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Medicine Y3 TCD 13-24 > 13. Acute Kidney Injury (AKI) > Flashcards

13. Acute Kidney Injury (AKI) Flashcards

1
Q

Give me a brief overview of the function of a kidney

A

They make urine, regulate salt and water (make 3-4 pints a day)
remove waste products from blood into. urine
Produce hormones that regulate BP and also create erythropoietin to control the production of RBC
They activate vitamin D to keep bones healthy
They clean your blood and remove many drugs that some people take for their condition

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2
Q

What two criteria make up the staging of AKI

A 
serum creatinine (SCr)
urine output
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3
Q

what is the criteria for stage 1 AKI

A

SCr increase more than 26 micrnmol/L within 48 hours or increase between 1.5-1.9x reference value

urine output less than 0.5ml/kg/hour for more than 6 consecutive hours

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4
Q

what is the criteria for stage 2 AKI

A

increase between 2-2.9 x reference SCr

urine output less than 0.5ml/kg/hour for more than 12 hours

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5
Q

what is the criteria for stage 3 AKI

A

increase more than 3X reference range of SCr or increased greater than 354 micro mols/L or commenced on renal replacement therapy (RRT)

Urine output less than 0.3ml/kg/hr for more than 24 hours or anuria for 12 hours

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6
Q

In someone with suspected AKI what checklist is used to improve the care of someone with AKI

A

think SALFORD

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7
Q

What is think SALFORD

A

an institue AKI care bundle that is used in all patients with 26mmol/L or 1.5X rise in creatinine or oliguria (less than 0.5ml/kg/hr) for 6 hours

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8
Q

what does think SALFORD stand for

A

Sepsis and other causes - treat

ACE/ARB and NSAIDS suspend/review drugs

Labs (repeat creatinine within 24hours) & Leaflets (for the patient)

Fluid assessment and response (history and examination, initiate fluid chart, measure daily weights- if hypovolaemic give bolus IV 250mls and reassess)

Obstruction (USS within 24 hours for AKI 3)

Renal/critical care referral

Dip the urine and record it

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9
Q

Name some symptoms and signs of AKI

A

nausea and vomitting, or diarrhoea, evidence of dehydration
reduced urine output or changes in urine colour
confusion, fatigue and drowsiness
An acute illness with any of the risk factors (see other questions)

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10
Q

What is the NICE criteria for AKI

A
  • Rise in creatinine of ≥ 25 micromol/L in 48 hours
  • Rise in creatinine of ≥ 50% in 7 days
  • Urine output of < 0.5ml/kg/hour for > 6 hours – this is termed oliguria
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11
Q

What is oliguria

A

Urine output of < 0.5ml/kg/hour for > 6 hours

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12
Q

Name the various risk factors that would predispose a patient to developing AKI injury

A

chronic kidney disease
other organ failure/chronic diseases (heart failure, diabetes, liver disease)
Older age (above 65 years)
History of AKI
cognitive impairment
nephrotoxic medications such as NSAIDS, ACE inhibitors, ahminoglycosides, ARB, diuretics within the past week
Use of a contrast medium such as during CT scan
hypovolaemia
oliguria
sepsis

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13
Q

name some nephrotoxic medications

A

NSAIDS and ACE inhibitors, aminoglycosides, ARBs, diuretics

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14
Q

Whenever someone asks you the cause of renal impairment what can you split it into

A

pre-renal, renal and post-renal causes

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15
Q

what is the most common cause of AKI
pre-renal
renal
post-renal

A

pre-renal

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16
Q

why does pre-renal pathology cause AKI

A

it is due to inadequate blood supply to the kidneys which reduces the filtration of blood

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17
Q

name some pre-renal causes of AKI

A

Dehydration
hypotension (shock)
Heart failure
Hypovolaemia secondary to diarrhoea/vomiting
renal artery stenosis
Sepsis
hepatorenal syndrome (to do with liver cirrhosis)

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18
Q

Name some renal causes of AKI

A 
this is where there is an intrinsic disease in the kidney 
-glomerulonephritis 
- Interstitial nephritis 
- Acute tubular necrosis 
Rhabdomyolysis
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19
Q

