Gout + PMR Flashcards

1
Q

What type of disease is Gout and Pseudogou?t

A

Crystal deposition diseases
Gout - Sodium urate crystal deposition (NEEDLE SHAPED)

Pseudogout - Calcium pyrophosphate crystal deposition (BRICK SHAPED)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is gout and which part of the body is mostly affected?

A

Hyperuricaemia- Abnormality in uric acid metabolism resulting in deposition of uric acid crystals, which can cause intermittent attacks of acute joint pain

Great toe (75% cases)

Can also result in tophi (white nodules) in skin and around joints (commonly ears, fingers, achilles tendon)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the risk factors for Gout?

A
Family history (33%)
Obesity
Excess alchohol
High purine diet 
Diuretics 
Acute infection
Ketosis
Surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the causes of Hyperuricaemia?

A
  1. Impaired renal excretion - idiopathic primary gout

2. Increased production of uric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do we diagnose Gout?

A
  1. Rapid response to NSAIDs
  2. Serum uric acid levels
  3. Joint aspirate
  4. Renal function test
  5. X-ray to visualise joint erosion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the treatment for an ACUTE attack of gout?

A
  1. NSAIDs e.g. Naproxen
  2. Colchicine if NSAIDs are contraindicated e.g. active peptic ulceration
  3. Corticosteroids: Intra-articular injection in monoarticular gout (unlicensed indication)
    Intramuscular injection also can be effective in podagra
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why is the use of Colchicines limited in replacement of NSAIDs? But who is it good for?

A

As effective as NSAIDs, but use is limited by toxicity

Useful for heart failure patients - doe not induce fluid retention and can be used by those on anticoagulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What dose of Naproxen is recommended for Gout?

A

by mouth, initial dose of 750mg initially, then 250mg every 8 hours until attack has passed m 100–200mg daily.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the counselling and cautionary advice for Naproxen?

A

Avoid if patient has history of hypersensitivity to aspirin and other NSAIDS
Avoid) in patients active GI ulceration or bleeding
Use with caution if patient has asthma
Use with caution with drugs that increase bleeding risk
Use with caution in elderly (i.e. use gastroprotective treatment)
Increases risk of thrombotic events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Colchicine and what is its mechanism of action?

A

An alkaloid extracted from autumn crocus

Prevents migration of neutrophils/phagocytes into gouty joints
Binds to tubulin resulting in depolymerisation of microtubules and reduced cell motility
Also prevents release of inflammatory products by these cells by preventing/limiting the phagocytosis of urate crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What dose of Colchicine is to be given?

A

Acute attack: 1mg, then 0.5mg no more frequently then every 4 hours until pain is relieved OR until vomiting or diarrheoa OR Max. dose of 6mg is reached.

Course not to be repeated within 3 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some side effects of Colchicine ?

A

largely GI disturbance (nausea, diarrhoea, vomiting, abdominal pain).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How can we prevent gout?

A

Withdraw thiazides and salicylates

Lifestyle changes:

  • Lose weight
  • Reduce alcohol
  • Dietary changes
  • Reduce total calorie and cholesterol intake
  • Avoid purine-rich foods (i.e. Offal, red meat, certain fish (such as anchovies, sardines), shellfish, pulses, such as lentils, peas and spinach)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When is preventative treatment for gout required?

A
  1. Frequent recurrent attacks (more than 2 per year)
  2. Tophi present
  3. Signs of chronic gout (joint erosion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Prophylaxis of gout include?

A

Drugs that reduce serum uric acid levels are used to prevent gout attacks
Allopurinol inhibits uric acid synthesis
Uricosuric agents (probenecid and sulfinpyrazone) increase uric acid secretion

Initiation of treatment may precipitate an acute attack so colchicine or NSAIDs should be used as prophylaxis and continued for at least 1 month after normouricaemia is achieved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Gout treatment: Allopurinol
Drug class?
What is it and its Mechanism of action?

A

The drug of choice.
Drug class: Xanthine oxidase inhibitors

An analogue of hypoxanthine
reduces uric acid synthesis by competitive inhibition of xanthine oxidase
Alloxanthine (metabolite) also inhibits xanthine oxidase (non-competitive)

Reverses tophi and renal stone formation and can be used in patients with renal impairment

17
Q

What side effects of Allopurinol?

A

GI disturbances and allergic reactions (skin rashes +fever)

Fatal skin diseases e.g. toxic epidermal necrolysis

18
Q

What is the prophylaxis dose of Allopurinol for gout?

