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WVC Diabetes part 1
WVC IGGY chpt 67 to pg 1491
| Question | Answer |
|---|---|
| In the United States, diabetes mellitus (DM) is the leading cause of | new cases of blindness, end-stage kidney disease requiring dialysis or transplantation, and foot or leg amputations. |
| Studies show that __________ controls reduces complication of diabetes | glycemic |
| An essential part of preventing complications that occur with DM is | Treatment of hypertension and hyperlipidemia |
| The main feature of chronic DM is | hyperglycemia resulting from problems with insulin secretion, insulin action, or both. |
| DM is classified by | underlying problem causing a lack of insulin and the severity of the insulin deficiency. |
| The 2 types of islet cells that are responsible for insulin control | alpha and beta cells |
| Alpha cells produce ___________, beta cells produce _________ and ________ | glucagon; insulin and amylin. |
| A major “counterregulatory” hormone that has actions opposite those of insulin | glucagon, |
| It causes the release of glucose from cell storage sites whenever blood glucose levels are low | glucagon |
| This allows body cells to use and store carbohydrate, fat, and protein | insulin |
| TYPE 1 DIABETES | • Beta-cell destruction leading to absolute insulin deficiency • Autoimmune • Idiopathic |
| TYPE 2 DIABETES | • Ranges from insulin resistance with relative insulin deficiency to secretory deficit with insulin resistance |
| Other conditions resulting from hyperglycemia | • Genetic defects of beta-cell function/ insulin action•pancreatitis, trauma, neoplasia, cystic fibrosis, hemochromatosis•acromegaly, Cushing's disease, glucagonoma, pheochromocytoma, hyperthyroidism, aldosteronism• congenital rubella, cytomegalovirus• |
| GESTATIONAL DIABETES MELLITUS (GDM) | • Glucose intolerance with onset or first recognition during pregnancy • Diagnosis is based on results of a 100-g oral glucose tolerance test during pregnancy |
| Proinsulin, secreted by and stored in the beta cells of the islets of Langerhans in the pancreas, is transformed by | the liver into activated insulin. |
| Insulin attaches to receptors on target cells, where it promotes | glucose transport into the cells through the cell membranes. |
| C-peptide levels are used to measure | the rate that beta cells secrete insulin. |
| Insulin is allows | glucose in the blood to move into cells to generate energy. |
| The liver is the first major organ to be reached by insulin in the blood. In the liver, insulin promotes | glycogenesis at the same time that it inhibits glycogenolysis, protein and lipid synthesis and inhibits ketogenesis & gluconeogenesis |
| In muscle, insulin promotes | protein and glycogen synthesis. Keeps blood glucose levels in the norm |
| In fat cells, insulin promotes | triglyceride storage. Keeps blood lipid levels in the norm. |
| The pancreas secretes about | 40 to 50 units of insulin daily directly into liver circulation in a two-step manner (basal insulin secretion & prandial) |
| Glucose is the main fuel for central nervous system (CNS) cells.The brain needs a continuous supply from circulation to prevent | neuronal dysfunction and cell death. |
| ______ _________can be used as fuel by some cells when glucose is not available. | fatty acids |
| Glucose and free fatty acids are stored inside cells as | glycogen in the liver and muscles |
| In the fat cells, glycogen is stored as | triglyceride |
| The most efficient means of storing energy is in the form of | triglyceride |
| During a prolonged fast or after illness or injury | proteins are broken down and some amino acids are converted into glucose. |
| During a fasting state, plasma glucose is maintained by | a balance between glucose uptake by cells and glucose production by the liver. |
| During a fasting state, liver processes are regulated by glucagon release from | pancreatic alpha cells that stimulate glucose production. |
| During fasting, insulin is released from | pancreatic beta cells to prevent excessive liver glucose output. |
| Glucose in the blood after a meal is controlled by | the emptying rate of the stomach and delivery of nutrients to the small intestine, where they are absorbed into circulation |
| In response to food in the stomach, Incretin hormones | increase secretion of insulin and slow the rate of gastric emptying, preventing hyperglycemia after meals |
| In type 2 diabetes, hyperglycemia results from | excessive liver glucose production and reduced glucose uptake in other cells due to a combination of INSULIN RESISTANCE and DEFICIENT INSULIN SECRETION. |
| With DM II, during a meal, the rate of gastric emptying is | faster than normal. Stomach contents reach the intestine & the rate of glucose entry into circulation increase →hyperglycemia. The ↑rate of gastric emptying is thought due to ↓secretions of amylin and GLP-1 |
| Glucagon is the main | counterregulatory hormone. It increases blood glucose by actions opposite those of insulin when more energy is needed. |
