1. #Risk factors Diagnosis Clinical manifestations Acute complications

2. #Risk factors (LDL) Family history of diabetes Race
Obesity (BMI > 30)
Age
Hypertension
hyperlipidaemia
Tobacco, Smoking
IGT, IFG (prediabetes)
History of Gestational DM
Cataracts
Woman delivered of a baby > 4 kg
Polycystic ovary disease
Inactivity

3. Obesity and Pre-Diabetes
Diet high in fat, carbohydrates
Increase the insulin levels in body.
Beta cells pump out more and more insulin and the Beta cells become exhausted.
Insulin levels decline
Also pre-diabetics have a tendency toward insulin resistant cells
Result: diet abuse, less insulin, resistant cells = tips patient into Type II Diabetes.

4. DIABESITY Persons with diabetes who suffer from obesity

5. Carbohydrates
 Carbohydrates – Simple Sugars – contain 1or 2 units ( saccharied units )
Complex Carbohydrates- long chains of simple sugar: polysaccharide starch is a complex carbohydrate

6. Glycaemic Index (GI)
A food's GI indicates the rate at which the carbohydrate in that food is broken down into glucose and absorbed from the gut into the blood. In high GI foods, this occurs quickly, causing your blood glucose (sugar) level to rise rapidly.
The Glycaemic Index (GI) ranks food on a scale from according to the effect they have on blood glucose levels.
Lewis 1196

8. Diagnosis of DM occurs when…
Plasma random glucose > 11.1 mmol/L along with symptoms DM.
Plasma glucose > 7.0mmol/L after 8hrs fasting.
OGTT value > 11.1mmol/L 2 hrs after 75g glucose PO.
(Tests most reliable in morning and normally repeated on a different day for confirmation.)

9. Glucose testing

10. Glycosylated Haemoglobin (HbA1c)
Blood test measuring the average blood glucose level over a 2-3 month period.
Now the recommended test for screening and diagnosis of diabetes * NZSSD
Informs us of how well the patient’s diabetes is controlled.
Goal is < 7% or mmol/mol
Each 1% increase = 11mmol/mol
Fructosamine (reaction of glucose and plasma protein)
Autoantibody tests (islet cells)
Lewis 1186/1362

12. Clinical Manifestations Type 1
The manifestations of Type I diabetes often come on suddenly and very severely. They include:
Excessive thirst POLYDIPSIA
Excessive urination – POLYURIA
Excessive eating POLYPHAGIA
Weight loss (even though you may be hungry and eating well)
Feeling weak and tired
Blurred vision
Ketoacidosis

13. Clinical Manifestations Type 2
Sometimes, people with Type II diabetes don't notice any symptoms or the symptoms are experienced gradually. They include:
blurred vision
cuts or sores that are slow to heal
itchy skin, yeast infections
increased thirst
dry mouth
need to urinate often
leg pain
# 3 P’s

14. Osmotic diuresis Hyperglycemia
Blood glucose levels above renal threshold (10-12mmol/L
Kidneys excrete glucose along with water and electrolytes ( k+)
Polyuria
Dehydration

15. Short Term/Acute Complications
Acute hyperglycemic complications
HHNS (Hyperosmolar Hyperglycaemic Non- ketotic Syndrome) previously HONK
DKA (Diabetic Ketoacidosis)
Acute hypoglycemic complications
Diaphoresis, shakiness
LOC
Seizure activity, brain death
Somogyi effect (Low & High)
Dawn Phenomena

16. LDL
Compare hyperglycaemia with hypoglycaemia under the following headings
Clinical manifestations
Causes
Treatment
Preventative measures

17. Stress and Diabetes Mellitus
Stress causes release of hormones
- ACTH - corticosteroids
- Catecholamines
Increases:
Glucose
Heart rate
Cardiac contraction
Muscle contraction
Bronchial relaxation

18. HHS /HHNS (Hyperosmolar Hyperglycaemic [Nonketotic] Syndrome)
Metabolic derangement characterized by:
Principally in Type 2 diabetics
Hyperglycemia
Hyperosmolarity
Absence of ketones
Preceding probable:
Infection most common cause (Pneumonia, UTI)
hydration (Dementia, immobility, vomiting) MI
Some drugs (Diuretics, H2 blockers)

19. Diabetic Ketoacidosis (DKA)
Clinically, uncontrolled diabetes that requires emergency treatment with intravenous fluids and insulin
Biochemically, an increase in the serum concentration of ketones greater than 5 mEq/L, a blood glucose level of greater than 11.1mols, and a blood pH of less than 7.2
Disorder in the breakdown of carbohydrate, fat and protein
Hyperglycaemia, dehydration with electrolyte loss and acidosis

20. Diabetic ketoacidosis (DKA)
No glucose in cells to be used as source of energy
liver starts converting glycogen to glucose
Body starts breaking down fat stores ( lypolysis)
Ketones (acids) produced
Increased ketones and glucose in blood
Metabolic acidosis
Osmotic diuresis

22. Causes of DKA Poor compliance Concurrent illness (e.g., UTI, vomiting)
Medical, surgical, or emotional stress
Brittle diabetes
Idiopathic (no identifiable cause)
Insulin infusion catheter blockage
Mechanical failure of insulin infusion pump

24. DKA and HHNS

25. Hypoglycaemia
A reduction in plasma glucose concentration to a level that may induce symptoms of low blood sugar.
Caused by:
too much insulin or oral hypoglycaemics
too little food
excessive physical activity
stress

26. Treatment for hypoglycaemia
If conscious gm of fast acting concentrated carbohydrate orally ---
3 – 4 commercially prepared glucose tablets or
60 – 120 ml fruit juice or soft drink or
6 – 10 jelly beans or
2 – 3 teaspoons of sugar or honey
Retest after 15 minutes and if less than 3.8 – 4mmol
repeat above
Follow with a snack of protein and starch if not having a meal in the next 30 minutes

27. If unconscious ….. Glucagon 1mg subcutaneously or intramuscularly
May take up to 20 minutes to wake up.
Follow with a carbohydrate snack
If no response will require bolus IV glucose 50% 25 – 50ml

28. Hypoglycaemia

29. Somogyi Effect
Swing to high plasma glucose from overnight low plasma glucose
Rebound hyperglycaemia and ketosis
AM readings may cause night time adjustment of insulin and compound problem.
Treatment involves adjusting supper snacks and less insulin

30. Dawn Phenomenon
Hyperglycaemia in the morning due to release of counter-regulatory hormones
growth hormone, cortisol
Adolescence and young adulthood
RX – adjust times of insulin or increase