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20 Cards in this Set
- Front
- Back
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Generally speaking, do those with permanent neonatal diabetes generally end up on insulin for the rest of their lives?
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no, they generally can switch from I to sulfonylurea (high doses)
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How do sulfonylureas work?
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Sulfonylureas bind to an ATP-dependent K+ (KATP) channel on the cell membrane of pancreatic beta cells. This inhibits a tonic, hyperpolarizing efflux of potassium, thus causing the electric potential over the membrane to become more positive. This depolarization opens voltage-gated Ca2+ channels. The rise in intracellular calcium leads to increased fusion of insulin granulae with the cell membrane, and therefore increased secretion of (pro)insulin.
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What are the major metabolic defects that are present in type 2 diabetes mellitus which lead to glucose elevation?
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decreased glucose transport and utilization at the level of muscle and adipose tissue, increased glucose production by the liver and relatively decreased insulin secretion by the pancreas. Added to this abnormal flux is any dietary carbohydrate which is absorbed as glucose or converted to glucose during the absorption or postabsorptive process.
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Binding of insulin to insulin receptors in peripheral tissue (muscle) leads to what, biochemically speaking?
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autophosphorylation of Insulin receptors and phosphorylation of tyrosines on a variety of cellular proteins including members of the insulin receptor substrate family and Cbl-CAP.
- Cbl-CAP --> translocation of GLUT4 to membrane. IRS family --> alterations in glucose, lipid, and protein metabolism; and changes in gene expression and cell growth. |
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Genetics of Type 1 behave in what inheritance manner?
In type 1 DM, what is actually responsible for B-cell death? What % of B-cells must be destroyed before overt diabetes becomes apparent? |
autosomal recessive
Cell mediated immune response, even though autoantibodies are a marker for the dz process. 80-90% |
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Order the following stages in T1 DM:
- overt immunological abnormalities w/ normal insulin release - no c-peptide - overt diabetes w/ c-peptide - progressive loss of insulin release w/ normal glucose |
(1) immuno w/ normal Insulin
(2) progressive i loss, G normal (3) overt DM, C-peptide present (4) no C-peptide |
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What are often the 1st autoantibodies to appear on assay in T1 DM, esp in children?
Antibodies to which protein expressed in neuroendocrine cells (esp islets) is present in 60-80% of newly dx'ed t1dm? What is IA-2? What % of T1DM pts will have + ab? |
Insulin (30-40% of young children with t1dm)
Glutamic Acid Decarboxylase member of transmembrane protein-tyrosine phosphatase family, found in secretory vesicles of endocrine and neuronal cells (60-70% of t1dm) |
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Which type of dm is characterized by insulin deficiency and widely fluctuating BG?
What complication is generally only related to missed medication doses or increased insulin requirements w/ stress in t1dm pts? |
t1dm
diabetic ketoacidosis |
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From a pathophysiologic standpoint persons with type 2 diabetes consistently demonstrate four cardinal abnormalities - what are they?
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(1) resistance to i in peripheral tissues (mus, fat, & liv)
(2) ^ liv G production (3) defective i secretion esp i/ response to G stim (4) rapid/^^ abs of G from GI tract |
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Progression of Diabetes is related to progressive what?
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progressive B-cell failure
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What % of pts with t2dm are overweight?
- c peptide lvls? - risk of DKA and hypoglycemia? |
80%
- generally > 1mcg/L - both are rare |
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In non-diabetics, which is a stronger CVD risk?
- LDL cholesterol - high insulin lvls (insulin resistance) |
they are equally bad.
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Polycystic ovarian syndrome, acanthosis nigricans, hepatic steatosis, hyperuricemia, hyperCoag, dyslipidemia, hepatic steatosis... all are features of what?
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metabolic syndrome (insulin resistance syndrome / dysmetabolic syndrome)
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What are the % for having a close family member with diabetes in t1dm? t2dm?
In which is thyroid dz more prevalent? Is it possible in both? |
~10%, ~50%
t1dm, yes it's possible in both. |
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Are minorities more at risk for t2dm? Which has the highest?
What lipid profile lvls put you at risk for |
yes, hispanics.
HDL <35; TriG lvl >250 |
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In the absence of ANY risk factors, when should diabetes testing begin (age in years)?
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45y, If results are normal, testing should be repeated at least at 3-year intervals, with consideration of more frequent testing depending on initial results and risk status
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Do A1c lvls correlate well with risk non-proliferating diabetic retinopathy?
CVD? Are A1c lvls affect by acute (stress, illness, etc.) pertrubations in G lvls? |
yes, correlate well.
yes. no - it's got a long hl, so it's really a look at the last 2-3 months of G control. |
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What are the dx criterion for diabetes? (4 "or's")
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(1) A1C > 6.5%
or (2) FPG > 126 mg/dl or (3) 2hr PG >200mg/dl during an oral G tolerance test (OGTT) or (4) i/ a pt w/ classic sx of hyperG or hyperG crisis: random plasma glucose >200mg/dl |
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Fasting Plasma G of 100-125 mg/dl; 2hr PG i/OGTT 140-199mg/dl; A1c 5.7% to 6.4%...
all of these are categories of what? |
increased risk for diabetes: note that this increase in risk is incremental, and proportionate to the height of the lvls.
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Give the appropriate plan for the following cases:
- A1c >5.7% w/ IFG or IFT - >6.0% w/ IFG and IFT - Diabetes IFG: fasting (8 hours) plasma glucose 100-125 mg/dL IGT: 2-hour value in 75-g OGTT 140-199 mg/dL |
(1) lifestyle, follow @ 1y
(2) lifestyle +/- metformin; follow @6m. (3) lifestyle + metformin; follow @3m. |