| Other hormones that increase blood glucose levels are | epinephrine, norepinephrine, growth hormone, and cortisol |
| Insulin and counterregulatory hormones keep the level of blood glucose normally | 70 to 100 mg/dL |
| Gluconeogenesis, is the | conversion of amino acids into glucose. |
| Lipolysis, is the | breakdown of fat |
| Proteolysis, is the breakdown of | proteins, provide fuel for energy |
| Levels of counterregulatory hormones increase in an | attempt to make glucose from other sources |
| Hyperglycemia causes fluid and electrolyte imbalances, leading to the classic symptoms of diabetes: | polyuria, polydipsia, and polyphagia. |
| Polyuria results in excess | sodium, chloride & potassium being excreted In the urine→dehydration →polydipsia→ cell breakdown → polyphagia |
| With insulin deficiency, fats break down, releasing free fatty acids. Conversion of fatty acids to | ketone bodies provides a backup energy source. |
| Ketones are | abnormal breakdown products of fatty acids, |
| Collection of ketones in the blood when insulin is not available, results in | metabolic acidosis. |
| The dehydration that occurs with diabetes leads to | hemoconcentration, hypovolemia, hyperviscosity, hypoperfusion & hypoxia. |
| Physiologic Response to Insufficient Insulin | • Decreased glycogenesis• Increased glycogenolysis • Increased gluconeogenesis • Increased lipolysis • Increased ketogenesis • Proteolysis |
| Kussmaul respiration | an increase in respirations due to diabetic metabolic acidosis. Acetone is exhaled, giving the breath a “fruity” odor. |
| Hyperkalemia or hypokalemia in DM is related to | patients response to treatment, severity of acidosis and level of hydration. |
| Three glucose-related emergencies can occur in patients with diabetes | •Diabetic ketoacidosis (DKA) caused by lack of insulin and ketosis•Hyperglycemic-hyperosmolar state (HHS) caused by insulin deficiency and profound dehydration•Hypoglycemia from too much insulin or too little glucose |
| DM can lead to health problems and early death due to | macrovascular and microvascular |
| Macrovascular complications are | coronary heart disease, cerebrovascular disease, and peripheral vascular disease, lead to increased early death among those with diabetes. |
| Microvascular complications of blood vessel structure and function lead to | nephropathy (kidney dysfunction), neuropathy (nerve dysfunction), and retinopathy (vision problems). |
| Chronic hyperglycemia causes | irreversible basement membrane thickening and organ damage. |
| Glucose toxicity directly or indirectly affects | functional cell integrity. |
| Chronic ischemia in small blood vessels causes | connective tissue hypoxia and microischemia |
| Complications in patients with type 2 diabetes seem more related to | hypertension, a sedentary lifestyle, high blood lipid levels, and smoking than to hyperglycemia, and obesity |
| Many older diabetic patients have no classic signs of high blood glucose levels, and the diagnosis is made | when the patient seeks treatment for another illness or for complications of diabetes, such as visual problems. |
| The most common complication of DM is | cardiovascular disease |
| The leading cause of death in patients with DM is | MI, coronary artery disease, diabetic cardiomyopathy, and abnormal blood clotting. Left ventricular dysfunction with cardiac failure and fatal cardiac dysrhythmias are more common in diabetic patients after MI. |
| Diabetic patients often have a higher incidence of traditional cardiovascular risk factors of | obesity, HTN, dyslipidemia, and sedentary lifestyle. Cigarette smoking / positive family history also increase risk for cardiovascular disease. Renal disease, indicated by albuminuria, increases the risk for coronary heart disease and mortality from MI. |
| Patients with diabetes tend to have higher levels of C-reactive protein (CRP), | an acute-phase inflammatory marker associated with increased risk for future cardiovascular problems and death. |
| Cardiovascular disease complication rates can be reduced through | aggressive management of hyperglycemia, hypertension, and hyperlipidemia.. |
| Considerations for stroke in pt with DM are | Hypertension, hyperlipidemia, nephropathy, peripheral vascular disease, and alcohol and tobacco abuse |
| The cause and progression of diabetic retinopathy are related to | problems that block retinal blood vessels and cause them to leak, leading to retinal hypoxia |
| Retinopathy is linked to fasting blood glucose levels | above 129 mg/dL |
| _______________ & ___________________increase the rate of retinopathy development in patients with type 1 diabetes | Hyperglycemia and hypertension |
| Vision loss also occurs from | macular degeneration, corneal scarring, and changes in lens shape or clarity |
| Hyperglycemia may cause | blurred vision even with glasses |
| Hypoglycemia may cause | double vision |
