Treatment of Diabetes pt1 Flashcards
Plainly describe what is Diabetes mellitus
- a metabolic disorder due to defects in insulin secretion , action or both
- results in chronic hyperglycaemia and disturbances to carb, fat and protein metabolism
What are the late associated complications of diabetes
1- Microvascular : kidneys & retinopathy
2- Microvascular : atherosclerosis, MI , stroke
3- Neuropathy : loss of sensation
List the Onset , Nutritional status , Prevalence, genetic predisposition and defect of Type 1 diabetes
- childhood / puberty
- normally malnourished
- 10-20% worldwide
- moderate genetic predisposition
- defect in pancreatic B cell
List the Onset , Nutritional status , Prevalence, genetic predisposition and defect of Type 2 diabetes
- 35 +
- normally obese
- 80-90% diagnosed
- strong genetic predisposition
- Insulin resistance , insufficient
How are insulin levels measured
- Insulin is measured using C-peptide ( ELISA )
- proinsulin is made of an A, B and C chain. the C chain is cleaved off to produce mature insulin
- C chain is what’s measured to determine insulin levels because we’re only looking at level of active insulin in blood
Explain the phases of insulin secretion
Phase 1 : rapid peak trigger by increased glucose levels (meal)
Phase 2 : slow, sustained until blood glucose is back to normal : pulsatile release into portal vein
Where is a lot of insulin produced lost
- Liver
What is the half life of insulin
5-6 minutes
Explain the Mechanism by which Insulin is stimulated ( 5 steps )
1- glucose taken up by pancreatic B cell by GLUT2 transports
2- metabolized to generate ATP
3- ATP blocks ATP sensitive K+ channel
4- membrane depolarization because K can’t get out of cell so Ca influx into cell
5- increase in Calcium ions triggers release of insulin into prepackaged vesicles
What happens with beta cells in type 2 diabetes
- less insulin granules are being released each time the B cell depolarizes
Explain the mechanism of insulin secretion during low blood glucose levels
1- no glucose taken up 2- no ATP metabolized 3- Regular K+ efflux 4- hyper polarization 5- decrease Ca influx 6- decrease in Insulin secretion
How does insulin stimulate glucose uptake
- insulin binds to insulin receptors which signal glucose uptake via GLUT4 in liver, muscle and fat
- GLUT 4 is translocated from cytosol to membrane and then opens up to take in glucose
Does the heart and brain need GLUT 4
- they do not require insulin for glucose uptake since they are very metabolically active
How insulin works In liver
1- increase Glycolysis 2- increase glycogen synthesis 3- decrease gluconeogenesis 4- decrease glycogenolysis overall effect : increased storage of glycogen in liver
How insulin works in muscle
1- increase glucose uptake via GLUT 4 2- increases glycogen synthesis 3- increase glycolysis 4- increases amino acid uptake 5- increases protein synthesis
How insulin works in Adipose tissue
1- Increase glucose uptake via GLUT 4
2- increase triglyceride formation ( storage of fat )
Overall effect : fat deposition / storage for when there is no food
How insulin works In Brain
1- increase Hunger
2- decrease Hepatic glucose production
3- decrease lipoprotein production
How is insulin taken up in brain
via GLUT 1
In the case of monozygotic twins where one twin develops T1DM , what is the likelihood of the other twin developing T1DM
- 25 %
- not likely
Does insulin occur in a biphasic manner
- yes
Are insulin levels measured Bia C peptide PCR
- no , ELISA not PCR
What are the medical indications of Insulin
- type 1 diabetes
- emergency keto acidosis treatment
- type 2 diabetes control or pre-surgery
- pregnancy
- emergency treatment of hyperkalaemia
Why can insulin not be given as tablet
- it’s a peptide and would be degraded by GIT
How is insulin administered by patients
- subcutaneously
