Type 2 Diabetes Mellitus Flashcards

1
Q

what is type 2 diabetes mellitus?

A

condition in which the combination of insulin resistance and beta-cell failure result in hyperglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

T2DM is associated with?

A

obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The resultant chronic hyperglycaemia from T2DM may initially be managed by?

A

diet

weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

With time, T2DM will need what treatment?

A

insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

WHO diabetes classification

A
T1DM
T2DM
hybrid forms
other
unclassified
during pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is LADA?

A

Autoimmune diabetes leading to insulin deficiency can present later in life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what can be a feature of T2DM?

A

diabetic ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is MODY?

A

maturity onset diabetes of the young

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diabetes may present following what diseases?

A

pancreatic damage

other endocrine disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

epidemiology of diabetes

A

globally varies enormously
increasing prevalence
occurring/being diagnosed younger
greatest in ethnic groups that move from rural to urban lifestyle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are normal fasting glucose levels?

A

less than 6mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are normal 2 hr glucose (OGTT) levels?

A

less than 7.7mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are normal HbA1c levels?

A

less than 42 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

describe beta cell function (%) as time progresses with T2DM

A

beta cell function is decreasing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

relative insulin deficiency

A

insulin is produced by pancreatic beta cells but not enough to overcome insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are fasting glucose levels for T2DM?

A

more than 7mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are 2 hr glucose (OGTT) levels for T2DM?

A

more than 11mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are HbA1c levels for T2DM?

A

more than 48mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

the intermediate state for fasting glucose levels is called?

A

impaired fasting glycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

the intermediate state for 2hr glucose levels is called?

A

impaired glucose tolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

the intermediate state for HbA1c is called?

A

pre diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

why is their usually no diabetic ketoacidosis in relative insulin deficiency?

A

usually enough insulin to compensate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

overview pathophysiology of T2DM

A

genetic risk, intrauterine environment and adult environment
insulin resistance/secretion
fatty acids important in pathophysiology
T2DM is heterogenous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

pathophysiology of T2DM

A

first phase insulin response is lost

still get hepatic glucose production > drives progression

25
Q

draw the relationship between insulin secretion and sensitivity

A

secretion on y axis
sensitivity on x axis
curve starts high, sharp decrease then plateaus

26
Q

consequences to insulin resistance in the liver

A

production of hepatic glucose from glycogen

27
Q

consequences to insulin resistance in the muscle

A

no glucose uptake

stays in the circulation

28
Q

consequences to insulin resistance in the adipocytes

A

disrupts lipid metabolism
no glucose uptake
increased triglycerides because insulin promotes conversion to NEFA

29
Q

list inflammatory adipokines that are involved in T2DM

A

TNF-alpha, IL-6, glucocorticoids, visfatin, endocannabinoids, adiponectin, leptin, fatty acids, resistin, apelin

30
Q

monogenic diabetes

A

single gene mutation > MODY

31
Q

polygenic diabetes

A

polymorphisms that increase risk of development

32
Q

how does the strength of genetic risk affect the chance of developing T2DM?

A

low genetic risk requires a high environmental trigger

high genetic risk requires a low environmental trigger

33
Q

what is the role of obesity in T2DM?

A

major risk factor

fatty acids + adipocytokines important in pathophysiology

34
Q

which puts you at a higher risk of development of T2DM: central or visceral obesity?

A

visceral

35
Q

other than obesity, list other associations with the development of T2DM?

A

perturbations in gut microbiota

intra-uterine growth retardation

36
Q

list major risk factors for T2DM

A
age
increased BMI
ethnicity
PCOS
family Hx
inactivity
37
Q

typical presentation of T2DM

A
hyperglycaemia
overweight
dyslipidaemia
fewer osmotic symptoms than type 1 
w/ complications
insulin resistance
later insulin deficiency
38
Q

what is the first line test for the diagnosis of T2DM?

A

HbA1c
no fasting required
quick
cheap

39
Q

diagnosis of T2DM w/ HbA1c

A

1x HbA1c >=48mmol/L + symptoms

2x HbA1c >=48mmol/L if asymptomatic

40
Q

T2DM usually diagnosed in patients when?

A

osmotic symptoms
infections
screening: incidental finding
presentation of complication (acute or chronic)

41
Q

hyperosmolar hyperglycaemic state

A

presents commonly w/ renal failure, profoundly dehydrated
insufficient insulin for preventing hyperglycaemia but enough to suppress lipolysis/ketogenesis
absence of acidosis
often identifiable precipitating event (infection, MI)

42
Q

management of T1DM

A

exogenous insulin (basal-bolus) regime
self-monitoring of glucose
structured education
technology

43
Q

management of T2DM

A
diet
oral meds
structured education
may need insulin
remission/reversal
44
Q

list diabetic complications

A

retinopathy
neuropathy
nephropathy
CVS

45
Q

principles of a T2DM consultation

A

glycaemia > HbA1c, review meds, glucose monitor
weight assessment
blood pressure
dyslipidaemia > cholesterol profile
screening for complications > foot check, retinal screening

46
Q

dietary recommendations

A
total calorie control
reduce fats, refined carbs
increase complex carbs
increase soluble fibre
decrease sodium
47
Q

list four main facets of pathophysiology of T2DM

A

excess hepatic glucose production
resistance to action of circulating insulin
inadequate insulin production for extent of insulin resistance
excess glucose in circulation

48
Q

drug treatment to reduce hepatic glucose production

A

metformin

49
Q

drug treatment to improve insulin sensitivity

A

metformin

thiozolidinediones

50
Q

drug treatment to boost insulin secretion

A

sulphonylureas
DPP4-inhibitors
GLP-1 agonists

51
Q

drug treatment to inhibit carb gut absorption/inhibit renal glucose resorption

A

alpha glucosidase inhibitor

SGLT-2 inhibitor

52
Q

first line T2DM drug treatment

A

metformin

53
Q

main side effects of metformin

A

GI side effects

54
Q

metformin is contraindicated in?

A

severe liver, sever cardiac or moderate renal failure

55
Q

how do sulphonylureas work?

A

bind to ATP-sensitive K+ channel and close it, independent of glucose/ATP

56
Q

what is pioglitazone?

A

peroxisome proliferator-actived receptor agonists (PPAR- gamma)

57
Q

side effects of pioglitazone

A

older types hepatitis, heart failure, mild weight gain

58
Q

function of pioglitazone

A

insulin sensitiser

59
Q

what procedures have the potential to induce remission of T2DM?

A

gastric bypass surgery

low calorie diet for 3-6 months