| Open-angle glaucoma and cataracts are | more common in patients with diabetes |
| The older patient with retinopathy may have | blurred vision, distorted central vision, fluctuating vision, loss of color perception, and mobility problems resulting from loss of depth perception. |
| It is especially important to assess the ability of the patient to | perform tasks such as measurement and injection of insulin and blood glucose monitoring to determine if adaptive devices are needed to assist in self-management activities. |
| It is a common complication of diabetes and often involves all parts of the body. | neuropathy |
| Damage to sensory nerve fibers results in | either pain or loss of sensation. |
| Damage to motor nerve fibers results in | muscle weakness. |
| Damage to nerve fibers in the autonomic nervous system can cause | dysfunction in every part of the body. |
| the most common neuropathies in diabetes and involve widespread nerve function loss | Diffuse neuropathies |
| They have a slow onset, affect both sides of the body, involve motor and sensory nerves, progress slowly, are permanent, and include autonomic nerve dysfunction. | Diffuse neuropathies |
| Late complications include foot ulcers and deformities | Diffuse neuropathies |
| They usually are caused by an acute ischemic event or by the physical trapping of a nerve and effect a single nerve or nerve group | Focal neuropathies |
| The symptoms begin suddenly, affect only one side of the body or body area, and are self-limiting | ischemic neuropathies |
| These stem from compression of a nerve in a body compartment or between tissues. Symptoms begin gradually and can occur anywhere. They may be bilateral, having a waxing and waning course without spontaneous recovery | Focal entrapment neuropathy (ie:CTS) |
| Autonomic nervous system neuropathy leads to problems in | cardiovascular, GI, and urinary function. |
| Hyperglycemia leads to neuropathy through | blood vessel changes that cause nerve hypoxia |
| Orthostatic hypotention and syncope | increase the risk for falls, especially among older adults |
| Common GI symptoms from diabetic neuropathy are | dysphagia N/V, and bowel elimination problems. Diarrhea often occuring at night. Constipation, Gastroparesis |
| The most common GI symptom of DM is | Constipation, intermittent and may alternate with bouts of diarrhea. |
| Gastroparesis a cause of | hypoglycemia |
| Loss of nerve input to the bladder results in | incomplete emptying, which leads to urinary infection and kidney problems |
| Diabetes is the leading cause of | end-stage kidney disease (ESKD) and kidney failure in the United States |
| Risk factors for nephropathy | a 10- to 15-year history of diabetes, diabetic retinopathy, poor blood glucose control, uncontrolled hypertension, and genetic predisposition. |
| The earliest clinical sign of nephropathy is | microalbuminuria |
| Diffuse neuropathies | Distal symmetric polyneuropathy, Autonomic neuropathy |
| Sensory alterations of distal symmetric polyneuropathy | Paresthesias: burning/tingling sensations, starting in toes and moving up legs. Dysesthesias: burning, stinging, or stabbing pain. Anesthesia: loss of sensation |
| Motor alterations in intrinsic muscles of foot in distal symmetric polyneuropathy | Foot deformities: high arch, claw toes, hammertoes; shift of weight-bearing to metatarsal heads and tips of toes |
| Focal ischemia manifests as | Thoracolumbar radiculopathy w/sensory&reflex loss: Pain across back/side/front of chest/abdomen. Cranial nerve palsies, third/sixth nerves: Sudden diplopia/ptosis; eye pain. Amyotrophy Pain; asymmetric weakness; wasting of iliopsoas, quads/adductors |
| Autonomic neuropathy manifestations | :Gastroparesis/constipation, nausea/anorexia. Diabetic diarrhea; Diarrhea/bowel incontinence, bladder/urinary ret. Impotence, ED, Orthohypotension, resting tachycardia, Defective counterregulation, Loss of warning signs of hypoglycemia |
| Entrapment neuropathies | Carpal tunnel syndrome. Popliteal nerve/knee; Footdrop; Posterior tibial nerve at tarsal tunnel; Tarsal tunnel syndrome: sensory impairment in sole of foot; weakness of intrinsic muscles of foot; burning pain and paresthesias at ankle and plantar surface |
| Chronic high blood glucose levels cause | hypertension in kidney blood vessels and excess kidney perfusion |
| Increased pressure from hypertension in the kidney have what effect on the system | leaky blood vessels,→filtration of lg particles→ deposits in kidney tissue/blood vessels→vessels narrow ↓kidney oxy→kidney cell hypoxia/cell death. Time→ scarring in blood vessels in the glomerulus → unable to filter urine from the blood, →renal failure. |
| What items are included in the filtration of larger particles resulting from damage of kidney hypertension | albumin and other proteins |
| What disease process speeds the process of diabetic nephropathy | cardiac disease, both systolic and diastolic hypertension greatly speed the progression of diabetic nephropathy |
