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The kidneys are responsible for… Fluid/electrolyte regulation Na and fluid balance Potassium balance Phosphate elimination What does this mean for calcium? Secretion of erythropoetin Secretion of HCO3 (bicarb) Excretion of toxins/waste Activation of Vitamin D |
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Renal ischemia resulting in direct cellular death Nephrotoxic injury – necrotic tubules slough and plug Type of ARF |
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accumulation of nitrogenous waste in blood stream (BUN, creatinine) |
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H&P Laboratory tests BUN Serum Crt Serum elytes Urinalysis/culture Hemoglobin/Hematocrit |
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Body Water Regulation Fluid volume is altered when the kidney loses its ability to excrete water FVO How is sodium affected? Other factors: proteinuria Proteinuria occurs in response to damage of the glomeruli loss of albumin in the urine: fluid shifts from intravascular space to interstitial space because of decreased oncotic pressure Due to decreased GFR, aldosterone released from adrenal cortex so kidneys to reabsorb sodium and water Fluid retention results in development of respiratory and cardiovascular clinical manifestations Assessment Findings When damaged, kidneys do not secrete potassium well. Leads to hyperkalemia EKG changes R/f decreased CO Lack of phosphate excretion Causes hypocalcemia Manifestations: Can be recalled by the mnemonic "CATS go numb"- Convulsions, Arrhythmias, Tetany and numbness/parasthesias in hands, feet, around mouth and lips. Chvostek’s sign/Trousseau’s sign Laryngospasm Cardiac—prlonged QT Hyperparathyroid due to hypocalcemia Kidneys normally convert inactive vitamin D to its active form: 1,25- dihydroxycholecalciferol Impaired vitamin D synthesis results in decreased absorption of calcium in the gastrointestinal tract When the serum level of calcium decreases, the parathyroid gland increases its secretion of parathyroid hormone, causing calcium to be released from the bone and compensating for the decreased serum level of calcium Anemia and Bleeding Anemia kidneys produces erythropoietin to stimulate bone marrow to release red blood cells normochromic, normocytic anemia Bleeding Altered platelet function and increased gastric acid secretion from increased release of parathyroid hormone Metabolic acidosis Tubules cannot excrete hydrogen ions (H+) Bicarb not secreted effectively What are s/s of metablic acidosis? Assessment Findings Uremia Syndrome that incorporates all signs and symptoms seen in various systems throughout the body Azotemia Nitrogenous waste products from protein metabolism are retained in the body Evidenced by the increased serum levels of urea nitrogen and creatinine Causes confusion, metallic taste in mouth, halitosis, and ulcers in the mouth (bacteria break down urea into ammonia) Pruritus excretion of waste products (and phosphate) through the skin Assessment Findings Other symptoms Depression |
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Fluid Volume Overload Decreased Cardiac Output Altered Tissue Perfusion Risk for Injury |
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Correction of fluid volume overload Nutritional therapy Erythropoietin therapy Calcium supplementation, phosphate binders Antihypertensive therapy Measures to lower potassium Adjustment of drug dosages to degree of renal function Independent nursing interventions |
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IV insulin IV glucose to manage hypoglycemia IV 10% calcium gluconate Raises threshold for excitation Sodium bicarbonate Shift potassium into cells Correct acidosis Sodium polystyrene sulfonate (Kayexalate) Cation-exchange resin Resin in bowel exchanges potassium for sodium Evacuates potassium-rich stool from body Educate patient that diarrhea may occur due to laxative in preparation Antihypertensive drugs Diuretics β blockers Calcium channel blockers Angiotensin-converting enzyme (ACE)
inhibitors Angiotensin receptor blocker agents Drug Therapy Phosphate problems Phosphate binders Calcium carbonate (Tums) Bind phosphate in bowel and excreted Sevelamer hydrochloride (Renagel) Lowers cholesterol and LDLs Should be administered with each meal Side effect: Constipation Supplementing vitamin D Calcitriol (Rocaltrol) Serum phosphate level must be lowered before administering calcium or vitamin D Drug Therapy Anemia Erythropoietin Epoetin alfa (Epogen, Procrit) Administered IV or subcutaneously Increased hemoglobin and hematocrit in
2 to 3 weeks Side effect: Hypertension Iron supplements If plasma ferritin <100 ng/ml Side effect: Gastric irritation,
constipation May make stool dark in color Folic acid supplements Needed for RBC formation Removed by dialysis |
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Protein restriction 0.6 to 0.8 g/kg body weight/day Sodium restriction Diets vary from 2 to 4 g depending on
degree of edema and hypertension Sodium and salt should not be equated Patient should be instructed to avoid
