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Blwyddyn 1; Tymor 3 > 137; Monoarthritis, Gout & Pseudogout > Flashcards

137; Monoarthritis, Gout & Pseudogout Flashcards

1
Q

List some possible causes of Monoarthritis

A

Septic arthritis

Gout

Pseudogout

Trauma/haemoarthritis

Sero-neg arthritis (psoriasis/IBD)

Reactive arthritis

Sarcoid

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2
Q

What is septic arthritis?

A

Acute inflammation of the joint caused by direct infection

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3
Q

What are the main bacterial causes of septic arthritis?

A
  1. Strep Aureus; from local damage to skin
  2. Gonococcus
  3. Streptococcus
  4. E.Coli
  5. Mycobacteria- TB
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4
Q

What are the predisposing factors for developing Septic Arthritis?

A

Prosthetic joint

Immunosupressed/elderly

Diabetic

Rheumatoid arthritis

Joint damage

IV drug abuse

Source of infection from elsewhere

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5
Q

What are the outcomes of Septic Arthritis; untreated and treated?

A

Untreated;

Rapid, irreversible joint destruction

Sinus/Abscess formation

Osteonecrosis

Septicaemia- organ failure

Treated;

50% Morbidity

10% Mortality

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6
Q

How should a monoarthritis be investigated?

A
  1. Aspirate joint fluid

Gram stain

Macroscopic appearance

Crystals

  1. Blood test

Urate

CRP

FBC

Blood cultures

  1. X-ray
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7
Q

How should a case of Septic Arthritis be treated?

A

Abx; 2wk IV & 4wk oral

Identification of infection source

Washout surgery *gold standard*

Drainage (when surgery not viable)

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8
Q

What is Gout?

A

Inflammatory response to Monosodium Urate Monohydrate Crystals;

HyperUricaemia

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9
Q

Epidemiology of Gout?

A

Male gender (oestrogen is protective)

Age

Impaired renal function

Hyperuricaemia

High purine diet

Regular alcohol

Obesity

Drugs (some diuretics)

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10
Q

What is Uric Acid a break down product of?

A

Purine

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11
Q

How is uric acid excreted?

A

1/3 in faeces

2/3 in urine

90% of gout patients have impaired Urate excretion

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12
Q

What are the modifiable risk factors for gout?

A

Purine-rich diet

Hyperuricaemia

Regular alcohol consumption

Obesity

Medications (diuretics)

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13
Q

What clinical features are associated with the chronic form of Gout?

A

Tophi

Bone & joint destruction

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14
Q

Which joint does Gout most commonly affect?

A

1st MCP joint

>50% of cases

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15
Q

What are the investigations for Gout?

A

Fluid examination

Urate crystals; wit negative birefringance

Bloods

Hyperuricaemia

Urinalysis

Urea levels may be normal during an acute attack

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16
Q

How is Gout treated?

A

Correcting Hyperuricaemia

Prevention; low purine diet, regulate alcohol, weight loss, treat hypertension

Urate lowering drugs

NSAIDs

Colchicine

Steroids; oral and intra-articular

17
Q

Which patients should use urate-lowering drugs?

A

Second attack within a year

Renal impairement orUrate stones

Tophi tissue damage

18
Q

What are the 2 main Urate lowering drugs?

A
  1. Xanthine Oxidase inhibitors

Reduce Uric acid production

  1. Uricosuric agents

Increase Uric acid secretion

Urate Lowering drugs should not be commenced during an attack; wait 1-2 weeks after for inflammation to subside

19
Q

Give 2 examples of Xanthine Oxidase inhibitors

A
  1. Allopurinol
  2. Febuxostat
20
Q

Name 3 Uricosuric agents

A
  1. Sulphinpyrazone
  2. Probenectid
  3. Benzobromarone
21
Q

What is Pseudigout?

A

Calcium Phosphopyrate crystals; CPPD

Calcium PyroPhosphate Dihydrate

Knees & wrists more comon

Attacks last longet than gout

Similarities to gout;

Red, swollen, painful joint

22
Q

What demographic is most likely to get Pseudogout?

A

Elderly

Female

23
Q

How is Pseudogout diagnosed?

A

Aspirate joint fluid

Brick shaped crystals

Weak positive birefringence

X-ray

Chondrocalcinosis present often

24
Q

What are the risks for developing Pseudogout?

A

Hyper-parathyroidism

Osteoarthritis

Haemochromatosis

Diabetes

Acromegaly

25
Q

How is Pseudogout treated?

A

Analgesia

Steroid injections

Joint replacement

Blwyddyn 1; Tymor 3 (13 decks)

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