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34 OCTOBER 2015 | EMSWORLD.com the blood before it enters systemic circula- tion via the hepatic veins. Hepatocytes in the liver monitor the circulating levels of nutrients such as car- bohydrates, amino acids and lipids (fats). Excess nutrients are removed from the blood and stored, and deficiencies can be corrected by tapping into stored reserves or synthesizing required nutrients. Excess glucose is stored in the liver as glycogen, and excess fatty acids as lipids, which can be utilized when deficiencies exist. In addi- tion, fat-soluble vitamins such as A, D, K and E are absorbed by and stored in the liver, as are minerals such as iron and copper. Metabolic waste products and toxins are removed from circulation by the liver and deactivated, excreted and/or stored. The liver plays a major role in the break- down of not only toxins from the environ- ment (for example, some hydrocarbons or poison from an ingested mushroom) but also in the metabolism of alcohol, drugs and medications. It is also responsible for the breakdown of hormones such as estrogen, testosterone and even insulin. The liver plays an important role in blood pressure regulation via the synthesis of the inactive hormone angiotensinogen. When activated by renin (secreted by the kidney), angiotensinogen is converted to angiotensin, a hormone that will go on to increase blood pressure through a variety of functions. Hematologic Regulation As blood passes through the liver, many important processes take place. Phagocytic cells in the liver remove cellular debris, damaged and/or old RBCs, and pathogens from circulation. In addition, cells in the liver synthesize plasma proteins. The major plasma protein in the human body is albu- min. Albumin is a relatively large molecule and helps create and maintain the colloidal osmotic pressure of the blood that keeps f luid (plasma) in the vasculature and out of the surrounding tissues. The liver plays an important role in the production of numerous clotting factors required for normal function of coagulation as well as the complement protein components of the immune system. Synthesis and Secretion of Bile Bile is synthesized by the liver, stored in the gallbladder and excreted into the proximal small intestine (duodenum). It is composed mostly of water (97%) and contains smaller amounts of bilirubin, ions and bile salts. Bile salts assist in the breakdown of lipids and absorption of fatty acids. The bile emulsifies fats entering the small intestine from the stomach, aiding in digestion. Key functions of the liver described here (Table 2) are but a small fraction of the total number it provides. As such, any condi- tion that damages the liver and prevents it from performing its role in the body can result in a serious, life-threatening condi- tion. Cirrhosis of the liver and chronic liver failure is one such condition. Epidemiology, Etiology and Pathophysiology The most recent data from the CDC reveals the overall mortality from chronic liver dis- ease and cirrhosis in the United States in 2013 was 36,427 persons. 2 The age groups with highest mortalities were 45–54 (8,785) and 55–64 (11,951); these accounted for more than half the deaths. Of persons who died of chronic liver disease and cirrhosis in 2013, 65% were male. 2 Caucasians accounted for 87.4% of all deaths from chronic liver disease and cirrhosis. 2 Caucasian males accounted for 57.2% of all deaths, while black males accounted for only 2.5%. Of the deaths in the U.S. in 2013 from liver disease and cir- rhosis, alcoholic liver disease accounted for 49.8%, while other chronic liver disease and cirrhosis accounted for 50.2%. 2 There are numerous etiologies of liver disease that can lead to cirrhosis, and the most common causes in the U.S. are hepatitis C, alcoholic liver disease and nonalcoholic liver disease. Together these three etiologies accounted for about 80% of patients on the liver transplant wait list between 2004–2013. 3 While cirrhosis can be treated if identified in the early stages and its underlying cause corrected, late-stage cirrhosis is irreversible, and the only treatment option is a liver trans- plant. Patients with cirrhosis of the liver are thus subject to a wide range of complications and have decreased life expectancy. Cirrhosis is a slowly progressing, indo- lent disease in which healthy tissue in the liver is injured and replaced with scar tis- sue and ultimately progresses to hepatic fibrosis. This fibrosis interrupts the normal flow of blood through the liver, resulting in impaired function. As a result, vital func- tions such as the synthesizing and storage of nutrients, the secretion of clotting factors and plasma proteins, and the clearing of tox- ins in the blood cannot occur. In addition, the impaired flow of blood through the liver results in a backup of blood into the hepatic portal circulation. This backup results in an increase of pressure into the portal, gastric, esophageal and mesenteric veins, a condi- tion termed portal hypertension. 4 Portacaval anastomoses are connections between veins of the portal system and the systemic circulation. The most important anastomoses are in the esophagus and rec- tum, but there are others as well. When por- tal hypertension occurs, blood f low from the gastrointestinal tract is directed away from the liver and directly into systemic circulation, a condition termed portosys- temic shunting. This can result in dilation of these anastomotic vessels and the creation of internal hemorrhoids, as well as gastric and esophageal varices. TABLE 2: SIGNS AND SYMPTOMS OF CIRRHOSIS Weakness, fatigue, weight loss; Jaundice, pruritis; Pale, greasy, floating feces; Upper gastrointestinal bleeding; Dark urine; Ascites, abdominal distension; Caput medusae, palmar erythema, spider angiomas; Altered mental status; Bruising, bleeding; Gynecomastia; Hypotension; Hepatomegaly, splenomegaly; Asterixis; Pain. CONTINUING EDUCATION