Type 1 diabetes Flashcards

(35 cards)

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?

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?

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
What is the effect of genetically modifying short acting insulin variants?
Speed up their subcutaneous absorption
25
What MHC is most strongly associated with type I diabetes?
HLA-DQ8
26
Which part of the insulin protein do most T cells recognise?
The C-peptide in the context of HLA-DQ8
27
What does insulin deficiency do to protein and lipid homeostasis?
Increase lipolysis and protein degradation for energy
28
How do you test for retinopathy and how often do you test for it?
Examine the retina Annually
29
How can a hypoglycaemic event cause AMI?
Hypoglycaemia \> Stim. of sympathetic NS \> Tachycardia \> Silent angina \> AMI
31
How can you tell if autoimmunity is antibody mediated?
If there a neonatal syndromes - mother passing autoantibodies to children
32
What is the ideal HbA1c level to reduce complications?
7%
33
How long does it take for ketoacidosis to occur in a long term T1DM patient who is without insulin?
1 day
34
What are the three components required for an artificial pancreas?
Glucose sensor Glucagon pump Insulin pump
35
Why must potassium be administered in the treatment of ketoacidosis?
Because insulin causes it to enter cells