Hepatorenal syndrome Flashcards

1
Q

renal failure in liver disease causes

A

sepsis (chronic liver disease increases susceptibility to infection) (can lead to AKI)

hepatorenal syndrome

hypovolemia- diuretics, GI bleeding

nephrotoxic drugs

parenchymal renal disease

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2
Q

hepatorenal syndrome

A

renal failure that occurs in patients with severe liver disease in the absence of any pathological cause for the development of renal failure

People with hepatorenal syndrome have narrowed and constricted blood vessels in their kidneys in response to liver failure, which reduces blood flow to the kidneys.

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3
Q

cause of hepatorenal syndrome

A

serious complication of liver cirrhosis

functional renal failure, kidneys stop working, reduced renal blood flow and glomerular filtration rate

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4
Q

HRS reversibility

A

reversible with liver transplant

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5
Q

AKI

A

acute kidney injury
an acute significant reduction in the glomerular filtration rate

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6
Q

serum creatinine

A

biomarker of renal function

influenced by bodyweight, race, age (less muscle as u age), gender

patients with cirrhosis:
less creatinine in muscles (muscle wasting)
increased renal tubular secretion of creatinine
interference w assays for sCr by elevated bilirubin

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7
Q

diagnosing AKI

A

inc in sCr from baseline

3 stages
stage 3 requires dialysis and renal replacement

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8
Q

main features of hepatorenal syndrome HRS

A

functional renal failure (replace liver and kidney will work) caused by intra-renal vasoconstriction in patients with end stage liver disease and circulatory dysfunction

circulatory dysfunction caused by splanchnic vasodilation and insufficient cardiac output
leads to hypovolemia

spontaneous w deteriorating liver function
or secondary to precipitating event such as bacterial infection

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9
Q

ascites

A

accumulation of fluid in peritoneal cavity
causes abdominal swelling

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10
Q

main factors in pathogenesis of HRS

A

hemodynamic factors (lowering of BP)

impaired cardiac output

increased activation of sympathetic NS

increased formation of vasoactive mediators

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11
Q

diagnosing HRS

A

lowered mean arterial pressure
lowered bp
lowered renal blood flow (because ascites increases renal venous pressure, compresses renal vein)
low cardiac output (increases risk of hrs)

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12
Q

vasoactive mediators

A

can lead to intra-renal vasoconstriction

can cause mesangial / smooth muscle cell contraction and reduce glomerular filtration rate by decreasing the single nephron glomerular filtration rate

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13
Q

pathophysiology of low glomerular filtration rate GFR

A

normal:
mesangial cell relaxation
prostaglandin E2

low gfr:
mesangial cell contraction
lowered surface area
no prostaglandin E2

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14
Q

NSAIDS effect

A

NSAIDs cause renal failure in ascites

reversible inhibitor of cyclooxygenase

blocks production of prostaglandin E2

AKI

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15
Q

management of hrs

A

treat underlying precipitating cause-
fluid challenge, review drugs, culture and antibiotics

support renal function until recovery of liver failure or liver transplant

optimise bp- vasoconstrictor drugs

paracentesis for tense ascites (removing fluid)

renal support (hemofiltration or dialysis)

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16
Q

terlipressin

A

terlipressin improves GFR and renal function in HRS

suppresses catecholamines and activation of RAAS