GI - Hepatomegaly and Liver cancer Flashcards
Malignant Ddx of hepatomegaly
Primary liver tumour
Hepatocellular carcinoma (HCC, 85%)
Cholangiocarcinoma (CC)
Secondary tumours
Solid organ malignancies: GI, other primaries
Haematological: leukaemia, lymphoma
Benign ddx of hepatomegaly
Infiltrative/replacement of parenchyma
Fat: alcoholic liver disease, NAFLD
Metabolic: Wilson’s disease, haemochromatosis, amyloidosis, other infiltrative diseases
Cysts: simple liver cysts, polycystic liver
Abscess: pyogenic, amoebic
Benign tumours:
Expansion of parenchyma
Hepatitis: infective, ischaemic, metabolic, autoimmune
‘Obstructive’
Vascular: Rt HF, TR, Budd-Chiari syndrome
Biliary: PBC, biliary atresia
Outline brief history taking for hepatomegaly
Pain: usually indicates significant enlargement stretching the liver capsule
Jaundice ± obstructive jaundice
GI symptoms, esp changes in bowel habits
Constitutional symptoms and fever
Systemic screen for any primary
Hx and RFs for chronic liver disease
FHx for malignancy
Outline P/E for hepatomegaly
General: cachexia, pallor, jaundice
Cervical LNs
Peripheral stigmata of chronic liver disease
Hepatomegaly itself: upper and lower border, surface, edge, consistency, tenderness, bruit
Other abd findings: splenomegaly, other masses, ascites
PR exam for rectal masses
Ddx diffuse smooth, firm hepatomegaly
Alcoholic liver disease
Haematological malignancies
Ddx irregular, hard hepatomegaly
HCC
Cholangiocarcinoma
Secondary malignancies
First-line investigations for hepatomegaly
□ Bloods: CBC, L/RFT, clotting profile, Viral hepatitis serology, tumour markers (AFP, CEA, CA19-9)***
□ Imaging: CXR, USG, triphasic CT, dynamic contrast MRI
□ Endoscopy: upper and lower (if suspicious for GI primaries)
□ Biopsy: plan for palliative radio-chemotherapy, defining cancer type for operability
- US-guided FNAC
- Tru-cut core biopsy
Liver anatomy:
Arterial and venous supply
Portal hepatis structure
□ Blood supply: 80% from portal v., 20% from hepatic artery
□ Venous drainage via left, middle and right hepatic veins
□ Porta hepatis structures:
→ CBD: towards the Right
→ Hepatic Artery: towards the Left
→ Portal Vein: towards the Inferior side
→ Divides into left and right branches 2cm from liver
Liver anatomy:
Ligaments and peritoneal reflections
→ Triangular ligament superiorly fixing superior surface of liver onto diaphragm
→ Falciform ligament anteriorly attaching anterior surface of liver onto abd wall
→ Ligamentum teres as remnant of umbilical v. running within falciform ligament to umbilicus
→ Ligamentum venosum as remnant of ductus venosus running along posterior surface of liver from lig. teres to IVC
→ Hepatoduodenal lig (lesser omentum) running from posteroinferior surface of liver to stomach, laterally bound by hilar vessels (f. of Winslow)
List benign liver tumors
Hepatic Haemangioma
Hepatic Adenoma
Focal Nodular Hyperplasia (FNH)
Hepatic Haemangioma /
Demographic
Pathogenesis
S/S
Complications
Demographic: Most common benign liver cancer, 30-50y, M:F ≈ 1:3
Pathogenesis: congenital vascular malformation, enlarge by ectasia (not hyperplastic), well-circumscribed lesion
S/S;
- Asymptomatic, incidental finding
- Vague RUQ discomfort/fullness: due to liver capsule stretch
- Mass effect: nausea, anorexia, early satiety
- Acute abd pain due to intra-tumour thrombosis/bleeding
- cutaneous haemangioma
Complications
- High output HF
- Hypothyroidism: ↑T3 deiodinase activity
- Kasabach-Merritt syndrome
Hepatic haemangioma /
Dx investigations with typical findings
Mx
Dx:
- USG: well-demarcated, homogeneous, hyperechoic mass with high vascularity
- Triphasic CT
Pre-contrast: well-demarcated hypodense lesion
Early phase: characteristic peripheral nodular enhancement
Delayed phase: remains enhancing - MRI: smooth, well-demarcated homogenous mass
***FNAC: contraindicated! (risk of severe haemorrhage)***
Mx:
Observation for asymptomatic esp if small, eg. <1.5cm
Serial imaging for larger asymptomatic tumours >5cm
Surgical resection for symptomatic or complicated lesions
Non-surgical Tx: low dose RT, arterial embolization, IFN-α-2A if large, unresectable
Hepatic Adenoma /
Demographic
Risk factors
Pathogenesis
Demographics: uncommon, usually in young women (M:F = 10:1)
RFs:
→ Strongly a/w oestrogen use (HRT/OCP
→ Anabolic androgen use
→ Others: glycogen storage diseases, genetic mutations, pregnancy
Pathology: benign proliferation of hepatocytes (NOT ‘hepatoma’), 70-80% solitary
Hepatic adenoma /
S/S
□ Asymptomatic in majority
□ Episodic RUQ/epigastric pain due to hepatomegaly, bleeding or tumour necrosis
□ Spontaneous rupture + intra-abd bleed: sudden severe pain + hypotension
□ Abdominal mass or hepatomegaly
□ Malignant transformation: risk ~8-13%,
Hepatic adenoma /
Dx investigations with typical results
Mx
Dx:
□ USG: non-specific well-demarcated hyperechoic SOL of liver
□ Triphasic CT: iso/hypodense (precontrast) → peripheral enhancement (early) → centripetal flow (portal venous) → iso/hypodense (late)
□ Others: MRI, 99mTc sulphur colloid scan, angiography
Mx:
□ Cessation of OCP + interval imaging for asymptomatic small adenomas
□ Surgical resection if symptomatic or >5cm
□ Avoid pregnancy/ undergo RFA before attempting pregnancy
Focal Nodular Hyperplasia of liver /
Demographic
Pathogenesis
S/S
Dx and Mx