| What is an autoimmune disorder in which beta cells are destroyed in a genetically susceptible person | DM I |
| Describe the autoimmune disease process in type 1 diabetes | immune system cells, mediators, and antibodies attack and destroy insulin-secreting cells in the islets. |
| Antigen pattern for DM 1 and viral considerations | HLA-DR or HLA-DQ, mumps, congenital rubella, and coxsackievirus infection, appear to trigger autoimmune destruction of pancreatic beta cells |
| Development of the DM 1 is an interactive effect of | genetic predisposition and exposure to certain environmental factors. |
| Most patients with type 1-diabetes have what antibodies/markers | islet cell antibodies (ICAs), insulin autoantibodies (IAAs), autoantibodies to glutamic acid decarboxylase (GAD), or autoantibodies to tyrosine phosphates. Circulating ICA and IAA may be present before manifestations of DM1 develop. (key feature) |
| DM 1, average age at onset | Usually younger than 30 yr, occurs at any age |
| DM II average age at onset | Peaks in 50s; may occur earlier |
| Main symptoms of DM 1 | Abrupt onset, thirst, weight loss |
| Main symptoms of DM II | Frequently none; thirst, fatigue, visual blurring, vascular or neural complications |
| Etiology of DM 1 | Viral infection |
| Etiology of DM II | unknown |
| Basic pathology of DM II | Insulin resistance & Dysfunctional pancreatic beta cell |
| What antigen patterns/antibodies are present in DM II | none |
| Endogenous insulin and C-peptide in DM 1 and DMII | DM 1-none; DMII-Low, normal, or high |
| Is inheritance in DM1 recessive or dominant | recessive |
| Is inheritance in DMII recessive or dominant | dominant and multifactorial |
| How does nutritional status affect the onset of DM1 | non-factorial, usually non-obese |
| What percentage of DMII patients are insulin dependent | 20-30% |
| Sulfonylurea therapy is used in what type of DM | DMII |
| A progressive disorder in which the pancreas makes less insulin over time | DMII |
| A reduced ability of most cells to respond to insulin, poor control of liver glucose output, and decreased beta-cell function, eventually leading to beta-cell failure | insulin resistance |
| The simultaneous presence of metabolic factors known to increase risk for developing type 2 diabetes and cardiovascular disease | metabolic syndrome (syndrome X) |
| Features of metabolic syndrome are | Abdominal obesity: waist men >40” ; women >35” •Hyperglycemia: FBS> 100 mg/dL •HTN: systolic BP > 130, diastolic BP > 85 •Dyslipidemia: triglyceride > 150, HDL< 40 (men) or < 50 (women) |
| Any the features of metabolic syndrome can cause | atherosclerosis and the risk for stroke, coronary heart disease, and early death |
| What would you teach a client with DM | lifestyle changes: ↓wt to 20% of ideal BMI; modifying diet and exercising more will reduce cardiovascular risk. Drug therapy may be required to achieve desired lipid and blood pressure outcomes. |
| What would you teach for healthcare promotion in a patient with DM1 | control of blood glucose levels, regularly follow-up with their HCP; regular yearly eye/urine microalbumin tested; Early diagnosis of changes allows adjustments in treatment regimens to be made that slow progression of eye and kidney problems |
| The major focus for healthcare promotion of DM1 is | Control of diabetes and its complications |
| The major focus for healthcare promotion of DMII is | prevention |
| What would you teach for healthcare promotion in DMII | maintain appropriate weight, reduce cardiovascular risk factors of tobacco use, hypertension, and high blood lipid levels reduce onset of DMII & and its long-term complications. |
| What is the percentage of heredity incidents of DMII | 15% |
| In assessing the history of a patient, what are important questions to ask | about risk factors and symptoms related to diabetes (age, how large their children were at birth or if they were glucose intolerant); Asses for fatigue, polyuria, and polydipsia; vision/touch changes, infections (yeast too), ↑time to heal |
| The preferred test for DM in non-pregnant adults is | Fasting plasma glucose (FPG) NPO 8hrs; A diagnosis of diabetes is made with THREE separate test results > 126 mg/dL even with older adults |
| The classic symptoms of diabetes include | polyuria, polydipsia, and unexplained weight loss. |
| How is DMII diagnosed | Symptoms of diabetes plus casual blood glucose concentration > 200 mg/dL OR FPG OR 2-hr plasma glucose > 200 mg/dL (oral glucose tolerance test of 75 g glucose dissolved in water) |
| Normal ranges for FBG | 100 mg/dL (older adults rise 1 mg/dL per decade) |
| Impaired fasting glucose(IFG) is defined as | >100 mg/dL but <126 mg/dL |
| Normal ranges for (GTT) Glucose tolerance test (2-hr post-load result) | <140 mg/dL |
| Impaired glucose tolerance test (IGT) are | >140 mg/dL but <200 mg/dL |
| IGT provisional diagnosis leves | 200 mg/dL |
| Normal values for Glycosylated hemoglobin (hemoglobin A1c [HbA1c]) test | <7% |
