Rheumatology Flashcards

1
Q

Name some medications that might precipitate gout

A

Thiazide and loop diuretics (reduce excretion of uric acid)

Certain chemotherapy agents

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2
Q

Inflammatory arthritides can be classified as either seropositiv, seronegative, infectious or crystal-induced

What are the seropositive arthropathies?

A

Rheumatoid arthritis

Juvenile RA

SLE

Scleroderma

Vasculitis

Sjogren’s

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3
Q

Inflammatory arthritides can be classified as either seropositiv, seronegative, infectious or crystal-induced

What are the seronegative arthropathies?

A

Ankylosing spondylitis

Psoriatic arthritis

Reiter’s syndrome (reactive arthritis)

Inflammatory bowel disease arthritis

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4
Q

When considering gout as a diagnosis, what important past medical history questions might you ask a patient?

A

History of gout

History of renal disease

History of renal stones

Heart failure or hypertension managed with diuretics

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5
Q

Other than the affected joint in question, where else would you look on a patient with suspected gout?

A

Appearance of gouty tophi which indicate chronic hyperuricaemia (pinnae of the ears and fingers)

May also have olecranon bursitis

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6
Q

Suspect gout? What investigations would you perform?

A

Joint aspirate for microscopy, gram-staining and culture - most important investigation, confirms diagnosis of gout or pseudogout and culture will help to rule out septic arthritis

FBC - usually shows neutrophilia and raised inflammatory markers

Serum uric acid - may be raised, but normal in 25-40% of patients with acute attack

Blood cultures sent at the same time as aspirate cultures

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7
Q

Acute gout diagnosed! How do you treat it?

A

Attacks can be very painful and last 5-7 days. Best managed with COX-2 inhibitors and NSAIDs - Diclofenac, Naproxen and Indomethacin can all be used

For some patients e.g. renal failure, the above may not be appropriate, so Colchicine can be used (500 micrograms 4 times/day)

Steroids are also useful - once SA excluded, intra-articular steroid injections can prove useful in monoarticular disease

Once acute attack has passed, allopurinol can be commenced to lower uric acid levels

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8
Q

What condition would the following bloods indicate?

Anti-dsDNA - raised

Anti-Ro - raised

Anti-La - normal

A

SLE

Anti-dsDNA is associated with SLE

Anti-Ro may also be raised, as well as in Sjogren’s, but anti-La is much more specific for Sjogren’s

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9
Q

SLE has numerous associated complications

What investigations would you perform to explore these?

A

Urinalysis - glomerulonephritis (GN) in SLE often presents with proteinuria and/or haematuria before any derangement in U&Es. Presence of red cell casts indicates GN

Baseline CXR and pulmonary function tests - done to exclude interstitial lung disease

Baseline echocardiogram - pulmonary hypertension may be seen in severe autoimmune disease

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10
Q

How is SLE treated?

A

Based on degree of organ involvement

Hydroxychloroquine is started in every patient - reduces photosensitivity, fatigue, arthralgia and reduces likelihood of progression to other organ involvement

Short courses of steroids/IM steroids can be given to patients with synovitis

NSAIDs can be used to treat arthralgia

Long-term steroids should be reserved for patients with major organ involvement

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11
Q

In a patient with SLE, what advice would you give them regarding pregnancy?

A

Active disease? Avoid pregnancy as associated with poor maternal and foetal outcomes

Immunosuppressive therapy? Methotrexate and Mycophenolate are highly teratogenic - should be stopped for at least 3 months prior to conception

Does she have antiphospholipid antibodies? If so, she should be given aspirin and LMWH once pregnancy confirmed

Does she have anti-Ro antibodies? Associated with congenital heart block in 2-5% of foetuses

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12
Q

Woman in her 60s presents with new-onset pain in her arms for the last 6 weeks, and some weight loss. Recently started on a statin for high cholesterol

What questions do you ask?

A

Establish if muscular pain or joint pain

Muscular diseases are characterised by pain, weakness and wasting of muscles. Generally there is no stiffness in the joint Examples include polymyositis, dermatomyositis, inclusion body myositis, limb girdle muscle dystrophy or statin-induced necrotising myositis

Able to get up from a chair?

Stiffness in the morning?

Swelling/stiffness in the small joints of the hands?

Anyone in the family with a muscle disease?

Systemic Enquiry - difficulty swallowing? Regurgitation? SoB? Chest pains etc.

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13
Q

What are Gottron’s papules?

What condition are they associated with?

A

Red bumps forming on the ouside of the joints of the hand

Seen in dermatomyositis

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14
Q

What is one of the telling features of polymyalgia rheumatica that separates it from muscle diseases?

What bloods are classically raised in the acute phase?

A

Muscle diseases exhibit muscle weakness, but there is no muscle weakness in PMR, it is a disease of the joints

ESR/CRP will be elevated

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15
Q

What blood test is really important when trying to establish if a patient is suffering from a muscle disease?

A

Creatinine Kinase

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16
Q

Inflammatory pain and stiffness is usually worse in the morning/evening and after activity/inactivity

A

Inflammatory pain is usually worse in the morning and in inactivity

It usually gets better as the day progresses, as opposed to mechanical back pain which gets worse as the day progresses

17
Q

Back pain that radiates down the legs indicates an inflammatory/mechanical source

Parasthesia, bowel and bladder symtoms indicate an inflammatory/mechanical source

A

Mechanical source

Again, mechanical source

18
Q

Inflammatory back pain responds very well/poorly to NSAIDs

Mechanical back pain responds very well/poorly to NSAIDs

A

Inflammatory - very well to NSAIDs

Mechanical - poorly to NSAIDs

19
Q

Seronegative spondylarthropathies are more commonly symmetric/asymmetric poly/oligoarthropathies

A

More commonly oligoarthropathies (fewer than 4 joints involved), and more commonly asymmetric

20
Q

Can DIP joints be affected in seronegative spondyloarthropathies?

A

Yes - useful to differentiate from RA which doesn’t affect DIPs

21
Q

What are the two most common organisms associated with reactive arthritis in the UK?

A

Campylobacter

Chlamydia

22
Q

What is the gold standard investigation of choice when investigating a patient presenting with back pain deemed likely to be the result of a seronegative spondyloarthropathy?

A

MRI of Spine and SI joints

Also HLA typing - HLA-B27 is present in 95% of patients with ank. spond. and is also v. high in patients with reactive arthritis

23
Q

How is ankylosing spondylitis best treated?

A

NSAIDs and physiotherapy for spinal disease. There is no role for steroids or DMARDs

For peripheral disease, IA or IM steroids, short courses of oral steroids or DMARDs such as sulfasalazine, methotrexate and leflunomide

24
Q

According to the Chapel Hill Consensus Critera, what are the types of large cell vasculitis?

A

Takayasu arteritis

Giant cell arteritis

25
Q

According to the Chapel Hill Consensus Critera, what are the types of medium cell vasculitis?

A

Polyarteritis nodosa

Kawasaki disease

26
Q

According to the Chapel Hill Consensus Critera, what are the types of small cell vasculitis (ANCA-associated)?

A

Microscopic polyangiitis

Granulomatosis with Polyangiitis (formerly Wegener’s)

eosinophilic Granulomatosis with Polyangiitis, (formerly Churg-Strauss)

27
Q

According to the Chapel Hill Consensus Critera, what are the types of immune complex small cell vasculitis?

A

Henoch-Schonlein purpura aka IgA Vasculitis

Cryoglobulinaemic vasculitis

Hypocomplemenetemic Urticarial vasculitis