2.5 Renal, Urinary Elimination Flashcards
Describe the anatomy, physiology, and functions of the kidney
Kidney function:
Regulate Fluid Volume:
Concentrate/dilute urine
Affected y ADH and blood volume
Aldosterone (released from adrenal cortex)
Metabolic and endocrine functions: Synthesize prostaglandins Produce an enzyme that activates the precursor to vit D need for small intestine to absorb/maintain Ca Synthesizes erythropoietin Maintains acid/base
Urea:
End product of protein metabolism; increased in dehydration, infection, GI bleeding, increased protein intake
Creatinine:
End product of muscle metabolism
BUN and creatinine:
Levels are elevated in kidney failure
GFR:
Rate of kidney filtration, determine kidney function
Review the normal levels and significance of the following diagnostic tests
BUN-CREATININE RATIO
BUN-Creatinine Ratio:
Normal ration is 10:1
Higher ratio (20:1 or higher) with prerenal causes, after GI bleed
Lower-low protein intake, acute tubular necrosis, severe liver disease
Review the normal levels and significance of the following diagnostic tests
URINE SPECIFIC GRAVITY
Urine specific gravity (1.003-1.030 osm/kg):
Compares weight of urine against the weight of distilled water
Indicates concentration of urine
High= concentration
Low= diluted
Review the normal levels and significance of the following diagnostic tests
URINE SPOT SODIUM
Urine spot sodium:
Decreased urine Na in prerenal AKI
Increased urine Na in intrarenal AKI
**like specific gravity but Na specific
Review the normal levels and significance of the following diagnostic tests
CREATININE CLEARANCE
Creatinine Clearance (59-137 ml/min/m2):
Measures kidney’s ability to remove creatinine from plasma in one minute
Procedure:
Collect all urine for 12-24 hr
Draw fasting blood sample at sometime during collection of urine
Start test by having pt void and discarding urine
Collect all urine during the 12-24 hr period
Have patient void at end of test and save urine
Label and send to lab
Review the normal levels and significance of the following diagnostic tests
RENAL BIOPSY
.
Review the normal levels and significance of the following diagnostic tests
GLOMERULAR FILTRATION RATE
GFR (>60):
Decreases:
Occlusion of the afferent arteriole
Decreased permeability of the membrane
Increased intra capsular pressure
Increases:
Increased BP, declined blood protein osmotic pressure, increased glomerular permeability
Review the normal levels and significance of the following diagnostic tests
RENAL US
.
Compare and contrast the following:
a. Azotemia
b. Uremic Syndrome
c. Oliguria
d. Anuria
a. Azotemia: accumulation of nitrogenous waste in blood (BUN, creatinine) may be begin before urine output falls. Medication, disease, medication interaction, etc.
b. Uremic Syndrome: renal function declines to point where symptoms develop in multiple body systems. Loss may be sudden or developed over long period. May include blood in the urine
c. Oliguria: Urine output <140 ml/24 hr
d. Anuria: without urine, urine output <100 ml/24 hr
Compare and contract assessment findings in acute kidney injury (AKI) / acute renal failure (ARF)
with chronic renal failure (CRF).
Acute kidney injury (AKI):
Onset: hours today, invariably reversible
Cause: pre renal or post renal.
Infections, antibiotics, extensive burns, poisoning, shock, MI surgery.
