digit) and entesopathies are common

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34
Q

Two types of entesopathies that are very common in seronegative arthritis?

A

Achilles insertional tendonitis

Plantar fasciitis

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35
Q

Testing for spondyloarthritis?

A

Patients are often HLA-B27 +ve, although only a minority of these people develop one (it is not a useful diagnostic test)

CRP and ESR usually raised

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36
Q

What is ankylosing spondylitis?

A

Chronic inflammatory disease of the spine and sacroiliac joints, which can lead to eventual fusion of the intervertebral and SI joints

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37
Q

Occurrence of ankylosing spondylitis?

A

MALES are more commonly affected

Age of onset typically between 20-40 years

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38
Q

Symptoms of ankylosing spondylitis?

A

Spinal pain and stiffness; may also develop knee/hip arthritis

Spinal morning stiffness that IMPROVES with EXERCISE

Eventually, loss of spinal movement and ? mark spine develops (loss of lumbar lordosis and increased thoracic kyphosis)

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39
Q

Test for lumbar spinal flexion?

A

Schobers test inv. measuring 5cm below PSIS and 10cm above, whilst the patient is upright

Ask them to bend forward and remeasure the distance

Normally, it should extend beyond 20 cm

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40
Q

Conditions assoc. with ankylosing spondylitis?

A

Anterior uveitis
Aortitis,
Pulmonary fibrosis Amyloidosis

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41
Q

X-ray signs of ankylosing spondylitis?

A

Commonly normal at the time of presentation.

  • Sclerosis and fusion of the sacroiliac joints
  • Bony spurs from the vertebral bodies, known as syndesmophytes, which can bridge the intervertebral disc

Result is fusion, producing a “bamboo spine”

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42
Q

HLA-B27 in ankylosing spondylitis?

A

90% of patients are +ve

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43
Q

Treatment of ankylosing spondylitis?

A
  • Physiotherapy, exercise, NSAIDs and anti-TNF inhibitors for more aggressive disease
  • DMARDs do not have any impact on spinal disease but may be used if there is peripheral joint inflammation
  • Surgery is mainly reserved for hip and knee arthritis
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44
Q

Describe psoriatic arthritis

A

Occurs in 30% of psoriasis patients

Arthritis is usually an ASYMMETRICAL oligoarthritis; can affect the DIP joints (only inflammatory arthritis to do this)

Patients usually have nail changes, inc. pitting and onycholysis

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45
Q

Other features of psoriatic arthritis?

A

Spondylitis, dactylitis and enthesitis commonly occur

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46
Q

Treatment of psoriatic arthritis?

A

DMARDs, usually methotrexate; anti-TNF therapy is available for those who do not respond

Joint replacement can be considered in severely affected larger joints and DIP joint fusion can occasionally help

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47
Q

What is enteropathic arthritis?

A

Inflammatory arthritis involving the peripheral joints and sometimes spine, occurring in patients with IBD (Crohn’s or UC)

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48
Q

Presentation of enteropathic arthritis?

A

Large joint ASYMMETRICAL oligoarthritis

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49
Q

Treatment of enteropathic arthritis?

A

Medication to manage both the IBD and arthritis

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50
Q

What is reactive arthritis?

A

Tends to occur after an infection, commonly genitourinary (Chlamydia, Neisseria) or GI infections (Salmonella, Campylobacter); this triggers an autoimmune arthropathy

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51
Q

Presentation of arthritis?

A

Large joints, e.g: the knee become inflamed 1‐3 weeks following the infection

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52
Q

What is Reiter’s syndrome?

A

Triad of symptoms of urethritis, uveitis/conjunctivitis and arthritis

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53
Q

Treatment of Reiter’s syndrome?

A

Most cases are self‐limiting; others have a chronic form OR frequent relapses

Treatment is aimed at the underlying infectious cause and symptomatic relief, inc. IA/IM steroid injections; occasionally DMARDs are required in chronic cases

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54
Q

Different types of connective tissue disease?

