Lecture 4 - Diabetes & Exercise Flashcards
Prevalence in Australia
Self reported data:
- 1.2mil aus diagnosed with diabetes
- 13% reported having type 1
- 86% reported having type 2
Proportion of people reporting diabetes increased with age
Highest prevalence for aged 75 and above years
Males had a higher prevalence than females
$10,000 - $15,000 cost per T2DM patient per year
In total over $3 billion per year in Australia
Define diabetes
It’s a metabolic disorder of multiple aetiology characterised by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action or both.
What is Insulin?
- polypeptide hormone
- synthesized in the pancreatic B-islet cells
- primary hormone responsible for control of uptake, utilisation, storage of cellular nutrients
- stimulates transport of glucose and fatty acids into muscle and adipose tissue
- cellular actions of insulin mediated by insulin binding to “insulin receptor”
- secretion tightly regulated process controlled by various nutrients, gastrointestinal hormones, pancreatic hormones and autonomic neurotransmitters
- glucose is the primary stimulators factor that releases insulin
What is the action of Insulin?
Muscle, increases:
- glucose entry
- glycogen synthesis
- amino acid entry
- protein synthesis
- ketone uptake
Decreases:
-protein catabolism
Liver- Increases:
- protein synthesis
- lipid synthesis
Decreases:
- ketogenesis
- glucose output, due to decrease gluconeogenesis and increases glycogen synthesis
Diabetes: how the pancreas reacts
Pancreas secrete 40-50units of insulin daily in 2 steps:
- Secreted at low levels during fasting [basal insulin secretion]
- following the ingestion of a meal portal blood insulin levels ride rapidly w/ a parallel but smaller rise in peripheral blood insulin levels
- an early burst of insulin occurs within 10min of eating
- then proceeds with increasing release as long as hyperglycaemia is present
Successful insulin therapy tries to mimic this process.
Glucose-insulin interaction
The glucose level in the blood that passes through the pancreas process the feedback mechanism to regulate insulin secretion
Glucagon has the opposite response
General classification of Types
Type 1 Diabetes:
- destruction of b-cells leads to absolute insulin definciency
- autoimmune or idiopathic
- 5-10% [13% australia]
Type 2 Diabetes:
- relative insulin deficiency. Predominantly insulin resistant, with relative insulin deficiency, to having a predominantly insulin-secretary defect with only mild to moderate insulin resistance
- 90% [86% australia]
Impaired Glucose tolerance [IGT] and Impaired Fasting Glucose [IFG] - Prediabetes
Gestational diabetes mellitus
- DM appears during 2nd or 3rd trimester
- may develop into type 2
- 2-5%
Type 1 Diabetes
5-10% [13% Aus] of diabetics
Childhood and adolescence
Eventual complete lack of endogenous insulin
Autoimmune destruction of beta cells in Islets of Langerhans in Pancreas
Insulin: hormone central to glucose transport and metabolism
Exogenous insulin administration requires
Type 2 Diabetes
90% of all cases [86% in AUS]
10 fold increase in adolescence
Linked to genetic & lifestyle factors [inactivity of skeletal muscle is the major driver in the pathogens is of T2DM]
Characterised by:
- diminished insulin response to blood glucose stimulus
- peripheral insulin resistance
Both type 1&2 lead to chronic hyperglycaemia if left unchecked
Diabetes: Treatment
Treatment of diabetes [Type 1&2]: maintain blood glucose to near ‘normal’ levels [-5mmol/L]
Home monitoring and glycosylated Hb [HbA1c]
-HbA1c = 3 month window of glucose control
Normal 4-6%
Patients <7%
Poorly controlled diabetes results in micro and macrovascular complications [eyes, kidneys, nerves, heart & blood vessles]
Major risk factor for heart disease, stroke, renal failure, blindness, peripheral vascular disease and most common cause of non-traumatic lower limb amputations
Symptoms of Hyperglycaemia
Polydipsia [thirst] Polyphagia [hunger] Hot, dry skin Acetone breath [ketosis= acidosis and respiratory failure] Fatigue Drowsiness Unconsciousness
Diabetes: Signs and symptoms
Polyuria:
- frequent and excessive urination
- osmotic diuresis caused by excess glucose in urine
- water loss can be severe along w/ Ca, Cl, & K
Polydipsia:
-excessive thirst associated w/ dehydration
Polyphagia:
- cells don’t relieve glucose leading to starvation which triggers excessive eating
- eating doesn’t provide glucose needed due to decreased insulin
Signs and Symptoms associated with hyperglycaemia:
Ketone bodies:
- breakdown of fat leads to ketones [small acids]
- accumulate in blood with no insulin
- caused metabolic acidosis
Acetone breath - Kussmaul respirations:
- excess acids cause increased H and CO levels
- stimulate brain to increase rate and depth of respirations to excrete acid and CO2
- acetone is exhaled thus breath has “fruity” door
- ultimately, pH will drop
Hyper/hypokalemia:
- lack of insulin causes depletion of K
- high K levels may occur due to shifting of K from inside the cells to blood
Long term complications of Chronic Hyperglycaemia
Microvascular complications:
- potential loss of vision
- chronic renal failure
- damage to peripheral nerves leading to loss of sensation- Charcot joints
- foot ulcers
- risk of amputation
- damage to autonomic nervous system causing: genitourinary, and cardiovascular symptoms
Macrovascular diseases:
- CAD
- Cerebrovascular disease
- PVD
Co-Risk factors for CVD: Hypertension Hyperlipidemia Obesity Insulin resistance Alterations in regulations of thrombosis and fibrinolysis
Hypoglycaemia: symptoms [treat with glucose]
Dizziness Weakness, trembling Hunger Numbness and tingling in fingers and lips Increase heart rate and arrhythmias Profuse sweating Coma and death
