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Renal System Contains
- -2 Kidneys
- -2 Ureters
- -Urinary bladder
- -Urethra
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Kidneys
- -Paired, bean-shaped
- -Retroperitoneal
- -Each side of your spine around T12-L3
- -Right kidney is lower than the left (Liver)
- -Weigh 4-6 oz & 5 inches long
- Adrenal gland on top of each kidney
- -20% of each of the blood pumped by the heart per minute goes to the kidneys
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Purpose of the kidneys
- -Regulate the volume and composition of ECF
- -Excrete waste products from the body
- -Control BP
- -Produce erythropoietin
- -Activate vitamin D
- -Regulate acid base balance
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Microstructure of the Kidneys
- Nephrons
- **Glomerulus
- **Bowman's capsule
- **Tubular system
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Tubular System
- -Proximal convoluted tubule
- -Loop of Henle
- -Distal convoluted tubule
- -Collecting Tubule
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Glomerular Filtration Rate (GFR)
- -Amount of blood filtered by glomeruli
- -Normal GFR is ~125 mL/min
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Kidneys Role in BP Regulation
Regulated through the Renin Angiotensin Aldosterone System (RAAS)
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Renin
- -Excreted by the Kidneys in response to: decreased ECF, decreased BP, decreased renal perfusion, decreased sodium or stimulation of the SNS.
- -Renin does not fix any of these problems; BUT it causes angiotensinogen from the liver to convert to angiotensin I
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Renin Angiotensin System
- -Renin causes angiotensinogen from the liver to be converted in angiotensin I
- -Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE)
- -Angiotensin II causes peripheral vasoconstriction = increased BP
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Angiotensin Converting Enzyme (ACE)
- -Causes angiotensin I to be converted to angiotensin II
- -ACE is located on the surface of blood vessels especially in the lungs
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Aldosterone
- -The renin angiotensin system causes the adrenal cortex to secrete aldosterone
- -Aldosterone increases the absorption of sodium and water
- -Secretion of aldosterone can be influenced by circulating blood volume and plasma concentrations.
- -Decreased blood volume causes increased aldosterone.
- -Increased K levels cause increased aldosterone which leads to Na and H2O retention leading to increased ECF causing increased BP which causes excretion of K
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Erythropoietin
- -Produced and released by the Kidneys when O2 levels are low (hypoxia) or when there is decreased renal blood flow.
- -Erythropoietin travels to the bone marrow where it stimulates RBC production.
- -Deficiency of erythropoietin occurs in renal failure and leads to anemia.
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Kidneys Role in Vitamin D Activation
- -Vitamin D can be obtained through the diet or UV radiation or cholesterol in the skin
- -Both forms have to be activated in the liver and then in the kidney. (Need vitamin D to absorb calcium from the GI tract)
- -By regulating Vit D we regulate calcium and phosphorous
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Kidneys Role in Acid-Base Balance
- -Kidney's can increase reabsorption of bicarb and even make more bicarb to buffer acids
- -Secretes excess hydrogen
- -pH of urine can be anywhere from 4-8
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Gerontological Considerations
- -Decreased size and weight of kidneys
- -After 70 y/o almost 1/2 of the glomeruli have lost function
- -Decreased blood flow
- -Decreased GFR
- -Decreased ability to concentrate urine
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Anuria
- -Technically no urination in a 24 hr period
- -Less than 100 mL in 24 hr
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Oliguria
-Decrease in urinary output to less than 400 mL/day
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Azotemia
- -The accumulation of nitrogenous waste products such as urea nitrogen and creatinine in the blood
- -Electrolyte and fluid status also change but few symptoms may be seen in patients at this stage
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Uremia
- -A condition in which renal function declines to the point that symptoms develop in multiple body systems
- -Azotemia with clinical manifestations
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Nonoliguria
- -A normal or increased urinary output
- -Occurs in about 50% of cases of ARF
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Renal impairment
Renal function reduced; no accumulation of metabolic waste products
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Renal insufficiency
