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)
Risk factors for diabetic retinopathy
- Long duration of DM
- Poor glycaemic control (higher HbA1c)
- HTN
- On insulin treatment
- Pregnancy
Treatment for retinopathy
Laser therapy main treatment (stabilises changes, does not fix)
Symptoms of diabetic nephropathy
- Hallmark is proteinuria
- Polyuria
- Fatigue
- Headaches
- Malaise
- Nausea
- HTN
Risk factors for diabetic nephropathy
- Poor BP control
- Poor BG control
Risk factors for diabetic neuropathy
- HTN
- Smoking
- HbA1c
- Duration of diabetes
- BMI
- Triglycerides
- Total cholesterol levels
Precipitating factors for DKA
- Infection
- Stress
- Non-adherence to insulin treatment
- Comorbid conditions
- Other medications (corticosteroids and duiretics)
- Binge drinking and illegal drung use
Symptoms of DKA develop more quickly or slowly than symptoms of HHS?
Quickly
Area for quickest absorption of insulin?
Abdomen
How is insulin administered and why?
Subcutaneously as insulin can be broken down in the GI tract
What does a bolus regimen consist of?
Taking rapid acting insulin before every meals to counteract post-meal increase in BG
What does a basal insulin regimen consist of?
Intermediate acting, long-acting and ultra-long acting insulins to maintain a steady dose of background insulin throughout the day, typically taken once of twice daily to regulate BG levels
What are the benefits and drawbacks to patients of a basal insulin regimen?
- Simple for patient
- Less risk of hypo overnight
- Doesnt cover meals
- Best used with long-acting insulin analogues which are expensive
What does basal-bolus regimen consist of?
Basal insulin (long acting) to maintain fasting BG levels and bolus taken before meals
What regimen is considered the best treatment for T1DM? What are the negatives for patients of this regimen?
Basal-bolus regimen
- Needs high level of patient education and carb counting, exercise consideration etc.
- risk of hypo
- need to measure BG before every meal and take insulins before food
What is a Sliding Scale Regimen?
- Typically reserved for hospital settings where a diabetics BG could fluctuate quickly due to metabolic stressors (infection, illness)
- Every 4-6 hours a persons BG is measured and an appropriate dose of short acting insulin and glucose is given to maintain good BG levels
- Risk of hypo’s and hyper’s
Humalog, aspart and glulisine are examples of what type of insulin?
Rapid acting
Detemir and glargine are examples of what type of insulin?
Long acting
