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LCRS Endocrinology > Type 2 diabetes > Flashcards

Type 2 diabetes Flashcards

1
Q

What is the definition of diabetes?

A

A state of chronic hyperglycaemia sufficient to cause long term damage to specific tissues notably the retina, kidneys, nerves and arteries

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2
Q

What is the clinical definition of diabetes?

A

Fasting blood glucose > 7mmol/l

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3
Q

What is impaired fasting glucose?

A

Space in between the defining markers for diabetes and normal when measuring fasting blood glucose

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4
Q

What is impaired glucose tolerance?

A

Space in between the defining markers for diabetes and normal when measuring the 2 hour response in a glucose tolerance test

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5
Q

What factors affect pathophysiology of T2DM?

A

Genetic
Intrauterine environment
Adult environment

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6
Q

What is the aetiology of Maturity Onset Diabetes of the Young?

A

Several hereditary forms- autosomal dominant for ineffective pancreatic beta cell insulin production

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7
Q

As a baby, what makes you more likely to develop T2DM?

A

Being small- intrauterine growth restriction (IUGR)

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8
Q

What other problems apart from an increase in blood glucose does insulin resistance cause?

A

Dyslipidaemia which stimulates the mitogenic pathway causing smooth muscle hypertrophy and an increase in blood pressure which increases the risk of microvascular disease

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9
Q

What happens to insulin production and resistance as we get older?

A

Production decreases and resistance increases

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10
Q

Eventually, insulin production will intersect with insulin resistance and the insulin production won’t be enough to overcome the resistance, when does this happen in caucasians?

A

110 years

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11
Q

What percentage of patients with T2DM are obese?

A

80%

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12
Q

What are the 2 phases of insulin release in a normal person?

A

1st phase- stored insulin that is ready to be released in one go
2nd phase- over a period of time, more insulin is produced and released

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13
Q

What happens to the insulin phases in people developing diabetes?

A

They will still have some insulin production but will lose their 1st phase response

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14
Q

How can diabetes get round their lack of a 1st phase response?

A

Eating complex carbohydrates which release the glucose slowly and decrease the need for a 1st phase response

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15
Q

What are triglycerides broken down into?

A

Glycerol and non-esterified fatty acids (NEFA)

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16
Q

What is insulin’s effect on the breakdown of triglycerides?

A

It inhibits it because you don’t need to break down fat stores after a meal

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17
Q

Where does the glycerol and NEFA go after formation?

A

To the liver

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18
Q

What happens to the glycerol in the liver?

A

Converted to glucose (gluconeogenesis)

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19
Q

How is glucose released from the liver?

A

Glycogenolysis

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20
Q

What happens to the NEFA when they get to the liver?

A

They are chopped up into 2-carbon segments which can’t be used to make glucose but are used to make very low density lipoprotein triglycerides which are atherogenic

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21
Q

What is insulin resistance modulated by?

A

Adipocytokines

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22
Q

What system is thought to be associated with obesity, insulin resistance and T2DM?

A

Gut microbiota

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23
Q

What is a common side effect of diabetes treatment and what is the only treatment that doesn’t cause this side effect?

A

Weight gain and metformin

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24
Q

How does T2DM present?

A

Microvascular:
Retinopathy
Nephropathy
Neuropathy

Microvascular:
Ischaemic heart disease
Cerebrovascular
Renal artery stenosis
PVD

Metabolic:
Lactic acidosis
Hyperosmolar

25
Q

In terms of metabolic issues, how often do they present in T2DM compared to T1DM?

A

Much more common in T1DM with ketoacidosis

26
Q

What is the basis of management of T2DM?

A

Education
Diet
Pharmacological treatment
Complication screening

27
Q

How should someone with T2DM control their diet?

A 
Control total calories/increase exercise
Reduce refined carbohydrates
Increase complex carbohydrates
Reduce fat as proportion of calories
Increase unsaturated fat as proportion of fat
Increase soluble fibre
28
Q

How do you monitor T2DM?

A

Weight
Glycaemia
Blood pressure
Dyslipidaemia

29
Q

What is orlistat and how does it work?

A

Pancreatic lipase inhibitor- it stops the breakdown of fat thus restricting fat absorption in the gut

30
Q

What is metformin and how does it work?

A

Biguanide- Treats insulin resistance in the liver

31
Q

How do sulphonylureas work?

A

Makes the existing pancreas secrete more insulin

32
Q

How do alpha glucosidase inhibitors work?

A

Delay glucose inhibition

33
Q

How do thiazolidinediones work?

A

They act on the adipocytes and addresses insulin resistance peripherally in fat and muscle

34
Q

How common is metformin as a treatment?

A

Used in more or less everyone with T2DM in particular overweight patients

35
Q

When would metformin not be used?

A

Severe liver failure
Severe cardiac failure
Mild renal failure

36
Q

How can beta cells gage the blood glucose levels and what does it lead to?

A

Glucokinase and insulin secretion

37
Q

How do sulphonylureas work?

A

They act on specific receptors and block the ATP sensitive potassium channel and cause the influx of calcium which leads to insulin secretion

38
Q

What is glibenclamide?

A

Sulphonylurea and insulin secretagogue

39
Q

What are the side effects of glibenclamide?

A

Hypoglycaemia

Weight gain

40
Q

What is acarbose?

A

Alpha gluconidase inhibitor

41
Q

How does acarbose work?

A

Prolongs the absorption of oligosaccharides which allows insulin secretion to cope following the loss of the first phase insulin response

42
Q

What are the side effects of acarbose?

A

Sugars reach the large intestine where they are fermented so flatus (gas) is an issue

43
Q

What are thiazolidinediones?

A

Peroxisome proliferator-activated receptor (PPAR-y) agonists

44
Q

What is an example of a thiazolidinedione?

A

Pioglitazone

45
Q

How do thiazolidinediones work?

A

They are an insulin sensitiser- mainly peripheral and cause weight gain- improvement in glycaemia and lipids

46
Q

What are the side effects of thiazolidinediones?

A

Hepatitis and heart failure

47
Q

What is the incretin effect?

A

Oral glucose load triggers a bigger release in insulin than IV glucose

48
Q

Why does the incretin effect occur?

A

Due to GLP-1 which is a gut hormone that is released on response to food in the gut and stimulate insulin and suppresses glucagon

49
Q

Where and how is GLP-1 produced?

A

It is produced by L-cells and is the transcription product of pro-glucagon gene

50
Q

What is a problem with GLP-1?

A

Short half life as it is rapidly degenerated by dipeptidyl peptidase-4 (DPP-IV)

51
Q

How do Gliptins work?

A

They make the GLP-1 that is present last longer because they are DPP-IV inhibitors

52
Q

What is gestational diabetes?

A

Temporary diabetes that is present in some pregnant women- helps identify women that are high risk for diabetes later in life

53
Q

In which type of diabetes is weight loss common in?

A

Type 1

54
Q

Which type of diabetes is ketone prone?

A

Type 1

55
Q

In which type of diabetes is serum insulin low or absent?

A

Type 1

56
Q

Which type of diabetes has HLA association?

A

Type 1- DR3 and DR4

57
Q

In which type of diabetes do islet B cells function?

A

Type 2

58
Q

In which type of diabetes are islet cell antibodies present?

A

Type 1

LCRS Endocrinology (18 decks)

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