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REN > Acute kidney injury > Flashcards

Acute kidney injury Flashcards

1
Q

Concept of AKI

What is acute kidney injury

A

Sudden deterioration in kidney function

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2
Q

What is timing for AKI

A

Timing
Can be Hours / days / weeks

so it has to be less than three months

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3
Q

What can hapeen in AKI

A

Mild drop in renal function to complete loss of kidney function (kidney failure)

May result in failure to maintain, fluid, electrolyte and acid base balance

use to called acute renal failure

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4
Q

Identification

How to stage AKI

A
  • RIFLE Criteria – 2004
  • Risk – Injury – Failure – Loss – ESRD

Kidney Disease Improving Global Outcomes (KDIGO) Group Clinical
Practice Guideline - 2012

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5
Q

Identification

what are the stages of AKI

A

Stage 1: mild increase in creatnine
stage 2: doubling of creatjnine
stage 3: more than double ot if the creatnine goes to 357 (you may need dialysis)

if urine output decreases, tells you something is up with the kidneys

once creatnine goes to stage 3, you start to experience the loss of kidney function

can also use urine output, harder to do, may not be accurate,

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6
Q

How common is AKI

A

very common
I in 5 emergency admissions into hospital have or develop
AKI

we have incidence of AKI increasing, because of increase of detection, increasing elderly population

costs about 1% of NHS budget (1 billion

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7
Q

What are the consequences of AKI

A

there is a high mortality rate
16.6% increase mortality for stage 1

there are 100,00 deaths associated with AKI

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8
Q

What other conditions cause mortality when you have AKI

A

sepsis

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9
Q

True or False

AKI can cause CKD

A

Patients with AKI are more likely to develop stage 5 renal disease

Patients with AKI and CKD are even more likely to develop stage 5 renal disease

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10
Q

CKD links to AKI

true or false

CKD and protienuria do not increase risk of AKI

A

False

it does

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11
Q

Risk factors

What are the risk factors of AKI

Do history ones

A

Age > 65 years

Having a history of
* Chronic Kidney Disease
* Diabetes
* Heart failure
* Liver disease
* if you rely on others for fluid intake

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12
Q

Risk factors

What are the risk factors of AKI

things that could be in a hospital that affect BP

A

-sepsis
-hypotension
-hypovolaemia
-dehydration
-reduced fluid intake

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13
Q

Risk factors

What drugs can increase risk of AKI

A
  • Diuretics
  • ACE inhibitors / ARBs
  • BP medication
  • Metformin
  • NSAIDs (pain relief, reduce inflammation)
  • gentamicin (used to treat bacterial infections)
  • acyclovir (used to treat herpes infections)
  • contrast
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14
Q

Causes

How do we classify causes of AKI

A

PRE-renal: perfusion failure
INTRINSIC: intrinsic disease of kidney
POST renal: obstruction of urinary system

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15
Q

Pre renal causes

What are the pre renal causes

perfusion

A
  • Hypovolaemia
  • Hypotension
  • Renal artery occlusion
  • heart failure, liver failure (hypervolaemic states)
  • Drugs
  • -ones that reduce BP, circulating volume (direuetics) or renal blood flow

  1. E.g. dehydration, gastrointestinal losses, haemorrhage, burns
  2. E.g. sepsis
  3. E.g. ACE inhibitors, NSAIDs, diuretics, anti-hypertensives
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16
Q

Causes (PRE)

What dilates the afferent aterioles in kidney

A

ANP
Prostoglandins

increases GFR

17
Q

Pre renal causes

What can vasoconstrict the afferent ateriole

A

NSAIDs

think about nsaids block prostoglandins, which means you vasocinstrict
which as a result decreases GFR

18
Q

Pre Renal causes

What vasoconstricts the efferent ateriole?

