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Phase 4 > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Define ankylosing spondylitis.

A

Chronic progressive inflammatory disease of spine and sacroiliac joints.

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2
Q

Is ankylosing spondylitis more common in males or females?

A

M>F

6: 1 at 16 years old
2: 1 at 30 years old

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3
Q

Which HLA type is normally present in ankylosing spondylitis?

A

90% HLA B27 positive

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4
Q

What is the pathophysiology of ankylosing spondylitis?

A

Inflammation in the axial skeleton is initially dominated by mononuclear cell infiltrates and by increased number of osteoclasts at bone cartilage interface.
AS involves: inflammation, cartilage erosion, ossification.

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5
Q

What are the symptoms of ankylosing spondylitis?

A 
Gradual onset severe low back pain. 
Worse at night. 
Spinal morning stiffness.
Relieved by exercise. 
Better towards end of day. 
Ultimately may lead to spinal fusion.
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6
Q

What are the investigations for ankylosing spondylitis?

A 
FBC
ESR
CRP
RF
HLAB27
X-ray
MRI
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7
Q

What are the complications of ankylosing spondylitis?

A 
Asymmetrical oligoarthropathy
Restrictive lung disease
Enthesitis
Acute iritis
Osteeoporosis
Aortic valve incompetence
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8
Q

What is the management of ankylosing spondylitis?

A 
Exercise
NSAIDs
Sulphasalazine
TNF alpha blockers (infliximab, adalimumab, etanercept)
Local steroid injections
Joint replacements
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9
Q

What are the symptoms of polymyalgia rheumatica?

A 
Acute onset
Muscle aches, tenderness, morning stiffness
Fatigue
Fever - low grade
Weight loss and anorexia
Malaise
Night sweats
Depression may be present
The patient may report asymmetrical joint pain, carpal tunnel sydrome symptoms and swelling of the hands and feet.
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10
Q

Who is polymyalgia rheumatica more common in?

A

Women

>50s

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11
Q

What investigations would you do in suspected polymyalgia rheumatica?

A 
ESR
CRP
TFTs
Immunoglobulins
CK (to rule out myositis)
Ultrasound
MRI (to check for synovitis/bursitis, will be absent in PMR)
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12
Q

What is the management of polymyalgia rheumatica?

A

Prednisolone 15mg per day with marked response.
Failure of response should be a cause to question diagnosis.
Gradually reduce as symptoms improve and CRP normalised.
Methotrexate may be needed.
NSAIDs not indicated long term.

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13
Q

Define temporal arteritis.

A

Immune mediated vasculitis characterised by granulomatous inflammation in the wall of medium sized and large arteries.

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14
Q

What is the pathophysiology of temporal arteritis?

A

T cell and macrophages.
IL-6 plays a role
Inflammation starts from outer layer and moves in.
Thickening and narrowing of lumen with subsequent ischaemia occurs due to healing.

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15
Q

Which other illness is temporal arteritis associated with?

A

Polymyalgia rheumatica.

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16
Q

Which age group is temporal arteritis associated with?

A

Over 50s

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17
Q

What are the symptoms of temporal arteritis?

A 
Headache
Temporal artery tenderness
Jaw claudication
Amaurosis fugax
PMR
Low grade fever
Weight loss and fatigue
Neurological manifestations occur in about one third of patients and may include stroke, TIA, or neuropathy.
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18
Q

What are the examination findings in temporal arteritis?

A

Temporal artery thickening, tenderness and nodularity
Pallor and oedema of the optic disc (Possibly with cotton-wool patches and haemorrhages. Optic neuropathy is irreversible).
Carotid or subclavian arteries bruits in patients with large vessel involvement: pulses in the neck or the arms may be decreased or absent in this subset of giant cell arteritis.
Patients with large-vessel stenoses may have asymmetric blood pressures or decreased pulses.

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19
Q

What would be the investigation findings in a patient with temporal arteritis?

A

ESR >50
Most patients have normochromic, normocytic anaemia - related to chronic inflammation and elevated platelet count.
1/3 of patients have mildly abnormal results on LFTs, particularly ALP.
Temporal artery biopsy is definitive test.
If systemic large vessel involvement suspected then CT/MRI angio.

20
Q

What is the management of temporal arteritis?

A

Prednisolone 60mg
Usually 2 year course.
Reduce steroids if symptoms reduce.

21
Q

What is the pathophysiology of rheumatoid arthritis?

A

Inflamed synovium is central to the pathogenesis.
Increased angiogenesis, cellular hyperplasia, influx of inflammatory cells, changes in the expression of cell surface adhesion molecules, many cytokines.
T cells, B cells, macrophages and plasma cells.
High levels of metalloproteinase activity are thought to contribute to joint destruction.

22
Q

What is the intra-articular presentation of rheumatoid arthritis?

A

Symmetrical, swollen, painful and stiff small joints.
>6 weeks.
Lasts >1 hour after waking
Larger joints may become involved.

23
Q

What is the extra-articular presentation of rheumatoid arthritis?

A 
Weight loss
Fatigue
Fever
Pericarditis
Nodules
Vasculitic skin disorders
Lymphadenopathy
Fibrosing alveolitis
Obliterative bronchiolitis
Pleural and pericardial effusion
Raynaud's
Carpal tunnel syndrome
Peripheral neuropathy
Splenomegaly
24
Q

Which signs may be visible in a patient with rheumatoid arthritis?

