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32 Cards in this Set
- Front
- Back
contrast agents
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Nephrotoxic
direct afferent arteriole constrictor |
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renal dysfunction populations at risk
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DM, HTN, certain malignancies, Nephrotoxic Rx, congenital disorders
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NSAIDS as nephrotoxic agent
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-inhibit production of vasodilatory prostaglandins,
-frequent culprit in pt's with preexisting renal insufficiencies |
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Nephrotoxic Drugs
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aminoglycosides: gentamycin, tobramycin
amphoteracin B acyclovir, sulfonamides, cyclosporin, tacrolimus, antineoplastic agents: methotrexate, hemoglobin, myoglobin, uric acid(tumon lysis syndrome)~released when cells die |
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Acute renal failure def.
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rapid decrease in Renal function
accumulation of metabolic waste Pt. w/ renal insufficincy may result in ESRD |
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Acute renal failure 3 mechanismns
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1) prerenal: decr. renal perfusion
2)intrarenal: tissue damage wwithin kidneys (ATN(acute tubular necrosis) 3) post renal: obstructed urine flow |
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Prerenal ARF concepts
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#1 cause
decr. blood flow = cell death, dying cells obstruct tubules, decr. GFR, oliguria. Recovery depends on establishing blood flow. oliguria.anuria |
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Intrarenal ARF caused by
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Acute tubular necrosis-damage to tubules varying degrees of damage/cellular death
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Acute tubular necrosis 2 main causes
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Ischemia
Nephrotoxic substances: contrast dyes, heavy metals antibiotics. |
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Acute tubular necrosis Tx
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must be immediate to minimize damage. Not always reversible, may lead to chronic renal failure
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Post renal ARF causes
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blockage of urine
Elderly male s/p prostatectomy** calculi, clots, BPH, gyn surgery, crystal formation: acyclovir, methotrexate, triamterene (k sparing diuretic)indinavir, sulfonamides |
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postrenal ARF and urine output
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decr. UO. < 100 ml/day
Tx to correct cause or may lead to permanent damage |
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ARF clinical course (4 phases)
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-onset
-oliguric phase -diuresis phase -recovery phase |
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ARF phase 1- onset
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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. |
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ARF phase 2- oliguria
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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.
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ARF phase 2- oliguria Labs
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Incr. BUN and serum Cr
Metabloic acidosis (decreased HCO3-) Hyper: K, PO4, Mg Hypo: Ca, Na |
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ARF phase 2- oliguria Metabolic Waste symptoms
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N/V
Drowsy, confusion, coma GI bleed Asterixis Pericarditis |
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ARF phase 2- oliguria electrolyte imbalance symptoms
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N/V
Drowsy, confusion, coma Kussmaul ECG changes (Inc K+) |
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Asterixis
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(flapping tremor) is a tremor of the wrist when the wrist is extended (dorsiflexion), sometimes said to resemble a bird flapping its wings
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oliguria definition pediatrics
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UO < 1 mL/kg/hr in infants
<0.5 mL/kg/hr in children |
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oliguria definition by UO output- adults
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<400 mL/day
< 30 cc/hr |
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GFR calculation
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(140- age in years) *Wt in kg/(72*Serum Cr)
for women *0.85 |
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Acute renal Failure phase III- diuretic phase
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polyuia (22-4L/day) ends when BUN and Cr stop rising.
lasts 2-6 weeks, Inc in GFR, but no improvement of cleared waste |
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Acute renal Failure phase III- diuretic phase Interventions
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strict I&O, daily weights, and electrolyte monitoring
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Acute renal Failure phase III- diuretic phase symptoms of volume depletion
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hypovolemia, dec. Na, K, continued incr. in BUN and Cr, hypotension, tachycardia, thirst, Increased mental acuity.
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Acute renal Failure phase IV- recovery phase
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return to normal limits, labs WNL, renal Fn continues improving, very vulnerable to renal injury.
Some do not recover= CRF |
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Acute renal failure Therapy goal
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Tx underlying cause
correct fluid/electrolyte imbalances prevent complications including nutritional deficiencies |
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Fluid challenge in ARF
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promotes renal perfusion- furosemide used.
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CCB use in ARF
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improves GFR and helps to maintain nephron cell integrity
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Diet therapy in ARF
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Pt. often in catabolic state, muscle breakdown, increased BUN
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Dietary orders for ARF
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They will be specific.
protein0.6g/kg or 40g/day, if dialysis,then1-1.5 g/kg. Na+ and fluid should =UO+500cc |
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indications for dialysis
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BUN >100 mg/dL, Cr > 5-10 mg/dL, intractible acidosis, electrolyte disturbances not responding to therapy.
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