Type 2 Diabetes Flashcards Preview

Endocrinology > Type 2 Diabetes > Flashcards

Flashcards in Type 2 Diabetes Deck (64)
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1
Q

what are the key physiological changes in T2DM?

A

insulin resistance

beta cell dysfunction

2
Q

what happens in a normal person when insulin binds to a receptor on a cell?

A

triggers production of glucose transport proteins to allow glucose to enter the cell

3
Q

what happens if someone is insulin resistant?

A

receptor is not as responsive to the insulin molecule & therefore less glucose enters the cell causes a build up of glucose in blood

4
Q

PCOS

A

polycystic ovarian syndrome

5
Q

what is beta cell dysfunction?

A

major defect in individuals with T2DM, reduced ability of beta-cells to secrete insulin in response to hyperglycaemia

6
Q

what happens initially for increasing insulin resistance?

A

initially the beta cells compensate

7
Q

what does insulin resistance lead to?

A

glucotoxicity (hyperglycaemia)

lipotoxicity (elevated FFA, TG)

8
Q

what do glucotoxicity & lipotoxicity lead to?

A

declining beta cell function

9
Q

which body shape is most commonly associated with T2DM?

A

apple body shape

10
Q

what is the metabolic syndrome?

A

high blood pressure
high triglycerides
low HDL
insulin resistance

11
Q

what 4 complications of T2DM can be present at time of diagnosis?

A

retinopathy
neuropathy
erectile dysfunction
nephropathy

12
Q

what 4 lifestyle changes can be made to help with T2DM?

A

weight loss
exercise
smoking cessation
improve diet

13
Q

which ethnicity have lower BMI targets due to increased risk of diabetes?

A

SE Asian populations

14
Q

what can we do to help patients better their self-management?

A

education
behaviour change
motivational interviewing
personal information sharing

15
Q

health literacy

A

the wide range or skills & competencies that people develop to seek out, comprehend, evaluate & use health information & concepts to make informed choices, reduce health risks & increase quality of life

16
Q

give an example of a biguanide?

A

metformin

17
Q

give some examples of sulphonylureas

A

glicazide
glibenclamide
glimeparide

18
Q

give an example of thiazolidinediones

A

pioglitazone

19
Q

what is metformin derived form

A

guanidine

20
Q

what does metformin do

A

improves sensitivty to insulin

21
Q

what are the doses of metformin tablets that can be given

A

500mg
850mg
1000mg

22
Q

what is the normal starting dose of metformin?

A

500mg od or bd

23
Q

what are the effects of metformin

A

reduces HbA1c by lowering insulin resistance

prevents microvascular & macrovascular complications

24
Q

when metformin is used as a monotherapy, does it cause hypos?

A

no

25
Q

is metformin do in pregnancy?

A

nothing it’s safe

26
Q

what does metformin do to BP?

A

minor reduction

27
Q

what does metformin to to triglycerides & LDL?

A

reduces them

28
Q

what GI side effects does metformin do?

A

anorexia, nausea, vomiting, diarrhoea, abdo pain, taste disturbance

29
Q

what substances does metformin interfere with?

A

Vit. B12 & folic acid absorption

30
Q

what other adverse affects can metformin do?

A

rarely lactic acidosis
liver failure
rash

31
Q

at what eGFR/serum creatinine should metformin be stopped?

A

eGFR 150

32
Q

at what level of eGFR should metformin dose be halved?

A

30-45 ml/min

33
Q

what is 1st line management of T2DM?

A

lifestyle changes

34
Q

what is 1st line therapeutic in T2DM?

A

metformin

35
Q

what are the 2 most widely used sulphonylureas (SUs)?

A

glicazide

glipizide

36
Q

what effects do SUs have?

A

reduced HbA1c
more rapid reduction in hyperglycaemia compared to insulin sensitisers
prevents microvascular & macrovascular complications

37
Q

how do SUs work?

A

increase insulin secretion

38
Q

what are the adverse affects of SUs?

A

hypoglycaemia
weight gain
GI upset
headaches

39
Q

when would SUs be first line?

A

in underweight T2DM

40
Q

what are the rarer adverse effects of SUs?

A

hypersensitivity
blood dyscrasias
live dysfunction

41
Q

when should SUs be avoided?

A

severe renal or hepatic failure

42
Q

why was rosiglitazone taken off the market?

A

concerns over increased risk of MI

43
Q

what are the effects of thiazolidinedones (TZDs)?

A

reduces HbA1c

prevents macrovascular complications

44
Q

do TZDs cause hypos?

A

not if used without an SU

45
Q

what happens to weight with TZDs?

A

increase is very common

46
Q

what is the effect of TZDs on heart conditions?

A

reduces heart attacks but will make heart failure worse

47
Q

how do TZDs work?

A

increase insulin sensitisation

48
Q

what MSK problem do glitazone drugs increase the risk of?

A

hip fractures

49
Q

give an example of an SGLT2 inhibitor?

A

dapagliflozin

empagliflozin

50
Q

give an example of a drug based on incretins (GLP-1 receptors agonists)?

A

exenatide
exendin
liraglutide
lixisenatide

51
Q

what is the incretin effect?

A

the amount of glucose given intravenously to bring the glucose blood level to the same as that of oral glucose will stimulate less insulin to be produced

52
Q

what are incretins?

A

intestinal secretions of insulin or hormones that help this

53
Q

what cells secrete GIP?

A

K cells

54
Q

what cells secrete GLP-1?

A

L cells

55
Q

what is the issue for patients with GLP-1 receptor agonists?

A

they have to be given by injection

56
Q

give an example of a glitazone

A

pioglitazone

57
Q

what are the benefits of GLP-1 receptor agonists?

A

promote insulin secretion from pancreas without hypoglycaemia
suppress glucagon
decrease gastric emptying (early satiety)
act on hypothalamus to reduce appetite, results in weight loss

58
Q

what are the problems with GLP-1 receptor agonists?

A

nausea
injectable
pancreatitis

59
Q

give an example of a drug based on incretins (DPP4 inhibitors)?

A

vildagliptin
sitagliptin
saxagliptin
linagliptin

60
Q

what are the benefits of DPP4 inhibitors?

A
promote insulin secretion from pancreas without hypoglycaemia 
suppress glucagon 
weight neutral
can be taken orally
nausea not as bad as other drugs
61
Q

what are the problems with DPP4 inhibitors?

A

not that potent
no weight loss
pancreatitis

62
Q

where in the body do SGLT2 inhibitors act?

A

in the kidneys to reduce uptake of sugar by about one quarter

63
Q

what’s the downside of SGLT2 inhibitors?

A

causes sugar in the urine which increases thrush & UTIs

64
Q

what insulin regimen is used in T2DM?

A

basal inulin