Porth's Essentials of Pathophysiology, 4e

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Gastrointestinal and Hepatobiliary Function

U N I T 8

obstructions. 3,4 Prehepatic causes of portal hypertension include obstructive thrombosis, narrowing of the portal vein before it enters the liver, and massive splenomegaly with increased splenic blood flow. The main posthepatic causes are right-sided heart failure and hepatic vein outflow obstruction. The dominant intrahepatic cause of portal hypertension is cirrhosis, in which bands of fibrous tissue and fibrous nodules distort the architec- ture of the liver and increase the resistance to blood flow. The major clinical consequences of portal hyperten- sion arise from the increased pressure and dilation of the venous channels behind the obstruction. In addition, col- lateral channels open that connect the portal circulation with the systemic venous circulation. The complications of the increased portal vein pressure and the opening of collateral channels are ascites, congestive splenomegaly, and the formation of portosystemic shunts with bleed- ing from esophageal varices (Fig. 30-12). Ascites. Ascites occurs when the amount of fluid in the peritoneal cavity is increased. It is a late-stage manifes- tation of cirrhosis and portal hypertension. 3,4,34 Ascites usually becomes clinically evident when at least 500 mL of fluid has accumulated. However, the amount may be so great (frequently several liters) that it not only dis- tends the abdomen, but also interferes with breathing. The fluid is generally serous, having less than 3 g of protein (largely albumin) and a concentration of solutes (glucose, sodium, and potassium) similar to that in the blood. Although the mechanisms responsible for the devel- opment of ascites are not completely understood, sev- eral factors appear to contribute to fluid accumulation, including an increase in hydrostatic pressure due to por- tal hypertension, salt and water retention by the kid- ney, and decreased colloidal osmotic pressure due to impaired synthesis of albumin by the liver. Diminished blood volume (i.e., underfill theory) and excessive blood volume (i.e., overfill theory) have been used to explain the increased salt and water retention by the kidney. According to the underfill theory, a contraction in the effective blood volume causes the kidney to retain salt and water. The effective blood volume may be reduced because of loss of fluid into the peritoneal cavity or because of vasodilation caused by the presence of cir- culating vasodilating substances. The overfill theory proposes that the initial event in the development of ascites is renal retention of salt and water caused by dis- turbances in the liver itself. These disturbances include failure of the liver to metabolize aldosterone, causing an increase in salt and water retention by the kidney. Another likely contributing factor in the pathogenesis of ascites is a decreased colloidal osmotic pressure, which limits reabsorption of fluid from the peritoneal cavity (see Chapter 8). Treatment of ascites usually focuses on dietary restric- tion of sodium and administration of diuretics. 34 Water intake also may need to be restricted. Because of the many limitations in sodium restriction, the use of diuret- ics has become the mainstay of treatment for ascites.

Hepatic encephalopathy

Facial telangiectasia

Jaundice

Fetor hepaticus

Spider nevi

Esophageal varices

Gynecomastia

Muscle wasting

Splenomegaly

Fibrotic liver changes

Periumbilical caput medusae

Palmar erythema

Ascites

Hemorrhoids

Testicular atrophy

Purpura

Edema

FIGURE 30-11. Clinical manifestations of cirrhosis.

to decreased clotting factors, thrombocytopenia due to splenomegaly, gynecomastia, and a feminizing pattern of pubic hair distribution in men because of testicular atrophy, spider angiomas, palmar erythema, and hepatic encephalopathy. Portal Hypertension Portal hypertension is characterized by increased resis- tance to flow in the portal venous system and sus- tained increase in portal venous pressure. 3,4,33 Normally, venous blood returning to the heart from the abdominal organs collects in the portal vein and travels through the liver before entering the vena cava (see Fig. 30-2). Portal hypertension can be caused by a variety of con- ditions that increase resistance to hepatic blood flow, including prehepatic, posthepatic, and intrahepatic