WVC IGGY chpt 67 to pg 1491
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| show | new cases of blindness, end-stage kidney disease requiring dialysis or transplantation, and foot or leg amputations.
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| Studies show that __________ controls reduces complication of diabetes | show 🗑
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| show | Treatment of hypertension and hyperlipidemia
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| show | hyperglycemia resulting from problems with insulin secretion, insulin action, or both.
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| show | underlying problem causing a lack of insulin and the severity of the insulin deficiency.
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| The 2 types of islet cells that are responsible for insulin control | show 🗑
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| Alpha cells produce ___________, beta cells produce _________ and ________ | show 🗑
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| show | glucagon,
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| It causes the release of glucose from cell storage sites whenever blood glucose levels are low | show 🗑
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| This allows body cells to use and store carbohydrate, fat, and protein | show 🗑
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| show | • Beta-cell destruction leading to absolute insulin deficiency • Autoimmune • Idiopathic
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| show | • Ranges from insulin resistance with relative insulin deficiency to secretory deficit with insulin resistance
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| Other conditions resulting from hyperglycemia | show 🗑
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| show | • Glucose intolerance with onset or first recognition during pregnancy • Diagnosis is based on results of a 100-g oral glucose tolerance test during pregnancy
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| show | the liver into activated insulin.
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| Insulin attaches to receptors on target cells, where it promotes | show 🗑
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| show | the rate that beta cells secrete insulin.
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| show | glucose in the blood to move into cells to generate energy.
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| show | glycogenesis at the same time that it inhibits glycogenolysis, protein and lipid synthesis and inhibits ketogenesis & gluconeogenesis
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| In muscle, insulin promotes | show 🗑
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| In fat cells, insulin promotes | show 🗑
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| The pancreas secretes about | show 🗑
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| show | neuronal dysfunction and cell death.
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| ______ _________can be used as fuel by some cells when glucose is not available. | show 🗑
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| Glucose and free fatty acids are stored inside cells as | show 🗑
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| In the fat cells, glycogen is stored as | show 🗑
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| The most efficient means of storing energy is in the form of | show 🗑
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| During a prolonged fast or after illness or injury | show 🗑
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| During a fasting state, plasma glucose is maintained by | show 🗑
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| show | pancreatic alpha cells that stimulate glucose production.
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| show | pancreatic beta cells to prevent excessive liver glucose output.
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| show | the emptying rate of the stomach and delivery of nutrients to the small intestine, where they are absorbed into circulation
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| show | increase secretion of insulin and slow the rate of gastric emptying, preventing hyperglycemia after meals
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| show | excessive liver glucose production and reduced glucose uptake in other cells due to a combination of INSULIN RESISTANCE and DEFICIENT INSULIN SECRETION.
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| show | 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
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| show | counterregulatory hormone. It increases blood glucose by actions opposite those of insulin when more energy is needed.
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| show | epinephrine, norepinephrine, growth hormone, and cortisol
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| show | 70 to 100 mg/dL
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| Gluconeogenesis, is the | show 🗑
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| Lipolysis, is the | show 🗑
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| Proteolysis, is the breakdown of | show 🗑
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| Levels of counterregulatory hormones increase in an | show 🗑
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| Hyperglycemia causes fluid and electrolyte imbalances, leading to the classic symptoms of diabetes: | show 🗑
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| show | sodium, chloride & potassium being excreted In the urine→dehydration →polydipsia→ cell breakdown → polyphagia
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| With insulin deficiency, fats break down, releasing free fatty acids. Conversion of fatty acids to | show 🗑
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| show | abnormal breakdown products of fatty acids,
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| Collection of ketones in the blood when insulin is not available, results in | show 🗑
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| The dehydration that occurs with diabetes leads to | show 🗑
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| Physiologic Response to Insufficient Insulin | show 🗑
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| show | an increase in respirations due to diabetic metabolic acidosis. Acetone is exhaled, giving the breath a “fruity” odor.
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| show | patients response to treatment, severity of acidosis and level of hydration.
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| Three glucose-related emergencies can occur in patients with diabetes | show 🗑
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| show | macrovascular and microvascular
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| Macrovascular complications are | show 🗑
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| show | nephropathy (kidney dysfunction), neuropathy (nerve dysfunction), and retinopathy (vision problems).
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| show | irreversible basement membrane thickening and organ damage.
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| show | functional cell integrity.
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| show | connective tissue hypoxia and microischemia
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| show | hypertension, a sedentary lifestyle, high blood lipid levels, and smoking than to hyperglycemia, and obesity
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| Many older diabetic patients have no classic signs of high blood glucose levels, and the diagnosis is made | show 🗑
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| show | cardiovascular disease
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| show | 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.