A
  • Systemic lupus erythematosus (SLE)
  • Sjogrens syndrome
  • Systemic sclerosis

Mixed connective tissue disease

• Anti-phospholipid syndrome.

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55
Q

What is SLE?

A

Prototype connective tissue disease; it is chronic and autoimmune and inv. skin, joints kidneys, blood cells and NS (can affect almost any system)

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56
Q

Classification criteria of SLE?

A

≥ 4 criteria in total but at least 1 clinical and 1 laboratory

OR

Biopsy proven lupus nephritis with +ve ANA or anti-DNA

PICTURE 8 IN UNI

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57
Q

Pathogenesis of SLE?

A

Defective apoptosis causes increased cell death and disturbed immune tolerance

Defective clearance of apoptotic cell debris allows for antigen persistence and immune complex production

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58
Q

Occurrence of SLE?

A

High in Black people of the US and UK, but not in African Blacks

WOMEN (90%) are affected more, frequently starting at child-bearing age

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59
Q

Constitutional symptoms of SLE?

A

Fever, fatigue and weight loss

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60
Q

MSK symptoms of SLE?

A

Arthralgia, myalgia and inflammatory arthritis

Avascular necrosis of the femoral head may be related to steroid use

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61
Q

Mucocutaneous symptoms of SLE?

A

Malar rash (SPARES THE NASO-LABIAL FOLDS) and photsensitivity

Discoid lupus

Subacute cutaneous lupus

Oral/nasal ulceration

Raynaud’s phenomenon

Alopecia

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62
Q

Renal symptoms of SLE?

A

LUPUS NEPHRITIS (must screen for this)

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63
Q

Respiratory symptoms of SLE?

A 
Pleurisy
Pleural effusion
Pneumonitis
PE
Pulmonary hypertension
Interstitial lung disease (ILD)
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64
Q

Haematological symptoms of SLE?

A

Leukopenia, lymphopenia, anaemia (may be haemolytic), and thrombocytopenia

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65
Q

Neuropsychiatric symptoms of SLE?

A

Seizures, psychosis, headache, aseptic meningitis

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66
Q

Cardiac symptoms of SLE?

A

Pericarditis (most common cardiac sign), pericardial effusion, pulmonary hypertension, sterile endocarditis (Libman-Sacks endocarditis) and accelerated ischaemic heart disease

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67
Q

GI symptoms of SLE?

A

Uncommon but inc. autoimmune hepatitis, pancreatitis and mesenteric vasculitis

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68
Q

Ix for SLE?

A

FBC (for anaemia, leucopaenia and thrombocytopaenia)

Antibody testing:
Anti-ANA (not specific)
Anti-dsDNA (specific)
Anti-Sm (specific by low sensitivity)
Anti-Ro, anti-La and anti-RNP (non-specific)

Urinalysis and RENAL BIOPSY to look for lupus nephritis

Imaging for damage to other organs

69
Q

How to monitor SLE disease activity?

A

Anti-dsDNA Ab varies with disease activity

C3/4 levels are low when the disease is active, esp. renal disease, as complement is consumed

Urinalysis to check for renal involvement

Manage CV risk factors

70
Q

Management of SLE?

A

Skin disease and arthralgia:
Hydroxychloroquine, topical steroids and NSAIDs

Inflammatory arthritis/some organ involvement, e.g: pericardial disease - immunosuppression (azathioprine) with corticosteroids at moderate doses and for short periods

Severe organ disease, e.g: lupus nephritis or CNS lupus then treatment tend to involve IV steroids and cyclophosphamide

In unresponsive cases, IV Ig and Rituximab may be used

71
Q

Monitoring of SLE?

A

Check anti-dsDNA antibodies and complement levels

Check urinalysis for blood or protein (may indicate glomerulonephritis)

Evaluate and manage CV risk factors, like BP and cholesterol (one of the major causes of mortality)

72
Q

What is Sjogren’s syndrome?

A

Autoimmune condition characterised by lymphocytic infiltrates in EXOCRINE organs

It can be a primary conditions OR can occur secondary to RA or SLE, etc

73
Q

Symptoms of Sjogren’s?

