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Y2 Endocrinology > Type 1 Diabetes Mellitus > Flashcards

Type 1 Diabetes Mellitus Flashcards

1
Q

How is T1DM classified (WHO)

A

Autoimmune destruction of islet cells from an environmental trigger. Leads to insulin deficiency and hyperglycaemia

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2
Q

Describe the pathogenesis of T1DM

A
  1. Environmental triggers and regulators along with immune dysregulation leads to destruction of beta cells.
  2. Eventually auto-antibodies are produced- further destruction
  3. Patients lose first phase insulin
  4. All beta cells are destroyed over time.
  5. Hyperglycaemia
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3
Q

What is the importance of the immune basis of T1DM

A

Increased prevalence of other autoimmune disease
Risk of autoimmunity in relatives
More complete destruction of B-cells
Auto antibodies can be useful clinically
Immune modulation offers the possibility of novel treatments

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4
Q

Describe the epidemiology of T1DM

A

10% of people with diabetes have T1
Slightly more M than F diagnosed
15x greater risk if first degree relative has diabetes

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5
Q

What are the immune markers for T1DM

A

Auto-antibodies can be a marker for diagnosis, disease progress, immune modulation treatment:

  • Islet cell antibodies (ICA)- grp O human pancreas
  • Insulin antibodies (IAA)
  • Glutamic acid decarboxylase (GADA) – widespread nuerotransmitter
  • Insulinoma-associated-2 autoantibodies (IA-2A)-receptor like family
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6
Q

What are the symptoms of diabetes

A 
polyuria 
nocturia
polydipsia 
blurring of vision
‘thrush’ 
weight loss
fatigue
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7
Q

What are the signs of diabetes

A 
dehydration 
cachexia
hyperventilation
smell of ketones
glycosuria 
ketonuria
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8
Q

What are the aims of T1DM treatment

A

Reduce early mortality

Avoid acute metabolic decompensation

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9
Q

What are some long term complications of T1DM

A

Retinopathy
Nephropathy
Neuropathy
Vascular disease

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10
Q

What are the diet restrictions recommended for T1DM patients

A

reduce calories as fat
reduce calories as refined carbohydrate
increase calories as complex carbohydrate
increase soluble fibre
balanced distribution of food over course of day with regular meals and snacks

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11
Q

Describe insulin treatment with meals

A

Short acting
Human insulin
Insulin analogue (Lispro, Aspart, Glulisine)

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12
Q

Describe background insulin treatment

A

Long acting
Non-c bound to zinc or protamine
Insulin analogue (Glargine, Determir, Degludec)

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13
Q

Describe the insulin pump

A

Continuous insulin delivery
Preprogrammed basal rates and bolus for meals
Does not measure glucose, no completion of feedback loop

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14
Q

How can diabetes treatment be monitored

A

Capillary monitoring

HbA1c

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15
Q

What does the reaction of HbA1c red cells with glucose depend on

A

Lifespan of red cell, about 120 days
Rate of glycation, faster in some individuals
Haemoglobinopathy, renal failure etc

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16
Q

What is the HbA1c test

A

Forms ideal measure of long term glycaemic control and has been shown to be related to risk of complications.
Furthermore lowering HbA1c associated lower risk of complication particularly microvascular complication

17
Q

What are the acute complications of T1DM

A

Ketoacidosis
Hyperglycaemia
Metabolic acidosis

18
Q

What does hyperglycaemia lead to

A

reduced tissue glucose utilisation

increased hepatic glucose production

19
Q

What doe metabolic acidosis do

A

circulating acetoacetate & hydroxybutyrate

osmotic dehydration and poor tissue perfusion

20
Q

What is the definition of hypoglycaemia

A

plasma glucose <3.6 mmol/l

severe hypoglycaemia - any hypo requiring help of another person to treat

21
Q

When can a hypoglycaemic episode occur

A

Can occur at anytime but often a clear pattern
Pre-lunch hypos common
Nocturnal hypos very common and often not recognised

22
Q

Which patients are more at risk of hypoglycaemic episodes

A

Low HbA1c

23
Q

What may cause a hypoglycaemic episode

A 
unaccustomed exercise
missed meals
inadequate snacks
alcohol
inappropriate insulin regime
24
Q

What are the symptoms of signs of hypoglycaemia due to increased autonomic activity`activation

A 
palpitations (tachycardia)
tremor
sweating
pallor / cold extremities
anxiety
25
Q

What are the symptoms of signs of hypoglycaemia due to impaired CNS function

A 
drowsiness
confusion
altered behaviour
focal neurology
coma
26
Q

What is the oral treatment for hypoglycaemia

A

glucose
- rapidly absorbed as solution or tablets
complex CHO
- to maintain blood glucose after initial treatment

27
Q

What is the parenteral treatment for hypoglycaemia

A

IV dextrose e.g 10% glucose infusion
1mg Glucagon IM
avoid concentrated solutions if possible (e.g 50% glucose)

28
Q

Describe the genetic aetiology of T1DM

A

Genetic susceptibility/ protection if you have certain HLA-DR alleles (chrom 6)
Specifically HLA-DR3 and HLA-DR4 increase risk while DR2 is protective

29
Q

What are the actions of insulin

A

Reduces:
Hepatic glucose output
Protein breakdown in muscle
Glycerol being taken out of fatty tissue into the periphery

Increases glucose being taken up by the muscle

30
Q

Describe the mechanism of diabetic ketoacidosis

A
  1. Insulin deficiency
  2. Increased lipolysis
  3. Fatty acids leave the adipocytes and form ketone bodies instead of glucose
  4. As fatty acids cannot pass the BBB, ketones are produced for the brain
  5. Ketones cause an acidic environment
  6. Osmotic dehydration due to brain enzyme dysfunction
  7. Poor tissue diffusion
31
Q

What is LADA

A

Latent autoimmune diabetes in adults - presentation of autoimmune type 1 diabetes that leads to insulin deficiency

32
Q

What is the relapsing and remitting disease theory

A

levels of effector T cells (that cause destruction of beta cells) and regulatory T cells (that control this destruction) fluctuate but over time effector T cells increase in number

Y2 Endocrinology (19 decks)

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