type 1 diabetes

Question 1

what are the differences between type 1 and type 2 diabetes

Answer 1

Type 1:
B cells in pancreas cant produce sufficient amounts of insulin
(insulin deficiency)
autoimmune, islet of Langerhans beta cells destruction leads to low levels of insulin
treated with insulin injections
usually diagnosed before age of 40

type 2:
impaired b cell function or loss of insulin sensitivity on insulin receptors
(insulin resistance)
treated with medicines that lower blood sugar and improve insulin sensitivity

both types cause inappropriate glucose homeostasis (chronic hyperglycaemia)

Question 2

what are consequences of high blood glucose levels

Answer 2

glucosuria (glucose presence in urine)
polyuria (osmotic diuresis) (pee a lot)
polydipsia (thirst)
visual disturbances (altered refractive index of lens)
urinogenital infections

Question 3

what are consequences of impaired glucose utilization in muscle

Answer 3

lethargy and weakness
weight loss (type 1)
ketoacidosis (increased fat metabolism, type 1)

Question 4

what are long term complications of diabetes

Answer 4

microvascular:
retinopathy
neuropathy
nephropathy
(high blood glucose levels damage vessels)

macrovascular:
ischaemic heart disease
stroke
peripheral vascular disease

good gylcemic control decreases chances for these complications

Question 5

what are diet and lifestyle changes for diabetes

Answer 5

healthy diet
regular meals
low fat sugar and salt
high in fibre and complex carbs
fruit and veg
regular exercise (improves sensitivity and reduces cardiovascular risk)

Question 6

describe the mechanism of insulin release and insulin synthesis

Answer 6

pancreatic beta cells have GLUT-2 transporters, GLP-1 (incretins) receptors M3 and alpha adrenoceptors.

glut 2 transporters transport glucose into cell. this leads to the production of ATP in the cell via glycolysis TCA and oxidative phosphorylation. this blocks KATP channels on the cell blocking hyperpolarization via decreasing potassium efflux. this leads to calcium influx into cell via calcium channels. there is also intracellular calcium influx. the influx causes insulin granules to release insulin via exocytosis.

incretins are gut hormones released when eating. incretin (GLP-1) acts at GLP1 receptors to stimulate insulin release

the M3 receptors are innervated by the parasympathetic nervous system which stimulates insulin release

the alpha adrenoceptors are innervated by the sympathetic nervous system which blocks insulin release.

insulin in vesicles are produced from preproinsulin > proinsulin > insulin
preproinsulin: signalling peptide, B chain, A chain and C peptide
proinsulin: b chain a chain and c peptide
insulin: b chain and a chain with sulfide bonds

Question 7

what is the role of insulin

Answer 7

binds to tyrosine kinase receptor: insulin receptor
stimulates glucose uptake into skeletal muscle via glut-4 transporter increases
stimulates conversion of glucose into glycogen in liver
prevents glycogen breakdown
inhibits glucose synthesis
stimulates fat storage
inhibits food intake
stimulates potassium uptake into cells

Question 8

how are insulins classified

Answer 8

based on duration of action

1. short acting (insulin analogues)
   soluble and rapid acting. normally insulin forms hexamers that break into monomers to be absorbed. these recombinant analogues are modified to remain as monomers
   ex: aspart/lispro
2. intermediate (mix of insulin and other ingredients)
   gradually absorbed into blood stream
   insulin isophane: complex with protamine
3. long lasting (mix of insulin and other ingredients)
   gradually absorbed into blood stream
   ex: insulin glargine/detemir taken every 24 hours
   detemir promotes binding to albumin. slowly dissociates
   glargine changes structure of insulin molecule to make it less soluble in physiological pH

insulin treatment is biphasic (mix of different types)
ex: basal/bolus once long acting
3 times short acting at each meal twice daily

intermediate and short acting given before breakfast and dinner