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CSI 1a > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Which glands are included in salivary glands?

A

Parotid, submandibular and sublingual glands (produce amylase)

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2
Q

How does glucose enter the blood stream from the small intestine?

A

Through GLUT-2 receptors

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3
Q

Which type of transport does glucose use?

A

Secondary active transport using Na+/K+ ATPase

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4
Q

Where are GLUT1 transporters distributed and what is it’s affinity for glucose?

A

Endothelium, erythrocytes.

Baseline affinity.

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5
Q

Where are GLUT2 transporters distributed and what is it’s affinity for glucose?

A

Kidney, small intestine, liver, pancreatic beta cells.

Low affinity.

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6
Q

Where are GLUT3 transporters distributed and what is it’s affinity for glucose?

A

Neurones, placenta.

High affinity.

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7
Q

Where are GLUT4 transporters distributed and what is it’s affinity for glucose?

A

Skeletal muscle, adipose tissue.

High affinity.

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8
Q

Which is the only glucose transporter that is insulin dependent?

A

GLUT4

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9
Q

How does glucose enter a muscle cell during hyperglycaemia?

A
  1. Insulin is released from the pancreas (beta cells)
  2. Insulin binds to extracellular insulin receptor on muscle cell.
  3. This activates a signalling cascade (2nd messenger, cAMP).
  4. Translocation of GLUT4 to cell surface membrane.
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10
Q

What is the fate of glucose in a muscle cell?

A
  1. Glucose -> Pyruvate (glycolysis)
  2. Pyruvate -> Acetyl CoA (Pyruvate Oxidation)
  3. Acetyl CoA (TCA Cycle)
  4. Oxidative Phosphorylation.

30 ATP produced.

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11
Q

What form is insulin released in?

A

Proinsulin.

Must be cleaved to form insulin and C-Peptide.

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12
Q

Why do beta cells start the formation of proinsulin?

A

Glucose and Ca2+ influx through GLUT2 transporters trigger it.

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13
Q

What processes does insulin lead to?

A

Increased glucose uptake, increased glycogenesis, decreased gluconeogenesis, increased lipogenesis.

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14
Q

What 2 things does type 2 diabetes cause?

A
  1. Insulin resistance
  2. Pancreatic beta cell dysfunction
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15
Q

How does insulin resistance cause hyperglycaemia?

A
  1. Insulin is unable to bind to insulin receptors on skeletal muscle and adipocytes.
  2. Increased insulin production.
  3. Increase in glucose in the blood due to no translocation of GLUT4.
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16
Q

How does beta cell dysfunction cause hyperglycaemia?

A
  1. Increase in the glucose in the bloodstream that cannot enter cells via GLUT4.
  2. Enters other cells via insulin independent GLUT channels, including the GLUT2 to the pancreas.
  3. Beta cells become worn down and are unable to produce enough insulin.
17
Q

What is the incretin effect?

A

Oral glucose elicits higher insulin secretory response than intravenous glucose does (GLP-1)

18
Q

What are some causes of hyperglycaemia?

A
  • neurotransmitter dysfunction
  • inflammation
  • decreased insulin, increased glucagon, increased lipolysis
  • decreased incretin effect
19
Q

What are some osmotic symptoms of type 2 diabetes?

A

Polydipsia, glycosuria, polyuria, nocturia.

20
Q

How does T2DM get diagnosed?

A
  1. Osmotic symptoms and 1 red glucose reading
    Or
  2. No symptoms and 2 red glucose readings
21
Q

What are some microvascular long term complications with T2DM?

A

Retinopathy, nephropathy, neuropathy.

22
Q

What are some macrovascular long term complications with T2DM?

A

Heart attack, stroke, peripheral vascular disease.

23
Q

What is a urine dipstick test?

A

Looking at the renal threshold. Poor sensitivity.

24
Q

What is impaired fasting glucose?

A

Hepatic insulin resistance. Leads to continuous glucose output from the liver.

Can’t handle glucose in fasting state.

Cannot suppress gluconeogenesis in liver.

25
Q

What is impaired glucose tolerance?

A

Mostly muscle insulin resistance plus impaired post-prandial insulin release. Poor cellular glucose uptake.

Glucose cannot enter skeletal muscle so stays in the circulation.

26
Q

What is glycosylated haemoglobin?

A

Haemoglobin A1C (HbA1C)

Hb with glucose/fructose stuck to it. Survives for 120 days so shows an average.

If >48 mmol/L, suggests T2DM.

Between 42-47 mmol/L, suggests pre diabetes.

27
Q

What are some non-modifiable risk factors for T2DM?

A
  • age >40
  • south Asian and African-Caribbean descent
  • family history
  • predisposition to certain conditions (eg PCOS)
  • gestational diabetes
28
Q

What are modifiable risk factors for T2DM?

A
  • exercise
  • smoking
  • stress/mood
  • diet
  • alcohol
29
Q

What is part of the NHS diabetes prevention programme?

A
  • Physical activity
  • Healthy weight
  • Diet

PHD

30
Q

Who is eligible for the prevention programme?

A

‘Non-diabetic hyperglycaemia’
- HbA1C of 42-47
- fasting plasma glucose of 5.5-6.9 within last 12 months
- 18 or over
- most recent blood result

31
Q

What are positives of Metformin?

A
  • does not cause weight gain unlike other diabetes medications
  • cheap
  • positive associations with reducing LDL and cardiovascular events
32
Q

What is the mechanism of action of metformin?

A

Stimulates movement of GLUT4 to apical side of the membrane, allowing glucose to enter the cell via AMPK (low specificity).

  • suppresses enzymatic reactions of gluconeogenesis
  • inhibits glucagon action
  • downregulates gluconeogenic genes
33
Q

What is AMPK?

A

A second messenger, increases insulin sensitivity.

34
Q

What is the fasting glucose, post prandial glucose, and random glucose of normal metabolism?

A

FG - <6.1 mmol/L
PPG - <7.8 mmol/L
R - <11.1 mmol/L

35
Q

What are the glucose values for impaired fasting glucose?

A

FG - 6.1-6.9
PPG - <7.8
R - <11.1

36
Q

What are the values for impaired glucose tolerance?

A

FG - <7
PPG - 7.8-11.1
R - <11.1

37
Q

What are the glucose values for diabetes?

A

FG - >7
PPG - >11.1
R - >11.1

CSI 1a (8 decks)

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