Liver
A retired PVC factory machinist develops a large, irregular liver tumor on CT. Which lesion is most likely?
- ((Liposarcoma::Primary hepatic liposarcoma is rare; not associated with PVC exposure))
- ((Angiosarcoma::☑️ Vinyl chloride exposure is a classic risk factor for hepatic angiosarcoma))
- ((Hamartoma::Benign lesion, typically incidental and not linked to occupational exposure))
- ((Hydatid liver disease::Parasitic cystic lesion; not related to vinyl chloride exposure))
- ((Benign angioma::Usually small cavernous haemangioma; not large irregular malignant mass))
💡 Hepatic angiosarcoma is linked to vinyl chloride and arsenic exposure, presenting as aggressive vascular tumours.
A vitally stable patient undergoes exploratory laparotomy and is found to have a Grade III liver laceration that is not bleeding. What is the most appropriate management?
- ((Washout and close with drain monitoring::Not required if there is no active bleeding and patient is stable))
- ((Laparotomy and packing::Indicated for active bleeding or haemodynamic instability))
- ((Refer to hepatobiliary centre::Reserved for complex injuries or ongoing haemorrhage))
- ((Transfer to high-dependency for strict care::☑️ Stable, non-bleeding Grade I–III liver injuries are managed non-operatively with close observation in HDU/ICU))
💡 Indications for surgery in liver trauma (from WSES & ATLS principles):
- Absolute indications
- Hemodynamic instability despite resuscitation
- Peritonitis
- Evisceration / impalement
- Associated intra-abdominal injuries requiring surgery e.g., bowel perforation
- Relative/situational indications
- Failure of non-operative management: ongoing bleeding, transfusion requirement > 2-4 units/24h
- Expanding or pulsatile intra-abdominal hematoma
- Severe head or spinal cord injury, so clinical monitoring for NOM isn’t reliable
A child with kwashiorkor developed hepatomegaly. What is deposited in the liver?
- ((Glycogen::Hepatomegaly in kwashiorkor is not due to glycogen accumulation))
- ((Fat::☑️ Protein deficiency → ↓ Apolipoprotein synthesis → Impaired lipid export → Fatty liver → Hepatomegaly))
- ((Iron::Iron deposition causes hepatomegaly in haemochromatosis))
- ((Amyloid::Amyloid deposition causes hepatomegaly in amyloidosis))
💡 Kwashiorkor is a severe protein-energy malnutrition in children who are not getting enough protein in their diets, even if they get enough calories, especially from carbohydrates. Without enough protein, the liver cannot produce apolipoproteins needed to export fat, so fat accumulates in liver cells, leading to fatty liver and hepatomegaly.
A 50-year-old alcoholic woman with liver cirrhosis and platelet count < 50, splenomegaly present. What is the most common cause of thrombocytopenia?
- ((Ineffective production in bone marrow::Alcohol can suppress bone marrow, but this is not the most common cause in cirrhosis with splenomegaly))
- ((Platelet destruction in the liver::Platelets are not primarily destroyed in the liver in cirrhosis))
- ((Platelet destruction in the spleen::Immune destruction can occur, but this is not the main mechanism in portal hypertension))
- ((Platelet sequestration in the spleen::☑️ Portal hypertension leads to splenomegaly and hypersplenism, causing increased sequestration of platelets))
A 45-year-old man with established cirrhosis has splenomegaly and persistent thrombocytopenia. Bone marrow shows megakaryocyte hyperplasia. What is the most likely cause of his thrombocytopenia?
- ((Ineffective production in the bone marrow::Megakaryocyte hyperplasia indicates increased platelet production, not ineffective production))
- ((Platelet destruction in the bone marrow::Platelets are not destroyed in the bone marrow))
- ((Platelet destruction in the liver::The liver is not the primary site of platelet destruction in cirrhosis))
- ((Platelet sequestration in the spleen::☑️ Portal hypertension causes congestive splenomegaly and hypersplenism, leading to increased platelet sequestration; bone marrow responds with megakaryocyte hyperplasia))
💡 The splenic vein normally drains into the portal vein, thus high portal venous pressure [from cirrhosis] transmits backwards into the spleen, causing increased congestive splenomegaly, expansion of the red pulp, and eventually fibrosis of the splenic trabeculae. Red pulp expansion in massive splenomegaly can sequester up to 90% of the body’s platelets. Bone marrow responds with megakaryocyte hyperplasia.
A 50-year-old shepherd presents with weight loss and tender hepatomegaly. MRI shows a well-rounded calcified lesion in the liver. FBC reveals eosinophilia. What is the most likely diagnosis?
- ((Hepatocellular carcinoma::Does not typically cause eosinophilia and calcified cystic lesions are not characteristic))
- ((Pyogenic liver abscess::Usually presents with fever and inflammatory markers; calcified wall and eosinophilia are not typical))
- ((Hydatid disease of the liver::☑️ Caused by Echinococcus granulosus (sheep/dog exposure); classically presents as a cystic liver lesion with calcified wall and eosinophilia))
- ((Cholangiocarcinoma::Does not cause eosinophilia and typically presents with obstructive jaundice rather than calcified cystic lesions))
💡 Hydatid cyst △ Sheep exposure + calcified cystic lesion + eosinophilia