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)
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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
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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
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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
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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
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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
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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
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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
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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
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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
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pyelonephritis is
more common in DM
more severe in DM
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