high-sodium foods Salt substitutes should not be used because they contain potassium chloride Nutritional Therapy Potassium restriction 2 to 4 g High-potassium foods should be avoided Oranges Bananas Tomatoes Green vegetables Phosphate restriction 1000 mg/day Foods high in phosphate Dairy products Coffee Most foods high in phosphate are also high in calcium Nutritional Therapy Fluid restriction Fluid volume intake is based on 500 mL/day (insensiblefluid loss) plus fluid equal to the urine output of the preceding 24 hours. |
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Must occur when GFR can no longer sustain life (<15 ml/hr). ESRD Acts as an external/”fake” kidney Used to correct fluid/electrolyte imbalances and to remove waste products in renal failure |
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Peritoneal dialysis Hemodialysis Cleans the blood What does this mean for medication administration? Blood from patient leaves and is sent outside the body Enters dialyzer, where semipermeable membrane separates blood from dialysate Hemodialysis Relies on a permanent fistula/graft in patient. Assessment: Bruit Thrill No B/P or sticks Hemodialysis Graft/fistula is accessed and connected to dialysis machine. Usually run ~4 hours 3 times per week, depending on severity. Complications Hypotension Bleeding Infection Cramping
http://www.youtube.com/watch?v=Dza8sTJixog Hemodialysis Can be done with temporary catheter in acute situation |
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Peritoneal access is obtained by inserting a catheter through the anterior wall. Uses patient’s peritoneum as the membrane across which fluids and dissolved substances are exchanged from the blood. Three phases of PD cycle Called an exchange Inflow Dwell Drain Dwell Diffusion and osmosis occur between patient’s blood and peritoneal cavity Duration of time varies Drain 15 to 30 minutes May be facilitated by changing position Exit site infection Peritonitis s/s? Abdominal pain Outflow problems Hernias Bleeding Pulmonary complications Protein loss |
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ARF Etiology and Pathophysiology |
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Acute renal failure is a life threatening illness with high mortality despite advances in supportive care A sudden loss of kidney function caused by failure or renal circulation or damage to the tubules or glomeruli Can be reversible, with spontaneous recovery in a few days to weeks Ischemia is primary cause: when allowed to persist for more than 2 hours, produces irreversible damage to tubules Acute Renal Failure Three major types: Prerenal decreased renal blood flow (40–70% of cases) R/T decr. Blood flow to kidneys R/T severe dehydration or hypovolemia Intrarenal direct renal parenchymal damage (intrinsic renal causes; 10–50% of cases) Postrenal obstructed urine flow (post-renal or obstructive causes; 10% of cases) |
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Lack of perfusion to kidneys People at high risk include elderly patients with atherosclerotic cardiovascular disease patients with pre-existing chronic kidney disease and patients with renal hypoperfusion caused by volume depletion, hypotension, or renal artery stenosis |
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Caused by diseases affecting the glomeruli, renal tubules, interstitium, or vasculature. Most common cause is acute tubular necrosis. Medications/Contrast dye aminoglycosides Rhabdomylolysis Infection/pyelonephritis |
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Obstructive nephropathy presents as acute renal failure relatively infrequently At risk populations include older men with prostate disease and patients with intra-abdominal, particularly pelvic, malignancy Stones Clinical consequence is the substantial diuresis that generally occurs once obstruction is relieved, which needs careful monitoring and appropriate fluid replacement to avoid volume depletion |
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Acute Renal Failure Presentation and Clinical Course |
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Presentation: Depends on underlying etiology (pre/intra/post) S/S as with CKD—differing etiologies Clinical course Oliguria (8-14 days) Diuretic phase (7-14 days) Nephrons cannot concentrate urine Recovery phase (several months-1 year) |
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H &P Serum elytes Imaging studies Aim is to find underlying etiology and treat it |
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As with CKD Fluid vol. deficit (in diuretic phase) Health maintenance—prevention |
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Depends on underlying etiology May or may not involve dialysis |
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A type of continuous, at-the-bedside hemodialysis that is safer for hemodynamically unstable patients Acid–base status/electrolytes adjusted slowly and continuously Can be used in conjunction with HD Contraindication Presence of manifestations of uremia requiring rapid resolution Can be continued for 30 to 40 days 1:1 nurse to patient ratio required |
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Continuous rather than intermittent Solute removal by convection (no dialysate required) in addition to osmosis and diffusion Less hemodynamic instability Does not require constant monitoring by HD nurse Does not require complicated HD equipment |
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