Acute Kidney Injury: Pathophysiology & Response - Edubirdie

University:
Western Sydney University
Course:
MEDI 2003 | Clinical Sciences 2
Academic year:

2024
Views:

292

Pages:

2
Author:

Mariam A. A.

AKI Subtitles: Define AKI. Understand different subtypes. Understand progressive effects on renal hypoperfusion causing renal then renal AKI. Understand the basis for clinical assessment of AKI & basic treatment. See mechanism & pathogenesis & pathophysiology. Why AKI is important? Systemic Response to Low Perfusion States. Graded Renal Response to Low Perfusion. Nodes and Text: Definition: AKI is related to renal injury and can be reversible. Based on either Cr or oliguria. Systemic Response to Low Perfusion States: Total organs over non-vital. ↑ cardiac contractility. ↓ L ventricular EF. Systemic arteriolar vasoconstriction. Graded Renal Response to Low Perfusion: Attempt to maintain GFR. Turn off GFR → pressure tubules. Renal necrosis (ATN). Cortical necrosis. Permanent damage. Renal Adaptations in Pre-Renal Phase Subtitles: Myogenic Reflex. Role of RAAS. Ischemia. Post-Renal AKI. Nodes and Text: Myogenic Reflex: Renal autoregulation changes to are of self-preservation. Role of RAAS: Is assisted by pg. Ischemia: Kidneys need to turn off GFR to ischemia. Reninina + fluid loss of salt & water reabsorption impaired. Oliguria: <400-800 mL/day. Pre-renal AKI: ↓ GFR, ↑ creatinine, oliguria, ↓ Na+ & K+. Post-Renal AKI: Unilateral complete obstruction of ureter. Loss of renal function on ipsilateral side. Hyperkalemia on opposite side. Small changes in Cr, GFR, & UO. Duration >2 weeks vs. incomplete stenosis. Only causes AKI if it's bilateral obstruction of ureter. Complete obstruction causes progressive & potentially reversible damage. Renal functional capacity affected early due to tubular damage. Full recovery of renal function after 12 weeks.

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