A

Typically, DRY EYES (keratoconjunctivitis sicca) AND MOUTH (xerostomia); due to dry mouth, dental problems can occur (e.g: high risk of caries)

Other symptoms:
• Arthralgia
• Fatigue 
• Vaginal dryness
• Parotid gland swelling
74
Q

Complications of Sjogren’s?

A

Peripheral neuropathy
ILD
Increased risk of lymphoma

75
Q

Diagnosis of Sjogren’s?

A

Confirmation of ocular dryness using Schirmer’s test

+ve anti-Ro and anti-La antibodies

Typical features of a lip? gland biopsy

76
Q

Classification criteria for diagnosis of Sjogren’s?

A

Diagnosis requires 4 of:
1. Ocular symptoms - dry eyes for > 3 months, foreign-body sensation, use of tear substitutes > 3 times daily

  1. Oral symptoms - feeling of dry mouth, recurrently swollen salivary glands, frequent use of liquids to aid swallowing
  2. Ocular signs - Schirmer test performed without anesthesia (< 5 mm in 5 min), +ve vital dye staining results
  3. Oral signs - abnormal salivary scintigraphy findings, abnormal parotid sialography findings, abnormal sialometry findings
  4. Positive minor salivary gland biopsy findings
  5. Positive anti–Ro or La antibodies
77
Q

Management of Sjogren’s?

A

Symptomatic management:
• Lubricating eyedrops

  • Saliva replacement products and regular dental care
  • Pilocarpine can stimulate saliva production but side effects inc. flushing
  • Hydroxychloroquine can help with arthralgia and fatigue
  • Other immunosuppression would only be used for organ inv. like ILD
78
Q

What is systemic sclerosis?

A

Systemic CTD where excess collagen deposition leads to skin and internal organ changes

79
Q

Presentation of systemic sclerosis?

A

CREST:
Calcinosis (subcutaneous deposits of Ca may be seen on digits)
Raynaud’s phenomenon (tends to be the presenting feature)
Esophageal dysmotility
Sclerodatyly (skin becomes thick, tight and shiny)
Telangiectasia

80
Q

Major and minor cutaneous features of systemic sclerosis?

A

Major:
Centrally located skin sclerosis affecting the arms, face and/or neck

Minor:
Sclerodactyly and atrophy o the fingertips and bilateral lung fibrosis

Diagnosis is made when the patient has 1 major 2 minor features

81
Q

Facial signs of systemic sclerosis?

A

Pinching of the skin of the nose (“BEAKING”) and tightening of the skin around the mouth

Telangiectasia can also be seen

82
Q

Organ involvement in systemic sclerosis?

A

Pulmonary hypertension, fibrosis and accelerated hypertension leading to renal crisis

Gut inv. can lead to dyaphagia, malabsorption and small bowel bacterial overgrowth

Inflammatory arthritis and myositis may occur

83
Q

2 classifications of systemic sclerosis?

A

Limited - skin inv. tends to be confined tot he face, hands, forearms and feet; organ inv. occur latera

Diffuse - skin changes occur more rapidly and can inv. the trunk; there is early signification organ inv.

84
Q

Which antibodies are assoc. with which types of systemic sclerosis?

A

Limited: anti-centromere antibody

Diffuse: anti-Scl-70 antibody

85
Q

Ix for systemic sclerosis?

A

Anti-centromere Ab and anti-Scl-70 Ab

86
Q

Monitoring of systemic sclerosis?

A

Organ screening regularly occurs, inc. PFTs, echo and monitoring of renal function

87
Q

Management of systemic sclerosis?

A

Raynaud’s/digital ulcers: CCBs, iloprost, bosentan

Renal involvement: ACEIs

GI involvement: PPIs for reflux

ILD: immunosuppression (usually cyclophosphamide)

88
Q

What is Mixed Connective Tissue Disease (MCTD)?

