1. Home
  2. Flashcards
  3. Preview

Exam 2 - ARF

  1. Renal System Contains
    • -2 Kidneys
    • -2 Ureters
    • -Urinary bladder
    • -Urethra
  2. 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
  3. 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
  4. Microstructure of the Kidneys
    • Nephrons
    • **Glomerulus
    • **Bowman's capsule
    • **Tubular system
  5. Tubular System
    • -Proximal convoluted tubule
    • -Loop of Henle
    • -Distal convoluted tubule
    • -Collecting Tubule
  6. Glomerular Filtration Rate (GFR)
    • -Amount of blood filtered by glomeruli
    • -Normal GFR is ~125 mL/min
  7. Kidneys Role in BP Regulation
    Regulated through the Renin Angiotensin Aldosterone System (RAAS)
  8. 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
  9. 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
  10. 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
  11. 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
  12. 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.
  13. 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
  14. 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
  15. 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
  16. Anuria
    • -Technically no urination in a 24 hr period
    • -Less than 100 mL in 24 hr
  17. Oliguria
    -Decrease in urinary output to less than 400 mL/day
  18. 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
  19. Uremia
    • -A condition in which renal function declines to the point that symptoms develop in multiple body systems
    • -Azotemia with clinical manifestations
  20. Nonoliguria
    • -A normal or increased urinary output
    • -Occurs in about 50% of cases of ARF
  21. Renal impairment
    Renal function reduced; no accumulation of metabolic waste products
  22. Renal insufficiency
    • -Metabolic waste products begin to accumulate in the blood
    • -Decreasing GFR
    • -Can be mild moderate or severe
  23. 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
  24. Serum Creatinine
    • -Normal range = 0.5 - 1.5 mg/dL
    • -More relable than BUN at detecting impaired kidney function
    • -By product of muscle catabolism
  25. Acute Renal Failure (ARF)
    • -Progressive azotemia
    • -Uremia
    • -Oliguria vs Nonoliguria
    • -Develops over hours to days
    • -Progressive increase in BUN, Cr, K+
  26. 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
  27. Types of ARF
    Image Upload 2
  28. 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
  29. 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
  30. Prerenal Oliguria
    • -Urine output = low
    • -BUN = Elevated
    • -Serum creatinine = normal or slightly elevated
    • -Urine specific gravity = High
    • -Urine Sodium = Low
  31. Oliguria of ARF
    • -Urine output = low
    • -BUN = Elevated
    • -Serum creatinine = Elevated
    • -Urine specific gravity = fixed at 1.010
    • -Urine sodium = high
  32. 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)
  33. Initiating Phase
    • -Occurs at the time of insult amd continues until the signs and symptoms become apparent.
    • -Can last hours to days
  34. 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
  35. 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
  36. 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
  37. Common Causes of AFR - Postrenal
    • Benign prostatic hyperplasia
    • Bladder cancer
    • Calculi formation
    • Neuromuscular disorders
    • Prostate cancer
    • Spinal cord disease
    • Strictures
    • Trauma (bacl, pelvis, perineum)
  38. 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
  39. 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.
  40. 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.
  41. 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.
  42. 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.
  43. 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.
  44. Sodium (Na+)
    -Normal Range = 135-145 mEq/L
  45. Potassium (K-)
    -Normal range = 3.5 - 5.0 mEq/L
  46. Calcium (Ca2+)
    -Normal Range = 9 - 11 mg/100mL
  47. Phosphate (PO43-)
    -Normal Range = 2.8 - 4.5 mg/dL
  48. Blood Urea Nitrogen (BUN)
    -Normal Range = 10 - 30 mg/dL
  49. Serum Creatinine (Cr)
    -Normal Range = 0.5 - 1.5 mg/dL
  50. Magnesium (Mg2+)
    -Normal Range = 1.5 - 2.5 mEq/L
  51. Bicarbonate (HCO3-)
    -Normal Range = 22 - 26 mEq/L
  52. 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.
  53. 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
  54. 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
  55. 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.
  56. 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.
  57. 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
  58. 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
  59. 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
  60. ARF - Diagnostic Exams
    • -History
    • *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
    • *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
  61. 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
  62. ARF - Nursing Assesment
    • -VS / I&O
    • -History
    • -Urine characteristics
    • -Energy level
    • -Mental status / LOC
    • -Neuromuscular
    • -Mucosa
    • -Lungs
    • -Heart
    • -Edema
    • -Review lab values
  63. 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
  64. 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.
  65. Manifestations of ARF - Urinary
    • -Decreased urinary output
    • -Proteinuria
    • -Casts
    • -Decreased specific gravity
    • -Decreased osmolality
    • -Increased urinary sodium
  66. Manifestations of ARF - Cardiovascular
    • -Volume overload
    • -Heart failure
    • -Hypotension (early)
    • -Hypertension (after development of fluid overload)
    • -Pericarditis
    • -Pericardial effusion
    • -Dysrhythmias
  67. Manifestations of ARF - Respiratory
    • -Pulmonary edema
    • -Kussmauls respirations
    • -Plueral effusions
  68. Manifestations of ARF - GI
    • -N/V
    • -Anorexia
    • -Stomatitis
    • -Bleeding
    • -Diarrhea
    • -Constipation
  69. Manifestations of ARF - Hematologic
    • -Anemia (development w/in 48 hr)
    • -Increased susceptibility to infection
    • -Leukocytosis
    • -Defect in platelet functioning
  70. Manifestations of ARF - Neurologic
    • -Lethargy
    • -Seizures
    • -Asterixis
    • -Memory impairment
  71. Manifestations of ARF - Metabolic
    • -Increased BUN
    • -Increased creatinine
    • -Decreased sodium
    • -Increased potassium
    • -Decreased pH
    • -Decreased bicarbonate
    • -Decreased calcium
    • -Increased phosphate
  72. Clinical Manifestations for Hyperkalemia
    • -Dysrhythmias
    • -Neuromuscular impairment
  73. Treatment for Hyperkalemia
    • -Regular Insulin IV Administration
    • -Sodium Bicarbonate
    • -Calcium Gluconate
    • -Dialysis
    • -Sodium Polystryrene Sulfonate (Kayexelate)
    • -Dietary Restriction
  74. 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.
  75. Treatment for Hyperkalemia - Sodium Bicarbonate
    • Sodium Bicarbonate
    • Therapy can correct acidosis and causes shift of K into cells
  76. 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.
  77. Treatment for Hyperkalemia - Dialysis
    • Dialysis
    • Hemodialysis can bring K levels to normal within 30 min to 2 hours
  78. 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.
  79. Treatment for Hyperkalemia - Dietary Restriction
    • Dietary Restriction
    • Daily potassium intake is limited to 40 mEq.
  80. Gerontological Considerations
    • -Nephron function decreases with age
    • -Impaired function of other organ systems
    • -Diuretics should be used with extreme caution
    • -Mortality rate is higher
  81. 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
  82. 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.
Author
oneofgreatlight
ID
104046
Card Set
Exam 2 - ARF
Description
Exam 2 - Renal
Updated

  1. Home
  2. Flashcards
  3. Preview