Chronic liver disease
Carcinoma Stomach
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Introduction? Gastric cancer is endemic in Japan
? Late stage at diagnosis because of
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? Low incidence? Non specific symptoms
? Risk factors not definable
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? Biological y more aggressive
? Increasing incidence of adenocarcinomas of proximal
stomach and distal esophagus
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Etiology
? Low acid production
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Body of stomach? H pylori infection
? Low acid production
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Esophagus & Cardia
? Reflux
? Obesity
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? High BMI? High glycaemic load diet
? GERD
? Smoking
? Alcohol
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? TobaccoAlthough no normal lymphoid tissue is found in the
gastric mucosa, the stomach is the most common site
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for lymphomas of the gastrointestinal tract
Borrmann classification(depending on
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macroscopic appearance)
? Type I: polypoid or fungating cancers
? Type II: ulcerating lesions surrounded by elevated
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borders
? Type II : ulcerated lesions infiltrating the gastric wall
? Type IV: diffusely infiltrating tumors
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? Type V: unclassifiable cancersPatterns of Spread
? Local extension
? Lymphatic metastases
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? left supraclavicular fossa (Virchow's node)
? left axil a (Irish's node)
? S/c periumbilical tumour deposits (Sister Mary Joseph's nodes)
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? Peritoneal metastases? Distant metastases
Clinical Presentation
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? Weight Loss? Anorexia
? Early satiety (Diffusely infiltrative type)
? Recurrent Vomiting (pyloric involvement )
? Dysphagia
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? Bleeding? Anemia
? Fatigue
? Epigastric pain
? Ascites, jaundice, or palpable mass indicates incurable
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disease
? Transverse colon is a potential site of malignant
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fistulization and obstruction from gastric primary tumor? Diffuse peritoneal spread of disease frequently produces
other sites of intestinal obstruction
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? Large ovarian mass ( krukenberg's tumor)
? Large peritoneal implant in the pelvis ( blumer's shelf)
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? Macroscopic description of the tumor? Extent of peritoneal metastases (P0-1)
? Extent of hepatic metastases (H0-1)
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? Peritoneal cytology findings
Resection Classification
? R0: no gross or microscopic residual disease
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? R1: microscopic residual disease (+ margins)
? R2: gross residual disease
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Diagnostic work up? Tumour Markers: CA 19.9,CA 72.4, CEA, CA 50
? Endoscopy & Biopsy:
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? Chromo endoscopy: identification of mucosal abnormalitiesthrough topical stains.
? Magnification Endoscopy: magnify standard endoscopic
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fields by 1.5- to 150-fold.
? Narrow band imaging: increased visualization of the
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microvasculature? Confocal laser Endomicroscopy : 3D microscopy including
subsurface structures
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? Overexpression or amplification of HER2 (EGFR2):? occurs in approximately 20% of patients with
gastric cancer
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? Recommended in metastatic, recurrent gastric
cancer
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? Trastuzumab used in Her 2 neu + cancers? Endoscopic ultrasound (EUS)
? Computed Tomography
? Magnetic Resonance Imaging:
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? to characterize liver lesions on CT scan
? Positron Emission Tomography:
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? 50% of primary tumors are FDG-negative? diffuse (signet cel ) subtype most likely to be non-FDG
avid
? Staging Laparoscopy and Peritoneal Cytology:
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? directly inspects the peritoneal and visceral surfaces
? done to spare nontherapeutic operations
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Treatment? Surgery (Gastrectomy with lymph node
dissection) `
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? Radical Gastrectomy (Proximal gastric cancer)
? Subtotal Gastrectomy (mid & distal gastric cancer)
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When the oncologic goal of an R0 resection can be achieved by a gastric-preserving approach, partial gastrectomy is preferred over total
gastrectomy
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A: Subtotal gastrectomy with a Bil roth II anastomosis
B: Total gastrectomy with a Roux-en-Y anastomosis
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? Lymphadenectomy? 15 nodes for adequate pathologic staging
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? Partial Pancreatectomy and Splenectomy--Resect or
Preserve?
