14- Diabetes Mellitus Flashcards

1
Q
  • 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.
A

-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)

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2
Q
  • 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?
A
  • 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.
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3
Q
  • 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?
A
  • 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.
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4
Q
  • give some acute complications of diabetes.
  • give some chronic complications of diabetes.
  • define metabolic syndrome.
A
  • 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.
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