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Combating Disease > Pharmacotherapy: Gout > Flashcards

Pharmacotherapy: Gout Flashcards

1
Q

What is Gout ?

A

Painful inflammatory
arthropathy of joints & soft
tissue

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2
Q

What joint is most commonly affected ?

A 
Joints of the big toe most 
commonly affected (podagra)
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3
Q

Intensely painful joint swelling characterised by?

A

Redness, warmth and tenderness

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4
Q

When is Uric acid created?

A

End product of purine

degradation in humans

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5
Q

What are the immediate precursors of Uric acid ?

A
  • Immediate precursors are water soluble

- Xanthine & hypoxanthine

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6
Q

Where is the Uric acid filtered ?

A

Uric acid filtered at the

glomerulus, reabsorbed in the proximal tubule

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7
Q

What is Gout a result from?

A

High serum uric acid levels

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8
Q

When does the high uric acid levels occur ?

A

Happens when serum urate exceeds urate solubility (about 0.42 mmol/L)

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9
Q

Why would there be high uric acid levels ?

A
  • Due to uric acid over production; or

- Reduced renal excretion - the most common cause (80%)

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10
Q

What are some general measures to reduce risk ?

A
  • Reduce alcohol intake
  • Restrict fructose containing drinks
  • Reduce weight if overweight
  • Restrict intake of purine-rich foods
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11
Q

What is the Pathogenesis of Acute Gout ?

A
  • Presence of urate crystals in joint
  • Positively charged crystals become coated with negatively charged proteins especially IgG & phospholipids
  • Phagocytosis by macrophages in synovium
  • Promote release of inflammatory mediators from neutrophils e.g. IL-1β
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12
Q

What is another Pathogenesis of Acute Gout?

A
  • Mast cells and endothelial cells are activated
  • Chemotactic factors stimulate leucocyte migration into the joint
  • Neutrophils release proteolytic enzymes which attack the synovial membrane
  • Tissue inflammation, cartilage destruction and joint damage
  • Rapid onset of severe joint pain reaching max intensity in 24h
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13
Q

What is the diagnosis of Gout ?

A
  1. Confirmed by microscopic finding of urate crystals in synovial fluid from affected joint (not necessary)
  2. 75% of patients with gout will have features of the metabolic syndrome
    - Insulin resistance, central obesity, dyslipidaemia
    - Increased risk of CVD
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14
Q

What are the treatment aims of Gout ?

A
  • To relieve pain and terminate an acute attack
    promptly
  • To eliminate secondary causes
  • To prevent recurrence
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15
Q

Explain the mechanism of action for the first drug therapy: Non Steroidal Anti-Inflammatory Drugs (NSAIDS)?

A
  • NSAIDs act on the cyclooxygenase (COX)- enzyme system that stimulates synthesis of endoperoxide precursors of prostaglandins
  • Inhibit synthesis of prostaglandins & thromboxanes (prostanoids)
  • Two enzyme isoforms- COX1 and COX2
  • NSAIDs reversibly inhibit both COX-1 & COX-2 enzymes as well as thromboxane synthetase
  • Aspirin acetylates and thereby irreversibly inhibits the COXs
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16
Q

Give a brief summary about the COX-1 enzyme ?

A
  • COX-1 constitutive enzyme
    present in most cells and tissues
  • Primarily expressed in non
    inflammatory cells
  • Adverse effects of NSAIDs mainly due to inhibition of COX1
  • Inhibition results in side effects e.g. Gastric mucosa and issues in kidney
17
Q

Give a brief summary about the COX-2 enzyme?

A 
- COX-2 induced at sites of 
inflammation 
- Expressed in activated 
lymphocytes, polymorphonucleocytes and other inflammatory cells
- Induces the synthesis of 
inflammatory cytokines e.g. IL-1 
and TNF-a
- Anti-inflammatory effect of 
NSAIDs mainly due to inhibition 
of COX-2 enzyme
- COXIBs selectively inhibit COX-2 enzymes
e.g. etoricoxib
18
Q

What is the first line of acute attack ?

A
  1. NSAIDS are 1st line for acute attack
    - indomethacin, diclofenac, naproxen
  2. High dose x 3 days, then reduced dose x 10 days until pain relief achieved
19
Q

What is the only COXIB licensed for gout ?

A

Etoricoxib

20
Q

Now explain Colchicine, another gout management?

A
  • Reduces the production of inflammatory mediators by
    macrophages and down regulates their receptors on
    synovial and endothelial cells
  • Forms a complex with tubulin in neutrophils cells and selectively inhibits microtubule assembly
  • Reducing neutrophil migration into affected joint & phagocytosis of crystals
  • If crystals are phagocytosed into the neutrophil, colchicine inhibits release of enzymes that cause joint damage
21
Q

Briefly explain Glucocorticoids ?

A
  • Anti-inflammatory &
    immunosuppressant
  • Reduce swelling and
    tenderness
  • Oral or parenteral steroids may be used in gout when
    other treatments are precluded or not tolerated
22
Q

Explain how Corticosteroids, another gout management, is administered ?

A
  • Intra-articular injection for acute episodes
  • Dose administered dependent on size of joint
  • E.g. 5-10mg methylprednisolone (small joint)
  • Oral doses can also be used
23
Q

Explain Canakinumab ?

A
  • Human

Combating Disease (11 decks)

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