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| show | 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.
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| Patients with diabetes tend to have higher levels of C-reactive protein (CRP), | show 🗑
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| Cardiovascular disease complication rates can be reduced through | show 🗑
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| show | Hypertension, hyperlipidemia, nephropathy, peripheral vascular disease, and alcohol and tobacco abuse
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| show | problems that block retinal blood vessels and cause them to leak, leading to retinal hypoxia
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| Retinopathy is linked to fasting blood glucose levels | show 🗑
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| _______________ & ___________________increase the rate of retinopathy development in patients with type 1 diabetes | show 🗑
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| show | macular degeneration, corneal scarring, and changes in lens shape or clarity
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| Hyperglycemia may cause | show 🗑
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| Hypoglycemia may cause | show 🗑
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| show | more common in patients with diabetes
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| The older patient with retinopathy may have | show 🗑
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| show | 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.
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| show | neuropathy
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| Damage to sensory nerve fibers results in | show 🗑
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| show | muscle weakness.
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| show | dysfunction in every part of the body.
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| the most common neuropathies in diabetes and involve widespread nerve function loss | show 🗑
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| show | Diffuse neuropathies
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| show | Diffuse neuropathies
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| 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 | show 🗑
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| show | ischemic neuropathies
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| 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 | show 🗑
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| show | cardiovascular, GI, and urinary function.
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| Hyperglycemia leads to neuropathy through | show 🗑
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| Orthostatic hypotention and syncope | show 🗑
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| show | dysphagia N/V, and bowel elimination problems. Diarrhea often occuring at night. Constipation, Gastroparesis
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| The most common GI symptom of DM is | show 🗑
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| Gastroparesis a cause of | show 🗑
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| Loss of nerve input to the bladder results in | show 🗑
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| show | end-stage kidney disease (ESKD) and kidney failure in the United States
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| show | a 10- to 15-year history of diabetes, diabetic retinopathy, poor blood glucose control, uncontrolled hypertension, and genetic predisposition.
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| The earliest clinical sign of nephropathy is | show 🗑
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| show | Distal symmetric polyneuropathy, Autonomic neuropathy
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| show | Paresthesias: burning/tingling sensations, starting in toes and moving up legs. Dysesthesias: burning, stinging, or stabbing pain. Anesthesia: loss of sensation
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| Motor alterations in intrinsic muscles of foot in distal symmetric polyneuropathy | show 🗑
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| Focal ischemia manifests as | show 🗑
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| show | :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
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| show | 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
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| Chronic high blood glucose levels cause | show 🗑
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| show | 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.
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| What items are included in the filtration of larger particles resulting from damage of kidney hypertension | show 🗑
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| What disease process speeds the process of diabetic nephropathy | show 🗑
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| What is an autoimmune disorder in which beta cells are destroyed in a genetically susceptible person | show 🗑
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| show | immune system cells, mediators, and antibodies attack and destroy insulin-secreting cells in the islets.
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| Antigen pattern for DM 1 and viral considerations | show 🗑
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| Development of the DM 1 is an interactive effect of | show 🗑
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| Most patients with type 1-diabetes have what antibodies/markers | show 🗑
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| DM 1, average age at onset | show 🗑
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| show | Peaks in 50s; may occur earlier
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| Main symptoms of DM 1 | show 🗑
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| show | Frequently none; thirst, fatigue, visual blurring, vascular or neural complications
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| show | Viral infection
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| show | unknown
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| Basic pathology of DM II | show 🗑
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| What antigen patterns/antibodies are present in DM II | show 🗑
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| Endogenous insulin and C-peptide in DM 1 and DMII | show 🗑
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| Is inheritance in DM1 recessive or dominant | show 🗑
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| Is inheritance in DMII recessive or dominant | show 🗑
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| How does nutritional status affect the onset of DM1 | show 🗑
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| show | 20-30%
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| Sulfonylurea therapy is used in what type of DM | show 🗑
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| show | DMII
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| 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 | show 🗑
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| The simultaneous presence of metabolic factors known to increase risk for developing type 2 diabetes and cardiovascular disease | show 🗑
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| Features of metabolic syndrome are | show 🗑
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| Any the features of metabolic syndrome can cause | show 🗑
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| What would you teach a client with DM | show 🗑
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| show | 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
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| The major focus for healthcare promotion of DM1 is | show 🗑
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| The major focus for healthcare promotion of DMII is | show 🗑
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| What would you teach for healthcare promotion in DMII | show 🗑
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| What is the percentage of heredity incidents of DMII | show 🗑
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| show | 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
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| The preferred test for DM in non-pregnant adults is | show 🗑
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| show | polyuria, polydipsia, and unexplained weight loss.