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Splenectomy:? Intraoperative evidence of direct tumor extension into the
spleen
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? Primary tumor is located in the proximal stomach along
the greater curvature
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Partial Pancreatectomy:? direct tumor extension into the pancreas
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Stage specific Survival rates for gastric adenocarcinoma arehigher in Japan than in Western countries because:
? Better-prognosis intestinal-type tumors are more common
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? Poorer-prognosis proximal gastric cancers are less frequent
? Widespread use of extensive D2 or D3 lymphadenectomy
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Chemotherapy
? Adjuvant
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? Neoadjuvant:
? Higher rate of R0 resections
? Early treatment of micro metastatic disease
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? Periperative
Adjuvant Intraperitoneal Chemotherapy
? Hyperthermic intraoperative peritoneal chemotherapy
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(HIPEC)
? Normothermic intraoperative chemotherapy (NI C)
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? Early postoperative intraperitoneal chemotherapy (EPIC)? Delayed postoperative intraperitoneal chemotherapy (DPIC)
Chemotherapy Drugs
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? Cisplatin
? 5-Fluorouracil
? Taxanes
? Epirubicin
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? Irinotecan? Trastuzumab (targeted therapy in Her 2 neu + )
Radiotherapy
? Preoperative
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? Intraoperative
? Postoperative
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Liver TumoursBenign tumours
? Liver Cell Adenoma
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? Focal Nodular hyperplasia? Hemangioma
? Mesenchymal hamartomas
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Liver Cell Adenoma
? benign proliferation of hepatocytes
? young women (aged 20-40 years)
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? associated with use of oral contraceptive pills (OCPs)? usually singular
? Upper abdominal pain
? tumor markers are normal
? MRI scans of LCA have specific imaging characteristics
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? two major risks are rupture & malignant transformation? Hepatic artery embolization
? Resection of the mass
Focal nodular hyperplasia
? Second most common benign tumor
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? young women? small (<5 cm) nodular mass
? involves the right and left liver equally
? Related to developmental vascular malformation
? Nonspecific symptoms
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? Contrast-enhanced CT and MRI scan? Symptomatic pts: resection
Hemangioma
? Most common benign tumor of the liver
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? Women more common than men (3:1 ratio)? Mean age of about 45 years
? Occur equally in the right and left liver
? Usually single
? Lesions > 5 cm are arbitrarily called giant hemangiomas
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? Tumor markers are usually normal? CT and MRI scan
? Resection: enucleation with inflow control
Hepatocel ular carcinoma
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Introduction? Fifth most common malignancy worldwide
? Male-to-female ratio 2.4:1
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? Poor prognosis
Etiology
? Infections with hepatitis B and C viruses
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? Ethanol abuse? Obesity
? Type 2 diabetes
? Non-alcoholic fatty liver disease
? Aflatoxin B1
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Pathology
? Malignant epithelial neoplasms: 85% to 95%
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? Benign: 6 %to 12%? Malignant mesenchymal tumors: 1% to 3%
? Metastatic tumors
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? Tumors metastatic to the liver are:? Peripheral
? Multiple
? Cause umbilication of surface of the liver
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? Primary liver tumors are:
? Central
? Solitary
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? Exophytic? HCC spreads most commonly to
? Lymph nodes around the liver
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? Peritoneal cavity? Lung
Characteristic feature of HCC is invasion of the
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portal veinClinical Features
Symptoms
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Signs? Abdominal pain
? Hepatomegaly
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? Weight loss
? Hepatic bruit
? Ascites
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? Weakness
? Splenomegaly
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? Ful ness? Jaundice
? Anorexia
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? Wasting
? Abdominal swel ing
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? Fever? Jaundice
? Virchow-Troisier nodes
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? Vomiting
? Cutaneous metastases (red-blue nodules)
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Paraneoplastic Syndromes? Hypoglycemia
? Erythrocytosis
? Hypercalcemia
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? Hypercholesterolemia? Dysfibrinogenemia
? Carcinoid syndrome
? Increased thyroxin-binding globulin
? Sexual changes (gynecomastia, testicular atrophy, and
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precocious puberty)
? Porphyria cutanea tarda
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Diagnostic work up
? Liver function tests
? S. Alpha feto protein (70%)
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? S.Des--carboxy prothrombin protein (80%)? Four-phase CT scan: unenhanced, arterial, venous, and delayed
phases