| Levels >8% of glycosylated hemoglobin indicate | poor diabetic control and need for adherence to regimen or changes in therapy. |
| What instructions do you give your clients prior to undergoing an oral glucose tolerance test | good 3 day diet of at least 150 carbs and reg exercise, fast for 10-12 hrs prior to test, carb restriction, bedrest, acute illness, Phenytoin (Dilantin), anovulatory drugs, diuretics, nicotinic acid, and glucocorticoids adversely affect results |
| How will you explain an oral glucose test to your clients | after fasting for 10-12 hours, initial blood drawn, within 5 mins consume 300mL of glucose, then blood samples are drawn q 30mins for 2 hrs. During the test, you rest, no smoking/drinking |
| What are the indications for DMII testing | >45 yrs old, BMI >25%, 1st relative w/DM, inactive,↑risk ethnic pop, baby wt >9 lbs/GDM, HTN, HDL<35, trigl >250, polycystic ovarian syndrome, IGF/IGT previously, Hx of vascular disease |
| The most sensitive test for DM is | oral glucose tolerance testing (OGTT) |
| How is GDM tested | OGTT, with hourly tests. Two or more of the venous plasma levels must be met or exceeded for a positive diagnosis |
| Screening for diabetes is done with either | fasting plasma glucose test or 2-hour OGTT |
| Glycosylated hemoglobin assays are useful because | blood glucose permanently attaches to hemoglobin |
| What shows the average blood glucose level during the previous 120 days—the life span of red blood cells. to evaluate the treatment plan | glycosylated hemoglobin assays (HbA1c ) LONG TERM |
| What test is used to assess long-term glycemic control, as well as to predict the risk for complications | HbA1c. Unlike the fasting blood glucose test, HbA1c test results are not altered by eating habits the day before the test. |
| What 2 conditions interfere with HbA1c | Hemolysis, blood loss, and pregnancy all increase red blood cell turnover and reduce HbA1c levels. Triglycerides and bilirubin interfere with the assay, leading to overestimation of HbA1c levels in patients with hypertriglyceridemia. |
| Glycosylated serum proteins and albumin | these proteins can indicate blood glucose control over a shorter period than HbA1c. |
| Glycosylated serum proteins and albumin measures are useful when | tight control of blood glucose is necessary (e.g., pregnancy) or in short-term follow-up of treatment changes. |
| What are the available tests for glycosylated serum proteins & albumin | glycosylated serum albumin (GSA), glycosylated serum protein (GSP), and fructosamine. |
| The presence of moderate to high urine ketones (hyperketonuria) indicates a | severe lack of insulin. |
| Hyperketonuria in the presence of hyperglycemia is a | medical emergency that, when detected early, can be treated with insulin and careful monitoring. |
| When should urine testing be performed | acute illness, stress, when blood glucose levels consistently exceed 300 mg/dL, during pregnancy, or when any symptoms of ketoacidosis are present. Ketone testing also is recommended for diabetic patients participating in a weight-loss program |
| Hyperketonuria without hyperglycemia suggests that | weight loss is occurring without disrupting blood glucose control |
| Tests for kidney function are important because the presence | of urine protein without kidney symptoms may indicate microvascular changes in the kidney |
| Urine albumin excretion rates of 20 to 200 g/min (30 to 300 mg/hr) indicate | microalbuminuria. Even minor elevations of albumin are associated with increased mortality. |
| Once clinical proteinuria has been detected, kidney function (e.g., glomerular filtration rate) is assessed by | creatinine clearance tests . In patients with nephropathy, a rise in serum creatinine level is related to both poor blood glucose control and hypertension |
| This test may be appropriate for a quick screening but should not be used for monitoring diabetes management. | Urine glucose testing is an indirect measurement of blood glucose and is much less precise than blood glucose testing. Fluid intake, urine elimination patterns, and certain drugs affect the results. |
| The long-term value is the | HbA1c Normal range 7% or below, correlate to an glucose level >135 mg/dL |
| The short-term values are the | FPG and the postmeal levels |
| Norman short-term value ranges | FPG: > 100 mg/dL even with older adults and post-meal >150 |
| The management of diabetes mellitus is complicated and involves considerable | patient involvement and education. |
| Nonsurgical management of diabetes mellitus involves | nutritional interventions, blood glucose monitoring, a planned exercise program, and in some instances, drugs to lower blood glucose levels. |
| Who plans, coordinates, and delivers care to the diabetic | The nurse, together with the patient, physician, nutritionist, pharmacist, case manager, and in some cases, physical therapist |
| Sulfonylurea agents are classified as | insulin secretagogues and are used for patients with some remaining pancreatic beta-cell function. |
