Diabetes Flashcards

0
Q

What metabolism pathways does diabetes cause abnormalities in?

A

Carbohydrate, fat, and protein.

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1
Q

What is the definition of diabetes?

A

Chronic hereditary disorder characterized by an abnormally high level of glucose in the blood and excretion of sugar in the urine. The basic defect is an absolute or relative lack of insulin.

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2
Q

When there is no fed signal (insulin), what happens to the lean body mass?

A

Broken down.

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3
Q

Define type 1 diabetes.

A

Pancreas stops producing insulin, resulting in hyperglycemia

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4
Q

Define type 2 diabetes.

A

Pancreas may not make sufficient insulin. Cells of the body do not use insulin effectively (insulin resistance). Insulin levels may look normal or high. Cells don’t receive enough glucose,resulting in hyperglycemia.

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5
Q

Is any other cell uptake affected by insulin resistance or lack of insulin?

A

Muscle uptake of amino acid (especially branch chain) also inhibited.

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6
Q

What are some common causes of normal weight type 2 diabetes?

A

Hereditary, virus, alcoholism, low birth weight.

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7
Q

Out of the ketosis resistant type 2’s what proportion use what treatments?

A

25 % diet, 50% oral hyperglycemic agents, 25% insulin.

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8
Q

What causes the pancreatic beta cells to release insulin?

A

Gut hormones prime them, but blood glucose causes the release.

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9
Q

What aspect of a mixed meal can slow insulin uptake?

A

Free fatty acids

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10
Q

What is the diagnostic criteria for diabetes? (3 possible).

A

Symptoms of diabetes + random plasma glucose >200 mg/dL.
Fasting (8 hr) plasma glucose >126 mg/dL.
2 hr post prandial >200 mg/dL. (75 g glucose)

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11
Q

What is the conversion from mg/dL to mmol/L?

A

Divide by 18.

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12
Q

What three tests are used to guide glycemic control in the Canadian guidelines?

A

HbA1C, fasting glucose, and 2 hr post prandial.

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13
Q

What is the lifespan of HbA1C? What is the ideal?

A

120 days. 0.04-0.06 or <100%

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14
Q

What is the difference between ideal and optimal glycemic targets?

A

Ideal is for the non-diabetic patients. Optimal targets are for post diagnosis, little higher range because don’t want to be too aggressive with treatment and risk hypoglycemic reactions.

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15
Q

How to target lipid levels change with a diabetes diagnoses and other risk factors?

A

Targets become more aggressive, so tolerate less lipid elevation the more comorbidities a patient has.

16
Q

Self monitoring glucose levels are important for what types of diabetics?

A

Type 1, those taking OHA or insulin to prevent hypoglycemia.

17
Q

In the obese insulin resistant person, is there more or less insulin secreted than a normal adult?

A

Way more!

18
Q

In the type 2 lean diabetic is more or less insulin secreted than a normal adult?

A

Less, pancreas is getting exhausted and can’t maintain demand for glucose. Still have elevated concentrations, because release a large amount at a time and insulin is broken down at a fixed rate .

19
Q

Why might VLDL be elevated during glucose ingestion when there is insulin resistance?

A

More FFA delivered to the liver with glucose, insulin impacts flow of nutrients through liver which leads to greater output of VLDL, glycated LPL means that it stays in circulation longer.

20
Q

What are the initial observations and physical symptoms of diabetes?

A

Polydipsia, polyuria, polyphagia, weight loss or obesity

21
Q

What are some general factors that all contribute to insulin resistance?

A

Excessive food intake leading to hyperglycaemia and hyperinsulinemia, obesity, inadequate exercise, genetic predisposition.

22
Q

How might compensatory hyperinsulinemia directly contribute to obesity?

A

Constant “fed” stimulation, increases storage of glucose as fat cells.

23
Q

What are some common risk factors for type 2 diabetes?

A

Age, obesity, ethnicity, prediabetes, family history, history of gestational diabetes, sedentary lifestyle, child of a woman with poorly controlled diabetes during pregnancy, low birth weight babies, PCOS.

24
Q

What is insulin resistance at a receptor level?

A

Down regulation of receptor activity to protect against rising insulin levels.

25
Q

How can up regulation be accomplished to counter the effect of insulin resistance?

A

Drugs , exercise ( walk after eating ), losing weight (central adiposity drives high blood glucose)

26
Q

How does insulin resistance impact on a cellular level?

A

Proportional to the level of fasting ( rather than post prandial) hyperglycaemia. Causes second messenger defects.

27
Q

How does insulin resistance impact on a hepatic level?

A

Inappropriately high level of glucose production when fasted and low level of uptake when fed. Liver can uptake glucose independent of insulin, but insulin still enters liver and affects the trafficking of gluconeogenesis.

28
Q

How does insulin resistance impact on a muscle level?

A

Attributed to receptor defects. Any manipulation that lowers insulin secretion will increase receptor concentration and decrease insulin resistance .

29
Q

What drives hyperglycaemia?

A

High gluconeogensis, low cellular glucose uptake, high dietary intake

30
Q

What does hyperglycaemia drive?

A

Impairs beta cell function, basal hyperinsulinemia, decreased glucose transport.

31
Q

What are the “ABCs” of diabetes for heart health?

A

A1C test
Blood pressure
Cholesterol

32
Q

What is the mechanism for hyperlipidemia in type 1 diabetes?

A

High TG due to defective removal of chylomicrons and VLDL from impaired LPL activity (including glycation impairment),

33
Q

What is the mechanism for hyperlipidemia in type 2 diabetes?

A

High TG due to elevated de novo synthesis from glucose. Low HDL may be due to obesity.