14- Diabetes Mellitus Flashcards
- define diabetes.
- outline the pathophysiology of diabetes
- give reasons why blood glucose may rise
- give the difference in mechanism of type 1 and type 2 diabetes.
-diabetes=when blood glucose is too high (hyperglycaemia) and over years leads to damage of small and large BVs causing premature death from CVDs
-when we eat food it’s broken into glucose, blood glucose rises and body sends a signal to the pancreas to release insulin, insulin is a KEY that unlocks cells so glucose can pass from BVs to cells to be used for energy
-either an inability to produce any insulin or adequate insulin production but insulin resistance prevents them working
-type 1=autoimmune beta cell destruction therefore no insulin is made bc of autoantibodies (absolute insulin deficiency)
type 2=pancreas may not make enough insulin (relative insulin deficiency) or cells don’t use insulin properly (insulin resistance)
- how does diabetes mellitus present in general?
- how is it diagnosed?
- how does type 1 diabetes present & how is it treated?
- what are ketones and what is ketoacidosis?
- typical symptoms of hyperglycaemia (polyuria, polydipsia-drinking lots of water, blurred vision), symptoms of inadequate energy utilisation(tiredness, weakness, weight loss)
- lab test, fasting glucose measured, a couple of tests
- rapid onset of weight loss in weeks, polydipsia and polyuria, if later could be vomiting due to ketoacidosis, patient usually younger than 30, presence of ketones. Treat w subcutaneous insulin injections several times a day.
- when we are starving, we begin to metabolise FAs for energy which releases ketones, presence of ketones in urine means they have low insulin. Ketoacidosis=absolute or relative deficiency of insulin, increased lipolysis, lots of ketone bodies formed.
- what causes insulin resistance to develop in type 2 diabetes?
- how does type 2 diabetes present?
- after bariatric surgery or weight loss, what changes are seen?
- how do we treat type 2 diabetes?
- central obesity around the abdomen and liver, muscle and liver fat deposition, physical inactivity, genetic influences.
- very variable symptoms as there’s a slower rise in blood sugar or asymptomatic, polyuria, polydipsia, weight loss, no urinary ketones, patients are often older and 90% are obese.
- after bariatric surgery or v low calorie diets, fasting blood glucose normalises, massive drop in liver fat content, normalising B cell function, rate of insulin release goes back to normal.
- lifestyle; diet, patient education, look for other vascular factors eg hypertension, smoking, non insulin therapies.
- give some acute complications of diabetes.
- give some chronic complications of diabetes.
- define metabolic syndrome.
- acute=massive metabolic decompensation ie diabetic ketoacidosis in type 1, hyperosmolar non ketotic syndrome in type 2. Hypoglycaemia;coma.
- chronic=macrovascular or large vessel disease; brain, heart, peripheral vascular disease, stroke, heart attack, intermittent claudication, gangrene. Micro vascular or capillary;eyes, kidneys, nerves could cause blindness, need for kidney replacement, foot ulcer etc
- a cluster of the most dangerous risk factors associated w CVD: diabetes and raised fasting glucose conc, abdominal obesity, high cholesterol, hypertension.