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Sucrose--> fructose=more G6P(gluconeogenesis)
Lactose= galactose=glucose 6 phosphate( through action of galactose 1 p uridyltransferase and phosphoglucose mutase)

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Yes. The problem lies in the degradation of glycogen.

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Yes. The problem lies in the degradation of glycogen.

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No. Liver cells are dead, and would not be able to respond to glucagon.

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- Depends on the combination of alleles for the G6PD gene in both mother and father
- If male student has, it means that the mother at least has 1 copy of the recessive G6PD deficient allele
- It is unknown if the father has recessive allele on his X-chromosome
- If father has recessive allele, daughter will definitely be a carrier (at least)
- If mother is homozygous recessive, daughter will definitely be a carrier as well (at least)
- Daughter will only have the same problem if father has G6PD deficient allele and mother is homozygous recessive

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Aspirin broken down in the liver and the products formed are hepatotoxic and thus the products kill the hepatocytes in the liver. The liver cells are therefore dysfunctional and  are unable to break down glycogen to glucose, neither can they undergo gluconeogenesis. Hence blood sugar levels are low.

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Gluconeogenesis and Glycogen metabolism

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- In RBCs, G6PD/ NADPH is the only source of reduced glutathione
- Compromises the function of RBCs severely (need to be flexible to effectively transport oxygen throughout body)
- In other organs, NADPH can be produced from other pathways (?)

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- Student is G6PD deficient (10-60% of normal activity)
- Antimalarial drugs increase the levels of ROS
- Leads to increased levels of GSSG as GSH levels are depleted to reduce the levels of ROS
- Problem of G6PD deficiency is amplified as there is insufficient G6PD to reduced the increased levels of GSSG
- Consequentially, ROS are not eliminated; oxidise proteins that maintain RBC membrane plasticity, leading to haemolysis

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PC deficiency results in the inability of pyruvate to be converted to oxaloacetate. Accumulation of pyruvate is shunted to alternative metabolic pathways which results in increased production of lactate. (Conversion to lactate allows for regeneration of NAD+ and generation of ATP.) Due to the absence of oxaloacetate, acetyl CoA cannot produce citrate and is shunted to produce ketone bodies. 

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PC deficiency results in the inability of pyruvate to be converted to oxaloacetate. Accumulation of pyruvate is shunted to alternative metabolic pathways which results in increased production of lactate. (Conversion to lactate allows for regeneration of NAD+ and generation of ATP.) Due to the absence of oxaloacetate, acetyl CoA cannot produce citrate and is shunted to produce ketone bodies. 

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- HMP Shunt
- Oxidation of glucose-6-phosphate to 6-phosphoglucono-delta-lactone
- Production of NADH

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-Von Gierke
-Glucose-6-Phosphatase deficiency leads to accumulation as it is not converted into glucose
- This explains the hypoglycaemia as product of glycogen degradation does not fully convert to glucose to be used extracellularly
-G6P accumulation inhibits gluconeogenesis leading to accumulation of pyruvate and therefore lactate through anaerobic respiration. This explains the high level of pyruvate and lactate.
-HMP shunt produces uric acid through nucleotide metab.
-accumulation of G6P in liver cells results in accumulation of glycogen therefore organomegaly