- -Metabolic waste products begin to accumulate in the blood
- -Decreasing GFR
- -Can be mild moderate or severe
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Blood Urea Nitrogen (BUN)
- -Normal range = 10-30 mg/dL
- -Urea is the end product of protein metabolism
- -Kidneys are responsible for excreting urea
- -Increased urea concentration in the blood means renal disease, certain meds or dehydration
- -Decreased urea concentration in the blood means over hydration, malnourishment, or liver damage
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Serum Creatinine
- -Normal range = 0.5 - 1.5 mg/dL
- -More relable than BUN at detecting impaired kidney function
- -By product of muscle catabolism
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Acute Renal Failure (ARF)
- -Progressive azotemia
- -Uremia
- -Oliguria vs Nonoliguria
- -Develops over hours to days
- -Progressive increase in BUN, Cr, K+
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ARF Risk Factors
- -Advanced age
- -Baseline renal insufficiency due to HTN or DM
- -Massive trauma
- -Sepsis
- -Major surgical procedures
- -Extensive burns
- -Cardiac arrest
- -Obstetric complications
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Prerenal
- -No damage to renal tissue
- -Caused by decrease in circulating blood volume
- -Usually reversible
- -Urine specific gravity is increased (> 1.025)
- - Low sodium urine
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Intrarenal
- -Fixed specific gravity (1.010)
- -Increased urine sodium
- -Urine has tubular casts and WBC casts R/T sloughing of necrotic cells b/c of kidney damage
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Prerenal Oliguria
- -Urine output = low
- -BUN = Elevated
- -Serum creatinine = normal or slightly elevated
- -Urine specific gravity = High
- -Urine Sodium = Low
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Oliguria of ARF
- -Urine output = low
- -BUN = Elevated
- -Serum creatinine = Elevated
- -Urine specific gravity = fixed at 1.010
- -Urine sodium = high
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Clinical Course
- -Prerenal and postrenal with no intrarenal damage resolve quickly once the underlying cause is treated
- -Prerenal or postrenal with intrarenal damage and intrarenal failure (Acute Tubular Necrosis (ATN)
- -Prolonged recovery
- -Chronic kidney disease may occur
- -4 Phases (Initiating, Oliguric, Diuretic & Recovery)
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Initiating Phase
- -Occurs at the time of insult amd continues until the signs and symptoms become apparent.
- -Can last hours to days
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Oliguric Phase
- -Occurs within 1-7 days of initial injury/insult
- -Can occur in 1 day if ischemia is present
- -Can take up to one week with nephrotoxic drugs
- -Lasts up to 2 weeks
- -The longer the oliguric phase, the poorer the prognosis for complete recovery of renal function
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Common Causes of AFR - Prerenal
- -Vitamin D can be obtained through the diet or UV radiation or cholesterol in the skin
- -Both forms have to be activated in the liver and then in the kidney. (Need vitamin D to absorb calcium from the GI tract)
- -By regulating Vit D we regulate calcium and phosphorous
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Common Causes of AFR - Intrarenal
- Prolonged prerenal ischemia
- Nephrotoxic injury
- *Drugs (aminoglycosides [gentamicin, amikacin], amphotericin B)
- *Radiocontrast agents
- *Hemolytic blood transfusion reaction
- *Severe crush injury
- *Chemical exposure (ethylene glycol, lead, arsenic, carbon tetrachloride)
- Interstial nephritis*Allergies (antibiotics [sulfanamides, rifampin], non-steroidal antiinflammatory drugs, ACE inhibitors)
- *Infections (bacterial [acute pyelonephritis], viral [CMV], fungal [candidiasis])
- Acute gomerulonephritis
- Thrombotic disorders
- Toxemia of pregnancy
- Malignant hypertension
- Systemic lupus erythematosus
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Common Causes of AFR - Postrenal
- Benign prostatic hyperplasia
- Bladder cancer
- Calculi formation
Neuromuscular disordersProstate cancer- Spinal cord disease
- Strictures
- Trauma (bacl, pelvis, perineum)
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Oliguric Phase
- -UOP is decreased causing fluid volume excess
- -Loss of concentration ability
- -Metabolic acidosis
- -Sodium imbalance
- -Potassium excess
- -Hematologic disorders
- -Calcium deficit and phosphate excess
- -Waste product accumulation
- -Neuro disorders
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Oliguric Phase - Urinary Changes
- -Urinary output decreases to less than 400 mL/24 hr for about 50% of patients
- -Urinalysis may show casts, RBCs, WBCs, a specific gravity fixed at 1.010 and urine osmolality at about 300mOsm/kg. This is the same specific gravity and osmolality as for plasma reflecting tubular damage with loss of concentrating ability by the kidney.
