L19 - Diabetes and Hypoglycaemia Flashcards
(40 cards)
How are blood glucose levels maintained?
- through dietary carbohydrates
- glycogenolysis
- gluconeogenesis
Describe blood glucose homeostasis?
FED STATE:
after a meal is eaten, the plasma glucose rises and so does insulin.
A rise in insulin causes the liver to stop breaking down glycogen into glucose. The uptake of glucose in the liver to be converted increases. Periperral catabolism decreases (break down of lipids and protein)
FASTING STATE:
decrease in plasma glucose leads to decrease of insulin levels. This in turn causes an increase in liver glucuneogenesis and an increase in lipolysis and proteolysis. There is also a decrease in peripheral uptake of glucose in muscle.
What is the function of Glucagon?
mobilises fuel and maintains the blood glucose during fasting state.
It activates gluconeogenesis and glycogenolysis
It activates fatty acid release
What is the function of Epinephrine?
Mobilises fuels in acute stress
stimulates glycogenolysis and fatty acid release
What is the function of cortisol?
amino acid mobilisation and gluconeogenesis
What is the function of growth hormone?
inhibits insulin action and stimulates lipolysis
What is Diabetes Mellitus?
A metabolic disorder characterised by chronic hyperglycaemia, glycosuria and associated abnormalities of lipid and protein metabolism.
What are the classes of diabetes?
type 1 - deficiency in insulin secretion
type 2 - target organs have resistance to insulin
secondary - chronic pancreatitis or surgery.
gestational - occurs for the first time in pregnancy
What is type 1 diabetes?
predominantly in young children and young adults
sudden onset (days or weeks)
most common cause is autoimmune destruction of Beta cells in the pancreas. May be due to interaction between genetic and environmental factors.
Describe the pathogenesis of type 1 diabetes?
destruction of Beta cells starts with autoantigen formation. Autoantigens are presented to T lymphocytes to initiate autoimmune response. Activated T lymohocytes with secrete IL-2 and Interferon, which will then go onto activate auto-antigens that are specific to T-lymphocytes. They then destroy the Islet cells and produce IL-4 which stimulates the proliferation of islet cell auto-antibodies.
There will also be circulating auto-antibodies to various cell antigens against glutamic acid decarboxylase, tyrosine phosphatase-like molecule as well as islet auto-antigen
How does destruction of B-cells in pancreas lead to hyperglycaemia?
It leads to a deficiency in insulin which lowers plasma glucose levels.
It also leads to a decrease in amylin, which is a glucoregulatory peptide that is co secreted with insulin. Amylin lowers blood glucose by slowing gastric emptying and suppressing glucagon output from pancreatic cells.
Describe Glycosuria as a metabolic complication of type 1 diabetes?
as a result of hyperglycaemia, the kidney threshold is exceeded and it cannot reabsorb all the glucose from the blood so a lot of it excreted in the urine. Urine contains too much glucose
Describe Polysuria as a metabolic complication of type 1 diabetes?
polysuria is excessive urination. This occurs as a result of high blood suagr levels and glycosuria. When excess glucose ends up in the urine, it pulls more water, and therefore results in more urine.
Describe volume depletion and polydipsia as a metabolic complication of type 1 diabetes?
When polyuria occurs, more water leaves the body, known as volume depletion.
To compensate, the body’s thirst increases and more water is drunk. This is called polydipsia
How does type 1 diabetes cause ketoacidosis?
insulin deficiency results in increased lipolysis and an increase in free fatty acids in circulation. This leads to increased FFA oxidation in the liver and the production of ketone bodies. This is known as ketoacidosis
Describe the presentation of diabetes type 2?
there is a slow onset in patients (months/years)
patients are usually middle aged or elderly - prevalence increases with age.
strong familiar incidence.
Describe the pathophysiology of type 2 diabetes?
Genetic predisposition and obesity lifestyle factors together lead to insulin resistance. In compensation, beta cell hyperplasia will occur which will make more insulin. However this will eventually lead to Beta cell failure and impaired glucose tolerance
As more and more beta cells fail, this leads to diabetes.
Describe some metabolic complications of type 2 diabetes
low insulin leads an incfrease in both gluconeogenesis and glycogenolysis. These in turn lead to hyperglycaemia and glycosuria.
Osmotic diuresis and loss of water/electrolytes from the body, increases blood viscosity and increases the risk of thrombosis. It also leads to dehydration.
Hyperglycaemia itself also increases plasma osmolarity and this may lead to cerebral dehydration
What is Impaired Glucose Tolerance?
When plasma glucose level is higher than normal (7 mmol/L) and the OGTT (oral glucose tolerance test) has a value of 7.8-11.1 mmol
What is Impaired Fasting Glycaemia?
When fasting plasma glucose is between 6.1. to 6.9 mmol/L and the OGTT (oral glucose tolerance test) has a value less than 7.8 mmol
What is an OGTT and when should it be carried out?
Oral Glucose Tolerance Test.
when 75g of oral glucose is goven and blood samples are taken at 0 and 120 mins after glucose
should be carried out to check body’s ability of metabolising glucose. Done on patients with IFG, unexplained Glycosuria and in clinical features of diabetes with normal plasma glucose
State the stepwise treatment of type 2 diabetes?
1 - diet and excersise
2 - oral monotherapy
3 - oral combination
4 - insulin and oral agents
How does Metformin treat type 2 diabetes?
it decreases gluconeogenesis and also increases the utilisation of glucose at the periphery
How does Sulfonylureas treat type 2 diabetes?
Depolarises the beta cells of the pancreas to increase insulin release
