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Zero Rheum and Sex > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is nailfold capillaroscopy?

A

Technique to magnify and examine the skin at the base of the fingernail and the health of the peripheral capillaries.
Abnormal capillaries, avascular areas, and microhaemorrhages indicate systemic sclerosis.
Helps support systemic sclerosis diagnosis and investigate patient with primary Raynauds to exclude systemic sclerosis.

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2
Q

Diagnosis systemic sclerosis is based on what?

A

Clinical features, antibodies and nail fold capillaroscopy.

ACR and EULAR criteria.

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3
Q

Management of systemic sclerosis?

non-medical and medical

A

MDT, no standard treatment:

Steroids and immunosuppressants: started in diffuse disease and for complications such as pulmonary fibrosis.

Non medical:

  • avoid smoking
  • gentle skin stretching to maintain the range of motion
  • regular emollients
  • avoiding cold triggers for Raynauds
  • physiotherapy to maintain healthy joints
  • occupational therapy for adaptations to daily living to cope with the limitations

Medical management:
focuses on symptoms and complications.
- nifedipine can be used for Sx of Raynauds
- anti acid medications (eg PPIs) and pro-motility (eg metoclopramide) for GI symptoms.
- analgesia for joint pain
- antibiotics for skin infections
- antihypertensives can be used to treat hypertension (usually ACEi)
- treatment of pulmonary artery hypertension
- supportive management of pulmonary fibrosis

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4
Q

What is polymyalgia rheumatica? (PMR)

A

PMR is an inflammatory condition that causes pain and stiffness in the shoulders, pelvic girdle, and neck.
There is a strong association with giant cell arteritis and the two conditions often occur together. Both conditions respond well to treatment with steroids.

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5
Q

What demographic usually gets PMR?

A

Polymyalgia rheumatica usually affects:

  • old adults (over 50)
  • more common in women
  • more common in caucasians
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6
Q

What are the core features of PMR according to NICE CKS and what are some “other features”?

A

Core features to determine whether someone has PMR, should be present for at least 2 weeks:

  • bilateral shoulder pain that may radiate to the elbow
  • bilateral pelvic girdle pain
  • worse with movement
  • interferes with sleep
  • stiffness for at least 45 minutes in the morning

Other features:

  • systemic symptoms such as weight loss, fatigue, low grade fever and low mode
  • upper arm tenderness
  • carpel tunnel syndrome
  • pitting oedema
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7
Q

What are some differentials for PMR?

A

Key challenge is excluding other conditions that can cause similar symptoms and not to miss other diagnoses. Eg:

  • OA
  • RA
  • SLE
  • myositis (due to conditions like polymyositis or medications like statins)
  • cervical spondylosis
  • adhesive capsulitis of both shoulders
  • hyper or hypothyroidism
  • osteomalacia
  • fibromyalgia
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8
Q

Diagnosis of PMR?

A

clinical presentation and response to steroids.
May need to exclude other conditions.
Inflammatory markers (ESR, plasma viscosity, and CRP) are usually raised but could be normal.

Do investigations to exclude other conditions before starting steroids.

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9
Q

Investigations to do in polymyalgia rheumatica before starting steroids?

A
  • FBC
  • U+Es
  • LFTs
  • calcium (can be raised in hyperparathyroidism or cancer or low in osteomalacia)
  • serum protein electrophoresis (for myeloma and other protein disorders)
  • thyroid stimulating hormone for thyroid function
  • creatine kinase for myositis
  • RF for RA
  • urine dipstick

Additional investigations to consider:

  • ANA for SLE
  • anti-CCP for RA
  • urine Bence Jones protein for myeloma
  • chest x-ray fro lung and mediastinal abnormalities
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10
Q

Treatment of polymyalgia rheumatica?

A

Treatment is with steroids. NICE CKS has steroid regime you should follow:

Initially start of 15mg prednisolone daily.

Assess after 1 week. If there is poor response in symptoms it is probably not PMR and an alternative diagnosis needs to be considered. Stop the steroids.

Assess 3-4 weeks. You would expect a 70% improvement in symptoms and inflammatory markers to return to normal to make a working diagnosis of PMR.

