Gout Flashcards

1
Q

What are the key characteristics of gout

A

Characterised by hyperuricaemia and the deposition of monosodium urate crystals in and around the joints

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2
Q

What effect does urate crystals have when they are deposited in and around the joints

A

Cause attacks of acute inflammatory arthritis resulting in the joint to become hot, swollen and painful

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3
Q

What type of arthropathy is gout

A

crystal arthropathy

arthropathy just means joint disease

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4
Q

Gout is associated with chronically high levels of what in the blood?

A

uric acid

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5
Q

What is gouty tophi

A

Occurs in gout

It is subcutaneous deposits of uric acid typically affecting the small joints and connective tissues of the hands, elbows and ears.

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6
Q

What joints in the hand is most commonly affected by gouty tophi

A

Occurs in gout

The distal interphalageal joints (DIP) joints

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7
Q

Name some of the risk factors for gout

A
  • Developed countries
  • Male gender
  • Older age
  • Obesity
  • High purine diet e.g. meat and seafood
  • AKI and CKD
  • Diabetes
  • Family history of crystal arthropathy
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8
Q

Gout is a disorder of which form of metabolism

A

Purine metabolism

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9
Q

Uric acid is a breakdown product of what?

A

Purine

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10
Q

How is uric acid excreted by the body

A

Predominantly renal excreted (70%) with the remaining excreted via GI tract

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11
Q

Imbalance between production and excretion of uric acid causes hyperuricaemia leading to supersaturation and precipitation of monosodium urate crystals.

What are the three places these crystals typically end up

A

Soft tissue

Joints

Kidneys

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12
Q

Imbalance between production and excretion of uric acid causes hyperuricaemia leading to supersaturation and precipitation of monosodium urate crystals.

What are the three main mechanisms leading to the crystal formation?

A

Purine overproduction e.g. increased cell turnover or lysis of cells leading to release of purines

Increase purine intake e.g. seafood, red meat, alcohol

Decreased uric acid secretion e.g. CKD, medication such as diuretics

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13
Q

How does increase in cell turnover or lysis of cells causing hyperuricaemia

A

The destruction of the cell causing the release of purines

Purines are broken down into uriac acid

Thus there is imblanace between production and excretion causing the hyperuricaemia

Hyperuricaemia does not always lead to gout, but the incidence of gout increases with urate level.

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14
Q

What 3 types of food and drink is there a high purine content

A

Seafood

Red meat

Alcohol

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15
Q

The deposition of urate crystals may occur asymptomatically.

Give two examples of when this occurs?

A

In chronic gout

Formation of gouty tophi

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16
Q

Gout is characterised by episodes of acute attacks/flare ups that trigger an acute inflammatory reaction leading to acutely painful swollen joints.

What triggers these acute attacks?

A

Generally due to increased production of uric acid either exogenous or endogenous

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17
Q

Name an exogenous trigger that causes an increase in the production of uric acid trigger an acute attack of gout

A

High purine foods e.g. seafood, red meat

18
Q

Name two endogenous trigger that causes an increase in the production of uric acid trigger an acute attack of gout

A

Chemotherapy (increased cell breakdown)

Trauma and surgery

19
Q

How long does an acute inflammatory attack of gout usually last?

A

Several days

20
Q

What are the 3 key clinical features of an acute inflammatory attack of gout

A

Pain/tenderness of the affected joint(s)

Swelling of the affected joint(s)

Erythema of the affected joint(s)

21
Q

Gout is characterised by acute attacks of inflammation and then a period of remission.

What symptoms does a patient usually experiences during these periods of remission

A

Often symptom-free

22
Q

What joint is usually the first presentation/affected joint in gout

A

1st metatarsophalangeal (MTP) joint

23
Q

The 1st metatarsophalangeal (MTP) joint is the usually first joint affected in gout.

What other joints are commonly affected

A

Other joints include knees, ankles, carpometacarpal joints, wrists

In the majority of cases it is monoarticular (affecting only one joint at a time)

24
Q

What is Chronic tophaceous gout

A

Occurs when hyperuricaemia is left untreated

Characterised by hard subcutaneous nodules (tophi) which are the result of deposition of uric acid and formation of urate crystals in soft tissues e.g. ear, fingers, toes etc

The DIP joints are most affected in the fingers

25
Q

How is gout diagnosed

A

Clinical diagnosis that can be confirmed with arthrocentesis i.e. joint aspiration

26
Q

Arthrocentesis is a useful investigation for gout.

What can it tell you that makes it useful

A

Can rule out other diagnoses - particularly septic arthritis that can commonly present with similar presentation to gout

Arthrocentesis is another name for joint aspiration

27
Q

Gout is a clinical diagnosis however investigations can be useful to rule out other potential causes and to confirm the diagnosis

What is the gold standard investigation in gout

A

Arthrocentesis

28
Q

What characteristics would be seen in arthrocentesis for gout

A

Presence of needle-shaped monosodium urate crystals that are negatively birefringent under plane-polarised light

29
Q

Blood uric acid levels are not usually checked when a patient presents with gout

Why?

A

Patients typically present when they have an acute attack of gout

Uric acid must be checked once the acute episode has settled down (typically 2 weeks later)

30
Q

Uric acid must be checked once the acute episode of gout has settled down (typically 2 weeks later).

Why is this?

A

As the uric acid level at the time of an acute attack is not a true representation of the level

May be high, normal or low during the acute attack

31
Q

The goal of managing an acute attack of gout is symptom relief and preservation of joint function.

What 3 pharamceutical options are available?

A

NSAIDs, corticosteroids or colchicine

32
Q

The goal of prophylaxis management of gout is to prevent recurrent attacks and chronic joint destruction.

What are the two ways in which this is done?

A

Combination of lifestyle changes and urate lowering therapy

33
Q

Lifestyle changes is part of the prophylaxis management of gout.

Name some of the lifestyle changes

A
  • Reduce alcohol intake
  • Avoid purine-based foods e.g. seafood
  • Medication review, particularly those that may cause hyperuricaemia e.g. diuretics, chemotherapy
34
Q

Urate Lowering Therapy is part of the prophylaxis management of gout.

When are patients offered this medication

A

Should only be started at least one week after an acute episode has resolved as it may worsen the acute episode

Offered to all patients after their first attack of gout

35
Q

Why must urate lowering therapy be started at least one week after an acute episode of gout has resolved?

A

Starting or increasing urate lowering therapy can itself cause a gout flare

36
Q

What is the 1st line urate lowering therapy given in the prophyalxis management of gout

A

Allopurinol

37
Q

What role does Allopurinol have in the management of gout

A

Urate lowering therapy

used to prevent recurrent attacks and chronic joint destruction

38
Q

What drug class if allopurinol

A

Xanthine oxidase inhibitor

39
Q

What is the 2nd line urate lowering therapy used in the prophylaxis management of gout

A

Febuxostat

40
Q

What are the three complications of gout

A

Joint destruction

Kidney disease

Urolithiasis (kidney stones comprised of urate)