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? MR imagingCharacteristic feature of HCC: rapid enhancement during the
arterial phase of contrast administration and "washout" during
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the later portal venous and delayed phases
Portal venous phase of triphasic computed tomography scan
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? PET CT Scan: not recommended
? Core biopsy: hal mark feature of HCC is stromal invasion
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CHILD PUGH score for assessment of hepatic reserveQuantitative assessment of hepatic
reserve
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Indocyanine green clearance test? Retention rate <10%: all resections are possible
? 10% to 20%: bisegmentectomy is well tolerated
? 20% to 29%: single segment can be excised
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? 30% or more: risk of liver failure is highManagement
Stage I and II HCC
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? Surgical resection? Local ablation (radiofrequency ablation)
? Local injection therapies (ethanol injection):
? maximum size of tumor reliably treated is 3 cm
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? Transplantation
Child-Pugh A: Resection
Child-Pugh B and C patients with stage I HCC tumors : transplant, if
appropriate
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Adjuvant Therapy? Trans arterial chemotherapy (TACE)
? Systemic chemotherapy
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? Lipiodol? Doxorubicin
? Mitomycin
? Cisplatin
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Stage II and IV Tumors? TACE
? Regional Chemotherapy
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? Systemic Therapy? External Radiotherapy (< 8 cm)
? Hepatic Arterial Radioisotopes
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? yttrium-90 (90Y)
? 131 I antiferritin
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Portal HypertensionAnatomy
? The normal portal pressure is 5-7 mmHg (8-12
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cm of water).? Portal hypertension is present when the portal
vein pressure exceeds 12 mmHg
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Causes
? Presinusoidal
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? Sinusoidal? Postsinusoidal
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Sequelae & Clinical picture? Porto-systemic collaterals
? Splenomegaly
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? Congestion of the whole GIT
? Bleeding varices
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Intra-abdominal venous flow pathways leading to engorged veins(varices) from portal hypertension
Screening Tests for Portal Hypertension
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? Ultrasound with doppler blood flow assessment.
? MRI venogram
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? Contrast-enhanced helical CT scan
Detection of oesophageal varices
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Management
? Management of patients with actively bleeding
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oesophageal varices
? Resuscitation
? Correct coagulopathy
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? Prevent encephalopathy? Sclerotherapy
? Endoscopic Banding
? Drugs: Vasopressin,Somatostatin
? Balloon tamponade
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? Trans-juguJar Intra-hepatic Porto-Systemic Shunt
(TIPSS )
? Shunt operations
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? Portocaval shunt? Proximal spleno-renal shunt
? Mesocaval (Drapanas) shunt
? Selective shunt (Warren shunt)
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? Liver TransplantChronic Liver
Disease
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Catabolism of hormones
Glucose homeostasis;
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and other serum proteinsglycogenolysis & gluconeogenesis
Chronic Liver
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Disease
Synthesis:
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- Albumin- Coagulation factors
Storage:
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Bile excretion
- Glycogen
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- Iron- Cu, Iron, vitamins
Signs of CLD
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Chronic Liver
Disease
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Investigations
Bedside
? Observations, BM, fluid balance, weight
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Blood tests? LFTs (pre/post) (including albumin), INR
? FBC, U&Es, CRP
? Liver screen: autoantibodies, alpha-1 antitrypsin, caeruloplasmin,
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serum copper, ferritin, viral hepatitis serologyImaging
? US abdomen + portal vein doppler
? CXR, CT, MRI, MRCP
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Special tests? Ascitic tap, OGD (oesophageal varices), liver biopsy
What is your management plan?
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Conservative? Alcohol abstinence, optimise nutrition, low salt diet, fluid restriction
Medical
? Vitamin B supplementation (IV/PO), chlordiazepoxide
? Diuretics
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? Paracentesis (give albumin)? NG feeding
? Antibiotics (? SBP)
? Steroids + albumin (N.B. avoid NaCl)
? Lactulose (in hepatic encephalopathy)
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Surgical? TIPSS
? Liver transplantation
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Complications of CLD? Portal hypertension: oesophageal varices, ascites
? SBP
? Hepatic encephalopathy (constipation, GI bleed, infection, renal
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failure)
? Hepatocel ular carcinoma
? Coagulopathy
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? Hepato-renal syndrome? Liver failure
? 5 year survival rate in cirrhotic CLD 50%
? Child Pugh Score: bilirubin, INR, albumin, ascites, hepatic
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encephalopathy