How is post renal AKI caused

A

by obstruction to the outflow of urine from the kidney, causing a back pressure into the kidney and reduced kidney function aka “obstructive uropathy”

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20
Q

name some post-renal causes of AKI

A

kidney stones
masses scubas cancer. in the abdo or pelvis
ureter strictures
enlarged prostate or prostate cancer - benign prostatic hyperplasia

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21
Q

the first step to treating an AKI is to correct the underlying cause, how could you do this

A

fluid rehydration with IV fluids in pre-renal AKI

stop nephrotoxic medications such as NSAIDs and antihypertensives that reduce filtration pressure

relieve obstruction in a posit-renal AKI, for example insert a catheter for a patient in retention from an enlarged prostate

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22
Q

what are the main complications with AKI

A

hyperkalaemia
fluid overload, heart failure and pulmonary oedema
metabolic acidosis
Ureamia (high urea) can lead to encephalopathy or pericarditis

23
Q 
From the list below name the drugs that are usually safe to continue in AKI 
Paracetamol 
warfarin 
statins 
aspirin (at a cardio protective dose of 75mg OD)
Clopidogrel 
Beta-blockers 
NSAIDS (except if aspirin at cardiac dose eg 75mg OD) 
ahminoglycosides 
ACE inhibitors 
ARB
diuretics 
metformin 
lithium 
digoxin
A 
Paracetamol 
warfarin 
statins 
aspirin (at a cardio protective dose of 75mg OD)
Clopidogrel 
Beta-blockers
24
Q 
From the list below name the drugs that should be stopped in AKI as it may worsen renal function 
Paracetamol 
warfarin 
statins 
aspirin (at a cardio protective dose of 75mg OD)
Clopidogrel 
Beta-blockers 
NSAIDS (except if aspirin at cardiac dose eg 75mg OD) 
ahminoglycosides 
ACE inhibitors 
ARB
diuretics 
metformin 
lithium 
digoxin
A 
NSAIDS (except if aspirin at cardiac dose eg 75mg OD) 
ahminoglycosides 
ACE inhibitors 
ARB
diuretics
25
Q 
From the list below name the drugs that may have to be stoped in AKI as increased risk of toxicity (but does usually worsen the AKI itself) 
Paracetamol 
warfarin 
statins 
aspirin (at a cardio protective dose of 75mg OD)
Clopidogrel 
Beta-blockers 
NSAIDS (except if aspirin at cardiac dose eg 75mg OD) 
ahminoglycosides 
ACE inhibitors 
ARB
diuretics 
metformin 
lithium 
digoxin
A

metformin
lithium
digoxin

26
Q

Hyperkalaemia needs prompt treatment to avoid arrhythmias which could be life threatening;
which drug is used to stabilise the cardiac membrane

A

IV calcium glconate

27
Q

Hyperkalaemia needs prompt treatment to avoid arrhythmias which could be life threatening;
which drugs are used to shift potassium from extracellular to intracellular fluid compartments

A

combined insulin/dextrose infusion

nebulised salbutamol

28
Q

Hyperkalaemia needs prompt treatment to avoid arrhythmias which could be life threatening;
which drugs can be used to remove potassium from the body

A

calcium resonium (orally or enema)
Loop diuretics
Dialysis

29
Q

Hydration status examination:

name some causes of fluid overload

A

o Iatrogenic: whereby medical intervention/treatment has caused it ie too much fluids
o Cardiac failure
o Renal failure
o Increased ADH secretion

30
Q

Hydration status examination:

name some causes whereby your fluid output will be increased

A

 Diabetes
 Diarrhoea and vomiting
 Fever (excessive sweating)
 Drugs (anti diuretics)

31
Q

Hydration status examination:

name some broad causes of dehydration

A 
decreased input of fluids 
increased output of fluids 
insufficient replacement of fluids during surgery 
Haemorrhage 
Sepsis
32
Q

Hydration status examination:

before going to the patient what things can you look at (ie test results or charts)

