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Health.1 > AKI > Flashcards

AKI Flashcards

1
Q

What is the definition of acute kidney injury?

A

a rapid (hours to days) decline in kidney function

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2
Q

What parameters are used to differentiate between different stages of AKI?

A
  • creatinine increase

- urine output

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3
Q

What units are used for urine output?

A

ml/kg/hr

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4
Q

What units are used for creatinine?

A

μmol/L

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5
Q

What is the creatinine level increase for stage 1 AKI?

A

26μmol/L or 50-100% increase

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6
Q

What is the urine output for stage 1 AKI and in what timeframe?

A

<0.5ml/kg in 6 hours

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7
Q

What is the urine output for stage 2 AKI and in what timeframe?

A

<0.5ml/kg in 12 hours

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8
Q

What is the creatinine level increase for stage 2 AKI?

A

100-200%

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9
Q

What is the creatinine level increase for stage 2 AKI?

A

100-200%

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10
Q

What is the creatinine level increase for stage 3 AKI?

A
  • > 354μmol/L increase (if baseline <310) OR
  • > 200% increase OR
  • needs dialysis
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11
Q

What is the urine out for stage 3 AKI and in what timeframe?

A

<0.3ml/kg in 24 hours OR anuric (needs dialysis) OR anuric for 12 hours

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12
Q

Which of the AKI stages shows the worst renal function?

A

stage 3

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13
Q

What is the mortality rate for hospitalised patients with AKI?

A

26.3%

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14
Q

AKI serum creatinine is used as measure of what?

A

function NOT eGFR

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15
Q

How does hospital/ITU stay change with worsening renal function?

A

increases

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16
Q

What are the 3 main risk factors for AKI?

A
  • older age
  • disease states
  • drugs
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17
Q

What conditions are a risk factor for AKI?

A
  • diabetes mellitus
  • liver disease
  • heart disease
  • hypertension
  • chronic kidney disease
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18
Q

What drugs are a risk factor for AKI?

A
  • diuretics
  • ACE inhibitors
  • ARBs
  • NSAIDs
  • vancomycin
  • gentamicin
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19
Q

What are the 3 categories of AKI causes?

A
  • pre-renal
  • (intra-)renal
  • post-renal
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20
Q

What is pre-renal AKI caused by?

A

perfusion failure - blood flow to kidneys

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21
Q

What is intra-renal AKI caused by?

A

intrinsic disease of the kidney

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22
Q

What is post-renal AKI caused by?

A

urinary obstruction

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23
Q

What is the most common category cause of AKI?

A

intra-renal

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24
Q

What can cause the perfusion failure responsible for pre-renal AKI?

A
  • hypovoloemia
  • hypotension
  • renal artery occlusion
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25
Q

What can cause hypovolaemia?

A
  • diarrhoea
  • vomiting
  • haemorrhage
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26
Q

What drugs can worsen the perfusion failure responsible for pre-renal AKI?

A
  • any drugs that block the RAAS system
  • diuretics
  • NSAIDs
  • antihypertensives
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27
Q

What is meant by renal autoregulation?

A

the kidneys are able to maintain adequate perfusion and urine output despite an increase or decrease in blood pressure

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28
Q

When the BP and blood volume goes outside the range of renal autoregulation, what happens?

A

perfusion failure, as well as low urine output

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29
Q

diagram outlining how the RAAS system works

A

diagram should have:

  • renin produced by juxtaglomerular cells of kidneys in response to low BP/salt depletion
  • renin converts angiotensinogen to angiotensin I
  • angiotensin I converted by ACE to angiotensin II
  • ang II acts on brain to increase thirst, adrenal cortex to release aldosterone and vascular smooth muscle to cause vasoconstriction and efferent arteriolar constriction
  • aldosterone acts on kidneys to increase Na retention and sodium excretion
  • brain and kidney actions lead to increase in blood volume
  • vascular smooth muscle actions lead to increase in blood pressure
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30
Q

What does ang II do to afferent and efferent arterioles of the kidney? What does this cause?

A
  • causes vasoconstriction at efferent
  • causes vasoconstriction at afferent (but stimulates release of vasodilator NO2 so it stays dilated)

–> increase in blood pressure

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31
Q

What do prostaglandins do to the afferent arterioles in the kidney? What does this cause?

A
  • causes vasodilation

- causes an increase in kidney perfusion

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32
Q

Which do NSAIDs affect: the afferent arteriole or the efferent arteriole? What is the result?

A
  • affect afferent arteriole
  • block prostaglandin’s vasodilation of afferent arteriole
  • leads to reduced kidney perfusion
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33
Q

Which do ACEi/ARBs affect: the afferent or efferent arteriole? What is the result?

A

affect on both….
AA: block prostaglandin’s vasodilation of afferent arteriole
- leads to reduced kidney perfusion

EA: stop the vasoconstriction of the efferent leading to a reduction in BP needed to for ultrafiltration of the kidneys

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34
Q

Why does RAAS blockade lead to AKI?

A

lack of ability to compensate for BP drop

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35
Q

Perfusion failure can have consequences on the kidney nephron. What is this consequence?

