This is a histopathology slide of alcoholic steatohepatitis (ASH) in liver tissue, captured by bright-field light microscopy from a formalin-fixed biopsy. The image shows extensive macrovesicular steatosis with hepatocytes containing large fat vacuoles that displace the nucleus. Intermixed hepatocellular damage includes ballooning degeneration and cytoplasmic rarefaction. The parenchyma exhibits a mixed inflammatory infiltrate within the portal tracts and lobules, enriched by neutrophils and activated T-lymphocytes (CD4+/CD8+), consistent with alcohol-related inflammatory activity. A ductular reaction is visible at the periportal/transitional zones, indicating biliary epithelial proliferation and portal tract remodeling in response to injury. Fibrosis is present, typically pericentral or perisinular, reflecting evolving architectural distortion in chronic injury. The sample demonstrates a typical ASH spectrum: steatosis with inflammatory activity and early fibrotic changes, which differentiates from simple steatosis. Clinically, these features correlate with alcohol use disorder, elevated transaminases (AST>ALT with AST:ALT ratio >2), and higher risk of progression to cirrhosis if alcohol intake persists. This image is valuable for educational purposes in hepatology, pathology, and medical training, aiding differential diagnosis against nonalcoholic steatohepatitis (NASH), viral hepatitis, and DILI. The scale is not provided, so magnification is variable across panels; H&E staining provides cytoplasmic and nuclear detail. High clinical relevance for hepatology education.

Educational infographic regarding Autoimmune Hepatitis (AIH), summarizing clinical data and immunopathogenesis. The top section displays a liver illustration surrounded by diagnostic and epidemiological summaries. Epidemiology notes a female predominance (75-80%) and prevalence of 4-42.9/100,000. Diagnostic criteria include elevated ALT, AST, and IgG, interface hepatitis, and specific serology: AIH-1 (ANA, SMA, SLA, anti-actin) and AIH-2 (anti-LKM1, anti-LC). Treatment modalities listed include corticosteroids, azathioprine, tacrolimus, cyclosporin, and liver transplantation. The bottom panel illustrates 'Immune imbalance' mechanisms: an Antigen-Presenting Cell (APC) presents self-antigen via a T-cell receptor (TCR) to a naïve T helper cell (Th0). This triggers a pro-inflammatory cascade where CD4+ effector T cells (Teff), B cells, and CD8+ T cells are upregulated (indicated by red upward arrows), leading to increased inflammatory factors. Simultaneously, regulatory T cells (Tregs) are downregulated (indicated by a red downward arrow), resulting in a loss of suppression on Teff and CD8+ cells. This diagram effectively demonstrates the loss of immune tolerance and effector-to-regulatory cell imbalance characteristic of AIH.

This composite educational image illustrates hepatic injury markers and gross pathological changes following chronic exposure to hydroxynonenal (HNE). Section A contains three temporal line plots showing serum levels of AST, ALT, and γ-GTP measured over 11 months. Open circles represent baseline levels, while closed circles following the black arrow indicate elevated enzyme levels after the initiation of HNE injections, signifying hepatotoxicity. Section B presents a side-by-side comparison of liver autopsy specimens. The control specimen (Cont) shows a normal, uniform reddish-brown surface. In contrast, the HNE-treated liver (HNE) demonstrates marked architectural and color changes, characterized by heterogeneous, whitish-yellow discolored regions (indicated by black and green arrows) intermingled with dark-brown areas. These macroscopic findings correspond to severe hepatocyte degeneration and lipid accumulation. This visual resource is intended for medical education regarding chemical-induced liver injury, non-alcoholic fatty liver disease (NAFLD) models, and the correlation between biochemical biomarkers and gross clinical pathology.

This is a liver biopsy prepared for light microscopy displaying features of parenchymal injury associated with long-term total parenteral nutrition (TPN). The hepatic parenchyma shows prominent fatty change (steatosis) with hepatocytes containing lipid vacuoles of variable size, compatible with macrovesicular and microvesicular steatosis. In addition, there is evidence of cholestasis with inspissated bile pigments accumulating within canaliculi and small intrahepatic ducts, a pattern that can mimic bile duct obstruction. The combination of steatosis and cholestatic injury is characteristic of PN-associated liver disease and can progress to ductular reaction, fibrosis, and ultimately cirrhosis if PN exposure persists. Damaged hepatocytes may display cytoplasmic ballooning and eosinophilic change, reflecting hepatocellular injury. The density of lipid droplets and bile plugs contributes to a heterogeneous lobular appearance. Clinically, this morphological spectrum mirrors the reported evolution of TPN-induced hepatic injury: steatosis in early stages, cholestasis with cholangiolar proliferation over time, and fibrotic remodeling in advanced disease. This histology is critical to distinguish PN-related liver injury from alternative etiologies such as biliary obstruction, viral hepatitis, or drug-induced cholestasis. It underscores the need for multidisciplinary management including PN modification, enteral stimulation, and monitoring of hepatic function tests to mitigate progression to cirrhosis.

Light microscopy of a Hematoxylin and Eosin stained liver biopsy reveals marked hepatocellular steatosis. Both macrovesicular and microvesicular patterns are present: large, one-to-many fat vacuoles within hepatocytes often displacing nuclei (macrovesicular steatosis) alongside finely distributed intracellular lipid droplets (microvesicular steatosis). The steatotic hepatocytes are intermingled with inflammatory cells, consistent with steatohepatitis. Inflammation is mixed, with neutrophils and occasional lymphocytes within the lobular parenchyma, and ballooning degeneration may be evident in affected hepatocytes. In addition, focal inspissated bile plugs within small ducts indicate cholestasis, contributing to cholestatic injury. These histologic features are characteristic of drug- or nutrient-related liver injury, particularly total parenteral nutrition (TPN)-associated steatosis and cholestasis. The combined steatosis and inflammatory infiltrate reflect hepatocellular injury with altered lipid metabolism and impaired bile excretion, which may progress to fibrosis if exposure persists. Clinically, TPN-induced liver injury is associated with abnormalities in liver enzymes, hyperbilirubinemia, and potential progression to steatohepatitis if lipids are not optimized or weaned. This image is relevant for teaching and research on iatrogenic liver injury, nutritional biochemistry, pathophysiology of steatosis, and differential diagnosis including alcoholic-fatty liver disease and NAFLD. Correlation with clinical data and exclusion of other steatosis etiologies should guide management, and monitoring of liver function tests.