If 3-4 weeks of treatment with steroids has given a good response then start a reducing regime with the aim of getting the patient off steroids:

  • 15mg until symptoms are fully controlled, then
  • 12.5mg for 3 weeks, then
  • 10mg for 4-6 weeks, then
  • reduce by 1mg every 4-8weeks

If symptoms recur they may need to stay on dose for longer or increase dose. Can take 1-2 years to fully wean off. If there is doubt about Dx, difficulty weaning, difficulty controlling symptoms then refer to a rheumatologist.

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11
Q

What must you tell patients on steroids?

A

“Don’t STOP”
Don’t - don’t stop steroids as they will be steroid dependent after 3 weeks and at risk of an adrenal crisis is abruptly withdrawn.
S - Sick day rules: increase dose when ill.
T - Treatment card. Provide steroid treatment card to alert others they are steroid dependent.
O - Osteoporosis prevention. Consider osteoporosis prophylaxis whilst on steroids with bisphosphonates and calcium and vitamin D supplements.
P - Proton Pump Inhibitor: Consider gastric protection eg omeprazole.

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12
Q

What is giant cell arteritis?

Who is at risk?

A

it is a systemic vasculitis of the MEDIUM and LARGE arteries.
Typically presents affecting the temporal arteries and is also known as temporal arteritis.

There is a strong link with polymyalgia rheumatica. Tends to be female caucasians over 50.

Key complication is irreversible vision loss. High dose steroids are used immediately once a diagnosis is suspected to prevent the development or progression of vision loss.

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13
Q

Symptoms of giant cell arteritis?

A

Main presenting feature is a headache:

  • severe unilateral headache typically around temple and forehead.
  • scalp tenderness may be noticed when brushing hair.
  • jaw claudication.
  • blurred or double vision
  • irreversible painless complete sight loss can occur rapidly.

There may be associated systemic symptoms:

  • fever
  • muscle aches
  • fatigue
  • loss of appetite and weight loss
  • peripheral oedema
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14
Q

Diagnosis of giant cell arteritis?

A

Definitive diagnosis made on:

  • clinical presentation
  • raised ESR: usually 50mm/hour or more
  • temporal artery biopsy findings

TOM TIP: multinucleate giant cells are found on the temporal artery biopsy. This is what gives rise the giant cell arteritis name. Popular exam question.

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15
Q

What additional investigations / tests might you do or find in giant cell arteritis?

A
  • FBC may show a normocytic anaemia and thrombocytosis
  • LFTs can show a raised ALP
  • C reactive protein is usually raised
  • Duplex ultrasound of the temporal artery shows the hypo-echoic halo sign
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16
Q

Initial management of giant cell arteritis?

A

Steroids:
Start steroids immediately before confirming the diagnosis to reduce the risk of permanent sight loss. Start 40 or 60mg prednisolone per day. 60mg is given is there is jaw claudication or visual symptoms. Review response in 48 hours.

Other medications:

  • Aspirin 75mg daily decreases vision loss and strokes
  • PPI eg omeprazole for gastric protection whilst on steroids

Referrals:

  • vascular surgeons for a temporal artery biopsy in all patients with suspected GCA
  • rheumatology for specialist diagnosis and management
  • ophthalmology review as an emergency same day appointment if they develop visual symptoms
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17
Q

What is the Ongoing Management in GCA?

A

Once the diagnosis is confirmed they continue high dose steroids (40-60mg) until the symptoms have resolved. Then they slowly wean off steroids, this can take several years. Similar process to managing polymyalgia rheumatica.

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18
Q

Mnemonic to remember additional measures for patients on steroids?

A

Dont STOP

DONT - dont stop taking steroids abruptly, there is risk of adrenal crisis.
S - sick day rules
T treatment card
O - osteoporosis prevention with bisphosphonates and supplemental calcium and vitamin D
P - proton pump inhibitors for gastric prevention

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19
Q

Complications of GCA?

A

Early neuro-ophthalmic complications:

  • vision loss
  • cerebrovascular accident (stroke)

Late:

  • relapses of the condition are common
  • steroid related side effects and complications
  • CVA (stroke)
  • aortitis leading to aortic aneurysm and aortic dissection
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20
Q

What are polymyositis and dermatomyositis?

