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GERR > pathophysiology of Acute Kidney Disease > Flashcards

pathophysiology of Acute Kidney Disease Flashcards

1
Q

Why do patients get AKI

A
  • Sepsis

- Hypotension

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2
Q

What are the parameters used in NEWS readings?

A
  • Respiration rate
  • O2 saturation
  • Systolic BP
  • Pulse rate
  • Level of consciousness
  • Temperature
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3
Q

How can AKI be prevented?

A
  • Recognise those at risk for AKI
  • Review medication and stop any ‘bad’ drugs
  • ensure adequate hydration
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4
Q

How is renal function measured?

A
  • Urine volume per given time
  • Serum Creatinine
  • Glomerular filtration rate
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5
Q

What sample would be taken to look at GFR and serum creatinine?

A

U&E blood sample

GFR derived from serum creatinine

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6
Q

What is the relationship between serum creatinine and GFR?

A
  • Very low levels of Serum creatine will have low GFR

- However GFR needs to very low to see significant changes in serum creatinine (non-linear relationship)

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7
Q

What factors are used to estimate eGFR?

A
  • Age
  • Gender
  • Ethnicity
  • Serum Creatinine
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8
Q

What are the normal GFR fro young/older adults?

A

younger normal = 100 mL/min

Older normal = Below 100 mL/min

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9
Q

What are the markers used to measure GFR?

A
  • Creatinine
  • Cystatin C
    Special circumstances:
  • Inulin or lohexol clearance
  • Radio-isotope clearance
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10
Q

What is AKI?

A

decrease in GFR which occurs within hours to weeks and is potentially reversible

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11
Q

How is AKI recognised?

A
  • Deteriorating NEWS score
  • Rising serum creatinine
  • Falling urine output
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12
Q

How are AKIs managed/prevented?

A 
Address medication
Boost BP
Calculate fluid balance
Dip urine
Exclude obstruction
Fast-track to senior
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13
Q

What does normal kidney function depend on?

A
  • Perfusion of kidney with adequate pressure and O2
  • Intact nephrons
  • Free urinary drainage
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14
Q

What is pre-renal AKI?

A

disordered perfusion of a kidney which is structurally normal

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15
Q

What is renal AKI?

A

Damage to nephrons often after prolonged pre-renal insults

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16
Q

What is post-renal AKI?

A

urinary drainage obstruction

17
Q

What is the cause of pre-renal AKI?

A

Shock which is caused by:

  • Distributive (generalised vasodilation and decrease in peripheral resistance often caused by sepsis)
  • Hypovolaemic (loss circulating BV caused by internal or external losses)
  • Cariogenic (pump failure caused by MI, arrhythmias, valvular HF or cardiomyopathy
  • Obstructive (mechanical interference with BF caused by pulmonary embolism, cardiac tamponade or tension pneumothorax)
18
Q

How does a low GFR lead to increase in Ang II?

A
  • less glomerular filtrate entering tubules
  • less solute going through tubular lumen is sensed by macula densa cells
  • macula densa tell JGA to release renin
  • Renin increase Ang II release
19
Q

What is the benefit of increase in Ang II when a low GFR is sensed?

A
  • Ang II potent vasoconstrictor of efferent arteriole
    afferent arteriole will
  • vasodilator as a result of prostaglandins
  • These in combination will increase glomeruli capillary pressure toward normal
20
Q

What other hormone will be released as a result of renin and angiotensin II?

A
  • Aldosterone

which acts on collecting duct to increase reabsorption of sodium and chloride and water to restore BV

21
Q

What would the urine of a patient with pre-renal AKI show?

A
  • Increased tubular Na/H2O
  • Increased osmolarity
  • Increased urine specific gravity
  • Decreased urine
  • Reduced fractional excretion
22
Q

How is pre-renal kidney injury treated?

A
  • kidney function can be restored if respond rapidly as kidney still functionally intact
  • will respond well to fluids to improve BP
  • if not treated can then get renal AKI
23
Q

What is the pathology of renal AKI?

A
  • ischaemic/hypoxic renal injury impairs tubular sodium reabsorption
  • kidney structure very sensitive to hypoxia
  • function of kidney therefore compromised
  • sodium and water will not be reabsorbed and so get high levels in urine
24
Q

What will histology of renal AKI show?

A
  • lumen can’t be distinguished

- filled with cellular debris

25
Q

What are major causes of acute tubular necrosis?

A
  • Renal ischaemia followed by reperfusion (usually caused by pre-renal AKI)
  • Exposure to nephrotoxins e.g. Drugs, radio contrast dyes or heme pigments released in muscle injury
26
Q

What are the features of renal AKI?

A
  • Reduced tubular Na/H20 reabsorption
  • Reduced urine osmolarity
  • reduced S.G
  • Increased urine sodium concentration
  • Increased fractional excretion sodium
  • reduced tubular potassium and increased serum potassium
  • reduced H+ secretion and reduced HCO3- production causing metabolic acidosis
27
Q

Why should you not give fluids to patients with renal AKI?

A
  • don’t overload with infused fluid as will cause pulmonary oedema and hypoxia
  • kidneys won’t respond to fluid challenge
28
Q

Causes of Post-Renal AKI?

A

Obstruction:

  • within lumen e.g. renal calculi
  • within wall e.g. benign prostatic hyperplasia
  • outside wall e.g. tumour invading ureters
29
Q

How should post-renal AKIs be treated?

A
  • exclude/relieve obstruction (rule out urinary retention and if catheter present check functioning)
  • Obstruction may still be present above the level of bladder output
  • treat underlying cause of obstruction
  • prevent or treat any infections
30
Q

What scan can be used to check for a post-renal AKI?

A

ultrasound

31
Q

What other form of AKI is possible (not post, renal or pre)

A
  • AKI in patients with CKD
32
Q

What can kill patients with AKI?

A
  • Pulmonary oedema and respiratory failure
  • Hyperkalaemia causing arrhythmias due to loss of capacity of kidneys to excrete potassium (seen on ECG)
  • Acidosis caused by no H+ excretion
33
Q

What should be done if kidney do fail?

A
  • balance fluid carefully, monitor intake and urine output
  • avoid unnecessary drugs
  • treat hyperkalemia
  • seek senior help
34
Q

What AKI type is dialysis used for?

A

Put onto dialysis until renal function improves

35
Q

What investigations should be done for someone with AKI?

A
  • urine dipstick
  • U&E
  • ABG
  • ECG
  • CXR
  • Ultrasound
36
Q

What should be asked in the history of AKI?

A
  • prior CKD
  • Fluid losses
  • Thirst
  • Nephrotoxins
37
Q

What should be examined in patients with AKI?

A
  • Pulse
  • BP
  • O2 sats
  • urine output

GERR (49 decks)

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