Diabetes Flashcards
(21 cards)
What are the symptoms of TIIDM?
Polydypsia.
Polyuria.
Polyphagia.
Weight loss.
How would you diagnose TIIDM?
OGTT = > 11.1mmol/L.
Fasting glucose = > 7mmol/L.
HbA1c = > 48mmol/L or > 6.5%.
What factors may affect HbA1c?
Haemolysis. Iron deficiency anaemia. Renal impairment (i.e. reduced EPO). Pregnancy (increased RBC turnover). Blood transfusion.
Where is insulin produced?
Beta cells of the pancreas.
What are the main functions of insulin?
Stimulates uptake of glucose by peripheral tissue > reduced blood glucose.
Inhibits liver breakdown of glycogen & increases glycogenesis.
Increases protein synthesis.
Increases TG storage in adipose tissue.
Explain the mechanism of insulin secretion?
Glucose binds to the GLUT-2 receptor on beta cells.
Glucose forms ATP via glycolysis.
Increased ATP > closure ATP-sensitive K+ channels > depolarisation.
Depolarisation > opening of voltage-gated Ca2+ channels.
Ca2+ influx > insulin release.
Why is it difficult to measure blood insulin levels? What can be measured instead?
Insulin undergoes extensive first pass metabolism.
Measure C-peptide.
Where is glucagon produced?
Alpha cells of the pancreas.
What are the main functions of glucagon?
Releases glucose into blood.
Stimulates gluconeogenesis & glycogenolysis.
Where an incretins produced?
Intestinal L-cells of the ileum.
What are the main functions of incretins?
Bind to GLP-1 receptor on beta cells > insulin release.
Decrease glucagon release from alpha cells.
Explain how insulin causes glucose uptake in peripheral tissue?
Insulin binds to the insulin receptor > phosphorylation of PI-3K > expression of GLUT-4 transporter proteins on the cell surface > glucose uptake.
Explain how insulin resistance occurs in TIIDM?
Insulin binds to the insulin receptor > impaired PI-3K phosphorylation > GLUT-4 is not transported to the cell surface > no glucose uptake.
Explain how insulin resistance progresses?
Insulin resistance > reduced glucose uptake > hyperinsulinaemia > further resistance > hyperglycaemia > glucotoxicity > impaired B-cell function > impaired insulin secretion.
What happens to glucagon secretion in TIIDM?
Glucagon secretion is increased > hyperglycaemia.
Explain the role of the kidneys in TIIDM?
Increased filtration of blood glucose ( > 10mmol/L) > increased expression of SGLT-2 receptors > increased glucose reabsorption > hyperglycaemia.
Explain the role of adipose cells in TIIDM?
Adipose cells are resistant to insulins anti-lipolytic effects > lipolysis > increased plasma FFAs.
Chronically elevated plasma FFAs results in:
> Increased gluconeogensis.
> Hepatic/peripheral insulin resistance.
> Impaired insulin secretion.
Explain the role of adipose cells in TIIDM?
Adipose cells are resistant to the effects of insulin > lipolysis > increased plasma FFAs.
Chronically elevated plasma FFAs results in:
> Increased gluconeogensis.
> Hepatic/peripheral insulin resistance.
> Impaired insulin secretion.
What are the effects of hypoinsulinaemia?
Proteolysis in skeletal muscle > muscle wasting & weight loss.
TG breakdown in adipose tissue > increased FFAs & ketones.
Glycogenolysis in the liver > hyperglycaemia.
What are the effects of hypoinsulinaemia?
Proteolysis in skeletal muscle > muscle wasting & weight loss.
TG breakdown in adipose tissue > increased FFAs & ketones.
Glycogenolysis in the liver > hyperglycaemia.
What factors help differentiate between TIDM & TIIDM?
Ketoacidosis:
> Only usually occurs in TIDM due to no insulin production.
FH of diabetes:
> Suggests TIDM.
Obesity:
> Mainly associated with TIIDM.
