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DM I and II
Endocrinology Diabetes
| Question | Answer |
|---|---|
| _________is the 6th leading ccuase of death by disease in the US, accounting for 18% of all deaths in people over 25 years of age, and is the leading cause of blindness, ESRD and nontraumatic lower limb amputations | Diabetes |
| Diabetes reduces life expectancy in middle-aged patients by how many years? | 10-15 years |
| Type I Diabetes Symptomatic Presentation | Commonly present with classic acute symptoms of hyperglycemia: polysipsia, polyuria, weight loss, and less frequently, polyphagia, blurred vision, and pruritus, 25% for the first time in Ketoacidosis |
| Risk factors for T2DM | Sedentary lifestyle, poor nutrition, and overweight and obesity |
| T2DM Disease Presentation | The disease is present for an avg of 4-7 yrs before diagnosis, and as many as 50% have an established cardiovascular complication at teh same time as diagnosis. Lethargy and fatigue |
| Effects of chronic hyperglycemia | impairment of growth, susceptibility to infections (balanitis, vaginitis) and slow wound healing |
| HbA1C | is a measure of glycosylated hemoglobin; it is a useful tool for monitoring glycemic control and for making therapeutic decisions, but is not recommended for diagnostic purposes. Average blood glucose over last 2-3 mos |
| OGTT | Oral Glucose Tolerance Test: reamins the standard for diagnostic purposes and is used for diagnosis of gestational diabetes |
| FPG | Fasting plasma glucose is simpler, cheaper, equally accurate, faster to perform, more reproducible and convenient compared to OGTT and is used for routine diagnosis. |
| Criteria for Diagnosis of DM | Fasting Plasma Glucose > or equal to 1262-hour postload > or equal to 200Random > or equal to 200 with symptoms |
| People who are generally euglycemic but have abnormal glucose responses when challenged with a OGTT are considered | Prediabetic |
| Screening for T1DM involves the measurement of | Autoantibody markers (antibodies to islet cells, insulin, glutamic acid decarboxylase, and tyrosine phosphatase) |
| Why is it not advised to do routine screeening for T1DM in healthy children as well as those at high risk of developing T1DM (siblings of patients with T1DM)? | Lack of established cut-off values for immune markers, lack of consensus regarding effective therapy for patients with positive test, and lack of cost effectiveness |
| Is screening of certain high-risk populations for T2DM considered cost-effective? | YES. More than 1/3 of people with T2DM are undiagnosed. Because of the insidious nature of T2Dm, patients have a high risk of developing complications by the time of clinical diagnosis |
| Gestational Diabetes facts | Glucose intolerance that develops during pregnancy and usually returns to nl after delivery. 2-5% of all pregnant women. Approximately 25% of lean women and 50% of obese women will go on to develop overt diabetes (types 1 or 2), IFG, or IGT over 20 years |
| What is the underlying pathologic process in most patients with T1DM? | Autoimmune destruction of the pancreatic islet B cells with absolute loss of insulin secretion. The dz has strong human leukocyte antigen (HLA) associations and numerous antibody markers of immune destruction |
| What is the underlying pathologic process in most patients with T2DM? | T2DM results from variable combinations of insulin resistance and insulin secretory defects (b-cell dysfunction), with one or the other abnormality predominating in a given patient |
| What is the hallmark characteristic of diabetes? | Hyperglycemia; what changes in degree over time |
| Etiology of T1DM | Immune mediated, Idiopathic, LADA. Generally, T1DM is an autoimmune disease in which some environemental insult (microbial, chemical, or dietary) triggers an autoimmune reaction in a genetically susceptible person. HLA-DR3 and/or HLA-DR4 is present 90% |
| Etiology of T2DM | Genetic defects of B-cell function or in insulin action, diseases of the exocrine pancreas, Endocrinopathies, Drug or chemical induced, infections, Uncommon forms of immune-mediated diabetes, Gestational DM |
| MODY | Maturity-onset diabetes of the young; autosomal dominant, hyperglycemia appears before the age of 25 |
| Excess aldosterone production by a tumor, through induction of hypokalemia and increased production of somatostatin, may impair what? | insulin secretion and cause diabetes |
| Metabolic Syndrome | Is not a subclass of DM. It consists of a clear cluster of clinical findings and lab abnormalities that include obesity (central, abdominal or visceral), increased sympathetic nervous system activity, HTN, glucose intolerance, cont'd next slide |
| Metabolic Syndrome II | T2DM, hyperinsulinemia, dyslipidemia, fatty liver, enhanced post-prandial lipemia, and many others...(AHHHH!!!) |