- -Proteinuria may be present if the renal failure is R/T glomerular membrane dysfunction.
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Oliguric Phase - Fluid Volume Excess
- -When urinary output decreases, fuid retention occurs
- -The severity of the symptoms depends on the extent of the fluid overload.
- -The neck veins may be distended with a bounding pulse.
- -Edema and HTN may develop.
- -May eventually lead to HF, pulmonary edema, and pericardial and plueral effusions.
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Oliguric Phase - Metabolic Acidosis
- -In renal failure, the kidneys cannot synthesize ammonia, which is needed for hydrogen ion excretion or excrete acid products of metabolism.
- -The serum bicarb level decreases b/c bicarb is used up in buffering hydrogen ions.
- -In addition defective reabsorption and regeneration of bicarb occurs.
- -Patient may develop Kussmaul respirations (rapid, deep respirations) to increase excretion of CO2.
- -Lethargy and stupor will occur if treatment is not started.
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Oliguric Phase - Sodium Imbalance
- -Damaged tubules cannot conserve sodium which results in increased secretion of sodium leading to low serum sodium levels.
- -Excess intake of sodium should be avoided b/c ot can lead to voulume expansion, HTN, and HF.
- -Uncontrolled hyponatremia or water excess can lead to cerebral edema.
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Oliguric Phase - Potassium Excess
- -Serum K levels increase because the normal ability of the kidneys to excrete 80-90% of the body's K is impaired.
- -If the ARF is caused by massive tissue trauma, the damaged cells release additional K into the ECF.
- -Bleeding & blood transfusions can also cause cellular destruction releasing more K into the ECF
- -Acidosis worsens hyperkalemia as hydrogen enters and K is driven our of the cells into the ECF.
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Sodium (Na+)
-Normal Range = 135-145 mEq/L
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Potassium (K-)
-Normal range = 3.5 - 5.0 mEq/L
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Calcium (Ca2+)
-Normal Range = 9 - 11 mg/100mL
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Phosphate (PO43-)
-Normal Range = 2.8 - 4.5 mg/dL
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Blood Urea Nitrogen (BUN)
-Normal Range = 10 - 30 mg/dL
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Serum Creatinine (Cr)
-Normal Range = 0.5 - 1.5 mg/dL
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Magnesium (Mg2+)
-Normal Range = 1.5 - 2.5 mEq/L
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Bicarbonate (HCO3-)
-Normal Range = 22 - 26 mEq/L
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Oliguric Phase - Hematologic Disorders
- -Anemia occurs because RF results in impaired erythropoietin production.
- -Anemia may be compounded by platlet abnormalities that can lead to bleeding from multiple sources (brain, intestines)
- -WBCs are altered causing immunodifficiency leaving the patient susceptible to numerous systemic and local infections.
- -Infection and cardiopulmonary complications are the 2 leading causes of death in AFR.
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Oliguric Phase - Calcium Deficit
- -Decreased calcium levels are a result of decreased absorption of calcium in the intestine.
- -In order to absorb calcium, vitamin D needs to be activated by the kidneys.
- -When hypocalcemia occurs the PTH is secreted which stimulates bone demineralization, releasing calcium from the bones
- -Normally plasma calcium is ionized or free or bound to protein. In renal failure hypocalcemia is rarely symptomatic due to more ionized calcium than bound to protein.
- -Low ionized Ca2+ levels can lead to tetany
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Oliguric Phase - Phosphate Excess
- -When the PTH stimulates bone demineraliztion, phosphate is released as well leading to elevated levels.
- -Hyperphosphatemia also results from decreased phosphate excretion by the kidneys
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Oliguric Phase - Waste Product Accumulation
- -Kidneys are primary excretory organ for waste products.
- -BUN and serum creatinine are elevated in kidney failure.
