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Renal/Urology > Lecture 14 - Acute Kidney Injury > Flashcards

Lecture 14 - Acute Kidney Injury Flashcards

1
Q

What was the traditional definition of acute renal failure?

A

Rapid loss of glomerular filtration and tubular function over hours to days
(leading to retention of urea/creatinine and oliguria)

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2
Q

What is the current definition of acute renal failure based off of?

A

KDIGO

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3
Q

Define acute renal failure by the KDIGO definition

A

Increase in serum creatinine by >=26.5micromol/l (0.3mg/dl) within 48 hours or >=1.5x baseline which is known/presumed to have occurred within the last 7 days
Urine volume <0.5ml/kg/h for 6 hours

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4
Q

Define AKI stage 1

A

Serum creatinine:
- 1.5-1.9x baseline OR >=26.5 micromol/l increase

Urine output:
- <0.5ml/kg/h for 6-12h

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5
Q

Define AKI stage 2

A

Serum creatinine:
- 2-2.9x baseline

Urine output:
- <0.5ml/kg/h for 12h or more

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6
Q

Define AKI stage 3

A

Serum creatinine:
- 3x baseline OR >=354 micromol/l increase OR initiation of RRT

Urine output:
- <0.3ml/kg/h for 24h or more or anuria for 12h or more

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7
Q

1 in ____ hospital admissions are complicated by AKI

A

7

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8
Q

What are the immediately dangerous consequences of AKI?

A 
AEIOU
Acidosis
Electrolyte imbalance
Intoxication (TOXINS)
Overload
Uraemic omplications

Death and dialysis

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9
Q

What are the 3 types of AKI?

A

Pre-renal
Renal/intrinsic
Post-renal

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10
Q

What are pre-renal causes of AKI due to problems with?

A

Problems with blood flow to the kidneys

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11
Q

What are renal causes of AKI due to?

A

Damage to the renal parenchyma

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12
Q

What are post-renal causes of AKI due to?

A

Obstruction to urine exit –> backing up and affecting normal kidney function

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13
Q

What are pre-renal causes of AKI?

A 
Sepsis
Hypovolaemia (e.g. haemorrhage, burns, vomiting, diarrhoea, diuretics)
Hepatorenal syndrome
Cardiac failure
Hypotension, e.g. due to meds
Arterial occlusion
Vasomotor - e.g. NSAIDs/ACEi
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14
Q

What are intrinsic causes of AKI?

A

Acute tubular necrosis
Acute interstitial nephritis (many causes incl. drugs, e.g. PPIs)
GN
Myeloma
Intrarenal vascular obstruction (vasculitis, thrombotic micoangiopathy)
Toxin related - drugs (aminoglycosides, radiocontrast, rhabdomyolysis, snake venom, mushrooms etc.)

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15
Q

What are causes of post-renal AKI?

A

Intraluminal - kidney stones, clots, sloughed papilla
Intramural - malignancy, ureteric stricutre, radiation fibrosis, BPH
Extramural -retroperitoneal fibrosis, malignancy

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16
Q

What is the most common cause of AKI?

A

Pre-renal (e.g. hypotension/hypovolaemia) –> insufficient plasma flow, if treated promptly can resolve, if not can lead to acute tubular necrosis

(which is exacerbated by toxic drugs)

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17
Q

Why are the kidneys particularly susceptible to hypoperfusion?

A

Highly metabolic with all the activity

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18
Q

What are the three phases of ATN?

A

Initiation
Maintenance
Recovery

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19
Q

What is involved in the initiation phase of ATN?

A

Exposure to toxic/ischaemic insult
Renal parenchymal injury evolving
But reversible

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20
Q

What is involved in the maintenance phase of ATN?

A

Established parenchymal injury
Maximally oliguric
Lasts 1-2 weeks

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21
Q

What is involved in the recovery phase of ATN?

A

Gradual increase in urine output

Fall in serum creatinine

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22
Q

If in ATN the gFR recovers quicker than the tubule resorptive capacity what may occur?

A

Excessive diuresis (post-obstructive natriuresis)

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23
Q

What is radiocontrast nephropathy?

A

AKI follow administration of iodinated contrast agent

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24
Q

How does radiocontrast nephropathy tend to present?

A

As transient renal dysfunction usually resolving after 72h

May lead to permanent loss of function

25
Q

What are risk factors for radiocontrast nephropathy?

A 
DM
Renovascular disease
Impaired renal function
Paraprotein 
High volume of radiocontrast
26
Q

What can cause renal failure in myeloma?

A 
Cast nephropathy - myeloma kidney 
Light chain nephropathy
Amyloidosis
Hypercalcaemia
Hyperuricaemia
27
Q

What things should you ask in your history of someone with suspected AKI?

A 
Drugs they're on
Insults - e.g. D+V in last 10 days?
Pre/post-renal factors
Uraemic symptoms 
Timing of symptoms - SoB, UO, vomiting
Systemic diseases - e.g. rashes/nose bleeds, sore joints, eye pain
28
Q

What investigations should you do for someone in AKI?

A 
UE, Bicarb, LFTs, bone
Clotting
Urine dipstick
FBC - anaemia?
USS
Blood gas
?ANCA/Ig/C3 C4 dsDNA
?renal biopsy
29
Q

What are AKI risk events?

A

Sepsis
Toxins (e.g. contrast, aminoglycosides, ACEi, ARBs, diuretics use in last week)
Hypotension
Hypovolaemia (e.g. haemorrhage, diarrhoea)
Major surgery

30
Q

What are AKI risk factors?