A

They are autoimmune disorders where there is inflammation in the muscles. Polymyositis is a conditions of chronic inflammation of the muscles. Dermatomyositis is a connective tissue disorder where there is chronic inflammation of the skin and muscles.

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21
Q

What is a key investigation in polymyositis and dermatomyositis?

A

Creatine kinase blood test. CK is an enzyme found inside muscle cells. Inflammation to the muscle cells leads to the release of CK. CK is usually less than 300 U/L. IN polymyositis and dermatomyositis the result is usually over 1000, often in multiple of thousands.

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22
Q

Other than polymyositis and dermatomyositis, what are some other causes of raised CK?

A

Other than polymyositis and dermatomyositis:

  • rhabdomyolysis
  • acute kidney injury
  • MI
  • statins
  • strenuous exercise
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23
Q

What can cause polymyositis and dermatomyositis?

A

Can be caused by an underlying malignancy. This makes them paraneoplastic syndromes. The most common associated cancers are:

  • lung
  • breast
  • ovarian
  • gastric
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24
Q

Presentation of polymyositis and dermatomyositis?

A
  • muscle pain, fatigue and weakness
  • occurs bilaterally and typically affects the proximal muscles
  • mostly affects the shoulder and pelvic girdle
  • develops over weeks

polymyositis occurs without any skin features whereas dermatomyositis is associated with involvement of the skin.

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25
Q

What are some dermatomyositis skin features?

A
  • Gottron lesions (scary erythematous patches) on the knuckles, elbows and knees
  • photosensitive erythematous rash on the back, shoulders and neck
  • purple rash on the face and eyelids
  • periorbital oedema (swelling around the eyes)
  • subcutaneous calcinosis (calcium deposits in the subcutaneous tissue)
  • periungal telangiectasia or erythema
  • scalp rash
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26
Q

Antibodies found in polymyositis and dermatomyositis?

A
  • anti-Jo-1 antibodies: polymyositis (but often present in dermatomyositis)
  • anti-Mi-2 antibodies: dermatomyositis
  • anti-nuclear antibodies: dermatomyositis

(anti-Jo-1 antibodies are actually in the cytoplasm so ANA could be negative but if you still did an ENA you might then get a positive results. This antibody is also found in antisynthetase syndrome)

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27
Q

Diagnosis of polymyositis and dermatomyositis?

A
  • clinical presentation
  • elevated CK
  • autoantibodies
  • electromyography (EMG)

Muscle biopsy can be used to establish a definitive diagnosis.

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28
Q

Management of polymyositis and dermatomyositis?

A

Mangement is guided by a rheumatologist. New cases should be assessed for possible underlying cancer. They may require physiotherapy and occupational therapy to help with muscle strength and function.

Corticosteroids are the fist line treatment of both conditions.

Other medical options where the response to steroids is inadequate:

  • immunosuppressants (such a azathioprine)
  • IV immunoglobulins
  • biological therapy (such as infliximab or etanercept)
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29
Q

What is antiphospholipid syndrome?

A

A disorder associated with antiphospholipid antibodies where the blood becomes prone to clotting. The patient is in a hypercoaguable state. The main associations are with thrombosis and complications in pregnancy, particularly recurrent miscarriage.

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30
Q

What condition is associated with antiphospholipid syndrome?

A

Antiphospholipid syndrome can occur on its own or secondary to an autoimmune condition, particularly SLE

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31
Q

What antibodies are associated with antiphospholipid syndrome?

A

Antiphospholipid antibodies:

  • lupus anticoagulant
  • anticardiolipin antibodies
  • anti-beta-2 glycoprotein I antibodies

The antibodies interfere with coagulation and create a hyper coagulable state.

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32
Q

Associations / effects of antiphospholipid syndrome?

A

Venous thromboembolism

  • DVT
  • PE

Arterial thrombosis

  • stroke
  • MI
  • renal thrombosis

Pregnancy complications

  • recurrent miscarriage
  • stillbirth
  • preeclampsia

Livedo reticularis is a purple lace like rash that gives a mottled appearance to the skin.

Libmann-Sacks endocarditis is a type of non-bacterial endocarditis where there are vegetations on the valves of the heart. The mitral valve is commonly affected. It is associated with SLE and antiphospholipid syndrome.

