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Questions and Answers
What is the sole source of energy production in mature red blood cells (RBCs)?
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Which glucose transporter facilitates glucose uptake in RBCs?
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What is the primary function of 2,3-bisphosphoglycerate (2,3-BPG) in RBCs?
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What is the consequence of a genetic defect in pyruvate kinase in RBCs?
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Which pathway is the only source of NADPH in RBCs?
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What is the function of reduced glutathione (GSH) in RBCs?
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Which enzyme deficiency leads to reduced NADPH production and increased susceptibility to oxidative stress in RBCs?
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What triggers hemolysis in individuals with G6PD deficiency?
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Why are younger red blood cells less affected in G6PD deficiency?
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What is the role of NADPH in protecting RBCs from oxidative damage?
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Why do red blood cells rely solely on anaerobic glycolysis for energy production?
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What is the metabolic fate of lactate produced in RBCs?
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How does 2,3-BPG affect the oxygen-hemoglobin dissociation curve, and what is the physiological significance of this effect?
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Explain the relationship between blood storage and 2,3-BPG levels, and its implications for transfusion.
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What is the primary role of the pentose phosphate pathway in red blood cell metabolism?
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Explain the mechanism by which G6PD deficiency leads to hemolytic anemia.
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Why are individuals with G6PD deficiency usually asymptomatic until exposed to certain triggers?
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Which of the following can trigger hemolysis in individuals with G6PD deficiency?
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How does oxidative stress affect red blood cell membrane integrity?
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A patient presents with dark urine, jaundice, and weakness after taking primaquine for malaria. Laboratory findings reveal decreased hemoglobin, decreased RBC count, increased reticulocytes, and decreased G6PD levels. What is the most likely diagnosis?
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Study Notes
Red Blood Cell Energy Metabolism
- Mature red blood cells (RBCs) primarily generate energy through anaerobic glycolysis due to the absence of mitochondria.
- The glucose transporter GLUT-1 is responsible for glucose uptake in RBCs.
2,3-Bisphosphoglycerate (2,3-BPG) Function
- 2,3-BPG decreases hemoglobin's affinity for oxygen, facilitating effective oxygen unloading in tissues.
Genetic Disorders and Enzyme Deficiencies
- A genetic defect in pyruvate kinase results in hemolytic anemia, characterized by the breakdown of RBCs.
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency reduces NADPH production, increasing RBC susceptibility to oxidative damage and hemolysis.
Pathways for NADPH Production
- The pentose phosphate pathway is the sole source of NADPH in RBCs, crucial for maintaining antioxidant defenses.
- Reduced glutathione (GSH) protects RBCs against oxidative damage.
Responses to Oxidative Stress
- Hemolysis in G6PD deficiency can be triggered by oxidative agents, stress, or dietary factors such as fava beans.
- Younger RBCs are less affected by G6PD deficiency due to higher G6PD enzyme levels.
Impact of 2,3-BPG on Blood Storage
- Blood storage decreases levels of 2,3-BPG, which may impair oxygen delivery upon transfusion.
Role of Pentose Phosphate Pathway
- The primary function of the pentose phosphate pathway in RBCs is to produce NADPH for redox reactions.
Mechanism Leading to Hemolytic Anemia
- G6PD deficiency causes a compromise in antioxidant defense due to reduced NADPH, resulting in oxidative damage and hemolytic anemia.
Triggers for Hemolysis
- Common triggers for hemolysis in G6PD deficiency include certain medications (e.g., primaquine), fava beans, and infections.
Oxidative Stress and Membrane Integrity
- Oxidative stress damages the integrity of the RBC membrane via lipid peroxidation, leading to increased fragility and potential hemolysis.
Clinical Presentation of G6PD Deficiency
- Symptoms may manifest as dark urine, jaundice, and weakness following exposure to triggers such as primaquine; laboratory findings typically show decreased hemoglobin, decreased RBC count, increased reticulocytes, and decreased G6PD levels.
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