Insulin and Hypoglycaemics Flashcards
What is glucosuria
elevated glucose levels saturate the glucose re-uptake mechanisms in the kidneys
diagnostic of underlying pathology = diabetes mellitus
leads to osmotic diuresis = thirst, dehydration, increased urine output, unconsciousness, death!
Homeostasis of hypergylcaemia
food intake/endogenous glucose production =
increase in plasma glucose =
insulin release from pancreatic B cells =
insulin action in liver, muscles, CNS =
decrease plasma glucose
Homeostasis of hypoglycaemia
fasting =
decrease in plasma glucose =
glucagon release by pancreatic A cells =
endogenous glucose production, action on liver, muscles, CNS =
increase in plasma glucose
Pancreatic Islets of Langerhans
approx. 1.5 mil per pancreas contain different cell types: - B cells that release insulin - A cells that release glucagon PP cells that release pancreatic polypeptide E cells that release ghrelin
How does glucose stimulate insulin release?
food intake = digestion = glucose uptake by B cells = inhibition of Katp channels (molecules which close K-channels mimic actions of glucose, used to treat hyperglycaemia - insulin secretagogues - . molecules which open K-channels inhibit the actions of glucose, used to treat hypoglycaemia - hypeglycaemia-inducing drugs) = depolarization of the cell = calcium influx = insulin release.
Glucose homeostasis; integration with digestion
food intake =
digestion =
release of gut hormones =
rise in serum GLP-1 =
activation on the GLP-1 receptor (incretin effect)=
cell signalling =
insulin release.
oral glucose faster insulin response compared to i.v
- glucagon-like peptide 1 and gastric inhibitory peptide are incretin hormones
Functional effects of insulin
increases glucose - glycogen (stored in skeletal muscle, liver)
increases glucose - fat (stored as adipose tissue)
increases amino acids - proteins (muscle)
increases glucose and amino acid transport to cells
decreases glycogen breakdown
decreases glucose formation (gluceoneogenesis)
Insulin therapy
treatment for people with type 1 diabetes mellitus
3 preparations:
- short duration; rapid onset (30-60 mins)
soluble insulin and rapid onset insulin analogues: eg. insulin aspart, insulin glulisine, insulin lispro (s.c, i.v)
- intermediate action
eg. isophane insulin; can be porcine, human or bovine (s.c)
- longer lasting; slow onset and lasts for longer
eg. protamine zinc suspension - porcine, human or bovine (s.c)
insulin detemir, insulin glargine - recombinat human (s.c)
What are the 3 preparations in insulin therapy made up of?
short duration - insulin aspart, insulin glulisine, insulin lispro (s.c, i.v)
intermediate action - isophane insulin; can be porcine, human or bovine (s.c)
longer lasting - protamine zinc insulin, insulin zinc suspension - porcine, human or bovine (s.c)
insulin detemir, insulin glargine - recombinant human (s.c)
Short action insulin
peal action 2-4 hours
duration of 8 hours
injected just before or just after food, only lasts long enough for meal at which it was taken
Intermediate/longer acting insulin
onset 1-2 hours
peak action 4-12 hours
duration is 16-35 hours
Biphasic insulin preperations
mixture of intermediate and fast acting
rapid onset
longer-lasting actions
Eg. biphasic insulin aspart and lispro, biphasic isophane insulin
Other treatments for type 1 diabetes mellitus
islet/pancreas transplantation
prevention: immune-mediated destruction of B-cells
Insulin administration
subcut injection 3-4 times daily
- used needle/syringe pens
- portable infusion pump of continuous short acting insulin infusion
Glucagon therapy
for hyperglycaemia-inducing: first treatment for severe hypoglycaemia when oral glucose is not possible - given m=by i.m, i.v, s.c to increase plasma glucose levels - SE = nausea, headaches - glucagon promotes > glycogenolysis > gluconeogenesis > lipolysis
