Renal Dysfunction - Exam 2 Flashcards Preview

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Flashcards in Renal Dysfunction - Exam 2 Deck (60):
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Kidney Failure

The partial or complete impairment of kidney function. Results in an inability to excrete metabolic waste products and water, as well as contributing to disturbances of all body systems. Can be classfied as acute (Acute kidney injury aka AKI) or chronic (chronic kidney disease aka CKD)

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Acute kidney injury (acute kidney failure)

The term used to encompass the entire range of the syndrome including a very slight deterioration in kidney function to severe impairment. Characterized by a rapid loss of kidney function demonstrated by a rise in serum creatinine and/or a reduction in urine output. Usually develops over hours or days with progressive elevations of blood urea nitrogen (BUN), creatinine, and potassium with or without a reduction in urine output.

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Azotemia

An accumulation of nitrogenous waste products (urea, nitrogen, creatinine) in the blood that is severe enough to warrant renal replacement therapy. Develops from acute kidney disease.

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Prerenal causes of AKD

Factors external to the kidneys that reduce systemic circulation causing a reduction in renal blood flow and lead to decreased glomerular perfusion and filtration of the kidneys. No damage to the kidney tissue. Oliguria is caused by a decrease in circulating blood volume (ex. severe dehydration, decreased cardiac output, burns) and is usually reversible. Body attempts to preserve blood flow to essential organs. Results in the reduction of sodium (less that 20 meq/L), increased salt and water retention, and decreased urine output. Can lead to intrarenal disease if not treated because the kidneys lose their ability to compensate.

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Glomerulonephritis

Immune complexes are deposited in the glomerular basement membrane, causing decreased plasma filtration and thus water and sodium retention

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Nephrotic Syndrome

A disorder characterized by increased glomerular permeability to plasma protein, which results in massive urinary protein loss

proteinuria, edema, low blood protein

cause: damage to glomerulus

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Urosepsis

Febrile urinary tract infection coexisiting with systemic signs of bacterial illness

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Renal Lithiasis, Nephrolithiasis

Also called urinary calculi, these stones cause symptoms when they obstruct urinary flow

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Acute Tubular Necrosis (ATN)

May be caused by ischemia, nephrotoxins, hemolyzed RBCs or myoglobin released from necrotic muscle cells

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Hydroureter/Hydronephrosis

The backup of urine above an obstruction causing dilation of the renal pelvis from distention; eventually causes pressure destruction to renal parenchyma

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Pyelonephritis

Inflammation of the upper urinary tract and kidneys

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Urinary changes

Manifestations include changes in specific gravity and osmolality of the urine

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Fluid Volume Excess

Edema, hypertension, CHF, and pulmonary edema are symptoms

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Metabolic Acidosis

Hydrogen ions build up, serum bicarb is used up and lethargy and stupor result

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Sodium Balance

This vital electrolyte may not be conserved by the kidney

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Potassium Excess

The kidneys normally excrete 80-90% of this electrolyte. Thus this level rises, putting the heart at risk.

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Hematologic Disorders

Anemia results from decreased erythropoietin, while altered WBCs lead to infection

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Calcium deficit and phosphate excess

The failing kidney does not activate Vitamin D, and thus Ca++ is not absorbed and PO4 levels rise

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Waste produce accumulation

Serum creatinine or creatine clearance measures this best, but BUN (interpreted cautiously) is helpful

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Neurologic Disorders

Mild symptoms are fatigue and difficulty concentrating, seizures, stupor, and coma occur as condition worsens

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Uremia

The condition in which azotemia progresses to a symptomatic state

Symptoms include: N/V, lethargy, fatigue, impaired thought processes, headache

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Creatinine Clearance

Used as an indication of glomerular filtration rate. Compares the amount of creatinine in the urine with the amount in the blood.

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Glomerular filtration rate GFR

The amount of blood filtered by the glomeruli in a given time

Normal = 125 mL/hour which produces about 1mL/minute of urine

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Prerenal

Due to factors external to the kidneys that reduce renal blood flow and lead to decreased glomerular perfusion and filtration.

