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32 Cards in this Set

  • Front
  • Back
contrast agents
Nephrotoxic
direct afferent arteriole constrictor
renal dysfunction populations at risk
DM, HTN, certain malignancies, Nephrotoxic Rx, congenital disorders
NSAIDS as nephrotoxic agent
-inhibit production of vasodilatory prostaglandins,
-frequent culprit in pt's with preexisting renal insufficiencies
Nephrotoxic Drugs
aminoglycosides: gentamycin, tobramycin
amphoteracin B
acyclovir, sulfonamides, cyclosporin, tacrolimus, antineoplastic agents: methotrexate, hemoglobin, myoglobin, uric acid(tumon lysis syndrome)~released when cells die
Acute renal failure def.
rapid decrease in Renal function
accumulation of metabolic waste
Pt. w/ renal insufficincy may result in ESRD
Acute renal failure 3 mechanismns
1) prerenal: decr. renal perfusion
2)intrarenal: tissue damage wwithin kidneys (ATN(acute tubular necrosis)
3) post renal: obstructed urine flow
Prerenal ARF concepts
#1 cause
decr. blood flow = cell death, dying cells obstruct tubules, decr. GFR, oliguria. Recovery depends on establishing blood flow.
oliguria.anuria
Intrarenal ARF caused by
Acute tubular necrosis-damage to tubules varying degrees of damage/cellular death
Acute tubular necrosis 2 main causes
Ischemia
Nephrotoxic substances: contrast dyes, heavy metals antibiotics.
Acute tubular necrosis Tx
must be immediate to minimize damage. Not always reversible, may lead to chronic renal failure
Post renal ARF causes
blockage of urine
Elderly male s/p prostatectomy**
calculi, clots, BPH, gyn surgery, crystal formation: acyclovir, methotrexate, triamterene (k sparing diuretic)indinavir, sulfonamides
postrenal ARF and urine output
decr. UO. < 100 ml/day
Tx to correct cause or may lead to permanent damage
ARF clinical course (4 phases)
-onset
-oliguric phase
-diuresis phase
-recovery phase
ARF phase 1- onset
time of onset of insult until dev. of oliguria. Dec: renal blood flow, GFR, Incr: ser cr, BUN, wastes.
Onset suddenlasting hrs to days.
Quick Tx may alleviate irreversible damage.
ARF phase 2- oliguria
Dec. UO(<400 cc/day), does not respond to fluid/ diuretic challange, total support of ren. Fn required.. may last days to weeks, 8-15 day avg.
ARF phase 2- oliguria Labs
Incr. BUN and serum Cr
Metabloic acidosis (decreased HCO3-)
Hyper: K, PO4, Mg
Hypo: Ca, Na
ARF phase 2- oliguria Metabolic Waste symptoms
N/V
Drowsy, confusion, coma
GI bleed
Asterixis
Pericarditis
ARF phase 2- oliguria electrolyte imbalance symptoms
N/V
Drowsy, confusion, coma
Kussmaul
ECG changes (Inc K+)
Asterixis
(flapping tremor) is a tremor of the wrist when the wrist is extended (dorsiflexion), sometimes said to resemble a bird flapping its wings
oliguria definition pediatrics
UO < 1 mL/kg/hr in infants
<0.5 mL/kg/hr in children
oliguria definition by UO output- adults
<400 mL/day
< 30 cc/hr
GFR calculation
(140- age in years) *Wt in kg/(72*Serum Cr)
for women *0.85
Acute renal Failure phase III- diuretic phase
polyuia (22-4L/day) ends when BUN and Cr stop rising.
lasts 2-6 weeks, Inc in GFR, but no improvement of cleared waste
Acute renal Failure phase III- diuretic phase Interventions
strict I&O, daily weights, and electrolyte monitoring
Acute renal Failure phase III- diuretic phase symptoms of volume depletion
hypovolemia, dec. Na, K, continued incr. in BUN and Cr, hypotension, tachycardia, thirst, Increased mental acuity.
Acute renal Failure phase IV- recovery phase
return to normal limits, labs WNL, renal Fn continues improving, very vulnerable to renal injury.

Some do not recover= CRF
Acute renal failure Therapy goal
Tx underlying cause
correct fluid/electrolyte imbalances
prevent complications including nutritional deficiencies
Fluid challenge in ARF
promotes renal perfusion- furosemide used.
CCB use in ARF
improves GFR and helps to maintain nephron cell integrity
Diet therapy in ARF
Pt. often in catabolic state, muscle breakdown, increased BUN
Dietary orders for ARF
They will be specific.
protein0.6g/kg or 40g/day, if dialysis,then1-1.5 g/kg. Na+ and fluid should =UO+500cc
indications for dialysis
BUN >100 mg/dL, Cr > 5-10 mg/dL, intractible acidosis, electrolyte disturbances not responding to therapy.