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
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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:
Discuss criteria used in recipient and donor selection for renal transplantation
Recipient criteria:
Usually <70 yrs old with life expectancy of >2yrs
Improve quality of life
Prohibiting factors:
Extensive malignancy, untreated cardiac disease, chronic resp failure, extensive vascular disease, chronic infection
Donor criteria: Willing donor in excellent health Living related/unrelated/cadaver donor Emotional stable Same blood type Compatibility: ABO compatibility Human leukocyte antigen histocompatibility consists of 6 antigens ABO and HLA, removal of plasma containing components causing or thought cause disease, replace with fluids such as saline, FFP or albumin
Describe the transplant procedure
Transplant procedure:
Kidney is surgically placed extraperitoneal in the iliac fossa
Renal artery is anastomosed to recipient’s iliac vein
Usually kidney begins to function immediately
Hemodialysis may be performed until good function is established
Identify the major complications of renal transplant and the medical and nursing measures that
prevent & treat complications.
Major complications of renal transplant:
Graft rejection, 3 types:
Hyperacute: occurs within min-hr. TX: none, must remove kidney
Acute: occurs within first 6 mo., reversible, common to have one rejection episode. TX: immunotherapy, corticosteroids
Chronic: occurs over mo-yr, irreversible, pt needs to be put on transplant list. TX: supportive
Manifestations of rejection: fever, graft tenderness, anemia, malaise. TX: immunosuppressants, steroids, antibiotics
Other complications
Infection: most serious, bacterial/fungal/viral (wound, UTI, pneumonia. Immunosuppressive meds may mast symptoms
Urinary tract: rupture of kidney, leaking of urine from ureteral bladder, surgical repair may be necessary
Skin cancer
Delayed wound healing
Steroid induced DM, cataracts, glaucoma, retinitis
HTN
Gastric ulcers
Osteoporosis
Aseptic bone necrosis, hips/knees
From NUR 141B, review the action & rationale for the following meds used in care of a renal patient:
a. sodium polystyrene sulfonate
b. sevelamer
c. Diuretics – include a comparison of onset & peak action for the following:
i. furosemide IV & oral
ii. bumetanide IV and oral
iii. hydrochlorothiazide
d. erythropoietin
Action/rationale for renal pt medications:
a. sodium polystyrene sulfonate:
Hypokalemic electrolyte modifier, reduction of serum potassium levels
b. sevelamer:
Electrolyte modifier, phosphate binder, binds phosphate in GI tract preventing its absorption
c. Diuretics – include a comparison of onset & peak action for the following:
i. furosemide IV & oral: Loop diuretic, inhibits reabsorption of sodium nd chloride from the loop of Henle and distal renal tubule. Increases renal excretion of water/sodium/chloride, mag/potassium/calcium PO: Onset: 30-60 min Peak: 1-2 hr IV: Onset: 5 min Peak: 30 min
ii. bumetanide IV and oral: Loop diuretic, inhibits reabsorption of sodium nd chloride from the loop of Henle and distal renal tubule. Increases renal excretion of water/sodium/chloride, mag/potassium/calcium PO: Onset: 30-60 min Peak: 1-2 hr IV: Onset: 2-3 min Peak: 15-45 min
iii. hydrochlorothiazide: Antihypertensive, thiazide diuretic, treatment for edema associated with renal dysfunction. inhibits reabsorption of sodium nd chloride from the loop of Henle and distal renal tubule. Increases renal excretion of water/sodium/chloride, mag/potassium/calcium/hydrogen/phosphate/bicarbonate PO only: Onset: 2 hr Peak: 3-6 hr
d. erythropoietin:
Discuss the action and rationales for the following meds used in the care of the renal patient
CYCLOSPORINE
Cyclosporin use in renal pt:
Immunosuppressant
Prevention and treatment of rejection in renal transplant pt
Discuss the action and rationales for the following meds used in the care of the renal patient
AZATHIOPRINE
Azathioprine use in renal pt:
Immunosuppressant
Prevention of renal transplant rejection
Discuss the action and rationales for the following meds used in the care of the renal patient
PREDNISONE
Prednisone use in renal pt:
Anti-inflammatory
Immune modifier
Suppresses inflammation and the normal immune response
Suppresses adrenal function
Discuss the action and rationales for the following meds used in the care of the renal patient
SODIUM BICARBONATE
Sodium bicarbonate use in renal pt:
Antiulcer agent
Management of metabolic acidosis
Used to alkalinize urine and promote excretion
Stabilization of acid/base status and treatment of life threatening hyperkalemia
Discuss the action and rationales for the following meds used in the care of the renal patient
TACROLIMUS
Tacrolimus use in renal pt:
Immunosuppressant
Prevention of organ rejection of kidney
Discuss the action and rationales for the following meds used in the care of the renal patient
INTROPIN (Dopamine)
Intropin (Dopamine) use in renal pt:
Vasopressor
Increase renal perfusion during shock state
Describe the effect of renal disease and the reproductive health
Effects of AKI:
Fluid and electrolyte imbalances
- fluid excess/deficit
- HYPERkalemia and hypermagnesemia
- HYPOnatremia and hypocalcemia
Acidosis
- kidneys unable to synthesize NH3 needed for H ion excretion
- decreased HCO3 since it is used as buffer
- Kussmaul respirations to decrease CO2
Identify significance of abnormal assessment data from case study Sodium 149 K+ 6.4 BUN 90 Creat 6.9 Cl 105 CO2 18 WBC 25.9 Hgb 11.9 HCT 38% plts 245,000
Sodium 149 K+ 6.4 BUN 90 Creat 6.9 Cl 105 CO2 18 WBC 25.9 Hgb 11.9 HCT 38% plts 245,000
Identify the most significant actual and “risk for” patient problems and associated Nursing
Diagnoses for this patient. Identify his collaborative problems from case study
.
Explain your role in placement of HD catheter from case study
.
Define: Azotemia Uremia Oliguria Anuria
Azotemia:
Accumulation of N2 waste in blood (BUN and creatinine increase)
May begin before urine output decreases
Uremia:
Renal function decline to point where symptoms develop in multiple body systems.
Loss may be sudden or develop over long period
Oliguria:
Urine output <400mL/24 hr (72ml/hr)
Anuria:
Urine output <100mL/24 hr
BUN normal range, what is it
Creatinine normal range, what is it
BUN (6.20 mg/dl):
Urea is end product of protein metabolism normally excreted through kidneys
Any renal function impairment causes increase
Other factors
Creatinine (0.6-1.3 mg/dl):
Accurate indicator of renal function
Not affected significantly by dietary or fluid intake
Causes of AKI
Prerenal
Intrarenal
Postrenal
AKI (from book):
Prerenal: Hypovolemia Low cardiac output Altered vascular resistance Examples: hemorrhage, dehydration, excess fluid loss from GI tract, burns, wounds, HF, cardiogenic shock, sepsis, anaphylaxis, vasoactive drugs
Intrarenal: Glomerular/microvascular injury Acute tubular necrosis Interstitial nephritis Examples: glomerulonephritis, DIC, vasculitis, HTN, toxemia of pregnancy, hemolytic uremic syndrome ischemia due to conditions associated with prerenal AKI; toxin such as drugs, heavy metals, hemolysis, rhabdomyolysis, nephrotoxic drugs, infectious diseases, immunologic disorders, idiopathic
Postrenal:
Ureteral obstruction
Urethral obstruction
Examples: calculi, cancer, external compression, prostatic enlargement, stricture, blood clot
