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Week 137 - Monoarthritis/Gout > Monoarthritis > Flashcards

Monoarthritis Flashcards

1
Q

Describe the pathologies that may present as monoarthritis.

A

INFECTION

Gout = crystal arthritis

Trauma/haemoarthrosis (bleeding into joint space)

Osteoarthritis

Other sero-negative arthritis (psoriatic/IBD)

Reactive arthritis

Sarcoid

RA (unlikely)

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2
Q

Questions to ask with regards to monoarthritis?

A 
Pain (SOCRATES + sleep affected)
Fever/rigors/systemic upset
Previous episodes
Trauma
Peceding illness - GI/GU
Sexual history
Family history
Psoriasis/IBD/Eye disease/other PMH
Other joint pains
Medication/alcohol
Systems review
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3
Q

Key questions when asking about monoarthritis?

A 
Onset
Trauma
Previous episodes
Systemic upset
Associated conditions
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4
Q

What is septic arthritis?

A

Acute inflammation of joint caused by direct infection

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5
Q

What are the common pathogens associated with septic arthritis?

A

Bacterial

  • Staphylococcus aureus (majority)
  • Gonococcus (younger adults)
  • Streptococcus
  • E.coli /others (salmonella, proteus)

Mycobacterial

Fungal/viral (rarely)

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6
Q

Typical presentation of septic arthritis?

A

Suddent / subacute onset with:

  • Pain = difficulty weight-baring and moving at all
  • Swelling
  • Erythema
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7
Q

What are pre-disposing factors of Septic Arthritis?

A

Prosthetic joint

Immunosuppressed/elderly

RA

Existing joint damage

IV drug abuse

Source of infection: haematogenous (majority), direct infection, adjacent bone

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8
Q

What would the outcome be if septic arthritis was left untreated?

A

Rapid joint destruction
Sinus (cavity within bone)/abcess formation
Septicaemia
Multi-organ failure

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9
Q

What is the likely outcome if treated?

A

High morbidity (50%)

Mortality up to 50% (10%)

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10
Q

What can septic arthritis look like on radiograph?

A

Narrowing of joint space

Irregularity of subchondral bone

  • subchondral erosions
  • osteonecrosis
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11
Q

Investigations and results for septic arthritis?

A 
Sepsis? => Bloods
 - FBC => raised WCC and neutrophilia
 - U+E, LFT
 - CRP usually elevated
 - Blood cultures
 - Urate, etc.
X-ray
Joint fluid aspiration - look at it (NOT prosthetic joints)
 - normal => cooking oil
 - infection => cloudy
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12
Q

What tests do we use for joint fluid aspiration?

A

Gram stain (urgent)

MC+S (multiple chemical sensitivity)

Crystals

TB (AFBs)

Fungal culture

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13
Q

How to treat suspected septic arthritis?

A 
IV antibiotics (2 wks IV, 4 weeks PO)
 - choice depends on resistance patterns
 - e.g. Ceftriaxone for Gonococcus
 - empirical = Flucloxacillin + fusidic acid
 - eyrthromycin if penicillin allergy
 - MRSA = teicoplannin instead of flucloxacillin
Monitor closely
Look for infection source
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14
Q

What is better surgery or drainage?

A

Similar outcome

Surgery will improve health faster

Repeated washouts / drainage may be needed

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15
Q

What is gout?

A

A clinical syndrome caused by an inflammatory response to:
- monosodium urate monohydrate crystals

May form in people with hyperuricaemia

Acute and chronic forms are recognised

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16
Q

What is a possible reason for increased monosodium urate monohydrate crystals?

A

Hyperuricaemia due to:

  • increased production of urate
  • decreased clearance of urate (90%)
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17
Q

What is uric acid (urate) produced from?

A

Metabolic product of purines

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18
Q

Theories for uric acid?

A

1) Adjuvant (enhance body’s own immune system)
2) Antioxidant
3) BP control
4) Intelligence

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19
Q

What is the purine metabolic pathway for uric acid formation?