A

Boutonniere deformity
Swan neck deformity
Ulnar deviation

25
Q

Which investigations would be carried out for rheumatoid arthritis?

A 
Rheumatoid factor
Anti-cyclic citrullinated peptide antibodies (anti-CCP)
FBC (anaemia)
CRP
X-rays
US/MRI
26
Q

What are the x-ray findings of rheumatoid arthritis?

A

Juxta-articular osteopenia.
Soft tissue swelling
Joint deformity.
Loss of joint space.

27
Q

What is the diagnostic criteria for rheumatoid arthritis?

A 
4 out of 7:
Morning stiffness (>1 hour, lasting >6 weeks)
Arthritis >3 joints
Arthritis of hand joints
Symmetrical arthritis
Rheumatoid nodules
\+ve rheumatoid factor
Radiographic evidence
28
Q

What is the management of rheumatoid arthritis?

A 
DMARDS - methotrexate +/- hydroxychlorouine/sulfasalzine - monitor bloods
Biological agents - infliximab etc
Steroids
NSAIDs
Physio
OT
Surgery
29
Q

What is the pathophysiology of gout?

A

Urate is a metabolite of purines and the ionised form of uric acid. Hyperuricaemia is due to renal under-excretion of urate in 90% of cases and to over production in 10%,. High urate levels result in super-saturation and crystal formation. Crystals in the joint interact with undifferentiated phaocytes, this triggers an acute inflammatory response cuasing neutrophilic synovitis.
Urate crystals can induce chronic inflammation, leading to synovitis, cartilage loss and bone erosions.

30
Q

What are the risk factors for hyperuricaemia?

A

Dietary factors such as consumption of seafood, meat and alcohol, esp. beer.
High cell turnover, such as haematological cancer and chemotherapy.
Diuretics can increase urate levels.
Obesity.
Insulin resistance.
Hypertension.

31
Q

Who is gout most common in?

A

Men and pre-menopausal women.

32
Q

How is diagnosis confirmed?

A

Arthrocentesis showing monosodium urate crystals. Strongly negative birefringent crystals.

33
Q

Which are the most commonly affected joints in gout?

A

First metatarsophalangeal
Tarsometatarsal
Ankle
Knee joints

34
Q

What are the other clinical features of gout?

A

In older people, the disease may be polyarticular and associated with marked oedema and swelling of the hands and feet.

35
Q

What are the criteria for gout identified by the American College of Rheumatology?

A

6 or more of:
More than one attack of acute arthritis.
Maximum inflammation developed within 1 day.
Monoarthritis attack, redness observed over joints.
First metatarsophlaangeal joint painful or swollen.
Unilateral first metatarsophalangeal joint attack.
Unilateral tarsal joint attack.
Tophus (confirmed or suspected)
Hyperuricaemia
Asymmetric swelling with a joint on x-ray film.
Subcortical cyst without erosion on x-ray film.
Joint culture negative for organism during attack.

36
Q

What is the management of gout?

A

NSAIDs
Colchicine (interupts neutrophil-endothelial interaction)
Steroids
Allopurinol

37
Q

What are the indications for allopurinol?

A

Recurrent attacks (2-3 per year)
Tophaceous gout
Radiographic changes and chronic destructive joint disease.
Urate nephrolithiasis
Patient preference because of severe and debilitating polyarticular attacks.

38
Q

What is pseudogout?

A

The deposition of calcium pyrophosphate. It is associated with both acute and chronic arthritis.

39
Q

Describe the crystals found in pseudogout?

A

Positive birefringent rhomboid-shaped crystals under polarised light. Fluids are often bloody.

40
Q

What might be found on x-ray of a joint with pseudogout?

A

Cartilage calcification.

41
Q

Define psoriatic arthritis.

A

A chronic inflammatory joint disease associated with psoriasis.

42
Q

Describe the pathophysiological changes in psoriatic arthritis.

A

It is a seronegative inflammatory arthritis.
HLA-B27 is involved.
Psoriatic synovium is characterised by hypervascularity and morphologically tortuous vessels and inflammation leads to deformities.

43
Q

What are the x-ray changes seen in psoriatic arthritis?

A 
Loss of joint space
Deformity
Bony erosion
Periarticular osteopaenia
Soft tissue swelling
44
Q

How is psoriatic arthritis distinguished from rheumatoid arthritis?

A

By the presence of dactylitis and the absence of anticyclic citrullinated peptide antibodies. Dactylitis DIP involvement, monoarticular pattern.

45
Q

What are the clinical features of psoriatic arthritis?

A

In a patient with psoriasis: prolonged morning stiffness in joint (lasting >30 minutes), morning first-step foot pain, join or digit swelling.

46
Q

What is the management of psoriatic arthritis?

A

NSAIDs usually sufficient to treat limited disease.
Articular steroids
Physio
Patients with progressive peripheral arthritis or oligoarthritis refractory to NSAIDs and intraartiular corticosteroids: require disease-modifying antirheumatic disease therapy (e.g. methotrexate) early in disease course. Infliximab if 2 failed DMARDs.

Phase 4 (12 decks)

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