A 
Defined conditions which features symptoms also seen in other CTDs, inc.  :
• Raynaud's phenomenon
• Arthralgia/arthritis
• Myositis
• Sclerodactyly
• Pulmonary hypertension
• ILD
89
Q

Antibodies assoc. with MCTD?

A

Anti-RNP antibodies

90
Q

Monitoring of MCTD?

A

Due to the risk of pulmonary hypertension, regular echocardiograms (anually) are done

Screen for ILD with PFTs

91
Q

Management of MCTD?

A

CCBs may be helpful for Raynaud’s

Immunosuprpession if there is significant muscle/lung disease

92
Q

What is anti-phospholipid syndrome (APS)?

A

Autoimmune, hypercoagulable state manifesting as recurrent venous/arterial thrombosis and/or fetal loss

It can be assoc. with other disease, e.g: SLE or other autoimmune disorders, OR it can occur by itself

93
Q

Presentation of APS?

A

Increased frequency of stroke/MI (esp. in younger individuals)

Libman-Sacks enodcarditis (sterile); this can also lead to embolisation and stroke

Recurrent PE or thrombosis can lead to pulmonary hypertension

Catastrophic APS is rare and often a fatal manifestation, where there are multi-organ infarction over a period of days to week s

Late spontaneous fetal loss is common and recurrent early fetal loss can occur

Some patient have a migraine

Livedo reticularis (cutaneous finding)

94
Q

Ix for APS?

A

May find thrombocytopaenia

Prolongation of APTT

Lupus anticoagulant, anti-cardiolipin antibodies and anti-β2 glycoprotein may be +ve

95
Q

Management of APS?

A

Anticoagulation for those who have had an episode of thrombosis

LMWH is used during pregnancy for those who have had recurrent pregnancy loss (warfarin is teratogenic)

Patients who are found to have +ve antibodies but who have never had had an episode of thrombosis do not require anticoagulation

96
Q

What is gout?

A

A CRYSTAL ARHTROPATHY caused by urate crystal deposition within a joint; it tends to occur due to hyperuricaemia

97
Q

Describe why hyperuricaemia can occur

A

Uric acid is the final breakdown product of purines (adenine and guanine) in DNA metabolism

It can occur due to renal underexcretion (diuretics or renal failure) or due to excessive intake of alcohol, red meat or seafood

98
Q

How can gout be triggered?

A

Uric acid crystals precipitating into joints can be triggered by dehydration, trauma or surgery

99
Q

Joints affected by gout?

A

Any joint can be affected but it tends to be the 1st MTP joint (AKA Podagra)

Ankle and knee are also commonly affected

100
Q

Presentation of gout?

A

Intensely painful, red, hot and swollen joint; symptoms tend to last for 7-10 days, if untreated, before spontaneously resolving
(MIMICS septic arthritis)

Gouty tophi can be seen (painless, white accumulation of uric acid which can occur in soft tissue and occasionally erupt through skin)

101
Q

Consequences of chronic gout?

A

Destructive, erosive arthritis

102
Q

How can a definitive diagnosis of gout be made?

A

Joint synovial fluid aspirate with polarised microscopy shows NEEDLE-shaped uric acid crystals which display -ve birefringence (change from yellow to blue when lined across the direction of polarisation)

Fluid is also analysed with gram stain and culture to exclude infection

103
Q

Treatment of acute gout?

A

NSAIDs, corticosteroids and opioid analgesics

Colchicine for those who cannot tolerate NSAIDs

104
Q

Prophylaxis of gout?

A

For recurrent attacks, OR joint destruction OR tophy:
Allopurinol/other urate-lowering therapies can prevent attack

They should not be started until as acute attack has settled as they can potentiate a further flare

105
Q

What is pseudogout?

A

Crystal arthropathy causing an acute arthritis but, in contrast to gout, it is caused by calcium pyrophosphate crystals

106
Q

Diagnosis of pseudogout?

A

Joint aspirate shows +vely birefringent crystals

107
Q

What is chrondrocalcinosis?

A

Calcium pyrophosphate deposition occurs in cartilage and other soft tissues in the absence of acute inflammation

Both come under the umbrella of Calcium Pyrophosphate Deposition disease (CPPD), of which the exact cause is unknown

108
Q

Joints affected by CPPD?

