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39 Cards in this Set
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Insulin |
Produced by the Islets of Langerhands in Pancreas Allow glucose transport into cells for use as energy or storage as glycogen in the liver, acts as key Stimulates protein synthesis and free fatty acid storage in adipose tissue |
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Diabetes mellitus |
Characterized by disturbances in carbohydrate, protein and fat metabolism The effects of DM result from insulin deficiency or resistance to endogenous insulin Types: Type 1, Type 2, Gestational, Diabetes secondary to other conditions |
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Type 1 DM |
Insulin Dependent, 10% of cases Caused by autoimmune destruction of pancreatic beta cells Eventually resulting in total lack of insulin production Cell destruction may be present for years before onset of symptoms (impending ketoacidosis) after illness or stressor Genetic predisposition Commonly diagnosed in adolescents, often <40
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Type 1 DM Manifestation |
Onset is rapid and manifestations are acute Hyperglycemia (blood glucose >126mg/dL on two occasions), polyuria, polyphagia, polydipsia, glucosuria, weight loss and fatigue Test urine for ketones |
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Type 2 DM |
Non-insulin dependent, 90% of cases The pancreas continues to produce some endogenous insulin, but is insufficient or poorly used by tissues. Insulin peripheral resistance (receptors are unresponsive) Beta cells become fatigued from compensatory overproduction Inappropriate, haphazard glucose production by liver Cytokines by adipose tissue cause inflammation and insulin resistance |
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Type 2 DM Risk factors |
Overweight or obese esp. abdominal or visceral Older age, although increasing prevalence in childhood Family history Americans of African, Native and Hispanic descent |
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Type 2 DM Manifestation |
Onset is gradual, producing few symptoms. Many are diagnosed on routine lab testing. Polyuria, polydipsia, polyphagia, fatigue and weakness. Recurrent infections: yeast, UTI, slow healing Paresthesias of hands and feet, visual changes. Glucose molecules damage tiny capillaries by drawing water in. |
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Gestational diabetes |
Glucose intolerance onset during second or third trimester Hormones secreted during pregnancy increase blood sugar, resulting in insulin resistance Blood glucose levels return to normal after delivery Dietary management, avoid excessive weight gain, frequent monitoring, possibly insulin Anti-diabetic meds contraindicated in pregnancy |
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Pre-diabetes |
Fasting glucose >100 but <126 Higher risk of developing Type 2 in 10 years Often linked to metabolic syndrome Increases risk of cardiovascular disease No symptoms, but damage to heart/blood vessels may already be occurring. Healthy weight, exercise, healthy diet to reduce risk |
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Diagnosis of DM |
Fasting plasma glucose (FPG) >126 mg/dL Normal 70-100 mg/dL Random plasma glucose >200 mg/dL on more than one occassion 2 hr postprandial glucose >200 mg/dL HgA1C >6.5% IGT (impaired glucose tolerance) is prediabetes |
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Therapeutic management |
Frequent monitoring of blood glucose esp. Type 1 Individualized diet plan Oral antidiabetic medications &/or insulin Exercise |
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Diabetic Diet |
Intake must be balanced with energy output. Weight loss of 5% improves glycemic control for overweight DM2. Balanced nutrition: At least 130 g/day of carbohydrate, limit sweeteners, 25-30 g fiber, <7% saturated fat, <200mg cholesterol, minimize trans fat, 2+ servings of fish for polyunsaturated fat, 15-20% protein, moderate alcohol or none. May use carb counting (45-60g per meal) or exchange list (portion size). |
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Exercise |
30 min, 5 days a week of moderate intensity physical activity (light bicycling, dancing, gardening, walking briskly) and resistance training 3 times per week. Same time and intensity each day, monitor hypoglycemia, avoid hot/cold. Exercise deceases insulin resistance and can have direct effect on lowering blood glucose levels. Decreases cardiovascular risk factors. Alters blood lipid levels. |
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Monitoring Glucose Levels |
