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Robbins Liver & Biliary > Portal HTN > Flashcards

Portal HTN Flashcards

1
Q

What is portal hypertension and why does it develop?

A

Because of increased resistance to portal blood flow through the liver causing high blood pressure in the portal system

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2
Q

What are the 3 categories of portal HTN?

A

Prehepatic

Intrahepatic

Posthepatic

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3
Q

Does the portal vein account for half, or 2/3rds of hepatic blood flow?

A

2/3rds

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4
Q

What is the strict definition of portal HTN?

A

absolute increase in the blood pressure within the portal vein > 8mmHg

OR

increase in the pressure gradient between the portal vein and hepatic vein of 5 mmHg or more

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5
Q

How is pressure in the portal vein assessed?

A

Doppler ultrasound

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6
Q

What are the major posthepatic causes of portal HTN?

A

Severe right-sided heart failure (and other causes of vena cavae obstruction)

Restrictive pericarditis

Budd-Chiari syndrome (thrombosis of the hepatic veins)

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7
Q

What Is the major intrahepatic cause of portal HTN?

A

Cirrhosis

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8
Q

What are the major causes of prehepatic portal HTN?

A

Thrombosis of the portal vein/splenic vein (due to hypercoaguable states and malignancy, eg pancreatic cancer)

Narrowing of the portal vein before it ramifies within the liver

Massive splenomegaly with increased splenic vein blood flow

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9
Q

What is the most important and frequent cause of portal HTN?

A

Cirrhosis

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10
Q

What are the minor causes of intrahepatic portal HTN?

A

Shistosomiasis (presinusoidal portal HTN)

Massive fatty change

Sarcoidosis (and other diffuse fibrosing granulomatous diseases)

Diseases affecting portal microcirculation (eg, nodular regenerative hyperplasia)

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11
Q

How is the resistance to portal flow increased at the level of the sinusoids in portal HTN?

A

Contraction of vascular smooth muscle and myofibroblasts

Disruption to normal flow by scarring and nodules of parenchymal regeneration

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12
Q

How do intrahepatic endothelial cells contribute to intrahepatic portal HTN?

A

Vasoconstrict through decrease in NO production

Release of endothelin-1, angiotensinogen and eicosanoids

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13
Q

How does the arterial system of the liver worsen intrahepatic portal HTN, especially in cirrhosis?

A

Arterial and portal systems in the liver anastamose

These intrahepatic shunts in fibrous septa load arterial pressure into the low pressure portal venous system

Also negatively affect metabolic exchange between sinusoidal blood and hepatocytes

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14
Q

How would you describe splanchnic circulation in portal HTN?

A

Hyperdynamic (fast flow rate)

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15
Q

Why does splanchnic circulation change in portal HTN?

A

NO production causing arterial vasodilation

Stimulated by reduced bacterial DNA clearance due to mononuclear phagocyte function decreasing

Also because of intrahepatic arterial-portal shunting bypassing Kupffer cell populations

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16
Q

Are antibiotics possibly effective in some treatments of portal HTN?

A

Yes

Bacteria are thought to contribute to splanchnic hyperdynamic flow

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17
Q

What are the four major complications of portal HTN?

A

Ascites

Formation of portosystemic shunts

Congestive splenomegaly

Hepatic encephalopathy

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18
Q

What is the term for accumulation of fluid in the peritoneal cavity?

A

Ascites

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19
Q

What percentage of ascites cases is caused by cirrhosis?

A

85%

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20
Q

What is the concentration of protein in ascites fluid?

A

It’s mostly serous

<3g/dL

21
Q

T/F the solute concentrations (sodium, potassium, glucose) in ascites fluid is less than that of blood

A

False

Usually close to serum levels

22
Q

Are cells common in ascites fluid?

A

No

Sometimes a small amount of WBCs

23
Q

What does the presence of RBCs in ascites fluid usually mean?

A

Possible disseminated intra-abdominal cancer

24
Q

What is a complication of long standing ascites?

A

Seepage into transdiaphragmatic lymphatics

Produces hydrothorax, more often on the right side

25
Q

What are the three aetiologies of ascites?