A

acute tubular necrosis
-when the cells in the kidneys are not getting enough nutrients or fluid, - very low BP, so suffer damage

can be drug related etc

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36
Q

What are the treatment options of perfusion failure?

A

treat underlying cause

  • fluid volume replacement
  • blood pressure support (inotropic drugs)
  • restore arterial patency
  • stop RAAS blockade
  • stop NSAID
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37
Q

In what two ways can drugs be toxic to the kidneys? and cause AKI

A
  • if their serum levels are too high: monitor!

- if they crystallise in the tubules

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38
Q

What drugs can be toxic by having their serum levels too high?

A
  • gentamicin

- vancomycin

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39
Q

What drugs are toxic by being able to crystallise in the tubules?

A
  • aciclovir (synthetic nucleoside analogues)
  • indinavir
  • sulfadiazine

IV, can cause nephrotoxicity quickly

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40
Q

What is nephrocalcinosis?

A

calcium and phosphate deposition in the kidneys

41
Q

What can nephrocalcinosis be caused by?

A
  • sodium phosphate enemas, infusions can cause a massive phosphate load
  • OTC calcium antacids can deposit Ca and alkali
42
Q

What would be seen on a nephrocalcinosis X-ray?

A

the kidneys (which normally wouldn’t be visible) clogged up with Ca and P deposits

43
Q

What 3 drugs need monitoring in the context of AKI and why?

A
  • gentamicin
  • amikacin
  • vancomycin
  • they all have narrow therapeutic indexes and can damage the kidneys
    aminoglycoside: given 1x daily, monitored diff to those
44
Q

What are the adverse effects of gentamicin?

A
  • epithelial necrosis
  • glomerular toxicity
  • vascular toxicity
45
Q

What is interstitial nephritis?

how to treat/prevent?

A

the kidney having an ‘allergic’ reaction to a drug

unpredicatble but can prevent by cautious use. can cause AKI

46
Q

What 5 drugs is interstitial nephritis common with?

A
  • NSAIDs
  • Proton pump inhibitors
  • 5-aminosalicylates
  • other antibiotics
  • anti-retroviral drugs
47
Q

What is metformin used to treat?

A

type 2 diabetes mellitus

48
Q

How can metformin cause lactic acidosis?

A
  • reduces gluconeogenesis
  • decreased conversion of lactate to pyruvate
  • leads to lactate build-up
49
Q

Why should AKI patients not be treated with metformin?

A

damaged kidneys will not be able to remove lactate/pyruvate

50
Q

What drugs have reduced clearance in AKI?

A
  • penicillins
  • opiates
  • benzodiazepines
  • insulin (can cause hypoglycaemia)
  • aminoglycosides (increased tox and reduced clearance)
51
Q

in AKI, how can insulin cause hypoglycaemia?

A

increased levels… inc hypogly event risk, short term harm

as kidneys usually excrete insulin

52
Q

what else may lead to increased pyruvate (lactic acidosis and metformin)

A

sepsis

53
Q

What are the causes of death in AKI?

A
  • infection
  • pulmonary oedema
  • underlying disease
  • hyperkalaemia
  • acidosis
54
Q

In dialysis, what may be removed/added from the patient’s blood?

A

fluids and solutes

55
Q

Does dialysis occur inside or outside of the body? What special term is used to describe this?

A
  • outside the body

- extracorporeal

56
Q

What is dialysis?

A

an extracorporeal therapy where the patient’s blood and dialysis fluid is separated by a semi-permeable membrane

57
Q

What is used between the patient’s blood and dialysis fluid in dialysis?

A

a semi-permeable membrane

58
Q

How does the GFR rate compare between dialysis and the own kidneys?

A

dialysis is not as good as real kidneys; only has a GFR of <15mls/min

59
Q

What determines the permeability of semi-permeable membranes?

A
  • size of membrane

- charge of membrane

60
Q

How do the semi-permeable membranes compare between haemodialysis and peritoneal dialysis?

A

haemodialysis: external device

peritoneal dialysis: peritoneum

61
Q

What process determines how drugs are cleared?

A

diffusion: high to low conc

62
Q

In peritoneal dialysis, what is used to gain entry into the abdomen?

A

a peritoneal catheter

63
Q

How long is fluid left in before it’s drained in peritoneal dialysis?

A

30 mins

64
Q

How is peritoneal dialysis performed?

A
  • dialysis fluid inserted into abdomen via catheter
  • fluid left to dwell for 30 min
  • fluid drained into collection bag
65
Q

How often a day can peritoneal dialysis be performed?

A

up to 20 times

66
Q

Why is peritoneal dialysis favourable for some patients as opposed to haemodialysis?

A

can be done at home

67
Q

Peritoneal dialysis can lead to the loss of what macromolecule? Why?

A
  • proteins

- peritoneum allows albumin and other plasma proteins through

68
Q

What are the two options for the time of day that peritoneal dialysis can be performed?

A
  • continuous during the day

- overnight

69
Q

How long does peritoneal dialysis last?

