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157 Cards in this Set
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Clinical syndrome of sudden loss of renal function, occuring over hours to a few days, that results in derangements in fluid and electrolyte balance, acid-base hemostasis, calcium/phosphate metabolism, blood pressure regulation, and erythropoiesis.
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Acute renal failure
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Hallmarks of ARF
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- decreased GFR
- increased creatinine - increased BUN |
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oliguria
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urine output less than 400ml/24h or less than 0.5cc/kg/24hr
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Anuria
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urine output less than 50ml/day
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nonoliguria
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urine output greater than 400ml/24h
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any physiological event that results in renal hypoperfusion
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prerenal ARF
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acute damage to renal parenchyma
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intrarenal ARF
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any obstruction in flow of urine from the collecting ducts
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postrenal ARF
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pathophysiology of prerenal ARF
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decrease in renal perfusion--renin from afferent arterioles--R-A-A-S--angiotensin 2 from the adrenal cortex
angiotension 2--vasoconstriction--aldosterone---sodium and water retention |
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in this phase of ARF the kidneys will maintain the mechanism of autoregulation to preserve adequate blood flow to essential organs and maintain GFR over a wide range of MAPs---if renal perfusion is severly compromised, autoregulation mechanism is overwhelmed and GFR fails
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prerenal ARF
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hypoperfusion treated by
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volume replacement, CO improvement, dysrhythmia treatment or a combination or these
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improved renal perfusion will be seen clinically as
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increased urine output and decreased urine sodium
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* autoregulation capacity overwhelmed
* GFR decreases * tubular fluid decreases * increased sodium and water reabsorption * urine output reduced to <400ml/day * urine sodium increases |
prerenal ARF
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causes of prerenal ARF include
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dehydration
hemorrhage hypovolemic shock hypovolemia third-spacing CHF MI cardiogenic shock valvular heart disease ACE inhibitors NSAIDS calcineurin inhibitors sepsis cirrhosis neurogenic shock renal artery stenosis |
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Lab studies to diagnosis prerenal ARF
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urinalysis
urine sodium, specific gravity, osmolality BUN, creat and BUN/creat ratio |
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diagnostic studies to diagnosis prerenal ARF
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* renal ultrasonography
* CT * MRI * renal arteriogram |
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treatment of prerenal ARF includes
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* volume replacement (kidneys rely on volume)
* improve CO, CI, PAWP * treat cardiac dysrhythmias (they can often decrease CO) |
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calcineurin inhibitor
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prograf
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treat prerenal failure with
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* aggressive fluid therapy
* diuretic therapy * vasopressor therapy * nutritional therapy |
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aggressive fluid therapy of prerenal ARF includes
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* crystalloids usually first treatment (be careful with LR d/t potassium and lactic acid levels)
* extracellular volume expaders * blood products--if hemorrage or decreased H&H |
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diuretic therapy of prerenal ARF includes
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* lasix IVP, 100-200 mg q6-8hr
- or - * laxis continuous infusion |
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why is mannitol of no benefit with prerenal ARF
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it causes increased workload and increased oxygen consumption
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vasopressor therapy of prerenal ARF includes
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dopamine--low dose, 2-5mcg/kg/min
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best dose of dopamine in treatment of prerenal ARF
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3mcg/kg/min
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this drug improves renal blood flow, leads to less severe form of ARF but does not prevent ARF
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dopamine
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nutritional therapy in prerenal ARF will
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* minimize uremic symptoms
* reduce incidence of fluid, electrolyte, and acid-base imbalances * decrease pts vulnerability to infections * minimize symptoms of anemia |
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nutritional therapy of prerenal ARF includes
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* amino acids 1.5 to 1.7gm/kg/day to minimize catabolism
* daily continuous dialysis * nephro tube feedings * daily weights, level of mobility * monitor: creat, BUN, protein, albumin, urea, electrolytes, CBC |
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care with amino acids should be taken in treatment of prerenal ARF d/t
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camino acids breakdown to nitrogen and the kidneys inability to excrete
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most common hospital-acquired form of intrarenal ARF is
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ATN
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2 factors that contribute to ATN
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* ischemia
* nephrotoxicity |