Thrombocytopenia (low platelets) is common in antiphospholipid syndrome.

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33
Q

Diagnosis of antiphospholipid syndrome?

A

Dx is made when there is a history of thrombosis or pregnancy complications plus persistent antibodies:

  • lupus anticoagulant
  • anticardiolipin antibodies
  • anti-beta-2 glycoprotein I antibodies
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34
Q

Management of antiphospholipid syndrome?

A

Managed jointly between rheumatology, haematology and obstetrics (if pregnant).

Long term WARFARIN with an INR range of 2-3 is used to prevent thrombosis.

Pregnant women are started on low molecular weight heparin (eg enoxaparin) plus aspirin to reduce the risk of pregnancy complication. Warfarin is contraindicated in pregnancy.

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35
Q

What is Sjogren’s syndrome?

A

Sjogren’s syndrome is an autoimmune conditions that affect the exocrine glands. It leads to symptoms of dry mucous membranes such as dry mouth, dry eye and dry vagina.

Primary Sjogren’s is where the condition occurs in isolation.

Secondary Sjogren’s is where is occurs related to SLE or RA.

36
Q

What antibodies are associated with Sjogren’s syndrome?

A

Sjogren’s syndrome is associated with anti-Ro and anti-La

Ms RoLa is dry eyed

37
Q

What test can be done in Sjogrens syndrome and how is it done?

A

Schirmer test

It involves inserting a folded piece of paper under the lower eyelid with a strip hanging out over the eyelid. This is left for 5mins and the distance along the strip that becomes moist is measured.

The tears should travel 15mm in a healthy young adult.

A result of less than 10mm is significant.

38
Q

Management of Sjogren’s syndrome?

A
  • artificial tears
  • artificial saliva
  • vaginal lubricants
  • hydroxychloroquine is used to halt the progression of the disease
39
Q

Complications of Sjogren’s syndrome?

A
  • eye problems such as conjunctivitis and corneal ulcers
  • oral problems such a dental cavities and cadida infections
  • vaginal problems such as candidiasis and sexual dysfunction

Sjogren’s syndrome can rarely affect other organs causing complications such as:

  • pneumonia and bronchiectasis
  • non-Hodgkins lymphoma
  • peripheral neuropathy
  • vasculitis
  • renal impairment
40
Q

What is vasculitis?

A

Inflammation of the blood vessels.
Different types are categorised on whether they affect the small vessels, medium vessels or large vessels.
They each have some unique features to help you spot them in exams.

41
Q

What are the types of vasculitis affecting the small vessels?

A
  • Henoch-Schonlein purpura
  • eosinophilic granulmoatosis with polyangiitis (Churg-Strauss syndrome)
  • microscopic polyangitis
  • granulomatosis with polyangiitis (Wegener’s granulomatosis)
42
Q

What are the types of vasculitis affecting the medium vessels?

A
  • polyarteritis nodosa
  • eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
  • Kawasaki disease
43
Q

What are the types of vasculitis affecting the large vessels?

A
  • Giant cell arteritis

- Takayasu’s arteritis

44
Q

Presentation of vasculitis?

A

Generic features that should make you think vasculitis:

  • Purpura. These are purple-coloured non-blanching spots caused by blood leaking from the vessels under the skin
  • Joint and muscle pain
  • Peripheral neuropathy
  • Renal impairment
  • Gastrointestinal impairment
  • Gastrointestinal disturbance (diarrhoea, abdo pain, bleeding)
  • Anterior uveitis and scleritis
  • Hypertension

Also associated with systemic manifestations of:

  • fatigue
  • fever
  • weight loss
  • anorexia (loss of appetite)
  • anaemia

Features specific to different types are discussed later.

45
Q

Tests / finding in vasculitis?

A
  • inflammatory markers CRP/ESR are usually raised
  • anti neutrophil cytoplasmic antibodies (ANCA) is the blood test to remember

Two types of ANCA:

  • p-ANCA or anti-PR3 antibodie: Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) and Microscopic polyangiitis.
  • c-ANCA or anti-MPO antibodies: Granulomatosis with polyangiitis.
46
Q

Management of vasculitis?

A

Depends on the type and suspected cases should be referred to a specialist rheumatologist. Usually a combination of steroids and immunosuppressants.

