Endocrinology 15 - Type 1 Diabetes Mellitus Flashcards
1
Q
Why can diabetes mellitus be ambiguous?
A
- Autoimmune type 1 leading to insulin deficiency can be present decades into life (latent autoimmune diabetes in adults)
- T2DM may present in childhood
- Ketoacidosis can be a feature of T2DM, as well as T1DM (occurs in afro-Caribbean individuals)
- Monogenic diabetes can present phenotypically as type 1 or 2 (MODY or mitochondrial diabetes)
- Diabetes may present following pancreatic damage or other endocrine disease
2
Q
How are type 1 and 2 diabetes classified (aetiology)?
A
- Type 1 - environmental trigger and genetics result in autoimmune destruction of islet cells. Insulin deficiency leads to hyperglycaemia
- Type 2 - obesity and genetics lead to insulin resistance. B-cell failure results in hyperglycaemia.
3
Q
Describe the pathogenesis of type 1 diabetes
A
- Genes
- Immune disregulation
- Environmental triggers
- Fast onset to high glucose levels due to damage to beta cells of the pancreas.
4
Q
Why is the immune basis of type 1 diabetes important?
A
- Increased prevalence of other autoimmune disease
- Risk of autoimmunity in relatives
- Complete destruction of B-cells
- Auto antibodies can be used clinically (measure antibodies to diagnose type 1 diabetes)
- Immune modulation and novel treatments
5
Q
List the markers of T1D
A
- Islet cell antibodies
- Insulin antibodies
- Glutamic acid decarboxyase (widespread neurotransmitter)
- Insulinoma associated 2 autoantibodies
- HLA markers correlate with risk (DR3 and 4 significant risk of a patient developing type 1 diabetes) used in research
6
Q
List the symptoms of type 1 diabetes mellitus
A
- Polyurea
- Nocturia
- Polydipsia
- Blurring of vision
- Thrush
- Weight loss
- Fatigue
7
Q
List the signs of type 1 diabetes mellitus
A
- Dehydration
- Cachexia (weakness of the body due to weight and muscle loss)
- Hyperventilation
- Smell of ketones
- Glycosuria
- Ketonuria
8
Q
What are the aims of treatment in T1DM?
A
- Reduce early mortality
- Avoid acute metabolic decompensation
- Prevent long term complications (retinopathy, neuropathy, vascular disease and nephropathy)
9
Q
How is T1DM treated?
A
- Exogenous insulin to preserve life
- Insulin treatment with meals short acting (human insulin or insulin analogue) and basal insulin is long acting (given at the evening)
- Insulin pump
- Islet cell transplants (immunosuppressive agents for the rest of their life)
10
Q
Describe the diet changes in type 1 diabetes
A
- Reduce calories as fat
- Reduce calories as refined carbohydrate
- Increase calories as complex carbohydrate
- Increase soluble fibre
- Regular meals and snacks
11
Q
What is an insulin pump?
A
- Continuous insulin delivery
- Pre-programmed basal rates and bolus for meals
- Does not measure glucose, no completion of feedback loop
12
Q
How do you know how effective treatment of T1DM is?
A
- Capillary monitoring (finger prick, record glucose levels using a machine before insulin administration - not as accurate as venous glucose)
- Continuous glucose monitoring (sits on the abdomen and measures glucose levels continuously, with an alarm for hypoglycaemia)
- HbA1c red cells interact with glucose, which is irreversible. Levels of this can be measured to measure long term glycaemic control
13
Q
List the acute complications in T1DM
A
- Ketoacidosis resulting in metabolic acidosis (circulating acetoacetate and hydroxybutyrate, osmotic dehydration and poor tissue
perfusion) - Hyperglycaemia (rapid decompensation - reduced tissue glucose production, increased hepatic glucose production)
- Hypoglycaemia (as a result of treating diabetes)
14
Q
Define hypoglycaemia and severe hypoglycaemia
A
- Hypoglycaemia (plasma glucose of less than 3.6mmol/l)
- Severe hypoglycaemia (any hypo requiring help of another person to treat)
15
Q
What are the risks of hypoglycaemia?
A
- Mental processes impaired <3mmol/l
- Consciousness impaired at <2mmol/l
- May contribute to arrhythmia and sudden death
- Long term effects on the brain
- Loss of warning after reccurent hypos (long term patients, autonomic changes)
16
Q
Who is affected by hypos?
A
- Main risk factor is quality of glycaemic control (tight glycaemic control)
- More frequent in patients with low HbA1c
17
Q
When do hypos occur?
A
- Any time but often a clear pattern
- Pre-lunch hypos common
- Nocturnal hypos very common, and often not recognised
18
Q
Why do hypos occur?
A
- Unnacustomed exercise
- Missed meals
- Inadequate snacks
- Alcohol
- Innapropriate insulin regime
19
Q
List the signs and symptoms of hypoglycaemia
A
Increased autonomic activation
- Palpitations and tachycardia
- Tremor
- Sweating
- Pallor/cold extremities
- Anxiety
Impaired CNS function
- Drowsiness
- Confusion
- Altered behviour
- Focal neurology
- Coma
20
Q
How is hypoglycaemia treated?
A
- Orally by feeding the patient (glucose + complex CHO)
- Parenteral if consciousness is impaired (10% dextrose or 1mg glucagon IM)
21
Q
How is T1DM affected by the environment?
A
- Higher prevalence in the winter than the summer
- Higher prevalence in certain areas of the world suggesting environment affects T2DM
- May be related to viruses and bacteria in the winter
22
Q
How is glucose regulation affected by T1DM?
A
- Muscle cells (takes up glucose if there is insulin present. If insulin deficient amino acids from proteins in the muscle are used to make glucose in the liver)
- Liver (produces glucose)
- Adipose (If insulin deficient, glycerol is released from adipose tissue to make glucose. Fatty acids are converted to ketone bodies)
23
Q
How is insulin administered to T1DM patients?
A
- Background insulin throughout the day (mimicking normal insulin levels)
- Insulin administered with a meal (short acting)
24
Q
Describe the epidemiology of type 1 diabetes
A
- Northern europeans
- Lean
- Child/adolescent onset
- 10% of people with diabetes have type 1
