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30 Cards in this Set
- Front
- Back
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Define Type I DM
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immune mediated with antibodies to either islet cells or autoantibodies to insulin causes b cell distruction
ABSOLUTE insulin deficiency, ketosis prone |
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Defien Type II Diabets
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Insulin resistant or insulin secretory effect. NOT autoimmune
increase IR normal to increased Insulin levles not ketosis prone |
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What does the term impared glucose tolerance indicate?
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patients with glucose between 40 mg/dl to 199 mg/dl after orst. More clinical term than diagnostic.
'Pre-Diabetes" Associated with metabolic syndrome |
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What is the diagnostic criteria for diabetes?
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Sx of diabetes plus casual blood glucose >200
FPG >126 2 hour plasma glucose >200 |
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What are the clinical manifestations og Type I DM?
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Polydypsea, polyuria, polyphagia
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what is the treatmetn for Type I diabetes/
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Insulin, diet, exercise to help make tissues mroe sensitive to insulin.
Exercise in type I offers no glycemic control |
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what are the complications of type I DM?
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Hypoglycemia
Diabetic ketoacidosis Dawn phenomenon Somogyi effect ct |
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Describe the difficulty of counter-regulation in type I DM in regards to hypoglycemia
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increased insulin leveles may prevent glucagon from being released and neuropathy causes decreased epinephrine release. This hinders the body from beingable to counteract a hypergylcemic episode
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Describe diabetic ketoacidosis
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decreased insulin decreases tissue uptake by the cells causing hyperglycemina, aminoacidemia, and hyperlipidemia. lack of insulin -> increased glucagon increasing fat buringing and ketones. Dehydration -> Acidosis
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What factors contribute to ketoacidosis...
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1) decreaseg glucose uptake causes dehydration
2)Increased protein catabolism causes dehydration 3)burning FFA leads to ketogenisisand ketonuria |
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What is the somogyi effect?
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Hypoglycemia at night followed by rebound hyperglycemia in the morning
tx: decrease insulin amount or time of administration |
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What is the dawn phenomenon?
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early morniong rise in blood glucose believed to be from increase in GH that stimulates liver glucose production (coupled with decreased tissue use)
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What are the clinical manifestations of type I DM?
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recurrent infections
genital puritis visual changes paresthesia and fatigue |
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How do diet and exercise as a treatment of type II diabetes differ than that in type I?
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In type II it offers glycemic control
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How do Sulfonylureas/Meglitinides work?
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work on B cells in pancreas to close K+/ATPase cells so that the cell depolarizes and insulin is released (high Ca2+influx)
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How do biguanides work? Give and example of a common biguanide.
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Metformin
suppresses hepatic glucose production in liver increases glucose uptake in muscles by increasing sensitivty of insulin receptors |
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How do a glucosidase inhibitors work?
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they act on the small intestine to block glucosidases slowing and inhibitin CHO absorption
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How do Thiazolidenediones “glitizones” work?
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Bind to PPRY receptors to increase insulin sensitivity on muscle liver and adapose tissues
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name a GLP analogue
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Exenatide
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How do GLP analogus work?
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• Act on pancreas to increase insulin secretion Avia the “incretin effect”
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where is IR in type II Dm primarily occuring>?
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The muscle mostly, but also slightly at the adipose and liver cells
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What is insulin resistance the result of?
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reduction in insulin receptor content and tyrosine kinase activity
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Describe the pathway that is broken with insulin resistance...
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• defects in IRS1, IRS2 causes decreased activity of phosphoinositide-3OH kinase
(3IP--K, critical for glucose transport) and defective vesicular transport to insulin responsitive surface membranes |
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Explain the functions of calcium:
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-Muscular functiona nd excitability
-secretion of vessicles -blood clotting -thight junction function -Cardiac function -teeth and bone health |
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Explain the functions of phosphate:
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metabolic pathways of fuel
provision high energy transfer/storage cofactors (NAD etc) 2 nd messengers |
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What are the forms of Ca2+ in the blood?
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40% Protein bound
50% ionized Ca2+ (bioactive form) 10% complexed to ions like citrate, sulfate or PO4 |
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What is the approximate total amount of Ca2+in the blood.
How much is bioavailable |
8.6-10.6 and about half (5 mg/dl) is free
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What is calciums role in acidemia and alkalemia?
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Ca2+ and H+ compete for negative charges on plasma proteins (like albumin)
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Ca2+ role in Acidemia=
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: less Ca bound to
albumin |
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Ca2+ role in Alkalemia:
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more Ca bound to albumin
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