pathophys of AKI - amboss

Question 1

define AKI

Answer 1

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

Question 2

three main causes of AKI

Answer 2

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

Question 3

diagnosis of AKI is made based on

Answer 3

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

Question 4

prerenal causes of AKI

Answer 4

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

Question 5

pathophysiology of prerenal AKI

Answer 5

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

Question 6

azotaemia

Answer 6

high levels of nitrogen containing compounds in the blood

Question 7

signs of prerenal AKI

Answer 7

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

Question 8

intrarenal AKI is due to

Answer 8

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

Question 9

nephrotoxins

Answer 9

aminoglycosides (antibiotics)
lead
myoglobin released from damaged muscles
ethylene glycol
radiocontrast dye
uric acid (tumour lysis syndrome)

Question 10

glomerulonephritis

Answer 10

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

Question 11

cells lining glomerulus

Answer 11

podocytes

Question 12

signs of intrarenal AKI

Answer 12

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

Question 13

acute interstitial nephritis

Answer 13

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

Question 14

failure to cease medications causing acute interstitial nephiritis may lead to

Answer 14

renal papillary necrosis
where the renal papillae are destroyed

Question 15

how common in prerenal

Answer 15

60% of AKIs

Question 16

cardiorenal syndrome

Answer 16

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

Question 17

hepatorenal syndrome

Answer 17

kidney injury in patients with cirrhosis

Question 18

abdominal compartment syndrome

Answer 18

high abdominal pressure associated with organ dysfunction or failure

Question 19

causes of decreased circulating volume

Answer 19

cardiorenal syndrome
hepatorenal syndrome
abdominal compartment syndrome
nephrotic syndrome
acute pancreatitis

Question 20

how common is intrinsic acute kidney injury

Answer 20

35% of cases of AKI

Question 21

infections causing acute interstitial nephritis

Answer 21

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

infiltrative diseases eg. sarcoidosis, amyloidosis

Question 22

vascular diseases causing intrarenal AKI

Answer 22

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

Question 23

post renal acute kidney injury

Answer 23

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

Question 24

how common is post renal kidney injury

Answer 24

5% of AKI

Question 25

causes of acquired obstructions

Answer 25

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

Question 26

causes of post renal acute kidney injury

Answer 26

acquired obsructions
neurogenic bladder
congenital malformations

Question 27

serum creatinine levels in patients with unilteral ureteral obstruction

Answer 27

typically remain normal

Question 28

pathophysiology of prerenal kidney injury

Answer 28

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

Question 29

BUN:creatinine ratio in prerenal kidney injury

Answer 29

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

Question 30

pathophysiology of intrinsic kidney injury

Answer 30

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

Question 31

pathophysiology of post renal kidney injury

Answer 31

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

Question 32

GFR in post renal kidney injury

Answer 32

remains normal as long as one kidney is functioning normally

Question 33

anuria

Answer 33

<50ml/24 hours

Question 34

complications of oliguric/anuric phase of kidney injury

Answer 34

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

Question 35

phases of AKI

Answer 35

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

Question 36

complications of polyuric/diuretic phase

Answer 36

glomerular filtration returns to normal which increases urine production
tubular resorption remains distrubed
loss of electrolytes and water
dehydration, hyponatraemia, and hypokalaemia

Question 37

clinical features of AKI

Answer 37

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

Question 38

signs of fluid overload

Answer 38

peripheral or pulmonary oedema
hypertension
heart failure
shortness of breath

Question 39

signs of uremia

Answer 39

anorexia
nausea
encephalopathy, asterixis
pericarditis
platelet dysfunction

Question 40

signs of renal obstruction

Answer 40

distended bladder
incomplete voiding
pain over the bladder or flanks

Question 41

what happens during intrinsic aki

Answer 41

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

Question 42

membrane permeability in intrarenal damage

Answer 42

large molecules can get through causing proteinuria and haematuria

Question 43

clinical features of intrarenal AKI

Answer 43

azotemia
more circulating fluid - hypertension and edema
lower GFR

Question 44

causes of postrenal AKI

Answer 44

compression - BPH, intra abdominal tumours
blackage - kidney stones