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26 Cards in this Set
- Front
- Back
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Screening for DM
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Should be considered for all overweight adults who have other risk factors; screening all pts every 3 years starting at age 45
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Screening for Type 2 DM in kids
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Screen every 3 years starting at age 10 (or puberty if before age 10) if overweight and have 2 risk factors
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Risk factors for DM
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physical inactivity, first-degree relative with DM,
members of a high-risk ethnic population (e.g., African American, Latino, Native American, Asian American, Pacific Islander), women who delivered a baby weighing >9 lb. or were diagnosed with GDM, hypertension (≥140/90 mmHg or on therapy for hypertension), HDL cholesterol level <35 mg/dl and/or a triglyceride level >250 mg/dl women with PCOS, A1C ≥5.7%, IGT, or IFG on previous testing, other clinical conditions associated with insulin resistance (e.g., severe obesity, acanthosis nigricans), history of CVD |
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tools for screening
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FPG, OGTT, HA1C
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diagnostic criteria
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Need one of the following: HbA1C 6.5+ OR FPG 126+ OR 2-hour plasma glucose 200+ during OGTT OR classic sx of hyperglycemia, random plasma glucose of 200+
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glucose in fasting state
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glucagon from pancreas acts at liver to maintain FPG 60-90
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glucose in fed state
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blood glucose rises 90-140; incretins work in intestine to slow glucose uptake and promote satiety in stomach, stimulate release of insulin from pancreas. Insulin promotes glut2 transporters to uptake glucose from blood and turn it into G6P. Amylin acts at brain to suppress glucagon, slow gastric emptying.
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Type 1 DM
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pancreatic beta cell destruction >> no insulin secreted; glucagon is hypersecreted (it's normally suppressed by insulin) >> liver produces glucose >> hyperglycemia with inability to clear normally.
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stages of Type 1 DM
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genetic predisposition >> precipitating event >> immunologic abnormalities >> progressive loss of insulin >> overt DM, C-peptide present >> no C-peptide present
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type 1 DM pathophysiology
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AI destruction; triggering events could be something like CMV, cow's milk, enteroviruses
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AutoAB
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GAD, etc. Allow you to monitor progression to DM
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AI conditions associated w/ Type 1 DM
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Thyroiditis, Graves Dz, Celiac, Addison's, Pernicious Anemia
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Type 1 DM epi
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can occur at any age but more common in young adults; recessive genetic role; 2% have parent w/ dz; 10% have first-degree relative
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Type 1 DM clinical features
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characterized by insulin defic and widely fluctuating blood sugars; ketoacidosis can occur.
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Natural hx of Type 2 DM
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beta cells get blinded to glucose
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glucolipotoxicity
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hyperglycemia begets hyperglycemia; hyperglycemia impairs insulin secretion and action
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Type 2 DM epi
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seen mostly in adults but increasing in kids; 50% have affected 1st degree relative
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Type 2 DM clinical
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often insidious onset
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how to tell type 1 vs type 2
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C-peptide is low normal, then zero; Anti-GAD AB in type 1; C-peptide is high-normal then low-normal in Type 2
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Type 2
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can occur in thin people, may have fam hx, glucose tends to be more stable, w/ milder hypoglycemia. C peptide is nigh normal, then low. No AB seen
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Type 1 tx
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insulin
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type 2 tx
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orals, injectables +/- insulin
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preDM
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FPG 100-125 (IFG), OGTT 140-199 (IGT), A1C 5.7-6.4
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pre DM tx
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lifestyle intervention more effective than meds
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risk factors for DM
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inactivity, 1st degree relative w/ dz, high-risk ethnic group, gestational DM, HTN, low HDL, high TG, PCOS, A1c 5.7+
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most at risk group
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Latina females
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