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169 Cards in this Set
- Front
- Back
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What is the criteria for diagnosis of DM?
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fasting plasma glucose >/= 126mg/dL
2 hour value from a 75g oral glucose tolerance test >/= 200mg/dL or casual plasma glucose level of >/= 200mg/dL with symptoms of diabetes need to have it on 2 seperate days for diagnosis |
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What are microvascular complications?
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neuropathy, retinopathy, and nephropathy
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What is the result of HTN control in diabetes?
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reduced risk of retinopathy, nephropathy, and cardiovascular risk
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What is basal-bolus insulin therapy?
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basal insulin for fasting and postabsorptive control and rapid-acting bolus insulin for mealtime coverage.
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What prevention strategies for T1DM?
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none have proven successful
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Abnormalities in metabolism of what is present in DM?
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fat, carbs, protein
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How many DM pts have been diagnosed?
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2/3
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What is DM the leading cause of?
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blindness age 20-74
development of end-stage renal disease |
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What is responsible for 2/3s of deaths in T2DM?
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cardiovascular events
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When does T1DM typically develop?
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childhood or early adulthood
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What % of DM is Type 1?
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5-10%
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How is T1DM initiated?
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exposure of a genetically susceptible individual to an environmental agent
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What is associated with the development of T1DM?
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B-cell autoimmunity
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What is latent autoimmune diabetes of adults?
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when markers of autoimmunity are detected in T2DM and failure of PO agents and become insulin dependent
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What is T1DM idiopathic?
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nonimmune form of diabetes frequently seen in minoritites with intermittent insulin requirements
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Is T2DM more common in men or women?
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women
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What ethnic groups have an increased risk of T2DM?
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native americans, hispanic americans, asian americans, AA, pacific island people
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How common is gestational DM?
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7% or pregnancies
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How many gestational DM pts develop T2DM or glucose intolerance later in life?
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30-50%
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What causes T1DM?
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autoimmune destruction of the B cells of the pancreas
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What are markers of immune destruction of the B cells, and how often are they present in T1DM?
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present in 90%
islet cell antibodies, antibodies to glutamic acide decarboxylase, antibodies to insulin |
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How does type 1 present when develops in adults?
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maintain sufficient insulin secretion to prevent ketoacidosis for many years (LADA - latent autoimminue diabetes of adults)
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What is T2DM characterized by?
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insulin resistance and a relative lack of insulin secretion, with progressively lower insulin secretion over time
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What complications are T2DM pts at risk of developing?
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macrovascular complications
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What is included in metabolic syndrome?
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abdominal obesity, HTN, dylipidemia (high TG, low HDL), elevated plasminogen activator inhibitor type 1 (PAI-1)
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What is gestational DM?
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glucose intolerance first recognized during pregnancy
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What is mature onset diabetes of youth (MODY)?
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impaired insulin secretion with minimal or no insulin resistance
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How does mature onset diabetes of youth present?
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typically exhibit mild hyperglycemia at an early age
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How do you get mature onset diabetes of youth?
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inherited in an autosomal dominant pattern
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When do you see type A insulin resistance?
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acanthosis nigricans, virilization in women, polycystic ovaries, hyperinsulinemia
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What causes type b insulin resistance?
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autoantibodies to the insulin receptor
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Should you scrren for T1DM?
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not recommended
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When should screening for T2DM begin?
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every 3 years in all adults beginning at age 45 years
screen earlier if risk factors present |
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What is the recommended screening test for T2DM?
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fasting plasma glucose
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When should children be screened for T2DM?
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overweight with 2 risk factors
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What is considered overweight?
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BMI>85th percentile for age and sex
weight for height >85th percentile or weight >120% IBW for height |
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What risk factors for screening T2DM?
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family history of T2DM in 1st and 2nd degree relatives
native american, AA, hispanic, asian/south pacific islanders signs of insulin resistance conditions associated with insulin resistance (acanthosis nigricans, HTN, dylipidemia, polycystic ovary syndrome) |
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How often for screening of T2DM in children?
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every 2 years starting at 10 years of age
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What is the principal tool for the diagnosis of DM in nonpregnant adults?
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fasting glucose test
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What is used for diagnosis in pregnant?
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OGTT
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What is impaired fasting glucose?
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atleast 100mg/dl but less than 126mg/dl
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What is impaired glucose tolerance?
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OGTT: 2-hr glucose value >/= 140mg/dl but < 200mg/dl
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What are pts with impaired fasting glucose or impaired glucose tolerance classified as?
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prediabetes: higher risk of developing diabetes in the future
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What is normal fasting plasma glucose?
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<100mg/dL
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What is normal 2hr postload plasma glucose from OGTT?
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<140mg/dL
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What does fasting glucose reflect?
