BIOS 256 Week 3 Case Study Metabolism

Grace J.
August 6, 2025August 6, 2025
BIOS-256, CU BSN

Student Name

Chamberlain University

BIOS-256: Anatomy & Physiology IV with Lab

Prof. Name

Date

History

BT is a 36-year-old female presenting with complaints of dysuria (painful urination) for the past two days, accompanied by increased urinary frequency. She denies experiencing fever or any other systemic symptoms. BT reports a decrease in her usual water intake.

Physical Examination

On physical examination, the abdomen is soft, non-tender, and without any palpable masses, indicating no signs of acute abdominal pathology.

Laboratory Findings

A urinalysis using a dipstick test reveals the presence of leukocytes and nitrites, which are indicative of a urinary tract infection (UTI). Additionally, ketones are detected in the urine (ketonuria), an unexpected finding that requires further investigation to determine the underlying cause of ketone production.

Assessment

The patient is diagnosed with a urinary tract infection alongside ketonuria. The presence of ketones in the urine suggests that the body is utilizing fat as an energy source due to insufficient glucose availability. Ketones are typically excreted via the lungs and kidneys. Additional patient history and testing are necessary to explore the potential metabolic reasons behind the ketonuria.

1. Identify 2 potential causes of ketonuria.

Question: Identify 2 potential causes of ketonuria.
Answer:
Ketonuria can result from various metabolic conditions. Two potential causes include:

Cause	Description
Diabetes Mellitus	In uncontrolled diabetes, especially type 1, the lack of insulin prevents glucose from entering cells. This prompts the body to break down fats for energy, producing ketones as a by-product (Kitabchi et al., 2009).
Glycogen Storage Disease	This group of inherited disorders affects glycogen metabolism. In some types, the body is unable to access stored glucose, leading to fat metabolism and subsequent ketone production (Chen, 2001).

2. Identify the nutrient involved in the formation of ketones.

Question: Identify the nutrient involved in the formation of ketones.
Answer:
The nutrient primarily involved in ketone formation is fat. When the body lacks sufficient glucose, it begins breaking down fat stores for energy. The fatty acids released are then converted into ketones by the liver (Volek & Phinney, 2011). Thus, ketone production increases when carbohydrate intake is low or glucose availability is impaired.

3. Describe the process of lipolysis and formation of ketones.

Question: Describe the process of lipolysis and formation of ketones.
Answer:
Lipolysis is the catabolic process through which triglycerides, stored in fat cells, are broken down into glycerol and free fatty acids. The glycerol can be used for gluconeogenesis, while the free fatty acids are transported to the liver. In the liver, these fatty acids undergo beta-oxidation, forming acetyl-CoA. When acetyl-CoA accumulates beyond what the Krebs cycle can process, it is converted into ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone). This typically occurs during prolonged fasting, carbohydrate restriction, or insulin deficiency (Grabacka et al., 2016).

4. Is the process in Q3 anabolic or catabolic?

Question: Is the process in Q3 anabolic or catabolic?
Answer:
The process described in Question 3 is catabolic. Catabolism refers to the breakdown of complex molecules into simpler ones to release energy. Lipolysis and the subsequent formation of ketones involve the degradation of triglycerides and fatty acids for energy production, fitting the definition of a catabolic pathway (Berg et al., 2002).

5. Predict the effect of excess ketones on the blood pH?

Question: Predict the effect of excess ketones on the blood pH.
Answer:
Excessive accumulation of ketones in the blood can lead to a condition known as metabolic acidosis, specifically ketoacidosis. Ketone bodies are acidic in nature, and their overproduction reduces blood pH, making it more acidic. This is especially dangerous in diabetic ketoacidosis (DKA), where insufficient insulin causes unchecked ketone production, potentially leading to life-threatening acid-base imbalance (Kitabchi et al., 2009).

References

Berg, J. M., Tymoczko, J. L., & Stryer, L. (2002). Biochemistry (5th ed.). W.H. Freeman.

Chen, Y. T. (2001). Glycogen storage diseases. In The Metabolic and Molecular Bases of Inherited Disease (pp. 1521–1551). McGraw-Hill.

Grabacka, M., Pierzchalska, M., Dean, M., & Reiss, K. (2016). Regulation of ketone body metabolism and the role of PPARα. International Journal of Molecular Sciences, 17(12), 2093. https://doi.org/10.3390/ijms17122093