| The action of sulfonylurea agents are | stimulate insulin secretion from pancreatic beta cells and increase the number or sensitivity of cell receptor sites for interaction with insulin. The overall effect of sulfonylurea therapy is lowering of fasting plasma glucose levels. |
| Side effects of sulfonylurea agents include | weight gain and hypoglycemia. Hypoglycemic episodes are more likely to occur with chlorpropamide (Diabinese, Novo-Propamide) because of its long duration of action. |
| What type of patients are more susceptible to hypoglycemia | Underweight older patients with cardiovascular, liver, or kidney impairment |
| Oral Blood Glucose–Lowering Agents SULFONYLUREAS | Acetohexamide (Dymelor), Chlorpropamide (Diabinese), Tolazamide (Tolinase), Tolbutamide (Orinase, Mobenol) |
| SECOND-GENERATION SULFONYLUREA AGENTS | Glipizide (Glucotrol), Glyburide (DiaBeta/Micronase), Glimepiride (Amaryl) |
| MEGLITINIDE ANALOGUES | Repaglinide (Prandin), Nateglinide (Starlix), |
| BIGUANIDES | Metformin (Glucophage) |
| ALPHA-GLUCOSIDASE INHIBITORS | Acarbose (Precose), Miglitol (Glyset) |
| THIAZOLIDINEDIONES | Pioglitazone (Actose), Rosiglitazone (Avandia |
| FIXED COMBINATIONS | are combinations of metformin and other drugs |
| Post-meal glucose levels (postpradial) | Under 180 mg/dl (6.6 mmol/L) one or two hours after a meal. |
| Pre-meal glucose leves (prepradial) | 70-130 mg/dL |
| Blood glucose values at bedtime should be between | 100 and 140 mg/dL |
| Signs and symptoms of hypoglycemia | sweating, hunger, weakness, dizziness, tremor, tachycardia, anxiety |
| Meglitinide analogues are classified as | insulin secretagogues and have actions and adverse effects similar to those of sulfonylureas |
| Repaglinide (Prandin) and Nateglinide (Starlix) | lower blood glucose by triggering insulin secretion from pancreatic beta cells |
| These drugs were designed to increase meal-related insulin secretion. They are rapidly absorbed and have a short duration of action | Repaglinide (Prandin) and Nateglinide (Starlix) |
| ____________ is taken before meals, has a rapid onset w/limited duration of action,is used to treat fasting and postprandial hyperglycemia. | Repaglinide (Prandin) |
| _____________is rapidly absorbed and stimulates insulin secretion within 20 minutes of ingestion. It is taken just before meals to control mealtime hyperglycemia and improves overall glycemic control in patients with type 2 diabetes. | Nateglinide (Starlix) |
| ________________are antihyperglycemic agents and insulin sensitizers. | Biguanides |
| Metformin (Glucophage) is the major drug in this class. | Biguanides |
| Metformin’s action | It does not increase insulin secretion. It decreases liver glucose production, →↓FPG release, and improves insulin receptor sensitivity. |
| The ADA recommends metformin as | initial therapy for DMII b/c drug does not induce weight gain/hypoglycemia, low cost,few adverse effects. |
| The most common side effects of metformin are | abdominal discomfort and diarrhea. |
| Metformin should not be used in conditions that decrease drug clearance, such as | renal insufficiency, liver disease, alcoholism, or severe congestive heart failure or in patients older than 80 years. |
| Patient teaching for metformin | to report symptoms of fatigue, unusual muscle pain, difficulty breathing, unusual or unexpected stomach discomfort, dizziness, lightheadedness, or irregular heartbeats to the primary care provider. |
| Alpha-glucosidase inhibitors are agents that | prevent hyperglycemia by delaying absorption of carbohydrate from the small intestine. These drugs inhibit enzymes in the intestinal tract, reducing the rate of digestion of starches and the absorption of glucose. |
| Acarbose does what | delays rather than prevents glucose absorption and does not cause weight loss. |
| The most common side effects of Acarbos and Miglitol are | flatulence, diarrhea, and abdominal discomfort. These drugs do not cause hypoglycemia unless given with sulfonylureas or insulin. |
| Patient teaching for acarbose and miglitol | use oral glucose tablets, glucose gel, or low-fat milk to treat hypoglycemia. Severe hypoglycemia may require glucose infusion or glucagon injection. |
| _____________________ improve insulin sensitivity/reduce liver glucose production. ↑insulin action in muscle, fat, and liver tissue by stimulating an enzyme receptor that regulates glucose and lipid metabolism (peroxisome proliferator activated receptor) | Thiazolidinediones (TZDs) antihyperglycemic agents and insulin sensitizers |
| Although______________ is available, its use has been associated with an increased risk for heart-related deaths, bone fractures, and macular edema. | rosiglitazone |
| All Thiazolidinedions (TZDs) reduce blood lipid levels. Major side effects of TZD treatment are | an increase in adipose tissue and fluid retention, infection, headache, peripheral edema, and pain |