Ischemia, sepsis, nephrotoxic medications (NSAID’s)
Diagnosis:
Mortality:
Chronic kidney disease (CKD):
Onset: years Cause: Diagnosis: Mortality: Primary cause of death:
Discuss the difference between the following three categories of AKI:
a. Pre-renal
b. Intra-renal (true renal)
c. Post-renal
Acute Kidney Injury:
PRE-RENAL:
Urine has high specific gravity and osmolarity
Little or not proteinuria; sediment may be present
Minimal Na excretion
BUN-Creatinine Ratio is significantly elevated (10:1 to 40:1)
INTRA-RENAL (true renal):
Parenchymal changes from disease or nephrotoxic substances r/t:
-Nephrotoxins
-Hgb released from hemolyzed RBC’s
-Myoglobin released from necrotic muscle cells (rhabdomyolysis)
Acute tubular necrosis (ATN):
- Most common is contrast induced nephropathy and interstitial nephritis
- Ischemic causes: affect basement membrane
- Nephrotoxic agents: chemo, cephalosporins, PPI, gentamycin, vancomycin, cocaine, NSAIDs, antifungals, ACE’s, oral anticoagulants
Manifestations: Edema, wt gain, weakness, HTN High Na concentration and proteinuria Glomerulonephritis- hematuria ATN- muddy brown granular casts Elevated serum K and creatinine
POST-RENAL:
Urine with fixed specific gravity, elevated Na and little or no proteinuria
Urine sediment is normal
Obstruction identified
Fluctuations between anuria and polyuria may indicate intermittent urinary tract obstruction
Briefly describe the phases of AKI (initiation, maintenance, and recovery phase)
AKI phases
Non-oliguric (diuretic) phase (1-3 weeks): Accounts for 50% cases May excrete up to 2-5L of urine May lead to dehydration and hypotension Decreased Na and K Kidneys able to excrete waste May have fluid overload May have extracellular fluid depletion May be caused by acute interstitial nephritis or ATN
Oliguric phase (10-14 days):
Urine production falls below 400ml/day
50% patients may not develop oliguria
Prognosis worsens as length of time increases in the phase
Manifestations depends on cause, usually prerenal. Changes in urinary output, fluid and electrolyte imbalance, uremia
May require dialysis
Na HCO3
Recovery phase (up to 12 months): Kidneys may return to prerenal failure status Possible mild tubular abnormalities continue for years Continued risk for fluid and electrolyte imbalances especially during stress
Describe medical management of AKI
AKI medical management:
Primary intervention: adequate hydration and diuresis
Restoration of optimal renal function
Correct underlying condition (bleeding/obstruction)
Secondary infection (judicious use of foley)
Pericarditis: steroids, NSAID’s, pericardiocentesis or ‘ectomy
Seizures: increase BUN decrease seizure threshold
Anemia
Bleeding tendencies: increased BUN interferes with platelet aggregation, tx with Vit K
Fluid replacement: avoid overload, replace on previous days urine plus 600ml
Tx electrolyte imbalance: hyperkalemia most dangerous imbalance r/t cardiac arrhythmias and arrest.
Hyperkalemia imbalance caused by: inability to excrete K, release of K from cells due to acidosis, rapid tissue catabolism
Treat hyperkalemia with 50% glucose with reg insulin, HaHCO3 IV, Ca gluconate IV, dialysis, kayexalate with sorbitol, beat adrenergic agonist
Correct acidosis: r/t accumulation of acid waste products, prevent with hydration of NS, NaHCO3, dialysis for severe
Describe nursing management of AKI, including nursing diagnosis & interventions. Give rationale for
dietary changes or restrictions
Dietary changes/restriction for AKI
Protein: avoid protein wasting
Low: K, Na and P, Fats
Adequate CHO
Compare and contrast the following renal replacement therapies:
a. Dialysis
i. Hemodialysis (HD)
ii. Peritoneal dialysis (PB)
iii. Continuous dialysis (CVVHD)
b. Kidney transplant
Renal replacement therapies:
Dialysis types
Hemodialysis:
Peritoneal dialysis:
Automated: 4+ exchanged during night with 1-2 hour dwell time. Some pt’s might need to do manual during day time
Continuous dialysis: Exchanges done 4x/day with 4-10 hour dwelling time. Warmed dialysate instilled into peritoneal cavity by gravity. Fluid remains in cavity for prescribed time. Fluid is drained and amount of drained is recorded. Repeated as ordered.
Peritoneal dialysis complications:
Peritonitis: bacteria infection, fever, rebound tenderness, nausea, malaise, cloudy dialysate output, increased WBC/neutrophils, tx w/ antibiotics
Ab pain: r/t of decreased pH of dialysate, cath placement, rapid infusion, infusion of air. Tx change position of catheter, slow infusion
Outflow problem: <80% of fluid return, kinked/migrated cath. Tx change cath position
Hernias and lower back pain: r/t increased intra-abdominal pressure
Bleeding: poss. intraperitoneal bleeding
Pulmonary: atelectasis, pneumonia, bronchitis r/t lung volume
Protein loss: in peritoneal effluent; increase protein
Hyperglycemia: glucose absorbed by dialysate
Encapsulating Sclerosing Peritonitis or Loss of Ultrafiltration: tick fibrous membrane develop around bowel causing intestinal obstruction/strangulation and loss of ultrafiltration. Tx: change to hemodialysis
Kidney transplant:
