T2DM Flashcards
describe the pathophysiology of T2DM
Typically progresses from a preliminary phase of impaired glucose tolerance or impaired fasting glucose.
what are the effects of insulin resistance
what happens to risk of T2DM as BMI increases
increases
are females or males at greater risk of diabetes
females
describe the development of T2DM, including B cell mass, glucose levels, weight and insulin resistance
under the titles susceptibility, adaption and failure
Typically progresses from a preliminary phase of impaired glucose tolerance or impaired fasting glucose.
describe the changes in T2DM that lead to hyperglycaemia
describe the pattern of presentation
describe the synthesis of insulin
synthesised in the RER of pancreatic B cells, as a larger single chain preprohormone called preproinsulin
it is cleaved to form insulin which contains two polypeptide chains linked by disulphide bonds
there is a connecting C peptide which is a by product of cleavage and has no known physiological function
C peptide
amounts of it are generally found to be equal to that of insulin as they are linked during synthesis
can be used as a marker of insulin production
what effect does obesity have on the presentation of T2DM
accelerates it
how much function of B cells must be lost to develop DM
90% in T1DM to become hyperglycaemia
only 50% in T2DM
how can the incidence and progression of microvascular complications be reduced
intensive glucose control
weight loss
is there a stronger genetic influence on T1 or T2
T2 - ≥80% concordance in identical twins
microvascular disease and T2DM
T2DM is for most people predominantly a disease of the B cell, the rate of progression and severity of B cell dysfunction is affected by genetics and environment
B cell dysfunction leads to hyperglycaemia, which chronically can lead to microvascular disease
macrovascular disease and T2DM
There are lipid abnormalities, which include reduced HDL cholesterol, increased triglycerides and a predominance of small dense LDL particles. These are all associated with an increased risk of CV disease. Increase hepatic secretion of triglyceride rich VLDL and impaired clearance of this VLDL appears to be of central importance to the pathophysiology of this dyslipidaemia.