A chronic multisystem disease related to abnormal insulin production,
impaired insulin utilization, or both. Leading cause of: o End-stage renal disease o Adult blindness o Nontraumatic lower limb amputation Major contributing factor o Heart disease o Stroke Etiology/Pathophysiology o Theories link causes to single/combination of these factors: Genetic, autoimmune, viral, environmental o Two most common types: Type 1 & Type 2 Other types: gestational, prediabetes, secondary diabetes o Regardless of its cause, diabetes is primarily a disorder of glucose metabolism related to absent or insufficient insulin supply and/or poor utilization of available insulin. Normal insulin metabolism: Produced by beta cells (Islets of Langerhans) The insulin is continuously released into the bloodstream in small increments with larger amounts released after food. Stabilizes glucose range to 70-120 mg/dL Insulin Promotes glucose transport from the bloodstream across cell membrane to the cytoplasm of a cell. o Decreases glucose in the bloodstream. Insulin increases in the body after a meal o Stimulates storage of glucose as glycogen in liver and muscle. o Inhibits gluconeogenesis o Enhances fat deposition o Increases protein synthesis The fall in insulin level during normal overnight fasting facilitates the release of stored glucose from the liver, protein from muscle, and fat from adipose tissue.
o Counterregulatory Hormones Oppose effects of insulin Increases blood glucose levels Provide regulated release of glucose for energy Help maintain normal blood glucose levels Ex. Glucagon, epinephrine, growth hormone, cortisol Abnormal production of any or all of these hormones may be present in diabetes o Skeletal muscle and adipose tissue- insulin-dependent tissues o Other tissues (brain, liver, blood cells)- do not directly depend on insulin for glucose transport. Although liver cells are not considered insulin-dependent tissue, insulin receptor sites of the liver facilitate the hepatic uptake of glucose and its conversion to glycogen.
ALTERED MECHANISMS IN TYPE I & II DIABETES
Formerly known as juvenile-onset or insulin-dependent diabetes. Most often occurs in people younger than 40 years of age. o Occurs more frequently in younger children. o 40% of those with Type I-onset before age of 20. Incidence has increased by 3% to 5% over recent decades. o As a person grows older the Beta Cells take longer to respond; and this is why the incidence has become increased, as a person gets older. Accounts for 5-10% of all people with diabetes. Etiology and Pathophysiology- o End result of long-standing process Progressive destruction of pancreatic beta cells by the bodys own T cells. Auto antibodies cause a reduction of 80-90% in normal beta cell functioning before manifestations occur. o Causes: Genetic predisposition Related to human leukocyte antigens (HLAs) Exposure to a virus Idiopathic diabetes is a form of type 1 diabetes that is not related to autoimmunity but is strongly inherited. This occurs only in a small number of people with type 1 diabetes, and is most often in those of African or Asian ancestry.
RENAL FAILURE Chronic Kidney Disease (CKD) o Involves progressive, irreversible loss of kidney function o Definition: The presence of: Kidney damage Pathologic abnormalities Markers of damage (blood, urine, imaging tests) Glomerular filtration rate (GFR) <60 mL/min for 3 months or longer Disease staging based on decreased in GFR o Normal GFR 125 mL/min, which is reflected by urine creatinine clearance o Last stage of kidney failure End-stage renal disease (ESRD) occurs when GFR <15mL/min o Up to 80% of GFR may be lost with few changes in functioning of body. o Remaining nephrons hypertrophy to compensate. o End result is a systemic disease involving every organ. o Because the kidneys are highly adaptive, kidney diseases often are not recognized until considerable loss of nephrons has occurred. Because patients with CKD are frequently asymptomatic, it has been estimated that about 70% of people with CKD are unaware that they have the disease o Each year, 70,000 people die from causes related to renal failure. o More than 26 million Americans have CKD. o Mortality rates are 19% to 24% for those with stage 5 CKD on dialysis. o Leading causes of ESRD: Diabetes & Hypertension Diabetes about of cases and hypertension about 1/3 of cases.