- -Elevated BUN may be caused by dehydration, corticosteroids and catabolism resulting from infections, fever, severe injury or GI bleeding.
- -Best indicator of kidney function is serum creatinine b/c it is not significantly altered by other factors
- -Measuring creatinine clearance with a 24 hour urine study or using a radioactive tracer is the best method for assessing renal fuction.
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Oliguric Phase - Neurological Disorders
- -Neurological changes can occur as waste products accumulate in the brain and other nervous tissue
- -Mild = fatigue and difficulty concentrating
- -Severe = seizures, stupor & coma
- -Eventually all body systems become involved in the uremia of the ARF.
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Diuretic Phase
- -Begins with gradual increase in UOP of 1-3L/day (can be as much as 3-5 L/day
- -Can last for 1 to 3 weeks
- -In this phase the kidneys have recovered their ability to excrete wastes but not to concentrate urine.
- -Hypovolemia and hypotension may occur
- -Monitor for hyponatremia, hypokalemia and dehydration
- -Uremia may still be severe AMB low creatinine clearance, elevated serum creatinine, elevated BUN and persistant S/S
- -Near the end of the phase the electrolytes, acid-base balance and waste product values begin to normalize
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Recovery Phase
- -Begins when GFR increases allowing BUN and creatinine levels plateau and then decrease
- -Major improvements occur within 1-2 weeks
- -Can take up to one year to normalize
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Outcome of ARF
- -Depends on overall health, severity & complications
- -Some individuals do not recover and progress to chronic kidney disease
- -Those who do recover usually have normal kidney function w/o complications.
- -Older adults always have increased risk for increased recovery time
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ARF - Diagnostic Exams
- -History
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Prerenal causes should be considered when there is a hx of dehydration, blood loss or severe heart disease. - *Intrarenal causes may be suspected if a pt. has been taking nephrotoxic drugs or a recent hx or hypotension or hypovolemia..
- *Postrenal causes are suggested by a hx of changes in the urinary stream, stones, BPH, or cancer or the bladder or prostate
- -Urinalysis*Urine sediment containing abundant casts, cells or proteins suggests intrarenal disorders.
- *Urine sediment may be normal in both prerenal and postrenal ARF.
- *Hematuria, pyuria, and crystals may be seen in postrenal conditions.
- -Renal ultrasound*Often the firs test done
- *Useful for possible renal disease and obstruction or the urinary collection system
- -Renal Scan
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Assesses for renal blood flow, tubular function and integrity of the collecting system - -CT/MRI*Identify lesions and masses as well as obstructions and vascular abnormalities
- -Renal biopsy*Useful in the diagnosis of intrarenal causes of ARF
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Common Indications for Dialysis in ARF
- 1. Volume overload resulting in compromised cardiac and/or pulmonary status
- 2. Elevated K level with ECG changes
- 3. Metabolic acidosis (serum bicarb <15 mEq/L)
- 4. BUN level >120 mg/dL
- 5. Significant changes in mental status
- 6. Pericarditis, pericardial effusion or cardiac tamponade
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ARF - Nursing Assesment
- -VS / I&O
- -History
- -Urine characteristics
- -Energy level
- -Mental status / LOC
- -Neuromuscular
- -Mucosa
- -Lungs
- -Heart
- -Edema
- -Review lab values
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ARF - Overall Goals
- Patient will:
- -Recover without any loss of function
- -Not experience any complications
- -Maintain normal fluid and electrolyte balance
- -Have decreased anxiety
- -Comply with and understand the need for careful follow-up care
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Nursing Diagnosis - ARF
- -Excess fluid volume R/T renal failure and fluid retention
- -Risk for infection R/T invasive lines, uremic toxins, and altered immune responses secondary to kidney failure. (infection leading cause of death in ARF)
- -Imbalanced nutrition less than body requirements R/T altered metabolic state and dietary restrictions
- -Disturbed thought process R/T effects of erema toxins on CNS
- -Fatigue R/T anemia, metablic acidosis, and uremic toxins
- -Anxiety R/T disease process, theraputic interventions and uncertainty of prognosis
- -Risk for injury R/T altered mental status
- -Risk for dysrythmias R/T electrolyte imbalnces
- -Risk for metabolic acidosis R/T inability to excrete H+, impaired HCO3- reabsorption and decreased synthesis of ammonia.