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hepatic glucose production, which depends on insulin secretory capacity of the pancreas
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What does postprandial glucose reflect?
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uptake of glucose in peripheral tissues (muscle and fat) and depends on insulin sensitivity of these tissues
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What are the 4 main features of T1DM?
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- a long preclinical period marked by the presence of immune markers when B-cell destruction is thought to occur
- hyperglycemia when 80-90% of B cells are destroyed - transient remission (honeymoon phase) - established disease with associated risks for complications and death |
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What is the most commonly detected antibody associated with T1DM?
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islet cell antibody
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What percent of newly diagnosed T1DM pts have an antibody present?
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more than 90%, 3.5-4% of unaffected first degree relatives will also have antibodies
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How much earlier does preclinical B-cell autoimmunity occure before diagnosis of T1DM?
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9-13 years
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Are antibodies considered markers or mediators of B-cell destruction?
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markers
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What is a nonpancreatic autoimmune disorder associated with T1DM?
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Hashimoto thyroiditis
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Can certain human leukocyte antigens (HLAs) be predisposing or protective on chromosome 6?
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both, DQA and B genes have a strong genetic link also
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Why does destruction of pancreatic B-cell function cause hyperglycemia?
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absolute deficiency of both insulin and amylin
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How does insulin lower blood glucose?
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stimulation of tissue glucose uptake, suppression of glucose production by the liver, and suppression of free fatty acid release from fat cells
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What is the result of increased levels of free fatty acids?
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inhibit uptake of glucose by muscle and stimulate hepatic gluconeogenesis
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What is the result of Amylin?
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plays a role in lowering blood glucose by: slowing gastric emptying, suppressing glucagon output from pancreatic alpha cells, and increases satiety
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How is amylin production in T1DM?
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very low because of B cell destruction
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What percent of glucose metabolism is dependent on insulin?
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25%, it takes place in muscle
75% of glucose disposal takes place in non-insulin-dependent tissues (brain, splanchnic tissues or liver and GI |
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In the fasting state, where is 85% of glucose production derived?
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liver and remaining amount is produced in kidneys
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What is secreted in the fasting state to oppose the action of insulin and stimulate hepatic glucose production?
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glucagon, prevents hypoglycemia
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Where is glucagon produced?
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pancreatic alpha cells
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What is the result of carbohydrate ingestion?
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increase plasma glucose concentrationand stimulates insulin release from pancreatic B cells
results in hyperinsulinemia - suppresses hepatic glucose production and stimulates glucose uptake by peripheral tissues |
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Where is the majority of glucose taken up by peripheral tissues disposed?
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muscle, small part is metabolized by adipocytes
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What is glucagon in fed state?
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suppressed
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What is result of a decline in plasma FFA concentrations?
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increased glucose uptake in muscle and reduces hepatic glucose production
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What is the result of a decrease in plasma FFA concentration?
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lowers plasma glucose by decreasing production and enhancing uptake in muscle
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table 77-6 pg 1213
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table 77-6 pg 1213
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What percent of T1DM present with diabetic ketoacidosis?
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20-40% after several days of polyuria, polydipsia, polyphagia, and weight loss
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What is the "honeymoon" phase?
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in T1DM when their blood glucose concentrations are relatively easy to control and small amounts of insulin are needed . Once the residual insulin secretion wanes the patients are completely insulin deficient and tend to have more labile glycemia.
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What are the primary goals of DM management?
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reduce risk for microvascular and macrovascular disease complications, ameliorate symptoms, reduce mortality, improve quality of life
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How are microvascular disease complications reduced?
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near normal glycemia control: adherence to therapeutic lifestyle intervention (diet and exercise), drug therapy regimens, maintain BP near normal
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How are macrovascular disease complications reduced?
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aggressive management of traditional CV risk factors (smoking cessation, tx of dylipidemia, intensive BP control, antiplatelet therapy)
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What are adverse effects of hyperglycemia?
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microvascular disease, poor wound healing, compromises WBC function, leads to classic symptoms of DM
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What are considered severe manifestations of poor diabetes control?
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diabetic ketoacidosis and hyperosmolar hyperglycemic state
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What is the gold standard for following long-term glycemic control for the previous 2-3 months?
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HbA1c
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What can affect HbA1c measurements?
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hemoglobinopathies, anemia and red cell membrane defects
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What is measured if pt has states that affect HbA1c?
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fructosamine - correlates to glucose control ove the last 2-3 weeks
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What is the target HbA1c?
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<7%, lower if hypoglycemia and/or wt gain can be avoided
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How often should eye exams be performed in DM?
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yearly
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How often should the feet be examined and BP assessed?
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at each visit
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How often should a urine test be run for microalbumin?
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yearly
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How often for lipid test?
