Acute Kidney Injury 3 Flashcards
What are the main causes of prerenal AKI?
Hypovolemia, hypervolemia with decreased effective circulating volume, and hypotension.
What are examples of hypovolemic causes of prerenal AKI?
Hemorrhage, GI losses (vomiting, diarrhea), urinary or cutaneous losses.
What conditions cause hypervolemia with decreased effective circulating volume in prerenal AKI?
Nephrotic syndrome, cardiac dysfunction, and liver disease.
What types of shock can lead to prerenal AKI?
Septic and myocardial shock.
How does the body respond to decreased renal perfusion?
Increased sympathetic tone, and hormonal responses such as renin, angiotensin II, aldosterone, and ADH release.
What role do prostaglandins play in prerenal AKI?
They cause afferent arteriole dilation to maintain GFR.
How does angiotensin II affect renal arterioles?
It constricts efferent arterioles to preserve GFR.
Is the renal structure intact in prerenal AKI?
Yes, the glomeruli, interstitium, and tubular structures remain intact.
What happens if hypoperfusion persists in prerenal AKI?
It may progress to intrinsic AKI.
What are key historical features of prerenal AKI?
Hemorrhage, vomiting, diarrhea, fever, weight loss, and decreased urine output.
What physical signs indicate dehydration or hypoperfusion in prerenal AKI?
Tachycardia, hypotension, poor skin turgor, dry mucous membranes, sunken eyes/fontanelle, and prolonged capillary refill (>2 seconds).
What physical finding suggests nephrotic syndrome, cardiac dysfunction, or liver disease in prerenal AKI?
Edema.
What BUN-to-creatinine ratio suggests prerenal AKI?
Greater than 20.
What is the typical urine specific gravity in prerenal AKI?
Greater than 1.020.
What is the typical urine osmolality in prerenal AKI?
Greater than 500 mOsm/kg.