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Pathophysiology - Unit IV > Diabetes > Flashcards

Diabetes Flashcards

Glucose regulation, diabetes.

1
Q

What is diabetes?

A

Metabolic disease characterized by hyperglycemia.

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2
Q

Diabetes is the _th cause of death in the US.

A

7th.

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3
Q

What happens to insulin?

A

Insulin drives glucose into the cell, but the glucose cannot get into the cells without insulin.

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4
Q

Increased blood sugar and increased insulin secretion lead to?

A

Glycolysis = ATP. Storage as: glycogen (glycogenesis), fat, and protein.

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5
Q

Decreased blood sugar and increased glucagon secretion lead to?

A

Glucose release from cells (help from liver) by gluconeogenesis and glycogenolysis.

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6
Q

Glucagon comes from?

A

The liver.

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7
Q

Glucagon occurs when?

A

When glucose is gone, it causes the release of glucose into the blood for tissues that need it.

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8
Q

What is diabetes mellitus?

A

Decrease in insulin or insensitivity to insulin, therefore glucose can’t be driven into the cell.

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9
Q
  • Diabetes Mellitus causes?
A

Hyperglycemia and osmotic diuresis.

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10
Q

Signs and symptoms of diabetes mellitus?

A

Polyuria, polydipsia, polyphagia.

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11
Q

Type I Diabetes is also known as?

A

Juvenile-onset diabetes (because it generally happens at a younger age)

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12
Q
  • What is Type I Diabetes?
A

Autoimmune process that destroys the beta cells of the pancreas, leading to a loss of insulin production?

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13
Q
  • Type I Diabetes destroys what cells?
A

Beta cells of the pancreas, leading to loss of insulin production.

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14
Q

Type I Diabetes forms?

A

Ketones.

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15
Q

Ketones are caused by?

A

Decreased insulin, increased sugar, and increased lipids form ketones in the body.

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16
Q

A Type I Diabetic who is not in diabetic ketoacidosis is still likely to?

A

Develop ketones when their blood sugar is too high.

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17
Q

Hyperglycemia affects?

A

Fats, proteins, and carbohydrates.

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18
Q

Glucose accumulates in the blood and appears in?

A

The urine.

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19
Q

Hyperglycemia can lead to osmotic diuresis, which causes?

A

Polyuria and polydipsia.

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20
Q
  • Body uses free fatty acids for?
A

Energy, which causes high lipids.

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21
Q
  • Type II Diabetes is also known as?
A

Adult-onset diabetes.

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22
Q
  • The underlying pathophysiology for Type II Diabetes is?
A

Insulin Resistance.

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23
Q

Type II Diabetes is considered onset based on?

A

Lifestyle.

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24
Q

The risk of developing type II diabetes is correlated with?

A

Age, obesity, and family history.

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25
Q
  • Type II Diabetics increase insulin secretion to compensate for?
A

Peripheral tissue resistance, but at the end this system fails.

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26
Q

What happens when the pancreas “burns out” in a person with Type II Diabetes?

A

The Type II Diabetic will need insulin replacement just like the Type I Diabetic.

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27
Q

Diabetes has been defined as?

A

Starvation in the midst of plenty. Lol.

28
Q
  • Normal fasting blood glucose?
A

70-100 mg/dL

29
Q
  • Hb1Ac is also known as?
A

Glycosylated Hemoglobin.

30
Q
  • Normal Hb1Ac?
A

< 6.5%

31
Q
  • Hb1Ac is used for?
A

Identifying the average plasma glucose concentration over prolonged periods of time.

Glucose permanently attaches to the hemoglobin (RBC). RBCs live ~120 days (4 months). Hb1Ac records a four month period.

32
Q
  • Rate of fasting plasma glucose?
A

> 100 mg/dL

33
Q

Rate of random plasma glucose?

A

> 126 mg/dL with polyuria and polydipsia.

34
Q
  • Another name for OGTT is?
A

Oral Glucose Tolerance Test.

35
Q
  • OGTT in 1 hour?
A

< 200 mg/dL

36
Q
  • OGTT in 2 hours?
A

< 140 mg/dL

37
Q

OGTT is used to?

