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Endocrinology > 15. Type I diabetes mellitus > Flashcards

15. Type I diabetes mellitus Flashcards

1
Q

What type of people are likely to get type I diabetes?

A

Lean, young individuals

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2
Q

Why is there some ambiguity regarding the group of people most likely to suffer from type I diabetes?

A

• More and more older individuals diagnosed with insulin deficiency
- latent autoimmune diabetes in adults (LADA) - requires insulin as treatment
• Can present following pancreatic damage or other endocrine diseases

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3
Q

Can type II diabetes present in childhood?

A
  • Yes, prevalence of obesity is increasing

* Monogenic diabetes can present phenotypically as Type 1/2 diabetes e.g. MODY, mitochondrial diabetes

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4
Q

Is type I or II diabetes more common?

A

Type II diabetes

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5
Q

What factors can lead to autoimmune destruction of islet cells in T1D?

A
  • Environmental (trigger)

* Genetic

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6
Q

What factors can lead to insulin resistance in T2D?

A
  • Genetic (stronger influence)

* Obesity (associated)

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7
Q

Describe the pathogenesis of T1D

A
  • Patient gets pre-diabetes => overt diabetes, as beta cells start to malfunction (steadily)
  • Patients admit, sick from diabetic ketoacidosis (high risk effect of T1D)
  • Beta cells continue to decline over time
  • Relapsing remitting disease
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8
Q

What affect does T1D have on other conditions (same group of conditions)?

A
  • T1D is an autoimmune condition

* Therefore, increased prevalence of other autoimmune diseases

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9
Q

What other cells can you see near beta cells in T1D?

A
  • Lots of inflammatory cells (plasma cells)

* Lots of T-cells (role in destruction of beta cells)

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10
Q

What is the HLA-DR allele and what does it show?

A
  • Gene where a genetic abnormality can increase the risk of developing T1D
  • Haplotypes from DR1 to DR9
  • DR3 and DR4 are critical
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11
Q

What evidence suggests there is an environmental influence on T1D?

A
  • Higher prevalence in winter
  • Could be a viral pathogen that targets beta cells during this period
  • Also, certain places in the world with a higher prevalence
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12
Q

What clinical measurements can you make to try and diagnose T1D?

A
  • Islet cell antibodies (ICA) - grp O human pancreas
  • Insulin antibodies (IAA)
  • Glutamic acid decarboxylase antibodies (GADA) - widespread NT
  • Insulinoma-associated-2-autoantibodies (IA-2A)-receptor like family

(there are some individuals with T1D that don’t have antibodies)

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13
Q

What are the symptoms of diabetes?

A
  • Polyuria
  • Nocturia
  • Polydipsia
  • Blurred vision
  • Thrush
  • Weight loss
  • Fatigue
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14
Q

What are the signs of diabetes?

A
  • Dehydration
  • Cachexia (weakness and wasting of the body)
  • Hyperventilation
  • Smell of ketones
  • Glycosuria
  • Ketonuria
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15
Q

What affect does insulin usually have on the liver, muscle and adipose?

A

• Reduced hepatic glucose output
• Increased glucose uptake by the muscle
- increased protein synthesis
• Stops fatty acids/glycerol from leaving adipose

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16
Q

What affect does insulin deficiency have on the liver, muscle and adipose?

A

• Lot of glucose from the liver released into the circulation
• Glucose not taken up by the muscle
=> Hyperglycaemia
• Proteins released from muscle (increases glucose production in liver)
• Fatty acids in adipose tissue broken down
• Triglycerides release lots of fatty acids
• Fatty acids taken up by the liver, ketone bodies produced (which can go into the Kreb’s cycle to produce energy)

17
Q

What are the aims of treatment in T1D?

A
  • Reduce early mortality
  • Avoid acute metabolic decompensation
  • Prevent long term complications e.g. vascular disease
  • Need exogenous insulin to preserve life
18
Q

What diet do you need in T1D?

