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Biochem Exam 4 > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Is Diabetes just one disease?

A

No; heterogeneous group of multifactorial, polygenic syndromes characterized by elevated fasting blood glucose

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2
Q

How many people in US have diabetes?

A

28 million (8 mil undiagnosed)

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3
Q

What is diabetes a leading cause of?

A
  • Adult blindness + amputation
  • Renal failure
  • Nerve damage (neuropathy)
  • Heart attacks
  • Strokes
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4
Q

Age of onset in Type 1 vs 2?

A

1- childhood/puberty

2- after 35

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5
Q

Nutritional status at time of disease onset in type 1 vs 2?

A

1- undernourished

2- obesity

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6
Q

Prevalence of type 1 vs 2?

A

1- <10% diagnosed diabetics

2- >90% diagnosed diabetics

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7
Q

Genetic disposition in type 1 vs 2?

A

1- moderate

2- very strong

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8
Q

Defect/deficiency in type 1 vs 2?

A

1- beta cell destruction -> no insulin production

2- insulin resistance + inability of beta cells to produce appropriate amount of insulin

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9
Q

Frequency of ketosis in type 1 vs 2?

A

1- common

2- rare

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10
Q

Plasma insulin in type 1 vs 2?

A

1- low-absent

2- high early in disease; low-absent later

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11
Q

Acute complications in type 1 vs 2?

A

1- ketoacidosis

2- hyperosmolar hyperglycemic state

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12
Q

Response to oral hypoglycemic drugs in type 1 vs 2?

A

1- unresponsive

2- responsive

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13
Q

Treatment in type 1 vs 2?

A

1- insulin necessary

2- diet, exercise, oral hypoglyemic drugs, insulin (maybe), reduce risk factors (essential)

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14
Q

What is essential for type 1 diabetes to occur?

A 
Initiating event (virus/toxin) -> autoimmune attack on beta-cell of pancreas
-in individuals w/ genetic predisp
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15
Q

What are the sx of type 1?

A

1) Polyuria
2) Polydipsia
3) Polyphagia
- all develop suddenly

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16
Q

What is the diagnosis of type 1 confirmed by?

A

1) HbA1c (> or = 6.5 mg/dl)

2) Fasting blood glucose (FBG > or = 126 mg/dl, normal = 70-99)

17
Q

What is the biochemical diff between type 1 and 2?

A

1 has ketonemia (high blood KBs)

-body doesn’t have insulin -> TAG -> lipolysis -> FAs -> liver -> KBs

18
Q

What is increased metabolically in type 1?

A

1) Hyperglycemia (increased gluconeogenesis)
2) Ketonemia
3) Extra FAs in liver -> VLDLs accumulation
4) Extra FAs in intestine -> chylomicrons accumulate
5) Glucagon (b/c no insulin)

19
Q

What are the 2 treatments of type 1?

A

1) Standard: 1-2 daily injections

2) Intensive: 3+/day

20
Q

What does intensive therapy result in?

A

3-fold increase in freq. of hypoglycemia (>90% of patients)

-Caused by excess insulin

21
Q

Highest prevalance of type 2 is in what people?

A

A. Indians, Alaskan natives, hispanics, african amer, asian amer

22
Q

What sx are common in type 2?

A

1) Polyuria
2) Polydipsia
3) Polphagia
- May be asymptomatic

23
Q

What does insulin resistance cause in target tissues (liver, adipose, muscle)?

A
  • Increased adipose lipolysis
  • Decreased FA oxidation
  • Increased gluconeogenesis
  • Decreased glucose uptake by GLUT-4
24
Q

What is key in the development of insulin resistance?

A

Excess adipose tissue

-IR increases w/ weight gain, decreases w/ weight loss

25
Q

Up to 10 years as an obese individual, before diagnosis of diabetes what happens?

A

Develop insulin resistance w/ compensatory hyperinsulinemia

-Pancreas initially retains beta-cell capacity

26
Q

With time what happens in type 2?

A

Beta cell dysfunction w/ declining insulin secretion + worsening hyperglycemia

27
Q

What are microvascular complications of type 2?

A

Retinopathy, neuropathy, nephropathy

28
Q

What are macrovascular complications of type 2?

A

Cardiovascular disease + stroke

29
Q

What is increased metabolically in type 2?

A

All the same as in type 1 (hyperglycemia + dyslipidemia), but ketonemia is not nearly as high as in type 1

30
Q

What are the hypoglyemic agents used in treatment of type 2?

A

1) Metformin - decreases hepatic output of glucose
2) Sulfonylureas - increase insulin secretion
3) Thiazolidinediones - increase peripheral insulin sensitivity
4) Alpha-glucosidase inhibitors - decrease dietary carb absorption
5) Later on insulin therapy

31
Q

What can often correct type 2?

A

Weigh reduction, exercise and medical nutrition therapy

32
Q

Increased HbA1c is linked to?

A

Higher chance of microdisease

33
Q

What are chronic complications of type 2?

A

Premature atherosclerosis, cardiovascular disease + stroke, retinopathy, nephropathy/neuropathy

34
Q

What is directly correlated to incidence of type 2?

A

Obesity and exercise

Biochem Exam 4 (7 decks)

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