Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Management of patients with renal disorders •Primary glomerular disease •Renal failure Pathophysiology • Primary glomerular disease: Inflammation of glomerular capillaries • Antigen-antibody complexes—Deposition of these complexes in glomerular capillaries (IgG)—inducing inflammatory response • Major indicators of Glomerular Injury—proteinuria, hematuria, decreased GFR, hypertension, edema, decreased excretion of Na • Acute Nephritic Syndrome: clinical manifestations of glomerular inflammation • Glomerulonephritis: inflammation of glomerular capillaries that occurs in acute or chronic form Health assessment clinical manifestations • • • • • • Main manifestations of AGI: Hematuria, edema, azotemia, proteinuria, Hematuria could be microscopic or macroscopic Cola-colored urine because of RBCs Edema & hypertension Proteinuria due to increased permeability of glomerular membrane; with pitting edema • Headache, malaise, flank pain • In elderly, circulatory overload, with dyspnea, pulmonary edema AGI Clinical manifestations • In acute nephritic syndrome: the kidneys become large & edematous, congested • Elevated serum IgA • As urine out put decreases, BUN and creatinine in the blood increases • Kidney biopsy may be needed • If improvement: amount of urine increases; urinary protein diminish • Some may develop uremia and require dialysis for survival Complications • Hypertensive encephalopathy: emergency management of hypertension • Glomerulonephritis, without treatment, progresses to ESRD: S & S—hematuria, proteinuria • Heart failure & pulmonary edema Nursing management • Treat symptoms, preserve kidney function & treat complications: Antibiotic, Penicillin; if the cause is infection Corticosteriods; managing HTN; controlling proteinuria protein restriction, when renal insufficiency and increased BUN Na restriction, when HTN, edema & HF Liberal intake of CHOs, to provide energy & reduce catabolism of protein; Intake and output, daily weight, Fluid based on I & O Patient education Chronic glomerulonephritis • Secondary to repeated acute nephritic syndrome & other health conditions; hyperlipidemia • Kidneys are reduced to one-fifth of normal size—fibrous tissues; cortex shrinks to 1-2 mm in thickness • Glomeruli become scarred; renal artery branches are thickened • The result is sever glomeruli damage– ESRD • May discovered accidentally, when HTN, elevated BUN & Creatinine are detected • May report general symptoms: weight loss, increasing irritability, increased need to urinate at night, headache, digestive disturbances Chronic glomerulonephritis • As progresses, develop signs of chronic renal diseases or renal failure: poorly nourished with yellow-gray pigmentation of the skin Periorbital and peripheral edema Normal blood pressure or severe HTN retinal hemorrhage and exudates Anemia-pale mucous membrane Cardiomegaly, gallop rhythm, distended neck veins peripheral neuropathy & neurosensory changes Development of pericarditis; friction rub, pulsus paradoxus Assessment / diagnostic findings Urine, fixed specific gravity 1.010, variable proteinuria, urinary casts When GFR is below 50ml/min • Hyperkalemia, decreased K excretion • Metabolic acidosis, because of decreased acid secretion • Anemia, decreased production of erythropoiesis • Hypoalbuminemia – secondary to protein loss • Increased serum phosphorous level • Decreased calcium, the Ca binds with phosphorus • mental changes; and impaired nerve conduction due to electrolyte imbalances & uremia Management: symptoms management • Reduce hypertension: Na & water restrictions, antihypertensives; monitor Wt. daily, diuretics, • Protein of high biologic value—dairy products, eggs, meat to promote good nutritional status • Adequate calories—spare protein for tissue growth • Manage UTI • Initiation of dialysis may be required; in the early period of the disease process. • Nursing management Monitor fluid & electrolytes imbalances Report system changes reduce anxiety; Emotional support Nephrotic syndrome • A type of renal failure-increased glomerular permeability; is manifested by Massive proteinuria; Hypoalbuminemia; Diffuse edema Hyperlipidemia, increased serum cholesterol & LDL Caused by intrinsic renal disease or systemic diseases that cause glomerular damage Major manifestations Edema, pitting in dependent areas (periorbital), ascites Irritability, headache,-- malaise Nephrotic syndrome management • • • • • Treat underlying disease; slowing progression to CKD Typical treatment include: Diuretics for edema ACE inhibitors to reduce proteinuria Lipid lowering agents • Nursing management: • Instruct to follow medications & dietary regimen • Aware about and communicate health changes Renal Failure Acute Renal Failure • A rapid loss of renal functions related to kidney damage • A life-threatening metabolic complications can occur— metabolic acidosis, fluid & electrolyte imbalances • Accepted criterion for ARF: 50% or greater increase in serum creatinine; The normal is less than 1 mg/dL • Increased BUN • Changes in urine volume may occurs Oliguria, less than 500 ml/day Anuria, less than 50 ml/day Non-oliguria, greater than 800 ml/day ACUTE RENAL FAILURE • There is a specific underlying problem • Some of these factors—reduce blood flow to the kidney Hypovolemia; hypotension; reduced cardiac output Obstruction by tumor, blood clot, or renal stone Bilateral obstruction of renal arteries or veins • Should be treated before permanent damage occur Categories of ARF • Pre renal ARF; is the result of impaired blood flow, causing hypoperfusion and decreasing GFR • Intra renal ARF: is the result of actual parenchymal damage to glomeruli or tubules—abnormal reabsorption & decreased urine flow; leading to acute tubular necrosis; intra-tubular obstruction • Post renal ARF: obstruction distal to the kidney: pressure rises in the kidney, decreased GFR Read chart 44-4, P. 1321. Phases of ARF The initiation period: begins with insult and ends when oliguria develops The oliguria period: increase serum concentrations of substances that kidneys excretes Uremic symptoms appear and life-threatening condition, hyperkalemia, develops Some patients have decreased renal function but excrete 2L/day, non-oliguria renal failure; Occurs after exposure to nephrrotoxic agents, burn, trumatic injury Phases of ARF The diuresis period: gradual increase in urine—glomerular filtration starts to recover renal function may still abnormal; because uremic symptoms present—thus, needs expert attention Observe for dehydration The recovery period: Signals improvement of kidney function; may need 3-12 months; lab values return to normal Leave 1-3% reduction in the GFR—not clinically significant Assessment • • • • • • • • • Appears critically ill & lethargic; dry skin; dehydration CNS symptoms: drowsiness, headache, seizures Urine output: scant to normal; hematuria may be present Low specific gravity indicating inability to concentrate, a sign of tubular damage; an early sign Pre renal azotemia—decreased urinary Na to less than 20 mEq/L; Intra renal azotemia—urinary Na more the 40 mEq/L Increased BUN and creatinine Hyperkalemia with oliguria or anuria; metabolic acidosis, can not excrete acid metabolites phosphate high and calcium low—decreased absorption from GIT; Anemia; CT, MRI or ultrasonography Prevention of ARF • Careful history to identify exposure to nephrotoxic agents, medications: Blood tests for BUN & creatinine, 24 hours after initiation of nephrotoxic medications and 2 times a week • Adequate hydration for those at risk for dehydration • Prevent & treat shock promptly • For critically ill patients; monitor CVP, arterial pressure, urine output • Treat hypotension promptly • Prevent & treat infections • READ CHART 44-5, P 1322 Management principles • • • • Treat the underlying cause: pre renal azotemia by optimizing renal perfusion, post renal failure with removing obstruction, intra renal azotemia with supportive therapy; with Removal of causative agents, Aggressive management of pre and post-renal failure Avoidance of associated risk factors Prompt treatment of shock and infection