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prolonged hypoprofusion of prerenal ARF--ischemia to renal tubular epithelia--decreased ATP--intracellular K, Mg, PO4 and decreased intracellular Na, Cl, and Ca--cell injury and dysfunction--increase in O2 free radicals--tubular cells necrose--cells slough off and obstruct tubular lumen--backflow of tubular fluid--decreased GFR that further
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pathophysiology of ischemic ATN
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profound vasoconstriction that reduces renal blood flow up to 50% is the final contributor in this type of intrarenal ARF
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ischemic ATN
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hormones/chemicals released in ischemic ATN
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* norepinephrine (released by SNS)
* angiotensin 2 (converted by the lungs) * endothelin (released by damaged endothelial cells in the kidneys) |
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concentration of nephrotoxin in renal tubular cells--necrosis--cells sough off into tubular lumen--obstruction of tubular lumen--back flow of tubular fluid--decreased GFR and profound vasoconstriction reducing renal blood flow further
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pathophysiology of nephrotoxic ATN
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in this type of intrarenal ARF,
* basement membrane of renal cells remains intact * injured necrotic areas more localized * nonoliguria occurs more often * healing process is more rapid |
toxic ARF
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there is less morbidity with this type of intrarenal ARF
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toxic
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causes of ischemic ATN include
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* hemorrhagic hypotension
* sever volume depletion * surgical aortic cross-clamping * cardiac surgery * septic shock * pancreatitis * immunosuppression (cyclosporin, tacrolimus) * NSAIDS |
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causes of toxic ATN include
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* aminoglycoside nephrotoxicity
* drugs * heavy metals * radiologic contract agents * fungicides and pesticides * plant and animal substances * organic solvents |
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offending agents of aminoglycoside nephrotoxicity
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* neomycin
* tobramycin * gentamicin * amikacin * streptomycin |
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this antibiotic is nephrotoxic but it is not an aminoglycoside
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vanco
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increaed risk factors for toxicity when using aminoglycoside agents include
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* volume depletion
* advanced age * cardiac surgery * DM * pts with underlying renal insuff. |
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propholactic treatment of patients at high risk for aminoglycoside nephrotoxicity includes
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give them good IV fluids before, during, and after the drugs and monitor the peaks/troughs of drugs
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these drugs are ototoxic
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aminoglycosides
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dosage of aminoglycosides that kidneys do better with
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large dose rather than small divided doses
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drugs that cause toxic ATN include
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* aminoglycosides
* amphotericin * cyclosporin * anesthetics * chemo agents * vanco |
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heavy metals that cause toxic ATN include
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* mercury
* arsenic |
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plant and animal substances that can cause toxic ATN include
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* mushrooms
* snake venom |
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organic solvent that can cause toxic ATN
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carbon tetrachloride
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pts at greatest risk for developing radiocontract nephrotoxicity
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those with:
* diabetes * underlying renal insuff. * advanced age * volume depletion * multiple myelomas * large contrast loads |
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this occurs in
* 5-15% of hospitalized patients wih toxic ATN * usually develops 7-10 days after onset of therapy * is dose dependent since the agents are eliminated by the kidneys |
aminoglycoside nephrotoxicity
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* begins within 48hrs of administration
* peaks within 3-5 days * returns to baseline in 7-10 days |
radiocontrast nephrotoxicity
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this should be done before and after IV dye administration
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agressive hydration with IV NS
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this drug should be given before and after IV dye administration to protect the kidneys
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600-1200mg mucomyst bid
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cause of intrarenal ARF include
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* necrosis
* nephrotoxins |
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4 phases of ATN
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* onset phase
* oliguric or nonoliguric phase * diuretic phase * recovery phase |
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* begins with initial insult and last until cell injury occurs
* lasts hours to days * renal blood flow and O2 consumptoin reduced by 20% * healing can take 8 days to one year * signs of renal failure begin: decreased urine output and increase serum creatinine |
onset phase of ATN
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treatment goals of ATN include
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* determine cause
* initiate treatment to prevent irreversible tubular damage |
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patients in this phase of ATN
* more frequently require renal replacement therapy * are less likely to recover renal function * have a higher mortality rate |
oliguric
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this type of ATN is most likely the cause of ischemia
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oliguric
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this type of ATN lasts 12-30 days
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oliguric
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this will be seen in the oliguric phase of ATN
