Diabetes 2.0

To track trends and identify patterns

Improving insulin sensitivity

Hyperglycemia

Before, during, and after exercise

Developing Type 2 diabetes later in life

Type 1 diabetes

Type 1 diabetes

Weight loss, blurred vision, and polydipsia

Frequent urination

a group of metabolic diseases characterized by the inability to produce sufficient insulin or use it properly, resulting in hyperglycaemia

Hyperglycaemia and hypoglycaemia

1. blood glucose levels poorly managed
2. diabetic ketoacidosis
3. hyperosmolar nonketotic syndrome

High blood glucose levels cause the kidneys to excrete glucose and water

headache, blurred vision, increased thirst, weakness, and fatigue. These symptoms are due to the Kidney's attempt to excrete excess glucose from the blood by increasing urination

Fasting BGL ≥ 7.0 mmol/L OGTT > 11.1 mmol/L HbA1C ≥ 6.5%

Is a hormone produced by the beta cells of the pancreas. It is needed by the skeletal muscles, adipose tissue, and liver to absorb and use glucose

CVD, microvasculardiseases, and both autonomic and peripheral neuropathy (nerve damage)

Excess weight

It is where the body cannot effectively use insulin for the uptake of glucose into the muscle or liver. It is not a lack of insulin, its poor function of insulin.

False

occurs in patients whose diabetes is in poor control and in whom the amount of effective insulin is very low or absent

Type 1

abdominal pain, nausea, vomiting, rapid or deep breathing,sweet,or fruity smelling breath

when the body breaks down fat for energy because of a lack of carbohydrates

Elevated ketones in the blood

Ketones

is a metabolic process that occurs when the body breaks down fat for energy if its not getting enough CHOs

profound and prolonged hyperglycaemia because of the Kidney's attempt to excrete excess glucose

severe dehydration, excessive urination and can cause coma

1. too much insulin
2. too little carbohydrate intake
3. missed meals
4. excessive or poorly planned exercise

True

moderate to high intensity lasting longer than 30min

1. increase insulin sensitivity
2. on going glucose use. (occurs to replenish muscle and liver glycogen stores)
3. physiological replacement of glycogen stores through gluconeogenesis (biosynthesis of glucose from certain non-carbohydrate carbon substrates)

By releasing glucose-raising hormones such as glucagon, epinephrine, growth hormone, and cortisol. These hormones help increase circulating blood glucose levels

they are released as blood glucose decreases to help increase circulating blood glucose

Adrenergic and neuroglycopaenic

Shakiness, weakness, sweating, nervousness, anxiety, tingling of mouth and fingers, hunger

headache, visual disturbances, mental dullness, confusion, amnesia, seizures

decrease vasodilation, blood coagulation abnormalities, increased inflammation markers, sympathoadrenal responses

the inability to sense hypoglycaemia symptoms. It is the onset of neuroglycopaenic symptoms before the apperance of adrenergic warning symptoms

HU may result in many serious forms of morbidity including seizure, coma, fractures and joint dislocation and cardiac arrhythmias, and is occasionally fatal.

1. test blood glucose to confirm 2.consumption ~15g of CHO that contains minimal or no fat
2. wait 15-20 min to allow symptoms to resolve 4.re test blood glucose levels

hyperglycaemia

coronary artery disease, myocardial infarction, peripheral artery disease

retinopathy (eye disease) and nephropathy

Weakness, numbness and pain from nerve damage, usually in the hands and feet. Legs are affected before hands. Sensory symptoms include Ps&Ns and burning. Loss of sensory input to the feet can cause foot deformities affecting gait and increases risk of injury

it affects the non-voluntary, non-sensory nervous system, can affect any system of the body including the cardiovascular, respiratory, nueroendorcine, and gastrointestial.

high resting heart rate response and abnormal blood flow response during exercise

Acute= hypoglycaemia, hyperglycaemia, diabetic ketoacidosis, hypersomolar state Chronic= microvascular (retinopathy, nephropathy, neuropathy) and macrovascular(arteriosclerosis, myocardial infarction, stroke, lower extremity gangene)

Increased risk of stroke and cerebrovascular disease including transient ischemic attack and cognitive impairment. High BP and insulin resistance increase risk or coronary heart disease. Peripheral vascular disease resulting from narrowing blood vessels increasing risk for reduced blood flow.

-Polydipsia (excessive thirst) -Polyuria (frequent urination) -Polyphagia (excessive hunger) -Unexplained weight loss -Infections and cuts that are slow to heal -Blurry vision -Fatigue

-starting blood glucose level (self monitored) -amount, type, and timing of most recent food intake -medication use and timing

T1D is caused by alpha cell destruction

It always requires insulin therapy

Life management strategies

It is not influenced by genetics

All of the above

Diabetic Ketoacidosis

Too little CHO is consumed

Peripheral artery diseasse

Increased epinephrine release

15 gram of glucose and minimal fat

Abnormal sensory symptoms

High resting HR, low exercising HR

Impaired fasting glucose

Hyperglycaemic hyperosmolar non-ketotic syndrome

All of the above