Diabetes Flashcards

1
Q

Name and describe the two types of diabetes.

A
  1. Diabetes mellitus: Body doesn’t produce enough insulin or doesn’t properly respond to insulin
  2. Diabetes insipidus: Excessive thirst and excretion of large amounts of dulute urine. Results from malfunction of the vasopressin/antidiuretic hormone system
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2
Q

Describe the oral glucose tolerance test.

A

It determines the rate of glucose removal from the blood.

Patients fast, and then drink glucose. Blood glucose is measured before glucose consumption and at intervals thereafter.

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3
Q

What fasting blood glucose concentration suggests diabetes?

A

> 126 mg/dl (After 2 hours, >200)

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4
Q

Uncontrolled diabetes results in very high _______ concentration.

A

blood glucose

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5
Q

What are the two types of diabetes mellitus?

A
  1. Type I diabetes: Body produces little to no insulin
  2. Type II diabetes: Body becomes resistant to insulin
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6
Q

How does type I diabetes develop?

A

The body’s immune system destroys pancreatic beta cells, which produce insulin

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7
Q

Type I diabetes usually strikes which demographic?

A

Children and young adults

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8
Q

Which type of diabetes accounts for 90% of all cases?

A

Type II

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9
Q

How does type II diabetes develop?

A

It begins as insulin resistance. As the need for insulin rises, the pancreas gradually loses ability to produce it.

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10
Q

Type II diabetes is associated with what conditions?

A

Older age, obesity, family history of diabetes, and physical inactivity

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11
Q

Why do those with type I diabetes die without insulin?

A

Ketoacidosis

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12
Q

Those with type 2 diabetes can’t survive without insulin. True or false?

A

False. They can.

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13
Q

Where are glucose transporters stored?

A

Within the cell in membrane vesicles

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14
Q

What happens when insulin interacts with its receptor?

A

Vesicles move to the surface and fuse with the plasma membrane, bringing up the glucose transporters

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15
Q

When insulin levels drop, what happens to glucose transporters?

A

They’re removed from the plasma membrane via endocytosis, forming small vesicles.

These small vesicles fuse with a larger endosome, and patches of the endosome bud off to become small vesicles, ready to return to the surface when insulin levels rise again.

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16
Q

Insulin stimulates glycolysis. True or false?

A

True

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17
Q

Insulin inhibits fatty acid synthesis. True or false?

A

False

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18
Q

Insulin inhibits lipolysis. True or false?

A

True

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19
Q

Insulin stimulates lipogenesis. True or false?

A

True

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20
Q

During the fasting or diabetic state, _____ and _____ are elevated.

A

epinephrine; glucagon

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21
Q

Urea is exported to the _____ and excreted in _____.

A

kidney; urine

22
Q

Which TCA cycle intermediate is diverted to gluconeogenesis?

A

Oxaloacetate

23
Q

Glucose is exported via the bloodstream to the _____.

A

brain

24
Q

Fatty acids from adipose tissue are oxidized as fuel, producing what?

A

Acetyl-CoA

25
Q

Acetyl-CoA synthesis favors _____ synthesis.

A

ketone body

26
Q

Ketone bodies are exported to the brain to be used as what?

A

Fuel

27
Q

Where do excess ketone bodies end up?

A

Urine

28
Q

A lack of insulin secretin or response to insulin means what for glucose reabsorption?

A

It’s significantly reduced.

29
Q

What contributes to high blood glucose levels in diabetic patients aside from the reduced glucose absorption?

A

Gluconeogenesis in the liver still occurs even though there’s enough glucose available.

30
Q

In diabetic patients, lipoprotein lipase is [promoted/inhibited]. What does this result in?

A

inhibited

This results in high concentrations of VLDL and chylomicrons in the blood

31
Q

In type I diabetes, no insulin secretin leads to ____ and ____.

A

lipolysis; ketoacidosis (excessive production of ketone bodies)

32
Q

Type II diabetes patients are insulin resistant, which means what?

A

Receptors on liver/muscle cells are insensitive

33
Q

In type __ diabetes patients, beta cells don’t make enough insulin to either inhibit gluconeogenesis or stimulate glucose uptake.

A

II

34
Q

Why do insulin-resistant diabetic patients rarely have ketoacidosis?

A

Lipolysis in adipose cells is still inhibited by insulin.

35
Q

How does glucose regulate insulin secretion in beta cells?

A

Glucose enters the cell via GLUT2 and undergoes glycolysis, the TCA cycle, and oxidative phosphorylation, which increases [ATP].

The increase in ATP closes the ATP-gated K+ channel, which depolarizes the cell because K+ can’t leave.

Voltage-gated Ca2+ channels allow Ca2+ to flow in. The ER takes in the Ca2+, releasing insulin in secretory granules to be secreted outside the cell.

36
Q

What drugs treat type II diabetes?

A

Sulfonylurea drugs

37
Q

How do sulfonyl drugs work?

A

They target ATP-gated K+ channels and increase insulin release from pancreatic beta cells.

38
Q

What’s glycation?

A

A nonenzymatic attachment of glucose to proteins

39
Q

What leads to glycation? Why is this bad?

A

Elevated blood glucose levels leads to glycation of proteins, which negatively affects their function.

40
Q

Describe the glycation reaction.

A

It’s a nonenzymatic reaction of glucose with lysine residues and N-termini of proteins.

41
Q

Glycation leads to damage in what?

A

Kidneys, retinas, cardiovascular system (Small blood vessels)

42
Q

What is the glucose measuring device that determines your blood glucose concentrations called?

A

Glucometer

43
Q

Your blood glucose concentrations change [slowly/rapidly].

A

rapidly

44
Q

What is hemoglobin a1c? Does it change slowly or rapidly?

A

A glycated form of hemoglobin

It gives an indication of blood glucose concentrations over past weeks/months. It changes slowly.

45
Q

How does hemoglobin glycation relate to hemoglobin a1c tests?

A

Glycated protein level is proportional to blood glucose concentrations and used to estimate blood glucose concentrations over weeks (Hemoglobin a1c levels)

46
Q

Why is high glucose is bad?

A

It leads to inappropriate glycation of proteins, which causes blurred vision and increases the risk of cardiovascular disease

47
Q

What is hypoglycemia? How does it happen, and what does it result in?

A

Low blood sugar

It happens very fast when too much insulin is injected. It can lead to coma and death.

48
Q

What does diabetic ketoacidosis cause? How does it happen?

A

It causes dehydration, labored breathing, coma, and death.

It happens more slowly when insulin isn’t present or insulin response is too low. The liver makes an excessive amount of ketone bodies from lipolysis and fatty acid beta oxidation.

49
Q

What are some chronic diabetes-related complications?

A

Cardiovascular disease and stroke, high blood pressure, blindness, renal disease, nerve disease, and amputations

50
Q

What are some treatment options for type II diabetes?

A

Diet can control diabetes in some patients. Losing weight will increase the number of peripheral insulin receptors, improving insulin sensitivity.

Drugs and oral/inhaled insulin could also help.