Portal hypertensive gastropathy (PHG) occurs as a complication of cirrhotic or non-cirrhotic portal hypertension. Although the pathogenesis of PHG is not completely understood, evidence suggests that the key factor for the development of PHG is portal hypertension. PHG is clinically important because it may cause acute (and even) massive or insidious, blood loss. The diagnosis of PHG is (only) made endoscopically; it is most often characterized by an abnormality of the gastric mucosa described as a mosaic-like pattern resembling ‘snake-skin’, with or without red spots and the endoscopic pattern is key its diagnosis. Unfortunately, standardization of the endoscopic diagnostic criteria for PHG is poor and consensus is generally lacking, resulting in a wide range of reported prevalence. Pharmacological therapies, presumably reducing portal pressure and gastric blood flow, have been used to treat acute bleeding; propanolol, a non-selective β-blocker (24–480 mg/day), has been used most frequently. Endoscopic treatment for PHG bleeding plays a small, if any, role in the treatment of PHG. TIPS and shunt surgery have not been extensively analysed as a treatment for acute or chronic PHG bleeding, but they appear to lessen the severity of PHG. Secondary prophylaxis of PHG bleeding with non-selective β-blockers is recommended. There is not enough evidence to support the use of β-blockers in primary prophylaxis of PHG bleeding, even in cases of severe PHG (however, non-selective β-blockers are recommended if varices are present). Further studies are needed to clarify the role of PHG in suspected chronic gastrointestinal bleeding.