Flashcards in diabetes Deck (26):
how are insulin and insulin analogue preparations administered?
SC or IV injection
What is an example of a short-acting insulin?
What are three examples of ultra short-acting insulins?
insulin aspart, glulisine and lispro
What is an example of an intermediate-acting insulin?
protamine insuline (isophane)
What is an example of a long-acting insulin?
insulin glargine, detemir
MOA of short acting insulin?
hexamer insulin molecule is broken up before absorption
MOA of ultra-short acting insulin?
aa sequence of insulin is altered, no hexamer formation; monomers and dimers are ready for absorption from injection site.
MOA of long-acting insulin?
peak less basal levels: binds to albumin, slowly dissociates
ADRs of insulin and insulin analogues
hypoglycaemia, lipodystrophy, localised allergic reactions, insulin antibody formation
What does SC insulin infusion do to metabolic control?
MOA of sulphonylureas
cause depolarisation of pancreatic beta-cells by closing of KATP channels
Do sulphonylureas undergo hepatic metabolism?
ADR of sulphonylureas?
hypoglycaemia, stimulate appetite - leading to weight gain
MOA of metformin
activates AMPK causing increase of glucose uptake and decreased gluconeogenesis
advantages of metformin
euglycaemic rather than hypoglycaemic, excreted unchanged in the urine
ADRs of metformin
GI upset, lactic acidosis (rare), interferes with B12 absorption
MOA of glitazones
bind to and stimulate peroxisome proliferator-activated receptor-gamma (PPAR-gamma), PPAR binds to DNA to promote insulin signalling
ADRs of glitazones
hepatic impairment, fluid retention, weight gain
MOA alpha-glucosidase inhibitors
competes with di and polysaccharides in the gut for binding to carbohydrate enzyme
ADRs of alpha-glucosidase inhibitors
flatulence, diarrhoea, abdominal discomforts
MOA of incretin-enhancing agents (are injected)
increase insulin sensitivity of pancreatic beta cells, reduce food intake, increase glucose uptake, decrease nutrient reabsorption
ADRs of incretin-enhancing agents?
hypoglycaemia, GI upset, pancreatitis (rare)
MOA of DDP-4 (dipeptidylpeptidase-4) inhibitors?
potentiate endogenous incretin action by preventing their breakdown
ADRs of DDP-4
GI upset, headache, increased UTI, nasopharyngitis
MOA of Na+-glucose co-transporter 2 inhibitor
inhibit Na+-glucose transporter, increase glucose excretion from kidneys by preventing PCT reabsorption