Lecture 28: Diabetes Flashcards Preview

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Flashcards in Lecture 28: Diabetes Deck (61)
1

How many grams of FFAs in the body?

12,000

2

How many grams of glucose in the body? How much is circulating?

80
20 grams circulating = 80 kcal

3

What % of the body's total energy requirement does the brain consume? How many grams a day is that in the resting state?

25% = 120 g/day

4

What is the needed blood glucose level for the brain to maintain its normal function?

70 mg/dL

5

What is the blood glucose limit for danger for the brain?

50 mg/dL

6

What 3 types of cells are insensitive to insulin?

1. Brain
2. RBCs/WBCs
3. Renal medulla

7

Why do patients with sepsis often exhibit hypoglycemia?

Increase in WBCs which can only use glucose for energy

8

What is the renal medulla?

A deep part of the kidney which is not exposed to a lot of O2 so cannot oxidize FAs so only uses anaerobic glucose metabolism

9

Why is lactic acidosis often seen in extremely ill patients?

Because they rely on anaerobic glycolysis to get energy fast and produces a ton of lactate

10

What 4 types of cells are sensitive to insulin?

1. Liver
2. Muscle
3. Adipocytes
4. Heart

11

Grams of glycogen stored in muscleS?

400 g

12

Grams of glycogen stored in liver?

100 g

13

Grams of fat stores?

12,000

14

Grams of protein stores?

6,000

15

For how long after eating is exogenous glucose the main source of fuel?

4 hours

16

For how long after eating is glycogen the main source of fuel?

4-16 hours

17

For how long after eating is gluconeogenesis the main source of fuel?

16 hrs-40 days

18

What does the drop in gluconeogenesis after day 2 of fasting due to?

Ketogenesis helping out

19

Diabetes incidence?

1 in 3

20

How many people in the US have DM?

29.1 million

21

How many people in the US have pre-diabetes?

86 million

22

Range of normal FBG?

60-100

23

Range of impaired FBG?

101-125

24

Range of diabetes FBG?

Above 126

25

How is DM diagnosed?

1 of the following:
1. Random plasma glucose > 200 mg/dL* + DM symptoms
2. FPG > 126 mg/dL*
3. PG > 200 mg/dL 2 hrs after 75g glucose load*
4. Hb A1C > 6.5%

* need to be repeated the next day

26

By what age have we produced all of the beta cells for our lifetime?

12

27

What is putative trigger?

The autoimmune reaction that causes B-cell injury in T1DM

28

What % of beta cells are left when T1DM is diagnosed?

Usually about 10%

29

What could we do if we were able to diagnosis T1DM earlier?

Administer immunosuppressive drugs to stop disease progression

30

When is glucose used during a race?

When speeding and at the end of the race

31

What 3 tissues can use both glucose and FAs?

1. Heart
2. Muscles
3. Liver

32

What causes hyperglycemia in diabetes?

1. Insulin resistance
2. Gluconeogenesis

33

What 2 things happen during gestational diabetes?

1. β-cell dysfunction
2. Insulin resistance

34

How to go from mM to mg/dL?

Multiply by 18

35

What are the 2 types of insulins used to treat diabetics? What periods do they each cover?

1. Bolus: fast acting: covers 2 hrs after eating
2. Basal: longer effect: between meals and during sleep

36

Describe the basal glucose level during pregnancy.

Lower than normal because fetus uses glucose for growth: 60-90 mg/dL

37

Can fuels cross the placenta?

Yeah: glucose, FAs, ketone bodies, AAs

38

Can insulin cross the placenta?

NOPE

39

What happens if glucose levels are too high during pregnancy?

Before week 7: fetus does not have a pancreas so cannot control the high levels
After week 7: fetus will synthesize a lot of insulin causing increased growth, fat deposition, hypoxia, impaired lung maturation, or even macrosomia

40

Can a pregnant woman's DM be treated without baby being affected?

Yes because insulin cannot cross the placenta

41

What is the best way to measure insulin levels?

Glucose tolerance test: drink glucose and measure amount of insulin in the blood

42

What is the best way to measure insulin resistance?

Insulin euglycemic pump test:
1. Start constant insulin infusion in patient
2. Start variable glucose infusion to counter hypoglycemia
3. Once steady state is reached we can know the max amount of glucose tissues can absorb

43

What are glucose disposal rates?

Max rate of glucose absorbance at a certain insulin plasma concentration

44

Describe the trend of insulin secretion during the progression of T2DM.

- Normal at first
- Increases during the impaired glucose intolerance phase
- Reaches its peak during the undiagnosed T2DM phase
- Decreases back to normal levels during diagnosed T2DM phase (but not enough to control glucose levels because insulin resistance is now extremely high)

45

When do we start seeing a rise in post-prandial and fasting BG levels in T2DM progression?

When insulin secretion starts decreasing

46

At what phase of T2DM do we see micro and macrovascular complications?

Usually before it's diagnosed

47

What's the story with the Pima Indians?

Group of Indians who cultivated the desert before the 1850s. Then american settlers came west and took their land and moved them to a reservation where they had to eat what american ranchers ate: high fat meats and bread => huge rise in T2DM in these peeps because of genetic predisposition and environment: 34.2% of those in Arizona have T2DM compared to 6.4% of those living in Mexico (only due to genes)

48

How does visceral fat affect T2DM? Why?

Increase in visceral fat = increase in risk of T2DM because visceral fat releases substrate (like FFAs) and hormones (like TNF = tumor necrosis factor and resistin) that promote insulin resistance

49

What is visceral fat?

Body fat that is stored within the abdominal cavity and is therefore stored around a number of important internal organs such as the liver, pancreas and intestines.

50

What is insulin resistance syndrome?

Insulin resistance caused by increase in visceral fat

51

What causes atherosclerosis in insulin resistance syndrome? What does this put patients at risk of?

Insulin resistance causes dyslipidemia (low HDL, High TG) and hypertension both leading to atherosclerosis

2-4 x more at risk to have heart disease

52

What is atherosclerosis?

Plaque build-up inside arteries

53

What is the exact definition of insulin resistance?

Acquired abnormality related to an accumulation of visceral adipose tissue in genetically predisposed persons

54

What are the 2 genetic components of T2DM?

1. Diabetes-related genes
2. Diabetogenes

55

What are the 3 environmental components of T2DM?

1. Obesity
2. Activity
3. Diet

56

3 benefits of exercise for T2DM patients?

1. Improves insulin sensitivity
2. Mobilizes Visceral Fat
3. Improves Glucose Control

57

What is the UKPDS?

Study with T2DM patients: retinopathy, nephropathy, and possibly neuropathy are benefited by lowering blood glucose levels in type 2 diabetes with intensive therapy, which achieved a median HbA1c of 7.0% compared with conventional therapy with a median HbA1c of 7.9%. The overall microvascular complication rate was decreased by 25%.

58

What did the Diabetes Control and Complications Trial (DCCT) prove? With what patients?

Intensive management of T1D prevents complications:
1. Test blood glucose 4x/day
2. Insulin pump or injection 4x/day
3. Adjust insulin
4. Diet + exercise plan
5. See docs/monthly

59

What is a surrogate marker for risk of diabetic complications?

HbA1C

60

Which type of DM can obesity cause?

BOTH

61

How does heart disease affect the heart's metabolism? Why is this critical?

Looses ability to metabolize FAs, so hypoglycemia is very dangerous for them