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renal failure intro 374-402
Terms in this set (70)
what does the kidneys do for our body? select all that apply
a. it controls fluid and electrolyte balance.
b. it also controls acid-base balance
c. helps to control blood pressure.
d. helps to maintain homeostasis
a. it controls fluid and electrolyte balance.
b. it also controls acid-base balance
c. helps to control blood pressure.
d. helps to maintain homeostasis
what is renal failure?
it is a condition in which the kidneys are unable to remove accumulated metabolites from the blood, resulting in altered fluid,electrolyte and acid-base balance.
- it may be acute or chronic renal failure.
-both are characterized by azotemia.
what are the causes of renal failure
a. primary kidney disorder
b. may be secondary to a systemic disease or other urological defects.
increased levels of nitrogenous waste in the blood
-retention and build up of nitrogenous waste in the blood
-nitrogen being the breakdown of protein.
pt with this may not exhibit s/s of renal failure like seen with uremia or uremic syndrome.
acute renal failure
a. it has an abrupt onset and may be reversed with prompt intervention.
b. it is a rapid decline in renal function with azotemia and fluid and electrolyte imbalances.
c. the most common cause are ischemia and exposure to nephrotoxins
d. more accurate term for this disease is ACUTE KIDNEY INJURY.
insufficient blood supply
substances that damages the nerves or nerve tissue.
what are the kidneys particularly vulnerable to
ischemia and nephrotoxins.
acute kidney injury (AKI)
refers to the a sudden decline in kidney function that causes disturbances in fluid, electrolyte and acid-base balance.
acute kidney injury
A reversible syndrome caused by sudden loss of kidney function, characterized by decreased urine output and progressive azotemia (accumulation of metabolic wastes).
acute tubular necrosis
is a syndrome of abrupt and progressive decline in the tubular or glomerular function
Usually due to damage from prolonged ischemia or nephrotoxins causing cellular death
nsaids can lead to what
renal failure. They impair renal autoregulatory responses by blocking prostaglandin production. (remember from your CRF lecture that the kidneys are responsible for prostaglandin production)
So an individual who takes NSAIDS chronically should be monitor for renal function and those who's renal function is impaired should not receive NSAIDS
therapeutic mgmt of arf
1.The best way to treat ARF is to prevent it
2. Clients at risk should be monitored closely for their hydration status, I & O, lab values and use of nephrotoxic agents and underlying causes treated.
Stay vigilant - monitor labs that reflect poor kidney function - an early sign of renal injury is the kidney's inability to concentrate the urine - so you will see a decrease in specific gravity of the urine
3.Recognize the cause - so if it is volume depletion - should be corrected - or we need to manage their hypertension better
If it is prerenal -It can sometimes be prevented by giving a fluid challenge to increase GFR or by administering an osmotic diuretic to increase vascular volume and renal perfusion.
If diuretic therapy is used within 4-8 hours of onset, an oliguric presentation may be converted to a nonoliguric presentation - remember this has better prognosis.
Most clients will require some form of dialysis or continuous renal replacement therapy (CRRT).
The general trend is to initiate early and frequent dialysis to keep the client as free of symptoms as possible and to prevent complications while the kidneys repair themselves.
HD must be started when GFR is < 15 mL/Minute
what is the classification system for acute kidney injury that establishes the diagnostic criteria, outcome and treatment options to reduce kidney injury early.
it is RIFLE
R-risk of injury
L-loss of function
E-end-stage renal failure
what is the new biomarkers that has been established to identify acute kidney injury
interleukin 18 (IL- 18
neutrophil gelatinase-associate lipocalin
kidney injury molecule 1 or KIM-1
Who can give me an example of something nephrotoxic Nephrotoxins most commonly associated with ATN are
Aminoglycoside antibiotics such as
Amphotericin B - treats systemic fungal infections
Radiologic contrast media
And in some cases chemotherapeutic agents - cytoxin - have to hang IVF after the medication
the causes and pathophysiology of acute renal failure category
is the most common cause accounting for approximately 55 % of cases
-hypoperfusion leads to ARF without directly affecting the integrity of kidney tissues
intrarenal or intrinsic ARF
is caused by direct damage to functional kidney tissue.
