Final answer:
In the context of a urea cycle defect, hepatic coma, Reye's syndrome, and excessive exercise, the NPN substance that could be elevated is ammonia. This is because the urea cycle's function is to convert toxic ammonia to urea, and a defect in this cycle leads to ammonia accumulation in the blood.option c is correct answer.
Step-by-step explanation:
Understanding Non-Protein Nitrogenous Substances and the Urea Cycle
When evaluating conditions such as a urea cycle defect, hepatic coma, Reye's syndrome, and situations involving excessive exercise, it is crucial to understand which non-protein nitrogenous (NPN) substance could be elevated.
The urea cycle is responsible for converting toxic ammonia to urea for excretion. When there is a defect in this cycle, especially at the first or second steps, it leads to ammonia intoxication. Consequently, if the cycle is ineffective due to a defect, hepatic conditions, or excessive protein catabolism, as with rigorous exercise, accumulated ammonia cannot be adequately detoxified and thus results in increased levels of ammonia in the blood.
Conditions such as hyper-ammonemia type-I, associated with carbamoyl phosphate synthase-I deficiency, and type-II, associated with ornithine transcarbamoylase deficiency, both lead to the elevation of blood ammonia levels. Therefore, in the context of the given options, the NPN that could be elevated is c) Ammonia. Other NPNs like uric acid are more related to overproduction due to cell death or diseases like Von-Gierke's, whereas creatinine relates to muscle metabolism and renal function. Bilirubin increases signal issues with bilirubin uptake and conjugation in the liver, as seen in Crigler-Najjar and Gilbert's disease.