Portal Hypertension Flashcards

1
Q

Variceal hemorrhage, hepatic encephalopathy, and ascites—the major complications of cirrhosis of the liver

A

result from portal hypertension, defined as an increase in hepatic sinusoidal pressure to 6 mm Hg or greater

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2
Q

The portal vein is formed by the confluence

A

of the splenic vein and the superior mesenteric vein behind the neck of the pancreas

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3
Q

The portal vein

A

is approximately 7.5 cm in length and runs dorsal to the hepatic artery and bile duct into the hilum of the liver.

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4
Q

In the hilum of the liver,

A

the portal vein divides into the left and right portal vein branches, which supply the left and right sides of the liver

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5
Q

The umbilical vein

A

drains into the left portal vein, and the cystic vein from the gallbladder drains into the right portal vein.

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6
Q

The liver receives a dual blood supply from the

A

portal vein and the hepatic artery that constitutes nearly 30% of total cardiac output.

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7
Q

Portal venous blood derived from the

A

mesenteric venous circulation constitutes approximately 75% of total hepatic blood flow, whereas the remainder of blood to the liver is derived from the hepatic artery, which provides highly oxygenated blood directly from the celiac trunk of the aorta.

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8
Q

Other unique aspects of the hepatic sinusoids are

A

the space of Disse, a virtual space located extraluminal to the endothelial cell and adjacent to the hepatocyte, and its cellular constituents, the hepatic stellate cell (HSC) and the Kupffer cell

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9
Q

Four distinct zones of venous drainage at the gastroesophageal junction are particularly relevant to the formation of esophageal varices

A

The gastric zone, which extends for 2 to 3 cm below the gastroesophageal junction, comprises veins that are longitudinal and located in the submucosa and lamina propria. They come together at the upper end of the cardia of the stomach and drain into short gastric and left gastric veins.

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10
Q

Four distinct zones of venous drainage at the gastroesophageal junction are particularly relevant to the formation of esophageal varices

A

The palisade zone extends 2 to 3 cm proximal to the gastric zone into the lower esophagus.

The palisade zone is the dominant watershed area between the portal and systemic circulations.

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11
Q

Four distinct zones of venous drainage at the gastroesophageal junction are particularly relevant to the formation of esophageal varices

A

More proximal to the palisade zone in the esophagus is the perforating zone, where there is a network of veins. These veins are less likely to be longitudinal and are termed perforating veins because they connect the veins in the esophageal submucosa and the external veins.

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12
Q

Four distinct zones of venous drainage at the gastroesophageal junction are particularly relevant to the formation of esophageal varices

A

The truncal zone, the longest zone, is approximately 10 cm in length, located proximal to the perforating zone in the esophagus, and usually characterized by 4 longitudinal veins in the lamina propria.

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13
Q

The fundus of the stomach drains

A

through short gastric veins into the splenic vein.

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14
Q

progression of portal hypertension results from

A

1) the prominent obstructive resistance in the liver; (2) resistance within the collaterals themselves; and (3) continued increase in portal vein inflow.

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15
Q

Hepatic Vein Pressure Gradient

A

The HVPG is the difference between the wedged hepatic venous pressure (WHVP) and free hepatic vein pressure (FHVP).

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16
Q

Measurement of the HVPG has been proposed for the following indications:

A

1) to monitor portal pressure in patients
taking drugs used to prevent variceal bleeding; (2) as a prognostic marker (3) as an end point in trials using pharmacologic
agents for the treatment of portal hypertension; (4) to assess
the risk of hepatic resection in patients with cirrhosis; and (5) to
delineate the cause of portal hypertension (i.e., presinusoidal,
sinusoidal, or postsinusoidal usually in combination with venography, right-sided heart pressure measurements, and transjugular liver biopsy.

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17
Q

DETECTION OF VARICES

A

EGD is the most commonly used method to detect esophageal varices

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18
Q

If small varices are detected on the initial examination,

A

endoscopy should be repeated in 1 to 2 years.

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19
Q

In patients in whom no varices are detected on initial evaluation,

A

endoscopy to screen for varices should be repeated in 2 to 3 years.

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20
Q

a platelet count less than 110,000/mm3 and liver stiffness measurement by transient elastography greater than 25 kPa

A

may identify with a high degree of confidence the patients who may need therapy to prevent variceal bleeding.

21
Q

The best known criteria are those compiled by the Japanese Research Society for Portal Hypertension

A

descriptors include red color signs, color of the varix, form (size) of the varix, and location of the varix.
Red color signs include red “wale” markings, which are longitudinal whip-like marks on the varix;
cherry-red spots, which usually are 2 to 3 mm or less in diameter;
hematocystic spots, which are blood-filled blisters 4 mm or greater in diameter; and diffuse redness.
The color of the varix can be white or blue.

22
Q

Esophageal varices may be small and straight

A

Grade 1

23
Q

tortuous and occupying less than one third of the esophageal lumen

A

Grade 2

24
Q

or large and occupying more than one third of the esophageal lumen

A

Grade 3

25
Q

US

A

portal vein diameter greater
than 13 mm and the absence of respiratory variations in the
splenic and mesenteric veins are sensitive but nonspecific markers of portal hypertension

26
Q

Causes of Portal Hypertension

A

COMMON
Cirrhosis
Schistosomiasis
Extrahepatic portal vein thrombosis Idiopathic portal hypertension Cardiac fibrosis

27
Q

Schistosomiasis

A

Portal hypertension results from presinusoidal obstruction caused by deposition of eggs of Schistosoma mansoni or Schistosoma japonicum in the presinusoidal portal venules.