-it is responsible for another 40%
-urinary tract obstruction with resulting kidney damage is the precipitating factor for postrenal ARF which is the least common form.
prerenal ARF cause
a.hypovolemia- hemorrhage dehydration burns wounds
b.low cardiac output(heart failure, cardiogenic shock)
c.altered vascular resistance.(sepsis, anaphylaxis, vasoactive drugs)
intrarenal/intrinsic ARF cause
1.glumerular/ microvascular injury
ex. glomerulonephritis,disseminated intravascular coagulation, hypertension, vasculitis, hemolytic uremic syndrome
2. acute tubular necrosis
ex. hemolysis, rhabdomyolisis, ischemia associated with prerenal failure such as toxins drugs heavy metals.
acute pyelonephritis, toxins, metabolic imbalances, idiopathic
postrenal ARF causes
ex. calculi,cancer, external compression
2. urethral obstruction
ex. prostatic enlargement, calculi,cancer, stricture, blood clot.
-results from the conditions that affect renal blood flow and perfusion.
-it is common particularly in trauma surgical and critically ill patients
-there is a drop in the glomerular filtration rate due to a drop in renal blood flow to less than 20 % which is the normal cause of GFR to fall.
-it is rapidly reversed when renal blood flow is restored and the renal parenchyma remains undamaged.
obstructive causes are classified as postrenal.
-any condition that prevents urine excretion can lead to postrenal ARF.
-Benign prostatic hypertrophy is the most common precipitating factor,
-others include renal or urinary tract calculi and tumors.
-children may experience oliguria or normal/increased urine output.
-renal failure without oliguria indicates less severe renal injury.
it is characterized by acute damage to the renal parenchyma and nephrons.
-causes are disease of the kidney itself,tubular necrosis (most common cause)
-in acute glomerulonephritis-glomerular inflammation can reduce renal blood flow and cause ARF.
-vasculitis, malignant hypertension and arterial or venous occlusion damages nephrons sufficiently to result in ARF.
acute tubular necrosis (ATN).
( destruction of tubular epithelial cells ) causes an abrupt and progressive decline of renal function.
-prolonged ischemia is the primary cause of ATN.
if it occurs with nephrotoxins concurrently the risk for this is high.
risk factor for ischemia ATN
what is the most frequent cause of intrinsic renal failure in children
injury tubule to the tubule resulting in ATN
lasting more than 2 hours causes severe and irreversible damage to kidney tubules with patchy cellular necrosis and sloughing.
what are the common nephrotoxins associated with ATN
the aminoglycoside antibiotics and radiological contrast media
-it is higher when it is given to older adults or clients with preexisting renal insufficiency and when used in combination with other nephrotoxins.
vomiting and diarrhea
nonsteroidal anti-inflammatory drugs
angiotensin coverting enzyme inhibitors
allergic response to radiocontrast media
exposure to nephrotoxic drugs
benign prostatic hyperplasia
bladder outlet obstruction
risk factors for ARF
severe heart failure
severe liver disease
lower urinary tract obstruction.
drugs and radiological contrast media that are toxic to kidney
older adult-due to higher incidence of serious illness.decreased in kidney function.
child with renal insufficiency
acute renal failure prevention
identification of client at risk and implementation of prevention, protection against injury. knowledge of adverse effects of contrast media particularly contrast induced nephropathy.
contrast induced nephropathy
is the third most common cause of hospital acquired renal failure, after decreased real perfusion and administration of nephrotoxic medications.
three phases of the clinical manifestations of arf
initiation phase-last hours to days, begins with the initiating event such as hemorrhage and ends with tubular injury.if it is recognized and treated prognosis is good.
2. maintenance phase.
3. recovery phase.
maintenance phase of arf
charaterized by significant fall of gfr and tubular necrosis.
-oliguria may develop although many clients continue to produce normal or near nomal amounts of urine.
-azotemia fluid retention electrolyte imbalance occurs and metabolic acidosis develop.
-salt and water retention causes edema increases risk for heart failure and pulmonary edema.
-hyperkalemia, hyperphosphotemia, hypocalcemia.
-anemia develops after several days of aARF
-immune functions impaired increasing risk for infection.
recovery phase of arf
characterized by a process of tubule cell repair and regeneration and gradual return of the GFR to normal or pre-ARF levels.
-diuresis may occur as nephrons and gfr recover,
creatinine bun ppotassium and phosphate level remains high.
-renal function improves rapidly during the first 5-25 days of the recovery phase and continues to improve up to 1 yr.
anemia clinical manifestations
dizziness, confusion, lethargy
tachycardia tachypnea hypotension
anemia clinical therapies
administration of epoeitin for RBC
therapies aimed at treating the underlying cause of ARF
fluid volume excess
dependent pitting edema (edema that retains indentation caused by pressure.