A
  • Reduce calories as fat
  • Reduce calories as refined carbohydrate
  • Increase calories as complex carbohydrate
  • Increase soluble fibre
  • Balance distribution of food over course of day with regular meals and snacks
19
Q

What kind of insulin is used as treatment with meals and in the background?

A
  • With meals: short acting, human insulin, insulin analogues (lispro, aspart, glulisine)
  • Background: long actin, non-c bound to zinc/protamine, insulin analogues (glargine, determir, degludec)
20
Q

What does a diabetic patient inject themselves with when they eat?

A
  • Short and long acting insulin
  • Long acting insulin lasts until their next meal
  • Insulin analogues (long acting) give a good, 24-hour long profile
  • This is called a basal-bolus regime
21
Q

What percentage of diabetic patients have a basal-bolus regime?

A

90%

22
Q

How do insulin pumps work?

A
  • Administers continuous insulin
  • Pre-programmed basal rates and bolus for meals
  • Does not measure glucose
23
Q

How can T1D be invasively treated?

A

• Islet cell transplant
• Beta cells taken from donor pancreas
• Cells are isolated and injected into patient’s liver
• Move through hepatic veins and migrate around the body
- can then produce insulin
• Immunosuppresive agents needed

24
Q

How can you measure how successful treatment for T1D is?

A
  • Measure capillary glucose levels (vary dependent on tissue perfusion)
  • Glucose monitor - real time
  • Look at HbA1c
25
Q

What is the HbA1c test?

A

• Blood sample that relies on red cells attaching to the glucose monitor
• HbA1c red cells react with glucose - irreversible and non-covalent
• Lifespan of red cells in around 120 days, so test gives an idea of glucose levels over 3 months
• Ideal for long-term glycaemic control
• May not be accurate:
- rate of glycation is faster in some individuals
- haemaglobinopathy (SCA, thalassaemia) can change red cell half life
- renal failure, blood loss

26
Q

What does a high HbA1c mean?

A

Higher blood glucose

27
Q

At what blood glucose level is someone considered to be hypoglycaemic?

A

< 3.6 mmol/l

28
Q

Explain the significance of hypoglycaemia in diabetic patients?

A
  • Occasional hypoglycaemic episodes are inevitable as a result of treating diabetes
  • Major cause of anxiety in patients + families
  • Source of major misconceptions in media
  • Blood glucose < 3 mmol/l: most mental processes impaired
  • Blood glucose < 2 mmol/l: consciousness impaired
29
Q

When is hypoglycaemia defined as sever?

A
  • Any hypoglycaemic episode that requires the help of another person to treat it
  • May contribute to arrhythmia and sudden death
30
Q

What is the main risk factor of hypoglycaemia in diabetic patients?

A

Quality of glycaemic control

31
Q

When do hypoglycaemic episodes happen?

A
  • Can occur at any time

* Often a clear pattern e.g. pre-lunch, nocturnal

32
Q

Why does hypoglycaemia occur?

A
  • Patients may start going to the gym while not changing their insulin dose
  • May miss meals/inadequate snack
  • Alcohol
  • Inappropriate insulin regime
33
Q

What are the symptoms and signs of hypoglycaemia?

A 
Due to increased autonomic activation
• palpitations (tachycardia)
• tremor 
• sweating
• pallor/cold extremities
• anxiety
Due to impaired CNS function
• drowsiness
• confusion
• altered behaviour
• focal neurology
•coma
34
Q

How can hypoglycaemia be treated?

A

Oral (feed if patient is unconscious)
• quick acting glucogels
• complex CHO (to maintain blood glucose after initial treatment)

Parenteral (if unconscious)
• IV dextrose (10%) glucose infusion
• 1mg glucagon (IM)
• Avoid conc. solutions e.g. 50% glucose - can cause severe skin reactions

35
Q

A patient can be sent home with a glucagon emergency pack, but when might this not be useful?

A
  • Relies on the liver having enough glucose
  • If you have been fasting for days, glycogen stores in liver will be depleted
  • Glucagon may not work

Endocrinology (17 decks)

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