Type 1 diabetes Flashcards

1
Q

Why don’t autoantibodies play an important role in pathogenesis for type 1 diabetes?

A

Because the ag is intracellular

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1
Q

How do you diagnose type 1 diabetes?

A

Presenting symptoms: Weight loss, polyuria, polyphagia, polydipsia, fatigue, pain

Autoantibodies

Glucose tolerance test

HbA1c

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2
Q

When are autoantibdoies found in diabetes development?

A

Long before the onset of symptoms

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3
Q

Do you get polyuria because of polydipsia or vice versa?

A

Vice versa - polydipsia because of polyuria

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4
Q

Which tissues are preferentially damaged in diabetes?

A

The retina

The nerves

The kidney

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5
Q

When is glargine taken?

A

At bedtime - to control overnight blood glucose

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5
Q

What are the consequences of neuropathy?

A

Sensory disturbance:

Numb feet (+ poor circulation) + injury > gangrene > Amputation

Autonomic:

Gastric stasis

Impotence

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6
Q

What type of insulin therapy is determir?

A

Long acting

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6
Q

What does a fructosamine test tell you?

A

The level of glycosylation of amines - similar to HbA1c

  • may be indicated if there is blood loss
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7
Q

What is an example of an open loop system?

A

Insulin pump

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8
Q

What type of insulin therapy is isophane?

A

Long acting

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9
Q

Below what blood glucose level is hypoglycaemia an emergency?

A

4mmol/L

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10
Q

What type of insulin therapy is glulisine?

A

Short acting

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11
Q

High postprandal glucose but low HbA1c is indicative of what?

A

Unrecognised blood loss

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13
Q

How do we know type 1 diabetes is an autoimmune disease?

A
  • demonstrate presence of antibody to normal tissue
  • establish the molecular identity of antigen
  • induce/identify similar antibodies and pathology in animal model
  • benefit of immunosuppression,
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13
Q

Why is it thought that determir causes weight lose?

A

It can cross the BBB (due to the addition of a FA) allowing it to act on the hypothalamus to suppress apeptite

14
Q

What type of insulin therapy is glargine?

A

Long acting

15
Q

What are the two limitations of islet cell transplantation?

A
  1. Availability of Islet cells to donate
  2. Chronic immunosuppression
16
Q

What are some new treatments indevelopment?

A

Transplantation, regeneration of islets

Correct autoimmunity - avoid reccurrence

Artificial pancreas

17
Q

Describe the therapy regimen called basal bolus?

A

One long acting insulin given at bedtime - typically glargine or determir

One short acting prior to meals - Apart, glulisine or lispro

18
Q

How do you test for nephropathy? How often do you test for it?

A

Protein in urine

Annually

20
Q

What percentage of risk is accounted for by genetics?

A

30-40%

22
Q

Why do you get polyuria?

A

Because of the diuretic effect of glucose

23
Q

Whis is APS-1 syndrome?

A

Loss of thymic tolerance due to mutations of AIRE gene

24
Q

What is the effect of genetically modifying short acting insulin variants?

A

Speed up their subcutaneous absorption

25
Q

What MHC is most strongly associated with type I diabetes?

A

HLA-DQ8

26
Q

Which part of the insulin protein do most T cells recognise?

A

The C-peptide in the context of HLA-DQ8

27
Q

What does insulin deficiency do to protein and lipid homeostasis?

A

Increase lipolysis and protein degradation for energy

28
Q

How do you test for retinopathy and how often do you test for it?

A

Examine the retina

Annually

29
Q

How can a hypoglycaemic event cause AMI?

A

Hypoglycaemia > Stim. of sympathetic NS > Tachycardia > Silent angina > AMI

31
Q

How can you tell if autoimmunity is antibody mediated?

A

If there a neonatal syndromes - mother passing autoantibodies to children

32
Q

What is the ideal HbA1c level to reduce complications?

A

7%

33
Q

How long does it take for ketoacidosis to occur in a long term T1DM patient who is without insulin?

A

1 day

34
Q

What are the three components required for an artificial pancreas?

A

Glucose sensor

Glucagon pump

Insulin pump

35
Q

Why must potassium be administered in the treatment of ketoacidosis?

A

Because insulin causes it to enter cells