Term
what is the criteria for the dx of diabetes mellitus? |
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Definition
fasting plasma glucose >=126 mg/dL; 2 hour plasma glucose >=200 mg/dL |
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Term
what is the criteria for dx of "pre diabetic state"? |
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Definition
fasting plasma glucose >=100 and <126 mg/dL; 2 hour plasma glucose >=140 and <200 mg/dL |
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Term
what is metabolic syndrome? |
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Definition
clustering of sx: high visceral fat, high trigs, low HDL, impaired glucose tolerance, measure waist circumference at level of iliac crest (>40 in men and >35 in women). any 3 out of these 5 sx = metabolic syndrome |
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Term
what are the 3 most common organs affected by microvascular complications of db? |
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Definition
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Term
why do diabetics have an increase in CV disease? |
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Definition
hyperglycemia, hypertension, dyslipidemia, pro-coagulant state |
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Term
what HLA types are assoc with type 1 db? |
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Definition
HLA DR3 and HLA DR4 (HLA DR2 provides protection) |
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Term
what are the 3 autoantibodies assoc with type 1 db? |
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Definition
anti-insulin, anti-glutamic acid decarboxylase, anti-ICA512 (presence of one ab is mildly predicative of type 1 db, but presence of all 3 is highly predictive) |
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Term
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Definition
genetic cause for beta cell abnormality; usually type 2 db is beta cell abnormality + insulin resistance (from metabolic syndrome). metabolic syndrome --> increase in visceral adipodisity --> increased intracellular lipid in liver, muscle, pancreatic beta cell --> activates PKC and IKKB pathways to activate serine and threonine phosphorylases --> act on IRS and PI-3 kinase to reduce their availability to carry out intracellular insulin signaling --> reduces glucose uptake in muscle and adipose tissue, reduces glycogen synthesis in liver and NO prod in endothelial cells |
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Term
why do diabetics get fasting hyperglycemia (remember, first step is post-prandial then if it worsens get fasting)? |
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Definition
the liver is regulated by levels of INSULIN (not glucose). in diabetics, the liver becomes insulin resistant and therefore needs 3x as much insulin to regulate it --> B cell function decreases and it cannot put out that much insulin --> liver thinks it has low glucose --> overproduces glucose |
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Term
what are incretins and how do they contribute to db? |
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Definition
GI hormone that is secreted post-prandially --> acts on beta cells to amplify the insulin response to glucose (DB pts deficient incretin action) |
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Term
is fasting or post-prandial glucose primarily responsible for hyperglycemia in type 2 diabetes? |
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Definition
in poorly controlled diabetics, FASTING glucose is responsible for hyperglycemia. in WELL controlled diabetcis, POSTPRANDIAL glucose is responsible |
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Term
what do we use to decrease glucose in the fasting state? |
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Definition
sulfonylureas, metformin, nighttime basal insulin (glargine insuline) |
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Term
what do we use to treat hyperglycemia in the post-prandial state? |
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Definition
rapid acting insulin analogues and inhaled insulin (acarbose, nateglinide, pramlintide, exenatide) |
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Term
how do we decrease both fasting AND post-prandial glucose? |
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Definition
sulfonylrueas+metformin; thiazolindeinediones, repaglinide, exenatide, sitagliptin |
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Term
AE of thiazolidinediones? |
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Definition
most potent tx; small increase in edema and CHF, weight gain, bone fracture |
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Term
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Definition
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Term
how do sulfonylurea drugs work? |
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Definition
close the K channel independent of glucose (normally glu generates ATP --> ATP causes K channel to close --> Ca channel opens --> insulin secretion) |
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Term
how do GLP receptor drugs work? |
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Definition
stimulate insulin secretion by activating cAMP pathway in B cell --> AMPLIFY insulin secretion d/t glucose (GLP receptor = receptor on K channel that will lead to closure) so same amt of glucose will cause twice as much insulin output |
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Term
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Definition
decreases glucose (mechanism unknown) |
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Term
how do thiazolidinediones work? |
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Definition
activates PPAR which inhibits lipoprotein lipase which causes peripheral fat to make more smaller cells with less fat and causes apoptosis of visceral fat |
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