| Teach patients taking TZDs drugs | have periodic liver function studies because of the potential for liver damage. |
| Combining drugs with different mechanisms of action may be | highly effective in maintaining desired blood glucose control. Some patients may need a combination of oral agents and insulin to control blood glucose levels. |
| Drugs are started | at the lowest effective dose and increased every 1 to 2 weeks until the patient reaches desired blood glucose control or the maximum dosage |
| Insulin therapy is indicated when | blood glucose cannot be controlled after the use of two or three different oral agents. |
| Antidiabetic drugs are not a substitute for dietary modification and exercise. Teach the patient | about the need for continuing dietary restrictions and regular exercise. |
| To avoid adverse drug interactions, teach the patient to | consult with the primary care provider or pharmacist before using any over-the-counter drugs. |
| The choice of oral antidiabetic drug is based on | cost, the patient's ability to manage multiple drug doses, age, and response to the drugs. |
| Shorter-acting agents (e.g., glipizide) are preferable in | older patients, those with irregular eating schedules, or those with liver, kidney, or cardiac dysfunction |
| Longer-acting agents (e.g., glyburide, glimepiride) with once-a-day dosing are better for | adherence. Beta-cell function in type 2 diabetes often declines over time, reducing the effectiveness of some oral agents. The treatment regimen for the patient with type 2 diabetes may eventually require insulin therapy either alone or with oral agents. |
| Insulin therapy is needed for | type 1 diabetes and also may be used for type 2 diabetes. |
| The safety of insulin therapy in older patients may be affected by | reduced vision, mobility and coordination problems, and decreased memory. |
| Insulin is manufactured using DNA technology to synthesize | pure human insulin. |
| Insulin analogues are | genetically engineered human insulins in which the structure of the insulin molecule is altered to change the rate of absorption and duration of action within the body |
| Lispro insulin, | a rapid-acting insulin analogue that is created by switching the positions of lysine and proline in one area of the insulin molecule |
| Patient teaching for insulin | insulin types, injection tecs/sites. Patient response can all affect the absorption, onset, degree, and duration of insulin activity. Reinforce that changing insulins may affect blood glucose control and should be done only under supervision of the HCP |
| A usual insulin starting dose is | between 0.5 and 1 unit/kg of body weight per day. |
| What factors influence insulin absorption & availability | injection site; timing, type, or dose of insulin used; and physical activity. |
| Absorption is fastest in the | abdomen, followed by the deltoid, thigh, and buttocks |
| What is the preferred site for insulin injections | the abdomen, because it provides the most rapid insulin absorption. |
| Absorption rate is determined by | insulin properties. The longer the duration of action, the more unpredictable is absorption. Larger doses of insulin also prolong the absorption. |
| What increases insulin absorption | Factors that ↑blood flow from the injection site, such as local application of heat, massage of the area, and exercise of the injected area |
| Injection depth | changes insulin absorption |
| Timing of injection affects | blood glucose levels |
| The interval between premeal injections and eating, known as “lag time,” affects | blood glucose levels after meals. |
| Insulin lispro, insulin aspart, and insulin glulisine have rapid onsets of action and should | be given within 10 minutes before mealtime when blood glucose is in the target range. |
| Regular insulin should be given at least | 20 to 30 minutes before eating when glucose levels are within the target range. |
| Mixing insulins can | change the time of peak action. |
| When rapid-acting (Humalog or NovoLog) or short-acting (regular) insulin is mixed with a longer-acting insulin, draw the | shorter-acting dose into the syringe first |
| No other insulin should be mixed with insulin glargine or insulin detemir. Mixing | clouds the solution and makes the onset of action and peak effect time less predictable. |
| Lipoatrophy is | a loss of fat tissue in areas of repeated injection that results from an immune reaction to impurities in insulin. Treatment consists of injection of insulin at the edge of the atrophied area. |
| Lipohypertrophy is | an increased swelling of fat that occurs at the site of repeated insulin injections. Treatment consists of rotating the injection site among different body areas |
| Dawn phenomenon | results from a nighttime release of growth hormone that causes blood glucose elevations at about 5 to 6 AM fasting hyperglycemia. Give more insulin in night time |
