Type 1 Diabetes Flashcards
What type of reaction is T1DM?
Type 4 hypersensitivity reaction
What is T1DM characterised by?
Loss of beta cella due to autoimmune destruction where T cells attack the pancreas
When is T1DM commonly. diagnosed?
Childhood and adolescence
What is an important group of genes on chromosome 6 which encodes the MHC important in self tolerance and recognising foreign molecules?
HLA
People with T1DM often have which specific genes in common?
HLA-DR3 and HLA-DR4
What autoantibodies do we test for in T1DM?
- Anti GAD (Antibodies to glutamic acid decarboxylase (anti-GAD) are reliable serological markers of Insulin-dependent diabetes mellitus)
- Pancreatic islet cell Ab (present in 90% of patients with insulin dependent diabetes mellitus)
- Islet antigen-2 Ab
- ZnT8 (zinc transporter vastly expressed on the membrane β-cells and is required for the accumulation of zinc for proper insulin processing)
What are the symptoms of uncontrolled T1DM?
Polyphagia - frequent hunger Glycosuria - glucose in urine Polyuria - frequent urination Polydipsia - frequent thirst Blurred vision Leaner body mass (lower BMI)
What is the main emergency complication in T1DM?
DKA
What is DKA characterised by? (conditions and values)
- Hyperglycaemia (blood glucose >11mmol/L)
- Ketonaemia (blood ketones >3mmol/L or ketonuria >2mmol/L)
- Acidosis (bicarbonate <15mmol/L and or venous pH <7.3)
- High potassium
- Urea and creatinine raised due to pre-renal failure
How does DKA occur?
Body breaks down fat into free fatty acids (lipolysis) due to lack of insulin in body
Liver turns fatty acids into ketone bodies (acetoacetic acid and beta hydroxybutyric acid)
Ketone bodies used for energy but also increase acidity of blood
What are the signs and symptoms of DKA?
- Kussmaul respiration (deep laboured breathing)
- Hyperkalaemia (insulin stimulates sodium potassium ATPases in normal circumstances where potassium is pumped out of the cells so without insulin, there is less potassium being pumped into cells so more potassium in the fluid outside the cells. Increased potassium in fluid around cells moves into the blood stream = hyperkalaemia despite less potassium inside cells)
- Dehydration (high levels of glucose in blood)
- Hypotension
- Tachycardia
- Abdominal pain
- Nausea and vomiting
- Mental state changes and coma
- Weight loss
- Fruity smelling breath (acetone)
What are the complications of DKA?
- Cerebral oedema (children more at risk)
- Adult respiratory distress syndrome
- Thromboembolism
- Aspiration pneumonia (if drowsy or comatose patient)
- Death
Treatment of DKA
- Rehydration (3L in 3 hours)
- Replacement of electrolytes (potassium) to help reverse acidosis, if blood pH <7 = IV bicarbonate
- IV Insulin
- Treatment of underlying cause (infection)
What are the main micro vascular complications of T1DM?
- Diabetic nephropathy (30% of T1DM- damage to small vessels in kidneys leading to progressive loss of kidney function) (Major risk for CVD x30)
- Retinopathy (damage to small blood vessels in retina leading to progressive loss of vision)
- Neuropathy (Occurs in 30-50% of pt with DM - nerve damage causing pain and loss of sensation) (gloves and stocking distribution) (DM still a major cause of amputation)
Macrovascular complications of DM
- Higher CVD risk due to artherosclerosis (3-4x more likely to have MI, HF, stroke)
- Other associated autoimmune disorders (thyroid disease, pernicious anaemia, coeliac, addisons, autoimmune gastritis)
- Psychological complications - anxiety, depression, emotion stress, poorer QOL.
- Infections - UTI’s, skin infections, necrosis lipoidica (uncommon)