28
Q

he host reaction results in granulomatous inflammation, which causes presinusoidal and peri- portal fibrosis.
The fibrosis that results is sometimes called “clay pipestem” or simply “pipestem” fibrosis and is associated with sustained heavy infection.

A

Schistosomiasis

29
Q

the agents that decrease splanchnic blood flow acutely

A

vasopressin and its analogs and somatostatin and its analogs.

30
Q

DRUGS THAT DECREASE PORTAL BLOOD FLOW

A

Nonselective β-adrenergic blocking agents (e.g., propranolol, nadolol) Somatostatin and its analogs
Vasopressin and terlipressin

31
Q

DRUGS THAT DECREASE INTRAHEPATIC RESISTANCE

A

α1-Adrenergic blocking agents (e.g., prazosin) Angiotensin receptor blocking agents
Nitrates

32
Q

Diuretics,

A

ecreasing plasma volume, may reduce portal pressure but are not recommended if the patient does not have ascites.

33
Q

Vasopressin

A

is an endogenous peptide hormone that causes splanchnic vasoconstriction, reduces portal venous inflow, and decreases portal pressure.

34
Q

Nonselective beta blockers such as pro-

pranolol or nadolol are preferred.

A

Blockade of β1-adrenergic
receptors in the heart decreases cardiac output.
Blockade of
β2-adrenergic receptors, which cause vasodilatation in the mesenteric circulation, allows unopposed action of α1-adrenergic
receptors and results in decreased portal flow.

35
Q

Carvedilol

A

is a drug that has both nonselective beta blocker and weak α-receptor blockade activity.

known to have antioxidant as well as antiproliferative actions and may be superior to endoscopic variceal ligation in the prevention of a first variceal bleed.

Carvedilol is started at a dose of 3.125 mg twice daily, and the dose is increased stepwise to a maximum of 25 mg daily

36
Q

Nitrates

A

short-acting (nitroglycerin) or long-acting (isosorbide mononitrate) nitrates result in vasodilatation.

37
Q

Endoscopic variceal ligation

A

eferred endoscopic modality for control of acute esophageal variceal bleeding and prevention of rebleeding

38
Q

Control of Acute Bleeding

A

The approach to treating esophageal variceal hemorrhage also applies to acute gastric variceal hemorrhage and includes volume resuscitation, avoidance of overtransfusion, and antibiotic prophylaxis with norfloxacin, 400 mg twice daily, or ciprofloxacin, 500 mg twice daily, for 7 days.

39
Q

A diagnosis of gastric variceal hemorrhage should be considered if bleeding is noted from a gastric varix

A

blood is found to appear at the gastro- esophageal junction or the gastric fundus; blood is found in the stomach and gastric varices with a “white nipple sign” (indicating a fibrin-platelet plug) are seen in the absence of other causes of bleeding;

40
Q

The preferred endoscopic therapy for fundal gastric variceal bleeding

A

injection of polymers of cyanoacrylate, usually N-butyl-2-cyanoacrylate,

The mucosa overlying the varix injected eventually sloughs, and the hardened polymer is extruded.

41
Q

Prevention of Rebleeding

A

Cyanoacrylate glue injection may be superior to nonselective beta blockers in preventing gastric variceal rebleeding.

42
Q

Ectopic Varices

A

They also may manifest with hemobilia, hematuria, hemoperitoneum, or retroperitoneal bleeding.

The duodenum is a common site of ectopic varices, and varices typically are associated with portal vein obstruction, but in the West, the usual cause of duodenal varices is cirrhosis.

43
Q

Anorectal varices

A

reported in 10% to 40% of cirrhotic patients who undergo colonoscopy

Rectal varices are dilated superior and middle hemorrhoidal veins, whereas hemorrhoids are dilated vascular channels above the dentate line.
Rectal varices collapse with digital pressure, but hemorrhoids do not.

44
Q

Endoscopic glue injection or band ligation is the

A

preferred approach for bleeding duodenal varices.

45
Q

The diagnosis of PHG

A

mosaic-like pattern of the gastric mucosa on endoscopic examination.
This pattern is characterized by small polygonal areas with a depressed border. Superimposed on this mosaic- like pattern may be red point lesions that are usually greater than 2 mm in diameter.
PHG is considered mild when only a mosaic-like pattern is present and severe when superimposed discrete red spots are also seen.

46
Q

In GVE

A

aggregates of ectatic vessels can be seen on endoscopic examination as red spots without a mosaic background.

GVE appears histologically as dilated mucosal capillaries with focal areas of fibrin thrombi or ectasia in combination with proliferation of spindle cells.

47
Q

Treatment GVE

A

The more common presentation is one of chronic, slow bleeding and anemia.
Pharmacologic therapy to prevent bleeding (primary prophylaxis) in patients with severe PHG is not currently recommended.

48
Q

For GVE: If lesions are localized, the platelet count is greater than approximately 45,000/mm3, and the INR is less than 1.4,

A

thermoablative therapy, as with argon plasma coagulation, may be helpful

49
Q

When the vascular ectasias are diffuse and extensive in the stomach,

A

cryotherapy using liquid nitrogen or CO2 may be tried.

If endoscopic treatment fails, therapy with an oral estrogen-progesterone combination (estradiol 35 μg plus norethindrone 1 mg daily) may help reduce transfusion requirements.