APEX LIVER DOMAIN

which metabolic action of the liver enables the removal of ammonia from the body?

-glycogenolysis

-amino acid deamination

-urea formation

- beta-oxidation

Urea formation

Deamination of amino acids produces ammonia (NH3), which is converted into urea for excretion by the kidneys. in the absence of urea formation, ammonia accumulates, causing cerebral toxicity and potentially hepatic coma.

Beta oxidation transforms fatty acis into 2 carbon acetyl radicals that form acetyl coenzyme A.

Glycogenolysis is the breakdown of stored glycogen to form glucose.

which features of cirrhosis predispose to the development of bacterial peritonitis? select 2

-formation of portal systemic collaterals

-hepatic venous pressure gradient >or equal to 12 mmHg

-ascites

-splanchnic vasoconstriction

ascites and hepatic venous pressure gradient greater than or equal to 12 mmHg

What percentage of the liver's oxygen supply is provided by portal venous blood?

-25

-50

-75

-95

50%

Although portal blood makes up 75% of the total hepatic blood supply, it provides only 50% of the oxygen content.

The combined hepatic arterial and portal venous blood vessels receive 20-25% of cardiac output.

Decreases in portal blood supply cause reciprocal increases in hepatic arterial blood flow. The liver contains about 450 ml of blood and thus can be viewed as a blood reservoir.

the high cardiac output in a patient with cirrhosis is largely due to a/an: select 2

-elevated intravascular volume

-decreased systemic vascular resistance

-increased nitric oxide production

-enhanced sympathetic response

decreased systemic vascular resistance and increased nitric oxide production

R: the hyperdynamic circulation in cirrhotic patients is largely due to profound decreases in afterload. the peripheral vasculature is dilated due to the increased production of vasodilators as a result of portal hypertension. These vasodilators include nitric oxide, vasoactive intestinal peptides, natriuretic peptides, and glucagon.

CIrrhotic patients have an increase in total fluid volume but a decrease in effective circulating volume due to the pooling of blood in the excessively dilated splanchnic vasculature.

what is the primary hepatic defense against bacterial infectious disease?

-hepatocytes

-stellate cells

-space of disse

-kupffer cells

Kupffer cells

Kupffer cells are large phagocytic macrophages that line the hepatic venous sinuses. These cells act very rapidly (<0.01 second) to phagocytose and ultimately digest bacteria and other foreign matter that enter the liver from the intestines.

The space of Disse (the perisinusoidal space) connects with lymphatic vessels to remove excess fluids. Hepatic sinusoids are the vascular structures that permit the mixing of hepatic arterial and portal venous blood. These sinusoids provide exposure to blood to Kupffer cells (for cleansing) and the endothelial cells that surround the hepatocytes.

Hepatocytes make up about 80% of the liver's cellular volume and are responsible for extensive metabolic functions, including protein, fat, carbohydrates, and drug metabolism.

Stellate cells are typically quiet but are activated in response to liver injury. they ultimately contribute to hepatic inflammation and fibrosis.

what are the MOST common causes of jaundice? (select 2)

-hemochromatosis

-bile duct obstruction

-end stage liver disease

-erythrocyte destruction

Bile duct obstruction

and erythrocyte destruction

Jaundice or icterus ( a yellow tint of body tissue from the accumulation of bilirubin) is caused by either RBC destruction (hemolytic jaundice) or the inability of bile to be excreted into the GI tract (obstructive jaundice). Bile duct obstruction or damaged liver cells can lead to obstructive jaundice.

Hemochromatosis is a hereditary disease characterized by an excess of total body iron. Iron is deposited into liver, pancreatic, and cardiac cells. Hepatomegaly and cirrhosis can occur. It is not a common cause of jaundice.

is the diagnosis of cirrhosis required for the diagnosis of portapulmonary hypertension?

NO

High mean PAP and PVR with portal hypertension are features of portopulmonary hypertension.

what conditions are diagnosed with hepatopulmonary syndrome?

select 3

-intrapulmonary vascular dilation

-A-a gradient > 15 mmHg on room air

-cirrhotic liver disease

-mean pulmonary artery pressure >25 mmHg

-Portal Hypertension

-Pulmonary Vascular Resistance >240 dynes/sec/cm

-A-a gradient > 15 mmHg on room air

-intrapulmonary vascular dilation

-Portal Hypertension

a triad of features defines hepatopulmonary syndrome: an A-a gradient >15mmHg on Room Air or PaO2<80 mmHg, evidence of pulmonary vascular dilation (typically with demonstrable right to left shunt) and portal htn (HVPG >5 mmHg) A diagnosis of cirrhosis is not required for the diagnosis of HPS.

High mean PAP and PVR with portal hypertension are features of portopulmonary hypertension.

what is the END pathologic outcome of cirrhosis of the liver?

-regeneration of hepatocytes

-reduced hepatic arterial flow

-destruction of liver parenchymal cells

-portal hypertension

Portal Hypertension

Cirrhosis leads to the destruction of liver parenchymal cells and is replaced with fibrous tissue that contracts around blood vessels. This process impedes portal blood flow by significantly increasing vascular resistance in this normally very low-pressure system. Portal HTN is the end result.

Regeneration of hepatocytes occurs after liver resection or acute liver injury but not if viral infection or inflammation has occured. Thus, regeneration does not occur in cirrhotic livers.

which stimuli produce gallbladder contraction and bile release into the gastrointestinal tract (select 2)

-cholecystokinin

-secretin

-vagal input

-pepsinogen

Vagal input and cholecystokinin

The most potent stimulus for gallbladder contraction is the presence of fatty foods within the duodenum. Fatty foods stimulate the release of the hormone Cholecystokinin, which relaxes the sphincter of Oddi.

The gallbladder may also be stimulated by vagal and enteric neural input. Accordingly, during EGD and/or colonoscopy, when the upper or lower GI tract is stimulated by stretch, gallbladder contraction and emptying can occur and increase the risk of regurgitation and aspiration.

Secretin stimulates the secretion of water, sodium and bicarbonate from epithelial cells that line the bile ducts. This secretion can double the volume of secretory produce through the common bile duct.

Pepsinogen is secreted by peptic cells in response to vagal stimulation or acid in the stomach.

the amount of cholesterol in the bile is determined often by the amount of

-calcium ingested

-cholesterol ingested

-fat ingested

-urea excreated

fat ingested

the amount of cholesterol in the bile is in part determined by the amount of fat in one's diet. Liver cells synthesize cholesterol from fat. this is why patients with a high fat diet are prone to cholelithiasis.