Type 2 Diabetes Flashcards
what is the pathophysiology of T2DM
genetic disposition + obesity lifestyle factors
insulin resistance
=
compensatoy beta cell hyperplasia (normoglycemia)
=
early beta cell failure (impaired glucose tolerance- pre diabetes)
=
beta cell failure late (diabetes)
can also be caused by primary beta cell failure (rare)
what are the components of the ominous octet that contribute to hyperglycaemia in T2DM
decreased insulin secretion (pancreas) increased glucagon secretion (pancreas) decreased incretin effect (gut peptide) increased hepatic glucose production (liver) neurotransmitter dysfunction increased lipolysis increased glucose reabsorption (kidneys) decreased glucose uptake (muscles)
why is the prevalence of T2DM increasing more than the incidence
as people are living longer
what ethnic group has a higher risk of diabetes
eastern Asian
insulin resistance is more assocaited with micro/macro vascular disease
macro
hyperglycaemia is more associated with micro/macro vascular disease
micro
how is CVD risk most effectively treated
statins/ anti-hypertensives
when is one blood test diagnostic for diabetes
when its over diagnostic limit and patient is symptomatic
what is the treatment areas for T2DM
lifestyle changes
glycaemic management- metformin (most), insulin (last line)
blood pressure management
lipid management- statin
antiplatelet therapy- aspirin, clopidogrel
what is the treatment for acute T2DM
basal bolus insulin
metformin
what is the first line treatment give to most people for glycaemic control
metformin
what is the mechanism of metformin
decreases hepatic gluconeogenesis
increased peripheral glucose uptake
what outcomes does metformin usually have
decreases HbA1c
weight neutral
no hypoglycaemia control when used as monotherapy
decreased Cancer and CHD risk
what are some adverse effects of metformin
GI, lactic acidosis
what can metformin be combined with as a second step
SGLT2 glitazone gliptin GLP-1R SU basal insulin
what is the mechanism of sulphonylurea
blocks beta cell KATP channels , increased 1st and 2nd phase insulin secretion
what are the outcomes seen when using sulphonylurea
decrease in HbA1c
weight gain
hypoglycaemia
what are adverse effects of sulphonylurea
abnormal LFTs
increased CHD
name a sulphonylurea
gliclazide
what is the maximum effective dose of gliclazide
80-120mg
what happens as the dose of sulphonylureas is increased
efficacy is reduced
what are gliptins
e.g. GLP-1 receptor agonist and DPP4 inhibitors
how do DPP 4 inhibitors work
blocks action of DDP- an enzyme that destroys the hormone incretin
how does GLP-1 receptor work
is an incretin- increases secretion insulin and somatostatin, reduces secretion of glucagon
what are the outcomes of GLP-1 receptor agonists
lower HbA1c
increase in weight
can GLP-1 help with hypoglycaemia
when used in combination with metformin and/or a sulphonylurea
what is the outcome of DPP4 inhibitors
decrease HbA1c
weight neutral or decreased
what do SGLT-2 inhibitors do
reduce the amount of glucose being absorbed in the kidneys, passed out in the urine instead of being reabsorbed into the blood
how does glitazone work
lower insulin resistance, increasing peripheral glucose uptake via PPAYgamma activator
what are the outcomes of glitazone
decrease HbA1c
increase weight
what are the adverse affectes of glitazone
fracture risk increase
hepatoxicity
fluid retention
what should you consider if drugs not working
adding on another instead of titrating up the dosage
what is the max dosage or metformin
1000mg bid
what is given if there is a history of cardiovascular disease
metformin + SGLT2
