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GI 4 > Portal HTN > Flashcards

Portal HTN Flashcards

1
Q

2 general causes of portal HTN

A
  • increase in resistance to portal flow
  • increase in portal venous flow
  • P = R x F
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2
Q

main mechanism that leads to increased intrahepatic resistance

A
  • deposition of fibrous tissue and the formation of nodules disrupts the architecture of the liver leading to an increased resistance to flow and to portal HTN
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3
Q

most common cause of portal HTN and site of increased resistance

A
  • cirrhosis

- site of increased resistance is sinusoidal

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4
Q

examples of increased resistance in pre-hepatic

A
  • portal or splenic vein thrombosis
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5
Q

examples of increased resistance in pre-sinusoidal

A
  • schistosomiasis

- at the level of the portal triad

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6
Q

examples of increased resistance in post-sinusoidal

A
  • veno-occlusive disease where fibrosis occurs in the central veins
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7
Q

examples of increased resistance in post-hepatic

A
  • Budd-Chiari
  • right sided heart failure
  • hepatic vein thrombosis
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8
Q

increased intrahepatic resistance in cirrhosis is both structural and functional

A
  • structural: sinusoidal fibrosis and regenerative nodules

- functional: active vasoconstriction

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9
Q

levels of vasodilators and vasoconstrictors in during cirrhosis

A
  • NO activity is reduced

- endothelin-1(vasoconstrictor) activity is increased

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10
Q

3 main mechanisms of portal HTN in cirrhosis

A
  • increased intrahepatic resistance: structural (fibrosis) and functional (decreased NO)
  • increased splanchnic inflow (increased NO)
  • increased collateral resistance
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11
Q

paradox of portal HTN

A
  • in the intrahepatic vasculature there is a deficiency of NO leading to vasoconstriction but in the extrahepatic vasculature there is an overproduction leading to vasodilation
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12
Q

definition and cause of hyperdynamic circulatory state (HCS)

A
  • consequence of portal HTN that plays an important role in the development and/or worsening of the complications of cirrhosis
  • HCS results from systemic vasodilation, sodium retention, and blood volume expansion
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13
Q

splanchnic vasodilation as a consequence of HCS

A
  • subsequent increase in portal venous inflow maintains portal hypertension and leads to increase in blood flow through collaterals that lead to variceal growth and their eventual rupture
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14
Q

peripheral vasodilation as a consequence of HCS

A
  • leads to a decrease in effective blood volume that in turn leads to sodium retention which can lead to ascites
  • with further vasodilation there is renal vasoconstriction which can lead to hepatorenal syndrome
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15
Q

late result of HCS

A
  • high output heart failure with decreased peripheral utilization of O2
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16
Q

vasodilation in the pulmonary circulation as a consequence of HCS

A
  • leads to arterial hypoxemia and hepatopulmonary syndrome
17
Q

cerebral vasodilation as a consequence of HCS, especially in acute liver failure

A
  • leads to brain edema and hepatic encephalopathy
18
Q

factors associated with variceal growth

A
  • Child-Pugh B/C cirrhosis, alcoholic etiology, presence of red wale marks on initial endoscopy
19
Q

threshold portal pressure for variceal growth

A
  • 11-12 mmHg
  • the threshold HVPG level is necessary but not sufficient for the development of gastroesophageal varices
  • factors other than pressure, such as volume of blood flow and local anatomic factors may contribute to the formation of varices
20
Q

definitive method to diagnose portal HTN

A
  • portal pressure measurements
21
Q

portal pressure measurement equation

A
  • HVPG = WHVP - FHVP
  • hepatic venous pressure gradient (HVPG)
  • wedged venous hepatic pressure (WHVP)
  • free venous hepatic pressure (FHVP)
  • normal HVPG ranges from 3-6 mmHg
22
Q

when is HVPG normal

A
  • pre-hepatic and presinusoidal portal HTN

- post-hepatic HTN - WHVP and FVHP are both elevated making HVPG normal

23
Q

when is HVPG elevated

A
  • sinusoidal HTN secondary to blockage of intersinusoidal communications by fibrous tissue
  • post-sinusoidal HTN
24
Q

predictors of variceal hemorrhage

A
  • variceal size (larger ones are more likely to bleed)
  • cherry red signs
  • Child-Pugh B/C
  • variceal wall tension (increased pressure leads to increased radius and the wall becomes thinner)
25
Q

MOA of vasoconstrictors in treating HTN and varices

A
  • increase splanchnic arteriolar resistance thereby reducing portal venous inflow
26
Q

MOA of venodilators in treating HTN and varices

A
  • reduces mean arterial pressure and subsequent reduction of portal inflow
27
Q

MOA of TIPS/shunt surgery in treating HTN and varices

A
  • shunt that bypasses the site of increased resistance, normalizing pressure
  • however there is an increased incidence of hepatic encephalopathy and liver failure
28
Q

MOA of variceal band ligation/sclerotherapy

A
  • attempts to obliterate the variceal

- does not modify splanchnic flow or intrahepatic resistance so variceal recurrences is the rule

29
Q

prevention of varices

A
  • non-selective beta blockers DO NOT prevent the development of varices
30
Q

prevention of variceal hemorrhaging

A
  • non-selective beta blockers PREVENT first variceal hemorrhage
  • if beta blockers are contraindicated (asthma, COPD) then use band ligation therapy
31
Q

treatment of acute variceal hemorrhage

A
  • safe vasoactive drug (somatostatin, OCTREOTIDE, vapreotide), endoscopy, antibiotic prophylaxis
  • 2nd line: TIPS/shunt therapy
32
Q

most common AE of TIPS

A
  • hepatic encephalopathy
33
Q

treatment of recurrent hemorrhage

A
  • best treatment is beta blockers with band ligation
34
Q

90% of gastric varices can be controlled by

A
  • endoscopic cyanoacrylate injection

- TIPS

35
Q

treatment of hypertensive gastropathy

A
  • non-selective beta blockers

GI 4 (11 decks)

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