Acute Kidney Injury Flashcards

1
Q

what is hyperkalaemia and what are the symptoms?

A

muscle fatigue, weakness, paralysis, abnormal heart rhythm

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2
Q

what does an ECG show in a patient with hyperkalaemia, and why?

A

K+ affects action potentials
causes wide QRS and tall, tented t waves

= causes VF

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3
Q

how do you investigate and treat hyperkalaemia?

A

eGFR, ABG, ECG, blood glucose

stabilise myocardium using calcium gluconate 10%/10ml over 5 minutes

10 units of short acting insulin in 50 ml 50% dextrose solution and also 10ml nebulised salbutamol
= this shifts potassium back into cells

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4
Q

how do you treat hypokalaemia

A

consider other electrolyte abnormalities

administer potassium chloride in sodium chloride at max rate of 20mmol/hour

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5
Q

what is an AKI

A

clinical syndrome characterised by acute drop in kidney function

diagnosed by rise in creatinine of >25micromol in 48 hours or rise by >50% in 7 days
urine output of 0.5ml/kg > 6 hours
25% fall in eGFR in young people over 7 days

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6
Q

what are the risk factors of AKI

A
CKD 
heart failure
diabetes 
liver disease 
older age
oliguria 
nephrotoxic impairments such as NSAIDs and ACE-I
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7
Q

what are the pre-renal causes of AKI

A

inadequate blood supply to kidneys which reduces filtration

dehydration, hypotension, HF, sepsis, shock, hepatorenal failure

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8
Q

what are the renal causes of AKIs

A

intrinsic disease due to reduced filtration of blood

- glomerulonephritis, interstitial nephritis, acute tubular necrosis, NSAIDs, ACE-I

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9
Q

what are the post-renal causes of AKI

A

obstruction to outflow of urine from kidney

kidney stones, cancer mass, ureteral strictures, enlarged prostates

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10
Q

what are the clincial features of an AKI

A

fever, rash, joint pains, nausea, dehydration, confusion and drowsiness
uveitis, audible bruits

oliguria !!

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11
Q

how do you stage AKI?

A

stages 1-3, dependant on serum creatinine and urine output

look for table in notes

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12
Q

what are the investigations for an AKI?

A
  • urinalysis (protein and blood = nephritis)
  • glc for diabates
    -US of KUB
    ABGs = metabolic acidosis
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13
Q

how do you manage an AKI?

A
  • underlying pathology
  • support = treat sepsis, stop nephrotoxic meds (ACE-I, ARBs, NSAIDs)

pre renal: correct volume depletion and increase renal perfusion via circulatory or cardiac support

renal: biopsy and treat internal condition

post-renal: catheter and nephrostomy

also = FLUID for all

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14
Q

what are the complications of an AKI?

A
  • hyperkalaemia
  • fluid overload, heart faiure and pulmonary oedema
  • metabolic acidosis
  • uraemia
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15
Q

what is the SALFORD pneumonic for an AKI

A
S - sepsis
A - ACE-I, NSAIDs drug review
L - labs (creatinine) and leaflets
F - fluid assessment and response (history and examination 
Obstructive cause?
Renal care if specialist needed
Dip urine and record
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16
Q

what is the SALFORD pneumonic for an AKI

A
S - sepsis
A - ACE-I, NSAIDs drug review
L - labs (creatinine) and leaflets
F - fluid assessment and response (history and examination, fluid chart, measure daily weights, if hypovolemic give bolus IV 250mls and reasses)
O - obstruction (USS)
R - renal  referral, non resolving AKI 
Dip urine
17
Q

what are urea and creatinine?

A

urea = made from ammonia by liver, excreted into blood

creatinine = muscle breakdown product, equal concentrations released into blood each day
= creatinine is normally completely filtered out of blood into urine so hence used as marker of kidney damage bc none should be present in blood

18
Q

what is the formula used in pre-renal failure for eGFR

A

GFR = 1/creatinine

19
Q

what is acute tubular necrosis and what is shown on the histology?

A

combination of factors have caused renal ischaemia and toxicity = hypotension and dehydration

20
Q

how do you treat ATN?

A

supportive
recovery is 2-3 weeks; high mortality
no meds unless septic

21
Q

what are the 3 phases of ATN?

A

oligouric: high creatinine, low urine
maintenance: increased urinary output

polyuric recovery: large amounts of dilute urine, hypovolaemic, DCT and CD still recovering so do not allow water to be reabsorbed

22
Q

what is sepsis

A

sepsis is defined as a life threatening organ dysfunction caused by dysegulated host response to infection

caused by body mounting a systemic inflammatory response to infection

23
Q

what is the pathophysiology of sepsis

A
  • release of IL and TNF
  • nitrous oxide = vasodilation
  • BV increase permeability
  • space between blood and tissues - reduction in oxygen reaching tissues
  • coag system activated = compromising organ perfusion
  • thrombocytopenia
  • haemorrhages
  • DIC
24
Q

why does blood lactate rise in sepsis?

A

hypoperfusion of tissues that starves the tissue of oxygen = anaerobic respiration = waste product

25
Q

what is septic shock

A

defined when the arterial BP drops and you get hypoperfusion
systolic BP <90 despite fluid resuscitation
hyperlactaemia (>4)

26
Q

what are the risk factors for sepsis

A

immunocompromised patients , eg very young or very old

chemotherapy, steroids or immunosuppressants

surgery, trauma, burns

pregnancy

indwelling medical devices eg catheters or centrals

27
Q

what does sepsis present with?

A

NEWS score high
fever
high resp rate
confusion, drowsiness

may have: cellulitis, wound, cough, dysuria, non-blanching rash, mottled skin, reduced urine output

= kidneys often affected early in sepsis due to low blood flow in renal medulla

28
Q

what is the investigations you would do for sepsis?

A
- FBCs
U&Es
LFTs
CRP
clotting for DIC 
blood cultures for bactaraemia 
blood gases for lactate, pH and glucose
urine dipstick 
CXR
CT 

patients should be assessed and treated within ONE HOUR of suspected sepsis presentation

29
Q

what is the sepsis six?

A
  • blood lactate
  • blood cultures
  • urine output
  • oxygen to maintain sats 94-98
  • empirical broad spectrum AB
  • IV fluids