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* fluid overload
* azotemia * electrolyte abnomalities (increased K, increased PO4 and decreased Ca) * metabolic acidosis * uremia |
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electrolyte abnormalities seen in oliguirc phase of ATN
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* increased K
* increased PO4 * decreased Ca |
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Goals of treatment of oliguric ATN
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* support renal function
* keep pt alive until renal inury heals |
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this form of ATN is seen in 50% of patients with ATN
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nonoliguric
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this form of ATN is most commonly associated with toxic injury
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nonoliguric
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in this form of ATN the kidneys tend to retain the ability to concentrate urine to some degree
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nonoliguric
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in this form of ATN there is a decreased need for dialysis
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nonoliguric
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this form of ATN lasts 5-8 days
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nonoliguric
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with this form of ATN pts more frequently require renal replacement therapy
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oliguric
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with this form of ATN pts are less likely to recover renal function
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oliguric
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with this form of ATN there is a higher mortality rate
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oliguric
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this form of ATN is most commonly a result of ischmia
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oliguric
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this form of ATN lasts 12-30 days
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oliguric
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with nonoliguric ATN you will see
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* diuresis
* fluid complications are minimized * hyperkalemia |
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goals of treatment of nonoliguric ATN include
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* support renal function
* keep patient hydrated |
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in this phase of ATN there will be a gradual increase in urine output as renal function starts to return
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diuretic phase
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in the diuretic phase of ATN diuresis can exceed
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4-5 liters per day
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in the diuretic phase of ATN the renal concentrating ability is
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impaired
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how long does the diuretic phase of ATN last
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1-2 weeks
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pts in the diuretic phase of ATN have
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* risk for hypovolemia
* hyponatremia * hypokalemia |
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goals of treatment during diuretic phase of ATN include
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* maintain hydration
* prevent electrolyte depletion * continue to support renal function |
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the time it takes for renal function to return is know as the _____ phase of ATN
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recovery
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if the basement membrain is damaged this results
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residual renal impairment
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45% of pts with ATN will not recover
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full renal function
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5% of pts with ATN will require
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long term dialysis/transplant
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the recovery phase of ATN lasts
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several months to a year
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goals of treatment in the recovery phase of ATN
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* foster and maintain renal function
* pt and family education |
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pt/family education of ATN should include
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* what caused the renal failure
* follow-up care * preventative measures for recurrence |
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treatment of intrarenal ARF includes
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* aggressive fluid administration
* diuretics * vasopressors * nutritional therapy * skin care * meds * teaching * dialysis |
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medication treatment of intrarenal ARF includes
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* aminoglycosides
* IV NS before and after aminoglycosides and contrast dye * mucomyst with hydration before and after contrast dye |
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obstruction to urine flow from kidney to bladder--retrograde pressure through collecting system--decreased reate of tubular fluid flow--lowers the GFR--increase reabsorption of Na, H2O and urea--lowered urine Na concentration and increased urine osmolality, BUN and creat--entire collectin system dilaties and damages nephrons--dysfunction of concentrating/diluting mechanism--urine osmolality and Na concentration become similar to plasma
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pathophysiology of postrenal ARF
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acute renal failure from this cause must involve both kidneys (or pts with a single kidney) since a single functioning kidney can maintain homeostasis
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postrenal
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after relief of the obstruction in postrenal failure there is often diuresis as great as
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1 liter per hour
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in postrenal ARF replacement of electrolytes and water must take place or
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hypovolemia/shock are imminent
