Disorders of glucose metabolism/Questions and case studies
Questions[edit | edit source]
- During fasting, which enzyme is responsible for the production of free glucose in the liver
- A – Glucagon
- B – Glucose-6-phosphate dehydrogenase
- C – Glucokinase
- D – Hexokinase
- E – Glucose-6-phosphatase
- Which of the following metabolites cannot provide carbon atoms for gluconeogenesis?
- A – Alanine
- B – Pyruvate
- C – Lactate
- D – Palmitate
- E – Oxaloacetate
- Insulin accelerates
- A – glucose production by the liver
- B – uptake of glucose in the muscles
- C – excretion of fatty acids from adipose tissue
- D – conversion of glycogen into glucose in the liver
- E – conversion of amino acids to glucose in muscles
- Which of the following enzymes has a role in the Cori cycle?
- A – Lactate dehydrogenase
- B – Glucose-6-phosphate dehydrogenase
- C – Pyruvate dehydrogenase
- D – Glucokinase
- E – Hydroxymethylglutaryl–CoA reductase
- After taking food (mixed food), insulin is secreted. This rise in insulin causes a normal person to: (fill in correctly if something rises, falls or does not change)
- A – release of glucose from the liver...
- B – uptake of glucose by muscle and fat tissue...
- C – gluconeogenesis in the liver...
- D – synthesis of fatty acids...
- E – glucagon secretion...
- Glucagon controls the function of target cells by first binding to a specific membrane receptor and thus increases inside the cell:
- What are the metabolic causes of hyperglycemia in diabetes mellitus?
- A – Reduction of glucose utilization in tissues
- B – Gluconeogenesis in muscles
- C – Gluconeogenesis in the liver
- D – Glucose transfer across the hepatocyte membrane conditioned by insulin deficiency
- E – Increased renal threshold for glucose
- F – Increasing the effect of glucagon over the effect of insulin
- G – Inhibition lipolysis (breakdown of fatty acids)
- What are the metabolic causes diabetic ketoacidosis? (more options)
- A – Reduced degradation ketone body in the liver
- B – Combination of insulin deficiency with glucagon excess
- C – Conversion of acetoacetate to acetone
- D – Catabolism of fatty acids (lipolysis)
- E – Increased production of acetyl CoA in the liver
- F – Increased formation of hydroxymethylglutaryl-CoA in mitochondria
- What are the main causes of hyperosmolar coma in diabetes mellitus?
- A – Osmotic diuresis for hyperglycemia with insufficient water intake
- B – Complete lack of insulin combined with an excess of glucagon
- C – A lack of insulin will reduce the utilization of glucose in the brain, causing a malfunction in the brain's centers controlling water and electrolyte metabolism
- D – Glycation of collagen in the glomerular basement membrane, which leads to increased permeability
thumb|right|300px|Coriho cyklus Question 4.
Case reports[edit | edit source]
Female patient with overweight and abdominal pain[edit | edit source]
49-year-old woman, long history of obesity without dieting and weight reduction. She has pelvic pain. Gynecologist. find: chron. pelvic inflammation. At the last visit, elevated blood pressure, fasting blood glucose 15.8 mmol/l.
- What type of diabetes does the patient probably suffer from?
- What does elevated glucagon do?
- What is the cause of increased excretion of urea in the urine in diabetes mellitus?
Female, 21 years old with type 1 diabetes[edit | edit source]
Admitted to hospital in a delirious state with tachypnea. A fruity smell on the breath. History of acute respiratory infection. Laboratory findings:
- 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
- What diagnosis is involved
- How can a low bicarbonate level be explained (pathobiochemical basis)
- Why is the level of urea and K+ elevated.
Nurse, 24 years old[edit | edit source]
She had repeated episodes of hypoglycemia. Laboratory examination showed the following results: B-glucose repeatedly 0.9 - 1.1 mmol/l, C-peptide: 0.01 pmol/l to undetectable (repeatedly)
- What is the most likely cause of hypoglycemia?
Patient on parenteral nutrition[edit | edit source]
A 32-year-old man with an advanced stage of Crohn's disease (ileitis terminalis) and 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
- What is the explanation of the laboratory values
Links[edit | edit source]
Related Articles[edit | edit source]
Source[edit | edit source]
- MASOPUST, Jaroslav – PRŮŠA, Richard. Patobiochemie metabolických drah. 1. edition. Praha : Univerzita Karlova, 1999. 182 pp. pp. 24−33. ISBN 80-238-4589-6.