Question

A 28-year-old woman became severely depressed after the death of her first born child. According to her husband, the child was diagnosed as fetal demise due to no active cardiac activity during an ultrasound examination. Three m she was brought to the local hospital emergency room because of severe weakness and lethargy. The patient was observed to have pallor and body thinness. After being questioned by the emergency room doctor, it was determined that the patient had eaten very little for several weeks. The husban stated the patient who used to love to cook, now would not even enter the onths later, kitchen area at home. The emergency room physician determined that the rest of the patient's examination was within normal limits. Laboratory workup showed that the patient had elevated levels of alanine, acetoacetate, B hydroxyl butyrate, and a blood urea nitrogen (BUN). Her blood glucose level was in 45 mg/dL. The patient was admitted to the hospital and fec intravenously. given antidepressant medication, and had a consultation with a psychiatrist. Due to the feeding, the patient was shifted to an 1800 cal/day diet. Otherwise, her recovery time was uneventful. 1. What condition did the patient have after suffering the loss of her unborn child? 2. How was the patient obtaining energy during the period of time that she was not eating? How could this patient maintain plasma glucose within normal limits even though she was not eating? 3. 4. Why was the BUN level elevated? 5. What does the elevated levels of acetoacetate and B hydroxyl butyrate indicate about the energy metabolism of the patient?

Answer 1

1. She is suffering with depression after the death of her unborn child . But lately the patient is suffering with starvation in which she is not able to eat. Because of the absence of food, the plasma level variations could be noted.  
2. At the time of starvation the energy needed was obtained by three types of fuels such as glucose, fatty acids and ketone bodies. To provide sufficient glucose to brain and other tissues , the proteins will be broken down to use carbon skeleton of glucogenic amino acids and as a result BUN will be high.
Due to decreased insulin and increase in glucagon there will be mobiilization of tryacylglycerides in adipose tissue and gluconeogenesis in liver . But the liver will stop using this newly produced glucose so that it can be preserved for priority cells. And the muscle tissues will be using fatty acids as a substitute of glucose .
After a few days of startvation around 1/3 rd of energy needed by brain will be fulfilled by ketone bodies produced from liver into the blood

3. Even if the patient is starving the blood glucose level will be maintained, by the normal biological mechanism. Fatty acids cannot be converted into glucose but the triacylglycerol can be converted into glucose . Also amino acids by protein degradation can be used for glucose production . So the blood level can be maintained by shifting the fuel, used by other cells, from glucose to fatty acids and ketone bodies.  
4. For the production of essential glucose , the precursors of glucose are needed. The proteolysis of muscle protein give some of the precursor of glucose. While degradation of proteins , glucogenic amino acids will be converted into glucose and the nitrogen part of amino acids will be converted into urea, so that the blood urea nitrogen will be increased  

5. Degradation of fatty acids leads to increased production of acetyl units and the entry of acetyl coA is prevented by the reduced supply of oxaloacetate as a result of gluconeogenesis , which further results in the inability to oxidaze acetyl units. Thus there will be an excessive synthesis of ketone bodies such as acetoacetate and B hydroxybutyrate from the liver to the blood. After few days of starvation there will be an excessive amounts of ketone bodies and it becomes the major fuel of the brain .