diabetes Flashcards

1
Q

What is prediabetes?

A

Blood sugars are higher than usual, but not high enough to be diagnosed with T2DM.

Are at a high risk of developing T2DM.

(Not a clinical term recognised by WHO → Starting to be used more by healthcare professionals and in the media to describe people who are at high risk of T2DM.

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2
Q

What are other names for prediabetes?

A

Borderline Diabetes

Impaired Glucose Regulation (IGR)

Non-diabetic hyperglycaemia

Impaired fasting glucose (IFG) together with Impaired Glucose Tolerance (IGT)

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3
Q

What are the symptoms of prediabetes?

A

Don’t have any symptoms.

If you start to have any symptoms of T2DM it means you have probably already developed it.

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4
Q

List of modifiable factors that increase risk of diabetes

A

Smoking

History of high BP

Being overweight, especially with centripetal obesity

Sedentary lifestyle (physically inactive → Not doing enough physical activity; sedentary → sitting or lying down for long periods).

Alcohol

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5
Q

List of non-modifiable factors that increase risk of diabetes

A

Older age; more at risk of white and over 40 OR over 25 and Afro-Caribbean, Black African or South Asian.

Having a parent, brother, sister or child with diabetes

Polycystic Ovary Syndrome (PCOS associated with insulin resistance)

Mental health conditions (e.g. schizophrenia, bipolar disorder, depression)

Antipsychotic medication (risk is quite low)

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6
Q

Roughly what % of people who have diabetes have T2DM?

A

90%

(Can come on slowly (Insidious onset), usually over the age of 40. Signs may not be obvious or there may be no signs at all, therefore it might be up to 10 years before diagnosis

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7
Q

What is the NHS diabetes prevention programme?

A

Joint commitment from NHS England, Public Health England and Diabetes UK, to deliver at scale, evidence based behavioural interventions for individuals identified as being at high risk of developing T2MD.

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8
Q

Why implement the NHS diabetes prevention programme?

A

Strong international evidence that behavioural interventions can significantly reduce risk of developing condition, through reducing weight, increasing physical activity and improving the diet of those at high risk

Diabetes treatment → 10% of annual NHS budget.

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9
Q

What are the aims of the programme?

A
  • To reduce the incidence of Type 2 diabetes;
  • To reduce the incidence of complications associated with diabetes -
    heart, stroke, kidney, eye and foot problems related to diabetes; and
  • Over the longer term, to reduce health inequalities associated with
    incidence of diabetes.
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10
Q

How was the NHS DPP developed?

A

Developed by delivery team from NHS England, Public Health England, and Diabetes UK.

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11
Q

Interventions and goals:

A

The NHS DPP behavioural intervention is underpinned by three core goals:
* achieving a healthy weight
* achievement of dietary recommendations
* achievement of CMO physical activity recommendations

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12
Q

DPP model specification

A
  • must be made up of at least 13 sessions
  • at least 16 hours face to face contact time
  • spread across min 9 months
  • each session lasts between 1-2 hours

people will receive support on setting and achieving goals to making positive changes to lifestyles in order to reduce risk of developing T2DM.

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13
Q

Who is eligible to go on DPP?

A

Individuals eligible for inclusion have ‘non-diabetic hyperglycaemia’ (NDH), defined as having an HbA1c 42 – 47 mmol/mol (6.0 – 6.4%) or a fasting plasma glucose
(FPG) of 5.5 – 6.9 mmol/l.

The blood result indicating NDH must be within the last 12 months to be eligible for referral and only the most recent blood reading can be used.

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14
Q

Referral routes to DPP:

A
  • Those who have already been identified as having an appropriately
    elevated risk level (HbA1c or FPG) in the past and who have been
    included on a register of patients with high HbA1c or FPG;
  • The NHS Health Check programme, which is currently available for
    individuals between 40 and 74. NHS Health Checks includes a diabetes
    filter, those identified to be at high risk through stage 1 of the filter are
    offered a blood test to confirm risk; and
  • Those who are identified with non-diabetic hyperglycemia through
    opportunistic assessment as part of routine clinical care.
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15
Q

Which cells release insulin and which release glucagon?

