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Endocrinology > Type 1 Diabetes > Flashcards

Type 1 Diabetes Flashcards

1
Q

How much of all diabetes does T1DM account for?

A

10%

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2
Q

What age group does T1DM occur?

A

<30yrs

Peak 12yrs

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3
Q

Define T1DM

A

autoimmune destruction of pancreatic beta-cells via abnormal T-cell response

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4
Q

What are the precipitating causes of T1DM?

A
  • Viral infection (e.g. rubella)
  • Environmental toxins or foods
  • Autoimmune (hypersensitivity type 4) couple be initiated by cytokine response to infection
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5
Q

Can susceptibility to T1DM be inherited?

A

Yes

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6
Q

Where are the susceptibility genes for T1DM located?

A

Chromosome 6 in the major histocompatibility complex (MHC).

Approx. 50% of genetic susceptibility to diabetes resides in HLA genes (HLA genotypes DR 3/4 and DQ A1)

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7
Q

What genotypes cause T1DM?

A

HLA DR3/4

HLA DQ A1

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8
Q

Is the genetic region also a region of other autoimmune diseases?

A

Yes. Suggesting that T1DM patients are more susceptible to other autoimmune disorders such as Graves’ Disease, Addison’s Disease, and celiac disease

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9
Q

Can T1DM be caused by an autoimmune response?

A

Yes.
A proportion of patients demonstrate abnormal B-cell response with circulating antibodies against various beta-cell proteins

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10
Q

List the main autoantibodies in T1DM

A

IAA - Insulin autoantibody
GAD65 - glutamic acid decarboxylase
ICA - islet cell antibody

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11
Q

What is the major complication of T1DM? And how does it develop?

A

Diabetic Ketoacidosis

  1. lack of glucose in cells results in catabolism of fats and proteins
  2. excessive amounts of FAs and their metabolites (ketones) in the blood
  3. ketoacids (b-hydroxybutyic acid and acetoacetic acid) are excreted in the urine (ketouria)
  4. Ketones produced at a quicker rate than they are metabolised in the liver (ketoacidosis)
  5. As dehydration develops, GFR decreases, excretion of acids decreased, resulting in decompensated metabolic acidosis
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12
Q

What’s the pathophysiology and symptoms of T1DM?

A
  1. Insulin deficit
  2. Decreased transportation and use of glucose by body cells - causing hyperglycaemia
  3. excess glucose spills into urine - glucosuria
  4. Levels of glucose in the filtrate exceed the capacity of the renal tubular transport exerting an osmotic pressure in the filtrate, thus large volume of urine is excreted (polyuria) with loss of fluid and electrolyte
  5. Excessive fluid loss through the urine and hyperglycaemia (glucose is a solute) draws water from the cells resulting in dehydration, thus thirst (polydipsia)
  6. Lack of nutrients enter the cells stimulate appetite (polyphagia)
  7. If insulin deficit is severe or prolonged, additional consequences develop: ketoacidosis
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13
Q

How does glucosuria result?

A

decreased transportation and glucose by body cells results in hyperglycaemia, this in turn is filtered into the urine

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14
Q

How does polyuria result?

A
  • Levels of glucose in the filtrate exceed the capacity of renal tubular transport
  • This results in osmotic pressure in the filtrate and drives water into the urine
  • Large volumes of urine produced (with fluid and electrolyte loss)
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15
Q

How does polydipsia result?

A

Excessive loss of fluid through urine and hyperglycaemia draws water out of cells (glucose is a solute and this plasma has higher osmolality)
This results in dehydration
Stimulates thirst sensors

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16
Q

How does polyphagia result?

A

Lack of nutrients entering cells (due to severe loss) stimulate appetite

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17
Q

What is ketoacidosis?

A

Large amount of ketones in the body

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18
Q

What are ketones made of?

A

Acetone and 2 organic acids (b-hydroxybutyric acid and acetoacetic acid)

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19
Q

How does ketoacidosis result?

A
  1. Glucose can’t get into cells
  2. Cells resort to catabolism of proteins and fat for energy source
  3. Excessive amounts of ketones result in the blood due to FA oxidation
  4. Liver limited in the amount of lipids, FAs, and ketones it can process within a given time
  5. Excessive amounts of ketones accumulate in the blood
  6. Ketoacids bind to bicarbonate buffer in the blood, decrease its concentration
  7. Blood pH decreases and ketoacidosis results
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20
Q

How does dehydration result in T1DM patients?

A
  1. Decreased insulin
  2. Increase gluconeogenesis and decreased glucose uptake
  3. Hyperglycaemia
  4. Glucosuria
  5. Osmotic diuresis (+polyuria)
  6. Dehydration
21
Q

What are the main themes for treatment of T1DM?

A

1) Diet and exercise

2) Insulin replacement

22
Q

Comment on diet treatment for T1DM

A
  • Maintaining optimum body weight
  • More complex CHOs with lower GI
  • Maintaining low cholesterol and lipid levels
  • Food intake must match available insulin and metabolic needs, including activity level
23
Q

Comment on exercise treatment for T1DM

A
  • Can promote uptake of glucose by muscle cells

- Weight control, reduce stress, improve CV fitness

24
Q

What is the risk of exercise in T1DM patients

A

Hypoglycaemia with strenuous and prolonged exercise due to increased uptake of glucose by muscle and increased action of insulin

25
Q

What are the different forms of insulin treatment available for T1DM patients?

