pathophys of AKI - amboss Flashcards

1
Q

define AKI

A

sudden loss of renal function with a subsequent rise in creatinine and blood urea nitrogen BUN

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2
Q

three main causes of AKI

A

decreased renal perfusion (prerenal)
direct damage to kidneys (intrarenal/intrinsic)
inadequate urine drainage (post renal)

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3
Q

diagnosis of AKI is made based on

A

increase in serum creatinine concenration and/or decrease in urine output

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4
Q

prerenal causes of AKI

A

decreased blood flow into kidneys may be due to
- absolute loss of fluid: haemorrhage, vomiting, diarhoea, severe burns, poor oral intake, diuretics
- relative loss of fluid: hypotension, distributive shock, congestive heart failure
- local to the renal artery: renal artery stenosis, embolus

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5
Q

pathophysiology of prerenal AKI

A

less blood is pumped to glomeruli
less blood filtered
decreased glomerular filtration rate (GFR)

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6
Q

azotaemia

A

high levels of nitrogen containing compounds in the blood

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7
Q

signs of prerenal AKI

A

oliguria - low urine
azotaemia - high urea and creatinine in blood
BUN:creatinine ratio of >20:1
concentrated urine

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8
Q

intrarenal AKI is due to

A

damage to the tubules, glomerulus or interstitium
eg.
- acute tubular necrosis via ischaemia (usually due to a prerenal decrease in blood flow) or via nephrotoxins
- glomerulonephritis
- acute interstitial nephritis
- vascular diseases

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9
Q

causes of acute tubular necrosis

A

ischaemia eg. due to prolonged hypotension
nephrotoxic drugs:
aminoglycosides (antibiotics)
cisplatin, methotrexate
radiocontrast dye
poisons:
lead
ethylene glycol
endogenous toxins:
uric acid (tumour lysis syndrome)
haemoglobin in intravascular haemolysis
myoglobin released from damaged muscles n rhabdomyolysis

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10
Q

glomerulonephritis

A

inflammation of the glomerulus
often caused by antigen antibody complexes causing inflammation and damage

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11
Q

cells lining glomerulus

A

podocytes

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12
Q

signs of intrarenal AKI

A

proteinuria and haematuria due to damaged podocytes
decreased GFR due to fluid leakage causing. reduced pressure difference
oliguria
more fluid in the blood: oedema and. hypertension
azotaemia

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13
Q

acute interstitial nephritis

A

infiltration of immune cells
canbe caused by NSAIDs, diuretics, penecillin
oliguria and eosinophiluria

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14
Q

failure to cease medications causing acute interstitial nephiritis may lead to

A

renal papillary necrosis
where the renal papillae are destroyed

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15
Q

how common in prerenal

A

60% of AKIs

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16
Q

cardiorenal syndrome

A

a spectrum of conditions affecting cardiac and renal systems when dysfunction in one organ results in dysfunction of the other
eg. congestive heart failure causing poor renal perfusion

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17
Q

hepatorenal syndrome

A

kidney injury in patients with cirrhosis

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18
Q

abdominal compartment syndrome

A

high abdominal pressure associated with organ dysfunction or failure

19
Q

causes of decreased circulating volume

A

cardiorenal syndrome
hepatorenal syndrome
abdominal compartment syndrome
nephrotic syndrome
acute pancreatitis

20
Q

how common is intrinsic acute kidney injury

A

35% of cases of AKI

21
Q

infections causing acute interstitial nephritis

A

bacterial: legionella, strep
fungi: candida, histoplasma
viral: hepatitis C virus, cytomegalovirus, HIV

infiltrative diseases eg. sarcoidosis, amyloidosis

22
Q

vascular diseases causing intrarenal AKI

A

haemolytic uraemic syndrome
thrombotic thrombocytopaenic purpura
hypertensive emergency
vasculitis, scleroderma renal crisis
renal vein thrombosis, renal atheroemboli, renal infarction

23
Q

post renal acute kidney injury

A

any condition that results in bilateral obstruction of urinary flow from the renal pelvis to the urethra

24
Q

how common is post renal kidney injury

A

5% of AKI

25
Q

causes of acquired obstructions

A

benign prostatic hyperplasia BPH
iatrogenic eg. catheter associated injuries
tumours eg. bladder, prostate, cervical, metastases
stones
bleeding with subsequent blood clot formation

26
Q

causes of post renal acute kidney injury

A

acquired obsructions
neurogenic bladder
congenital malformations

27
Q

serum creatinine levels in patients with unilteral ureteral obstruction

A

typically remain normal as long as the contralateral kidney remains in tact

28
Q

pathophysiology of prerenal kidney injury

A

decreased blood supply to the kidneys due to hypovolaemia, hypotension, or renal vasoconstriction
failure of renal vascular autoregulation to maintain renal perfusion
decreased GFR
activation of renin angiotensin system
increased aldosterone release
increased resorption of Na+, H2O
increased urine osmolality
secretion of anti diuretic hormone
increased reabsorbtion H2O and urea
creatinine is still secreted inthe proximal tubules, so the blood BUN:creatinine ratio increases

29
Q

BUN:creatinine ratio in prerenal kidney injury

A

increases
creatinine is still secreted in the proximal tubules but there is increased resorbtion of urea

30
Q

pathophysiology of intrinsic kidney injury

A

damage to a vascular or tubular component of the nephron
necrosis or apoptosis of tubular cells
decreased resorption capacity of electrolytes (eg. Na, water and/or urea)
increased Na and H20 in the urine
decreased urine osmolality

31
Q

pathophysiology of post renal kidney injury

A

bilateral urinary outflow obstruction eg. stones, BPH, neoplasia, congenital anomalies
increased retrograde hydrostaticpressure within renal tubules
decreased GFR and compression of the renal vasculature
acidosis, fluid overload, and increased BUN, Na and K

32
Q

GFR in post renal kidney injury

A

remains normal as long as one kidney is functioning normally

33
Q

anuria

A

<50ml/24 hours

34
Q

complications of oliguric/anuric phase of kidney injury

A

fluid retention (pulmonary oedema)
hyperkalaemia
metabolic acidosis
uremia
lethargy
asterixis

35
Q

phases of AKI

A

initiating event
oliguric or anuric phase
polyuric/diuretic phase
recovery phase

36
Q

clinical features of AKI

A

oliguria or anuria
signs of volume depletion - reduced skin turgor, orthostatic or frank hypotension and tachycardia
signs of fluid overload (from Na and H2o retention)
signs of uremia
signs of renal obstruction
fatigue, confusion, and lethargy
in severe cases: seizures or coma
affected individuals have a higher risk of secondary infection throughout all phases

37
Q

signs of fluid overload

A

peripheral or pulmonary oedema
hypertension
heart failure
shortness of breath

38
Q

signs of uremia

A

anorexia
nausea
encephalopathy, asterixis
pericarditis
platelet dysfunction

39
Q

signs of renal obstruction

A

distended bladder
incomplete voiding
pain over the bladder or flanks

40
Q

what happens during intrinsic aki

A

dead podocytes block the tubules
decreases glomerular filtration rate
less urea and creatinine get filtered out
potassium and metabolic acids build up in the blood because they are not excreted by dead podocytes

41
Q

membrane permeability in intrarenal damage

A

large molecules can get through causing proteinuria and haematuria

42
Q

clinical features of intrarenal AKI

A

azotemia
more circulating fluid - hypertension and edema
lower GFR

43
Q

causes of postrenal AKI

A

compression - BPH, intra abdominal tumours
blackage - kidney stones

44
Q
A