Urology Flashcards
What is an AKI? What is its effect on homostasis. How is it measured?
A rapid reduction in kidney function over hours to days leading to a failure to maintain fluid, electrolyte and acid base balance. Measured by serum urea and creatine
What are the defining chemical changes in AKI? Over what timeframe
Rise in creatinine by more than 26micromoles/L in 48 hours Risk in creatinine by 1.5 baseline (lowest within 3 months) within one week (known or presumed) Urine output
Risk factors for aki
Age Ckd Chf Liver disease Pvd Dm Sepsis Drugs Poor fluid intake / increased loss Urinary symptoms
What drugs are nephrotoxic increasing aki risk?
Nsaids Acei Arbs Gentamycin Iodine contrast
How is AKI graded?
Stage 1 - as diagnostic criteria Stage 2 - rise 2 to 2.9 baseline or 3 baseline or >345 or RRT needed or
What are the three sub classifications of AKI?
Prerenal Renal Post renal
What are causes of pre renal AKI? What drugs may worsen it?
Shock/volume depletion (CHF, hypovolaemia, sepsis, dehydration etc.) Renal artery stenosis AAA Hepatorenal syndrome ACEi or NSAIDs
Why do ACEi cause AKI when given to a patient with renal artery stenosis?
Angiotensin II causes vasoconstriction of afferent and efferent arterioles in the kidney. In renal artery stenosis the afferent already has low flow so GFR is maintained by efferent constriction. ACEi stops efferent constriction via decreased ang II thus decreases GFR
What effect does prerenal AKI have on kidney function?
Decreased GFR Active reabsorption of Na (as high renin thus high angiotensin II due to poor perfusion) so low amount of Na passed in urine
How should pre renal AKI be treated?
Fluid replacement Treat underlying cause Stop nephrotoxic drugs, especially NSAIDs and ACEi
What are the four broad catagories of renal AKI cause?
Tubular Glomerular Interstitial Vascular
What is the general term for and what are causes of tubular renal aki?
Acute tubular necrosis Any cause of prerenal with progression Diuretics Myoglobinuria Haemoglobinuria Endotoxins Radiological contrast agents Nephrotixic drugs - aminoglycosides, acei, nsaids Poisons - weedkiller, antifreeze Preeclampsia and eclampsia
What is the pathology behind acute tubular necrosis
Ischemia or toxic insult to tubular cells causing damage Low atp in cells Decreased reabsorption due to na/katpase dysfunction and bleb formation blocking reabsorption so more sodium to macula densa so less gfr due to afferent arteriole constriction (Tubularglomerular feedback) Increased tubular hydrostatic pressure (backleak of filtrate) decreases gfr Obstruction of tubules by debris decreases gfr
What would help differentiate prerenal aki from acute tubular necrosis - test and clinical sign?
Fraction of excreted sodium high in atn Poor response to fluids with oedema
How may urine output change over the course of acute tubular necrosis? How long does it last?
Early - oliguria Late - polyuria as defective reabsorption despite low gfr Usually around 1-3 weeks post initial insult but can be up to 6