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Year 4 - MSK ANNA > MSK - Swollen Hand Joints (RA) > Flashcards

MSK - Swollen Hand Joints (RA) Flashcards

1
Q

With a joint stiffness history, what focussed SR Qs should you ask?

A
  1. Fever/sweats
  2. Weight loss
  3. Anorexia
  4. Fatigue
  5. Skin rashes
  6. Changes in bowel habit
  7. Red/painful eyes
  8. Joint problems in family
  9. Psoriasis in family/PMH
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2
Q

Name the 7 most common forms of Inflammatory Arthritis

A
  1. Rheumatoid arthritis
  2. Connective tissue disease
  3. Vaculitis
  4. Ankylosing Spondylitis
  5. Psoriatic arthritis
  6. Reactive arthritis
  7. Inflammatory bowel disease (IBS) arthritis
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3
Q

In rheumatology if a patient is seropositive what does that mean?

A

It means that their blood test is positive for one of, or both, of the autoantibodies used to detect Rheumatoid arthritis i.e.

  1. Rheumatoid Factor (RF)
  2. Anti-CCP
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4
Q

Gout:

  1. Does gout/pseudogout have an acute or chronic history?
  2. What other rheumatological condition is pseudogout associated with?
A
  1. Acute history
  2. Osteoarthritis
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5
Q

What are the main features of Gout?

A
  • Male (M:F 4:1)
  • Pain - Acute monoarthropathy (pain during flares lasts several days but symptom free between flares)
  • Swelling
  • Erythema
  • 1st MTP joint - >50% of 1st presentations affect the 1st MTP - traditionally called podagra
    • Other common areas: wrist, knee, ankle
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6
Q

What are common radiological features of Gout?

A
  • Joint effusion (early sign)
  • Well-define ‘punched-out’ erosions with sclerotic margins near the joint or margin of bone, with overhanging edges - also known as rat bite erosions
  • Preservation of joint space (until late disease)
  • Eccentric erosions
  • No periarticular osteopenia (opposite to RA)
  • Soft tissue tophi may be seen (deposit of crystalline uric acid over joint, in skin, or in cartilage)
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7
Q

What is the threshold for hyperuricaemia?

A

Uric acid > 0.45 mmol/L

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8
Q

What are the risk factors for Gout?

A
  1. Male
  2. Obesity (↑ BMI)
  3. Reduced urate excretion:
    • Impaired renal function e.g. CKD
    • Drugs e.g. diuretics (volume contraction + ↑ reabsorption of uric acid)
    • Lead toxicity
  4. Increased urate production:
    • Dietary (alcohol, sweeteners, red meat, seafood, yeast products e.g. marmite)
    • Psoriasis
    • Drugs e.g. warfarin, cytotoxics
    • Myeloproliferative / lymphoproliferative disorders –> overproduction of blood cells also means ↑ breakdown –> thus ↑ uric acid production
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9
Q

What genetic condition is linked to Gout?

A

Lesch-Nyhan syndrome

  • Gypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency
  • X-linked recessive –> thus only in boys
  • Features: gout, renal failure, neurological deficits, learning difficulties, self-mutilation
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10
Q

In a pt with suspected Gout what investigations might you do?

A
  • JOINT ASPIRATION! - Gold standard test for gout
    • Synovial fluid is aspirated –> gram-stained + cultured + polarising microscopy (for monosodium urate or calcium pyrophosphate dihydrate crystals)
    • MSU crystals = needles
    • CPPD crystals = rhomboid
    • Warfarin doesn’t contraindicate needle aspiration
    • Prothetic joint = referral to orthopaedic surgeon
    • Neither 1) absence of organisms on Gram stain nor 2) a negative synovial fluid culture excludes the diagnosis of septic arthritis –> thus if uncertain it is advised to treat as both septic arthritis and gout
  • FBC - rule out septic arthritis as a differential
  • LFTs & U+Es - renal impairment is risk factor for gout and these tests influence choice of medication
  • Blood Culture - if septic arthritis could be a differential
  • CRP / ESR - important for monitoring response to treatment of inflammatory conditon (more so in septic arthritis)
  • DON’T do serum urate –> often unhelpful
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11
Q

How is Gout managed acutely?

