diabetes

Question 1

how are insulin and insulin analogue preparations administered?

Answer 1

SC or IV injection

Question 2

What is an example of a short-acting insulin?

Answer 2

neutral/regular insulin

Question 3

What are three examples of ultra short-acting insulins?

Answer 3

insulin aspart, glulisine and lispro

Question 4

What is an example of an intermediate-acting insulin?

Answer 4

protamine insuline (isophane)

Question 5

What is an example of a long-acting insulin?

Answer 5

insulin glargine, detemir

Question 6

MOA of short acting insulin?

Answer 6

hexamer insulin molecule is broken up before absorption

Question 7

MOA of ultra-short acting insulin?

Answer 7

aa sequence of insulin is altered, no hexamer formation; monomers and dimers are ready for absorption from injection site.

Question 8

MOA of long-acting insulin?

Answer 8

peak less basal levels: binds to albumin, slowly dissociates

Question 9

ADRs of insulin and insulin analogues

Answer 9

hypoglycaemia, lipodystrophy, localised allergic reactions, insulin antibody formation

Question 10

What does SC insulin infusion do to metabolic control?

Answer 10

improves

Question 11

MOA of sulphonylureas

Answer 11

cause depolarisation of pancreatic beta-cells by closing of KATP channels

Question 12

Do sulphonylureas undergo hepatic metabolism?

Answer 12

yes

Question 13

ADR of sulphonylureas?

Answer 13

hypoglycaemia, stimulate appetite - leading to weight gain

Question 14

MOA of metformin

Answer 14

activates AMPK causing increase of glucose uptake and decreased gluconeogenesis

Question 15

advantages of metformin

Answer 15

euglycaemic rather than hypoglycaemic, excreted unchanged in the urine

Question 16

ADRs of metformin

Answer 16

GI upset, lactic acidosis (rare), interferes with B12 absorption

Question 17

MOA of glitazones

Answer 17

bind to and stimulate peroxisome proliferator-activated receptor-gamma (PPAR-gamma), PPAR binds to DNA to promote insulin signalling

Question 18

ADRs of glitazones

Answer 18

hepatic impairment, fluid retention, weight gain

Question 19

MOA alpha-glucosidase inhibitors

Answer 19

competes with di and polysaccharides in the gut for binding to carbohydrate enzyme

Question 20

ADRs of alpha-glucosidase inhibitors

Answer 20

flatulence, diarrhoea, abdominal discomforts

Question 21

MOA of incretin-enhancing agents (are injected)

Answer 21

increase insulin sensitivity of pancreatic beta cells, reduce food intake, increase glucose uptake, decrease nutrient reabsorption

Question 22

ADRs of incretin-enhancing agents?

Answer 22

hypoglycaemia, GI upset, pancreatitis (rare)

Question 23

MOA of DDP-4 (dipeptidylpeptidase-4) inhibitors?

Answer 23

potentiate endogenous incretin action by preventing their breakdown

Question 24

ADRs of DDP-4

Answer 24

GI upset, headache, increased UTI, nasopharyngitis

Question 25

MOA of Na+-glucose co-transporter 2 inhibitor

Answer 25

inhibit Na+-glucose transporter, increase glucose excretion from kidneys by preventing PCT reabsorption

Question 26

ADRs of Na+-glucose co-transporter 2 inhibitor

Answer 26

genital infection, polyuria, dysuria, increased haemocrit, increased risk of hypoglycaemia, UTI, volume depletion