A

Beta-cells → Insulin → Converts glucose into glycogen.

Alpha-cells → Glucagon → Converts glycogen into glucose.

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16
Q

What are the core defects in T2DM?

A

Insulin resistance in muscle and liver (hyperinsulinemia)

Impaired insulin secretion by the pancreatic Beta-cells

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17
Q

List causes of hyperglycaemia

A
  • increased glucose reabsorption
  • decreased glucose uptake
  • increased lipolysis
  • inflammation
  • NT dysfunction
  • increased glucagon secretion
  • increased hepatic glucose production
  • decreased insulin secretion
  • vascular insulin resistance
  • decreased incretin effect
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18
Q

Mechanism for increased glucose reabsorption

A

^ renal glucose reabsorption by sodium/glucose co-transporter 2 (SGLT2) and the ^ed threshold for glucose spillage in the urine contribute to the maintenance of hyperglycaemia.

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19
Q

Mechanism for decreased glucose uptake

A

Beta-cell failure therefore less insulin secreted

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20
Q

Mechanism for increased lipolysis

A

Insulin resistance in adipocytes results in accelerated lipolysis and ^ed plasma FFA levels, both of which aggravate the insulin resistance in muscle and the liver and contribute to Beta-cell failure.

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21
Q

Mechanism of Inflammation

A

Activates and ^ expression of several proteins that suppress insulin-signalling pathways making the body less responsive to insulin and increasing the risk for insulin resistance.

22
Q

NT Dysfunction mechanism

A

Resistance to appetite-suppressive effect of a number of hormones + low brain dopamine + increased brain serotonin level contribute to weight gain, which exacerbates the underlying resistance.

23
Q

Mechanism of increased glucagon secretion

A

insulin inhibits glucagon secretion from alpha cells-over time after lots of insulin is being produced, alpha cells become insulin resistant→ glucagon secretion increases→blood glucose increases

24
Q

Mechanism of increased hepatic glucose production

A

increased glucagon levels and enhanced hepatic sensitivity to glucagon contribute to the excessive glucose production by the liver

25
Q

Mechanism of decreased insulin secretion

A

Beta-cell failure due to:

  • GLP resistance
  • Insulin resistant adipose, muscle and liver tissue.
26
Q

Mechanism of vascular insulin resistance

A

prolonged exposure to high levels of insulin causes increased vasculature resistance

27
Q

Decreases incretin Effect

A

the incretin ‘glucagon-like peptide 1’ (GLP1) stimulates β-cells to secrete insulin

28
Q

How is insulin involved in glucose metabolism?

A
  • Insulin from blood binds to insulin receptor in myocytes
  • Induces blood glucose to be transported through GLUT4 receptor via facilitated diffusion
  • Glucose converted to pyruvate via glycolysis
  • Pyruvate converted to acetyl CoA via pyruvate oxidation
  • Acetyl CoA converted to ATP via TCA and oxidative phosphorylation
29
Q

Where are GLUT-receptors not found?

A

Kidney and SI

30
Q

How do GLUT and SGLT receptors transport glucose into our body cells, respectively?

A

GLUT - Facilitated diffusion

SGLT - Active Transport (glucose transported into luminal epithelial cells in the kidney and small intestine)

31
Q

What is the primary distribution and function of GLUT1 transporter?

A

Endothelium, erythrocytes

Used for basal transport (insulin independent)

32
Q

What is the primary distribution and function of GLUT2 transporter?

A

Kidney, SI, liver, pancreatic beta cells

Used for low affinity transport (insulin independent)

33
Q

What is the primary distribution and function of GLUT3 transporter?

A

Neurones, placenta

Used for high affinity transport (insulin independent)

34
Q

What is the primary distribution and function of GLUT4 transporter?

A

Skeletal muscle, adipose

Used for insulin-regulated glucose transport

35
Q

What happens if your blood glucose is high, but you are insulin resistant?

