Pathophysiology- Chronic Liver Failure Flashcards

1
Q

Liver blood flow contributions

A
  • 30% hepatic artery
  • 70% portal vein (splenic vein and splanchnic circulation)
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2
Q

how can you increase pressure?

A

increase flow and/or resistance because pressure = flow x resistance

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3
Q

portal hypertension blood flow

A
  • venous collaterals form from distal esophagus to rectum
  • anterior collaterals via umbilical vein
  • posterior collaterals via retroperitoneal veins, splenorenal shunts
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4
Q

what is a major cause of death in portal hypertension?

A
  • varices which are tortuous venous collaterals under high pressure. variceal bleeding is a major cause of death.
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5
Q

Tx for varices?

A
  • volume resuscitation
  • correction of coagulopathy
  • splanchnic vasoconstriction
  • decrease blood flow to stomach and intestine
  • decrease blood flow via collaterals.
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6
Q

what medication treatment used for variceal bleeding?

A
  • vasopressin
  • somatostatin- block vasodilators such as glucagon
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7
Q

how can you decrease portal pressure–medical treatement?

A
  • beta blockers
  • transjugular intrahepatic portosystemic shunt
  • liver transplantation
  • surgical portosystemic shunt
  • endoscopic therapy to sclerose or band the vairces
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8
Q

what is the child pugh classification?

A
  • looks at albumin, ascites, bilirubin, PT, encephalopathy
  • given scores and graded child a, b, c (A is good c is bad)

a is 5-6, c is 10-15

**better prognosis after variceal bleeding with child A

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9
Q

what can casue ascites?

A
  • increased resistance to portal venous flow
  • increased flow to portal vein
  • increased lymphatic flow
  • leakage of lymphatic flow from the liver and intestines.
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10
Q

Does vasodilation or vasoconstriction cause ascites?

A

systemic vasodilation

-increased portosystemic shunting of vasodilators

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11
Q

renal and ascites

A
  • decreased renal perfusion
  • increased renal vasoconstriction
  • increased renin-angiotensin activity
  • increased sodium reabsorption
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12
Q

what’s the revised underfill theory?

A
  • ascites formation –> decreased effective volume –> renal sodium retention –> ascites and edema
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13
Q

overflow hypothesis

A
  • primary renal tubular retention of sodium –> increased plasma volume –> translocation of fluid out of splanchnic circulation as ascites
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14
Q

revised underfill theory

A
  • primary peripheral vasodilation –> consequent imbalance of capacitance and volume. consituting “relative” underfilling –> renal sodium retention
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15
Q

do you have sodium retention or clearance with ascites?

A
  • decreased renal clearance
  • severe liver disease is associated with sodium retention and decreased creatinine clearance
  • hep c can also cause renal disease
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16
Q

complications with ascites?

A
  • tense ascites, pressure on diaphragms and stomach, difficulty breathing and eating
  • hepatic hydrothorax
  • spontaneous bacterial peritonitis
17
Q

spontaneous bacterial peritonitis

A
  • large amount of undrained fluid
  • low protein ascites
  • low complement
  • bacterial translocation from intestines to blood
  • transient bacteremia infects the ascites
18
Q

Tx of ascites

A
  • sodium restriction
  • diurectics
  • treat the liver disease
  • large volume paracentesis
19
Q
  • Tx of ascites
A
  • correct portal htn
  • transjugular portosystemic shunt
  • surgical portosystemic shunt
  • liver transplantation
20
Q
A