3a. Ascites

Question 1

increased hepatic resistance in cirrhosis

Answer 1

• First, the development of hepatic fibrosis, which defines cirrhosis, disrupts the normal architecture of the hepatic sinusoids and impedes normal blood flow through the liver.
• Second, activation of hepatic stellate cells, which mediate fibrogenesis, leads to smooth-muscle contraction and fibrosis.
• Finally, cirrhosis is associated with a decrease in endothelial nitric oxide synthetase (eNOS) production, which results in decreased nitric oxide production and increased intrahepatic vasoconstriction

Question 2

increased hepatic resistance causes

Answer 2

portal hypertesnion

Question 3

portal hypertension and renal salt and water retention causes

Answer 3

ascites

Question 4

ascites in patients with cirrhosis is caused by

Answer 4

portal hypertension and renal salt and water retention

Question 5

why does renal water and salt retention occur in liver cirrhosis

Answer 5

1. increased systemic levels of nitric oxide (in contrast to the decrease seen intrahepatically), and increased levels of vascular endothelial growth factor and tumor necrosis factor, that result in splanchnic arterial vasodilation.
2. Vasodilation of the splanchnic circulation results in pooling of blood and a decrease in the effective circulating volume, which is perceived by the kidneys as hypovolaemia.
3. Compensatory vasoconstriction via release of antidiuretic hormone ensues, causing free water retention and activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system, which lead to renal sodium and water retention

Question 6

pathogenesis of ascites in the absence of cirrhosis

Answer 6

generally results from peritoneal carcinomatosis, peritoneal infection, or pancreatic disease

Question 7

peritoneal carcinomatosis can result from

Answer 7

can result from primary peritoneal malignancies such as mesothelioma or sarcoma, abdominal malignancies such as gastric or colonic adenocarcinoma, or metastatic disease from breast or lung carcinoma or melanoma

Question 8

peritoneal carcinomatosis causes ascites by

Answer 8

The tumor cells lining the peritoneum produce a protein-rich fluid that contributes to the development of ascites. Fluid from the extracellular space is drawn into the peritoneum, further contributing to the development of ascites.

Question 9

Pancreatic ascites results from

Answer 9

leakage of pancreatic enzymes into the peritoneum.

Question 10

total causes of ascites

Answer 10

1. mainly cirrhosis
2. some others: Cardiac ascites, peritoneal carcinomatosis, and “mixed” ascites resulting from cirrhosis and a second disease
3. Less common: massive hepatic metastasis, infection (tuberculosis, Chlamydia infection), pancreatitis, and renal disease (nephrotic syndrome).
4. Rare causes of ascites include hypothyroidism and familial Mediterranean fever.

Question 11

aetiology of ascites is best determined by

Answer 11

paracentesis

Question 12

paracenesis is

Answer 12

procedure in which a needle or small catheter is passed transcutaneously to extract ascitic fluid from the peritoneum. The lower quadrants are the most frequent sites for paracentesis.

Question 13

preferred location for paracentesis

Answer 13

The left lower quadrant is preferred because of the greater depth of ascites and the thinner abdominal wall.

Question 14

risks of paracentesis

Answer 14

Paracentesis is a safe procedure even in patients with coagulopathy; complications, including abdominal wall hematomas, hypotension, hepatorenal syndrome, and infection, are infrequent.

Question 15

turbid fluid

Answer 15

result from the presence of infection or tumor cells

Question 16

white, milky fluid

Answer 16

indicates a triglyceride level >200 mg/dL (and often >1000 mg/dL), which is the hallmark of chylous ascites.

Question 17

chylous ascites

Answer 17

Chylous ascites results from lymphatic disruption that may occur with trauma, cirrhosis, tumor, tuberculosis, or certain congenital abnormalities.

Question 18

dark brown fluid

Answer 18

can reflect a high bilirubin concentration and indicates biliary tract perforation.

Question 19

black fluid

Answer 19

may indicate the presence of pancreatic necrosis or metastatic melanoma.

Question 20

testing ascitic fluid

Answer 20

should be sent for measurement of albumin and total protein levels, cell and differential counts, and, if infection is suspected, Gram’s stain and culture

Question 21

SAAG stands for

Answer 21

serum-ascites albumin gradient

Question 22

SAAG is useful for

Answer 22

distinguishing ascites caused by portal hypertension from nonportal hypertensive ascites

Question 23

SAAG reflects

Answer 23

the pressure within the hepatic sinusoids and correlates with the hepatic venous pressure gradient

Question 24

A SAAG ≥1.1 g/dL reflects

Answer 24

the presence of portal hypertension and indicates that the ascites is due to increased pressure in the hepatic sinusoids.
Possible causes include cirrhosis, cardiac ascites, hepatic vein thrombosis (Budd-Chiari syndrome), sinusoidal obstruction syndrome (veno-occlusive disease), or massive liver metastases

Question 25

A SAAG <1.1 g/dL indicates

Answer 25

ascites is not related to portal hypertension, as in tuberculous peritonitis, peritoneal carcinomatosis, or pancreatic ascites.

Question 26

treatment for cirrhotic ascites

Answer 26

is restriction of sodium intake to 2 g/d. When sodium restriction alone is inadequate to control ascites, oral diuretics—typically the combination of spironolactone and furosemide—are used to increase urinary sodium excretion

Question 27

Fluid intake may be restricted in patients with

Answer 27

hyponatraemia

Question 28

spironolactone

Answer 28

aldosterone antagonist that inhibits sodium resorption in the distal convoluted tubule of the kidney. Use of spironolactone may be limited by hyponatremia, hyperkalemia, and painful gynecomastia

Question 29

furosemide

Answer 29

is a loop diuretic that is generally combined with spironolactone in a ratio of 40:100; maximal daily doses of spironolactone and furosemide are 400 mg and 160 mg, respectively.

Question 30

common complication of cirrhotic ascites

Answer 30

Spontaneous bacterial peritonitis

Question 31

Spontaneous bacterial peritonitis presents as

Answer 31

Patients with SBP generally note an increase in abdominal girth; however, abdominal tenderness is found in only 40% of patients, and rebound tenderness is uncommon.
Patients may present with fever, nausea, vomiting, or the new onset or an exacerbation of preexisting hepatic encephalopathy.