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Manifestations of ARF - Urinary
- -Decreased urinary output
- -Proteinuria
- -Casts
- -Decreased specific gravity
- -Decreased osmolality
- -Increased urinary sodium
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Manifestations of ARF - Cardiovascular
- -Volume overload
- -Heart failure
- -Hypotension (early)
- -Hypertension (after development of fluid overload)
- -Pericarditis
- -Pericardial effusion
- -Dysrhythmias
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Manifestations of ARF - Respiratory
- -Pulmonary edema
- -Kussmauls respirations
- -Plueral effusions
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Manifestations of ARF - GI
- -N/V
- -Anorexia
- -Stomatitis
- -Bleeding
- -Diarrhea
- -Constipation
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Manifestations of ARF - Hematologic
- -Anemia (development w/in 48 hr)
- -Increased susceptibility to infection
- -Leukocytosis
- -Defect in platelet functioning
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Manifestations of ARF - Neurologic
- -Lethargy
- -Seizures
- -Asterixis
- -Memory impairment
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Manifestations of ARF - Metabolic
- -Increased BUN
- -Increased creatinine
- -Decreased sodium
- -Increased potassium
- -Decreased pH
- -Decreased bicarbonate
- -Decreased calcium
- -Increased phosphate
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Clinical Manifestations for Hyperkalemia
- -Dysrhythmias
- -Neuromuscular impairment
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Treatment for Hyperkalemia
- -Regular Insulin IV Administration
- -Sodium Bicarbonate-Calcium Gluconate-Dialysis
- -Sodium Polystryrene Sulfonate (Kayexelate)
- -Dietary Restriction
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Treatment for Hyperkalemia - Insulin
- Regular Insulin IV Administration
- K moves into cells when insulin is given. Glucose is given concurently to prevent hypoglycemia. When effects of insulin diminish, K shifts back out of cells.
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Treatment for Hyperkalemia - Sodium Bicarbonate
- Sodium Bicarbonate
- Therapy can correct acidosis and causes shift of K into cells
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Treatment for Hyperkalemia - Calcium Gluconate
- Calcium Gluconate
- Therapy is given IV and generally used in advanced cardiac toxicity. Calcium raises the threshold for excitation, resulting in dysrhythmias.
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Treatment for Hyperkalemia - Dialysis
- DialysisHemodialysis can bring K levels to normal within 30 min to 2 hours
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Treatment for Hyperkalemia - Sodium Polystryrene Sulfonate (Kayexelate)
- Sodium Polystryrene Sulfonate (Kayexelate)Cation-exhange resin is administered by mouth or retention enema. When resin is in the bowel, K is exchanged for sodium. Therapy removes 1 mEq of K per gram of drug. It is mixed in water with sorbitol to produce osmotic diarrhea, allowing for evacuation of K-rich stool from the body.
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Treatment for Hyperkalemia - Dietary Restriction
- Dietary RestrictionDaily potassium intake is limited to 40 mEq.
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Gerontological Considerations
- -Nephron function decreases with age
- -Impaired function of other organ systems
- -Diuretics should be used with extreme caution
- -Mortality rate is higher
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Health Promotion - ARF Prevention
- -Identify and monitor high risk populations
- -Controlling exposure to nephroxic drugs and industrial chemicals
- -Prevent prolonged periods of hypotension or hypovolemia. Must have prompt replacement of significant fluid loss.
- -Monitor I&O/weights (1kg is = 1000mL of fluid)
- -Prompt treatment of UTI
- -NSAIDs used sparingly in renal insufficiency
- -ACE inhibitors used springly: can decrease perfusionand decrease K levels
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Nutrition Therapy for ARF
- -Diet should be high in calories (about 30-35kcal/kg of body weight daily)
- -Most of energy should come from carbohydrates and fats. 30-40% of total calories should come from fat.
- -Protein intake can vary depening on pt condition but generally is 0.6 g/kg/day to control nitrogenous waste production and limit starvation ketosis
- -K and Na are regulated in accordance with plasma levels.
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