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ENDO > Diabetes > Flashcards

Diabetes Flashcards

0
Q

2 hr after 75g carb load= 150-200

A

impaired glucose tolerance- big vessel damage

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1
Q

three criteria for diabetes

A

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)

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2
Q

2 hrs after 75 g glycose load =>200

A

DM- small BV damage

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3
Q

predisone

A

increases risk for diabetes

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4
Q

percentage of people that develop DM overtime who have IGT?

A

25%

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5
Q

Metabolic syndrome must have greater than 3 of

A

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

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6
Q

DM 1 type 1a

A

autoimmune

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7
Q

DM1 type 1B

A

idiopathic

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8
Q

HLA association type 1 DM

A

HLA-DR, HLA-DQ

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9
Q

Autoimmune Polyglandular Syndrome

A 
dm type 1
hashimotos
addisons
premature ovarian failure
SLE, RA, pernicious anemia, etc
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10
Q

DR+Q vs DR3/4+DQ

A

Dr+Q is protective

DR3/4+DQ are at a high risk

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11
Q

DR and DQ are on chromsome

A

6

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12
Q

IDDM-2 insulin gene is on

A

chromsome 11

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13
Q

IDDM2 insulin gene

A

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

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14
Q

PTPN22 and CTLA4

A

genes associated with cytotoxic T cell function

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15
Q

breast feeding and DM1

A

protective

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16
Q

cytokine mechanism of DM

A

activation of TH1 is bad vs Th2 tell cells

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17
Q

what is the most predicative of DM1 development risk?

A

insulin antibodies in children

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

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18
Q

only primary prevention that was successful in diabetes

A

oral insult- delayed onset (but still occured)

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19
Q

promising secondary preventiont rials

A

heat-shocked protein 60 and CTLA 4 IG

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20
Q

quantitatively most important for stimualted glucose uptake

A

muscle

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21
Q

insulin increases and increases with glucose until

A

insulin maxes out and falls

22
Q

the heavier you are per height

A

the more insulin resistant you are

23
Q

Rare AD diseases that produce DM2

A

MODY- maturity onset diabetes of the young

24
Q

most common MODY

A

MODY3

25
Q

MODY easily treated with

A

sulfonylurea (insulin ineffective)

26
Q

MODY2

A

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

27
Q

normal fasting insulin level

A

<10 uU/L

28
Q

exercising vs resting muscle

A

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

29
Q

insulin does not do this with liver

A

regulate how much the liver can take up

30
Q

insulin does do this with liver

A

tells it to stop gluconeogenesis and glycogenolysis

during fastign, resting glucose is also higher

31
Q

insulin and fat

A

regulates glucose uptake

regulates FFA output

32
Q

adiponectin is equal to

A

1/BMI

33
Q

adiponectin

A

decreases insulin resistance and is LOW in type2 DM

34
Q

leptin

A

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

35
Q

functions of glucagon like peptide

A

decreases glucagon realse, increases insulin release and responsiveness
decreases appetite

36
Q

why is GLP1 released

A

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

37
Q

T2DM & GLP1

A

decreased levels

38
Q

acanthosis

A

skin rash common sign of insulin resistance

39
Q

three major complications of uncontrolled DM

A

microangiopathy
accelerated atherosclerosis
opportunistic infections

40
Q

kid target for opportunistic infections

A

kidney

41
Q

kidneys transplanted frm diabetic to normal patient

A

will be normal

42
Q

types of infections common in diabetics

A

fungal (candida, mucormycosis)

bacteria (pyelonephritis)

43
Q

mechanisms of retinal injury

A

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

44
Q

early changes Type 1 DM

A

autoimmune attack on B cells with lymphocyte infiltration

45
Q

late changes Type 1 DM

A

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

46
Q

Type II early changes

A

no changes in islets

47
Q

mid course Type II

A

b cell malfunction

48
Q

later type II

A

b cell depletion/atrophy, but not absent

49
Q

late changes Type II DM

A

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

50
Q

Malliard Reaction

A

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
Q

how do AGEs interaact with blood vessel

A

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
Q

pyelonephritis is

A

more common in DM

more severe in DM

53
Q

ischemia serves as a ___for infection

A

nidus

ENDO (5 decks)

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