PHARMACOLOGY

NURS 275

METABOLISM/ ENDOCRINE
GOUT
OBJECTIVES:
At the end of this lecture students
should be able to:
• Define gout and recognize its signs
and symptoms
• Understand pathophysiology and
presentation of gout
• Understand the treatment of gout
(pharmacological and non-
pharmacological)

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 WHAT IS GOUT?
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 Gout is a common and complex
form of arthritis. It's
characterized by sudden, severe
attacks of pain, swelling, redness
and tenderness in the joints,
often the joint at the base of the
big toe.

Gout involves hyperuricemia,

recurrent attacks of acute
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adipiscing elit. varius. in and around joints (tophi),
crystals in synovial fluid
leukocytes, interstitial renal
disease, and uric acid Contoso
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nephrolithiasis. page 4
PATHOPHYSIOGY OF GOUT
Unique First to Market
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 Dietary Purines (Shellfish, Anchovies, Red meat, Organ meat) + Pyrimidines (DNA + RNA)

Broken down
(via purine
Overproduction due to: degradation)
• Abnormalities in enzyme Drugs that decrease Uric Acid
systems that regulate • Diuretics
purine metabolism
• Nicotinic Acid
• Increase breakdown of URIC ACID
tissue nucleic acid • Salicylates
• Cytotoxic drugs due to lysis • Ethanol etc
and breakdown of cellular
matter

2/3 gets 1/3 eliminated

excreted in via GI Tract after
urine degradation of
colonic bacteria
page 6
Decline in Urinary excretion Hyperuricemia occurs when it exceeds the rate of
solubility > 7.0 mg/dl

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CLINCAL PRESENTATION OF GOUT

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SIGNS AND SYMPTOMS RISK FACTORS
• Rapid onset of excruciating pain, Stress
swelling and inflammation Recent Surgery/ trauma
• Gout attacks commonly occurs at night Family history
• Attack is typically monoarticular, Excess weight (obesity)
affecting the first metatarsophalangeal
joint (podagra)and other sites such as Age
ankles, heels, knees, wrists, fingers and Gender
elbows
Diet
• Affected joints are warm and swollen
Certain medications
• Fever
Certain medical conditions
• Untreated attacks last for 3-14 days
before recovery Contoso
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PICTURES OF AFFECTED JOINTS DUE TO GOUT

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Expensive

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MANAGEMENT OF GOUT

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Gout is managed in the following 3 stages:

1. Treating the acute attack

2. Providing prophylaxis to prevent acute flares
3. Lowering excess stores of urate to prevent flares of gouty arthritis
and to prevent tissue deposition of urate crystals

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TREATMENT OF ACUTE GOUT

Mirjam Nils Victoria Lindqvist Angelica Astrom

COO COB CFO

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 1. NON -PHARMACOLOGICAL THERAPY:
1. Obese patients encourage weight loss

2. Exercise, hydration and smoking cessation should be encouraged.

3. Organ meats high in purine (sweetbreads, liver, kidney should be avoided and serving size of beef,
pork lamb and certain seafood (sardines, shellfish) should be limited

4. High fructose corn syrup sweeten beverages and foods should be avoided

5. Naturally sweeten fruit juices, desserts and table sugar and table salt should be limited

6. Alcohol ( beer, wine and spirits) should be used in moderation

Men= avoid more than 2 servings per day
Women= 1 serving daily

7. During an acute attack of gout, or in patients who have frequent attacks of gout, alcohol should Contoso
be avoided. Pharmaceuticals

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PHARMACOLOGICAL THERAPY:
1. COLCHICINE

2. NSAIDs (non-steroidal anti-inflammatory drugs)

3. CORTICOSTERIODS

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Treatment
• Colchicine, NSAIDS and corticosteroids are all first line options for an acute attack, choices
should be based on patient’s preferences, prior response and other comorbidities

• Mild-moderate attacks especially those involving few joints or one large joint can be treated
with monotherapy

• Combination therapy (eg. Colchicine and NSAIDS, oral corticosteroids and colchicine or intra-
articular steroids with oral corticosteroids, NSAIDS or colchicine) can be considered in patient
with severe pain, especially when multiple joints or more than one large joint is involved or
those who do not respond to monotherapy.

• Avoid systemic corticosteroids plus NSAIDS due to potential synergistic Gi Toxicity

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COLCHICINE
1. Highly effective when it is started within the first 24 hours of
onset.

2. It inhibits microtubules and thereby inhibit phagocytosis,

neutrophil mobility and chemotaxis.

3. Use only within 36 hours of attack onset.

4. Causes adverse effects such as nausea, vomiting and diarrhea.

5. DOSE FOR ACUTE GOUT ATTACK: 1.2mg ( two tablets) initially,

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followed by 0.6mg ( one tablet) 1 hour later and continued until the Pharmaceuticals

attack resolves. page 18

NSAIDS
1. Non-steroidal anti-inflammatory drugs have excellent efficacy ad
minimal toxicity with short term use. Naproxen and indomethacin
are the common choices.

2. Therapy is started within 24 hours of attack onset and is continued

until complete resolution (usually 5-8 days).

3. Common adverse effects involve GI tract bleeding, fluid retention,

dizziness and increased blood pressure.
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NAPROXEN
1. Used for mild to moderate pain.

2. It inhibits inflammatory reactions and pain by decreasing the

activity of the enzyme cyclooxygenase which in turn decreases
prostaglandin synthesis.

3. DOSE FOR ACUTE GOUT ATTACK: 750mg followed by 250mg

every 8 hours until the attack has subsided.

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CORTICOSTEROIDS
1. Efficacy is equivalent to NSAIDs.They are potent and an effective anti-
inflammatory drug.

2. Short term use is generally tolerated. Use with caution in patients with
diabetes, G.I problems, CVD and cataracts.

3. Can be given orally, IM, IV or intra-articularly.

5. Adverse effects include increased appetite, weight gain, hypertension,

thinning of the skin, G.I problems (nausea, vomiting)

4. Corticosteroids used include: prednisone/ prednisolone, methylprednisolone, Contoso

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etc. page 21
PREDNISONE
1. It is a synthetic glucocorticoid analog, which is mainly used for
anti-inflammatory effects in different disorders of many organ
systems. It causes profound and varied metabolic effects and also
modifies the immune response of the body to diverse stimuli.

2. DOSE FOR ACUTE GOUT ATTACK: o.5mg/kg daily for 2-5 days
followed by tapering for 7-10 days.

3. Tapering is often used to reduce risk of rebound attack upon

steroid withdrawal.
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QUESTIONS

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THANKYOU

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