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CSI > 5. Diabetes > Flashcards

5. 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 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 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 T2D?

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

Many cases of T2DM are preventable.

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

Long-term:

  • Reduce incidence of T2DM
  • Reduce incidence of complications associated with diabetes- heart, stroke, kidney, eye and foot problems related to diabetes
  • Reduce health inequalities associated with incidence of diabetes
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10
Q

What is the intervention?

A

NHS DPP has 3 core goals:

  • Achieving a healthy weight
  • Achievement of dietary recommendations
  • Achievement of CMO physical activity
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11
Q

Who is eligible for the NHS DPP?

A

Individuals eligible for inclusion have ‘non-diabetic hyperglycaemia’ [NDH] defined as → HbA1c 42-47 mmol/mol or a fasting plasma glucose (FPG) of 5.5-6.9 mmol/L.

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.

Only individuals 18+

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12
Q

What are the referral routes into the programme?

A
  • Those who have already been identified as having an appropriately HbA1c 42 – 47 mmol/mol 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 FPG 5.5 - 6.9 mmol/l 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
  • Those who are identified with non-diabetic hyperglycaemia through opportunistic assessment as part of routine clinical care
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13
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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14
Q

What are the core defects in T2DM?

A

Insulin resistance in muscle and liver

Impaired insulin secretion by the pancreatic Beta-cells

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15
Q

List all the causes of hyperglycaemia and explain the mechanism of each (check notion)

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 insulin Effect
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16
Q

How is insulin involved in glucose metabolism?

A

Insulin from the blood binds to insulin receptor on skeletal muscle/adipose cell this induces blood glucose to be transported through the Glut-4 receptor via facilitated diffusion into the skeletal muscle/adipose cell glucose is converted to pyruvate via glycolysis pyruvate is converted to acetyl CoA via the link reaction/pyruvate oxidation acetyl CoA is converted to ATP (C) via the Krebs cycle and oxidative phosphorylation when inside the cell, 1 molecule of glucose can gene rate ~30ATP

17
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)

18
Q

What is the primary distribution and function of each GLUT transporter?

A
  • 1
    • Primary distributionEndothelium, erythrocytes
    • FunctionBasal transport (insulin independent)
  • 2
    • Primary distributionKidney, SI, liver, pancreatic beta cells
    • FunctionLow affinity transport (insulin independent)
  • 3
    • Primary distributionNeurones, placenta
    • FunctionHigh affinity transport (insulin independent)
  • 4
    • Primary distributionSkeletal muscle, adipose
    • FunctionInsulin-regulated glucose transport
19
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
20
Q

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

A
  • Liver^ Glucose uptake^GlycogenesisDecreased gluconeogenesis and glycogenolysisDecreased lipolysis
  • Fat^ Glucose uptake and lipogenesisDecreased lipolysis
  • Muscle^ Glucose uptake^ Glycogenesis^ Protein synthesisDecreased protein catabolism
21
Q

What are the core impairments of T2DM?

A

Insulin resistance: Liver, fat and muscle don’t respond to insulin as well. This could cause a stage where lots of insulin is produced (hyperinsulinemia).

Beta-cells eventually become worn down, so they don’t produce as much insulin.

There isn’t enough insulin produced to overcome the resistance, so person becomes diabetic.

In T2DM liver, fat and muscle tissue become insulin resistant and beta-cells are unable to produce enough insulin to compensate so: Increased BG and FFAs

22
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.

23
Q

How is post-prandial glucose tested?

A

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

24
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

25
Q

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

A

Polydipsia: an increase in thirst; 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.

Polyuria: frequent urination; 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.

Polyphagia: a rise in appetite; 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.

26
Q

How can you diagnose T2DM?

A

Symptoms + 1 red glucose range test

OR

No symptoms + multiple red glucose range tests

27
Q

What is the renal threshold for glucose (RTG)?

A

The proximal tubule can only reabsorb a limited 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).

28
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
29
Q

What are the advantages and disadvantages of the HbA1c test?

A
  • Advantages:Takes into account blood glucose for 2-3 monthsEasy to measure (fasting is not needed for A1C assessment and no acute perturbations (e.g., stress, diet, exercise) affect A1C)Cheap
  • Disadvantages: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
30
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

31
Q

What are the most common side effects of Metformin?

A

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

32
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.

33
Q

EAST Framework for behavioural change:

A

https://www.notion.so/aa658c0f43e643ce9219366a96aeb0eb?v=c7fdae19084e435d9d61a46ed0e1ca5f

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