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EDIC academy > AKI (Part III) > Flashcards

AKI (Part III) Flashcards

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?

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;

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

Renal blood flow ?

A

Kidneys receive about 20-25% of cardiac output

22
Q

What are the principles underlying glomerular ultrafiltration?

A
  • Proportional to pressure gradient between glomerular capillary & tubular space
  • Permeability of glomerular capillary wall
  • Colloid osmotic gradient
23
Q

What is the mean pressure gradient driving ultrafiltration?

24
Q

Glomerular capillary pressure & regulation?

A

Needs to be tightly autoregulated to maintain GFR.

25
Q

What determines glomerular capillary pressure ?

A
  • Glomerular efferent / afferent arteriolar resistance
  • Renal perfusion pressure
26
Q

Factors increasing glomerular filtration?

A
  • Vasodilation of afferent arterioles
  • Normal systemic blood pressure
  • Vasoconstriction of efferent arterioles
  • Restricting outflow thus increase capillary pressure
27
Q

Factors decreasing glomerular filtration?

A
  • Vasoconstriction of afferent arterioles
  • Reduction in glomerular capillary pressure
  • Reduction in renal plasma flow
  • Efferent vasodilation
28
Q

Mechanism of autoregulation of renal perfusion in a hypotensive patient?

A
  • Myogenic reflex vasodilation of afferent arterioles
  • Preferential efferent vasoconstriction - Angiotensin & renal sympathetic innervation mediated
  • Maintenance of RBF & GFR
29
Q

Is its possible for the renal myogenic compensatory mechanism to fail?

A

Yes!
If the systemic perfusion drops below a critical level . Compensatory mechanisms will fail and GFR will rapidly decline.

30
Q

Sustained AKI is related to what renal structure?

A

Renal tubules

31
Q

Which are the highly metabolically active segments of the nephron?

A
  • Distal proximal tubule
  • Thick ascending limb of LoH
32
Q

What is the location of the metabolically active segments of the nephron?

A

Renal cortico-medullary junction

33
Q

The distribution of renal injury reflects the supply-demand for ?

A
  • Oxygen
  • Metabolites
34
Q

There is progressive decrease in oxygenation from cortex to medulla ?

A

True

  • Regional distribution of blood flow
  • Loop structure of vasa recta
35
Q

The inner medulla has limited metabolic activity?

36
Q

What structures are at high risk for ischaemic injury and tubular necrosis?

A
  • Distal proximal tubules
  • Thick ascending limb
37
Q

What are the potential causes for tubular cellular injury?

A
  • Alteration in microvascular flow
  • Inflammation
  • Reduced oxidative stress
  • Exposure to nephrotoxins
38
Q

Review the structure of the kidney?

A

See image attached

39
Q

Renal response to systemic hypotension?

A
  • Myogenic reflex vasodilatation - Afferent A
  • Efferent arteriole vasoconstriction
  • Angiotensin & renal sympathetic nerves
  • GFR & RBF maintained
40
Q

What happens to the cardiac output in hyperdynamic septic shock

A

It is elevated

41
Q

In hyperdynamic septic shock, CO is elevated - In the context if vasodilatation and hypotension, what happens to the arterioles ?

A
  • Efferent arteriole vasodilatation
  • High flow, low pressure renal circulation
  • GFR uncouples from elevation in RBF
42
Q

Upload picture of shock states of the kidney - Page 17

43
Q

AKI suppression of glomerular filtration is the most important mechanism mediating?

A

Reduction in renal clearance

44
Q

What is the mechanism of pathologic activation of tubulo-glomerular feedback mechanism?

A
  • Tubular dysfunction
  • Reduced reabsorption
  • Increased chloride load - Macular densa
  • Afferent arteriole vasoconstriction
  • Marked reduction in GFR.
45
Q

Characteristics of sepsis ?

A
  • Systemic vasodilation
  • Altered micro & macro circulation
  • Heterogenicity of regional blood flow dist
  • Decrease in functional capillary density
46
Q

What is the relationship between GFR & RBF and how do they dissociate ?

A

Alterations in the balance of efferent and afferent glomerular arteriolar tone and decreased renal perfusion pressures

47
Q

What are the most common setting of AKi?

A
  • Mixed inflammtory
  • Ishcaemic
  • Direct toxin mediated

EDIC academy (19 decks)

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