A

Tends to affect the knee, wrist and ankle

109
Q

Which conditions can coexist with CPPD?

A

Hyperparathyroidism, hypothyroidism

Renal osteodystrophy

Haemochromatosis

Wilson’s disease

Can also occur in some OA cases; however, chronic CPPD can also cause osteoarthritic change

110
Q

Treatment of acute pseudogout?

A

NSAIDs, corticosteroids (systemic and intra-articular) and occasionally colchicine

No medications can be used as prophylaxis

111
Q

What is polymyalgia rheumatica?

A

Fairly common chronic inflammatory condition of unknown aetiology that affects elderly individuals (rare <50 years)

112
Q

Symptoms of polymyalgia rheumatica?

A

PROXIMAL myalgia of the hip and shoulder girdles with accompanying morning stiffness of > 1 hour

Symptoms tend to IMPROVE as the day goes on and with MOVEMENT

113
Q

Assoc. conditions with polymyalgia rheumatica?

A

~15% of patient develop giant cell arteritis (GCA)

40-50% of GCA patients have assoc. PMR

114
Q

Diagnosis of PMR?

A

No specific diagnostic test for PMR but it tends to be assoc. with a raised CRP and PV/ESR

Symptoms respond dramatically to low-dose steroids (prednisolone 15 mg daily) and this is used as a diagnostic tool

115
Q

Treatment of PMR?

A

Prednisolone 15mg daily; dose is gradually reduced over 18 months

After this, conditions tends to have resolved

116
Q

What is Giant Cell Arteritis (GCA)?

A

Most common form of systemic vasculitis in adults; it has an unknown aetiology and occurs in ELDERLY patients

117
Q

Histopathology of GCA?

A

Transmural inflammation of the intima, media and adventitia of affected arteries

Patchy inflammation by lymphocytes, macrophages and multinucleated giant cells

Vessel wall thickening can result in arterial lumen narrowing, resulting in distal ischaemia

118
Q

Presentation of GCA?

A

Visual disturbances, headache, jaw claudication and scalp tenderness (with hair combing)

Constitutional symptoms, such as fatigue, malaise and fever may also be present

119
Q

When should GCA be considered?

A

Always consider it in the DD of a new-onset headache in patients >50 years, with an elevated ESR/CRP/PV

120
Q

Visual symptoms of GCA?

A

Visual loss is one of the most significant causes of morbidity, e.g: unilateral vision blurring/loss, often painless, and sometimes diplopia (double vision)

Permanent visual impairment can occur

121
Q

Describe the headache of GCA

A

Headache is usually continuous and located in the temporal or occipital areas

Focal tenderness on direct palpation is typically present, with a thickened, prominent and tender to touch temporal artery

122
Q

Describe jaw claudication in GCA

A

Fatigue/discomfort of jaw muscles during chewing of firm foods

It is caused by ischaemia of the maxillary artery

123
Q

Diagnosis of GCA?

A

Raised inflammatory markers

Temporal artery biopsy (most definitive test), which has 100% specificity for GCA but low sensitivity

124
Q

Why does a temporal artery biopsy have low specificity for GCA?

A

Skip lesions mean that some segments of the artery are normal

125
Q

Typical temporal artery biopsy findings in GCA?

A

Mononuclear infiltration or granulomatous inflammation, usually with multinucleated giant cells

126
Q

Treatment of GCA?

A

NO VISUAL IMPAIRMENT:
Prednisolone 40 mg gradually reduced over 18 months to 2 years

WITH VISUAL SYMPTOMS:
Prednisolone 60 mg gradually reduced over 18 months to 2 years

Treatment is started as soon as the diagnosis is suspected and should not be delayed for the biopsy results

127
Q

What are polymyositis and dermatomyositis?

A

Polymyositis - idiopathic inflammatory myopathy that causes symmetrical, proximal muscle weakness

Dermatomyositis - clinically similar but also has typical cutaneous manifestations

128
Q

Occurrence of dermato/polymyositis?

