Gastroenterology

Mary has non-alcoholic fatty liver disease, which is a type of chronic liver disease (NAFLD). Non-alcoholic fatty liver disease is intimately associated with metabolic syndrome, as risk factors for non-alcoholic fatty liver disease are also metabolic syndrome components. The presence of risk factors such as obesity, hypertension, type 2 diabetes, and hyperlipidemia characterizes metabolic syndrome. Mary's BMI is 46.7, which puts her in the obese class III category, according to the World Health Organization's (WHO) International Body Mass Index Classification. This is the highest classification for people who have a BMI of more than 40. Using the International Diabetes Federation's (IDF) classification for metabolic syndrome, a large waist circumference and any of the following 2 risk factors as mentioned above would be highly confirmative of metabolic syndrome. Mary’s waist circumference is 123cm, which is more than the cut off point of 80cm. She has high triglycerides level at 2.8mmol/l (cut of point <1.7mmol/l), low HDL at 0.8mmol/l (cut of point >1.0mmol/l) and a high LDL at 3.9mmol/l (cut of point <2.5mmol/l), confirming the presence of hyperlipidaemia. She also has hypertension, where her blood pressure measures at 145/95 mmHg; over the cut of point of 130/85mmHg. She has also been diagnosed with type 2 diabetes mellitus which is a component of metabolic syndrome. Another strong indication that Mary has metabolic syndrome is that Mary is on medication for hypertension, diabetes mellitus and hyperlipidaemia. As a conclusion, Mary has a total of all the risk factors for metabolic syndrome and she is therefore consistent with the diagnosis of non-alcoholic fatty liver disease(NAFLD) type chronic liver disease which has close association with metabolic syndrome.
Mary’s chronic liver disease can cause the occurrence of haematemesis due to the presence of oesophageal varices. Oesophageal varices are dilated submucosal veins around the lower third of the oesophagus where there is anastomoses between the systemic veins and the portal veins which were form due to increase portal pressure. When the portal pressure increases, the venous dilation occurs between the oesophageal branch of the left gastric vein and the left azygos vein from the systemic circulation. As the collaterals form are superficial in nature, these oesophageal varices tend to rupture easily, therefore causing haematemesis.
In this case where Mary’s haematemesis had persisted for a duration, other pathology that relates to a normal liver function should be investigated. Some of the more common differential diagnosis are gastric or duodenal ulcer, gastric erosions, and reflux oesophagitis. Frequent drug use such as aspirin and other non – steroidal anti-inflammatory drugs (NSAIDS) for other usage should be ruled out as well. Peptic ulceration accounts for more than 50% of haematemesis cases, hence endoscopy and appropriate management should be taken.
Mary’s ascites has resulted due to a complication of chronic liver disease caused by the resistance in portal blood flow also known as portal hypertension. When the portal pressure increases, aside from causing portal anastomoses to form and splanchnic blood flow to increase; local hydrostatic pressure also increases, causing leakage of fluid into the third space, or in this case peritoneum causing ascites. A concurrent reduced plasma oncotic pressure and hypoalbuminaemia also contributes to the accumulation of fluid in the peritoneal cavity. The peripheral vasodilation in chronic liver disease also causes activation of the renin-angiotensin system as it detects hypo-perfusion thus stimulating salt and water retention. This mechanism then further contributes to Mary’s ascites.