Lewis Ch 47 1172-1197 Grodner Ch 21 Ch 47 study guide ATI ch 68
Clinical Manifestations o Result of retained substances Urea Creatinine Phenois Hormones Electrolytes Water Other substances o Uremia Syndrome that incorporates all signs and symptoms seen in various systems throughout the body
o Urinary System Polyuria Results from inability of kidneys to concentrate urine Occurs most often at night Specific gravity fixed around 1.0.10 Oliguria Occurs as CKD worsens Anuria Urine output <40 mL per 24 hours o Metabolic Disturbances Waste product accumulation As GFR , BUN and serum creatinine levels
o BUN Not only by kidney failure but by protein intake, fever, corticosteroids, and catabolism N/V, lethargy, fatigue, impaired thought processes, and headache may occur Altered carbohydrate metabolism Caused by impaired glucose use o From cellular insensitivity to the normal action of insulin Defective carbohydrate metabolism Pts with diabetes who become uremic may require less insulin than before the onset of CKD. Insulin dependent on kidneys for excretion Serum creatinine and creatinine clearance determinations (calculated glomerular filtration rate) are considered more accurate indicators of kidney function than BUN or creatinine. Efforts are made to initiate renal replacement therapy before a patient becomes severely symptomatic. Elevated Triglycerides Hyperinsulinemia stimulates hepatic production of triglycerides. o Elevated glucose levels lead to increased insulin levels, and insulin stimulates hepatic production of triglycerides. Altered lipid metabolism o levels of enzyme lipoprotein lipase Important in breakdown of lipoproteins Almost all patients with uremia develop dyslipidemia, with elevated very-low-density lipoproteins (VLDLs), normal or decreased low- density lipoproteins (LDLs), and decreased high- density lipoproteins (HDLs). Most pts with CKD die from cardiovascular disease. o Electrolyte/Acid-Base Imbalances Potassium Hyperkalemia o Most serious electrolyte disorder in kidney disease o Fatal dysrhythmias Fatal dysrhythmias can occur when the serum potassium level reaches 7 to 8 mEq/L (7 to 8 mmol/L). Hyperkalemia results from decreased excretion of potassium by the kidneys, breakdown of cellular protein, bleeding, and metabolic acidosis. Potassium may come from the food consumed, dietary supplements, drugs, and IV infusions. Sodium May be normal or low Because of impaired excretion, sodium retained o Water is retained Edema Hypertension CHF Calcium and Phosphate alterations Magnesium alterations Hypermagnesemia generally is not a problem unless the patient is ingesting magnesium (e.g., milk of magnesia, magnesium citrate, antacids containing magnesium). Clinical manifestations of hypermagnesemia: o can include absence of reflexes, decreased mentalstatus, cardiac dysrhythmias, hypotension, and respiratory failure. Metabolic acidosis Results from: o Inability of kidneys to excrete acid load (primary ammonia) o Defective reabsorption/regeneration of bicarbonate o Hematologic System Anemia Due to production of erythropoietin o From in functioning renal tubular cells Other factors contributing to anemia: o nutritional deficiencies, decreased RBC life span, increased hemolysis of RBCs, frequent blood samplings, and bleeding from the GI tract. Bleeding tendencies Defect in platelet function Defects in platelet function are caused by impaired platelet aggregation and impaired release of platelet factor III. Infection Changes in leukocyte function Altered immune response and function Diminished inflammatory response o Cardiovascular System Hypertension Heart failure Left ventricular hypertrophy Peripheral edema Dysrhythmias Uremic pericarditis The most common cause of death in patients with CKD is cardiovascular disease. Even a slight reduction in GFR has been associated with a greater risk for development of coronary artery disease. Traditional CV risk factors such as hypertension and elevated lipids are common in patients with CKD. However, much of the CV disease may be related to nontraditional CV risk factors such as vascular calcification and arterial stiffness. o Respiratory System Kussmaul respiration Dyspnea Pulmonary edema Uremic pleuritis Pleural effusion Predisposition to respiratory infection o Gastrointestinal System Every part of the GI is affected Due to excessive urea o Mucosal ulcerations o Stomatitis Found with exudates and ulcerations A metallic taste in the mouth o Uremic fetor (urinous odor of breath) o GI bleeding o Anorexia, nausea, vomiting May develop if CKD progresses to ESRD and is not treated with dialysis.