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yearly and more frequently if needed to achieve lipid goals
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What must pt do to make self monitoring of blood glucose beneficial?
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pt must be empowered to change therapeutic regimen in response to test results
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What is recommended diet for T1DM?
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a meal plan that is moderate in carbs and low in sat. fat (<7% total calories) with a focus on balanced meals
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What percent does the ADA recommend of calories from carbs?
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45-65% of total daily intake, does not recommend <130g of carbs/day
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What is the benefit or aerobic exercise?
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improves insulin resistance and glycemic control, reduces cv risk factors, contributes to wt loss or maintenance, improves well-being
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What pts should have cv evaluation including an ECG and graded exercise test with imaging before moderate to intense exercise?
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older pts, pts with long standing disease (age > 35 years, or >25 years with DM >/= 10 years), multiple CV risk factors, presence of microvascular disease, previous evidence of atherosclerotic disease
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What is the physical activity goal?
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150min/week of moderate (50-70% max HR) intensity exercise
also 30minutes/week resistance training in pts with retinal contraindications |
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What kind of hormone is insulin?
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anabolic and anticatabolic hormone
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What kind of metabolism does insulin play a role in?
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protein, carbs, and fat
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How is insulin produced endogenously?
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in the B cell proinsulin is cleaved to insulin and C-peptide
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What can C-peptide measure?
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marker for endogenous insulin production
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table 77-9 pg 1216
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yea
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What strengths of insulin are available?
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100units/ml and 500units/ml
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Where did insulin originally come from?
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beef and pork
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How different is beef and pork insulin from human?
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beef differs by 3 AA and pork by 1 AA
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What does Eli Lilly, Pfizer, and Sanofi-Aventis use to manufacture insulin?
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Escherichia coli
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What does Novo Nordisk use for synthesis of insulin?
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Saccharomyces cerevisiae or bakers' yeast
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How much proinsulin is in purified preparations of insulin?
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<1ppm
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What happens when regular insulin is injected SC?
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self-associates into a hexameric structure and must dissociate first to dimers and then monomers before absorption through blood capillary
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What are the rapid acting insulins and why are they rapid?
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lispro, aspart, and glulisine insulins, they dissociate rapidly to monomers then absorption is rapid
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What AA transposed in lispro?
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B-28 lysine and B-29 proline human insulin monomeric
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What AA replaced in in aspart?
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B-28 aspartic acid human insulin; mono and dimeric
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What AA replaced in glulisine?
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B-3 lysine and B29 glutamic acid
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What action do rapid acting insulins have compared to regular?
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rapidly absorbed, peak faster, have shorter durations of action
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What is human insulins isoelectric point?
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5.4
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What is glargine isoelectric point?
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6.8
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What color is glargine in the bottle?
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clear because buffered to a pH of 4 where it is completely soluble
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How does glargine work?
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when injected into neutral pH of the body it rapidly forms microprecipitates that slowly dissolve into monomers and dimers which are subsequently absorbed, results in a long acting peakless 24hr duration insulin analog
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How is detemir formed?
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attaches a C14 fatty acid to the B-29 position and removes B-30 AA
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How does detemir work?
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fatty acid side chain binds to interstitial albumin at the SC injection site, the formulation also has stronger hexamer associations which prolong absorption, once it dissociates from interstitial albumin it travels to site of action
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table 77-10 pg 1217
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table 77-10 pg 1217
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What factors determine the absorption of insulin from a SC depot?
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source of insulin, concentration of insulin, additives to insulin preparations (zinc, protamine, etc), blood flow to the area (rubbing injection site, increased skin temp, exercise in muscles near the injection site can enhance absorption), and injection site
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Where is regular and neutral protamine Hagedorn (NPH) injected from most rapid to slowest acting?
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abdominal fat, posterior upper arms, lateral thigh area, superior buttocks area
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Do insulin analogs retain their kinetic profile at all site of injection?
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yes, unlike regular and NPH
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How does action of 500units/mL differ from 100unit/mL regular insulin?
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delayed onset, peak, and a longer duration of action
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Which insulins of protamine added?
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NPH, lispro, and aspart
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When have excess zinc?
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lente or ultralente
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What action does protamine or zinc have on insulin?
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delay onset, peak, and duration of insulin's effect
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How should NPH be prepared to resuspend the insulin prior to each use?
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invert or roll gently at least 10x to fully resuspend the insulin prior to each use
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How does action of detemir change as dose changes?
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onset is consistent across doses, peak is delayed with higher dosing, duration is 14hrs for low dose and 24 hrs for higher dose
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What is the t1/2 of IV regular insulin?
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9 minutes
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When does IV regular insulin reach SS?
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45 minutes
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Why IV regular insulin over other insulins?
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kinetics are similar to regular but have no advantage over regular and cost more
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Where is insulin degraded?
