Flashcards in Diabetes Deck (54)
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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
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2 hrs after 75 g glycose load =>200
DM- small BV damage
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predisone
increases risk for diabetes
4
percentage of people that develop DM overtime who have IGT?
25%
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Metabolic syndrome must have greater than 3 of
obesity (increase waist circumference)
lipids (increase TG, decrease HDL)
BP >130/85
glucose >100
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DM 1 type 1a
autoimmune
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DM1 type 1B
idiopathic
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HLA association type 1 DM
HLA-DR, HLA-DQ
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Autoimmune Polyglandular Syndrome
dm type 1
hashimotos
addisons
premature ovarian failure
SLE, RA, pernicious anemia, etc
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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
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IDDM2 insulin gene
class of variable number of tandem repeats at that locus (class III protective, class I predisposing)
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PTPN22 and CTLA4
genes associated with cytotoxic T cell function
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breast feeding and DM1
protective
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cytokine mechanism of DM
activation of TH1 is bad vs Th2 tell cells
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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)
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promising secondary preventiont rials
heat-shocked protein 60 and CTLA 4 IG
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quantitatively most important for stimualted glucose uptake
muscle
21
insulin increases and increases with glucose until
insulin maxes out and falls
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the heavier you are per height
the more insulin resistant you are
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Rare AD diseases that produce DM2
MODY- maturity onset diabetes of the young
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most common MODY
MODY3
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MODY easily treated with
sulfonylurea (insulin ineffective)
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MODY2
mutation of glucokinase- glucose sensor; islet enzyme which converts G-->G6P, which increases insulin release
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normal fasting insulin level
<10 uU/L
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exercising vs resting muscle
exercisign muscle can take glucose up without needing insulin but resting muscle is under control of insulin
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insulin does not do this with liver
regulate how much the liver can take up
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insulin does do this with liver
tells it to stop gluconeogenesis and glycogenolysis
during fastign, resting glucose is also higher
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insulin and fat
regulates glucose uptake
regulates FFA output
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adiponectin is equal to
1/BMI
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adiponectin
decreases insulin resistance and is LOW in type2 DM
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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
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why is GLP1 released
neural reflex (via enteroendocrine cells) in jejunum in response to eating
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T2DM & GLP1
decreased levels
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acanthosis
skin rash common sign of insulin resistance
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three major complications of uncontrolled DM
microangiopathy
accelerated atherosclerosis
opportunistic infections
40
kid target for opportunistic infections
kidney
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kidneys transplanted frm diabetic to normal patient
will be normal
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types of infections common in diabetics
fungal (candida, mucormycosis)
bacteria (pyelonephritis)
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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
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early changes Type 1 DM
autoimmune attack on B cells with lymphocyte infiltration
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late changes Type 1 DM
islet atrophy- absence of B cells, seen with IHC stain for insulin
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Type II early changes
no changes in islets
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mid course Type II
b cell malfunction
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later type II
b cell depletion/atrophy, but not absent
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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
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