Diabetes Flashcards Preview

ENDO > Diabetes > Flashcards

Flashcards in Diabetes Deck (54)
Loading flashcards...
0

three criteria for diabetes

symptoms + random >200

fasting glucose >125 2 xs

after a 75 g glucose load, a plasma glucose at or above 200 after 2 hrs (need to be low carb for two days before)

1

2 hr after 75g carb load= 150-200

impaired glucose tolerance- big vessel damage

2

2 hrs after 75 g glycose load =>200

DM- small BV damage

3

predisone

increases risk for diabetes

4

percentage of people that develop DM overtime who have IGT?

25%

5

Metabolic syndrome must have greater than 3 of

obesity (increase waist circumference)
lipids (increase TG, decrease HDL)
BP >130/85
glucose >100

6

DM 1 type 1a

autoimmune

7

DM1 type 1B

idiopathic

8

HLA association type 1 DM

HLA-DR, HLA-DQ

9

Autoimmune Polyglandular Syndrome

dm type 1
hashimotos
addisons
premature ovarian failure
SLE, RA, pernicious anemia, etc

10

DR+Q vs DR3/4+DQ

Dr+Q is protective
DR3/4+DQ are at a high risk

11

DR and DQ are on chromsome

6

12

IDDM-2 insulin gene is on

chromsome 11

13

IDDM2 insulin gene

class of variable number of tandem repeats at that locus (class III protective, class I predisposing)

14

PTPN22 and CTLA4

genes associated with cytotoxic T cell function

15

breast feeding and DM1

protective

16

cytokine mechanism of DM

activation of TH1 is bad vs Th2 tell cells

17

what is the most predicative of DM1 development risk?

insulin antibodies in children
glutamic a decarboxylase (GAD) autoAb are most pesistent are thus the only ones tested in adulthood

18

only primary prevention that was successful in diabetes

oral insult- delayed onset (but still occured)

19

promising secondary preventiont rials

heat-shocked protein 60 and CTLA 4 IG

20

quantitatively most important for stimualted glucose uptake

muscle

21

insulin increases and increases with glucose until

insulin maxes out and falls

22

the heavier you are per height

the more insulin resistant you are

23

Rare AD diseases that produce DM2

MODY- maturity onset diabetes of the young

24

most common MODY

MODY3

25

MODY easily treated with

sulfonylurea (insulin ineffective)

26

MODY2

mutation of glucokinase- glucose sensor; islet enzyme which converts G-->G6P, which increases insulin release

27

normal fasting insulin level

<10 uU/L

28

exercising vs resting muscle

exercisign muscle can take glucose up without needing insulin but resting muscle is under control of insulin

29

insulin does not do this with liver

regulate how much the liver can take up

30

insulin does do this with liver

tells it to stop gluconeogenesis and glycogenolysis
during fastign, resting glucose is also higher

31

insulin and fat

regulates glucose uptake
regulates FFA output

32

adiponectin is equal to

1/BMI

33

adiponectin

decreases insulin resistance and is LOW in type2 DM

34

leptin

signals satiety and increase with increasing fat mass, so obese individuals must have some resistance to it

35

functions of glucagon like peptide

decreases glucagon realse, increases insulin release and responsiveness
decreases appetite

36

why is GLP1 released

neural reflex (via enteroendocrine cells) in jejunum in response to eating

37

T2DM & GLP1

decreased levels

38

acanthosis

skin rash common sign of insulin resistance

39

three major complications of uncontrolled DM

microangiopathy
accelerated atherosclerosis
opportunistic infections

40

kid target for opportunistic infections

kidney

41

kidneys transplanted frm diabetic to normal patient

will be normal

42

types of infections common in diabetics

fungal (candida, mucormycosis)
bacteria (pyelonephritis)

43

mechanisms of retinal injury

fluid retention by glucose (can be reversed with good control)
microangiopathy-->occlusion-->thickened endothelial cell prolif-->angiogensis
eventual ischemia and infacrts

44

early changes Type 1 DM

autoimmune attack on B cells with lymphocyte infiltration

45

late changes Type 1 DM

islet atrophy- absence of B cells, seen with IHC stain for insulin

46

Type II early changes

no changes in islets

47

mid course Type II

b cell malfunction

48

later type II

b cell depletion/atrophy, but not absent

49

late changes Type II DM

amyloid deposition in islets, which is not specific to, but is very common in end stage DM2

50

Malliard Reaction

browning in cells
glucose becomes reactive-->interacts with lipids-->bicarb structures not stable-->less function-->AGEs accumulate inside and outside cell

**cannot be cleared and effects are worse with aging

51

how do AGEs interaact with blood vessel

get put out in the extravascular space (basement membrane)--Bind stable proteins (collagen IV, laminin)-->ECM no longer degraded properly-->increase BM that is stiffer and less permeable

this causes INTRACELLULAR TF, TGFB inflam, NO gen
and endothelial cell swells-->looses fx-->dies

52

pyelonephritis is

more common in DM
more severe in DM

53

ischemia serves as a ___for infection

nidus