Purine Metabolism Overview

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Questions and Answers

What is the primary mechanism by which hyperuricemia leads to gouty arthritis?

Inflammation from bacterial infection

Deposition of monosodium urate crystals (correct)

Formation of calcium phosphate crystals

Destruction of joint cartilage

Which diagnostic method is essential for confirming gout?

Ultrasound examination of soft tissues

X-ray imaging of affected joints

Blood uric acid level measurement

Synovial fluid aspiration and polarized light microscopy (correct)

What is the main treatment goal for managing gout over the long term?

Promoting the formation of kidney stones

Increasing dietary purine intake

Lowering uric acid levels below saturation point (correct)

Reducing inflammation in the joints

What characterizes patients with Xanthine Oxidase Deficiency (Xanthinuria)?

Hypouricemia with excretion of xanthine in urine Signup and view all the answers

What is a life-saving treatment for patients with Adenosine deaminase (ADA) deficiency?

Antibiotics and periodic immunoglobulin injections Signup and view all the answers

Which enzyme is specifically inhibited by hydroxyurea in purine metabolism?

Ribonucleotide reductase Signup and view all the answers

What is the primary role of sulfonamides in medical treatment?

To inhibit growth of rapidly dividing microorganisms Signup and view all the answers

Which condition is characterized by a deficiency in hypoxanthine-guanine phospho-ribosyl transferase (HGPRT)?

Lesch-Nyhan syndrome Signup and view all the answers

What is the primary substrate utilized by both adenine phospho-ribosyl transferase and hypoxanthine-guanine phospho-ribosyl transferase?

PRPP Signup and view all the answers

What is a major pathway for purine salvage in cells?

Recycling of purine bases to nucleotides using specific enzymes Signup and view all the answers

Which of the following statements is true regarding methotrexate?

It inhibits dihydrofolate reductase to control cancer spread. Signup and view all the answers

In purine metabolism, what is a characteristic of the salvage pathway?

It conserves energy by recycling nucleotides. Signup and view all the answers

What is the primary consequence of Lesch-Nyhan syndrome related to uric acid?

Excessive uric acid production leading to kidney stones Signup and view all the answers

Which enzyme family is responsible for hydrolyzing nucleic acids in the small intestine?

Nucleases Signup and view all the answers

How does uric acid contribute to tissue healing?

By mobilizing progenitor endothelial cells Signup and view all the answers

What can excessive alcohol consumption lead to regarding uric acid levels?

Development of hyperuricemia Signup and view all the answers

What is the process by which dietary purine bases are primarily converted in intestinal mucosal cells?

Conversion into free bases Signup and view all the answers

Which neurological and behavioral symptom is associated with Lesch-Nyhan syndrome?

Self-mutilation behaviors Signup and view all the answers

What role does uric acid play in the body besides being a waste product?

A strong antioxidant Signup and view all the answers

Which genetic condition is NOT associated with purine degradation?

Galactose uridyltransferase deficiency Signup and view all the answers

What is the main end product of purine nucleotide degradation in humans?

Uric acid Signup and view all the answers

Which condition is characterized by high uric acid levels in blood due to the underexcretion of uric acid?

Gout Signup and view all the answers

Study Notes

Purine Metabolism

De novo synthesis is the synthesis of purine nucleotides from simpler precursors.
Salvage pathway is the recycling of purine bases from the breakdown of nucleic acids.
Ribonucleotide reductase converts ribonucleoside diphosphates to deoxyribonucleotides, which are essential for DNA synthesis.
Hydroxyurea inhibits ribonucleotide reductase.
Thymidylate synthase is involved in pyrimidine synthesis and is inhibited by 5-fluorouracil.
Dihydrofolate reductase is involved in folate metabolism and is inhibited by methotrexate (eukaryotes), trimethoprim (prokaryotes), and pyrimethamine (protozoa).
Sulfonamides are structural analogs of para-aminobenzoic acid (PABA).
Sulfonamides inhibit bacterial synthesis of folic acid by inhibiting dihydropteroate synthase.
Methotrexate is a structural analog of folic acid used to inhibit nucleotide synthesis in cancer cells.
Methotrexate inhibits dihydrofolate reductase.
Adenine phosphoribosyltransferase (APRT) and hypoxanthine-guanine phosphoribosyltransferase (HGPRT) are enzymes involved in the salvage pathway.
APRT and HGPRT use phosphoribosyl pyrophosphate (PRPP) as a source of ribose 5-phosphate.
Lesch-Nyhan syndrome is an X-linked recessive disorder caused by a deficiency in HGPRT.
Lesch-Nyhan syndrome leads to hyperuricemia, gout, urolithiasis, and neurological abnormalities including self-mutilation.
Hyperuricemia is an elevated level of uric acid in the blood.
Hyperuricemia can be caused by excessive cell death, alcohol consumption, dietary nucleic acid intake, and underexcretion by the kidneys.
Gout is a painful inflammatory condition caused by the deposition of monosodium urate crystals in joints.
Gout is characterized by hyperuricemia.
Tophi are nodular masses of monosodium urate crystals that can deposit in soft tissues.
Gout is diagnosed by examining synovial fluid for needle-shaped monosodium urate crystals using polarized light microscopy.
Gout is treated by lowering uric acid levels below its saturation point.
Urate oxidase is a potential treatment for gout.
Hypouricemia is a low level of uric acid in the blood.
Xanthinuria is a genetic defect caused by a deficiency in xanthine oxidase.
Xanthinuria leads to hypouricemia and liver damage.
Adenosine deaminase (ADA) deficiency is an autosomal recessive disorder that leads to a buildup of adenosine and deoxyadenosine.
ADA deficiency causes severe combined immunodeficiency (SCID).
SCID involves a decrease in T cells, B cells, and natural killer (NK) cells.
Treatment for ADA deficiency includes antibiotics, immunoglobulin injections, enzyme replacement therapy (ERT), and bone marrow transplantation (BMT).

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Description

This quiz covers the intricacies of purine metabolism, including de novo synthesis, salvage pathways, and the role of key enzymes like ribonucleotide reductase. Additionally, it explores the impact of inhibitors such as methotrexate and sulfonamides on nucleotide synthesis. Test your knowledge on these essential biochemical processes!