Diabetes Mellitus Flashcards

(34 cards)

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
Up to 10 years as an obese individual, before diagnosis of diabetes what happens?
Develop insulin resistance w/ compensatory hyperinsulinemia | -Pancreas initially retains beta-cell capacity
26
With time what happens in type 2?
Beta cell dysfunction w/ declining insulin secretion + worsening hyperglycemia
27
What are microvascular complications of type 2?
Retinopathy, neuropathy, nephropathy
28
What are macrovascular complications of type 2?
Cardiovascular disease + stroke
29
What is increased metabolically in type 2?
All the same as in type 1 (hyperglycemia + dyslipidemia), but ketonemia is not nearly as high as in type 1
30
What are the hypoglyemic agents used in treatment of type 2?
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
What can often correct type 2?
Weigh reduction, exercise and medical nutrition therapy
32
Increased HbA1c is linked to?
Higher chance of microdisease
33
What are chronic complications of type 2?
Premature atherosclerosis, cardiovascular disease + stroke, retinopathy, nephropathy/neuropathy
34
What is directly correlated to incidence of type 2?
Obesity and exercise