A
  1. Rapid-onest, short acting insulin
  2. Intermediate-onset insulin
  3. Slow-onset, long-acting insulin
26
Q

How is insulin administered?

A

Subcutaneous injection

27
Q

What type of insulin is currently used for treatment?

A

Recombinant human insulin (Humulin)

28
Q

Define hypoglycaemia

A

Plasma [Glucose] <4mmol/L

Insulin shock

29
Q

Describe the onset of hypoglycaemia

A

Occurs suddenly following exercise, dosage error, vomiting, skipped meal

30
Q

What are the complications of hypoglycaemia

A

1) Impaired neurological function: poor concentration, slurred speech, lack of coordination, staggering gait - patient has the same appearance as a drunken individual
2) Over stimulation of sympathetic nervous system (adrenaline and glucagon): Increased pulse rate, moist skin, tachycardia, tremers.

If untreated and plasma [glucose] <2.5mmol/L will cause neuroglycopenia resulting in:

  1. Loss of conciousness
  2. Seizures
  3. Coma
  4. Death
31
Q

How would you treat hypoglycaemia?

A

If conscious:
Give high GI CHO immediately (fizzy non-diet drink or choclate)

Or

Glucogel 40% dextrose

If unconcious
IV 50% dextrose

32
Q

What tests can be used for Dx?

A

Fasting blood glucose (min. 8hrs no food/drink)
<= 6 - Normal
6.1-6.9 - Impaired
>=7 - Diabetes

Oral glucose tolerance test (OGTT)
<=7.7 - Normal
7.8-11 - Impaired
>=11.1 - Diabetes

HbA1c
42-47 - pre-diabetes
>48 - diabetic

33
Q

What is the significance of HbAc1?

A

HbAc1 is a form of haemoglobin that is measured primarily to identify 3month average of [Glucose]plasma

Test is limited to 3months lifespan of RBCs

Formed in a non-enzymatic glycation pathway by haemoglobin exposure to glucose

NOT YET IN USE IN GLASGOW

34
Q

What is the genetic predisposition to T1DM?

A
  • 1/3rd of patients
  • Polygenic (multiple genes required)
  • Main gene on chromosome 6: MHC-HLA genotypes DR 3/4 and DQ A1
35
Q

What is the environmental predisposition to T1DM?

A
  • Idiopathic

- Either direct beta-cell toxicity or immune-stimulating toxicity (mumps, Coxsakie)

36
Q

What’s the pathology of T1DM?

A
  1. Pancreatic islets are infiltrated with lymphocytes (insulitis)
  2. After inflammation islets becomes atrophic
  3. Immune destruction of beta-cells follow (insulin deficiency)

*Marked hyperglycaemia only occurs when 80-90% of beta-cell functionality is lost

37
Q

When does hypeglycaemia occur with respect to pancreatic function?

A

Marked hyperglycaemia only occurs when 80-90% of beta-cell functionality is lost

38
Q

List the T1DM-associated autoantibodies

A

Insulin associated antibody (IAA)
Islet cell antibody (ICA)
Glutamic acid decarboxylase (GAD65)

39
Q

What are the symptoms of T1DM?

A
  1. Hyperglycaemia
  2. Glucosuria
  3. Polyuria
  4. Polydipsia
  5. Polyphagia
  6. Weight loss
40
Q

What’s the biochemistry profile of T1DM

A

Fasting (hr) glucose >= 7mmol/L
Random glucose >= 11.1mmol/L
HbA1c >= 48mmol/L
OGTT >=11.1mmol/L

Test for C-peptide deficiency to determine decline in B-cell function

1 + symtoms = diabetic
2 + no symptoms = diabetic

41
Q

What’s the biochemical significance of C-peptide?

A

C-peptide is produced and released into the blood during insulin synthesis in beta-pancreatic cells.

It is produced in equal concentrations to insulin produced

As insulin cannot be measured in the blood, C-peptide acts as a clinical measure of insulin present.

42
Q

What does management of T1DM involve?

A
  1. Achieving good glyacemic control

2. Advice regarding regular physical activity

43
Q

Treatment for T1DM?

A

Insulin injections

44
Q

Types of insulin injections?

A
  1. Short-acting insulin rapid onset
  2. Short acting insulin analogues
  3. Longer-acting slow onset insulin
45
Q

Describe short-acting rapid-onset insulin

A

Starts working within30-60minutes and lasts 4-6hrs

Taken 15-30min before meal

46
Q

Describe short-acting insulin analogues

A

Faster onset and shorter duration
Does not improve diabetic control
Used with evening meals in patients prone to nocturnal hypoglycemia

47
Q

Describe Longer-acting slow onset insulin

A

Insulin premixed with retarding agents (e.g. zinc)
intermediate or long-acting
Slow release

48
Q

What is the basal-bolus routine?

A

A basal-bolus routine involves taking a longer acting form of insulin to keep blood glucose levels stable through periods of fasting and separate injections for shorter-acting insulin to prevent rises in blood glucose levels resulting from meals.

Basal = background
Bolus = at meal time

Endocrinology (11 decks)

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