Diabetes Type 2 Flashcards

1
Q

What is type 2 diabetes?

A

where repeated exposure to glucose and insulin makes the body more resistant to the effect of glucose so more and more insulin is required to stimulate glucose uptake, eventually making the pancreas fatigued and damaged

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2
Q

Give 6 risk factors for T2 diabetes:

A

1) older age
2) ethnicity (Black African, South Asian, Caribbean)
3) sedentary life style
4) family history
5) high carbohydrate diet
6) obesity

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3
Q

Give 8 presentations associated with T2 diabetes:

A

1) polyuria
2) polydipsia
3) fatigue
4) unintentional weight loss
5) opportunistic infections e.g. oral thrush
6) slow wound healing
7) glucose in urine
8) acanthosis nigricans

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4
Q

What is acanthosis nigricans?

A

thickening and darkening of the skin in the neck/axilla/groin, giving it a velvety appearance which is associated with insulin resistance

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5
Q

What HbA1c range indicates pre-diabetes?

A

42-47mmol/mol

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6
Q

What HbA1c range indicates diabetes?

A

48+ mmol/mol

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7
Q

Is the genetic link stronger in type 1 or type 2 diabetes?

A

Type 2

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8
Q

What is MODY?

A

MODY – maturity onset diabetes of the young – this is a rare type of type 2 diabetes. It will present in young people who have a family history of type 2 diabetes. It is dominantly inherited.

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9
Q

What is the prevalence of T2DM in the Uk?

A

The overall prevalence of this disease in the UK is about 5%. This rises to 10% by the age of 70.
Excepted to double by 2030

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10
Q

What can the onset of type 2 DM be accelerated by?

A
  1. Stress
  2. Pregnancy
  3. illness
  4. Certain drugs
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11
Q

What is the pathology behind T2DM?

A

Initially insulin is still released normally, and will still bind to insulin receptors, but it will not cause the normal physiological changes inside the cell. This occurs in genetically susceptible individuals due to modifiable lifestyle related factors. This is known as insulin resistance
Type-2 diabetes results when a person cannot secrete enough insulin to overcome this ‘resistance’.
Muscle cells in particular show increased insulin resistance and decreased glucose uptake

The secretory failure of insulin occurs when there is increase Beta-islet cell apoptosis, and the remaining cells fail to respond to insulin signalling
Increased lipolysis with elevated free fatty acids
Alpha-cell dysfunction – elevated glucagon levels
Increased glucose reabsorption by the kidneys
Altered cerebral responses to insulin and apetite

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12
Q

Why does elevated glucose production in the liver occur?

A

not only does a high blood glucose occur because normal digested glucose cant be taken up by cells, but it has a secondary effect on the liver; there is less glucose entering liver cells, and so the liver reacts as if blood glucose were low, and begins glycogenolysis, and raises blood glucose even more.

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13
Q

What are the 3 methods that diagnosis can be confirmed by?

A

HbA1c >6.5% – on at least two occasions

Fasting blood glucose (FBG) >7.0 mmol/L
OR – Random blood glucose >11.0 mmol.L, with subsequent elevated FBG on a separate day

Oral glucose tolerance test (OGTT)
Initial fasting blood sugar level (BSL) >7.0 mmol/L
End of test (after 75g of oral glucose, retested at 2 hours) >11.0 mmol/L

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14
Q

What is HbA1c?

A

HbA1c is a type of ‘glycated haemoglobin’ – essentially haemoglobin that has been altered due to the presence of glucose in the bloodstream.
The higher the glucose level, the greater the amount of glycated haemoglobin – or HbA1c – in the blood. And, as red blood cells have a lifespan of about 90 days, the HbA1c value is in indicator of what glucose levels have been doing for the past 90 days.

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15
Q

What is the screening guidelines for T2DM?

A

Screen everyone over 40
Consider screening anyone over 25 if likely high risk – e.g. high risk ethnic group (South Asian, Chinese, African-Caribbean, Black African origin)
Use a verified screening assessment tool – for example the Diabetes Risk Assessment Tool
If low or intermediate risk, screen every 5 years
If high risk, perform HbA1c or fasting glucose

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16
Q
A
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17
Q

What is the classic acute triad presentation of T2DM?