A

~8-10 years

70
Q

What is there a risk of with peritoneal dialysis?

A

peritonitis

71
Q

Haemodialysis and peritoneal dialysis both require permanent access to different parts of the body. What does haemodialysis require permanent access to?

A

the circulation

72
Q

What are two possible ways permanent access to the circulation is gained in haemodialysis?

A
  • AV fistula

- central venous catheter

73
Q

How often is haemodialysis carried out and for what condition?

A
  • 3x a week

- CKD5, or severe AKI

74
Q

How long does each haemodialysis session last for?

A

4 hours

75
Q

How long can haemodialysis last?

A

as long as there is permanent access to the circulation

76
Q

Explain the journey of the blood in haemodialysis.

A
  • leaves patient’s vein
  • enters dialysis machine via blood pump
  • thinned via heparin pump
  • waste from the plasma leaves at dialysis filter
  • dialysate fluid enters at dialysis filter
  • blood re-enters patient’s vein
77
Q

whats there a risk of with haemodialysis?

A

infection

78
Q

Patients with what two conditions need dialysis?

A
  • CKD

- AKI

79
Q

What GFR in CKD the need for dialysis?

A

<10ml/min/1.73m^2

depends on symtoms and fluid volume control

80
Q

Before what in patients with CKD is dialysis initiated?

A

before the patient becomes ill

81
Q

What creatinine levels in AKI and level of urination is required to initiate dialysis?

A

> 500mcmol/L

  • or oligo/anuric
    = low urine output/ lack of urine produced
82
Q

What condition due to AKI initiates dialysis?

what mat are complications of this? (2)

A

uraemia (buildup of toxins in your blood)

  • pericarditis
  • encephalopathy
83
Q

The following signal the initiation of AKI if they’re not controlled medically. What are they?

A
  • hyperkalaemia
  • metabolic acidosis
  • pulmonary oedema
84
Q

Why does AKI cause hyperkalaemia?

treatment?

A
  • reduced urinary excretion
  • increased intracellular K+ release

want to improve K before dialysis.
if results in inc K, treat using insuling dextrose, dialyse after so K made safe.

85
Q

In dialysis, what will the clearance of a drug depend on?

A
  • nature of the drug: solubility, size, charge
  • nature of the membrane: size, charge
  • non-renal and renal metabolism
  • type of dialysis
  • duration of dialysis
  • drug distribution
86
Q

what should be done with metabolic acidosis- when its causing AKI?
when?

A

manage bicarbonate
IV/ orally
before dialysis

87
Q

What is the drug class of vancomycin?

A

glycopeptide antibiotic

88
Q

What type of therapeutic window does vancomycin have?

A

narrow

89
Q

How much vancomycin is excreted unchanged by the kidneys?

A

90%

90
Q

What is the half-life of vancomycin

a) normally?
b) in CKD5?
c) with no kidneys?
d) in haemodialysis?

A

a) 4-6 hours
b) 54-180 hours
c) 7.5 days
d) 6 hours (high flux) to 7 days (standard)

91
Q

How do the plasma levels of vancomycin change during haemodialysis treatment?

A

they drop, maybe even below the MIC (minimum inhib conc)

- want ABOVE MIC, steady line

92
Q

Dialysis helps to maintain the homeostasis of what? (3)

A
  • fluid
  • acid-base
  • electrolyte
93
Q

How/ when must vancomycin be dosed in haemodialysis?

A

it needs to be dosed after haemodialysis due to the plasma levels dropping after a session

94
Q

dialysis access to circulation: 2 types?

A

Arterio-Venous Fistula

  • Superficial vein used.
  • Local/general anaethetic.
  • 6 weeks for healing

Central venous catheter
- Risk of infection, thrombosis, sclerosis.
350ml/min or more capable

95
Q

Diffusion in haemodialysis semi-permeable memb allows what?

A

equilibrium and transfer.

96
Q

what does semi-permeable allow.
describe processes of blood movement and water?

(how is AMOUNT of water controlled)?

A
  • blood cells and large components remain in blood
  • Ultrafiltration- water removal
    Water takes some solutes. Reduction of volume in patient circulation

Pressure gradient created: causes water movement. By changing this, can control HOW MUCH WATER removed

97
Q

Acid load cant be removed by filtration alone, whats added to patient from dialysis soln?

what does it allow?

A

Alkali (buffer) added
o Conc of alkali greater than in plasma
o Alkalis used: bicarbonate, acetate, or lactate
o Acetate and lactate: metabolised to bicarbonate

Allows correction of metabolic acidosis

98
Q

How to choose type of Dialysis

A

• Patient decision made on lifestyle factors
• Haemodialysis better for:
oDependant patients
oPatients who previously had peritoneal dialysis

99
Q

Complications of ahemodialysis?

A

Repeated access to circulation and/or permanent intra-vascular catheters
- Increased risk of infection

Hypotension caused by rapid fluid removal

Vascular damage (central vein occlusion) caused by repeated access procedures

Risk of blood borne virus
- May be risk for patients dialysing on holiday outside UK esp. HBV endemic areas

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