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Ganong's Review of Medical Physiology, 23rd Edition

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CHAPTER SUMMARY<br />

■ The liver conducts a huge number <strong>of</strong> metabolic reactions and<br />

serves to detoxify and dispose <strong>of</strong> many exogenous substances, as<br />

well as metabolites endogenous to the body that would be harmful<br />

if allowed to accumulate.<br />

■ The structure <strong>of</strong> the liver is such that it can filter large volumes<br />

<strong>of</strong> blood and remove even hydrophobic substances that are<br />

protein-bound. This function is provided for by a fenestrated<br />

endothelium. The liver also receives essentially all venous blood<br />

from the intestine prior to its delivery to the remainder <strong>of</strong> the<br />

body.<br />

■ The liver serves to buffer blood glucose, synthesize the majority<br />

<strong>of</strong> plasma proteins, contribute to lipid metabolism, and preserve<br />

cholesterol homeostasis.<br />

■ Bilirubin is an end product <strong>of</strong> heme metabolism that is glucuronidated<br />

by the hepatocyte to permit its excretion in bile. Bilirubin<br />

and its metabolites impart color to the bile and stools.<br />

■ The liver removes ammonia from the blood and converts it to<br />

urea for excretion by the kidneys. An accumulation <strong>of</strong> ammonia<br />

as well as other toxins causes hepatic encephalopathy in the<br />

setting <strong>of</strong> liver failure.<br />

■ Bile contains substances actively secreted across the canalicular<br />

membrane by hepatocytes, and notably bile acids, phosphatidylcholine,<br />

and cholesterol. The composition <strong>of</strong> bile is modified as<br />

it passes through the bile ducts and is stored in the gallbladder.<br />

Gallbladder contraction is regulated to coordinate bile availability<br />

with the timing <strong>of</strong> meals.<br />

MULTIPLE-CHOICE QUESTIONS<br />

For all questions, select the single best answer unless otherwise directed.<br />

1. Removal <strong>of</strong> the entire colon would be expected to cause<br />

A) death.<br />

B) megaloblastic anemia.<br />

C) severe malnutrition.<br />

D) a decrease in the blood level <strong>of</strong> ammonia in patients with<br />

cirrhosis <strong>of</strong> the liver.<br />

E) decreased urinary urobilinogen.<br />

CHAPTER 29 Transport & Metabolic Functions <strong>of</strong> the Liver 487<br />

2. After complete hepatectomy, a rise would be expected in the<br />

blood level <strong>of</strong><br />

A) glucose.<br />

B) fibrinogen.<br />

C) 25-hydroxycholecalciferol.<br />

D) conjugated bilirubin.<br />

E) estrogens.<br />

3. Which <strong>of</strong> the following cell types protects against sepsis secondary<br />

to translocation <strong>of</strong> intestinal bacteria?<br />

A) hepatic stellate cell<br />

B) cholangiocyte<br />

C) Kupffer cell<br />

D) hepatocyte<br />

E) gallbladder epithelial cell<br />

4. P450s (CYPs) are found in many parts <strong>of</strong> the body. In which <strong>of</strong><br />

the following do they not play an important role?<br />

A) bile acid formation<br />

B) carcinogenesis<br />

C) steroid hormone formation<br />

D) detoxification <strong>of</strong> drugs<br />

E) glycogen synthesis<br />

CHAPTER RESOURCES<br />

Ankoma-Sey V: Hepatic regeneration—Revising the myth <strong>of</strong><br />

Prometheus. News Physiol Sci 1999;14:149.<br />

Arias JM, et al (editors): The Liver: Biology and Pathology, 3rd ed.<br />

Raven Press, 1994.<br />

Chong L, Marx J (editors): Lipids in the limelight. Science<br />

2001;294:1861.<br />

H<strong>of</strong>mann AF: Bile acids: The good, the bad, and the ugly. News<br />

Physiol Sci 1999;14:24.<br />

Lee WM: Drug-induced hepatoxicity. N Engl J Med 2003;349:474.<br />

Meier PJ, Stieger B: Molecular mechanisms <strong>of</strong> bile formation. News<br />

Physiol Sci 2000;15:89.<br />

Michalopoulos GK, DeFrances MC: Liver regeneration. Science<br />

1997;276:60.<br />

Trauner M, Meier PJ, Boyer JL: Molecular mechanisms <strong>of</strong> cholestasis.<br />

N Engl J Med 1998;339:1217.

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