Glucose metabolism disorders / Questions and case reports

Questions

 * 1) During fasting, which enzyme is responsible for the production of free glucose in the liver
 * 2) * A – Glucagon
 * 3) * B – Glucose-6-phosphate dehydrogenase
 * 4) * C – Glucokinase
 * 5) * D – Hexokinase
 * 6) * E – Glucose-6-fosfatase
 * 7) Which of the following metabolites cannot provide carbon atoms for gluconeogenesis?
 * 8) * A – Alanine
 * 9) * B – Pyruvate
 * 10) * C – Lactate
 * 11) * D – Palmitate
 * 12) * E – Oxalacetate
 * 13) Insulin accelerates
 * 14) * A – hepatic glucose production
 * 15) * B – glucose uptake in muscles
 * 16) * C – excretion of fatty acids from adipose tissue
 * 17) * D – conversion of glycogen to glucose in the liver
 * 18) * E – conversion of amino acids to glucose in muscles
 * 19) Which of the following enzymes plays a role in the Cori cycle?
 * 20) * A – Lactate dehydrogenase
 * 21) * B – Glucose-6-phosphate dehydrogenase
 * 22) * C – Pyruvate dehydrogenase
 * 23) * D – Glucokinase
 * 24) * E – Hydroxymethylglutaryl–CoA reduktase
 * 25) Insulin is secreted after a meal (mixed diet). This increase in insulin causes a normal person to: (fill incorrectly if something is rising, falling or not changing)
 * 26) * A – release of glucose from the liver ...
 * 27) * B – glucose uptake by muscle and adipose tissue ...
 * 28) * C – gluconeogenesis in the liver ...
 * 29) * D – synthesis of fatty acids ...
 * 30) * E – secretion of glucagon ...
 * 31) Glucagon controls the function of target cells by first binding to a specific membrane receptor, thereby increasing within the cell:
 * 32) * A – neurotransmitter
 * 33) * B – a specific peptide that activates certain enzymes
 * 34) * C – cAMP (cyclic adenosine monophosphate)
 * 35) * D – nucleic acids
 * 36) * E – synthesis of enzymes
 * 37) What are the metabolic causes of hyperglycemia in diabetes mellitus?
 * 38) * A – Reduction of glucose utilization in tissues
 * 39) * B – Gluconeogenesis in muscles
 * 40) * C – Gluconeogenesis in the liver
 * 41) * D – Glucose transfer across the hepatocyte membrane due to insulin deficiency
 * 42) * E – Increase of renal threshold for glucose
 * 43) * F – Increased glucagon effect over insulin
 * 44) * G – Inhibition of lipolýysis (breakdown of fatty acids)
 * 45) What are the metabolic causes of diabetic ketoacidosis? (more options)
 * 46) * A – Reduced breakdown of ketone bodies in the liver
 * 47) * B – Combination of insulin deficiency with glucagon excess
 * 48) * C – Conversion of acetoacetate to acetone
 * 49) * D – Fatty acid catabolism (lipolysis)
 * 50) * E – Increased acetyl CoA production in the liver
 * 51) * F – Increased hydroxymethylglutaryl-CoA production in mitochondria
 * 52) What are the main causes of hyperosmolar coma in diabetes mellitus?
 * 53) * A – Osmotic diuresis for hyperglycemia with insufficient water supply
 * 54) * B – Complete lack of insulin combined with excess glucagon
 * 55) * C – Insulin deficiency reduces glucose utilization in the brain, causing disruption in the brain centres controlling water and electrolyte metabolism
 * 56) * D – Glycation of collagen in the basement membrane of glomeruli, which leads to increased permeability

Overweight patient with abdominal pain
A 49-year-old woman with a long history of thickness without attempting to diet and reduce weight. She has pelvic pain. Gynaecologist finding: chronic pelvic inflammation. At the last visit, increased blood pressure, and fasting blood glucose 15.8 mmol / l.

Questions:
 * 1) What type of diabetes is the patient likely to suffer from?
 * 2) What causes elevated glucagon?
 * 3) What causes increased urinary urea excretion in diabetes mellitus?

Woman, 21 years old with type 1 diabetes
Admitted to the hospitalizations in an obsessive state with tachypnea. Feel the fruity smell on your breath. A history of acute respiratory infections. Laboratory finding:
 * blood: glucose 22 mmol/l, bicarbonate 9,5 mmol/l
 * serum: urea 11,8 mmol/l, Na+ 136 mmol/l, K+ 5,7 mmol/l

Questions:
 * 1) What is the diagnosis?
 * 2) How would you explain the low level of bicarbonate (pathobiochemical background)?
 * 3) Why are urea and K+ levels increased?

Nurse, 24 years old
She used to have recurrent hypoglycemia. Laboratory examination showed the following results: β-glucose repeated 0.9 - 1.1 mmol / l, C-peptide: 0.01 pmol / l to undetectable (repeated)

Question:
 * 1) What is the most likely cause of hypoglycemia?

Patient on parenteral nutrition
Man, 32 years old, in advanced Crohn's disease (ileitis terminalis), in a state of severe malnutrition was on parenteral nutrition. Laboratory examination:
 * B-glucose (not fasting): 9,8 mmol/l
 * S-phosphate: 0,3 mmol/l
 * S-albumin: 27 g/l
 * S-Ca: 1,96 mmol/l

Question:
 * 1) What is the explanation of laboratory values?

Links
Other chapters from the book MASOPUST, J., PRŮŠA, R .: Pathobiochemistry of metabolic pathways

Source

 * MASOPUST, Jaroslav and Richard PRŮŠA. Pathobiochemistry of metabolic pathways. 1st edition. Prague: Charles University, 1999. 182 pp. 24–33.  ISBN 80-238-4589-6.