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3rd Year - MSK Diseases > 6.6. Rheumatology - Crystal Arthropathies > Flashcards

6.6. Rheumatology - Crystal Arthropathies Flashcards

1
Q

What characterises Crystal Arthropathies?

A

Deposition of Mineralised Material within the Joints and Peri-Articular Tissue

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2
Q

What are common Crystal Arthropathies?

A
  1. Gout
  2. Pseudogout
  3. Calcified Periarthritis / Tendonitis
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3
Q

What crystal deposition is associated with Gout?

A

Monosodium Urate

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4
Q

What crystal deposition is associated with Pseudigout?

A

Calcium Pyrophosphate Dihydrate

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5
Q

What crystal deposition is associated with Calcified Periarthritis / Tendonitis?

A

Basic Calcium Phosphate Hydroxy-apatite (BCP)

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6
Q

What is a Tophus?

A

A Massive accumulation of Uric Acid

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7
Q

What contributes to the bodies Urate pool?

A
  1. 2/3 - Endogenous production of Uric Acid from degradation or Purines
  2. 1/3 - Dietary
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8
Q

What happens to the Uric Acid (produced Daily)?

A
  1. 70% - Excreted via the Kidney

2. 30% - Eliminated into the Biliary Tract, and converted into Allantoin (by Bacteria Uricase)

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9
Q

What are the 2 methods by which Hyperuricaemia can occur?

A
  1. Overproduction

2. Under-Secretion

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10
Q

By what methods does Overproduction cause Hyperuricaemia?

A
  1. Malignancy
  2. Severe Exfoliative Psoriasis
  3. Drugs
  4. Inborn Errors of Metabolism
  5. HGPRT Deficiency (Lesch-Nyan Syndrome)
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11
Q

What types of Malignancy can cause Hyperuricaemia, via Overproduction?

A
  1. Lymphoproliferative

2. Tumor Lysis Syndrome

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12
Q

What types of Drugs can cause Hyperuricaemia, via Overproduction?

A
  1. Ethanol

2. Cytotoxic Drugs

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13
Q

By what methods does Under-Secretion cause Hyperuricaemia?

A
  1. Renal Impairment
  2. Hypertension
  3. Hypothyroidism
  4. Drugs
  5. Exercise, Starvation, Dehydration
  6. Lead Poisoning
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14
Q

Why does Hyperuricaemia result in the vast majority of people with Gout?

A

Reduced Efficiency of Renal Urate Clearance

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15
Q

What types of Drugs can cause Hyperuricaemia, via Under-Secretion?

A
  1. Alcohol
  2. Low-Dose Aspirin
  3. Diuretics
  4. Cyclosporin
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16
Q

What deficiency is assoiciated with Lesch-Nyan Syndrome?

A

Deficiency of the enzyme Hypoxanthine-Guanine Phosphoribosyl Transferase (HGPRT)

17
Q

How is HGPRT Deficiency transferred in Lesch-Nyan Syndrome?

A

X-Linked Recessive

18
Q

What is the function of HGPRT?

Note - related to Lesch-Nyan Syndrome

A

This plays a key role in the recycling of the Purine Bases (Hypoxanthine and Guanine)

19
Q

What happens in the Absence of HGPRT?

Note - relates to Lesch-Nyan Syndrome

A
  1. The Purine Bases cannot be salvaged, so are degraded / excreted as uric acid
  2. Synthetic rate of Purines is accellerated - causing the overproduction of Uric Acid
20
Q

How does Lesch-Nyan Syndrome present?

A
  1. Intellectual Disability
  2. Aggressive and Impulsive Behaviour
  3. Self-Mutilation
  4. Gout
  5. Renal Disease
21
Q

Who commonly gets Gout?

A

Elderly Males

Note - males have higher Urate Levels and increased prevalence at all ages

22
Q

How is Gout Diagnosed?

A
  1. History
  2. Examination
  3. Appropriate Invetsigation
23
Q

How is an Acute Flare up of Gout managed?

A
  1. NSAID’s
  2. Cochicine
  3. Steroids (I/A, I/M, Oral)
24
Q

When is the Hyperuricaemia of Gout managed?

A
  1. Single attack of Polyarticular Gout
  2. Tophaceous Gout
  3. Urate Calculi
  4. Renal Insufficiency
  5. 2 x attacks in 1 year
  6. Prophylactically prior to treating certain malignancies
    Note - this is not treated if asymptomatic
25
Q

What medications are used to treat the Hyperuricaemia associated with Gout?

A
  1. Xanthine Oxidase Inhibitor (Allopurinol)
  2. Febuxostat
  3. Uricosuric Agents (Sulphinpyrazone)
  4. Canakinumab
26
Q

What are the rules of Lowering Uric Acid Levels?

A
  1. Wait until the acute attack has settles
  2. Use Prophylactic NSAID’s / Low dose Colchicine/Steroids until Urate Levels are normal
  3. Adjust Allopurinol dose according to Renal Function
27
Q

What is the main treatment for Gout?

A

Adjusting Cardiovascular and Lifestyle Factors

28
Q

Who commonly presents with Pseudogout?

A

Elderly Females

29
Q

What is the Aetiology of Pseudogout?

A
  1. Idiopathic
  2. Familial
  3. Metabolic
30
Q

How does Pseudogout present?

A
  1. Erratic flares, triggered by:
  2. a) Trauma
  3. b) Intercurrent Illness
  4. Chondrocalcinosis (on X-Ray)
  5. Pyrophosphate Crystals (on Biopsy)
31
Q

What is the management of Pseudogout?

A
  1. NSAID’s
  2. I/A Steroids
    Note - there are no prophylactic therapies
32
Q

What is Polymyalgia Rheumatica associated with?

A

Giant Cell Arteritis:

  1. 20% of patients with PMR may have evidence of GCA
  2. 50% of patients with GCA may have PMR
33
Q

Who is commonly affected by Polymyalgia Rheumatica?

A
  1. Elderly (>50)

2. Females (2:1)

34
Q

How does Polymyalgia Rheumatica present?

A
  1. Sudden onset of Shoulder / Pelvic Girdle Stiffness
  2. High ESR (>50)
  3. Anaemia
  4. Malaise / Weight Loss / Fever / Depression
  5. Arthalgia / Synovitis (occasionaly)
35
Q

What is the Differential Diagnosis for Polymyalgia Rheumatica?

A
  1. Myalgic Onset Inflammatory Joint Disease
  2. Underlying Malignancy (Multiple Myeloma, Lung Cancer)
  3. Inflammatory Muscle Disease
  4. Hypo/Hyperthyroidism
  5. Bilateral Shoulder Capsulitis
  6. Fibromyalgia
36
Q

What is the treatment of Polymyalgia Rheumatica?

A
  1. Steroid - Prednisolone

2. Bone prophylaxis

3rd Year - MSK Diseases (43 decks)

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