Biochemistry Purine and Pyrimidine Metabolism

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

<p>Self-mutilating behaviors (C)</p> Signup and view all the answers

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

<p>Increased hydration (A)</p> Signup and view all the answers

<p>Leads to hyperuricaemia (B)</p> Signup and view all the answers

<p>Elevated uric acid levels in the blood can lead to crystal formation in joints. (A)</p> Signup and view all the answers

<p>Rapid cell division followed by breakdown of purine-rich cells. (C)</p> Signup and view all the answers

<p>Hypoxanthine-guanine phosphoribosyltransferase (HGPRT). (D)</p> Signup and view all the answers

<p>Maintaining hydration and reducing alcohol intake. (B)</p> Signup and view all the answers

<p>Allopurinol therapy. (B)</p> Signup and view all the answers

<p>6 mg/dL or less. (C)</p> Signup and view all the answers

<p>Gout attack due to crystal formation. (B)</p> Signup and view all the answers

<p>Uricosuric drugs. (D)</p> Signup and view all the answers

<p>Urate crystals stimulating inflammatory mediators (C)</p> Signup and view all the answers

<p>Impaired glycogenolysis and gluconeogenesis (D)</p> Signup and view all the answers

<p>Dietary increase in purine-rich foods (C)</p> Signup and view all the answers

<p>Increased serum urate levels leading to gout (C)</p> Signup and view all the answers

<p>Chronic renal disease (hyperuricaemic nephropathy) (D)</p> Signup and view all the answers

<p>It converts to lactic acid inhibiting uric acid excretion (B)</p> Signup and view all the answers

<p>It is characterized by self-mutilation and neurological disorders (A)</p> Signup and view all the answers

<p>Increase unsaturated fats and protein (B)</p> Signup and view all the answers

Impaired glycogenolysis and gluconeogenesis, leading to problems breaking down and creating glucose.

Characterized by enlarged liver (hepatomegaly), low blood sugar (hypoglycemia), high blood fat (hyperlipidemia), and even high lactic acid (lactic acidosis).

High levels of uric acid in the blood (hyperuricemia), causing crystals to form in joints and tissues.

Includes acute and chronic joint pain (arthritis), kidney stones (nephrolithiasis), and possible kidney damage.

Rest, ice, avoiding alcohol, adjusting diet to minimize purines (meat, seafood), and lower carbohydrates.

Enzyme necessary to convert glucose-6-phosphate to glucose, enabling the release of glucose into the bloodstream.

Uric acid production is increased by conditions like leukemia, cancer, and psoriasis; decreased excretion is tied to chronic kidney disease, lactic acidosis, and certain drugs.

Urate crystals trigger an inflammatory response, involving neutrophils and resulting in joint and tissue damage.

A metabolic disease characterized by high levels of uric acid in the blood (hyperuricemia).

Elevated uric acid levels in the blood.

A genetic defect in the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRT), leading to hyperuricemia.

A severe genetic disorder caused by a complete HGPRT deficiency, characterized by hyperuricemia and neurological problems.

An enzyme involved in the production of purines; increased activity leads to increased uric acid.

The creation of uric acid from purine metabolism, increased production contributes to higher serum uric acid.

The process of removing uric acid from the body; problems in this process can result in high levels of uric acid in the blood.

Ranges from 2-9 mg/dL, depending on gender (3-9 mg/dL in males, 2-7 mg/dL in females).

Drugs used to decrease the amount of uric acid in the blood, often targeting 6mg/dL or less.

A xanthine oxidase inhibitor that stops the body from making uric acid

Drugs that prevent the enzyme xanthine oxidase from converting xanthine to uric acid, thus lowering uric acid levels.

Drugs that increase the removal of uric acid from the body by preventing its reabsorption in the kidneys.

The amount of uric acid found in the blood plasma.

(In the leukemia case) Rapid cell death during cancer treatment can lead to a burst of uric acid.

(In the leukemia case) Damaged, dying cells can release excessive amounts from proteins during treatment, causing a build-up in urea.

Anticancer treatments might harm cells and cause them to release waste materials into the blood, leading to high levels of urea and uric acid after the treatment.