Clinical Diabetes Flashcards
how can diabetes be diagnosed?
fasting blood sugar with venous blood sugar sample
why cant a fingerprick test diagnose diabetes?
this is capillary blood sugar
what are normal blood glucose levels compared to diabetic ones?
5 mmol/L is normal
7+ is diabetic
what is an oral glucose tolerance test?
give 75mg of glucose and test blood sugar again 2 hours later. 11.1 mmol/L + is diabetic
what is polyuria?
frequent urination
what is polydipsia?
frequent thirst/dehydration
what is glycosuria?
excess sugar in urine
what is type I diabetes?
beta cell destruction
what is type II diabetes?
insulin resistance or deficiency due to beta cell disfunction
most common cause of type I diabetes mellitus?
autoimmune destruction of beta cells leading to no beta cell function
what are environmental factors contributing to type I?
viruses that can destroy beta cells (mumps, rubella), diet, stress, drugs
what is type II diabetes mellitus linked to?
insulin resistance and high BMI
what is the difference between white patients and indian patients in onset of type II diabetes?
younger age of onset with earlier proteinuria and renal disease.
what percentage of diabetes incidence is type II?
85%
where does insulin act?
adipose tissue, muscle and liver
what does lack of insulin lead to?
raised blood glucose levels. adipose tissue breaks down leading to diabetic ketoacidosis
what can intensive insulin treatment lead to?
hypoglycaemia
what would be an ideal diabetes treatment?
pancreatic transplant or beta cell transplant
what is type II diabetes mellitus a combination of?
insulin resistance and beta cell dysfunction
how does beta cell dysfunction come about?
genetic/environmental factors lead to insulin resistance so the beta cells release very large amounts causing hyperinsulinaemia . eventually beta cells stop working and cannot cope so they begin to dysfunction. the beta cells work so hard, they cant cope and dysfunction –> hyperglycemia
which type has more severe insulin deficiency?
type I
what are aims of treatment in type II diabetes mellitus?
- abolish symptoms/complications of hyperglycemia
- reduce threat of complications
- increase life expectancy
- restore life quality
what are early treatments of diabetes?
encourage patients to lose weight and exercise
what are insulin sensitisers?
decrease insulin resistance at target tissues so pancreas produces more insulin
what do effects of insulin sensitisers achieve?
- decrease plasma glucose levels
- decrease excessive lipolysis and reduce FFAs
- decrease hepatic gluconeogensis
- improve insulin mediated glucose uptake
what are the steps of treatment?
diet and exercise –> oral monotherapy –> oral combination –> insulin +- oral agents
what is metformin?
decreases hepatic glucose output and decreases fatty acid oxidation
how does metformin work?
increases kinase activity of insulin receptor and increases expression of GLUT-4 transporter and increases glycogen storage
what are glitazones (thiazolidnediones)?
oral insulin sensitising agents that lower blood glucose and insulin levels
what is glitazone mechanism of action?
PPAR- gamma
what do both metformin and glitazones do?
increase sensitivity of body to insulin
what do sulphonylureas do?
help beta cells produce insulin. they block K+ ATP channels –> depolarisation –> increase insulin release
what happens if you stop type I DM insulin treatment?
diabetic ketoacidosis
what happens if you stop type II DM treatment?
HONK hyperosmolar non-ketotic coma
what are complications of undiagnosed type 2?
cerebrovascular disease, retinopathy, cardiovascular disease, nephropathy, neuropathy, peripheral vascular disease
what are microvascular complications (directly related to blood sugar)?
nephropathy, retinopathy, neuropathy
what are macrovascular complications (where other things like cholesterol are important)?
CHD/Stroke, Peripheral vascular disease, blood pressure
