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Rheumatological conditions > Lupus, Gout, Reactive Arthritis & CPPD > Flashcards

Lupus, Gout, Reactive Arthritis & CPPD Flashcards

1
Q

What is Systemtic Lupus Erthematosus?

A

An auto-immune disease that is usually characterized by clinical manifestations that are multi-system.

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2
Q

What is the pathogenesis of SLE?

A
  • Results from recurrent activation of the immune system
  • Production of antibodies and protein products that then contribute to high levels of inflammation and tissue destruction
  • Activation of B & T cells (adaptive immune response)
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3
Q

What are the risk factors for SLE?

A
  • Genetic: Siblings of someone with SLE are 30% more likely to have the disease.
  • Environmental (UV over, Epstein-Barr Virus, Drug induced Lupus)
  • Hormonal (High Oestrogen, OCP use, Pregnancy)
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4
Q

How does SLE present?

A 
CAN AFFECT ANY ORGAN SYSTEM 
Most common key clinical features:
o	Cutaneous manifestations
o	Malar and/or Discoid rash 
o	Usually photosensitive
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5
Q

How is SLE Diagnosed?

A

Blood testing

  • Serological hallmark (98% sensitive)
  • Antinuclear antibodies (ANA)
  • Double Stranded DNA (dsDNA)
  • ENA antibodies
  • Raised ESR/CRP
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6
Q

How is ‘mild’ Lupus managed?

A
  • Reduce environmental triggers
  • UV, hormone therapy, CV risk
  • NSAIDs Antimalarials
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7
Q

How is ‘severe’ Lupus managed?

A
  • Corticosteroids
  • Be aware of osteoporosis risk.
  • Immunosuppressive drugs
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8
Q

What is reactive arthritis?

A

“Reactive arthritis (or Reiter’s syndrome) is a form of inflammatory arthritis that develops in response to an infection in another part of the body (cross-reactivity). Coming into contact with bacteria and developing an infection can trigger the disease.

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9
Q

What condition does reactive arthritis present similarly to?

A

Septic Arthritis

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10
Q

Reactive arthritis is associated with an acute monoarthitis, what does this mean?

A

Affecting one joint, usually in the lower limb (knee or talocrural)

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11
Q

What two bodily systems usually respond to reactive arthritis?

A

Seronegative spondyloarthropathy secondary to a bacterial infection in the GI or GU tract

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12
Q

Postulated pathogenesis of Reactive Arthritis?

A

Unclear but the common theories postulate that:

  • Immune response to the bacteria in systemic circulation
  • T-cell activation, leading to synovitis, monoarticular arthritis
  • Cross-reactivity with HLA-B27
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13
Q

Common pathogens to trigger reactive arthritis?

A

Most common: chlamydia, salmonella and shingella

Less common: Ecoli

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14
Q

What are some clinical manifestations of reactive arthritis?

A
  • Asymmetrical Oliglioarthritis
  • Ocular involvement
  • Penile Lesions
  • Skin Lesions
  • Cardiac Involvement
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15
Q

What does “The patient cant see, cant pee, cant climb a tree” refer to for reactive arthritis?

A 
It refers to the clinical manifestations
- Ocular: Uveitis, Conjunctivitis 
- Penile lesions: Urethritis,
Balanitis circinate
- Oliglioarthritis: Larger joints of lower extremity, Dactylitis, Enthesitis (achillies or PF), Bursitis, Sacroiliitis
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16
Q

How is reactive arthritis diagnosed?

A

No specific testing or imaging!

  • Hx taking and clinical features ensuring to rule out other causes of arthritis and the presence of predisposing infection
  • Blood testing: ESR and CRP to rule out an inflammatory arthritis
  • Testing for specific infection
17
Q

What is the suggested treatment and management for reactive arthritis?

A
  • Management of underlying infection with antibiotics
  • NSAIDs and paracetamol: NSAID use may be contraindicated in patients with gastric issues
  • DMARDs: For late-stage diseases
  • General mobility and treatment of arthritis compensations
18
Q

What is GOUT?

A

A form of arthritis characterised by severe pain, redness and tenderness in joints.

19
Q

What is a Monosodium urate crystal disorder?

A

An abnormality of uric acid metabolism that results in hyperuricemia and urate crystal deposition
(Inflammatory crystal monoarthropathy)

20
Q

Where do the crystals usually deposit in the body?

A
  • Joints- acute gout arthritis
  • Soft tissue- tophi and tenosynovitis
  • Urinary tract- urate stones
21
Q

What age group/ sex is most likely to suffer from gout?

A

Mainly a disorder of men between 40-50

In women onset is usually 60+

22
Q

What nationalities are at an increased risk for gout?

A

More common in Maori, Pacific Islander and Indigenous Australians

23
Q

What is the enzyme that transforms xanthine into uric acid?

A

Xanthine oxidase

24
Q

Pathogenesis of gout?

