Episode one of the Steatotic Liver Disease chapter reframes fatty liver as MASLD, a positive diagnosis built on hepatic steatosis plus at least one of five cardiometabolic criteria rather than an exclusion. The organizing idea: fibrosis stage, not the transaminase or the degree of steatosis, is the prognostic anchor, so the workup runs a tiered noninvasive sequence and management is graded by how much fibrosis is present. It walks the biology of insulin resistance and lipotoxicity, the PNPLA3 and TM6SF2 variants, lean disease and cryptogenic cirrhosis as the same entity, then the FIB-4 into elastography algorithm. Management climbs from weight-loss targets through bariatric surgery, including compensated cirrhosis, to the newly on-label drugs resmetirom and semaglutide. Topics covered Positive cardiometabolic diagnosis and the five criteria Steatohepatitis versus bland steatosis and fibrosis as the prognostic anchor Alcohol continuum and the intermediate category Insulin resistance, lipotoxicity, and the PNPLA3 and TM6SF2 variants Lean disease and cryptogenic cirrhosis Noninvasive fibrosis testing: FIB-4, transient elastography, MR elastography Lifestyle, diet, and weight-loss targets Bariatric surgery including compensated cirrhosis Pharmacotherapy: resmetirom, semaglutide, pioglitazone, vitamin E Key decisions MASLD requires hepatic steatosis on imaging or biopsy PLUS at least one of five cardiometabolic criteria; one criterion is enough, a deliberate change from metabolic syndrome requiring three. Read prognosis through fibrosis stage, not the inflammatory grade or the transaminase level, because liver-related mortality climbs steeply with fibrosis while ALT does not track outcome. FIB-4 under one point three rules out advanced fibrosis and over two point six seven flags high risk, with the cutoff shifting to two point zero over age sixty-five; transient elastography under eight kilopascals rules out advanced fibrosis and over twelve to fourteen suggests cirrhosis. Stiffness over twenty kilopascals with a platelet count under a hundred fifty thousand indicates clinically significant portal hypertension and triggers variceal screening. Weight loss is dose-responsive: five percent reduces steatosis, seven to ten percent resolves steatohepatitis, and ten percent or more produces fibrosis regression, with the target shifted to three to five percent in lean disease. Compensated steatohepatitis cirrhosis can undergo bariatric surgery at experienced centers when synthetic function is preserved and there is no significant portal hypertension; a hepatic venous pressure gradient over fifteen is an absolute contraindication, with sleeve gastrectomy generally preferred. Resmetirom and semaglutide are on-label for non-cirrhotic moderate-fibrosis steatohepatitis, chosen by dominant comorbidity, while pioglitazone is for the diabetic and vitamin E at eight hundred international units for the non-diabetic biopsy-proven patient, avoided in diabetics and cirrhosis. 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 organizing idea (00:25) - Positive diagnosis on cardiometabolic criteria (02:10) - Fibrosis as the prognostic anchor (03:23) - Mechanism and the genetic variants (05:19) - Lean disease and cryptogenic cirrhosis (06:50) - Noninvasive fibrosis assessment (10:08) - Lifestyle, diet, and weight-loss targets (12:23) - Bariatric surgery and cirrhosis (14:05) - Pharmacotherapy: the new on-label drugs

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