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EDIC academy > AKI (Part III) > Flashcards

AKI (Part III) Flashcards

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1
Q

Etiology of AKI ?

A

See image attached

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2
Q

AKI by aetiology ?

A

See image attached

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3
Q

Which are the highly metabolically active segments in a nephron?

A
  • Distal proximal tubules
  • Thick ascending loop

They are present at the renal-corticomedullary junction

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4
Q

Oxygen supply from cortex to medulla of the kidney ?

A

The is progressive decrease in oxygenation from cortex to medulla. Related to ;

  • Regional distribution of blood flow
  • Loop structure of vasa recta
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4
Q

The inner medulla of the kidney metabolic activity ?

A

Limited metabolic activity

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4
Q

renal-corticomedullary junction & ischaemic injury?

A

They are at highest risk of ischaemic injury & tubular necrosis - Distal proximal tubule & thick ascending limb

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5
Q

Structure of the nephron?

A

See image attached

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6
Q

Renal injury ?

A

See image attached

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7
Q

What is glomerular ultrafiltration ?

A

It is proportional to the pressure gradient between the glomerular capillary and tubular space

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8
Q

What is the mean pressure gradient driving ultrafiltration ?

A

10mmHg

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9
Q

Glomerular capillary & filtration ?

A

It is autoregulated to maintain GFR

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10
Q

Determinant of glomerular capillary pressure?

A
  • Glomerular afferent and efferent arteriole resistance
  • Systemic renal perfusion pressure
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11
Q

Afferent arterioles ?

A
  • Vasodilation causes increased GFR
  • Vasoconstriction reduces GFR (Decreased glomerular capillary pressure and renal plasma flow)
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12
Q

Efferent arterioles ?

A
  • Vasoconstriction will increase glomerular capillary pressure
  • Vasodilation will cause low pressure renal perfusion
  • Ultrafiltration is reduced
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13
Q

Effects of systemic hypotension on arterioles?

A
  • Myogenic relfex vasodilation of afferent arterioles
  • Preferential efferent vasoconstriction - (Mediated - Angiotensin & renal sympathetic innervation)
  • Both of the above act to maintain GFR & RBF
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14
Q

Glomerular and systemic haemodynamic abnormalities

A

See image attached

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15
Q

Mechanisms of loss of glomerular filtration?

A
  • Pathological activation of tubulo-glomerular feedback
  • Tubular obstruction
  • Tubular back leaks
  • Tubular stasis
  • Renal oedema
  • Altered glomerular permeability
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16
Q

Mechanism of pathological activation of tubulo-glomerular feedback ?

A
  • Tubular dysfunction with decreased reabsorption
  • Increased chloride load delivered to macula densa
  • Afferent arteriole vasoconstriction
  • Marked reduction in GFR
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17
Q

Characteristics of sustained oliguric AKI?

A
  • Tubular dilation
  • Reduction is glomerular UF gradient
  • Elevated tubule and interstitial pressures
  • Local & systemic inflammatory response
  • Fluid overload 7 raised CVP
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18
Q

Mechanism of filtration failure in established AKI ?

A

See attached image

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19
Q

Characteristics of sepsis?

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A
  • Systemic vasodilation
  • Altered macro & micro circulation
  • Difference in regional blood flow
  • Increased CO in initial stages
20
Q

The dissociation between RBF and glomerular filtration can be explained by;

Study These Flashcards
A
  • Alteration in afferent & efferent arteriolar tone
  • Decreased renal perfusion
21
Q

Renal blood flow ?

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A

Kidneys receive about 20-25% of cardiac output

22
Q

What are the principles underlying glomerular ultrafiltration?

Study These Flashcards
A
  • Proportional to pressure gradient between glomerular capillary & tubular space
  • Permeability of glomerular capillary wall
  • Colloid osmotic gradient
23
What is the mean pressure gradient driving ultrafiltration?
10mmHg
24
Glomerular capillary pressure & regulation?
Needs to be tightly autoregulated to maintain GFR.
25
What determines glomerular capillary pressure ?
- Glomerular efferent / afferent arteriolar resistance - Renal perfusion pressure
26
Factors increasing glomerular filtration?
- Vasodilation of afferent arterioles - Normal systemic blood pressure - Vasoconstriction of efferent arterioles - Restricting outflow thus increase capillary pressure
27
Factors decreasing glomerular filtration?
- Vasoconstriction of afferent arterioles - Reduction in glomerular capillary pressure - Reduction in renal plasma flow - Efferent vasodilation
28
Mechanism of autoregulation of renal perfusion in a hypotensive patient?
- Myogenic reflex vasodilation of afferent arterioles - Preferential efferent vasoconstriction - Angiotensin & renal sympathetic innervation mediated - Maintenance of RBF & GFR
29
Is its possible for the renal myogenic compensatory mechanism to fail?
Yes! If the systemic perfusion drops below a critical level . Compensatory mechanisms will fail and GFR will rapidly decline.
30
Sustained AKI is related to what renal structure?
Renal tubules
31
Which are the highly metabolically active segments of the nephron?
- Distal proximal tubule - Thick ascending limb of LoH
32
What is the location of the metabolically active segments of the nephron?
Renal cortico-medullary junction
33
The distribution of renal injury reflects the supply-demand for ?
- Oxygen - Metabolites
34
There is progressive decrease in oxygenation from cortex to medulla ?
True - Regional distribution of blood flow - Loop structure of vasa recta
35
The inner medulla has limited metabolic activity?
True
36
What structures are at high risk for ischaemic injury and tubular necrosis?
- Distal proximal tubules - Thick ascending limb
37
What are the potential causes for tubular cellular injury?
- Alteration in microvascular flow - Inflammation - Reduced oxidative stress - Exposure to nephrotoxins
38
Review the structure of the kidney?
See image attached
39
Renal response to systemic hypotension?
- Myogenic reflex vasodilatation - Afferent A - Efferent arteriole vasoconstriction - Angiotensin & renal sympathetic nerves - GFR & RBF maintained
40
What happens to the cardiac output in hyperdynamic septic shock
It is elevated
41
In hyperdynamic septic shock, CO is elevated - In the context if vasodilatation and hypotension, what happens to the arterioles ?
- Efferent arteriole vasodilatation - High flow, low pressure renal circulation - GFR uncouples from elevation in RBF
42
Upload picture of shock states of the kidney - Page 17
43
AKI suppression of glomerular filtration is the most important mechanism mediating?
Reduction in renal clearance
44
What is the mechanism of pathologic activation of tubulo-glomerular feedback mechanism?
- Tubular dysfunction - Reduced reabsorption - Increased chloride load - Macular densa - Afferent arteriole vasoconstriction - Marked reduction in GFR.
45
Characteristics of sepsis ?
- Systemic vasodilation - Altered micro & macro circulation - Heterogenicity of regional blood flow dist - Decrease in functional capillary density
46
What is the relationship between GFR & RBF and how do they dissociate ?
Alterations in the balance of efferent and afferent glomerular arteriolar tone and decreased renal perfusion pressures
47
What are the most common setting of AKi?
- Mixed inflammtory - Ishcaemic - Direct toxin mediated
48

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