A

ANP
Angiotensin 2
noradrenaline

vasoconstricting increases GFR (think hose pipe analogy)

if you stand at the end of hosepipe, then you back up the fluid

19
Q

PRE renal causes

What vasodilates efferent ateriole

A

ACE 1

lose ablity to vasocnsotirct, which decreases GFR

20
Q

Renal autoregulation

What is the blood pressure in the autoregulation zone of kidneys

A

around 80 to 180 mmHg

21
Q

Pre renal

what happens when blod volume decreaes

A

your perfusin reduces
because unable to autoregulate, to vasdoilate/constrict afferent or efferent enough

22
Q

PRE renal

What is the treatment of perfusion failure

A

keep the tissue perfusion
-replacing fluids (blood, IV fluid)
-restorin
- giving blod pressure support (giving inotropic drugs)
- restoring aterial patency (means something about blockages)

stop the use of
- NSAIDS
- or blocking the RAAS system

23
Q

POST renal

what are the causes of post renal causes

usually obstruction

A
  • Benign prostatic hypertrophy
  • Tumours
  • Fibrosis
  • Stones (would need to be biltaeral which is quite rare

Tumours: Intrinsic e.g. bladder, ureter
Extrinsic e.g. prostate, cervix

24
Q

Treatment (POST renal)

How would you treat obsrutcuon

A

Nephromstomy
Bladder cathereter
urinary stent

25
Q

INTRINSIC renal causes

What are the ‘renal’ causes

Tubules

A

Acute Tubular Necrosis (consequence prolonged pre renal perfusion problems)

Acute interstitial nephritis

sarcodsis, and TB

Drugs (NSAIDS, ABs)

infection (HIV, hepatitis B/C, Post streptococcal, Endocarditis, Covid)

Systemic diseases like (vasculitis, Lupus, Myeloma)

Glomerulonephritis

can be reversible
may need dialysis until kidneys restore function

AIN:
caused by drugs, set of an allergic reaction of kidney (eoisonphlils etc), because of inflmamtio causes tubular damage -> treat with steriods

26
Q

INTRINSIC renal causes

What is the difference between nephrotic vs nephrictic

A

Onset: Nephrotic (insidious), nephritic (abrupt)
Odema: Nephrotic (lots), nephritic (some)
BP: Nephrotic (normal), nephritic (raised)
Serum albumin: Nephrotic (raised), nephritic (normal)
Haematuria: Nephrotic (can be there), nephritic (its there)

Nephrotic: where there is loss of filtraion barrierm leak proteins, lose proteins from blood

Nephritis: more inflmmation, rapid reduction in urine output and kidney function), blood in urine

27
Q

INTRINSIC renal causes

What can cause death in AKI

AKI patients dont usually die from AKI there’s usally other reasons

A

Infection, cancer, cardiovascular disease

28
Q

What are the complications of AKI

A

Hyperkalaemia
Acidosis
Pulmonary oedema

can be managed, using dialysus, pottassium loweing drugs etc

29
Q

Natural history of AKI

What are the differenet histories

A
  1. Can make a full recovery
  2. Can go from AKI to CKD
  3. Acute on chronic kidney disease
  4. Can go from AKI to end stage renal disease
30
Q

Prevention

How do we prevent AKI

A

we need to identify those at risk of AKI early
* Patient related risk factors (age, co-morbidies)
* Admission related risk factors (sepsis, infections)
* Intervention / treatment related risk factors (are they gettings ABs like gentimycin, NSAIDs etc)

31
Q

Asssess

How do we monitor AKI

A

Urine output
Input / Output
Weights

32
Q

Mangement

How do we manage AKIs

A
  • Starts with identification and recognition of AKI risk (or indeed AKI)
  • Fluid balance
  • Fluid intervention (Oral and IV)
  • Exclude obstruction (sorted with catherter)
  • Urine Dipstick
  • Treatment of underlying problems
  • Stopping nephrotoxic drugs and context specific nephrotoxic drugs (like NSAIDs if not needed)
  • Ongoing monitoring and treatment adjustment
  • Ongoing monitoring and fluid intervention adjustment
  • Referral
33
Q

What are the indictaions for dialysis

A

Fluid overload (not sorted by diuretics)
* Hyperkalaemia (not sorted by perfusion)
* Severe metabolic acidosis
* Severe uraemia

-removal of poisons of toxins (can give antidotes, and use dialysis to remove toxins)

REN (6 decks)

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