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pts with a history of abdominal tumors, calculi, BPH, distended bladder, kinked or obstructed foley may have this diagnosis of ARF
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postrenal ARF
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pts with a history of events or conditions of prolonged hypoperfusion, nephrotoxins, systemic disease, rhabdomyolysis, atheroembolic intrarenal diseases may have this form of ARF
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intrarenal ARF
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diagnostic and lab studies to diagnosis intrarenal failure
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same as those used to diagnosis prerenal failure
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lab studies used to diagnosis postrenal ARF
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same as those for pre and intrarenal ARF
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diagnostic studies used to diagnosis postrenal ARF
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same as those for pre and intrarenal failure plus an IVP
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slow, progressive, irreversible deterioration in renal function that results in the kidney's inability to eliminate waste products and maintain fluid and electrolyte balance
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CRF
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ulitmately leads to ESRD
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CRF
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ESRD leads to need for
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renal replacement therapy or renal transplant
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to prevent progression of CRF
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* avoid nephrotoxins
* strict control of HbA1c with diabetes * BP control with ACE and ARBs * control serum lipids especially in DM and nephrotic syndrome * control CHF |
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these drugs for control of BP drop renin
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ACE and ARBs
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etiology of CRF includes
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* vascular
* glomerular * interstitial * congenital * genetic |
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vascular causes of CRF
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* HTN (untreated or poorly controlled)
* Kimmelstiel-Wilson syndrome (atherosclerosis of renal artery) * renal artery stenosis * renal artery thrombosis/sclerosis * AAA * cardiovascular disease * Type 1 DM * scleroderma |
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glomerular causes of CRF include
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* beta streptococci infection
* immunologic glomerular disease * systemic lupus erythematosus * type 1 DM |
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interstitial causes of CRF include
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* pyelonephritis
* recurrent infections * autoimmune processes * allergic interstitial nephritis * phenacetin (pain reliever) |
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congenital lesion causes of CRF include
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* horseshoe kidney
* reflux * hydronephrosis |
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genetic disease causes of CRF include
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* polycystic renal disease
* medullary cystic kidney disease |
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other cuases of CRF include
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* obstructive uropathy
* neoplasms/tumors * transplant rejection * hepatorenal syndrome |
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three stages of CRF
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* decreased renal reserve
* renal insufficiency * ESRD |
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in this stage of CRF there is a 40-50% loss of renal function
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decreased renal reserve
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this stage of CRF is typically asymptomatic since kidneys can maintain excretory and regulatory function
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decreased renal reserve
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in this stage of CRF the BUN and creat remain normal
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decreased renal reserve
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in this stage of CRF there is only 20-40% of normal renal function remaining
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renal insufficiency
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in this stage of CRF solute clearance, ability to concentrate urine, and hormone secretion are compromised
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renal insufficiency
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in the renal insufficiency stage of CRF, these signs of renal failure begin to be seen
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* azotemia
* electrolyte imbalances * anemai * fatigue * polyuria * nocturia |
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in this stage of CRF there is <15% renal function remaining
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ESRD
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in this stage of CRF regulatory function, excretory function, and hormonal function are severely impaired
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ESRD
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in this stage of CRF, uremic symptoms become evident
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ESRD
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uremic symptoms evident in ESRD include
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* N/V and anorexia
* altered sensorium * weakness and fatigue |
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evident signs of renal failure include
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* elevated BUN/creat
* anemia * hypocalcemia * hyperkalemia * hyperphosphatemia * fluid overload |
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neuro assessment of pt with CRF will reveal
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* lethargy
* muscle irritability * general irritability * LOC * fatigue * alterations in short term memory and concentration * fogginess with thought process * blurred or vision changes * burning feet syndrome * restless leg syndrome * seizures |
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cardiovascular assessment of pt with CRF will reveal
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* CP
* hypervolemia * peripheral edema * abnormal shape of chest wall, sternum, and ribs * tachycardia * dysrhythmias |