| Metabolic Syndrome is associated with higher risk of | atherosclerosis, vascular disease, coronary artery disease, diabetes, and PCOS |
| Genetic predisposition is a stronger factor in type I or type II? | Type II. |
| Early hyperinsulinemia is found in Type I or Type II? | Type II. In the preclinical phase, the pancreatic B cells compensate for genetically predetermined peripheral insulin resistance by producing more insulin to maintain euglycemia. Some patients are identified at this stage while they are clinically asymp |
| Name the five main elements that characterize the pathophysiology of T2DM | Insuline resistance, B-cell dysfunction, dysregulated hepatic glucose production (HGP), abnormal intestinal glucose absorption, and obesity |
| Describe the pathology of T2DM | Classically, early loss of the first phase of glucose-stimulated insulin secretion occurs (peaking at 10min), with subsequent gradual loss of the second phase (starting 30 minutes after glucose stimulus and peaking at 60 minutes). |
| What is glucotoxicity? | Glucotoxicity refers to the effect of chronic hyperglycemia in decreasing insulin secretion and insulin activity. It is a function of the duration and magnitude of the hyperglycemia and contributes to the progressive worsening of hyperglycemia |
| Describe the role of FFA in T2DM | Elevated FFA levels, the result of unrestrained adipose tissue lipolysis in the relative absensce of insulin, also have a tox effect on B-cell (lipotoxicity) and together with intracellular protein glycation, contribute to further failure of these cells |
| Role of FFAs in T2DM continued | FFas exacerbate hyperglycemia through increased oxidation in skeletal muscle and liver, where they decresae glucose utilization and incresae gluconeogenesis, respectively. Also increase hepatic synthesis of triglycerides |
| HGP | Hepatic Glucose Production; results from inadequate suppression of hepatic gluconeogenesis |
| Gastric Dysmotility | In T2DM, hyperglycemia may cause this and increase glucose absorption |
| Name the cornerstones of a comprehensive diabetes management plan for DM | W.E.A.N.S D.WeightEducationActivityNutritionSelf-monitoring blood glucoseDrugs |
| HbA1C monitoring in Type I and Type II | Type I - four or more times per yearType II - two or more times per years if stable, 4 or more times per year if unstable |
| Elevated Post Prandial Glucose (PPG) is... | a risk factor for cardiovascular disease and cause mortality |
| Falsely low HbA1C levels can be seen in which conditions? | B-Thalassemia and sick cell trait b/c of the frequency of hemolysis |
| Regular patient assessment includes | weight, bp, pulse, SMBG records, foot examination, and discussion about smoking cessation at every office visit, with quarterly assessment of HbA1C |
| Standards of care | micro-albuminuria, SrCr, Dilated retinal exam, general physical, neurolog, cardiac, nephrology, dental, foot eval yearly. Influenza yearly and Pneumovax every 5 years |
| Optimal LDL level | <100, or <70 in patients with established cardiovascular disease |
| Optimal HDL level | over 45 for men, over 55 for women |
| Optimal Triglyceride level | under 150 |
| ______are highly effective in the management of diabetic dyslipidemia and, together with their anti-inflammatory actions and improvement in endothelial function, may reduced the risk of cardiovascular events by 30% | Statins |
| As little as __ to ____ % wegith loss in overweight and obese patients reduces the risk of diabetes and leads to increased insulin sensitivity, with improvement in glycemic control, and the possibility of a reduction or cessation of antihyperglycemics | 5-10% |
| Gastroinstestinal Surgical procedures exist for the management of obese patients with a BMI above ____ | 35; 83% of patients undergoing gastric bypass surgery exhibit resolution of their diabetes, and 86% show resolution at 5 years. |
| Every percentage point reduction in HbA1C is associated with | a 40% reduction of complications in T1DM, and 35% reduction of complicatoins in T2DM |
| ________ women should have tighter HbA1C control | Pregnant. |
| New data suggests that ______ is safe for pregnant women with gestational diabetes | metformin |
| Standard Insulin therapy in T1DM | consists of one to two injection per day using intermediate or long-acting insulin with or without short or rapid-acting insulin |
| Intensive insulin therapy in T1DM | refers to multiple (three or more) daily in jections or CSII. Typically regular or rapid acting insulin three times daily in combination with NPH 2x dily or at bedtime or glargine insulin once daily at bedtime |
| Diabetic ketoacidosis characteristics | Hyperglycemia (greater than 250), Ketosis, and Acidosis (pH less than or equal to 7.3 or bicarbonate less than or equal to 15) |
