15. Type I and II Diabetes Mellitus - Clinical and Management Aspects Flashcards
How many people were estimated to have diabetes in 2013?
382 million.
What is the estimate for people with diabetes in 2035?
592 million.
What are the two causes of hyperglycaemia?
Inability to produce insulting due to B cell failure or insulin production is adequate but insulin resistance prevents it working effectively.
What are some typical symptoms of hyperglycaemia?
Polyuria, polydipsia, blurring of vision and urogenital infections.
How is diabetes diagnosed?
Symptoms and one abnormal test or asymptomatic and two abnormal tests. Tests: fasting blood glucose, HbA1c (type II predominantly), oral glucose tolerance test.
Other than type I and type II, what are some forms of diabetes mellitus?
Genetic defects of beta cell or insulin action, drug induced diabetes, association with other hormone disorders, iron overload or pancreatectomy.
What are the three key areas of action of insulin?
Glucose metabolism - enhances glucose up take in liver, muscle and a adipose tissue, inhibits liver glycogen breakdown.
Fat metabolism - promotes clearance of free fatty acids and prevents lipolysis.
Amino acid metabolism - active transport of amino acids into cells, inhibits catabolism of proteins and gluconeogenesis in the liver.
How can insulin deficiency lead to CV collapse?
It leads to hyperglycaemia and lipolysis. Hyperglycaemia leads to glucosuria, dehydration then renal failure that can lead to shock. Lipolysis leads to increased free fatty acids, then ketones which leads to acidosis.
Shock and acidosis can lead to CV collapse.
How is insulin deficiency induced CV collapse treated?
Insulin and fluids.
How is type I diabetes treated?
Exogenous insulin, subcutaneous injections several times a day.
What percentage of type II diabetics are overweight or obese?
90%.
Why does obesity lead to type II diabetes?
Obesity causes an insulin resistance. At first, this leads to secretion of more insulin but eventually the pancreas can’t keep up with it and there’s pancreatic exhaustion. This means that hyperglycaemia develops.
In what way could type II diabetes be considered as a potentially reversible metabolic disorder?
Within 7 days of fasting, blood glucose can normalise and there is a massive fall in liver fat content and return of normal insulin sensitivity. Over 8 weeks insulin release is normal and there is decreased pancreatic fat which normalises B cell function.
What causes improvements in glucose and insulin resistance after a very low calorie diet or post bariatric surgery?
There is a profound change in intracellular concentration of fat metabolites. Fat is mobilised first from the liver and ectopic sites. Fasting glucose improves because of an 81% decrease in liver fat content and normalisation in haptic insulin sensitivity.
Why is there an absence of ketones in the urine in type II diabetes?
There is still some B cell insulin production but just not enough to control glucose levels.