Common Causes:

Hypovolemia: dehydration, hemorrhage, GI losses, excessive diuresis

Decreased Cardiac Output: cardiac dysrhythmias, cardiogenic shock, heart failure, myocardial infarcation

Decreased Peripheral Vascular Resistance: anaphylaxis, septic shock

Decreased Renovascular Blood Flow: thrombosis, embolism, hepatorenal syndrome

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Intrarenal

Acute tubular necrosis (ATN)- responisble for 50% of intrarenal  ARF: Ischemia, nephrotoxcitity

Include conditions that cause direct damage to renal tissue (parenchyma) resulting in impaired nephron function

Common Causes:

Drugs, radiocontrast (IV dye), hemolytic blood tx, severe crush injury, chemical exposure, interstitial nephritis, acute glomerulonephritis

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Postrenal

Involves mechanical obstruction of urine outflow

Common Causes:

Benign  prostate hypertrophy, bladder cancer, calculi (stone) formation

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Oliguric Phase

Usually occurs within 1 (more common) to 7 days of the causitive event. Can be prerenal, intrarenal or postrenal in origin. Clinical manifestations include:

Urinary changes

Fluid volume excess

Metabolic acidosis

Sodium balance

Potassium excess

Hematologic disorders

Calcium deficit and phosphate excess

Waste product accumulation

Neurologic disorders

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Diuretic Phase

Gradual increase in daily urinary output, up to 5L/day. Signals beginning recovery, as kidneys have regained the ability to excrete wastes, but not to concentrate urine (reabsorb water). This phase may last 1-3 weeks. Assess for Fluid Volume Deficit as evidenced by hypovolemia and hypotension.

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Recovery Phase

May last up to 12 weeks. GFR increases, so BUN and creatinine gradually decrease

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Fluid Challenge

If a patient is thought to have a prerenal cause of decreased urinary output of elevated BUN, a "bolus" or rapid infusion (usually over 30-60 minutes) of IV fluid (200-500 mL for adults) may be ordered to "challenge" the kidneys. If the kidneys can function normally, they will respond with an increased urine output. This procedure may be repeated more than once and be followed by the administration of furosemide (Lasix) or other diuertic. Nursing implications are to assess for signs of fluid volume excess and pulmonary edema by monitoring:

Vital signs: increased BP, increased pulse, increased respirations

Lung sounds: Rales, dyspnea

Jugular Veins: distended

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Oliguric Phase: Urinary Changes

Manifestations include changes in specific gravity and osmolality of the urine.

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Oliguric Phase: Fluid Volume Excess

Edema, hypertension, CHF, and pulmonary edema are symptoms

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Oliguric Phase: Metabolic Acidosis

Hydrogen ions build up, serum bicarb is used up and lethargy and stupor result

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Oliguric Phase: Sodium balance

This vital electrolyte may not be conserved by the kidney. If Na increases, potassium decreases. May be low, high, or normal.

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Oliguric Phase: Potassium Excess

The kidneys normally excrete 80-90% of this electrolyte. Thus this level rises, putting the heart at risk.

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Oliguric Phase: Hematologic Disorders

Anemia results from decreased erythopoietin, while altered WBCs lead to infection

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Oliguric Phase: Calcium deficit and phosphate excess

The failing kidney does not activate vitamin D and thus Ca++ is not abosrbed and PO4 levels increase.

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Oliguric Phase: Waste product accumulation

Serum creatinine or creatinine clearance measures this best, but BUN (interpreted cautiously) is helpful

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Oliguric Phase: Neurologic disorders

Mild symptoms are fatigue and difficult concentreating, seizures, stupor, and coma occur as condition worsens

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Chronic Renal insufficiency (CRI) <25% of function

When GFR is about 25% of normal, the BUN and creatinine begin to rise in the blood. Symptoms of easy fatigue, weakness, HA, nausea and pruritis appear. Considered stage 4.

