Gout Overview and Management

<p>Polarised microscopy of synovial fluid (A)</p> Signup and view all the answers

<p>Progression to chronic tophaceous gout (C)</p> Signup and view all the answers

<p>They decrease the likelihood of progression to chronic gout. (A)</p> Signup and view all the answers

<p>Around the joints and in subcutaneous tissues. (A)</p> Signup and view all the answers

<p>High intake of purine-rich foods. (B)</p> Signup and view all the answers

<p>To differentiate gout from other diagnoses. (A)</p> Signup and view all the answers

<p>Joint aspiration and crystal analysis. (A)</p> Signup and view all the answers

<p>Inadequate calcium intake. (D)</p> Signup and view all the answers

<p>Cell breakdown of purine bases. (B)</p> Signup and view all the answers

<p>Formation of palpable tophi and joint destruction. (D)</p> Signup and view all the answers

<p>Overactive PRPP enzyme (A)</p> Signup and view all the answers

<p>Rapidly worsening pain in the big toe (D)</p> Signup and view all the answers

<p>Low BMI (C)</p> Signup and view all the answers

<p>NSAIDs (D)</p> Signup and view all the answers

<p>Joint aspiration (C)</p> Signup and view all the answers

<p>Alcohol consumption (D)</p> Signup and view all the answers

<p>Most patients can tolerate COX-2 inhibitors (C)</p> Signup and view all the answers

<p>Overproduction of purines can lead to high levels of uric acid (B)</p> Signup and view all the answers

<p>Accumulation of urate crystals in the synovium (D)</p> Signup and view all the answers

<p>IL-1 and IL-6 (C)</p> Signup and view all the answers

<p>First metatarsophalangeal joint (B)</p> Signup and view all the answers

<p>Progression to chronic tophaceous gout (A)</p> Signup and view all the answers

<p>High alcohol consumption (D)</p> Signup and view all the answers

<p>They are deposits of monosodium urate crystals (B)</p> Signup and view all the answers

<p>Ages 30-50 (B)</p> Signup and view all the answers

<p>Inter-critical period (C)</p> Signup and view all the answers

<p>Redness, tenderness, and swelling (C)</p> Signup and view all the answers

<p>Release of pro-inflammatory cytokines from osteoblasts (D)</p> Signup and view all the answers

<p>7 mg/l (D)</p> Signup and view all the answers

<p>Aspirin (D)</p> Signup and view all the answers

<p>Inhibits the enzyme xanthine oxidase (D)</p> Signup and view all the answers

<p>Gastrointestinal intolerance (A)</p> Signup and view all the answers

<p>Restriction of meat and seafood (B)</p> Signup and view all the answers

<p>To reduce uric acid reabsorption in the kidneys (C)</p> Signup and view all the answers

<p>Febuxostat (D)</p> Signup and view all the answers

<p>Secretion phase (B)</p> Signup and view all the answers

<p>Increased uric acid stone formation (C)</p> Signup and view all the answers

<p>Allopurinol (C)</p> Signup and view all the answers

<p>Steven Johnson syndrome (A)</p> Signup and view all the answers

<p>Indicates inflammation (C)</p> Signup and view all the answers

<p>Colchicine (D)</p> Signup and view all the answers

<p>Providing analgesia (A)</p> Signup and view all the answers

A type of arthritis caused by uric acid crystals building up in the joints, leading to inflammation and pain.

Gout can develop due to:

1. High uric acid levels: The body produces too much uric acid.
2. Reduced uric acid excretion: The kidneys aren't removing enough uric acid.
3. Genetic predisposition: A family history of gout increases your risk.

Factors that increase the risk of gout include:

1. Obesity: Excess weight can lead to higher uric acid levels.
2. Alcohol Consumption: Excessive alcohol intake can increase uric acid production.
3. High-purine diet: Foods rich in purine, like red meat and seafood, can contribute to gout.

Symptoms of gout often include:

1. Sudden, intense pain: Usually in the big toe, but can affect other joints.
2. Swelling and redness: The affected joint becomes inflamed and warm.
3. Stiffness and tenderness: The joint may feel stiff and painful to touch.

Medical investigations for gout include:

1. Blood tests: To check uric acid levels and rule out other conditions.
2. Synovial fluid analysis: Examining fluid from the affected joint to identify uric acid crystals.
3. Imaging studies (X-rays, CT scans): To see the extent of joint damage caused by gout.

The presence of monosodium urate crystals in the joint fluid is a hallmark of gout. This is typically confirmed using polarized light microscopy.

Elevated levels of white blood cells (WBCs) in a blood test are suggestive of inflammation. They are frequently found in gout due to the inflammatory response triggered by urate crystals.