A
  • glucose is not taken into skeletal muscle and adipose cells
  • glut 1, 2, 3 cells (i.e. endothelium, erythrocytes, kidney, small intestine, liver, pancreatic beta cells, neurones, placenta) will take in lots of glucose
36
Q

What are the additional functional effect of insulin on the liver, muscle and fat?

A
37
Q

What are the differences in pathogenesis between T1DM and T2DM?

A

T1DM → Very little/no insulin produced at all

T2DM → Little insulin produced + insulin resistant cells.

38
Q

How is post-prandial glucose tested?

A

OGTT - get patient to fast for 8 hrs then give them a 75g oral glucose load, then measure their blood sugar 2 hours after.

39
Q

What is the difference between impaired fasting glucose vs. impaired glucose tolerance?

A

Impaired fasting glucose: predominantly hepatic insulin resistance leads to continuous glucose output from the liver

Impaired glucose tolerance: predominantly muscle insulin resistance plus impaired post-prandial insulin release results in poor cellular glucose uptake.

Impaired fasting glucose and impaired glucose tolerance can occur together or separately, one could occur first

40
Q

What are the symptoms of T2DM (can also be T1DM)?

A

Polydipsia (increase in thirst), Polyuria (frequent urination), Polyphagia (rise in appetite)

41
Q

Why does polydipsia occur in T2DM?

A

when blood glucose levels get high, your kidneys produce more urine in an effort to remove the extra glucose from your body, leaving you feeling dehydrated.

42
Q

Why does polyuria occur in T2DM?

A

when blood glucose levels are too high, your body will try to remove some of the excess glucose via urination. This also leads to your kidneys filtering out more water, which leads to an increased need to urinate.

43
Q

Why does polyphagia occur in T2DM?

A

in people with diabetes, glucose can’t enter cells to be used for energy. This can be due to either low insulin levels or insulin resistance. Because your body can’t convert this glucose to energy, you’ll begin to feel very hungry.

44
Q

How can you diagnose T2DM?

A

Symptoms + 1 red glucose range test

OR

No symptoms + multiple red glucose range tests

45
Q

What is the renal threshold for glucose (RTG)?

A

The proximal tubule can only reabsorb alimited amount of glucose (~375 mg/min),
known as the transport maximum.

When the blood glucose level exceeds about 60–180 mg/dL, the proximal tubule becomes overwhelmed and begins to excrete glucose in the urine. This point is called the renal threshold for glucose (RTG).

46
Q

What is the HbA1c test?

A

HbA1c → Hb that has been glycosylated.

  • this process occurs non-enzymatically and can occur with the monosaccharides glucose,
    fructose, and galactose
    (although glucose least easily)
  • formation of HbA1C occurs proportionately to plasma glucose levels
  • therefore, HbA1C levels can be used to diagnose and monitor diabetes
47
Q

Advantages of HbA1c test

A

Takes into account blood glucose for 2-3 months

Easy to measure (fasting is not needed for A1C assessment and no acute perturbations (e.g., stress, diet, exercise) affect A1C)

Cheap

48
Q

Disadvantages of HbA1c

A

Only an approximate measure.

Not reliable in certain conditions e.g. Pregnancy (amount of Hb changes/rapid changes in glucose management) → Renal failure + Sickle cell

49
Q

What is used for first-line treatment of T2DM and how does it work?

A

Metformin

Reduces the amount of sugar your liver releases into your blood. It makes your body respond better to insulin by stimulating GLUT-4 translocation

It doesn’t cause weight gain, unlike some other diabetes medicines

Lower risk to hypoglycaemia

Best to take with a meal to reduce the side effects

50
Q

What are the most common side effects of Metformin?

A

Sick, diarrhoea, stomach-ache and going off your food.

51
Q

What is the behavioural insight approach?

A

Approach that uses knowledge of how and why people behave, to encourage positive behaviour change.

Behavioural insights consider all aspect of behaviour (e.g. psychology, social anthropology and behavioural economics) and acknowledge the importance of the fast and intuitive automatic system driving behaviour.

Behavioural insights are most helpful where individuals want to make positive behaviour changes but struggle to do so.