A
  1. Polyuria
  2. Thirst
  3. Weight loss
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18
Q

What are the common subacute presentation of a T2DM patient?

A
  1. Lack of energy
  2. Polyuria, polydipsia
  3. Vision blurring
  4. Frequent fungal/ bacterial infections - often of the genitals
  5. Loss of sensation
19
Q

Give 3 non-pharmaceutical interventions for T2 diabetes:

A

1) exercise
2) weight loss
3) low glycaemia, high fibre diet

20
Q

What is the first line drug for T2 diabetes treatment?

A

metformin
with a SGLT-2 inhibitor if patient has existing CVD

21
Q

List 4 second line diabetes drugs:

A

1) sulfonylurea
2) pioglitazone
3) DPP-4 inhibitor
4) SGLT-2 inhibitor

22
Q

What is the third line drug management for T2 diabetes?

A

1) triple therapy (metformin and 2 second line drugs)
OR
2) insulin therapy

23
Q

When are GLP-1 mimetics indicated?

A

where triple therapy for T2 diabetes fails and the patient’s BMIi is over 35 kg/m^2

24
Q

Describe the action of metformin:

A

it increases insulin sensitivity and decreases glucose production in the liver

25
Q

Give 4 side effects of metformin:

A

1) abdominal pain
2) nausea
3) diarrhoea
4) lactic acidosis secondary to AKI

26
Q

Give 3 examples of SGLT-2 inhibitors:

A

1) dapagliflozin
2) empagliflozin
3) canagliflozin

27
Q

Describe the action of SGLT-2 inhibitors:

A

they block the action of sodium-glucose contransporter-2 proteins found in the proximal tubules of the kidney which act to reabsorb glucose, meaning SGLT-2 inhibitors cause increased glucose to be excreted in urine

28
Q

Give 4 side effects of SGLT-2 inhibitors:

A

1) increased urine output
2) UTIs
3) diabetic ketoacidosis
4) genital thrush

29
Q

What type of drug is pioglitazone?

A

Thiazolidinedione

30
Q

Describe the action of pioglitazone:

A

it increases insulin sensitivity and decreases glucose production in the liver

31
Q

Give 3 side effects of pioglitazone:

A
  1. Weight gain
  2. Heart failure
  3. Increased risk of bone fractures
32
Q

Give an example of a sulfonylureas:

A

gliclazide

33
Q

Describe the action of sulfonylureas?

A

stimulate insulin release

34
Q

Give 2 side effects of sulfonylureas:

A

1) weight gain
2) hypoglycaemia

35
Q

Describe the action of DPP-4 inhibitors:

A

they inhibit DPP-4 which acts to inhibit incretins (hormones produced by the GI tract after eating to increase insulin secretion and inhibit glucagon production), therefore increasing incretin activity

36
Q

Give two examples of DPP-4 inhibitors:

A

1) sitagliptin
2) alogliptin

37
Q

Give 2 side effects of DPP-4 inhibitors:

A

1) headaches
2) low risk of acute pancreatitis

38
Q

Describe the action of GLP-1 mimetics:

A

the mimic the action of glucagon-like peptide-1 (the main incretin which acts to increase insulin secretion and inhibits glucagon production)

39
Q

Give two examples of GLP-1 mimetics:

A

1) exenatide
2) liraglutide

40
Q

Give 4 side effects of GLP-1 mimetics:

A

1) reduced appetite
2) weight loss
3) nausea
4) vomiting

41
Q

True or false: T2 diabetics on insulin have to pass a strict criteria in order to drive

A

True

42
Q

Give 8 complications of type 2 diabetes:

A

1) CKD
2) infection
3) gastroparesis
4) diabetic retinopathy
5) diabetic foot
6) autonomic neuropathy
7) peripheral neuropathy
8) hyperosmolar hyperglycaemic state

43
Q

What is the step wise approach for treatment of T2DM patients?

A

Lifestyle
Lifestyle + metformin
Lifestyle + metformin + secondary drug agent &laquo_space;start here if HbA1c >8.5% at diagnosis
Lifestyle + metformin + secondary drug agent + insulin (+/- third line agent – most commonly GLP-1 agonists)