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pulmonary assessent of pt with CRF will reveal
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* SOB
* DOE or at rest * use of accessory muscles * decreased sats * Kussmaul resps |
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hematology assessment of pt with CRF will reveal
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* fatigue
* increased sleep * sensations of cold * bruising pallor of conjunctiva, skin and mucous membranes * decreased body temp |
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GI assessment of pt with CRF will reveal
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* indigestion
* N/V/D * anorexia * metalic taste * weight loss * heme pos. stool and emesis * GI bleed * diverticulitis * hemorrhoids |
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electrolyte assessment of pt with CRF will reveal
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* hyperkalemia
* hypermag |
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skin assessment of pt with CRF wil reveal
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* dry skin
* pruritis * tingling of skin * lesions * uremic frost * bruising * pallor |
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may hear a friction rub in pts with CRF due to
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uremic pericarditis or recurrent pericarditis
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management of CRF includes
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* prevention of fluid overload
* management of acid-base balance * management of cardiovascular alterations * control of HTN * management of electrolytes |
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interventions to prevent fluid overload in CRF includes
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* fluid restriction
* Na restriction * give diuretics (but monitor K) * accurate I&O * daily weight * monitor for peripheral and pulmonary edema |
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to manage acid-base balance of pt with CRF give alkaline meds for a pH <7.2 and HCO3 <14, such as
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sodium bicarb drip and antacids
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acid base balance can be maintained in pts with CRF by
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* HD or CRRT
* peritoneal dialysis |
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symptoms of uremic pericarditis
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* CP
* fever * pericardial friction rub * ST elevations on EKG * dyspnea * tachycardia * confusion * JVD * weakness * peripheral edema * tamponade (Becks triad) * narrowed pulse pressure |
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treat LVH with
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inotropic drugs such as dopamine, dobutamine, and dig
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control HTN in pts with CRF with
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* fluid and Na restriction
* diuretics * dialysis * antihypertensive meds (BB, CCB, ACE inhibitors, ARBs) |
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if this is not recognized and treated it will lead to fatal dysrhythmias
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potassium imbalance
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interventions for K <6
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* restrict dietary K
* diuretics * K binding resins PO or enema (kay exelate) |
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interventions for K >6
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calcium gluconate or calcium chloride IV, IV insulin, D50W, sodium bicarb
* diuretics * dialysis |
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treat restless leg syndrome with
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mirapex
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treat burning feet syndrome with
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* cotton socks
* open comfortale shoes * vitamin B |
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treat cognitive impairments by
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* correct electrolytes
* correct BUN and creat imbalances |
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treat cerebral edema by
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correction of fluid overload
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this is a major cause of mortality in ARF and CRF
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infections
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impairment in the immune system of pts with ARF and CRF is caused by
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* malnutrution
* effecst of uremia on WBCs |
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baseline temp in uremic pts is ____ so _____
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low so any increase above baseline is significant
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as GFR decreases, PO4 increases and Ca decreases resulting in
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renal osteoporosis and osteodystrophy
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when Ca and PO4 crystals precipitate in the brain, eyes, gums, heart valves, myocardium, lungs, joints, blood vessels, and skin it is a condition called
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metastatic calcification
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xerosis
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dryness
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renal diet consists of
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* fluid restrictions
* Na, K, PO4 restriction * iron, Ca, folic acid, and vitamin supplements * high cal (30-44 kcal/kg/day) * most calories form carbs and lipids * essential and nonessential amino acids * protein restriction |
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protein restriction for a pt not on dialysis
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0.8g/kg/day
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protein restiction for a pt on dialysis
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1.5g/kg/day
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interventions for pt on renal diet
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* monitor serum protein, albumin, prealbumin, elecrolytes, H&H, urea
* monitor daily weight * strict I&O * nutritional education |
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if a pt with CRF is not able to take po this should be condidered
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tpn or tube feeding
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tube feeding of choice for pt with RF
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nephro
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