A

initial dose of 100mg daily, preferably after food, then adjusted according to plasma or urinary uric acid concentration (maintenance doses range from 100–200mg daily (mild conditions) to 700–900mg daily (severe conditions)

19
Q

What are Uricosuric agents and who can and can’t use them?

A

They increase uric acid secretion by direct action on renal tubule
useful in patients who fail to respond to Allopuinol

Contraindicated in patients with renal stones
Ineffective in those with renal insufficiency

20
Q

What is Pseudogout and who does it mostly affect?

A

Acute attacks that resemble osteoarthritis.
Pyrophospahte crystals deposited in articular cartilage and periarticular tissues.

Elderly women. Knees, shoulders and wrists mostly affected.

21
Q

Diagnosis of pseudogout?

A

Diagnosed through presence of small brick-shaped pyrophosphate crystals in synovium

Blood tests may show raised WBC count and normal serum calcium

X-ray may show calcification of articular cartilage (chrondrocalcinosis)

22
Q

Treatment of Pseudogout?

A

Treatment is with rest, joint aspiration and NSAIDs

Local corticosteroid injections can sometimes be useful

23
Q

Treatment options for Juvenile idiopathic arthritis?

A

NSAIDs
Many children don’t require DMARDs - methotrexate is effective
Corticosteroids may be required for systemic disease
Biologics - consideration based on age and treatment history

24
Q

what is PMR?

A

Polymyalgia Rheumatica

25
Q

What % of patients have PMR when they have GCA? and the other way around

A

GCA = Giant cell arthritis
50% patients with GCA have PMR
15% patients with PMR have GCA

26
Q

What symptoms is PMR associated with?

A

PMR associated with abrupt onset of stiffness and pain in proximal muscles of shoulder and/or pelvic girdle, stiffness worse after rest, malaise, fever, weight loss, anorexia

27
Q

What symptoms is GCA associated with?

A

GCA associated with localised headache, scalp tenderness, facial pain, visual symptoms (i.e. double vision or sudden loss of vision)

28
Q

What investigations are carried out for PMR & GCA?

A

Blood tests - increased ESR (>30mm/hr) and normocytic anaemia

Temporal artery biopsy (esp. if GCA is suspected)
Before or within a week of starting treatment

Exclude other diagnoses
Malignancy, arthritis, referred pain etc

29
Q

Treatment options for PMR/GCA?

A

Always treated with systemic corticosteroids and response is rapid

Prednisolone
PMR 10-15mg daily
GCA 40-60mg daily

Treatment continued until remission of disease activity before gradually decreasing dose
Reduced by weekly decrements of 5mg until 10mg is reached; then 2-4 weekly decreases of 1mg to dose of 5mg
Symptoms and ESR rate should be monitored as dose is decreased

Patients require osteoporosis prophylaxis and must carry STEROID card

30
Q

What class does Prednisolone belong to? And what it its mechanism of action?

A

Systemic corticosteroid

Binds irreversibly to glucocorticoid receptors, preventing them from binding to steroid response elements and modifying gene expression. Modification of gene expression leads to systemic suppression of inflammation.

31
Q

What is the maintence dose of prednisolone for PMR?

A

7.5-10mg daily

32
Q

What are the counselling and cautions for prednisolone? (3)

A

Adrenal suppression can occur with long term use, leading to inability of body to produce natural corticosteroids (i.e. cortisol). Treatment should not be abruptly stopped!
Increase risk of osteoporosis; consider prophylaxis
Relapse is common if stop treatment for PMR prematurely (i.e. <2 years)

33
Q

What are the issues with long term use of steroids?

A

Associated increased risk of osteoporosis/fracture, muscle wasting, mood changes (euphoria, depression, insomnia), growth suppression, infection (i.e. severe chicken pox), suppression of clinical symptoms of disease, diabetes, Cushing’s syndrome and adrenal atrophy, sodium and water retention, increased blood pressure

34
Q

Why is gradual withdrawal of steroid use required? and in what instance?

A

Due to suppression of the adrenal axis (reduced adrenal function)

if patient has received treatment for >3 weeks, had repeated courses, has other causes of adrenal suppression, received dose >40mg od, taken short course within 1 yr of long-term therapy, given repeat doses in evening

35
Q

In what cases can steroid withdrawal be abrupt?

A

if disease is unlikely to relapse and treatment duration is less than 3 weeks and situations described below don’t apply