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| How is DMII diagnosed | show 🗑
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| Normal ranges for FBG | show 🗑
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| Impaired fasting glucose(IFG) is defined as | show 🗑
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| show | <140 mg/dL
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| Impaired glucose tolerance test (IGT) are | show 🗑
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| show | 200 mg/dL
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| show | <7%
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| show | poor diabetic control and need for adherence to regimen or changes in therapy.
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| What instructions do you give your clients prior to undergoing an oral glucose tolerance test | show 🗑
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| How will you explain an oral glucose test to your clients | show 🗑
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| show | >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
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| show | oral glucose tolerance testing (OGTT)
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| show | OGTT, with hourly tests. Two or more of the venous plasma levels must be met or exceeded for a positive diagnosis
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| show | fasting plasma glucose test or 2-hour OGTT
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| show | blood glucose permanently attaches to hemoglobin
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| What shows the average blood glucose level during the previous 120 days—the life span of red blood cells. to evaluate the treatment plan | show 🗑
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| show | HbA1c. Unlike the fasting blood glucose test, HbA1c test results are not altered by eating habits the day before the test.
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| show | 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.
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| Glycosylated serum proteins and albumin | show 🗑
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| Glycosylated serum proteins and albumin measures are useful when | show 🗑
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| What are the available tests for glycosylated serum proteins & albumin | show 🗑
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| The presence of moderate to high urine ketones (hyperketonuria) indicates a | show 🗑
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| Hyperketonuria in the presence of hyperglycemia is a | show 🗑
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| When should urine testing be performed | show 🗑
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| Hyperketonuria without hyperglycemia suggests that | show 🗑
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| show | of urine protein without kidney symptoms may indicate microvascular changes in the kidney
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| show | microalbuminuria. Even minor elevations of albumin are associated with increased mortality.
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| Once clinical proteinuria has been detected, kidney function (e.g., glomerular filtration rate) is assessed by | show 🗑
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| This test may be appropriate for a quick screening but should not be used for monitoring diabetes management. | show 🗑
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| The long-term value is the | show 🗑
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| The short-term values are the | show 🗑
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| show | FPG: > 100 mg/dL even with older adults and post-meal >150
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| The management of diabetes mellitus is complicated and involves considerable | show 🗑
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| show | nutritional interventions, blood glucose monitoring, a planned exercise program, and in some instances, drugs to lower blood glucose levels.
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| show | The nurse, together with the patient, physician, nutritionist, pharmacist, case manager, and in some cases, physical therapist
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| show | insulin secretagogues and are used for patients with some remaining pancreatic beta-cell function.
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| The action of sulfonylurea agents are | show 🗑
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| show | weight gain and hypoglycemia. Hypoglycemic episodes are more likely to occur with chlorpropamide (Diabinese, Novo-Propamide) because of its long duration of action.
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| What type of patients are more susceptible to hypoglycemia | show 🗑
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| Oral Blood Glucose–Lowering Agents SULFONYLUREAS | show 🗑
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| show | Glipizide (Glucotrol), Glyburide (DiaBeta/Micronase), Glimepiride (Amaryl)
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| MEGLITINIDE ANALOGUES | show 🗑
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| BIGUANIDES | show 🗑
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| show | Acarbose (Precose), Miglitol (Glyset)
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| show | Pioglitazone (Actose), Rosiglitazone (Avandia
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| FIXED COMBINATIONS | show 🗑
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| Post-meal glucose levels (postpradial) | show 🗑
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| Pre-meal glucose leves (prepradial) | show 🗑
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| show | 100 and 140 mg/dL
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| Signs and symptoms of hypoglycemia | show 🗑
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| show | insulin secretagogues and have actions and adverse effects similar to those of sulfonylureas
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| show | lower blood glucose by triggering insulin secretion from pancreatic beta cells
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| show | Repaglinide (Prandin) and Nateglinide (Starlix)
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| show | Repaglinide (Prandin)
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| _____________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. | show 🗑
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| show | Biguanides
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| Metformin (Glucophage) is the major drug in this class. | show 🗑
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| Metformin’s action | show 🗑
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| The ADA recommends metformin as | show 🗑
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| show | abdominal discomfort and diarrhea.
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| Metformin should not be used in conditions that decrease drug clearance, such as | show 🗑
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| Patient teaching for metformin | show 🗑
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| Alpha-glucosidase inhibitors are agents that | show 🗑
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| Acarbose does what | show 🗑
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| The most common side effects of Acarbos and Miglitol are | show 🗑
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| show | use oral glucose tablets, glucose gel, or low-fat milk to treat hypoglycemia. Severe hypoglycemia may require glucose infusion or glucagon injection.
