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Endo/Repro Exam 2 > Type I and Type II Diabetes > Flashcards

Type I and Type II Diabetes Flashcards

1
Q

What is Type I known as?

A

Insulin dependent

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2
Q

What is Type II known as?

A

Insulin resistant

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3
Q

What typically causes Type I?

A

Autoimmune destruction of beta cells

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4
Q

What typically causes Type II?

A

Loss of insulin’s effectiveness on metabolism effector cells become less receptive to insulin

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5
Q

When does Type I typically present?

A

Early in life but may develop in adults 30-40s

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6
Q

When does Type II typically present?

A

Adults typically due to obesity

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7
Q

Four characteristic symptoms of diabetes:

A
  1. ) Polyphagia
  2. ) Polydipsia
  3. ) Polyuria
  4. ) Glucosuria
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8
Q

What occurs in Type I if untreated?

A

Development of ketoacidosis

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9
Q

What occurs in Type II if untreated?

A

Persistent hyperglycemia but rarely ketoacidosis

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10
Q

What occurs to glycogen stores without insulin?

A

They are depleted and not replenished

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11
Q

What occurs to fatty acids without insulin?

A

They are depleted and excess glucose cannot be stored as fatty acids

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12
Q

What causes ketoacidosis?

A

Triglyceride stores are mobilized and ketone bodies are produced in the liver

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13
Q

What is the effect of insulin on alpha cells?

A

Suppresses secretion of glucagon

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14
Q

What is the effect of alpha cells in Type I diabetes?

A

Lack of insulin causes the alpha cells to continue to secrete glucagon resulting in uncontrolled hyperglycemia from stimulated gluconeogenesis

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15
Q

Why does ketoacidosis not occur in Type II diabetics?

A

Insulin increases proportionally to glucose levels in the blood and cells are somewhat responsive enough to insulin so that enough glucose enters the cells to suppress the need for ketones as energy

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16
Q

Diabetes risk factors in males:

A

BMI > 25
Waist circumference > 40 inches
Older than 40

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17
Q

How can large amounts of fructose cause insulin resistance?

A

Fructose does not stimulate insulin release

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18
Q

What is fructose used for in the body?

A

Mostly for acetyl-CoA and fat (locally in the liver causing non-alcoholic fatty liver disease)

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19
Q

Fasting blood glucose test levels:

A

> 126 mg/dL after 8 hours or more without food

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20
Q

Casual/random blood glucose levels:

A

> 200 mg/dL at any time

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21
Q

What does glucose cause in hemoglobin?

A

Irreversible binding with N-terminus of beta chain

22
Q

What is A1c dependent on?

A

Exposure of erythrocyte to glucose over 8-12 weeks

23
Q

What is the target A1c level?

A

Less than 6.5% to 7% of Hb being A1c

24
Q

What does fructosamine test do?

A

Tests the glycosylation of proteins typically albumin

25
Q

What does fructosamine test tell you?

A

Rapid changes in blood glucose levels over 2-3 weeks

26
Q

Normal values of fructosamine test?

A

200-285 micromoles/L

27
Q

When would you use fructosamine test?

A
  1. ) Rapid changes in diabetes treatment
  2. ) Diabetic pregnancy
  3. ) Shortened RBC life span
  4. ) Abnormal forms of hemoglobin
28
Q

What does elevated blood glucose levels cause in blood vessels?

A

Increase in osmotic pressure causing potential bursting of small capillaries

29
Q

When is gestational diabetes screening test done?

A

24-26 weeks into pregnancy

30
Q

What levels denote gestational diabetes?

A

> 126 mg/dL fasting

>200 mg/dL casual/random

31
Q

Two hormones that are noted to be involved in normal gestational insulin resistance?

A

Human placental lactogen (hPL)

Human placental growth hormone (PGH)

32
Q

How does hPL and PGH have affect on mother?

A

Produced by placenta and enter the mother’s bloodstream

33
Q

What week does PGH dominate?

A

12 weeks through term

34
Q

What affect does hPL and PGH have?

A

Conserves glucose by increasing lipolysis

35
Q

Cause of diabetes insipidus?

A

Defect in ADH

36
Q

Two types of diabetes insipidus?

A

Central

Nephrogenic

37
Q

When does neonatal (NDM) diabetes mellitus occur?

A

In the first 6 months of life

38
Q

Three defective proteins in NDM, their age of onset, their treatment and their inheritance patterns:

A

SUR1: 1-3 months, sulfonylureas, autosomal recessive
Kir6.2: 3-6 months, sulfonylureas, autosomal dominant
Glucokinase: 1 week, insulin, autosomal recessive

39
Q

What is maturity-onset diabetes of the young (MODY)?

A

Defective MODY gene which are involved in beta-cell development

40
Q

MODY inheritance patterns?

A

Autosomal dominant

41
Q

What is Diabulimia?

A

An eating disorder associated with Type I diabetes

42
Q

What occurs in Diabulimia?

A

Diabetics withholding insulin doses to lose weight

43
Q

How is metabolic syndrome diagnosed?

A

As having 3/5 medical conditions

44
Q

What are the medical conditions in metabolic syndrome?

A
  1. ) Elevated fasting blood glucose levels
  2. ) Abdominal obesity
  3. ) Elevated blood pressure
  4. ) High serum triacylgylcerides (> 150 mg/dL)
  5. ) Abnormally low HDL cholesterol levels (
45
Q

What occurs when TAG intake is greater than TAG oxidation for energy?

A

Adipocytes enlarge to store the excess TAGs

46
Q

What occurs when adipocytes reach their maximum capacity?

A

They secrete macrophage chemotaxis protein (MCP-1)

47
Q

What does MCP-1 cause?

A

Macrophage infiltration and production of TNF-alpha

48
Q

What does TNF-alpha cause?

A

TAG hydrolysis and fatty acid release

49
Q

What is a theory for metabolic syndrome?

A

Lipid toxicity hypothesis

50
Q

What occurs when TNF-alpha causes a large release of FA?

A

The FFA overwhelm muscle cells and accumulate forming small lipid droplets

51
Q

What does the ectopic storage of FFA result in?

A

Results in muscle cells being resistant to insulin which decreases glycogen stores

Endo/Repro Exam 2 (18 decks)

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