Homeostasis in action Flashcards
feedforward of insulin
amino acids and GI hormones can also increase insulin secretion before BGL have increased = physiological feedforward
polyuria
large volumes of urine
polydipsia
excessive drinking/ thirst
polyphagia
excessive hunger
why do diabetics have the symptoms they do of polyuria, polydipsia and polyphagia?
normally the kidneys don’t want glucose in the urine so the kidney cells reabsorb the glucose and its taken back into the bloodstream. when the concentration gets around 10mmol/L the cells become saturated and cant absorb anymore. the osmolarity of the urine will be high ad this will drag water out from cells, making the person hungry and the cells aren’t getting the glucose they need so this makes you hungry
hyperglycaemia
less fat breakdown and ketone production
insulin levels may still be adequate but not sufficient enough to control BGL.
beta cells eventually become exhausted and insulin therapy may be needed
diabetes insipidus
lots of dilute urine but not glucose in it
due to altered secretion of ADH (antidiuretic hormone) or decreased responsiveness to it.
often associated with brain injury or tumor in region of the pituitary gland.
gastrointestinal diabetes
often occurs in women during pregnancy may resolve after pregnancy large increase in risk of - birth injuries - neonatal hypoglycaemia - congenital malformations - child /adult obesity
Acute consequences of no insulin
glycosuria - renal tubes cant absorb the excess glucose being filtered.
polyuria- lots of urine
thirst - due to dehydration which stimulates the osmo-receptors in the thirst centres of the brain.
breakdown of protein and fat
- muscle wasting and weight loss
- amino acids released from protein breakdown provides substrates for gluconeogenesis in the liver and increases hyperglycaemia.
- elevated blood lipid levels from fat lipolysis.
ketoacidosis (DKA)
Ketones are acidic and cause acidosis when produced in excess. acetone like smell on breathe and can also be detected in urine
acidosis causes hyperventilation - deep loathed breathing pattern often associated with DKA
acidosis can often cause hyperkalemia. - H+ concentration in ECF exchanged with K+ ions from ICF. total body K+ becomes depleted and lost in urine need to be careful when administering insulin in DKA.
chronic problems of no insulin
cardiovascular disease renal failure retinal damage poor wound healing peripheral nerve damage (somatic and autonomic) susceptibility to infection
chronic hyperglycaemia
increase in lipid levels
damage blood vessels and nerves predisposing to atherosclerosis (build up of fats and other substances in the artery walls)
impaired blood flow to various tissues, sensory and motor nerve damage and increased injury risk.
screening for Diabetes mellitus
fasting blood glucose
- it if is over 7mmol/L suggestive of diabetes mellitus, between 6.1 and 6.9 suggestive of impaired fasting glucose (IFG) .
oral glucose tolerance test
- 75g of glucose administered orally and BGL measured at intervals over following the hours.
- if over 11.1 after 2 hours = diabetes mellitus (not pregnant)
- 50g test screening at around 28 weeks pregnant.
HbA1C
HbA is the most common form of adult Hb (haemoglobin).
over RBC lifespan a small fraction of HbA becomes glycated and is known as HbA1c. (it has glucose permanently bound to it)
HbA1c reflects the average blood glucose concentration to which the RBC has been exposed over its lifespan (around 120 days)
can therefore be used as a screening test for diabetes mellitus or to access how well it is being managed.
42-53 mmol/L = good
97- 151 mmol/L = very bad
insulin treatment for type 1
insulin - human insulin manufactured using recombinant DNA technology, human insulin subsequently modified to slow absorption from subcutaneous injection sites.
typical regime - daily injection of long acting insulin based on anticipated food intake and energy expenditure (feedforward control)
additional doses of short acting insulin based on actual blood glucose measurements (negative feedback control)
