TQ2. Why is there glucose in MW’s urine (glucosuria)? How is the glucosuria related to her dehydrated state? TQ3. Why is the majority of the acetyl CoA from FA β-oxidation being used for ketogenesis rather than being oxidized in the tricarboxylic acid cycle? TQ4. Was MW in positive or negative nitrogen balance when she was brought to the hospital?
TQ5. What response to the DKA is apparent in MW? What response is likely occurring in the kidney? Hint: In addition to conversion to urea, how is toxic ammonia removed from the body?
TQ6. What would be true about the levels of ketone bodies and glucose during periods of physiologic stress in individuals with impaired FA oxidation?
Case 4: Hypoglycemia, Hyperketonemia, and Liver Dysfunction
Patient Presentation: AK, a 59-year-old male with slurred speech, ataxia (loss of skeletal muscle coordination), and abdominal pain, was dropped off at the Emergency Department (ED).
Focused History: AK is known to the ED staff from previous visits. He has a 6year history of chronic, excessive alcohol consumption. He is not known to take illicit drugs. At this ED visit, AK reports that he has been drinking heavily in the past day or so. He cannot recall having eaten anything in that time. There is evidence of recent vomiting, but no blood is apparent.
Physical Examination (Pertinent Findings): The physical examination was remarkable for AK’s emaciated appearance. (His body mass index was later determined to be 17.5, which put him in the underweight category.) His facial cheeks were erythematous (red in color) due to dilated blood vessels in the skin (telangiectasia). Eye movement was normal. Neither icterus (jaundice) nor edema (swelling due to fluid retention) was seen. The liver was slightly enlarged. Bedside tests revealed hypoglycemia and hyperketonemia (as acetoacetate). Blood was drawn and sent to the clinical laboratory.
Pertinent Test Results:
DUI = driving under the influence; H = High; L = Low.
Additional Tests: Complete blood count (CBC) and blood smear revealed a macrocytic anemia (see right image). Folate and B12 levels were ordered.
Diagnosis: AK is diagnosed with alcoholism.
Treatment (Immediate): Thiamine and glucose were given intravenously.
Prognosis: Alcoholism (alcohol dependence) is the third most common cause of preventable death in the United States. People with alcoholism are at increased risk for liver cirrhosis, pancreatitis, gastrointestinal bleeding, and some cancers.
Nutrition Nugget: Those with alcoholism are at risk for vitamin deficiencies as a result of decreased intake and absorption. Thiamine (vitamin B1) deficiency is common and can have serious consequences such as Wernicke-Korsakoff syndrome with its neurologic effects.
Thiamine pyrophosphate (TPP), the coenzyme form, is required for the dehydrogenase-mediated oxidation of α-keto acids (such as pyruvate) as well as the transfer of two-carbon ketol groups by transketolase in the reversible sugar interconversions in the pentose phosphate pathway.