Self-Monitoring of Blood Glucose (SMBG) Current blood glucose: make decisions about food intake, activity and medication dosages. Record of fluctuations. Use glucometer. Monitor 4+ times a day if multiple injections or illness. Glycosylated Hemoglobin readings HgbA1C Amount of hemoglobin with glucose attached to it, as percentage of total hemoglobin. Measures glycemic control for previous 2-3 months. No fasting required. Note RBC diseases. Goal is 6.5-7.0%. |
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Hyperglycemia |
Blood sugar >200 mg/dL (normal 70-130) Inadequate insulin, ingesting too much glucose or severe stress Symptoms: polyuria, and polydipsia, may be asymptomatic |
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Hypoglycemia signs |
Too much insulin compared to blood glucose. Related to mismatch between food intake and timing of peak action. Glucose levels <70 mg/dL. Hot & dry = sugar high Cold & clammy = need some candy Tachycardia and tremors Irritability Restless Excessive hunger Diaphoresis and dizziness |
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Hypoglycemia treatment |
Check blood glucose. <50mg/dL wo symptoms or <70 mg/dL w symptoms. Rule 15: ingest 15 g of simple carb i.e. 5oz fruit juice or regular soda, 4 glucose tablets, 10 lifesavers, 3 teaspoons sugar. Recheck 15 min. Repeat. Contact health care provider after 3 rounds. In acute care, may give 25-50mL of D50% or IM glucagon Protein snack when resolved. |
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Diabetic ketoacidosis (DKA) |
Profound insulin deficiency. Characterized by hyperglycemia, ketosis, acidosis, dehydration. Serum glucose >250, pH<7.35, urine + ketones and glucose Glucose is unable to enter the cells: lipids are used as energy source breaking down fatty acids, ketones are waste product Metabolic acidosis
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DKA causes |
Occurs primarily in patients with type 1 DM, may be seen in Type 2 during severe illness or stress. Precipitating factors: illness, infection, emotional stress, inadequate insulin dosage, undiagnosed type 1, poor self-management, neglect. |
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DKA signs |
Early symptoms: polyuria with dehydration, polydipsia, acetone (fruity) breath, fatigue If not treated: severe electrolyte depletion (Na, K, Cl, Mg, PO4), nausea/vomiting, hypovolemia, shock, renal failure, coma and death Kussmaul respiration attempt to compensate for acidosis |
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DKA management |
Goals: restore fluid, electrolyte and glucose balance. Establish IV: 0.45-0.9 NaCl (1-2L/hr) to restore urine output to 30-60mL/hr and raise BP, then 500mL/hr. Insulin bolus followed by IV drip. When blood glucose=250mg/dL, pH=7.3, add 5-10% dextrose to prevent sudden hypoglycemia (causes cerebral edema) and use sliding scale insulin. Assess for potassium imbalance: insulin causes K to move into cells. Monitor cardiac function and vital signs. |
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Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)
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Life-threatening syndrome: severe hyperglycemia, but able to produce enough insulin to prevent DKA. Usually Type 2. Triggered by meds, infection, illness, surgery. Osmotic diuresis and fluid volume deficit: electrolyte imbalance (loss of Na, K, PO4, Mg from tissues), dehydration and hypovolemia. Neurologic manifestations: somnolence, coma, seizures, hemiparesis, aphasia. |
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HHSN clinical manifestations |
Symptoms occurs over 24 hr to 2 weeks Decreased LOC Dry mucous membranes Polydipsia, hyperthermia Impaired sensory and motor function Positive Babinski sign, seizures
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HHSN diagnostics |
Serum osmolality >340mOsm/L Serum glucose >600 Serum K and Cl elevated due to dehydration Normal serum pH No serum ketones
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HHNS treatment |
High mortality rate. Treated similar to DKA: fluid replacement, electrolyte correction and insulin. Focus is more on fluid replacement. Neurological problems may linger after other problems are corrected. |
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Angiopathy |
Damage to blood vessels: macrovascular or microvascular Complication of chronic hyperglycemia due to: Accumulation of damaging by-products of glucose metabolism (sorbitol effects nerves); abnormal glucose molecules in basement membrane of small vessels (eye and kidney) and derangements of RBC function that leads to decrease in oxygenation to tissues. Complications reduced by keep glucose levels as near normal as possible |
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Macrovascular disease |