Steroids can be administered to the target area:

  • oral (ie prednisolone)
  • IV (ie hydrocortisone)
  • nasal spray for nasal symtoms
  • inhaled for lung involvement (eg Churg-Strauss)

Immunosuppressants that are used:

  • cyclophosphamide
  • methotraxate
  • azathioprine
  • rituximab and other MABs

Management of MSP and Kawasaki disease (types mostly affecting children) is different.

47
Q

What is Henoch-Schonlein purpura (HSP) and how does it commonly present?

A

HSP is an IgA vasculitis
Commonly presents with a purpuric rash affecting the lower limbs and buttocks in children. Inflammation occurs due to immunoglobulin A deposits in the blood vessels of the affected organs such as the skin, kidneys and GI tract.

Often triggered by an upper airway infection (eg tonsillitis) or a gastroenteritis.

Most common in children under 10.

48
Q

What are the four classic features of HSP?

A
  • purpura (100%)
  • joint pain (75%)
  • abdominal pain (50%)
  • renal involvement (50%)

HSP affects the kidneys in 50% of patients causing IgA nephritis.

49
Q

Management and course of HSP?

A

Management is supportive; simple analgesia, rest and hydrations. Benefits of steroids are unclear.

The abdominal pain usually settles within a few days. Patients without kidney involvement can expect to fully recover within 4 to 6 weeks. A third of patients have a recurrence of the disease within 6 months. 1% of patients with go on to develop end stage renal failure.

50
Q

What is eosinophilic granulomatous with polyangiitis also called?

A

eosinophilic granulomatous with polyangiitis aka Churg-Strauss syndrome

51
Q

What does eosinophilic granulomatous with polyangiitis aka Churg-Strauss syndrome affect?

A

It is a small and medium vessel vasculitis.

It is associated with lung and skin problems, but can affect other organs such as the kidneys. It often presents with severe asthma in late teenage years or adulthood.

A characteristic finding is elevated eosinophil levels on the FBC.

52
Q

What is microscopic polyangiitis?

A

It is a small vessels vasculitis.

The main feature of microscopic polyangiitis is renal failure.
It can also affect the lung causing SOB and haemoptysis.

53
Q

What is granulomatosis with polyangiitis also called?

A

granulomatosis with polyangiitis aka Wegener’s granulomatosis

54
Q

What are the features of granulomatosis with polyangiitis aka Wegener’s granulomatosis?

A

Small vessel vasculitis.
It affects the respiratory tract and kidneys.

Resp:
In the upper respiratory tract it commonly affects the nose causing nose bleeds (epistaxis) and crusty nasal secretions; ears causing hearing loss; and sinuses causes sinusitis.

A classic sign in exams in the saddle shaped nose due to a perforated nasal septum. This causes a dip halfway down the nose.

In the lungs it causes a cough, wheeze and haemoptysis.

CXR shows consolidation and may be misdiagnosed as pneumonia.

Kidneys:
In the kidneys it can cause a rapidly progressing glomerulonephritis (RPGN).

55
Q

What is polyarteritis nodosa (PAN)?

Associated with and what does it affect?

A

Polyarteritis nodosa (PAN) is a medium vessel vasculitis.

It is most associated with Hep B but can occur without a clear cause or with Hep C and HIV.

It affects the medium sized vessels in locations such as the skin, GI tract, kidneys and heart. This can cause renal impairment, strokes and MI.

It is associated with a rash called livedo reticularis. This is a mottled, purplish, lace like rash.

56
Q

What is Kawasaki disease?

Features?

A

Kawasaki disease is medium vessel vasculitis.

It affects young children, typically under 5. No clear cause.

Clinical features:

  • persistent high fever for more than 5 days
  • erythematous rash
  • bilateral conjunctivitis
  • erythema and desquamation (skin peeling) of palms and soles
  • “strawberry tongue” (red tongue with prominent papillae)

A key complication is coronary artery aneurysms. Treatment is with aspirin and IV immunoglobulins.

57
Q

What is Takayasu’s arteritis?

What does it affect and how does it present?

A

Takayasu’s arteritis is a large vessel vasculitis.

