Renal Dysfunction - Exam 2 Flashcards
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)
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.
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.
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.
Glomerulonephritis
Immune complexes are deposited in the glomerular basement membrane, causing decreased plasma filtration and thus water and sodium retention
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
Urosepsis
Febrile urinary tract infection coexisiting with systemic signs of bacterial illness
Renal Lithiasis, Nephrolithiasis
Also called urinary calculi, these stones cause symptoms when they obstruct urinary flow
Acute Tubular Necrosis (ATN)
May be caused by ischemia, nephrotoxins, hemolyzed RBCs or myoglobin released from necrotic muscle cells
Hydroureter/Hydronephrosis
The backup of urine above an obstruction causing dilation of the renal pelvis from distention; eventually causes pressure destruction to renal parenchyma
Pyelonephritis
Inflammation of the upper urinary tract and kidneys
Urinary changes
Manifestations include changes in specific gravity and osmolality of the urine
Fluid Volume Excess
Edema, hypertension, CHF, and pulmonary edema are symptoms
Metabolic Acidosis
Hydrogen ions build up, serum bicarb is used up and lethargy and stupor result
Sodium Balance
This vital electrolyte may not be conserved by the kidney
Potassium Excess
The kidneys normally excrete 80-90% of this electrolyte. Thus this level rises, putting the heart at risk.
Hematologic Disorders
Anemia results from decreased erythropoietin, while altered WBCs lead to infection
Calcium deficit and phosphate excess
The failing kidney does not activate Vitamin D, and thus Ca++ is not absorbed and PO4 levels rise
Waste produce accumulation
Serum creatinine or creatine clearance measures this best, but BUN (interpreted cautiously) is helpful
Neurologic Disorders
Mild symptoms are fatigue and difficulty concentrating, seizures, stupor, and coma occur as condition worsens
Uremia
The condition in which azotemia progresses to a symptomatic state
Symptoms include: N/V, lethargy, fatigue, impaired thought processes, headache
Creatinine Clearance
Used as an indication of glomerular filtration rate. Compares the amount of creatinine in the urine with the amount in the blood.
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
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
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
Postrenal
Involves mechanical obstruction of urine outflow
Common Causes:
Benign prostate hypertrophy, bladder cancer, calculi (stone) formation
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
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.
Recovery Phase
May last up to 12 weeks. GFR increases, so BUN and creatinine gradually decrease
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
Oliguric Phase: Urinary Changes
Manifestations include changes in specific gravity and osmolality of the urine.
Oliguric Phase: Fluid Volume Excess
Edema, hypertension, CHF, and pulmonary edema are symptoms
Oliguric Phase: Metabolic Acidosis
Hydrogen ions build up, serum bicarb is used up and lethargy and stupor result
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.
Oliguric Phase: Potassium Excess
The kidneys normally excrete 80-90% of this electrolyte. Thus this level rises, putting the heart at risk.
Oliguric Phase: Hematologic Disorders
Anemia results from decreased erythopoietin, while altered WBCs lead to infection
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.
Oliguric Phase: Waste product accumulation
Serum creatinine or creatinine clearance measures this best, but BUN (interpreted cautiously) is helpful
Oliguric Phase: Neurologic disorders
Mild symptoms are fatigue and difficult concentreating, seizures, stupor, and coma occur as condition worsens
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.
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
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
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
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
Normal Na
135-145
Normal K+
3.5-5
Normal Cl
95-105
Normal phosphate
2.8-4.5
Normal BUN
10-30/100mL
Normal Creatinine
0.6-1.5
Normal Calcium
9-11
What can be treated to reverse a high pH (acidosis)
IV sodium bicarb can be used to reverse acidosis. This is a temporary correction
CKD - Hyperkalemia Therapy Options
- Regular insulin (Fast, Temporary)
- Na+ HCO3 (Fast, Temporary)
- Calcium Gluconate (Protects heart)
- Dialysis (effective, but takes 0.5-2hours
- Sodium Polystyrene Sulfonate (Kayexalate) (effective, causes diarrhea) can take time to work
- Dietary Restriction (long term)
CKD - Hypertension Therapy Options
- Weight loss (if obese) (best to combine diet and exerecise)
- Therapeutic lifestyle changes (exercise, avoid alcohol, smoking cessation)
- Diet
- Antihypertension drugs
CKD - Renal Osteodystrophy Thearpy Options
CKD-MBD is a mineral and bone disorder due to CKD. Leads to fractures
- Limit dietary phosphorous
- Administer phosphate binders: Renagel
- Supplement vitamin D activated (works with calcium)
CKD - Anemia
Leads to activity intolerance
- Erythropoeitin (Epogen, Procrit or darbepoietin (Aranesp)
- Blood transfusion if acutely symptomatic
CKD - Dyslipidemia
Leads to CVD
- Medicaitons
- Lifestyle modification
Anuria
No urine. Every mL the patient drinks is retained
Oliguria
Scant urine output, some fluid is eliminated
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:
- Check labs before and after for potassium levels
- Monitor closely: for larger, faster doses place patient on cardiac monitor
- Give po doses with food
- Monitor peripheral infusions for irritation, apply warm compresses, dilute further, infuse more slowly at nurse’s discretion, assure patency of IV sites