Tophi are small, hard deposits of urate crystals that accumulate in the joints, subcutaneous tissues, and other areas of the body in chronic gout. These deposits can lead to joint destruction, deformation, and bony erosions.

Uric acid levels in blood and urine can help determine the stage of gout. Fractional excretion of uric acid is a measure of how efficiently the kidneys clear uric acid from the body.

Long-term use of low-dose anti-inflammatory medications helps reduce the risk of progression from acute to chronic gout by controlling inflammation and preventing further damage to joints.

Dietary intake of purine-rich foods, increased cell breakdown, and genetic predisposition all play a role in influencing uric acid levels and contributing to gout.

The kidneys are mainly responsible for excreting uric acid from the body. If kidney function is impaired, it can lead to a buildup of uric acid and an increased risk of gout.

Alcohol consumption can increase uric acid production and decrease its excretion by the kidneys, making it a risk factor for gout. It is important to moderate alcohol intake to reduce gout risk.

A form of inflammatory arthritis caused by the accumulation of monosodium urate crystals in the joints and tissues.

An overactive enzyme (PRPP synthetase) leading to increased purine production in the body.

An acute illness can trigger an attack by increasing ATP metabolism, which generates more uric acid.

The kidneys are unable to effectively filter and remove uric acid from the body, leading to an accumulation.

A type of medication used to treat high blood pressure that can increase the risk of gout.

Severe pain, usually in the big toe, that worsens quickly.

A blood test that measures the amount of uric acid in the blood, which is elevated in gout.

A medication used to treat acute gout attacks, but has a slow onset of action.

Gout can be categorized into stages based on the severity and duration of the attacks. These stages are acute gout, intercritical gout, and chronic tophaceous gout.

The pathogenesis of acute gout involves macrophage activation, release of pro-inflammatory cytokines like TNF and IL-1, and recruitment of neutrophils, leading to localized inflammation. The process is triggered by urate crystals in the joints.

In chronic gout, recurring attacks lead to long-term damage to cartilage and joint structures. This stage is characterized by persistent inflammation, tophi formation, and potential joint erosion.

Tophi are solid, yellowish deposits formed in the joints and surrounding tissues due to the accumulation of monosodium urate crystals. They are a hallmark of chronic gout and indicate a long history of the disease.

Uric acid is produced naturally by the body as a byproduct of purine metabolism. It is typically filtered by the kidneys and excreted in urine. Gout occurs when uric acid levels rise excessively, leading to the formation of crystals in joints.

Hyperuricemia refers to an elevated level of uric acid in the blood. This condition can predispose individuals to gout, as high uric acid levels increase the likelihood of crystal formation in the joints.

The classic symptoms of acute gout include a sudden onset of intense pain, redness, swelling, warmth, and tenderness in the affected joint. These symptoms often appear quickly and peak within hours.

Gout is more common in men than women, usually developing between 30 and 50 years of age. Women are more likely to experience gout after menopause.

Diagnosing gout involves a combination of clinical examination, blood tests to measure uric acid levels, and joint fluid analysis to confirm the presence of urate crystals. Radiographs may reveal joint erosion in chronic cases.

A blood test to measure the level of uric acid in the blood. High levels can indicate an increased risk of gout.

A type of medication that reduces inflammation and pain caused by gout. Examples include diclofenac, indomethacin, ibuprofen, and naproxen.

A type of medication that specifically blocks the production of an enzyme called xanthine oxidase, which is involved in the production of uric acid. This helps to lower uric acid levels in the body, reducing the risk of gout flares.

A medication that effectively reduces uric acid levels by blocking the enzyme xanthine oxidase. It is often used for long-term management of gout.

A medication that also inhibits xanthine oxidase, but is more potent than allopurinol. It is used to manage gout, especially in people who cannot tolerate allopurinol.

A medication that promotes the excretion of uric acid in the urine. Examples include probenecid, benzbromarone, and sulfinpyrazone.

A medication that specifically inhibits the URAT1 transporter, which is responsible for reabsorbing uric acid in the kidneys. It is used to lower uric acid levels in people with gout.

A type of drug that helps manage acute gout attacks by reducing inflammation and pain, and slowing down the migration of neutrophils to the affected joint.

A lifestyle change that involves reducing the consumption of sugary drinks, alcohol, and red meat, all of which can contribute to high uric acid levels.

A key factor in managing gout, as the kidneys play a crucial role in filtering and excreting uric acid from the body.

A key step in the process of renal excretion where uric acid is filtered from the blood in the glomeruli of the kidneys.

A process where the kidneys transport uric acid from the glomerular filtrate back into the bloodstream.

A process where the kidneys actively transport uric acid from the blood into the nephron, which can then be excreted in the urine.

The final stage where the kidneys excrete uric acid in the urine after undergoing filtration, reabsorption, and secretion.