It mainly affects the aorta and its branches. Also affects the pulmonary arteries.
These are large vessels and their branches can swell and form aneurysms or become narrowed and blocked. This leads to its other name of “pulseless disease”.

It usually presents before the ages of 40 with non-specific systemic symptoms, such as fever, malaise and muscle aches or with more specific symptoms of arm claudication or syncope.

Diagnosed using CT or MRI angiography. Doppler ultrasound of the carotids can be useful in detecting carotid disease.

58
Q

What is Behçet’s disease?

A

Behçet’s disease is a complex inflammatory condition.
Recurrent oral and genital ulcers.
Can also cause inflammation of other areas such as the skin, GI tract, lungs, blood vessels. MSK systems and CNS.
Presentation can vary a lot between patents with some mildly affected and other dramatically affected.

59
Q

Differential diagnosis for mouth ulcers?

A

Yes Behçet’s disease but ulcers are common:

  • simple aphthous ulcers are very common
  • squamous cell carcinoma
  • herpes simplex virus
  • hand, foot and mouth disease (Coxsackie A virus)
  • IBD (particularly Crohn’s)
  • inflammatory conditions such as RA
  • folate deficiency
60
Q

Features of Behçet’s can manifest in what areas?

A

Mouth ulcers

Genital ulcers

Skin

MSK system

GI system

CNS

Veins

Lungs

61
Q

In what way do the features of Behçet’s can manifest in each area?

A

Mouth ulcers:
At least 3 episodes of mouth ulcers a year. Painful, sharply circumscribed erosions with a red halo. Occur in the oral mucosa and heal over 2 to 4 weeks.

Genital ulcers:
Similar in appearance to oral ulcers. “Kissing ulcers” are when an ulcer develops on two opposing surfaces so that they are facing each other.

Skin:
Easily inflamed in Behçet's, finding may include:
- erythema nodosum
- papules and pustules (similar to acne)
- vasculitic type rashes
Eyes:
Eye manifestations need urgent ophthalmology review as they may ne sight saving.
- anterior or posterior uveitis
- retinal vasculitis
- retinal haemorrhage

MSK system:

  • morning stiffness
  • arthralgia
  • oligoarthritis often affecting the knee or ankle. This causes swelling without join destruction.
GI system:
Inflammation and ulceration can occur in the GI tract, this tends to affect the:
- ileum 
- caecum
- ascending colon

CNS:

  • memory impairment
  • headaches and migraines
  • aseptic meningitis
  • meningoencephalitis
Veins:
Can become inflamed leading to thrombosis. These don't embolise but stay in place. eg:
- Budd Chiari syndrome
- DVT
- thrombus in the pulmonary veins
- cerebral venous sinus thrombosis

Lungs:
Pulmonary artery aneurysms can develop. If they rupture they can be fatal.

62
Q

Investigations in Behçet’s disease?

A

Dx in clinical based on the features. On key investigation is the pathergy test.

Pathergy test involves using a needle to make an subcutaneous abrasion on the forearm. This is then reviewed 24-48 hours later to look for a weal 5mm or more in size.
It tests for non-specific hypersensitivity in the skin.

Pathergy test is positive in Behçet’s disease, Sweet’s syndrome and pyoderma gangrenosum.

63
Q

Management of Behçet’s disease?

A

Usually coordinated by a rheumatologist with input from derm, ophtho, neuro.

Manangement involves a combination of:

  • topical steroids (eg soluble betamethasone tablets)
  • systemic steroids (ie oral prednisolone)
  • colchicine is usually effective in treating symptoms (as an anti-inflammatory)
  • topical anaesthetics for genital ulcer (eg lidocaine ointment)
  • immunosuppressants such as azathioprine
  • biologic therapy such a infliximab
64
Q

Prognosis in Behçet

A

Behçet’s is a relapsing remitting condition. Patients generally have a normal life expectancy and may go into complete remission. Increased mortality with haemoptysis, neuro involvement and other major complications.

65
Q

What is gout?

How does it present?

A

Gout is a type of crystal arthropathy associated with chronically high uric acid levels.

Urate crystals are deposited in the joint causing it to become hot, swollen and painful.

Gouty tophi are subcutaneous deposits of uric acid, typically affecting the small joints and connective tissues of the hands, elbow and ears.
The DIP joints are the most affected joints in the hands.

