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home - Liver - Liver Masses - Nodular Regeneration Written by Dr Sebastian Zeki

Knows the epidemiology pathology clinical presentation and natural
history of benign tumours of the liver

Can define a programme of investigation and characterisation of
benign liver lesions including haemangioma focal modular
hyperplasia and adenoma

Demonstrates ability to make an appropriate differential diagnosis
Formulates appropriate plan of management
Recognises importance of the role of multidisciplinary team in
diagnosis and management



Understands the epidemiology risk factors pathology prevalence
and range of presentations of HCC

Knows the appropriate investigation and staging of the disease
Aware of treatment options including trans-arterial
chemoembolisation (TACE) radiofrequency ablation (RFA) local
ethanol injection

Appreciates the indications and contraindications of each and how
the most appropriate is selected Aware of surgical treatment options

Aware of role of surveillance and referral for specialist multidisciplinary management including liaison with oncology

Appreciates the indications and contraindications of each modality of
treatment and how the most appropriate is selected

Understands the process of selection of patients for liver resection or

Appreciates Involvement of multi-disciplinary team in management
decisions close liaison with surgical radiology oncology and
pathology colleagues

Nodular Regeneration

Treatment:Treat the underlying condition.Treat portal hypertension.Liver transplantation if liver failure co-exists. Consider NRH in non-cirrhotic portal hypertension.Diagnosis is histologicalNo need to survey Results in hypertrophy of less vulnerable peri-portal areas and subsequent nodulesTransient T-cell induced endothelial injury may also be the trigger for the development of NRH EpidemiologyThis has an overall prevalence of 1%. It is more common in the elderly.and M=F incidenceIt is sually asymptomatic and normal LFT’s / slowly progressive Nodular regenerative hyperplasia of the liver Drugs:Azathioprine Thioguanine Cyclophosphamide Chlorambucil Busulfan Doxyrubicin Cytosine Arabinoside Bleomycin Carmustine Interleukin-2 Haem/Onc:Liver cancers Sacrococcygial teratoma Essential thrombocytosis Polycythemia vera Lymphoproliferative / Myelo-proliferative disorders Multiple myeloma Spherocytosis Sickle cell disease Protein S deficiency Factor V Leiden mutation Hyperhomocysteinemia Antiphospholipid syndrome Immune PBCPolymyositis Sjögren's syndrome Scleroderma CREST Syndrome Still's syndrome Polyarteritis nodosa RA/PMR/ SLEBehcet's disease Cryoglobulinemia Idiopathic hypereosinophiliaTTP Celiac disease Myasthenia gravis HIV/ CVID Others Liver/ Renal transplantationASDVSDPulmonary vein anomalies Congenital portal venous anomalies VATER syndrome HHTCystinosis Turner's syndrome Nodules of 1 to 3 mm H H H H H H Nodules clustered around portal triads. The central part of the regenera-tive nodule consists of hypertro-phied hepatocytes arranged in multilayer (2-3 layers) plates. Peripheral cells are thin, atrophic, and arranged in parallel plates assoc. with some sinusoidal dilatation . No fibrosis between nodules Need reticulin staining Central event may be portal venopathy due to thrombosis/ obliteration due to hypercoagulability, endothelial injury, or autoimmune injury and subsequent ischaemia adjacent to central vein USS: isoechoic/ hypoechoic often with a hypoechoic rim, features that can mistakenly suggest hepatic metastases; CT: nonspe-cifically hypodense. MRI: isointense on T2-weighted images and contain foci of high intensity on T1-weighted images. PrognosisThis depends on development of PHTN.The relationship between NRH and HCC is unclear. Radiology Pathology Associations Written by Dr Sebastian Zeki

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