AKI (Part III) Flashcards
Etiology of AKI ?
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AKI by aetiology ?
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Which are the highly metabolically active segments in a nephron?
- Distal proximal tubules
- Thick ascending loop
They are present at the renal-corticomedullary junction
Oxygen supply from cortex to medulla of the kidney ?
The is progressive decrease in oxygenation from cortex to medulla. Related to ;
- Regional distribution of blood flow
- Loop structure of vasa recta
The inner medulla of the kidney metabolic activity ?
Limited metabolic activity
renal-corticomedullary junction & ischaemic injury?
They are at highest risk of ischaemic injury & tubular necrosis - Distal proximal tubule & thick ascending limb
Structure of the nephron?
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Renal injury ?
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What is glomerular ultrafiltration ?
It is proportional to the pressure gradient between the glomerular capillary and tubular space
What is the mean pressure gradient driving ultrafiltration ?
10mmHg
Glomerular capillary & filtration ?
It is autoregulated to maintain GFR
Determinant of glomerular capillary pressure?
- Glomerular afferent and efferent arteriole resistance
- Systemic renal perfusion pressure
Afferent arterioles ?
- Vasodilation causes increased GFR
- Vasoconstriction reduces GFR (Decreased glomerular capillary pressure and renal plasma flow)
Efferent arterioles ?
- Vasoconstriction will increase glomerular capillary pressure
- Vasodilation will cause low pressure renal perfusion
- Ultrafiltration is reduced
Effects of systemic hypotension on arterioles?
- Myogenic relfex vasodilation of afferent arterioles
- Preferential efferent vasoconstriction - (Mediated - Angiotensin & renal sympathetic innervation)
- Both of the above act to maintain GFR & RBF
Glomerular and systemic haemodynamic abnormalities
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Mechanisms of loss of glomerular filtration?
- Pathological activation of tubulo-glomerular feedback
- Tubular obstruction
- Tubular back leaks
- Tubular stasis
- Renal oedema
- Altered glomerular permeability
Mechanism of pathological activation of tubulo-glomerular feedback ?
- Tubular dysfunction with decreased reabsorption
- Increased chloride load delivered to macula densa
- Afferent arteriole vasoconstriction
- Marked reduction in GFR
Characteristics of sustained oliguric AKI?
- Tubular dilation
- Reduction is glomerular UF gradient
- Elevated tubule and interstitial pressures
- Local & systemic inflammatory response
- Fluid overload 7 raised CVP
Mechanism of filtration failure in established AKI ?
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