Typically presents: with a single acute hot, swollen and painful joints. The obvious and extremely important Ddx is septic arthritis.

66
Q

Risk factors for gout?

A
  • male
  • obesity
  • high purine diet (eg meat and seafood)
  • alcohol
  • diuretics
  • existing cardiovascular or kidney disease
  • family history
67
Q

Typical joints affected in gout?

A
  • base of the big toe (metatarso-phalangeal joint)
  • wrists
  • base of the thumb (carpometacarpal joint CMC)

Gout also affects big joints like the knee and the ankle.

68
Q

Diagnosis of gout?

A

Dx clinical or by aspiration of fluid from the joint.
Excluding septic arthritis is essential as this is a potentially joint- and life- saving diagnosis.

Aspiration fluid will show:

  • no bacterial growth
  • needle shaped crystals
  • negative birefringent of polarised light
  • monosodium urate crystical

Joint x-ray:

  • typically the joint space is maintained
  • lytic lesions in the bone
  • punched out erosions
  • erosions can have sclerotic borders with overhanging edges
69
Q

Management of gout?

A

During and acute flare:

  • NSAIDs are first line
  • colchicine is second line
  • steroids can be considered third line

Colchicine is used in patients that are inappropriate for NSAIDs, such as those with renal impairment or significant heart disease. A notable side effect is GI upset. Diarrhoea is a very common side effect. This is dose dependent, mean lower doses cause less upset than higher doses.

70
Q

Gout prophylaxis?

Tip?

A

Allopurinol is a xanthine oxidate inhibitor used for the prophylaxis of gout. It reduces uric acid levels.

Lifestyle changes can reduce the risk of developing gout. This involves loosing weight, staying hydrated and minimising the consumption of alcohol and purine-based food (such as meat and seafood).

TOM TIP: do not initiate allopurinol prophylaxis until after the acute attack is settled. Once treatment of allupurinol has been started then it can be continued during an acute attack.

71
Q

What is pseudogout?

A

Pseudogout is a crystal arthropathy caused by calcium pyrophosphate crystals.
Calcium pyrophosphate crystals are deposited in the joint causing joint problems. It is also known as chondrocalcinosis.

72
Q

Presentation of pseudogout?

A

Typical presentation of pseudogout is an older adult with a hot, swollen, stiff, painful knee. Other joints that are commonly affected are the shoulders, wrists and hips.

It can be a chronic condition and affect multiple joints.It can also be asymptomatic and picked up incidentally on an xray of the joint.

73
Q

Diagnosis of pseudogout?

A

In any patient presenting with a hot, painful and swollen joint, septic arthritis needs to be excluded as it is a medical emergency that is joint- and life- threatening. It tends to be the milder in the presentation compared with gout and septic arthritis.

To establish a definitive diagnosis the join needs to be aspirated for synovial fluid. Aspirated fluid will show:

  • no bacterial growth
  • calcium pyrophospate crystals
  • rhomboid shaped crystals
  • positive birefringent of polarised light

Chondrocalcinosis is the classic xray change in pseudogout. It appears as a thin white line in the middle of the joint space caused by the calcium deposition. This is pathognomic (diagnostic) of pseudogout.
Other changes may be similar to osteoarthritis, remember the mnemonic LOSS
- Loss of joint space
- Osteophytes
- Subarticular sclerosis
- Subchondral cysts

74
Q

Management of pseudogout?

A

Chronic asymptomatic changes found on an xray do not require any action.

Symptoms usually resolve spontaneously over several weeks. Sx management involves:

  • NSAIDs
  • colchicine
  • joint aspiration
  • steroid injections
  • oral steroids

Joint washout (arthrocentesis) is an option in severe cases.

75
Q

Osteopenia vs osteoporosis?

A

Ostepenia is a less severe form of osteoporosis.

Osteoporosis is a reduction in bone density meaning bones are more prone to fractures.

76
Q

Risk factors for osteoporosis?

A
  • older age
  • female
  • reduced mobility and activity
  • low BMI (under 18.5kg/m2)
  • rheumatoid arthritis
  • alcohol and smoking
  • long term corticosteroids (NICE says risk increases significantly with equivalent of more than 7.5mg of prednisolone per day for more than 3 months)
  • other medications such as SSRIs, PPIs, anti-epileptics and anti-oestrogens.