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liver, muscle, and kidney
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How does inhalation insulin work?
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bronchial tubes are impermeable to insulin, but easily absorbed across alveoli
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How does onset, peak, and duration of inhalation insulin compare to others?
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onset and peak similar to rapid acting, duration similar to regular insulin
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What strength is the inhaled insulin?
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1mg (3 units) and 3mg (8 units)
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Is one puff of 3mg equal to 3 puffs of 1mg?
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no
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When should inhalation insulin be given?
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prandial, efficacy equivalent to rapid acting
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Why is usefulness of inhalation insulin restricted?
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the smallest increment between doses is 2-3units
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When is inhalation insulin CI?
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chronic smoking last 6 months (increases absorption 2-5 fold), chronic passive smoke (reduces absorption of insulin inhalation), asthma (decreases absorption, bronchodilator use prior to use increase absorption), COPD (increases absorption), other chronic lung diseases
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What are the most common SE of inhalation insulin?
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dry cough near inhalation, increased sputum, dyspnea
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How do hypoglycemia rates of inhalation insulin compare to regular insulin?
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similar
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Hod does inhalation insulin affect FEV1 and diffusing capacity of the lung for carbon monoxide (DLCO) in T1DM?
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decrease (small, occure within first 3 months, reversible if d/c)
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Are pulmonary function tests needed when using inhalation insulin?
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baseline, 6 months, annually
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When should inhaled insulin be d/c?
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if FEV1 or DLCO declines by >/= 20% on 2 tests
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Are analog insulins superior to traditional insulins at controling HbA1c?
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non
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What insulins can be given within 10 minutes of a meal?
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lispro, aspart, glulisine, and Exubera, regular insulin is 30 minutes
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What insulins have shown the most postprandial lowering of glucose?
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rapid acting analogs
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Which insulins have shown less nocturnal hypoglycemia?
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detemir and glargine
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What are the most common AE for insulin?
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hypoglycemia and wt gain
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Do T1DM or T2DM have more hypoglycemia?
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T1DM
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What is hypoglycemia unawareness?
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pt doesn't experience the normal sympathetic symptoms of hypoglycemia (tachycardia, tremulousness, and sweating). Initial symptoms are neuroglycopenic (confusion, agitation, loss of consciousness, and/or progression to coma)
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What should pts with hypoglycemia unawareness do?
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temporarily raise glycemic goals (reduce insulin dose) and check blood glucose level prior to activities
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How do you treat hypoglycemia?
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ingestion of carbs, preferably glucose
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How do you treat hypoglycemia that causes unconsciousnes?
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IV glucose or glucagon injection (increases glycogenolysis), glucagon used if can't get IV access
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How long for glucagon to start working?
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10-15 minutes
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What SE from glucagon?
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vomitting, position so pt doesnt aspirate
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Why does insulin cause wt gain?
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increased truncal fat, related to daily dose and plasma insulin levels
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What is lipohypertrophy?
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caused by many injections into the same injection site, a raised fat mass at injection site
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What is lipoatrophy?
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caused by insulin antibodies, destruction of fat at site of injection, recommend more purified insulin
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What insulin has caused lipoatrophy?
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lispro
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table 77-11 pt 1219
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yea
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What is average daily dose of insulin for T1DM?
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0.5-0.6units/kg, 50% basal and 50% meal coverage
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What does pramlintide do?
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antihyperglycemic agent that suppresses inappropriately high postprandial glucagon secretion, reduces food intake (wt loss), slows gastric emptying (glucose in plasma matches glucose disposition)
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What is duration of pramlintide?
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3-4hrs
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How is pramlintide metabolized?
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kidneys, no accumulation seen in renal insufficiency
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Where is pramlintide injected?
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abdomen or thigh
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What is the main advantage of pramlintide?
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stabilizes wide postprandial glycemic swings, also can cause wt loss
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How does pramlintide cause wt loss?
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decrease appetite and slowing gastric empying reduces number of calories
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What effect does pramlintide have on microvascular complications?
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reduces HbA1c that reduces microvascular complications
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What AE for pramlintide?
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GI, nausea, anorexia (dose related and decrease over time), doesn't cause hypoglycemia but used whith insulin that can
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What DI?
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delay gastric empying so can delay absorption of medications (oral pain meds and AB)
if rapid absorption needed take 1hr before or 3hrs after pramlintide injection |
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How should insulin be adjusted when starting pramlintide?
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prandial insulin reduce 30-50% to reduce hypoglycemia, adjust basal only if FPG close to normal
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What is starting dose of pramlintide for T1DM?
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15mcg prior to each meal up to max 60mcg prior to each meal
2.5units on a 100unit/ml syringe equal to 15mcg |
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Can pramlintide and insulin be mixed?
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no
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