Exam 3 Flashcards
(155 cards)
Function of the kidneys
-BP management
-Fluid balance
-Filtering and excreting waste
-Acid base balance
-Vitamin D is activated in the kidneys (needed to absorb calcium in gut)
characteristics of acute kidney injury
-sudden onset
-May not progress
-Good prognosis
-High mortality if RRT is required or prolonged illness
characteristics of chronic kidney disease
-gradual onset
-progressive to permanent
-prognosis depends
-ESKD fatal without RRT
Three types of AKI
prerenal, intrarenal, postrenal
prerenal AKI cause
Hypoperfusion to the kidneys or diminished bloodflow
-volume depletion, vasodilation, decreased cardiac output
examples of prerenal AKI causes
hemorrhage, low blood volume, poor perfusion, HF, decreased cardiac output, MI, shock, sepsis, dehydration
intrarenal AKI causes
kidney tissue is affected directly; hematological, glomerular, or vascular issue
intrarenal AKI causes examples
acute tubular necrosis (most common), ischemia, nephrotoxic meds/agents(NSAIDs, abx contrast dye), glomerulonephritis, pyelonephritis
postrenal aki causes
obstruction of flow; reverses when obstruction is removed
postrenal AKI causes examples
kidney stones, BPH, cystitis, uti, prostate cancer, bladder cancer, cervical cancer, colon cancer, increased tubular pressure leading to dec GFR
Initiation phase of AKI
time from event to signs of decreased renal perfusion; several hours to two days; potentially reversible
maintenance phase of AKI
BUN and creatinine increased daily, oliguria is common (UOP < 400mL per day), FVO, electrolyte imbalances and acidoses, RRT required
recovery phase of AKI
return of tubular function, 4-6 mo for BUN and creatinine to return to normal, Residual impairment of GFR.
-early dialysis may prevent the traditional diuretic phase of AKI
Assessment findings for AKI
oliguria (dec UOP)
HTN
Edema, FVO
Azotemia
SOB
Confusion
S/S of uremia
S/S dehydration
Bruising
Petechiae
s/s uremia
malaise, fatigue, disorientation, drowsiness
what should you compare with a pt who is admitted with an AKI?
baseline vs current:
Weight
Intake and output
Fluid status
Lab values
lab/diagnostic findings for AKI
-elevated serum creatinine and BUN
-BUN:creatinine ratio may be normal
- creatinine clearance=decreased
-decreased GFR
-inc potassium and sodium and phosphorus
-Dec calcium
-ABG=metabolic acidosis
-Dec H&H
fluids and electrolyte status with AKI
-hyerkalemia (d/t low excretion)
-Hyponatremia (d/t fluid retention)
-hypocalcemia(d/t low excretion)
-hypermagnesemia(d/t low excretion)
-hyperphosphatemia(d/t low excretion)
-hypocalcemia (low excretion of phosphorus, decreased level of vitamin D)
overall interventions for AKI
figure out the underlying cause and treat it!
-maintain BP and normal fluid/electrolyte status(fluids or diuretics)
-AVOID nephrotoxic agents
-nutrition
-dialysis
prerenal AKI management
early recognition is key
-fluids and electrolyte/volume replacement
-caution in those with underlying cardiac disease
-may require inotropes, antidysrhythmic agents, preload/afterload reducers, intraaortic balloon pump
-may require hemodynamic monitoring to guide tx
intrarenal AKI management
treat the infection (acute tubular necrosis, glomerularnephritis, pyelonephritis, etc).
-diet low in protein and restrictions on electrolytes
-balance fluids and electrolytes
-hemodialysis
postrenal AKI management
alleviate the obstruction
-stent may be needed
-lithotripsy
-BPH meds
-stone removal
nutrition therapy for AKI
increased rate of protein breakdown in muscles
-registered dietitian needed to calculate protein and caloric needs
-oral supplements, enteral or parenteral nutrition
-kidney specific formulations
stages of CKD
Stages 1-5