Episode one of the Portal Hypertension and Cirrhosis Complications chapter treats portal hypertension as a pressure problem first, then follows that pressure into varices and bleeding. The organizing idea: the hepatic venous pressure gradient is the hemodynamic gold standard, and liver stiffness plus platelets give the noninvasive translation that now drives beta-blocker and screening decisions. Screening thresholds, primary prophylaxis, and the acute variceal hemorrhage bundle all key off the same physiology, with the restrictive transfusion target, mandatory ceftriaxone, and the early-TIPS decision as the cirrhosis-specific layers. It closes on gastric varices, portal hypertensive gastropathy, and GAVE, where anatomy and drainage pick the therapy, not appearance. Topics covered Portal hypertension hemodynamics and HVPG thresholds Beta-blocker response and presinusoidal versus postsinusoidal causes Noninvasive CSPH detection and the rule of five Variceal screening and surveillance intervals Primary prophylaxis: carvedilol versus band ligation The acute variceal hemorrhage bundle Early TIPS during the index admission Gastric varices, portal hypertensive gastropathy, and GAVE Key decisions An HVPG over five defines portal hypertension, ten or higher defines clinically significant portal hypertension and identifies who will develop varices and decompensation, and over twelve marks the variceal bleeding threshold; a beta-blocker responder drops the gradient more than a fifth or below twelve. By the rule of five, a liver stiffness of twenty-five kilopascals or higher rules in clinically significant portal hypertension while stiffness of fifteen or lower with platelets of a hundred fifty thousand or higher rules it out; defer screening endoscopy when stiffness is under twenty and platelets over a hundred fifty thousand. In compensated cirrhosis with clinically significant portal hypertension, a beta-blocker reduces first decompensation even without high-risk varices, a different indication from variceal prophylaxis, and cirrhosis without CSPH is not an indication. For medium or large varices choose a nonselective beta-blocker or band ligation, with carvedilol preferred because its alpha-blockade lowers intrahepatic resistance in addition to inflow; hold nonselective beta-blockers when systolic pressure drops under ninety, sodium falls under a hundred thirty, or acute kidney injury develops. In acute variceal hemorrhage transfuse to a hemoglobin around seven, not higher, and give octreotide plus mandatory ceftriaxone with endoscopic band ligation within twelve hours. Early TIPS within seventy-two hours improves one-year survival in high-risk bleeds, Child C in the ten-to-thirteen range or Child B with active bleeding, and the decision is made during the index admission rather than after the second bleed. Isolated fundal varices without esophageal varices should prompt evaluation for splenic vein thrombosis, and GAVE breaks the portal-pressure logic because TIPS is not effective. For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: [email protected]. (00:00) - Introduction and the hemodynamic root (00:31) - Portal hypertension as a pressure problem (01:08) - HVPG thresholds and their meaning (03:13) - The noninvasive framework and rule of five (05:32) - Variceal screening and surveillance (06:28) - Primary prophylaxis choices (08:17) - The acute hemorrhage bundle (09:46) - Early TIPS in the index admission (11:57) - Gastric varices, gastropathy, and GAVE

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“What did the council decide on item 42?” — answered with the speaker and the moment.

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