Acute Kidney Injury (Acute Renal Failure) Flashcards

1
Q

define acute kidney injury

A

acute kidney injury represents a rapid decline in kidney function that happens within a few hours or within a day.
it causes a build up of nitrogenous waste products and impairs fluid and electrolyte balance.

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2
Q

list types of acute kidney injury and include causes for each type
pre-renal acute kidney injury

What’s happening in the blood/vascular space??

A

prerenal-acute kidney injury: characterized by a marked decrease in renal blood flow.
causes: profound depletion of vascular volume (hemorrhage, loss of extracellular fluid volume), impair perfusion because of heart failure and cardiogenic shock, and decreased vascular filling because of increased vascular capacity (anaphylaxis or sepsis).

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3
Q

list types of acute kidney injury and causes for each

intra-renal acute kidney injury

A

results from conditions that cause damage to structures within the kidney.
causes: prerenal AKI, toxic insult to the tubular structures of the nephron, intratubular obstruction.
Acute glomerulonephritis, acute pyelonephritis are also causes of intra-renal acute kidney injury.

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4
Q

list types of acute kidney injury and the causes

post-renal AKI

A

results from obstruction of urine outflow from the kidneys.

causes can include: calculi and strictures, tumors or neurogenic bladder, prostatic hyperplasia.

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5
Q

define prerenal AKI and explain how conditions of decreased cardiac output can cause a pre-renal AKI

A

definition: an acute kidney injury characterized by a marked decrease in renal blood flow.

if there is no blood flow from the heart to go throughout the body and perfuse the kidneys, then a prerenal AKI could occur.

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6
Q

differentiate ischemic acute tubular necrosis from nephrotoxic ATN.

A

ischemic ATN occurs most frequently in people who have extensive surgery, severe hypovolemia, overwhelming sepsis, trauma, or burns.

nephrotoxic ATN occurs when a nephrotoxic drug decreases renal perfusion and/or causes tubular injury.

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7
Q

outline the four phases of AKI

A

onset phase: hours or days, time it takes the onset of the precipitating event until tubular injection occurs.

oliguric phase:
8-14 days or longer, marked decrease in GFR–>sudden retention of endogenous metabolites (urea, potassium, sulfite, and creatinine). Urine output lowest. Fluid retention–edema, water intoxication, pulmonary congestion. uremia can occur–BAD if untreated–seizures and death. hyperkalemia will happen but not symptomatic unless 6-6.5 or above.

diuretic phase: kidneys are trying to heal, so urine output increases, but tubule scarring and damage occur. BUN, serum creatinine, potassium and phosphate levels remain elevated/continue to rise. GFR increases, urine output increases to 400 mL/day, electrolytes are possibly depleted.

recovery phase: Tubular edema resolves, renal function improves. Normalized function of fluid and electrolyte balance. renal tubular function is eventually restored. BUN and creatinine return to normal, GFR returns to 70-80% normal. Mild to moderate kidney damage can still persist.

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8
Q

explain how the BUN/creatinine ratio is helpful in diagnosis

A

The BUN/Creatinine ratio is useful in the differential diagnosis of acute or chronic renal disease. Reduced renal perfusion, e.g. congestive heart failure or recent onset of urinary tract obstruction, will result in an increase in BUN/Creatinine ratio.

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9
Q

differentiate between the BUN and creatinine lab tests

A

creatinine: serum creatinine reflects the glomerular filtration rate (GFR)–how much is getting put out.

BUN: A blood urea nitrogen (BUN) test measures the amount of urea nitrogen in your blood–how much waste is being eliminated.

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10
Q

describe the impact of aging on risk AKI

A

Elderly patients are at risk of AKI due to decreased renal reserve and altered kidney function inhibiting kidney function recovery following acute injury.

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11
Q

explain how prevention and early diagnosis would impact treatment of AKI.

A

prevention and early diagnosis would help treatment be less aggressive and invasive, and could help reverse the effects of AKI.

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12
Q

relate how azotemia and GFR indicate AKI

A

azotemia: an accumulation of nitrogenous wastes in the blood indicates AKI. These wastes are: urea nitrogen, uric acid, and creatinine)

GFR: a decreased GFR indicates AKI

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