care of patients with acute/chronic kidney injury ch 71 Flashcards
onset
difference between acute/chronic
acute: sudden (hours to days)
chronic: gradual (months to years)
% of nephrons involved
difference between acute/chronic
acute: 50%
chronic: 90-95%
duration of disease
difference between acute/chronic
acute: 2-4 weeks, less than 3 months
chronic: permanent
prognosis of disease
difference between acute/chronic
acute: good for return of kidney function with supportive care. high mortality in some situations
chronic: fatal without a renal replacement therapy such as dialysis or transplantation
azotemia
the retention and buildup of nitrogenous wastes in the blood
When BUN rises faster than the serum creatinine level, the cause is usually related to ____
protein breakdown or dehydration
when both the BUN and creatinine levels rise and the ratio between the two remains constant, this indicates ____
kidney dysfunction
causes of pre renal AKI
any condition that decreases blood flow to the kidneys and leads to ischemia in the nephrons
shock (hypovolemia, hemorrhage, distributive, obstructive) HF PE anaphylaxis sepsis pericardial tamponade
most common: shock, HF
causes of intrarenal AKI
actual physical, chemical, hypoxic, immunologic image directly to the kidney tissue
usually occurs with damage to glomeruli, interstitial tissue, or tubules
acute interstitial nephritis exposure to nephrotoxins acute glomerular nephritis vasculitis acute tubular necrosis renal artery or vein stenosis renal artery or vein thrombosis formation of crystals or precipitates in the nephron tubules
normal osmolarity
270-300
HCO3 range
22-26
PaCO2
35-45
early AKI can often be revered by:
correcting blood volume
increasing BP
improving cardiac output
drugs that most often cause intrarenal AKI
aminoglycoside antibiotics (gentamicin, neomycin, streptomycin, kanamycin, tobramycin) NSAIDs
causes of postrenal AKI
obstruction of the urine collecting system anywhere from the calyces to the urethral meatus
obstruction must be bilateral to cause post renal failure, unless only 1 kidney is functional
ureter, bladder, urethral cancer kidney, ureter, bladder stone bladder atony prostatic hyperplasia or cancer urethral stricture cervical cancer
onset phase of AKI
- description
- characteristics
begins with precipitating event and continues until oliguria develops
last hours to days
the gradual accumulation of nitrogenous wastes, such as increasing serum creatinine and BUN
oliguric phase of AKI
- description
- characteristics
characterized by urine output of 100-400 mL/24 hr that does not respond to fluids or diuretics
lasts 1-3 weeks
increasing serum creatinine and BUN
hyperkalemia, metabolic acidosis, hyperphosphatemia, hypocalcemia, hypermagnesemia
sodium retention
urine specific gravity and urine osmolarity do not vary as plasma osmolarity changes
diuretic phase of AKI
- description
- characteristics
high output phase
often has a sudden onset within 2-6 wk after oliguric stage
urine flow increases rapidly over a period of several days
diuresis can result in an output of 10 L/day of dilute urine
BUN levels start to fall and continues till it reaches normal levels
normal kidney tubular function is re-established
recovery phase of AKI
- description
- characteristics
patient begins to return to normal levels of activity
complete recover can take up to 12 months
manifestations of volume depletion
yellow box 1541
low urine output decreased systolic BP decreased pulse pressure orthostatic hypotension thirst rising blood osmolarity
potential nephrotoxic substances
rifampin vancomycin ibuprofen ketorolac naproxen tylenol captopril metformin myoglobin
manifestations of prerenal azotemia AKI
hypotension tachycardia decreased cardiac output decreased central venous pressure decreased urine output lethargy
renal manifestations of intrarenal/postrenal AKI
oliguria or anuria
increased urine specific gravity
cardiac manifestations of intrarenal/postrenal AKI
HTN tachycardia JVD increased central venous pressure tall T waves
respiratory manifestations of intrarenal/postrenal AKI
SOB orthopnea crackles pulmonary edema friction rub
gastrointestinal manifestations of intrarenal/postrenal AKI
anorexia
n/v
flank pain
neurologic manifestations of intrarenal/postrenal AKI
lethargy
headache
tremors
confusion
lab values in pt with prerenal azotemia
BUN/creatine ration of greater than 20 sodium often less than 10-20 urine concentrated urine sediment (RBCs, RBC casts, tubular cells) myoglobin, hemoglobin
lab values for intrarenal problem
BUN/creatine ration less than 15
urine sodium less than 40
specific gravity less than 1.01
lab values for postrenal problem
urine sodium may be normal
specific gravity 1.000-1.010
main problems during the oliguric phase
close monitoring for life threatening electrolyte changes and nitrogen retention
problems during the diuretic phase
hypovolemia
electrolyte loss
what do calcium channel blockers do in AKI
can be given if caused by nephrotoxic acute tubular necrosis
prevent movement of calcium into the kidney cells, maintain kidney cell integrity, improve the GFR by improving kidney blood flow