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

25
causes of acquired obstructions
benign prostatic hyperplasia BPH iatrogenic eg. catheter associated injuries tumours eg. bladder, prostate, cervical, metastases stones bleeding with subsequent blood clot formation
26
causes of post renal acute kidney injury
acquired obsructions neurogenic bladder congenital malformations
27
serum creatinine levels in patients with unilteral ureteral obstruction
typically remain normal as long as the contralateral kidney remains in tact
28
pathophysiology of prerenal kidney injury
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
BUN:creatinine ratio in prerenal kidney injury
increases creatinine is still secreted in the proximal tubules but there is increased resorbtion of urea
30
pathophysiology of intrinsic kidney injury
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
pathophysiology of post renal kidney injury
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
GFR in post renal kidney injury
remains normal as long as one kidney is functioning normally
33
anuria
<50ml/24 hours
34
complications of oliguric/anuric phase of kidney injury
fluid retention (pulmonary oedema) hyperkalaemia metabolic acidosis uremia lethargy asterixis
35
phases of AKI
initiating event oliguric or anuric phase polyuric/diuretic phase recovery phase
36
clinical features of AKI
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
signs of fluid overload
peripheral or pulmonary oedema hypertension heart failure shortness of breath
38
signs of uremia
anorexia nausea encephalopathy, asterixis pericarditis platelet dysfunction
39
signs of renal obstruction
distended bladder incomplete voiding pain over the bladder or flanks
40
what happens during intrinsic aki
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
membrane permeability in intrarenal damage
large molecules can get through causing proteinuria and haematuria
42
clinical features of intrarenal AKI
azotemia more circulating fluid - hypertension and edema lower GFR
43
causes of postrenal AKI
compression - BPH, intra abdominal tumours blackage - kidney stones
44