-dyspnea, pulmonary edema, hypoxemia
jugular vein distention
fluid volume excess clinical therapies
tall,peaked t waves widened qrs
smooth muscle hyperactivity
nausea and vomiting
hyperkalemia clinical therapies
removal of all potassium from intravenous solutions
low potassium diet
administration of glucose and insulin to drive potassium into the cell.
potassium absorbing enema solutions
goals for a client that develops arf
maintain fluid and electrolyte balance (key goal)
2. identify and correct the underlying cause
3.restore the urine output and kidney function
4. prevent additional kidney damage
5. to compensate for renal impairment unti kidney function is restored.
diagnostic test for ARF
2.serum creatinne and BUN-evaluates renal function.
4.arterial blood gas
5.complete blood count
8.intravenous pyelography, retograde pyelography or antegrade pyelography- may be used to evaluate kidney structure and function.
10. radiographic studies-may be helpful in determining arf in pediatric clients
urinalysis of arf would show what
fixed specific gravity of 1.010
presence of rbs wbcs and renal tubular epithelial cells
cell cast-which are protein and cellular debri
serum creatinine and bun
this is checked in ARF conditions because it can increase rapidly within 24-48 hours of onset
this is checked for arf conditions to evaluate f and e status. potassium rises and often used to indicate the need for dialysis.
complete blood count
is checked due to anemia
used to identify obstructive causes of renal failure and important to differentiate arf from end stage chronic kidney disease.
-in arf, kidneys are enlarge while in chronic kidneys are small and shrunken.
in which contrast dye is injected into the ureters preffered- due to fewer nephrotoxin effects than intravenous pyelography
in which contrast medium is injected percutaneously into the renal pels are preffered- due to fewer nephrotoxin effects than intravenous pyelography
evaluate and differentiate between acute and chronic kidney disease.
complex bone disease process of chronic kidney disease in which increased sorption of bone is caued by chronic hyperparathyroidism.
IV fluids and blood volume expanders
given as needed to restore renal perfusion
administered in low doses by intravenous infusion increases renal blood flow
-it is a sympathetic neurotransmitter that improves cardiac output and dilates blood vessels of the mesentery and kidneys when given in low therapeutic doses.
furosemide (lasix) or osmotic diuretic.
potent loop diuretic is given if renal blood flow does not improve urinary output.
-it is also given if nephrotoxins are present to wash it out
-it also helps to establish urinary output to prevent oliguria, reduce the degree of azotemia and F and E imbalances.
it is also used to manage salt and water retention.
aluminum hydroxide (alternaGel, amphojel, nephrox
an antacid that is used to control hyperphosphatemia in renal failure.
-it binds with phosphates in the GI tract which are then excreted in the feces.
initial emergency tx of children with fluid depletion
focuses on rapid fluid replacement with ml./kg of saline or lactated ringers solution given over 5 to 10 minutes and repeat as needed to ensure renal perfusion and stabilize blood pressure.
may also be administered when blood loss os the cause of the clients circulatory depletion.
nutrition for renal insufficiency
proteins are limited to 0.6 kg of body weight per day to minimize the degree of azotemia.
carbohydrates are increased to maintain adequate calorie intake and provide protein sparing effect.
children with acute renal failure nutrition
1. parenteral or enteral feeding may be used initially to minimize protein catabolism.
2. diet is tailored to individual childs need for calories carbs fats and amino acids or protein hydrolysates. depends on the degree of renal failure sodium potassium and phosporus may be restricted.
3. oral feedings are initiated as soon as tolerated
4. a multidisciplinary team review with a nutritionist may be necessary.
AKI vs CKD
difference is CRF is not reversible and occurs over a long period of time when renal decline is sudden, functioning nephrons are overworked and renal failure can develop with loss of only 50% of functioning nephrons.
characteristics of AKI
50% of nephron involvement
weeks to less than 3 mos duration
good for return of renal function, high mortality in some situations for prognosis
characteristic of CKD
90-95% of nephrons are involved
prognosis-fatal without renal replacement therapy -HD, PD, transplant.
what happens to kidneys as we age
they atrophy and there is less nephrons so does not take as great of an insukt to cause acute renal failure and the existence of comorbidities such as DM heart disease vascular disease
kidneys receive how much of cardiac output
20-25% of cardiac output 1200 mls/min and are extremely sensitive to changes in blood flow.
THIS SET IS OFTEN IN FOLDERS WITH...
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