A 
fluid balance 
abs chart 
meds 
bloods 
CXR
33
Q

Hydration status examination:

what things can you comment on from the end of the bed

A

• What’s going into them
o IV lines, NGT, NBM, food or drink
• what’s going out
o Catheter, vomit bowels, drains, stomas

34
Q

Hydration status examination:

what can you comment on in the hands, arms and neck

A

Hands
Hands
• Warm, CRT, skin turgor
Arms
• Pulse (weak, increased in dehydration and overload)
• Lying/standing BP (more than 20 mmHg difference is significant)
Neck
• Carotid pulse (character- weak/thready)
• JVP (more than 4cm is significant and could this be overload)

35
Q

Hydration status examination:

what can you comment on in the face, chest and back/legs

A 
Chest 
•	Parasternal heave (RH dilatation)
•	Displaced apex beat (LH dilatation)
•	3rd heart sound (heart failure)
Back/legs 
•	Lung bases (crackles- LVF)
•	Sacral or ankle odema (RVF)
36
Q

Hydration status examination:

how could you finish off this exam

A
  • Review charts and bloods
  • Daily weights
  • Repeat bloods
  • CXR to look for pulmonary odema
37
Q

What ECG changes occur in a patient with hyperkalaemia

A
  • There are usually no P waves- but regular rhythm
  • Wide QRS complex (more than 3 small squares) with similar to, but no recognisable pattern of LBBB
  • Peaked T waves
38
Q

what happens if high levels of potassium are not treated

A

will go on to develop VF and have a cardiac arrest

39
Q

An ECG for hyperkalaemia is often mistaken for what other clinical abnormality

A

LBBB

40
Q

What drug is used to stabilise the myocardium in hyperkalemia

A

calcium glutinate

41
Q

which drugs are used to shift potassium back into the cells in hyperkalaemia

A

short acting insulin in dextrose

nebulised salbutamol

42
Q

How is hypokalaemia treated

A
  • Correct any other underlying electrolyte abnormalities such as hypomagnesaemia
  • Administer potassium chloride in NaCl at a maximum rate of 20mmol/hour
43
Q

in a patient with an AKI what could their ABG classically look like

A

partially compensated metabolic acidosis with low PH, low bicarbonate and compensatory low CO2

44
Q

Urine dipstick:

what does proteinuria 3+ indicate and on the flip side if it is negative what can you exclude

A

intrinsic renal disease

45
Q

Urine dipstick:

if there is blood and protein then what should you consider

A

glomerulonephritis

46
Q

Urine dipstick:

if dipstick is positive for blood but no RBC when what should you consider

A

myoglobin

47
Q

An AKI with negative urinalysis usually indicates what kind of AKI cause
pre-renal
renal
post renal

A

pre-renal

48
Q

Dialysis is considered for patients with kidney injury if. what kind of complications cannot be resolved

A

hyperkalaemia
pulmonary oedema
metabolic acidosis
uraemia encephalopathy (confusion, myoclonic jerks, seizures, coma) or uraemia pericarditis

49
Q

Why is the kidney susceptible to ischemic damage and necrosis

A

in order to have counter current multiplication mechanise in the renal tubules you need low and sluggish blood flow, especially in the renal medulla

50
Q

what is the protective mechanism that the kidney has which tries to prevent ischemia and maintain renal blood flow

A

the RAAS system (renin-angiotensin-aldosterone) mechanism

51
Q

where is the RAAS mechanism located

A

juxtaglomerular apparatus of the kidney

52
Q

how does the RAAS system work

A

it increases the overall effective circulation by increasing reabsorption of salt (Na) and water
also protects the nephron locally by vasoconstriction of efferent renal arteriole to maintain GFR

53
Q

Which drugs all prevent the protective RAASm mechanism making tubular ischemia and necrosis more likely

A

ACE-I, ARB and NSAIDS

54
Q

What are the 3 phases of acute tubular necrosis (ATN)

A

oliguric phase
maintenance phase
polyuric recovery phase

Medicine Y3 TCD 13-24 (32 decks)

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