Clinical aspects of Diabetes Mellitus and Complications Flashcards
What is Diabetes Mellitus and the complications associated with it ?
“Diabetes mellitus is a group of metabolic disorders
characterised by hyperglycaemia resulting from
defects in insulin secretion, insulin action or both.
The chronic hyperglycaemia is associated with long-
term damage, dysfunction, and failure of various
organs, especially the eyes, kidneys, nerves, heart and
blood vessels.”
1 in 20 have diabetes
What are the criteria for diagnosing Diabetes ?
Diagnosis;
- Glycated HaemogIobin >48mmoI/moI
- Fasting blood glucose > 7.Ommol/L
- 2hr blood glucose > I I . I mmol/L following OGTT
- Random blood glucose > 11.1 mmol/L in presence of symptoms
How do we classify Diabetes ?
Classification of DM:
Type 1 diabetes (B-cell destruction) - 10%
Type 2 diabetes (85%);
- Insulin resistance with relative insulin deficiency
- Secretory defect with insulin resistance
Other types (5%);
- Genetic (MODY etc)
- Pancreatic disease
- Endocrine disease
- Drugs
Gestational diabetes (Pregnancy is an insulin resistant state)
What are the features of Type 1 Diabetes ?
Type 1 Diabetes;
- Autoimmune disease
ß cell destruction;
- Symptoms when 80% cell mass lost
- Environmental factors e.g viral infection
Autoantibodies;
- Islet cell
- Insulin
- GAD (GAD65)
- Tyrosine phosphatases
85-90% individuals
Strong HLA associations;
- linkage to the DQA and DQB genes
- influenced by the DRB genes.
What is the typical history for Type 1 Diabetes?
Typical History;
- Thirst
- Polyuria
- Nocturia
- Weight loss 2stone
- Osmotic lens change
Signs;
- Clinically dry
- Blood sugar 44moI/L
- Urine ketones ++
How does the British Diet vary to a Diabetic Diet ?
British Diet;
- Protein = 12%
- Carbohydrate = 46%
- Fat = 42%
Diabetic Diet;
- Protein = 15%
- Carbohydrate = 50%; Starch (brown bread, brown rice)
- Fat = 35%
- Fibre
(Less fat, more Starch and Fibre)
What do we need to educate diabetic patients about ?
Education;
- Diet
- Hypoglycaemia
- Sick day rules ( more susceptible to flu due to low insulin, get sick more, more days off)
Monitoring;
- Blood
- (Urine)
- Driving
- Alcohol
- Smoking
- Insulin card
- Pregnancy/Contraception
Complications ;
- Acute
- Chronic
How can patients monitor their blood glucose ?
Glucose monitor, fingerpick
Freestyle libra - can use phone, digital glucose between cells also gives trends (interstitial glucose which gives a lag, may need to check blood sugar as well)
What does Glycated Haemoglobin (HbA1c) show?
Gives glucose level on average for the last little while
What are the types of Insulin Therapy and how can we adapt it for patients?
Trying to match insulin regime to patient and their lifestyle (twice day, etc)
We can give Multiple Injections or “Basal Bolus” regime
Give background insulin in background for day, titrate against morning sugar and every time you eat give yourself a shot of quick action insulin calculated for carbohydrates in meal (1 long acting in background, short acting after every meal)
What is a Continuous Subcutaneous Insulin Infusion (CSII) ?
In stomach, measures interstitial glucose
- can get patients on close loop symptoms/pump, and it regulates it itself - may need to tell before meal but relatively freeing
What are the risk factors for Type 2 diabetes ?
Type 2 Diabetes Mellitus Risk Factors;
Genetic factors;
- defect of B cell
- insulin resistance
Not making enough insulin for body
Environmental factors;
- Obesity
- Stress
- Reduced physical activity
What is the classical presentation of Type 2 diabetes ?
Classical presentation of Type 2 DM;
- Thirst, polyuria
- Malaise, fatigue
- Infections e.g. Candidiasis
- Blurred vision
- Complications
- Incidental finding
How does Visceral fat distribution vary in normal patients vs Type 2 diabetics?
Type 2 patient have a lot more intravisceral fat than healthy BMI patients
- Issue is that intravisceral fat is metabolically reactive
How does Type 2 Diabetes progress?
Insulin resistance is gradually increasing causing an increase in plasma insulin and blood glucose which is usually picked up at diagnosis.
The plasma insulin and blood glucose levels continue to rise until the plasma insulin plummets and this begins t cause complications and eventually lead to premature death, usually cardiovascular cause
As we all get older and fatter insulin resistance increases
How does Ketone body metabolism occur ?
- Muscles are broken down into amino acids, Leucine and Lysine and make their way to the liver for energy
- Adipose tissue is broken down into free fatty acids and sent to the liver and end organ for energy
- The liver produces Ketone Bodies for energy, but these are organic acids and cause acidosis affecting the end organ
What is the cellular causes of DKA?
Insulin deficiency leads to;
- Hyperglycaemia
- Glycosuria
- Osmotic diuresis
- Ketosis
- Acidosis
- Gastroparesis
These all cause Volume Depletion and Renal Hypoperfusion which leads to impaired excretion of H+ & Ketone bodies.
What are the Stages of Hypoglycaemia ?
Stages of Hypoglycaemia;
5mmoll - Normoglycemia
4mmoll - Autonomic reaction
3mmoll - Impaired cognitive function
2.5mmoll - EEG changes, Visual dysfunction
2.2mmoll - Neuroglycopaenia
~ 1mmol - Behavioural changes, reduced conscious level, EEG generalised slowing
<1mmol - Coma, brain death
What are the Human Counter Regulatory Mechanisms for Hypoglycaemia ?
Human Counter Regulatory Mechanisms
- Fall in blood glucose -> Vagal stimulation -> Activates Parasympathetics for Glucagon release and Adrenal Medulla stimulation
- Neuroglycopaenia -> Adrenal Medulla stimulation -> Activates Sympathetics for Adrenaline release
Both Glucagon and Adrenaline release cause Glycogen release by the Liver
This doesn’t happen when you’re drunk as you are less likely to detect hypo and then and as liver processing alcohol wont release glycogen - pickle