A

More common in women than men (2:1) and usually affects adults >20 years, esp. those 45-50 years

129
Q

Pathogenesis of polymyositis?

A

T-cell mediated cytotoxic process directed against unidentified muscle antigens (nuclear and cytoplasmic auto-antigens)

CD8+ T cells, along with macrophages, initially surround healthy non-necrotic muscle fibers and eventually invade and destroy them

130
Q

Antibodies found in polymyositis?

A

ANA and anti-RNP antibodies (shared with other autoimmune conditions)

Anti-Jo-1 and anti-SRP antibodies are unique to myositis

131
Q

Presentation of polymyositis?

A

SYMMETRICAL, proximal muscle WEAKNESS in the upper and lower extremities that is of insidious onset and tends to be noticed with, e.g: climbing stairs

Some patients have myalgia

Dysphagia can occur secondary to oropharyngeal and esophageal involvement occurs in about 1/3rd of patients with polymyositis and is a poor prognostic sign

ILD can occur, esp. in those +ve for anti-Jo-1 antibody

132
Q

Ix for polymyositis?

A

Raised inflammatory markers

Serum creatine kinase is usually raised

ANA, anti-Jo-1 and anti-SRP +ve

MRI for extent of muscle inv.

EMG findings are abnormal in most patients

MUSCLE BIOPSY

133
Q

Muscle biopsy findings in polymyositis?

A

Muscle fibres in varying stages of inflammation, necrosis and regeneration

There is a chronic inflammatory infiltrate of T cells, esp. CD8+

134
Q

Management of polymyositis?

A

Prednisolone (initially 40 mg)

COMBINED WITH

Immunosuppressive drugs, such as methotrexate or azathioprine

135
Q

Cutaneous features of dermatomyositis?

A

V-shaped rash over chest

Gottron’s papules, e.g; over fingers

Heliotrope rash

136
Q

Malignant assoc. with dermatomyositis?

A 
Common cancers inc:
Breast
Ovarian
Lung
Colon
Oesophagus
Bladder

Screen for malignancy at the time of diagnosis

137
Q

What is fibromyalgia?

A

Unexplained conditions causing widespread muscle pain and fatigue, commonly in young and middle-aged women

Can occur as a primary condition but can also be seen in patients with RA or SLE

138
Q

Potential causes of fibromyalgia?

A

Disorder of central pain processing or a syndrome of central sensitivity; patients tend to have a lower threshold for pain/other stimuli

139
Q

Signs and symptoms of fibromyalgia?

A

Persistent (≥ 3 months) widespread pain on both sides of the body, above and below the waist

Fatigue (disrupted and unrefreshing sleep)

Cognitive difficulties

Multiple other unexplained symptoms, anxiety and/or depression, and functional impairment ADLs

140
Q

Conditions assoc. with fibromyalgia?

A

Depression, IBS and migraines

141
Q

Ix for fibromyalgia?

A

CLINICAL DIAGNOSIS

Rule out other conditions, e.g: hypothyroidism, RA, SLE, PMR, etc

142
Q

Management of fibromyalgia?

A

Self-management techniques and education

Graded exercise

Atypical analgesia including tricyclics (e.g. amitriptyline), gabapentin and pregabalin may be of benefit

Cognitive behavioural therapy may help some patients

143
Q

What is vasculitis?

A

Inflammation of blood vessels that results in thickening, stenosis and occlusion with ischaemia

144
Q

Classifications of vasculitis?

A

ADD CLASSIFICATION PICTURE

145
Q

Describe large vessel vasculitis?

A

Primary vasculitis that causes chronic granulomatous inflammation predominantly of the aorta and its major branches

146
Q

Types of large vessel vasculitis?

A

Temporal (giant cell) arteritis - tends to be in >50 years and is far more common in east Asian countries

Takayasu arteritis - tends to be in young patients, rarely above 50 years

147
Q

Features of large vessel vasculitis?