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| _____________________ 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) | show 🗑
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| show | rosiglitazone
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| show | an increase in adipose tissue and fluid retention, infection, headache, peripheral edema, and pain
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| Teach patients taking TZDs drugs | show 🗑
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| show | highly effective in maintaining desired blood glucose control. Some patients may need a combination of oral agents and insulin to control blood glucose levels.
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| Drugs are started | show 🗑
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| show | blood glucose cannot be controlled after the use of two or three different oral agents.
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| show | about the need for continuing dietary restrictions and regular exercise.
🗑
|
||||
| show | consult with the primary care provider or pharmacist before using any over-the-counter drugs.
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| show | cost, the patient's ability to manage multiple drug doses, age, and response to the drugs.
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| show | older patients, those with irregular eating schedules, or those with liver, kidney, or cardiac dysfunction
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|
||||
| Longer-acting agents (e.g., glyburide, glimepiride) with once-a-day dosing are better for | show 🗑
|
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| show | type 1 diabetes and also may be used for type 2 diabetes.
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|
||||
| The safety of insulin therapy in older patients may be affected by | show 🗑
|
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| Insulin is manufactured using DNA technology to synthesize | show 🗑
|
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| Insulin analogues are | show 🗑
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| Lispro insulin, | show 🗑
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| Patient teaching for insulin | show 🗑
|
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| show | between 0.5 and 1 unit/kg of body weight per day.
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|
||||
| What factors influence insulin absorption & availability | show 🗑
|
||||
| show | abdomen, followed by the deltoid, thigh, and buttocks
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|
||||
| What is the preferred site for insulin injections | show 🗑
|
||||
| show | insulin properties. The longer the duration of action, the more unpredictable is absorption. Larger doses of insulin also prolong the absorption.
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| show | Factors that ↑blood flow from the injection site, such as local application of heat, massage of the area, and exercise of the injected area
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|
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| Injection depth | show 🗑
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| Timing of injection affects | show 🗑
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| show | blood glucose levels after meals.
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|
||||
| Insulin lispro, insulin aspart, and insulin glulisine have rapid onsets of action and should | show 🗑
|
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| Regular insulin should be given at least | show 🗑
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| show | change the time of peak action.
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|
||||
| When rapid-acting (Humalog or NovoLog) or short-acting (regular) insulin is mixed with a longer-acting insulin, draw the | show 🗑
|
||||
| show | clouds the solution and makes the onset of action and peak effect time less predictable.
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|
||||
| show | 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.
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| Lipohypertrophy is | show 🗑
|
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| Dawn phenomenon | show 🗑
|
||||
| show | 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
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|
||||
| show | lack of insulin, dawn phenom, somogyi phenom
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|
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| This method is more effective in controlling blood glucose levels than a multiple-injection schedule | show 🗑
|
||||
| show | 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.
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|
||||
| ___________insulin analogues are used with insulin infusion pumps | show 🗑
|
||||
| Problems with CSII include | show 🗑
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||||
| CSII may lead to more frequent and more severe ketoacidosis than other methods of insulin delivery because of | show 🗑
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||||
| show | 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
🗑
|
||||
| show | 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.
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|
||||
| Pramlintide (Symlin), an analogue of amylin, is approved for patients with | show 🗑
|
||||
| Pramlintide works by three mechanisms: | show 🗑
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||||
| show | gastric uptake
🗑
|
||||
| show | 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
🗑
|
||||
| show | NOT to be mixed in the same syringe because the pH of the two drugs is not compatible.
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|
||||
| show | Nausea, vomiting, and anorexia. It should not be used for patients with symptomatic gastroparesis
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|
||||
| Incretin agents are natural | show 🗑
|
||||
| show | 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
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|
||||
| Exenatide (Byetta) is a | show 🗑
|
||||
| show | 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 | show 🗑
|
||||
| show | slowing the inactivation of incretin hormones
🗑
|
||||
| Sitagliptin (Januvia) increases | show 🗑
|
||||
| show | 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
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| show | stuffy or runny nose, sore throat, upper respiratory infection, and GI effects of abdominal pain, nausea, and diarrhea. Monitor for symptoms of renal insufficiency.
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| show | Repaglinide (Prandin)
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| The major adverse effect is hypoglycemia. Patients who skip meals should also skip their scheduled dose of Starlix to reduce the risk for hypoglycemia | show 🗑
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| show | 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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Review the information in the table. When you are ready to quiz yourself you can hide individual columns or the entire table. Then you can click on the empty cells to reveal the answer. Try to recall what will be displayed before clicking the empty cell.
To hide a column, click on the column name.
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You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
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