A

Diagnose prediabetes/diabetes. Measure body’s ability to use a type of sugar (glucose). Most commonly used for gestational diabetes.

38
Q

Treatments of hyperglycemia are targeted to combat?

A
  1. High blood sugar.
  2. Inadequate insulin secretion.
  3. Insulin resistance.
39
Q

Treatment for high blood sugar?

A
  1. Reduce patient’s sugar intake.
  2. Decrease hepatic gluconeogenesis (Metformin).
  3. Increase insulin secretion: sulfonylyreas (i.e. glypizyde)
  4. Decrease insulin resistance: thiazolidinediones (i.e. actos, avandia)
40
Q

Action of Metformin?

A

Decreases hepatic gluconeogenesis.

Treats hyperglycemia.

41
Q

Action of sulfonylyreas?

A

Increases insulin secretion.
i.e. Glypizyde
Treats hyperglycemia.

42
Q

Action of thiazolidinediones?

A

Decreases insulin resistance
i.e. actos, avandia.
Treats hyperglycemia.

43
Q

Signs and symptoms of hyperglycemia?

A

Weight loss, polyphagia (excess appetite), elevated blood glucose, increased infections (i.e. vaginitis), polydipsia (increased thirst), polyuria (increased urine output).

44
Q

Adrenergic signs and symptoms of hypoglycemia?

A

Diaphoresis, weakness, hunge, headache, anxiety.

45
Q

Neroglucopenic signs and symptoms of hypoglycemia?

A

Confusion, slurred speech, coma, seizure.

46
Q

What is neuroglycopenia?

A

Shortage of glucose (glycopenia) in the brain, usually due to hypoglycemia.

47
Q

Why is hypoglycemia considered a real emergency to Susan Allen?

A

“Glucose is the only thing there to feed your brain. If it is not feeding the brain, you will die.”

48
Q

Causes of hypoglycemia?

A
  1. Excessive insulin due to excessive diabetes treatment or insulinoma.
  2. Too much insulin compared to glucose.
  3. Decreased glucagon, cortisol (i.e. adrenal insufficiency, or decreased growth hormone (hypopituitarism).
  4. Liver failure or glycogen storage decrease.
49
Q

Complications of hypoglycemia?

A

Weight loss, fatigue, prolonged wound healing, visual changes, neuropathies (no sensation to feet), formation of atherosclerosis.

50
Q

Treatment for hypoglycemia in DKA person?

A
  1. Low-dose insulin.

2. Electrolyte and fluid replacement (i.e. potassium)

51
Q

Treatment for hypoglycemia/insulin shock person?

A
  1. Fast-acting carbohydrates.
  2. IV glucose.
  3. SC glucagon.
52
Q

Blood sugar in person with DKA?

A

> 250 mg/dL

53
Q

Blood sugar in infant with hypoglycemia/insulin shock?

A

30 mg/dL or <

54
Q

Blood sugar in adults with hypoglycemia/insulin shock?

A

60 mg/dL or <

55
Q

Risk factors for hypoglycemia/insulin shock?

A
  1. Type I and Type II DM
  2. Insufficient food intake
  3. Excessive exercise
  4. Excessive insulin
56
Q

Risk factors for DKA?

A
  1. Type I DM

2. Stressful situation

57
Q

Mucous membranes in persons with hypoglycemia/insulin shock?

A

Normal.

58
Q

Respirations in persons with hypoglycemia/insulin shock?

A

Normal.

59
Q

Mucous membranes in persons with DKA?

A

Dry.

60
Q

Respirations in persons with DKA?

A

Hyperventilation, fruity or acetone odor to breath.

61
Q

Skin in person with hypoglycemia/insulin shock?

A

Perspiring.

62
Q

Skin in person with DKA?

A

Hot, flushed, dry.

63
Q

Symptoms of hypoglycemia/insulin shock?

A

Weak, anxious, confused, tachycardia.

64
Q

Symptoms of DKA?

A

N/V, polyuria, polyphagia, polydipsia, headache, irritability, comatose, fruity breath odor, SOB.

65
Q

Onset of hypoglycemia/insulin shock?

A

Rapid.

66
Q

Onset of DKA?

A

Slow.

Pathophysiology - Unit IV (4 decks)

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