A

Sinusoidal hypertension causing fluid to move into the space of Disse which is then removed by hepatic lymphatics (made worse by hypoalbuminaemia)

Percolation of hepatic lymph into the peritoneal cavity

Splinchnic vasodilation and hyperdynamic circulation caused by HR and CO unable to maintain BP when splanchnics dilated which activates RAAS -> HTN, vasodilation, Na and water retention increases perfusion pressure -> extravasation of liquid into abdomen

26
Q

How does hepatic lymph contribute to ascites?

A

Normal thoracic duct lymph flow is 800-1000mL/day

Cirrhosis can increase demand on thoracic duct flow to 20L/day, exceeding capacity

27
Q

Where do portosystemic shunts form in theory?

A

Where systemic and portal circulation share common capillary beds

28
Q

What are common places for portosystemic shunts?

A

Rectum

Oessophagogastric junction

Retroperitoneum

Falciform ligament of the liver (involving periumbilical and abdominal wall collaterals)

29
Q

Are portosystemic shunts in the rectum/anus clinically important?

A

No

Haemorrhoidal bleeding may occur, but is not usually massive or life-threatening

30
Q

How do abdominal wall portosystemic shunts appear clinically?

A

‘Caput medusae’

Dilated subcutaneous veins extending from the umbilicus toward the rib margins

Important clinical sign of portal HTN

31
Q

Are oesophageal varices important clinically?

A

Critically important

32
Q

How often do oesophageal varices occur in patients with cirrhosis?

A

40% of patients

33
Q

What is the major complication of oesophageal varices?

A

Rupture

Massive haematemesis and loss of blood

Hypovolaemia

Death

34
Q

How quickly do patients destabilise when oesophageal varices rupture?

A

Very quickly – minutes to hours

35
Q

What is the mortality rate of oesophageal varices?

A

30%

36
Q

What is the hepatic venous pressure gradient (HVPG)?

A

The difference in pressure between the portal vein and the IVC

37
Q

What is the wedged hepatic venous pressure (WHVP)?

A

The pressure in a hepatic vein

Can be used to estimate portal pressure because blood hits the balloon in the hepatic vein branch and the static column of blood transmits approximately the portal pressure directly to the balloon

38
Q

What is the free hepatic vein pressure (FHVP)?

A

IVC pressure

Used as a baseline

39
Q

How is HVPG (hepatic venous pressure) calculated?

A

WHVP - FHVP

Portal pressure minus normal IVC pressure, essentially

40
Q

What is the normal HVPG pressure range?

A

3-6 mmHg

41
Q

What is the definition of portal HTN in terms of actual pressure?

A

HVPG > 8 mmHg

HVPG > 12 mmHg is the threshold for the potential formation of varices, and higher levels increase risk for variceal haemorrhage

42
Q

How can ascites be classified?

A

Peritoneal or non-peritoneal

43
Q

How is the serum-ascites albumin gradient (SAAG) used in differentiating ascites classifications?

A

Nonperitoneal diseases produce ascites with a SAAG greates than 1.1 g/dL

44
Q

What are some causes of nonperitoneal ascites?

A

Intrahepatic and extrahepatic portal HTN

Hypoalbumaemia (nephrotic syndrome)

Myxoedema

Ovarian tumours

Pancreatic or biliary ascites

Chylous ascites (obstruction of thoracic duct or cisterna chyli)

45
Q

What are the causes of chylous ascites?

A

Mostly due to malignancy (eg lymphoma)

Can be seen post-operatively and following radiation injury

46
Q

What are some causes of peritoneal ascites?

A

Malignancy (primary peritoneal mesothelioma)

Granulomatous peritonitis

Vasculitis (SLE, Henoch-Schonlein purpura)

Whipple disease

Endometriosis

47
Q

What are 4 causes of granulomatous peritonitis?

A

TB

Fungal and parasitic infections (Candida, Cryptococcus, Schistosoma)

Sarcoidosis

Foreign bodies (talc, cotton, barium)

48
Q

Is massive ascites that does not respond to treatment a prognostic factor?

A

Yes

50% patient mortality within 6 months in patients exhibiting this feature

Robbins Liver & Biliary (6 decks)

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