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MEH > 10. Diabetes > Flashcards

10. Diabetes Flashcards

1
Q

What is diabetes?

A

Metabolic disorder characterised by hyperglycaemia due to insulin deficiency, insulin resistance or both.

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2
Q

What is type 1 diabetes characterised by?

A

Progressive loss of all or most of the pancreatic beta cells due to autoimmune attack.

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3
Q

When is type 1 diabetes usually diagnosed?

A

Children and teenage years

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4
Q

How is type 1 diabetes treated?

A

Life-long insulin treatment (must be injected)

Dietary management and exercise also key components

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5
Q

What is the cause of hyperglycaemia in type 2 diabetes?

A

Progressive loss of beta cells along with disorders of insulin secretion and resistance.

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6
Q

When is type 2 diabetes usually diagnosed?

A

Older patients, may be present for a long time before diagnosed.

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7
Q

How is type 2 diabetes managed?

A
  1. Diet
  2. Oral hypoglycaemia drugs
  3. Eventually insulin as it progresses
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8
Q

List the classic triad of symptoms you would expect to see in a patient with Type 1 diabetes mellitus.

A
  1. Polyuria
  2. Polydipsia
  3. Weight loss
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9
Q

Why is polyuria a feature of diabetes?

A

Glucose levels exceed renal threshold, and some glucose is excreted. Less water is reabsorbed into the nephron to account for the increased osmotic load.

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10
Q

Why is polydipsia a feature of diabetes?

A

Excessive water loss from polyuria and osmotic effects of glucose on the thirst centre.

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11
Q

Why is weight loss a feature of type 1 diabetes?

A

Increased proteolysis and lipolysis

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12
Q

How is diabetes easily diagnosed?

A

Measuring plasma glucose levels

Urine ketone and glucose levels

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13
Q

What life threatening crisis can untreated type 1 diabetes lead to?

A

Diabetic ketoacidosis

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14
Q

What affect does insulin deficiency have on the metabolism?

A

Rapid lipolysis, excess FA converted to ketone bodies in the liver.

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15
Q

How can type 1 diabetes result in ketoacidosis?

A

Increased rate of lipolysis in adipose tissue which releases large amounts of fatty acids, the substrate for ketone body formation. H+ associated with the ketones produces a metabolic acidosis.
Activation of the ketogenic enzymes in the liver.

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16
Q

How can ketoacidosis be detected on the breath?

A

Acetone is a volatile ketone body that can be smelt on the patients breath

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17
Q

What are the symptoms of ketoacidosis?

A 
Prostration - exhaustion
Hyperventilation
Nausea and vomiting
Dehydration
Abdo pain
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18
Q

Rather than the triad, which symptoms are patients with Type 2 diabetes more likely to be present with?

A

Lack of energy
Persistant infections (genital thrush)
Slow healing
Visual problems

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19
Q

If diet management fails, what oral hypoglycaemic drugs can be used to treat type 2 diabetes?

A

Sulphonylurea - increase insulin release from beta cells

Metformin - reduces gluconeogenesis

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20
Q

In which tissues is uptake of glucose determined purely by extracellular glucose concentration, what are the complications of this?

A

Peripheral nerves, eye and kidney.
During hyperglycaemia, the intracellular [glucose] increases and it metabolised by aldose reductase.
This reaction depletes NADH, increases disulphide bond formation in proteins, altering structure and function.
Accumulation of product sorbitol causes osmotic damage.

21
Q

What changes to the plasma proteins occur in persistant hyperglycaemia?

A

Glycation of plasma proteins such as lipoproteins and haemoglobin.

22
Q

How goes glycation of plasma proteins affect their function?

A

Forms stable covalent linkages, changing the charge and overall structure of the proteins, therefore affecting function.

23
Q

What is HbA1c?

A

Glucose reacts with Hb to form glycated Hb.

24
Q

How is HbA1c used clinically?