A
  • Lack the ability to degrade uric acid therefore deposited out of the urine
  • Hyperuricemia: Urate increases in the kidneys to a point where there is too much in the urine. It then congregates in the blood/ synovial fluid/ soft tissues then crystal precipitate and development of tophi.
  • Accumulation of crystals in the soft-tissues then leads to macrophages engulfing them
25
Q

What are the risk factors for gout?

A
  • Genetic factors: 35% increase in males if another male relative has had gout
  • Natonality: Maori, Pacific Islander and indigenous
  • Long term renal disease
  • Long term medication use: Diuretics, Salcylates
  • Diet: High purine diet (Shellfish, somefish, crab, lobster), Meats (especially bacon, turkey, veal and organ meats),
  • High alcohol consumption (Beer higher than spirits or wine)
  • High soft-drink consumption (Especially high fructose corn syrup)
26
Q

What are the four stages of gout?

A

Stage 1: Asymptomatic hyperuricaemia
Stage 2: Acute Gouty Arthritis
Stage 3: Intercrtial gout
Stage 4: Chronic tophacious gout and chronic gouty arthritis.

27
Q

How does Stage 1 (asymptomatic hyeruricaemia) present?

A

Usually no clinical manifestations and no treatment necessary other than lifestyle modifications.
Elevated serum uric acid:
o >0.42 mmol/L in men
o >0.36mmol/L in women

28
Q

How does Stage 2 (Acute gouty arthritis) present?

A
  • Acute attack of severe pain
  • Usually in great toe but can be elsewhere – knees, other toes, ankle
  • Often in the early hours of the morning and wakes the patient
  • Skin over the joint is red, shiny, hot and swollen
  • VERY tender to touch
  • Sheet overlying is too much- Can’t bear socks
  • May be precipitated by:
    o Alcohol or dietary excess
    o Starvation
    o Surgical operation
  • Can subside in 3-10 days
29
Q

How does Stage 3 (Intercritical gout) present?

A
  • Time between attacks.
  • Low to no pain.
  • Low-level inflammation causing joint destruction
  • Time for aggressive management strategies.
30
Q

How does Stage 4 (Chronic tophacious gout and chronic gouty arthritis) present?

A
  • Unlikely to be the first indication of Gout
  • Stone like deposits of monosodium urate in soft tissue, synovial tissue or in bone near joints (Ears, elbows, big toe, fingers)
  • Pathognomonic
  • Uric acid levels remain high over a number of years.
  • Attacks more frequent and more painful
  • Permanent joint destruction
31
Q

How is gout Diagnosed?

A 
Synovial fluid aspirate:
- Uric acid crystals present 
- Only real diaganostic feature
Elevated Serum Uric acid:
- Around 30% of all gout sufferers will be in normal limits.
Xray:
- Punched out joint erosions 
- Visible tophi and joint effusion
32
Q

What are some pharmaceutical management for gout?

A

NSAIDs

  • In acute attacks
  • Contraindicated in kidney disease

Corticosteroids
- For chronic inflammation

Allopurinol- Serious potential adverse reaction (hypersensitivity)

  • Xanthine oxidase inhibitor
  • Indicated when frequent attacks
  • Presence of tophi, kidney stones or uric acid nephropathy
  • Usually not indicated in kidney disease or elderly
  • Used as both a prophylaxis and a maintenance
33
Q

What is Calcium Pyrophosphate Deposition Disease (CPPD)?

A

A disease of crystal deposition in the joint and soft tissue, almost exclusive to articular cartilage.

34
Q

What are some risk factors for CPPD?

A
  • Disease of the elderly – most common in 65+ years
  • OA
  • Previous joint trauma
  • Metabolic disease – diabetes
  • Family Hx
35
Q

What is the pathophysiology of CPPD?

A

-Largely unknown how it is exactly caused but what occurs in the joint is an excess of pyrophosphate production in the cartilage

36
Q

What are the clinical features of CPPD?

A
  • Acute attacks that mimic gout
  • Pain, synovitis or tenderness in one OR multiple joints (Knee, MCP, wrist and hand most common)
  • Systemic features
  • Can also mimic RA, OA and tendonitis
37
Q

How is CPPD diagnosed?

A
  • Synovial fluid analysis (differs to gout via rhomboid shaped crystals)
  • X-ray (shows chondrocalcinosis which reduces joint space and forms new bone around the cartilage making it appear hyper-white)
38
Q

How is CPPD managed?

A
  • Treating acute flare ups and symptoms of an attack
  • After being diagnosed cortisone is usually injected into the joint
  • Managed with paracetamol/oral corticosteroids depending on age and co-morbidities
39
Q

How can you distinguish CPPD from GOUT?

A
  • Present with similar symptoms and often indistinguishable in early stages
  • Joint aspiration for fluid analysis necessary
  • Treatment is also similar in early stages
  • In chronic stage gout must be treated with hypouricemic agent to prevent severe deformity.

Rheumatological conditions (3 decks)

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