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End Stage Renal Disease (ESRD) < 10% of function

By this time GFR is less than 15mL/min. 10% of normal and patients are frankly uremic and activity is severely impaired. Some form of renal replacement must be begin, or death ensues. Considered stage 5

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sevalamer (Renagel)

Classification: non calcium phosphate blocker

Mechanism of action: binds phosphate from dietary sources to prevent absorption

Use: end stage renal disease

Side/adverse effects: monitor for changes in phosphate levels; monitor for allergy, constipation

Nursing implications: Must be taken with meals; if patient is NPO, no need to administer

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sodium polystyrene sulfonate (Kayexlate)

Classification: cation - exchange resin

Mechanism of action: sorbitol, a bulk laxative, ensures evaculation of potassium from the bowel, decreased K+ by exchanging Na+ for K+ in the gut for excretion

Use: to lower potassium levels

Route: by mouth or rectum, NG

Side/adverse effects: diarrhea, sodium and water retention

Nursing Implications: never give to a patient with hypoactive bowel sounds (paralytic illeus) fluid shifts can lead to bowel necrosis; monitor fluid shifts in patient with CHF. Check blood pressure and potassium level before administering

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darbepoetin alfa (Aranesp, Erythropoietin)

Classification: colony-stimulating factor responsible for stimulating growth of the erythroid precursors that mature into RBCs

Mechanism of action: hormonal action, normally made by the kidney

Use: chronic anemia of ESRD and chemothrapy-related anemia

Side/adverse effects: peripheral edema, HA, hyper and/or hypotension, arrhythmias, myelgas

Nursing Implications: correct deficiences of folic acid and B12 before beginning therapy, typically given weekly by direct IVP at the end of dialysis, or SC if patient is not being dialyzed, monitor blood pressure closely

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Normal Na

135-145

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Normal K+

3.5-5

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Normal Cl

95-105

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Normal phosphate

2.8-4.5

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Normal BUN

10-30/100mL

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Normal Creatinine

0.6-1.5

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Normal Calcium

9-11

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What can be treated to reverse a high pH (acidosis)

IV sodium bicarb can be used to reverse acidosis. This is a temporary correction

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CKD - Hyperkalemia Therapy Options

  1. Regular insulin (Fast, Temporary)
  2. Na+ HCO3 (Fast, Temporary)
  3. Calcium Gluconate (Protects heart)
  4. Dialysis (effective, but takes 0.5-2hours
  5. Sodium Polystyrene Sulfonate (Kayexalate) (effective, causes diarrhea) can take time to work
  6. Dietary Restriction (long term)

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CKD - Hypertension Therapy Options

  1. Weight loss (if obese) (best to combine diet and exerecise)
  2. Therapeutic lifestyle changes (exercise, avoid alcohol, smoking cessation)
  3. Diet
  4. Antihypertension drugs

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CKD - Renal Osteodystrophy Thearpy Options

CKD-MBD is a mineral and bone disorder due to CKD. Leads to fractures

  1. Limit dietary phosphorous
  2. Administer phosphate binders: Renagel
  3. Supplement vitamin D activated (works with calcium)

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CKD - Anemia

Leads to activity intolerance

  1. Erythropoeitin (Epogen, Procrit or darbepoietin (Aranesp)
  2. Blood transfusion if acutely symptomatic

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CKD - Dyslipidemia

Leads to CVD

  1. Medicaitons
  2. Lifestyle modification

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Anuria

No urine. Every mL the patient drinks is retained

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Oliguria

Scant urine output, some fluid is eliminated

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Administration of Potassium

PO: 40 mEq/dose

Central: Maximum dose and rate is 20mEq/50mL infused with electronic infusion device over 1 hour

Peripheral IVPB: Maximum dose and rate is 10mEq/50mL infused with EID over 1 hour

Continuous Peripheral Infusion: No more than 40mEq/liter

Side Effects: cardiac dysrhythmias, chemical phlebitis

Therapeutic Nursing Interventions:

  1. Check labs before and after for potassium levels
  2. Monitor closely: for larger, faster doses place patient on cardiac monitor
  3. Give po doses with food
  4. Monitor peripheral infusions for irritation, apply warm compresses, dilute further, infuse more slowly at nurse's discretion, assure patency of IV sites

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