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MD1 Metabolism > Autoimmune Insulin Dependent Diabetes > Flashcards

Autoimmune Insulin Dependent Diabetes Flashcards

1
Q

Is the trigger for coeliac disease endogenous or exogenous?

A

Exogenous

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2
Q

How is type 2 diabetes often picked up?

A

Not by clinical symptoms but by screening

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3
Q

What is C peptide?

A

Part of proinsulin

Cleaved off in beta cell and secreted with insulin

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4
Q

Why is C peptide measured?

A

Measure of endogenous insulin production

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5
Q

How much more common is type 2 diabetes than type 1?

A

10x

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6
Q

How is the incidence of type 1 diabetes changing?

A

Increasing

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7
Q

Is type 1 diabetes present at birth?

A

No

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8
Q

Why is there a significant burden of disease in type 1 diabetes?

A

Obligate use of exogenous insulin

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9
Q

How is type 1 diabetes treated?

A

Short- or long-acting insulin

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10
Q

What is the pattern of destruction of beta cells in the pancreas in type 1 diabetes?

A

From normal beta cell function to none at all

Not uniform destruction

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11
Q

What causes the disease process in type 1 diabetes?

A

Inflammatory infiltrate

  • T cells
  • B cells
  • Macrophages
  • DCs
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12
Q

Why are islets in type 1 diabetes called pseudo-atrophic?

A

Still have alpha cells and produce glucagon

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13
Q

What do CD8 T cells release to destroy beta cells in type 1 diabetes?

A

Perforin

Granzymes

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14
Q

What are the clinical features of type 1 diabetes?

A 
Symptoms
- Polyuria
- Polydipsia
- Polyphagia
Weight loss
Ketoacidosis
Insulin requirement
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15
Q

Do people with type 1 diabetes have autoantibodies?

A

Yes

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16
Q

What proportion of people with type 2 diabetes develop autoantibodies, and what does this mean?

A

10%

Progressing to T1D slowly

17
Q

What are some of the autoantibodies that can be detected in type 1 diabetes?

A

Insulin autoAbs
GAD autoAbs
IA-2 autoAbs

18
Q

What is the key self-antigen in the development of type 1 diabetes?

A

Insulin

19
Q

Are all the self-antigens recognised by autoantibodies in type 1 diabetes specific to beta pancreatic cells?

A

No - some are, some aren’t

20
Q

Does everyone with type 1 diabetes have all autoantibodies?

A

Not everyone has each autoAb but almost everyone does have them

21
Q

Why are autoantibodies in type 1 diabetes diagnostic of, but not disease causing?

A

Because Ags recognised intracellular > Abs can’t bind and block function

22
Q

How can babies get congenital autoimmunity?

A

Possibility of crossing placenta if mother has autoAbs

Wanes with half life of maternal Abs

23
Q

What is the relationship between the time course and disease process in type 1 diabetes?

A

Quite well > get sick very suddenly, but disease process going on for a long time

24
Q

Is there an age limit to developing type 1 diabetes?

A

No, but most common in childhood

25
Q

What is the risk of developing type 1 diabetes in monozygotic twins, where one sibling develops it in childhood?

A

In non-diabetic twin at start

  • Develop autoAbs
  • Increased risk of developing type 1 diabetes later in life
26
Q

What is the rate of loss of function in type 1 diabetes?

A

Unknown

27
Q

What are the stages proposed for type 1 diabetes?

A 
Variable genetic and environmental risk
Stage 1 - pre-symptomatic T1D
- Beta cell autoimmunity
- Normoglycaemia
Stage 2 - pre-symptomatic T1D
- Beta cell autoimmunity
- Dysglycaemia
- No symptoms
Stage 3 - symptomatic T1D
- Beta cell autoimmunity
- Dysglycaemia
- Symptoms
28
Q

What is APS-I syndrome?

A

Loss of thymic tolerance to peripheral Ags
Because of mutations in AIRE gene
Multiple autoimmune disorders
- 18% have T1D

29
Q

What is immune dysfunction, polyendocrinopathy, enteropathy, X-linked (IPEX)?

A

Mutation of FoxP3 gene

80% of children develop T1D

30
Q

What can reverse IPEX?

A

Bone marrow transplant

31
Q

Which gene associations are the strongest with type 1 diabetes?

A

HLA

Insulin - polymorphic expression in thymus

32
Q

Which two HLA are strongly associated with type 1 diabetes?

A

HLA-DQ2 and -DQ8

33
Q

What is the pathogenesis of type 1 diabetes?

A
  1. Proinsulin-reactive T cells escape negative selection
  2. Become activated due to high concentration/altererd Ag
  3. Recognition of beta cells
  4. CD8 T cell dominant destruction
  5. Spreading to other specifications
34
Q

What are possible environmental triggers for autoimmunity?

A 
UV
Diet
Drugs - not for T1D
Hygiene hypothesis
Infection
35
Q

What is wrong with the current treatment of type 1 diabetes?

A

Incapable of mimicking physiological glucose control > can’t prevent complications
Multiple injections per day

36
Q

What are the possible future therapies for type 1 diabetes?

A 
Restore insulin production
- Transplant/regenerate
Abolish disease recurrence
- Correct autoimmunity
In meantime
- Islet transplantation
- Artificial pancreas
37
Q

What are some possible avenues of correcting autoimmunity?

A 
Immunosuppression
Immunomodulatory drugs
Anti-inflammatory biologicals
Ag specific
Cell therapy
38
Q

Can hypoglycaemia unawareness be treated with islet transplantation?

A

Yes, with associated freedom from severe hypoglycaemic events

39
Q

What are the problems with islet transplantation?

A 
Availability of organ doners
Viability and function of islets
Immunosuppression - needed for
- Rejection
- Recurrence of T1D
Longevity of graft
All-sensitisation
Cost

MD1 Metabolism (18 decks)

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