| Precipitating factors for DKA | infection, URI, new-onset diabetes, problems with insulin administration, stress |
| Symptoms of DKA | Nausea, vomiting, thirst, polydipsia, polyuria, abdominal pain, weakness, fatigue, and anorexia. |
| Signs of DKA | tachycardia, orthostatic hypotension, poor skin turgor, warm or dry skin and mucous membranes, hyperventilation or Kussmaul's respiration, hypothermia or normothermia, ketones on breath, weight loss, Altered mentation, coma |
| Most important factor in the therapy of DKA | Restoration of circulating plasma volume, with maintenance of cardiac output and renal function. Give fluid and insulin |
| What is the most common cause of ESRD in developed countries? | Diabetic Nephropathy. 20% of T2DM, 75% of T1DM |
| Microalbuminuria is present after about how many years after the onset of diabetes | 15 years. Within 5 years of the appearance of macro-albuminuria, GFR will have declined by 50% in approximately 50% of patients; within a further 3-4 years, one have of these patients will have ESRD |
| When should screening of proteinuria occur? | Yearly for T2DM starting at diagnosis, and in T1DM starting 5 years post diagnosis. |
| Retinopathy Epidemiology in DM | 100% of T1DM and 60-80% of T2DM within 20 years. Incidence of retinopathy is higher in Mexican Americans and African Americans |
| When should eye exams be done in DM patients? | Annual diliated funduscopic examination by an opthalmologist should be performed in all patients with diabetes, starting 5 years after diagnosis in patients with T1DM. |
| Name the most common neuropathy associated with DM | Peripheral Neuropathy with glove and stocking distribution |
| What percentage of diabetics die from a macrovascular event? | 70-80%; the risk of such an event in people wtih diabetes is equivalent to that of nondiabetic patients with established cardiovascular disease. |
| _______ is the most important environmental factor causing insulin resistance | obesity |
| Which is a greater mortality risk in diabetics: death from HTN or hyperglycemia? | HTN |
| Aggressive treatment of HTN should start early with | an ACE I or an ARB |
| What is the risk of using BB in diabetics? | BBs may increase the severity of hypoglycemia by inhibiting glycogenolysis and gluconeogenesis and may mask the warning symptoms and signs of hypoglycemia by blunting the adrenergic response to hypoglycemia |
| Diabetic patients are in a procoagulant state and therefore taking ________ is recommended | low-dose Aspirin |
| ___________ is the single most important therapeutic intervention in addressing insulin resistance, glucose control, and overall cardiovascular risk. | Lifestyle modification |
| Glycemic control is a stronger risk for | microvascular dz than for macrovascular |
| What is the lifetime risk of developing diabetes for a Hispanic female? | 1 of 2! 1 of 3 Americans; 2 of 5 African Americans and Hispanics |
| Diabetes risk factors | Family Histroy, age greater than 45, obesity (greater than 120% ideal body weight or BMI greater or equal to 27), High-risk ethnic population, habitual inactivity |
| What is the risk increase of stroke in diabetics? | 2-6x |
| What is the risk increase of retinopathy in diabetics? | 25x |
| What is the risk increase of ESRD in diabetics? | 17x |
| What is the risk increase of heart disease in diabetics? | 2-4x |
| What is the risk increase of foot/leg amputations in diabetics? | 5x |
| Suggested range for blood glucose before meals in diabetics | 80-120 |
| Suggested range for blood glucose after meals in diabetics | 100-180 |
| Suggested range for blood glucose at bedtime in diabetics | 100-140 |
| A1C recommendation for diabetics | <7% |
| List the major metabolic defects in Type II diabetics | Peripheral insulin resistance in muscle and fat, decreased pancreatic insulin secretion, increased hepatic glucose output |
| Blood pressure goal for diabetics | <130/80mmHg |
| Total cholesterol goal for diabetics | <200mg/dL |
| In DKA, list the labs you should watch | Potassium, Creatinine, Sodium (pseudohyponatremia), WBC (demargination), Amylase |
| DKA treatment | NS or 1/2NS at 1 Liter for first 2 hours, then 500ml/hr. Follow CVP pressure (neck veins) or continue IV fluids until patient can take po. Potassium replacement. Can use KPO4 if phosphate is low. Follow EKG |
| Put the patient in the ICU not the floor if... | unconscious, marked hyperglycemia (>1000mg/dl), marked acidosis, Absence of frequent BG monitoring, acute concurrent event |
| Treatment of Hypoglycemia | 15gm of CH: 3 glucotabs, 1/2 C OJ, 5 lifesavers, 1/2 C regular soda, D50 IV, Glucagon 1mg IM, Recheck BG 20-30 minutes post treatment |
| Sulfonylurea with ACEI treatment has what effect of glucose level? | May increase risk of hypoglycemia. |
Created by:
ltm12