| Somogyi phenomenon is | morning hyperglycemia from the counterregulatory response to nighttime hypoglycemia. Teach adequate dietary intake at bedtime and evaluating the insulin dose and exercise programs to prevent conditions that lead to hypoglycemia |
| Three blood glucose phenomena in diabetic patients. | lack of insulin, dawn phenom, somogyi phenom |
| This method is more effective in controlling blood glucose levels than a multiple-injection schedule | Continuous subcutaneous infusion (CSII) |
| Teaching for CSII | adjust the #of insulin received based on data from blood glucose monitoring, monitor ketones when BGL’s are over 300mg/dL. Monitor the pump for problems, clogs/kinks. Do not abruptly d/c (hyperglycemia results). provide supplemental insulin schedule. |
| ___________insulin analogues are used with insulin infusion pumps | Rapid-acting |
| Problems with CSII include | skin infections that can occur when the infusion site is not cleaned or the needle is not changed every 2 to 3 days. |
| CSII may lead to more frequent and more severe ketoacidosis than other methods of insulin delivery because of | inexperience in pump use, infection, accidental cessation or obstruction of the infusion, or mechanical pump problems. |
| Patient education for diabetic drugs | store according to manufacture’s instructions, always have a spare bottle of each type of insulin used. inspect the insulin before each use for changes, always buy the same type of syringe, don’t reuse needles. Assess pt ability to administer |
| Amylin analogues are drugs similar to | amylin, a naturally occurring hormone produced by beta cells in the pancreas, that works with and is co-secreted with insulin in response to blood glucose elevation. |
| Pramlintide (Symlin), an analogue of amylin, is approved for patients with | either type 1 or type 2 diabetes treated with insulin. It is indicated as adjunct therapy for patients who use mealtime insulin delivery and have not achieved desirable glucose control despite optimum insulin therapy |
| Pramlintide works by three mechanisms: | delaying gastric emptying, reducing after-meal blood glucose levels, and by triggering satiety (in the brain), which leads to decreased caloric intake and weight loss. |
| Pramlintide alters | gastric uptake |
| Patient teaching for pramlintide | to take oral drugs in which rapid onset of action is important (e.g., analgesics) either 1 hour before or 2 hours after eating, inject pramlintide into a site different from where insulin is injected |
| Pramlintide and insulin are | NOT to be mixed in the same syringe because the pH of the two drugs is not compatible. |
| Common side effects of pramlintide | Nausea, vomiting, and anorexia. It should not be used for patients with symptomatic gastroparesis |
| Incretin agents are natural | “gut” hormones that, in addition to insulin, also lower plasma glucose levels |
| GLP-1 (incretin agent) has many effects on the stomach, liver, pancreas, and brain to work together to regulate blood glucose. It lowers | glucagon secretion from the pancreas, leading to reduced liver glucose production. It also delays gastric emptying, slows the rate of nutrient absorption into the blood, and reduces food intake, all of which lower blood glucose levels |
| Exenatide (Byetta) is a | long-acting analogue of GLP-1. It mimics the actions of GLP-1, stimulating insulin secretion only when blood glucose is high |
| The main side effect of exenatide | is nausea. It stimulates insulin secretion and may cause hypoglycemia when given with sulfonylurea drugs (which also stimulate insulin secretion) but not with metformin alone.) |
| Teach patients not to administer exenatide | after a meal and to keep the pen injectors refrigerated. |
| DPP-IV inhibitors work by | slowing the inactivation of incretin hormones |
| Sitagliptin (Januvia) increases | the body's active incretin hormone levels, reducing both before- and after-meal blood glucose levels. It works only when blood glucose is elevated. |
| Januvia is approved as single agent for patients with | type 2 diabetes unable to manage diabetes with diet and exercise alone and as add-on therapy for those patients with inadequate blood glucose control taking metformin or thiazolidinediones |
| Side effects of Januvia include | stuffy or runny nose, sore throat, upper respiratory infection, and GI effects of abdominal pain, nausea, and diarrhea. Monitor for symptoms of renal insufficiency. |
| Adverse effects include hypoglycemia, GI disturbances, upper respiratory tract infection, arthralgia or back pain, and headache | Repaglinide (Prandin) |
| The major adverse effect is hypoglycemia. Patients who skip meals should also skip their scheduled dose of Starlix to reduce the risk for hypoglycemia | Nateglinide (Starlix) |
| ADA recommends that metformin should not | be given to anyone with kidney disease and elevated blood creatinine levels. The drug should be withheld for 48 hours before and after using contrast material and surgical procedures requiring anesthesia. |
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