A

Acute Management:

  • Educate pts to understand that flare-ups should be treated as soon as they occur
  • General:
    • Affected joints rested, elevated and exposed in cool environment / ice pack
  • First line = NSAIDs or Colchicine
    • Max dose of NSAID should be prescribed until 1-2 days after the symptoms have settled
    • Choice of 1st line depends on: patient preference, renal function (can’t have NSAID) and co-morbidities e.g. diabetes
    • Co-prescribe PPI for gastroprotection from NSAID
  • Colchicine:
    • 500 µg bd-qds
    • Slower onset of action vs NSAIDS
    • Main side-effect = diarrhoea
  • Steroids:
    • Steroids (oral) 15mg/day if NSAIDs / colchicine are contraindicated - good in olig- or polyarticular gout
    • Intra-articular steroid injection - for monoarticular gout
    • Not suitbale if diabetic
  • If acute gout isn’t responsive to monotherapy then combinations are suitable
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12
Q

What drug is used for Urate-Lowering Therpay (ULT)?

A

Allopurinol (xanthine oxidase inhibitor) = 1st line

  • Initial dose 100mg OD –> titrate dose every 2-5 weeks
  • Aim for serum uric acid < 300 µmol/l
  • Max dose depends on achieving serum uric acid target - but not > 900 mg/day (300mg/day in significant renal impairment)
  • If pt has ↓ eGFR / CKD stage 4 or worse –> start at 50mg OD

Febuxostat = 2nd line

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13
Q

What adverse side effects are associated with Allopurinol?

A
  • 10% develop rash
  • Allopurinol hypersensitivity syndrome (rare) - 20-25% mortality
    • Highest risk in first few months of therapy
    • More common in south-east asia + Japanese - due to gene HLA B*5801 (only in 2% of caucasians)
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14
Q

What are the indications for Urate-Lowering Therapy in the prevention of Gout?

A
  • ULT is to be offered to all pts after 1st attack of gout
  • ULT should be introduced 2-4 weeks after an acute atack has subsided
  • ULT can precipitate acute gout attacks during first 6 months of therapy
    • Thus all patients who are to commence either allopurinol or febuxostat should be prescribed either colchicine (500 micrograms od-bd) or low dosage NSAID –> give for 2 weeks prior to ULT starting
    • Attacks of gout can occur up to 12 months after ULT start
  • ULT is recommended if:
    • ≥ 2 attacks in 12 months
    • Tophi
    • CKD disease stage II or worse
    • Uric acid renal stones (urolithiasis)
    • Prophylaxis if on cytotoxics or diuretics

Soft tissue tophi shown in image

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15
Q

What lifestyle modifications should a pt make for Gout?

A
  • ↓ alcohol
  • ↓ weight if obese
  • Avoid high purine food: liver, kidney, seafood, oily fish (mackrel, sardines) and yeast products
  • Exercise
  • Smoking cessation (gout ↑ CV risk)
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16
Q

Give a general review of the steps of escalation in Gout treatment

A
  • 1st line:
    • NSAID + PPI OR
    • Colchicine OR
    • Corticosteroid (oral, IM or intra-articular)
    • Affected joints rested, elevated and exposed in cool environment / ice pack
  • Review at 4-6 weeks:
    • Lifestyle factors: diet (↓ purines), exercise, alcohol, obesity
    • Assess CV risk factors (obesity, HTN, lipid profile, diabetes)
    • Stop diuretic medication if possible
    • Serum uric acid
    • Discuss ULT treatment
  • ULT treatment:
    • 1st line allopurinol - start 50-100mg OD, titrate up to effective dose
    • Target serum uric acid < 300 µmol/l
    • Do NOT stop allopurinol during acte attacks
    • 2nd line febuoxstat
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17
Q

Is the onset of Osteoarthritis sudden or slow?

How long are OA pts stiff for in the morning?

Is OA better or worse with activity?

A
  1. Slow (insidious)
  2. Stiffness < 30 mins in morning
  3. Worse with activity and at the end of the day
18
Q

Can any inflammatory arthritis cause tiredness?

A

Yes

19
Q

On examination of a pts hands, some of their joints feel “boggy” akin to a squashed grape - what is this suggestive of?