A

Percentage of Hb glycated is a good indicator of how effective glucose control has been.

25
Q

What does HbA1c indicate?

A

The average blood glucose concentration over the preceding 2-3 months (RBC lifespan).

26
Q

What percentage of Hb is glycated in normal healthy individuals?

A

4-6%

27
Q

What macrovascular complications are associated with diabetes?

A
  • Stroke risk
  • MI risk
  • Poor peripheral circulation - feet
28
Q

What microvascular complications are associated with diabetes?

A
  • Diabetic eye disease
  • Diabetic nephropathy
  • Diabetic neuropathy
  • Diabetic feet
29
Q

How does diabetes cause eye disease?

A

Retinopathy - damage to blood vessels in retina can lead to blindness
Glaucoma - osmotic effects of glucose can alter lens and cause visual problems
Cataracts

30
Q

How does diabetes cause nephropathy?

A

Damage to glomeruli, poor blood supply due to changes in the kidney blood vessels, or damage from UTI’s which are more common in diabetics.

31
Q

What is an early sign of nephropathy?

A

Increased protein in the urine - microalbuminuria

32
Q

How does diabetes cause neuropathy?

A

Damage to peripheral nerves - loss/changes in sensation, alteration in function of ANS

33
Q

What is diabetic feet?

A

Poor blood supply, damage to nerves and increased risk of infection make the feet vulnerable.
- Loss of feet through gangrene

34
Q

What is metabolic syndrome?

A

The co-occurance of multiple CVD risk factors in the same individual.

35
Q

Why are oral hyopglycaemic agents avoided in Type 1 diabetes?

A

Risk of hypoglycaemia

36
Q

How can C peptide be used to differentiate between T1 and T2 diabetes?

A

Present in patients with T2 but absent in patients with T1

37
Q

Which patients are at risk of spontaneous ketoacidosis?

A

Type 1

38
Q

Why is metformin given to T2 diabetics?

A

Inhibits gluconeogenesis

39
Q

Why are sulphonylureas given to T2 diabetics?

A

Binds directly to ATP sensitive K+ ATPase, causing it to close and triggering hyper polarisation and insulin release.

40
Q

How does insulin deficiency lead to hyperglycaemia?

A

Glycogenolysis increases
Gluconeogenesis increases
Peripheral glucose uptake reduced

41
Q

Briefly explain why insulin has to be injected and cannot be taken orally in pill form.

A

Insulin is a peptide hormone so would be broken down in the gastrointestinal tract to its consituent amino acids if it were to be taken orally.

42
Q

Is the glycation of haemoglobin to form HbA1c catalysed by an enzyme?

A

No, glycation is non-enzymatic.

43
Q

Name the two most significant factors underlying the aetiology of metabolic syndrome.

A
  1. Central obesity

2. Insulin resistance

44
Q

Why is tiredness/weakness a symptom of T1 diabetes?

A

loss of muscle mass, dehydration

45
Q

Outline the major ultrastructural features of the -cell that relate to the synthesis, storage and secretion of insulin

A

Many mitochondria – high energy requirement
Extensive RER
Extensive Golgi
Many storage vesicles
Many microtubules & microfilaments – active secretory tissue (exocytosis).

46
Q

How does insulin lower blood glucose concentration?

A

Glucose uptake into muscle and adipose tissue
 Stimulating glycogenesis in muscle and liver
 Stimulating glucose oxidation in liver.
 Stimulating lipogenesis in liver and adipose tissue.
 Inhibits gluconeogenesis in liver.

47
Q

What effect do catecholamines have on insulin secretion? Why is this beneficial?

A

Inhibit insulin secretion, enables a raise in blood glucose under stressful conditions

48
Q

What effect do gut hormones have on insulin secretion?

A

Stimulate insulin secretion after a meal, so the digestion components can be absorbed quickly to avoid major increases in their concentration.

MEH (19 decks)

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