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PA MS > MSPA: Rheumatology- The spondylarthropathies and crystalline arthropathies > Flashcards

MSPA: Rheumatology- The spondylarthropathies and crystalline arthropathies Flashcards

1
Q

What are the Major features of spondylarthropathies ?

A
  • Inflammation of the axial joints especially sacroiliitis.
    *Asymmetrical oligoarthritis
  • Dactylitis
  • Enthesitis
  • HLA-B27
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2
Q

What is Ankylosing Spondylitis?

A

It is a seronegative spondylarthropathy of unknown aetiology with strong correlation to HLAB-27 gene positivity. The inflammatory process is mediated by CD4+ and CD8+ T-Lymphocytes and macrophages inducing cytokine response through TNFα, TGF-β, and IL-17, which manifest as sacroiliitis and enthesitis along the spine causing the stiffness and bamboo spine appearance on X-Ray.

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3
Q

What is the epidemiology of ankylosing spondylitis ?

A

90% of the patients are HLAB-27 positive with 50% concordance rate. It is 3 times more common in men than in woman with a peak onset age range of 20-40.

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4
Q

What is the clinical presentation of ankylosing spondylitis ?

A

The hallmark is axial involvement which manifest as nocturnal back pain and stiffness that improves with exercise and not with rest. patients often have peripheral arthritis involving shoulder, hip , knee and ankle. The physical examination of the spine will often show kyphosis or kyphoscoliosis.

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4
Q

What are the systemic manifestations of ankylosing spondylitis ?

A

The patients often have constitutional symptoms, dactylitis, recurrent acute uveitis, IBD, and Achiliis tendinitis. The cardiovascular involvement may manifest as aortitis, Aortic regurgitation, and conduction abnormalities.

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5
Q

What are the Lab findings in Ankylosing spondylitis ?

A

Elevated ESR and CRP. All other markers of autoimmune or inflammatory diseases has to be negative ( seronegative).

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6
Q

What is the Tx of ankylosing spondylitis ?

A
  • PT ,OT interventions and smoking cessation.
  • NSAIDs
  • steroid injections
  • TNF alpha blockers such as Infliximab.
  • IL-17 antagonists such as Secukinumab
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7
Q

What is the pathophysiology of reactive arthritis ?

A

It is a seronegative arthritis triggered often in HLA B-27 positive people by infectious antigens from GI pathogens such as Shigella, Salmonella etc. STIs due to C.trachomatis, and GAS.

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8
Q

What is the symptomatology of Reactive Arthritis?

A

In most cases the symptom onset is 2 to 3 weeks post infection and often presents as Reiter’s syndrome which consist of conjunctivitis, urethritis and joint inflammation. The patients may also present with cervicitis and pericarditis.
The joint involvement may manifest as a single large joint involvement, ankle, hip and small joints or polyarticular.

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9
Q

What are the laboratory evaluations in reactive arthritis ?

A
  • Culture to rule out infections
  • HLA-B27 +
  • elevated ESR and CRP.
  • RF and ACPA negativity.
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10
Q

What is the management of reactive arthritis ?

A

*Antibiotics to treat underlying infection.
* NSAIDs for pain control.

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11
Q

What is Psoriatic arthritis clinical presentation?

A

The dermal psoriatic lesions + asymmetric oligoarticular (<5 joints) involvement is the most common presentation in PA. Th rheumatoid pattern of polyarticular ( >5 joint) presentation and axial arthritis presentation may also be seen. However, the lab works will be negative for RA.

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12
Q

What is the management of Psoriatic arthritis ?

A
  • NSAIDs
  • DMARDs
  • TNF antagonists
  • IL-17 antagonists
  • Surgery for hip and spine may be considered if medical management fails.
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13
Q

What is the pathophysiology of Gout ?

A

The under execration or over-production of uric acid causes the formation of MSU crystals, which gets deposited in and around the joints triggering humoral and cellular inflammatory process leading to acute gouty attacks.In chronic stage the disease causes MSU renal stone formation, interstitial nephritis, and most commonly tophi.

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14
Q

what are the causes of overproduction of uric acid ?

A
  • Diet
  • Genetics
  • Tumour Lysis Syndrome
  • Lymphoproliferative disorders
  • Psoriasis
  • Drugs: Warfarin, Cytotoxic agents
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15
Q

what are the causes of Underexcretion?