A

Synovitis

  • Inflammation of synovial membran which lines synovial joints (those with cavities)
  • Common (but not exclusive) to RA
20
Q

Which joints are most commonly affected in RA?

A

Wrists, MCP and PIP

  • DIP is more common to OA or psoriatic arthritis
  • Both OA and psoriatic arthritis are more likely to be asymmetrical compared to RA (more often symmetrical)
21
Q

You suspect a patient of having RA, what investigations would you do?

A
  • Baseline: FBC, LFTs, U+Es
  • Inflammatory markers: CRP + ESR
  • TFTs - if this is abnormal it can present with joint pain
  • Immunology screen
    • Rf + anti-CCP = RA
    • ANA = connective tissue disease e.g. SLE
22
Q

Inflammation can cause various blood tests to be deranged, name 5 and the direction of derangement

A
  1. CRP ↑
  2. ESR ↑
  3. Platelets ↑
  4. LFTs ↑
  5. Ferratin ↑
23
Q

You suspect a 55 year old woman of having RA, her FBC shows low Hb - name 5 possible causes of her anaemia

A
  1. Anaemia of chronic disease
  2. Iron deficiency anaemia
    • Secondary to use of NSAIDs
    • Due to menorrhagia
  3. Felty’s syndrome - anaemia, leucopaenia and enlarged spleen
  4. Pernicious anaemia (common autoimmune disease)
    • Patients who already have one autoimmune disease are much more likely than the general population to have a 2nd autoimmune condition
  5. Autoimmune haemolytic anaemia
24
Q

Does a normal Rheumatoid Factor test exclude RA?

A

No - RA is a clinical diagnosis made using ACR criteria, ~20% of RA pts will have negative rheumatoid factor

25
Q

What are common radiological features of RA?

A

Early x-ray findings:

  • Loss of joint space
  • Juxta-articular osteoporosis
  • Soft-tissue swelling

Late x-ray findings:

  • Periarticular erosions
  • Subluxation (significant structural displacement)
26
Q

ACR (American College of Rheumatology) criteria are used to diagnose RA - what are they?

A

Who should be tested?

  1. Have at least 1 joint with definite clinical synovitis (swelling)
  2. The synovitis is not better explained by another disease

A score of ≥6/10 is needed for classification of a patient as having definite RA

27
Q

A patient with newly diagnosed RA would like you to tell her about it, how common it is and why she develop it.

A

Rheumatoid arthritis is a chronic autoimmune condition. This means that the immune system which is usually very helpful in allowing us to fight infections becomes incorrectly activated and causes inflammation where we don’t want it i.e. in joints, leading to swelling, pain and stiffness.

It is relatively common affecting around 1% of women and around 0.5% of men. We don’t fully understand why patients develop it at a particular point but it is likely due to be due to a combination of factors including genes, the environment (possibly triggered by infection) and smoking (associated with the development of anti-CCP antibodies).

It is likely to need long term treatment but we would aim to control symptoms and prevent joint damage and disability.

28
Q

What is the DAS-28 and what element does it involve?

A

DAS-28 is a measure of disease acitivity in RA out of 10 (high, moderate or low)

DAS-28 is calculated using the following info:

  • Joint tenderness score = how many of the 28 joints are tender
  • No. of swollen joints out of 28
  • Patient’s global assesment of disease activity out of 100 (visual analogue scale)
  • Measure of acute phase response (ESR or CRP)

28 joints:

  • 2 shoulders
  • 2 elbows
  • 2 wrists
  • 2 knees
  • 20 hand joints
29
Q

In a patient with suspected RA, if there is uncertainty in the examination and on X-rays what would the next step be?

A

USS of the afflicted joint

  • USS is more sensitive than clinical examination in the identification of joint effusion and synovitis
  • USS is more sensitive than radiography at identifying bone erosions
30
Q

What are the nail features of Psoriatic arthritis?

A
  • Pitting - little indents
  • Onycholysis - when nail detachs from underlying skin
31
Q

How does Psoriatic skin appear and where are

common areas for psoriatic lesions?

