3c. Pancreas (Diabetes Mellitus) Flashcards
what is/occurs in type 1 diabetes mellitus
INSULIN DEPENDENT
autoimmune destruction of the pancreatic beta-cells
destroys the ability to produce insulin and seriously compromises the patients ability to absorb glucose from the plasma
diabetes is similar to starvation in the lack of nutrients - what happens in the body when nutrients are scare
body relies on stores for energy - adipose tissue broken down and fatty acids are released
How are FFAs used by the body in type 1
used by most tissues to produce energy - liver converts excess into ketone bodies which provide additional energy source for muscles and the BRAIN
what is ketoacidosis
the build up of acidic ketone bodies in the plasma - create life threatening acidosis with plasma pH <7.1
dead can occur in hours if untreated
how does ketoacidosis come about in type 1
poorly controlled insulin-dependent type 1 diabetes causes a lack of insulin - this depresses ketone body uptake so they build up in the plasma
how can ketoacidosis be detected
detectable in urine and produce distinctive acetone smell on the breath
what is/occurs in type 2 diabetes mellitus
NON-INSULIN DEPENEDENT
peripheral tissues become insensitive to insulin = INSULIN RESISTANCE
muscle and fat no longer respond to normal levels of insulin
what are the two causes of insulin resistance in type 2
- abnormal response of insulin receptors in tissues
2. reduction in number of insulin receptors in tissues
are beta cells affected in type 2
beta cells are NOT affected - remain intact and appear normal - there may even be hyperinsulinaemia
what percentage of patients have type 1 and 2 diabetes mellitus
10% type 1
90% type 2
what is the first line treatment for type 2
trying to restore insulin sensitivity of tissues with exercise and dietary chang
what is the second line treatment for type 2
oral hypoglycaemic drugs -
- Metformin is the first line treatment
- then Sulphonylureas
how does metformin work
inhibits hepatic gluconeogenesis and antagonises action of glucagon
how do sulphonylureas
act to close the KATP in cells and therefore stimulate Ca2+ entry and insulin secretion.
(obviously requires functioning beta cells so can’t be used in type 1)
why do many type 2 patients end up taking insulin
to prevent hyperglycaemia