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