o Neurologic System Expected as renal failure progresses. Attributed to: nitrogenous waste products Electrolyte imbalance Metabolic acidosis Axonal atrophy Demyelination of nerve fibers Restless leg syndrome Muscle twitching Irritability Decreased ability to concentrate Peripheral neuropathy Altered mental ability Seizures Coma Dialysis encephalopathy The treatment for neurologic problems is dialysis or transplantation. Altered mental status is often the signal that dialysis must be initiated. Dialysis should improve general CNS symptoms and may slow or halt the progression of neuropathies. o Musculoskeletal System CKD mineral and bone disorder Systemic disorder of mineral and bone metabolism Results in skeletal complications o (osteomalacia, ostetis fibrosa) and extraskeletal (vascular) calcifications o Integumentary System Pruritus Cause is multifactorial Includes dry skin, calcium-phosphate deposition in skin, and sensory neuropathy The itching may be so intense that it can lead to bleeding or infection secondary to scratching Uremic frost Rare o Reproductive System Infertility Both sexes Decreased libido Low Sperm Counts Sexual dysfunction o Psychologic Changes Personality and behavioral changes Emotional ability Withdrawal Depression Changes in body image caused by edema, integumentary disturbances, and access devices (e.g., fistulae, catheters) may contribute to the development of anxiety and depression. Diagnostic Studies o History and physical examination o Dipstick evaluation o Albumin-creatinine ratio (first morning void) o GFR o Renal ultrasound o Renal scan o CT scan o Renal biopsy o A person with persistent proteinuria (1+ protein on standard dipstick testing two or more times over a 3- month period) should have further assessment of risk factors and a diagnostic workup with blood and urine tests. o The two equations used most frequently to estimate GFR are the Cockcroft-Gault formula and the Modification of Diet in Renal Disease (MDRD) Study equation (see Table 47-8). Collaborative Therapy Correction of extracellular fluid volume overload or deficit Nutritional therapy Erythropoietin therapy Calcium supplementation, phosphate binders Antihypertensive therapy Measures to lower potassium Adjustment of drug dosages to degree of renal function. o Drug Therapy Hyperkalemia IV insulin o IV glucose to manage hypoglycemia IV 10% calcium gluconate Sodium polystyrene sulfonate (Kayexalate) o Cation-exchange resin o Resin in bowel exchanges potassium for sodium. Hypertension Weight loss Lifestyle changes Diet recommendations Sodium and fluid restrictions Antihypertensive drugs o Diuretics o Calcium channel blockers o ACE inhibitors o ARB agents It is recommended that the target BP should be <130/80 mm Hg for patients with CKD and 125/75 for patients with significant proteinuria. The BP should be measured periodically in supine, sitting, and standing positions to effectively monitor the effects of antihypertensive drugs. CKD-MBD Phosphate intake restricted to <1000 mg/day Phosphate binders o Should be administered with each meal o Side effect: constipation o Calcium carbonate (caltrate) Binds phosphate in bowel and excretes o Sevelamer hydrochloride (Renagel) Lowers cholesterol and LDLs Interventions for CKD mineral and bone disorder include limiting dietary phosphorus, administering phosphate binders, supplementing vitamin D, and controlling hyperparathyroidism. Supplementing Vitamin D o Calcitriol (Rocaltrol) o Serum phosphate level must be lowered before calcium or vitamin D is administered. Controlling secondary hyperparathyroidism o Calcimimetic agents Cinacalcet (Sensipar) sensitivity of calcium receptors in parathyroid glands o Subtotal parathyroidectomy Anemia o Erythropoietin Epoetin alfa (Epogen, Procrit) Administered IV or subcutaneously Increased hemoglobin and hematocrit in 2 to 3 weeks Side effect: Hypertension o Iron Supplements If plasma ferritin <100 ng/mL Side effects: gastric irritation, constipation May make stool look dark in color Another side effect of EPO therapy is the development of iron deficiency resulting from increased demand for iron to support erythropoiesis. Orally administered iron should not be taken at the same time as phosphate binders because calcium binds the iron, preventing its absorption. o Folic Acid Supplements Needed for RBC formation Removed by dialysis o *Avoid blood transfusions Dyslipidemia Goal: o Lowering LDL below 100 mg/dL o Triglyceride level below 200 mg/dL Statins o MHG-CoA reductase inhibitors Most effective for lowering LDL Evidence supports the use of statins in patients with CKD (especially diabetics) not yet on dialysis. The effectiveness of statins in patients on dialysis is still being studied. Fibrates (fibric acid derivatives) such as