Large and medium-sized blood vessels diseases: cerebrovascular, cardiovascular and peripheral vascular disease. Risk for stroke and heart disease 2-4 times higher. Chronic hyperglycemia promotes plaque build up (cholesterol and lipids) in arterioles, under endothelium. Risk increased by obesity, smoking, hypertension, hyperlipidemia, sedentary lifestyle, BP <130/80. Statins often prescribed. |
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Microvascular disease |
Thickening of vessel basement membranes in capillaries and arterioles in response to chronic hyperglycemia. Leaky and non-elastic. Leads to local tissue ischemia. Complications are specific to diabetes: retinopathy, nephropathy and neuropathy. |
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Diabetic retinopathy |
Microvascular damage to retina, causing edema or vitreous contraction. Partial occlusion causes capillary fluid to leak out, causing edema. Ischemia may cause new vessels to form that hemorrhage easily. Causes glaucoma, cataracts and blindness. Annual eye exam with specialist opthamologist. |
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Nephropathy |
Damage to small blood vessels that supply glomeruli of kidney. Leading cause of end-stage kidney disease. Risk factors: hyperglycemia, smoking and hypertension. Screened for albuminuria and serum albumin:creatinine for estimate GFR. End-stage renal disease leads to dialysis. |
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Neuropathy |
Nerve damage that occurs because of metabolic derangements. Sensory (peripheral): loss of sensation in fingers and toes including hot/cold and pain, paresthesia (tingling, burning) and increased sensitivity. Increases risk of foot ulcers and lower limb amputation. Autonomic: does not feel angina, gastroparesis, orthostatic hypotension, sexual function, resting tachycardia. Teach alternate signs of heart attack: SOB, sweating, extreme fatigue. |
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Dawn phenomena |
Hyperglycemia in morning due to GH and cortisol increase. Normal blood glucose until 3am and then begins to rise. High glucose 2-4am. Treatment: increase or add intermediate-acting insulin at bedtime.
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Somogyi Effect |
Hyperglycemia in morning due to a high dose of insulin at night. The decline in blood glucose causes the release of counter-regulatory hormones (cortisol, glucagon) and rebound hyperglycemia. Low glucose 2-4am. Treatment: decrease evening dose of intermediate-acting insulin and bedtime snack. Danger may be an increase in nightly insulin.
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Hospitalized diabetic patient |
Diabetes may not be primary diagnoses, but complicates treatment Stress, illness, infection, new medications Alterations in diet and timing (NPO, clear liquids, late trays) Type 2 may need insulin coverage while hospitalized Teaching opportunity |
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Geriatric diabetic patient |
Higher incidence of diabetes in elderly Goals may change Age-related factors may management more difficult: disabilities, co-morbidities, delayed psychomotor function, cognitive function May not experience hypoglycemic effects Involve family in teaching |
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Diabetes nursing diagnoses |
Ineffective health maintenance Risk for infection Risk for impaired skin integrity Risk for injury Risk for disturbed body image Knowledge deficit |
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Client education |
Type of diabetes, symptoms to report, Medic alert bracelet Regular exams with specialists Diligent skin and dental hygiene, including foot care Diet plan Sick day management plan Hypoglycemia: s&s, actions to take, causes, methods to prevent Finger-stick glucose monitoring and medication administration Treatment and prevention of acute and chronic complications |
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Glycogenoses |
Hereditary disorder in which body in unable to convert stored glycogen into glucose Due to missing enzyme i.e. pyruvate carboxylase, PEP carboxykinase Symptoms: failure to thrive (infants), growth and development issues, kidney stones, confusion, weakness If severe: chronic gout, seizures, coma, kidney failure Treated with timing carbohydrate consumption |
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Metabolic Syndrome (Syndrome X) |
3+ comorbid cardiovascular and insulin-related conditions due to obesity or underlying condition (polycystic ovary syndrome or DM) Hypertension Elevated fasting blood glucose Low HDL High Triglycerides Excess belly fat At increased risk of organ failure, MI, strokes. Weight loss, diet and exercise are key. |
