4Th Year Nutrition - Diabetes

Front 1

what are the other names for T2 DM?

Back 1

adult-onset and non-insulin dependent diabetes

Front 2

diabetes is a chronic condition that affects the ability of the body to ________.

Back 2

metabolize glucose

Front 3

is diabetes curable?

Back 3

no

Front 4

when is diabetes managable?

Back 4

throughout, especially in the early stages

Front 5

T2 DM accounts for ____ of diabetes cases.

Back 5

90%

Front 6

what are the other 2 types of diabetes?

Back 6

type 1 DM and gestational diabetes

Front 7

what tissues are affected by T2 DM?

Back 7

- skeletal muscle
- pancreas
- adipose tissue
- GI tract
- brain
and more

Front 8

what effect does T2 DM have on the pancreas?

Back 8

decreased insulin secretion

Front 9

what effect does T2 DM have on the kidney?

Back 9

increased glucose reabsorbtion

Front 10

what effect does T2 DM have on the brain?

Back 10

neurotransmitter dysfunction

Front 11

what effect does T2 DM have on adipose tissue?

Back 11

increased lipolysis

Front 12

what effect does T2 DM have on the digestive system?

Back 12

decreased incetin effect

Front 13

what effect does T2 DM have on the liver?

Back 13

increased hepatic glucose production and decreased hepatic glucose uptake

Front 14

what effect does T2 DM have on the musce tissue?

Back 14

decreased glucose uptake

Front 15

what effect does T2 DM have on Islet-a cells?

Back 15

increased glucagon secretion

Front 16

what is the main effect of T2 DM on the entire body?

Back 16

hyperglycemia

Front 17

what are the clinical syndromes of T2 DM

Back 17

- metabolic syndrome
- insulin resistance
- high fasting glucose
- high fasting insulin
- dyslipidemia
- impaired glucose tolerance
- hypertention

Front 18

what are the risk factors of T2 DM?

Back 18

- obesity
- inactivity
- abdominal obesity
- family history/ Genetics
- race/ age

Front 19

what ar the complications of T2 DM?

Back 19

- cardiovascular disease
- neuropathy (amputation)
- Nepropathy (kidney failure)
- retinopathy (blindness)
- alzheimer's disease

Front 20

what guidelines are used to diagnosed T2 DM?

Back 20

WHO

Front 21

what is the range for fasting glucose for impaired glucose intolerance?

Back 21

6.1 - 7 mmol/L

Front 22

what is the range for 2h - glucose for impaired glucose intolerance?

Back 22

7 - 11.1 mmol/L

Front 23

what is HbA1c ?

Back 23

glycosylated hemoglobin

Front 24

what is the range for fasting glucose for diabetes?

Back 24

> 7 mmol/L

Front 25

what is the range for 2h - glucose for diabetes?

Back 25

> 11.1 mmol/L

Front 26

what does HbA1c measure?

Back 26

the amount of hemoglobin that is bound by glucose (%)

Front 27

what does the level of HbA1c represent?

Back 27

the average blood glucose over a 2-3 month period (long term glucoregulation)

Front 28

what are the pros to HbA1c test?

Back 28

- no need to fast
- good correlation with diabetes severity
- can be used as a monitoring tool

Front 29

what are the cons to HbA1c test?

Back 29

- technically difficults test (not available in developing countries)
- results influenced by anemia, alcoholism, age, ethnicity and pregnancy

Front 30

why is 2h-glucose needed?

Back 30

- fasting plasma glucose fails to diagnose T2 DM in 30% of cases

Front 31

how long do humans spend in postprandial state?

Back 31

18 hours daily

Front 32

what is the oral glucose tolerance test (OGTT)?

Back 32

consumption of 50g of glucose and monitoring over 2 h.

Front 33

what is the treatment of T2 DM?

Back 33

control of glucose hormones

Front 34

what hormones are involved in the treatment of T2 DM?

Back 34

insulin and plamsa glucose

Front 35

where is glucose input in the fasting state in T2 DM?

Back 35

- hepatic glucose production

Front 36

in fasting, where is glucose utilization?

Back 36

- brain glucose uptake (+++)
- skeletal muscle glucose uptake (+/-)

Front 37

in fasting, the level of insulin is ______?

Back 37

- independent

Front 38

in T2 DM, heptic glucose production is _______ and can explain the elevated fasting glucose and insulin levels.

Back 38

increased

Front 39

in postprandial state, glucose input comes from?

Back 39

- glucose from meal (+)
- hepatic glucose production

Front 40

in postprandial state, where is the glucose utilization?

Back 40

- skeletal muscle glucose uptake (+++)
- glucose uptake by other tissues (adipose tissue and liver)

Front 41

in postprandial state, the level of insulin is ________.

Back 41

dependent

Front 42

in T2 DM, postprandial hyperglycemia can be explained by?

Back 42

1. impaired suppression of hepatic glucose production
2. decreased glucose uptake by SM and other tissues

Front 43

what happens during postprandial metabolism in the liver in full blown T2DM?

Back 43

decreased suppression of endogenous glucose production after a meal

Front 44

what happens during postprandial metabolism in the skeletal muscel in full blown T2DM?

Back 44

decreased insulin-stimulated glucose disposal

Front 45

in T2DM insulin secretion is _______ and ______.

Back 45

decreased and delayed

Front 46

in full blown T2DM, beta cell mass is _______, probably due to increased apoptosis. this leades to reduction in insulin secretion.

Back 46

decreased

Front 47

when is medication necessary for T2 DM?

Back 47

when imparied glucose tolerance becomes diabetes

Front 48

what is the prevalence of T2DM in North Americans, Europeans and Africans?

Back 48

2%

Front 49

what is the prevalence of T2DM in Pima Indians, Pacific Islanders (Nauru)?

Back 49

41 - 50%

Front 50

what is the prevalence of T2DM in chinese and Japanese?

Back 50

6-25%

Front 51

what is the obesity prevalence in diabetic population of north americans, europeans and africans

Back 51

60-80%

Front 52

what is the obesity prevalence in diabetic popultion in pima indians, pacific islanders (Nauru)?

Back 52

100%

Front 53

what is the obesity prevalence in diabetic population in chinese and japanese?

Back 53

30%

Front 54

if 1 of your siblings have T2DM, you risk of having T2DM increases by...?

Back 54

4 fold

Front 55

if 1 or your parents have T2DM, your risk of having T2DM increases by...?

Back 55

3.4-3.5 fold

Front 56

if both of your parents have T2DM, your risk of having T2DM increases by...?

Back 56

6.1 fold

Front 57

what is the concordance rates for T2DM for monozygotic twins?

Back 57

0.29 - 1.00

Front 58

what in the concordance rates for T2DM for dizygotic twins?

Back 58

0.10 - 0.43

Front 59

what are the envirnomental factors associated with the risk of T2DM?

Back 59

- nutrition (resistant starch, fatty acids, coffee/caffeine, reservatrol)
- minerals and vitamin intake
- physical inactivity/exercise
- sleep patterns
- stress/glucocorticoids hormones
- heavy metals and pesticides
intrauterine environment
- lots more

Front 60

what is the definition of dietary fibre?

Back 60

carbohydrates polymers (10+ units) that are not hydrolyzed by the endogenous enzymes of the small intestines of humans.