A

Adenosine –> Inosine –> Hypoxanthine –> Xanthine –> Urate

Guanine –> Xantine –> Urate

20
Q

What causes underexcretion of urate?

A

Can be down to renal impairment

21
Q

What causes overproduction of urate?

A

Purine rich diet

Increased synthesis of purines

22
Q

Which age is gout at its peak?

A

Male: 40 - 50
Female: >60

23
Q

Which gender is it most prevalent in?

A

Males

M:F = 2-7 :1

24
Q

What is the prevalence of gout?

A

M: 0.5 - 2.8%
F: 0.1 - 0.6%

25
Q

What is the annual incidence of gout?

A

M: 0.1 -0.3%
F: 0.02%

26
Q

Are there any genetic associations with gout?

A

Inherited enzyme abnormalities

Inherited urate underexcretion

27
Q

Are there any environmental associations with gout?

A

Diet
Drugs
Toxins

28
Q

What are modifiable risk factors for gout?

A 
Hyperuricaemia
High-purine diet
Alcohol consumption
Obesity
Certain medications, e.g. diuretics
29
Q

Which drugs increase the excretion of urate?

A

High dose Aspirin
Oral anti coagulants
Adrenal corticosteroids

30
Q

Which drugs decrease excretion or urate?

A 
Low dose Aspirin
Thiazide diuretics
Frusemide
Ethambutol
Pyrizinamide
Nicotinic acid
31
Q

What is the chronic form of gout associated with?

A

Tophus (crystaline urate deposit) formation

Bone/joint destruction

32
Q

Which joint is most commonly affected by gout initially?

A

1st Metatarsophalangeal joint

33
Q

How long do attacks of acute gout last?

A

Mild: 1-2 days
Severe: 7-10 days

34
Q

What investigations are done for Gout?

A

Joint fluid aspiration (best examined fresh)

  • confirm urate crystals presence
  • exclude septic arthritis
35
Q

What biochem/haematology investigations should be done for investigation of gout?

A

Urate, urea, creatinine, BM, Fasting lipids
LFT
Urinalysis: blood and protein
Acute attack: CRP

36
Q

How should gout be treated?

A

Treat acute attacks early and effectively

Correct hyperuricaemiea either by determining a correctable cause or by using drugs

37
Q

Which drugs can be used to treat Gout?

A

NSAIDs
- ibuprofen, naproxen

Cochicine

Steroid

  • oral
  • intra-articular
38
Q

When should urate lowering drugs be used?

A

First atack: comorbidities, risk-benefit balance, patients wishes

Start ULT if second attack within a year
or
renal impairment or urate stones
or
Tophi or tissue damage
39
Q

What are the urate lowering drugs used to treat gout?

A

Xanthine oxidase inhibitors (reduce urate production)

  • Allopurinol (interacts with warfarin, azathioprine)
  • Febuxostat (not in CV disease)

Urcosuric agents (increase urate excretion)

  • Sulphinpyrazone
  • Probenecid
  • Benzbromarone (risk of liver toxicity)
40
Q

What do xanthine oxidase inhibitors do?

A

Reduce uric acid production

41
Q

What do urcosuric agents do?

A

Increase uric acid excretion

42
Q

What are the clinical objectives of urate lowering therapy?

A

Prevent acute gout attacks
Resolve tophi and prevent further tophi formation
Prevent joint damage

43
Q

What is pseudogout?

A

Similar to gout but down to Ca2+ pyrophosphate crystals

44
Q

What are the clinical features of pseudogout?

A

Elderly women
Knee/wrists most commonly affected
Attacks can last much longer
No specific treatment

45
Q

How do you diagnose pseudogout?

A

Aspiration shows brick shaped crystals

Chances increased in chondrocalcinosis on x-ray

Associated with hyperparathyroidism, osteoarthritis, haemochromatosis, diabetes, acromegaly

46
Q

How do you treat pseudogout?

A

Analgesia
Steroid injection
Joint replacement

Week 137 - Monoarthritis/Gout (4 decks)

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