Post-menopausal women are at risk. Oestrogen is protective against osteoporosis and unless they are on HRT then post-menopausal women will have less oestrogen. Also tend to be older and have other risk factors.

77
Q

What is the FRAX tool?

A

Gives a prediction of the risk of a fragility fracture over the next 10 years. Usually the first step in assessing someones osteoporosis.

78
Q

What is involved in using the FRAX tool / how do you do it?

A

Input information such as their age, BMI, co-morbities, smoking, alcohol and FH. Can also enter bone mineral density result from a DEXA scan for a more acurate result but not necessary.

It give results as a percentage 10 year probability of a:

  • major osteoporotic fracture
  • hip fracture
79
Q

How is bone mineral density measured?

A

BMD is measured using a DEXA scan which stands for: dual-energy xray absorptiometry. Brief xray scans that measure how much radiation is absorbed by the bones, indicating how dense the bone is.

The BMD can be measured at any location on the skeleton, but the reading at the hip is key for classification and management of osteoporosis.

80
Q

How are bone density scores represented?

A

Z score or a T score.

Z score represents the number of standard deviations the patients bone density falls below the mean for their age.

T score represents the number of standard deviations below the means for a health young adult their bone density is.

The most clinically important outcome is the T score at the hip. This forms the basis for the WHO classification of osteoporosis.

81
Q

Who classifications for T score?

A

> -1 = normal

-1 to -2.5 = osteopenia

82
Q

When an how do you assess for osteoporosis?

A

First step is to perform a FRAX assessment on patients at risk of osteoporosis:

  • women over 65
  • men over 75
  • younger patients with risk factors scubas a previous fragility fracture, history of falls, low BMI, long term steroids, endocrine disorders and RA

NOGG Guidelines 2017 suggest next step based on FRAX score:

FRAX outcome without a BMD will suggest either:

  • low risk = reassure
  • intermediate risk = offer DEXA scan and recalculate the risk with the results
  • high risk = offer treatment

FRAX outcome with a BMD will suggest:

  • treat
  • lifestyle advice and reassure
83
Q

Lifestyle changes for osteoporosis?

A
  • activity and exercise
  • maintain a healthy weight
  • adequate calcium intake
  • adequate vitamin D
  • avoiding falls
  • stop smoking
  • reduce alcohol consumption
84
Q

Medical management of osteoporosis?

A

Vitamin D and calcium:
Patients at risk of fragility fractures with indequate intake of calcium should have calcium and vitamin D supplementation eg Calcichew-D3 which has 1000mg calcium and 800 units of vitamin D (colecalciferol). Adequate calcium but lacking sun exposure should have vit D.

Bisphosphonates:
First line treatment for osteoporosis. Interfere with osteoclasts, reducing their activity and therefore less bone resorption. Key side effects:
- reflux and oesophageal erosions. Oral tablets are to be taken on an empty stomach sitting up for 30mins before moving or eating to prevent this.
- atypical fractures (eg atypical femoral fractures)
- osteonecrosis of the jaw
- osteonecrosis of the external auditory canal

85
Q

Other medical management in osteoporosis aside from vitD+calcium and bisphosponates?

A

Other medical options:
If bisphosphonates are contraindicated, not tolerated or not effective:
- Denosumab is a MAB that works by blocking the activity of osteoclasts
- Strontium ranelate is similar calcium that stimulates osteoblasts and blocks osteoclasts but increase the risk of DVT, PE and MI.
- Raloxifene as secondary prevention only. It is a selective oestrogen receptor modulator that stimulate oestrogen receptors on bone but blocks them in the breasts and uterus.
- HRT should be considered in any women that go through the menopause early.

86
Q

Follow up on osteoporosis?

A

Low risk patients not on treatment should be given lifestyle advice and followed up within 5 years for a repeat assessment.
Patients on bisphosphonates should have a repeat FRAX and DEXA scan after 3 to 5 years.
A treatment holiday should be considered if their BMD have improved and they have no suffered fragility fractures. This means a break from treatment for 18months to 3 years before repeating the assessment.

Zero Rheum and Sex (2 decks)

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