A 
Age >=65
Previous AKI
Heart failure
Liver disease
CKD
DM
Vascular disease
Cognitive impairment
31
Q

In the presence of a risk event and 1+ risk factors for AKI what should you consider activating?

A 
STOP AKI Bundle - 
Sepsis - treat if suspected
Toxins - avoid
Optimise BP + volume status
Prevent harm - daily UE, fluid balance, med review
32
Q

What is the basic principle of treating AKI?

A

Removing the cause

33
Q

What are the 5 questions you should ask yourself whilst treating someone with an AKI?

A 
Do they need fluid?
Can you remove the precipitant?
Can you stop it getting worse?
Do they need a catheter?
How to make it safe?
34
Q

What is involved in maintaining someone’s fluid balance whilst they are in AKI?

A 
Volume resus if deplete, fluid restriction if overload
Optimise BP (give fluid/vasopressors, stop ACEi/antiHTNs)
35
Q

What drugs should be stopped in AKI?

A

Nephrotoxic drugs, e.g. NSAIDs/gentamicin

36
Q

What is resuscitation fluid?

A

IV fluids to urgently restore circulation with hypovolaemia

37
Q

What is routine maintenance fluid for?

A

IV fluids for those who cannot take orally/enterally to meet maintenance requirements

38
Q

What is replacement fluid for?

A

Those not requiring urgent IV resus but do not additional to maintenance to correct existing deficit, e.g. diarrhoea

39
Q

What do NICE recommend for maintenance fluids in adults?

A

25-30ml/kg/day water and 1mmol/kg/day of K, Na and Cl, 50-100g/day glucose

40
Q

What specific point should you remember about Hartmann’s fluid?

A

Contains K - do not give in hyperkalaemia

41
Q

If large volumes of 0.9% saline are given what is there a risk of?

A

Hypercholraemic metabolic acidosis

42
Q

What may be involved in removing the precipitant in AKI?

A

Stop causative drugs
Treating sepsis
Diagnose GN/other interstitial disease + give therapy

43
Q

What can you do to stop AKI getting worse?

A 
Support BP (vasopressors, stop anti-HTNs)
Reduce further insults, e.g. try to avoid IV radiocontrast
44
Q

What ECG changes do you see in hyperkalaemia?

A 
Peaked T waves usually the earliest sign
Tall tented T waves
P wave widens and flattens
PR segment lengthens
P waves eventually disappear
Prolonged QRS
High grade AV block with slow junctional and ventricular escape rhythms
Any conduction block
Sinus brady/slow AF
Sine wave (pre-terminal)
VF --> cardiac arrest
45
Q

How do you treat hyperkalaemia?

A

Stabilise myocardium - IV calcium gluconate
Shift K intracellularly - salbutamol, insulin-dextrose
Remove - diuresis, dialysis, anion exchange resins

46
Q

What are indications for dialysis in AKI?

A

Low bicarb, high lactate or pCO2
High K, high or low Na, high Ca, high uric acid, high phosphate or mg
To remove toxins, e.g. aspirin, theophylline, lithium, ethylene glycol, methanol, metformin
Overload, e..g pulmonary oedema
Pericarditis due to uraemia

47
Q

What are the signs and symptoms of AKI?

A

Reduce UO
Pulmonary/peripheral oedema
Arrhythmias (2ndary to K and acid base balance)
Features of uraemia (e.g. pericarditis, encephalopathy)

48
Q

What electrolytes are looked at in a U and E?

A

Na
K
Urea
Creatinine

49
Q

How does NICE recommend making a diagnosis of AKI?

A

In line with the (p)RIFLE, AKIN or KDIGO definitions, by using any of the following criteria:
a rise in serum creatinine of 26 micromol/litre or greater within 48 hours OR
a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days OR
a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than OR
>=25% fall in eGFR in children/young adults in 7 days

50
Q

Which AKI patients should have imaging?

A

If no identifiable cause for deterioration or risk of urinary tract obstruction they should have a renal USS within 24h of assessment

51
Q

List some drugs which are usually safe to continue in AKI

A 
Paracetamol
Warfarin 
Statins
Aspirin (75mg)
Clopidogrel
Betablockers
52
Q

List some drugs which should be stopped in AKI as they may worsen renal function

A 
NSAIDs
Aminoglycosides
ACEi
ARBs
Diuretics
53
Q

List some drugs which may have to be stopped in AKI not because they worse AKI but because there is an increased risk of toxicity

A

Lithium
Digoxin
Metformin

54
Q

Name 3 ways by which K can be removed from the body in hyperkalaemia?

A

Dialysis
Loop diuretics
Calcium resonium (oral/enema)

55
Q

Which part of the kidney is particularly susceptible for renal tubular hypoxia and why?

A

Medulla as it is already a relatively hypoxic environment

56
Q

Post-operative renal failure is more likely to occur in which patients?

A

Elderly, with PVD, high BMI, COPD, on vasopressors or nephrotoxic meds and undergo emergency surgery

57
Q

When should you refer to a nephrologist in AKI?

A

If any of the following apply:

  1. renal transplant
  2. ITU patient with unknown AKI cause
  3. vasculitis/GN/tubulointerstitial nephritis/myeloma
  4. AKI with no known cause
  5. Inadequate response to treatment
  6. complication of AKI
  7. stage 3 AKI
  8. CKD stage 4 or 5
  9. quality for renal replacement hyperkalaemia/metabolic acidosis/complications of uraemia/fluid overload
58
Q

What are the different investigation results you should see in pre-renal uraemia vs acute tubular necrosis?

A

Kidneys hold on to sodium in pre-renal uraemia to try to preserve volume

Renal/Urology (29 decks)

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