A

*Age (elderly)
* Male sex
* Post-menopausal female sex
* Impaired renal function
* Metabolic syndrome
* Hypertension
* Drugs:Antihypertensives,Diuretics, Aspirin

16
Q

What is the epidemiology of Gout ?

A

The uric acid levels tends to be more in men than in woman. But the risk of gout is equal in both gender. It is rarely seen before the age of 30 in men and woman rarely get it before menopause.

17
Q

What is the presentation of acute gout attack ?

A

The first gout attack is usually monoarticular for example podagra. The recurrent gouty attacks can be polyartritic. The attack itself presents with cardinal signs of inflammation and progressive intense pain. It usually peaks within 1 to 2 days and prolongs approximately 7-10 days.

18
Q

What are the chronic effects of Gout ?

A
  • Most patients develop Tophis after ~ 10 years from initial attack and it cause Chronic pain, deformity, joint
    destruction.
  • Chronic gout also cause Nephrolithiasis due to MSU stones or it can act as a nidus for calcium oxalate stones.
  • It can also cause urate nephropathy marked by uric acid crystals in renal parenchyma reducing kidney’s ability to concentrate urine.
19
Q

What should be the laboratory work up in Gout ?

A
  • FBC to rule out lymphoproliferative or myeloproliferative disorders.
  • Blood culture to rule out infectious causes.
  • BUN and creatinine to rule out renal under excretion causes.
  • Serum uric acid- which may not be elevated.
  • Joint aspirate will show synovial fluid, which is often turbid with low viscosity.
  • The light microscopy of joint aspirate will show negatively birefringent needle-shaped
    crystals.
20
Q

What is the colour of MUS needles under light microscopy ?

A

Under polarizing light microscopy, urate crystals are yellow when aligned parallel to the axis of the red compensator and blue when aligned across the direction of polarization

21
Q

What are the radiological findings in gout ?

A

The plain film will show erosive disease, rat bite lesions, overhanging edges and tophi.

22
Q

What is the non pharmacological management of gout ? *

A
  • Rest and elevate joint
  • Ice packs
  • Bed cage
  • Reduce intake of purine-rich food
  • Weight loss
    Indirect treatment
  • Treat hypertension and hyperlipidaemia
23
Q

What is the Treatment of Acute gout Attack?

A
  • NSAIDs – generally effective but can’t use if renal insufficiency
  • Colchicine – anti-inflammatory, can also be used long-term for
    prevention.
  • Steroids – oral or intra-articular
24
Q

What is the Tx approach to chronic gout and gout attack prevention?

A

If > 1 acute attack per year, tophi
or renal stones, treat it pharmacologically with Xanthine oxidase inhibitors and Low dose colchicine.

25
Q

What are the factors to consider while treating chronic gout with xanthine oxidase inhibitors ?

A

The goal is to reduce uric acid production. The Tx should only be started at least after 3 weeks form the acute gout symptoms resolution. Continue NSAIDs for the first several weeks. Start low and increase dose over time. Titrate to serum uric acid < 0.3 mmol/L. Low dose colchicine can be continued for up to 6 months.

26
Q

What is the epidemiology of CPPD ?

A

It is commonly seen in people over the age of 50. Vast majority of the cases are in people over the age of 85.

27
Q

What are the risk factors for CPPD ?

A
  • Trauma to joint
  • Hyperparathyroidism
  • Hypomagnesemia
  • Hypothyroidism
  • Hypophosphatemia
  • Hemochromatosis
28
Q

What is the pathophysiology of CPPD?

A

Idiopathic excessive pyrophosphate
production causes calcium pyrophosphate dihydrate crystal deposition on joints and soft tissues which stimulate inflammatory responses.

29
Q

What is the clinical presentation of CPPD?

A

It has a similar presentation as gout. The most common joints affected are the knee followed by elbow, shoulder and wrist. The patients typically presents with Red, tender, swollen joint with limited mobility. It can co-occur with RA and OA.

30
Q

What are the findings in the synovial fluid analysis in CPPD?

A

It will show Weakly positive birefringent rhomboidal crystals in polarizing filter.

31
Q

What are the radiological findings in CPPD ?

A

It is not necessary unless there is diagnostic uncertainty. The hallmark finding in X-ray will be chondrocalcinosis.

32
Q

What is the treatment of CPPD ?

A
  • NSAIDS – first-line therapy in those with intact renal function
  • Colchicine – may be useful for long-term therapy at low doses
  • Steroids
  • No agents for decreasing pyrophosphate exist.

PA MS (44 decks)

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