A

Non-specific, e.g: low-grade fever, malaise, night sweats, weight loss, arthralgia and fatigue

Following this, claudication symptoms occur in upper and lower limbs

148
Q

Consequences of untreated large vessel vasculitis?

A

Vascular stenosis and aneurysms can occur, causing pulses and bruits

149
Q

Ix for large vessel vasculitis?

A

ESR/PV/CRP raised

MR angiography shows thickened vessel walls and stenosis

PET CT shows increased metabolic activity in the large vessels

150
Q

Treatment of large vessel vasculitis?

A

40-60 mg of prednisolone gradually reduced

Steroid-sparing agents, e.g: methotrexate and azathioprine

151
Q

How to differentiate between different types of small to medium vessel vasculitis?

A

ADD VASCULITIS PICTURE

152
Q

Similar presenting features of small to medium vessel vasculitis?

A
  • Fever and weight loss
  • Raised, non blanching purpuric rash (vasculitic rash)
  • Arthralgia/arthritis
  • Mononeuritis multiplex
  • Glomerulonephritis
  • Lung opacities on X-ray
153
Q

4 types of ANCA assoc. vasculitis?

A

Granulomatosis with polyangiitis (GPA), AKA Wegener’s

Microscopic polyangiitis (MPA)

Renal limited vasculitis (RLV)

Churg-Strauss syndrome (CSS)

154
Q

Describe GPA

A

Granulomatous inflammation inc. the resp tract and necrotising vasulitis affecting small to medium sized vessels, e.g: capillaries, venules, arterioles and arteries

Necrotising glomerulonephritis is common

155
Q

Describe MPA

A

Necrotising vasculitis, with few/no immune deposits, affecting small vessel, i.e: capillaries, venules or arterioles

Necrotising arteritis involving small and medium sized arteries may be present; necrotising glomerulonephritis is very common

Pulmonary capillaritis often occurs

156
Q

Describe RLV

A

Pauci-immune necrotising glomerulonephritis with no apparent extra-renal features at presentation

157
Q

Describe CSS

A

EOSINOPHIL-rich granulomatous inflammation, inv. the resp tract, necrotising vasculitis affecting the small to medium-sized vessel and assoc. with asthma and eosinophilia

158
Q

Symptoms of GPA?

A

ENT symptoms are common, inc. nosebleeds, deafness, recurrent sinusitis and nasal crusting (over time, there may be collapse of nasal cartilage)

Resp symptoms such as haemoptysis and cavitating lesions on CXR are seen

159
Q

Antibodies assoc. with GPA?

A

cANCA and anti-proteinase 3 (anti-PR3) antibodies

160
Q

Characteristics of EGPA?

A

Late onset asthma

Rhinitis

Raised eosinophil count

Neurological symptoms, such as mononeuritis multiplex are common

161
Q

Most important complication of MPA?

A

Glomerulonephritis is common

162
Q

How to differentiate between ANCA-assoc. vasculitides?

A

ADD ANCA TABLE

163
Q

Ix for small to medium vessel vasculitides?

A

ESR/PV/CRP raised

Anaemia of chronic disease

U&Es for renal inv.

cANCA antibodies

Urinalysis

CXR

Biopsy of affected area, e.g: renal, skin, etc

164
Q

Management of ANCA-assoc vasculitis?

A

IV steroids and cyclophosphamide

165
Q

What is Henoch-Schonlein purpura?

A

Acute IgA-mediated disorder characterized by a generalised vasculitis inv. the small vessels of the skin, GI tract, kidneys, joints and, rarely, lungs and CNS

166
Q

Occurrence of Henoch-Schonlein purpura?

A

Commonly affects children

Tends to be a history of upper resp tract infection (a few weeks prior to symptoms)

167
Q

Symptoms of Henoch-Schonlein purpura?

A

Purpuric rash over buttocks and lower limbs, abdominal pain and vomiting and joint pain

168
Q

Treatment of Henoch-Schonelin purpura?

A

Self-limiting conditions not requiring specific treatment

Usually settles over a course of weeks to months

Year 2 Clinical (119 decks)

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