gemfibrozil (Lopid) are used to lower triglyceride levels and can also increase HDLs. o Complications of Drug Therapy Drug toxicity Digitalis Antibiotics Pain medications (Demerol, NSAIDS) o Nutritional Therapy Protein restriction (benefits are being studied) Water restriction (intake depends on daily urine output) Calorie-protein malnutrition A potential and serious problem that results from altered metabolism, anemia, proteinuria, anorexia, and nausea. Additional factors leading to malnutrition include depression and complex diets that restrict protein, phosphorus, potassium, and sodium. For the patient who is undergoing dialysis, protein is not routinely restricted. Although some evidence suggests that protein restriction has benefits, many patients find these diets difficult to adhere to. For CKD stages 1 through 4, many clinicians just encourage a diet with normal protein intake. Generally, 600 mL (from insensible loss) plus an amount equal to the previous days urine output is allowed for a patient receiving hemodialysis. Sodium restriction Diets vary from 2 to 4 g, depending on the degree of edema and hypertension Sodium and salt should not be equated. Salt substitutes should not be used because they contain potassium chloride. Instruct the patient to avoid high-sodium foods such as cured meats, pickled foods, canned soups and stews, frankfurters, cold cuts, soy sauce, and salad dressings. Potassium restriction 2 to 3 g High potassium foods should be avoided. o Foods with high potassium content that should be avoided include oranges, bananas, melons, tomatoes, prunes, raisins, deep green and yellow vegetables, beans, and legumes. Phosphate therapy 1000 mg/day Foods high in phosphate (dairy products) Most foods high in phosphate are also high in protein. Nursing Management: o Nursing Assessment/Diagnosis o Complete hx or any existing renal disease, family history o Long-term health problems o Dietary habits o Excess fluid volume o Risk for injury o Imbalanced nutrition: Less than body requirements o Grieving o Risk for infection o Because many drugs are potentially nephrotoxic, the nurse should ask the patient about both current and past use of prescription and over-the-counter drugs and herbal preparations. o Medications of concern: Antacids, NSAIDs, decongestants, and antihistamines. o Planning/Implementation o Overall goals: Demonstrate knowledge and ability to comply wth therapeutic regimen. Participate in decision making Demonstrate effective coping strategies Continue with ADLs within psychologic limitations o Health Promotion ID individuals at risk for CKD History of renal disease Hypertension Diabetes Mellitus Repeated UTI Regular checkups and changes in urinary appearance, frequency, and volume should be reported o Nursing Implementation o Acute Intervention Daily weight Daily BPs ID s/s of fluid overload ID s/s of hyperkalemia Strict dietary adherence Medication education Motivate patients in management of their diseases o Ambulatory & Home Care When conservative therapy is no longer effective, HD, PD, and transplantation are treatment options Patient/family need clear expectation of dialysis and transplantation. o Evaluation Maintenance of ideal body weight Acceptance of chronic disease No infection No edema Hematocrit, hemoglobin, and serum albumin levels in acceptable range Dialysis o Half of patients with CRF eventually will require dialysis o Diffuse harmful waste out of body o Controls BP o Keeps safe levels of chemicals in the body o Two types: Hemodialysis 3-4 times a week Takes 2-4 hours Machine filters blood and returns it to the body. Types of Access: o Temporary site: Perm cath- THIS IS THEIR LIFELINE..DO NOT ACCESS IT!
o AV fistula Surgeon constructs by combining an artery and a vein 3-6 months to mature o AV graft Man-made tube inserted by a surgeon to connect artery and vein 2-6 weeks to mature
What this means for ME as a NURSE Cannot take BP on the same arm as the fistula Protect the arm from injury Control obvious hemorrhage o Bleeding will be arterial o Maintain direct pressure No IV on same arm as fistula A thrill will be felt-this is normal Check for bruit every shift Access Problems: o AV graft thrombosis o AV fistula or graft bleeding o AV graft infection o Steal phenomenon Early post-op Ischemic distally Apply a small amount of pressure to reverse symptoms Peritoneal dialysis
Abdominal lining filters the blood 3 Types: o Continuous ambulatory o Continous cyclical o Intermittent Considerations: o Make sure the dressing remains intact o Do not push or pull on the catheter o Do not disconnect any of the catheters o Always transport the patient and bags/catheters as one piece o Never inject anything into the catheter
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