Flashcards in Type 2 Diabetes Deck (28):
Simple definition of insulin resistance?
Cells don't take up glucose in response to insulin.
Normally people make more insulin when their cells become more insulin resistant. What happens in Type 2 Diabetes (T2D)?
People are insulin resistant and don't make enough insulin.
What are 2 quantifiable measures altered in pre-diabetes?
Impaired glucose tolerance (post-prandial hyperglycemia).
Impaired fasting glucose (fasting hyperglycemia).
What differentiates pre-diabetes from diabetes? (not talking about numbers)
In pre-diabetes, increased insulin secretion is still somewhat compensating for decreased insulin sensitivity.
By the time T2D gets diagnosed, about how much beta cell function is usually lost?
Usually about 50% is lost by then.
What are the cutoffs of fasting glucose for "impaired" (pre-diabetes) and diabetes?
100 mg/dL for pre-diabetes.
126 mg/dL for diabtes.
What are the cutoffs for glucose tolerance (2hrs after glucose load) for pre-diabetes and diabetes?
140 mg/dL for pre-diabetes.
200 mg/dL for diabetes.
What percentage of US adults over 20 have pre-diabetes?
Is T2D just a pancreatic defect?
Nope. All sorts of things (like insulin resistance, increased gluconeogenesis, etc.) are going on.
What has been shown, surprising, to happen to glucagon in T2D?
Glucagon levels paradoxically rise after eating.
What are the 2 phases of insulin secretion? How is this altered in T2D?
1st phase - pre-formed granules of insulin release
2nd phase - more gradual release.
In T2D, the 1st phase doesn't occur.
Mechanism for altered glucagon activity in T2D?
Amyloid deposition in the islets impairs the ability of beta cells to suppress glucagon release by alpha cells.
What are incretins? What are 2 specific molecules?
Incretins are intestinal hormones that stimulate insulin secretion in response to food in the gut.
Glucagon-like peptide 1 (GLP-1)
Gastric inhibitory polypeptide (GIP)
How much of the insulin response to eating are incretins responsible for? How do we know this?
We know this because IV glucose does not increase insulin nearly as much as oral glucose. ("The Incretin Effect")
How is the incretin effect different in T2D?
The incretin effect is blunted in T2D.
What's the biggest single risk factor for T2D?
What's a pregnancy-related risk factor for diabetes?
Gestational diabetes - strong association with later development of T2D.
What kind of genetic associations are seen with risk for T2D?
Having one parent with T2D increases risk, both even more. (the way this is stated doesn't separate out environmental differences)
GWAS's have revealed some loci....
What are the 4 "classic" symptoms of T2D?
Polydypsia (excessive thirst)
Polyphagia (excessive hunger)
Unexplained Weight Loss
Non-specific symptoms of T2D? (name 5ish)
Dry mucous membranes / itchy skin
Recurrent infections (esp. candidiasis)
Poor wound healing
6 categories of signs of T2D?
Recurrent yeast infections.
Fundoscopic (eye exam) changes.
Neuro changes (sensation)
Foot problems (ulcers)
3 skin changes seen in T2D?
Ancanthosis nigricans (increased pigmentation in skin folds)
Carbuncles and furuncle.
4 diagnostic criteria, any of which are sufficient for Dx of T2D?
Fasting glucose > 126 mg/dL.
A1c > 6.5%
Random glucose > 200 mg/dL
2hr post-prandial glucose > 200 mg/dL
What is Hb A1c a product of? What is the time range for which is gives you information?
Hb A1c is a product of non-enzymatic glycosylation (sugar gets stuck on when there's too much).
A1c reflects average blood glucose over past 2-3 months.
How is A1c affected by post-prandial glucose rises?
It's more affected when A1c is low, it's less affected when A1c is high.
(It's biased toward higher values, and is more susceptible to being thrown off by meals when glucose is better controlled.)
(probably low yield)
Who should be screened for diabetes?
Everyone over 45.
People younger than that who have risk factors.
Can weight loss prevent overweight people with pre-diabetes from progressing to diabetes?