A

Skin: red, scaly patches with flaky silvery buildup (dead skin)

Common Locations:

  • Extensor surfaces, sacrum, scalp (most common locations)
  • Finger/nail changes
  • Palms + soles (pustular psoriasis)
32
Q

Do the symptoms of Psoriatic arthritis tend to come on acutely or insidiously?

A

Tend to be insidious (several weeks)

33
Q

Which joints are most likely to be affects in psoriatic arthritis compared to RA?

A

RA:

  • Often symmetry in affected joints
  • MCP / MTP
  • PIP
  • Interphalangeal joint of thumb / hallux
  • DIP (less likely / late stage)

Psoriatic arthritis:

  • More likely than RA to be assymetrical in joints affected
  • DIP (most common)
  • Can involve MCP/MTP and PIP - often all joints of a single digit in the case of dactylitis
  • Heel (achilles tendonitis)
  • Axial spine (spondilitis)
  • Sacrio-iliac (sacroilitis)
34
Q

What is dactylitis?

What can cause dactylitis?

A

Dactylitis = inflammation of an entire finger or toe

Conditions associated with dactylitis:

  • Seronegative arthropathies: psoriatic arthritis, ankylosing spondylitits, reactive arthritis (in reactive, sausage fingers occur due to synovitis)
  • Sickle-cell disease - as a result of vaso-occlusive crisis with bony infarcts
  • TB
  • Syphilis
  • Sarcoidosis
35
Q

What is Berchet’s Disease?

What is the classic triad of features?

What are other common features?

A

Berchet’s disease = complex multi-system inflammatory disorder with presumed auto-immune inflammation of artieres + veins

Classic Triad of Features:

  1. Oral ulcers
  2. Genital ulcers
  3. Anterior uveitis
    • ​Uvea = pigmented middle layer of eye, composed of (ant-post): iris, ciliary body, choroid –> thus anterior uveitis is inflammation of iris and ciliary bodies

Other Features:

  • Arthritis
  • Thrombophlebitis (vein inflammation relating to bloot clot) - associated with DVT and pulmonary aneurysms (leading cause of death)
  • Neurological involvement e.g. aseptic meningitis
  • GI: abdo pain, diarrhoea, colitis
  • Erythema nodosum - inflammation of fat cells under skin –> red, tender, nodules/patches, often on legs

Epidemiology:

  • Common young adults (20-40yrs)
  • 30% have +ve family Hx
  • More common in: middle east, east asian and eastern mediterranean (Turkey) peoples
  • Associated with HLA B51
36
Q

What is tenosynovitis?

A

Tenosynovitis is inflammation of the fluid-filled sheath (synovium) that surround the tendon

Features:

  • Joint pain
  • Swelling
  • Stiffness
37
Q

What are the most common types (pattern of joints) of Psoriatic arthritis?

A
  1. Rheumatoid-like polyarthritis (30-40% - most common)
  2. Asymmetrical oligoarthritis - typically affects hands and feet (20-30%)
  3. Sacroilitis
  4. DIP joint disease (10%)
  5. Arthritis mutilans (severe deformity fingers/hand, can occur in any severe inflammatory arthritis - rare)
38
Q

What is the classic triad of symptoms for Reactive Arthritis?

A
  1. Inflammatory arthritis post infection
  2. Urethritis / cervicitis
  3. Conjuctivitis / uveitis
39
Q

What are the counselling points for allopurinol (x6)?

A
  1. When you first take it:
    1. can worsen attack, co-prescribe NSAIDs/colchine for 6 months
    2. don’t start during attack, wait few weeks
  2. Take with food and lots of water (aim 2-3L / day)
  3. Don’t stop during an attack (makes worse)
  4. Check bloods (uric acid) in 4 weeks
  5. Common side-effect = rash
    1. BUT watch out for stephen johnson syndrome!
  6. lifelong medication
40
Q

Lifestyle advice for gout

A
  1. Diet: avoid high purines e.g. sardines, marmite
  2. Alcohol: decrease, avoid in attack entirely
  3. Fluids: 2-3L / day
  4. Weight loss
  5. Vit C
  6. stop medications that might be causing probs e.g. thiazide
  7. Smoking: stop, always just stop

Year 4 - MSK ANNA (13 decks)

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