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DanishMandi

This document discusses hepatocellular carcinoma (HCC). It begins with a case presentation of a 24-year-old male patient admitted with right hypochondriac pain, fever, weight loss, and vomiting who was initially diagnosed with liver abscess. Laboratory tests revealed elevated liver enzymes and AFP level over 1000 ng/L. Imaging showed multiple hypodense hepatic lesions. The patient was diagnosed with HCC. It then discusses HCC including risk factors like hepatitis B and C infection, cirrhosis from any cause. Pathogenesis involves chronic liver injury leading to cell regeneration and metabolic dysfunction increasing cancer risk. Symptoms include weakness, abdominal pain, and weight loss. Diagnosis is made through clinical presentation,

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CMH BWP
HEPATOCELLULAR CARCINOMA By Dr. Danish Rauf HOUSE SURGEON, CMH Bahawalpur Supervisor Col Malik Saeed Awan Consultant General and Laparoscopic Surgeon CMH BWP
CMH BWP SEQUENCE Case Presentation Case Discussion
CASE PRESENTATION CMH BWP
A 24-year-old patient was admitted to our hospital with a 2-month history of right hypochondriac pain and fever. He also reported decreased appetite, significant weight loss, and occasional vomiting but there were no other symptoms. He gave no history of chronic medical illnesses; there was no drug or family history of note. He denied cigarette smoking or alcohol consumption. Before presenting here, the patient was already previously seen in another hospital in which a diagnosis of liver abscess was made.
GENERAL PHYSICAL EXAMINATION Pulse: 98/ min Blood Pressure: 100/60 mmHg Respiratory rate: 15/ min Temperature: 103 尊F CMH BWP
ABDOMINAL EXAMINATION 1 )palpable liver (10 cm below the right costal margin, irregular, firm and tender) 2) No ascites or splenomegaly 3) no peripheral stigmata of chronic liver disease 4) No hepatic failure r disease CMH BWP
SYSTEMIC EXAMINATION Unremarkable CMH BWP
INVESTIGATION Laboratory Radiological CMH BWP
LABORATORY CBC : Hb 14.6 gm/dL, WBC of 11300/cmm, platelets of 291,000/cmm. LFTs : total bilirubin of 35 mmol/L (reference range 0-17), ALT 54 IU/L (30-65), AST 74 U/L (15-37), alkaline phosphatase 344 U/L (50-136), GGT 646 U/L (1-94), albumin 33 g/L (34-50) CMH BWP
Serum alpha-fetoprotein : >1000 ng/L Hepatitis Profile : Negative RFTs : Normal
RADIOLOGY Ultrasound Abdomen : multiple hypodense hepatic lesions CT : multiple hypodense hepatic lesions with ring enhancemen CMH BWP
DIAGNOSIS Hepatocellular Carcinoma CMH BWP
CASE DISCUSSION CMH BWP
hcc20-8-15-150824200958-lva1-app6892.pptx
hcc20-8-15-150824200958-lva1-app6892.pptx
hcc20-8-15-150824200958-lva1-app6892.pptx
INCIDENCE 28/100000 in SEA 10/100000 in SE 5/100000 IN NE Incidence is increasing day bydaydue to -chronic hepatitis B &C virus infection. -cirrhosis due toanycause. Thedisease is morecommon in male(4:1)usually in middleage group(50years).
hcc20-8-15-150824200958-lva1-app6892.pptx
PATHOGNESIS Theexact pathogenesis is unknown. Thedisease seems tooccur in stages: Chronic liver injury > cell death >regeneration> cellular metabolicdysfunction> release of inflammatory mediators> increase risk of transforming mutation of hepatocytes. Preneoplastic changes hepatocytes dysplasia can be seen.
CLINICAL PRESENTATION Symptoms: Weakness, malaise, abdominal chest pain,vomiting,jaundice,haematemesis. Anorexia,weightloss incaseof metastasis.
CONTD. Sign: Jaundice Ascites Hepatomegaly Periumbilical collateral veins Variceal bleeding Easy bruising Hepaticencephalopathy Shock
CONTD Local examination: Palpable mass in right upperabdomen which is hard,irregular,tender/nontender. Hepatic bruit
SPREAD invasion into vasculature mostly portal vein. lymphnode. Lung and bone metastasis in terminal cases.
DIAGNOSIS: Diagnosisof HCC is done by : 1. Clinical presentation 2.Investigation 3. Staging
IMAGES OF INVESTIGATION
El-Serag HB. N Engl J Med 2011;365:1118-1127 MRI Studies Showing the Effects of Hepatocellular Carcinoma at Different Stages of the Disease. A: Very early stage (one lesion 1.7cm), B: early stage (2 lesions 2.4 and 1.2 cm) C: Intermediate stage (multiple lesions, Childs B), D: Advanced (large mass and ascites)
CONTD.. Tumormarkers: AFP- measurement -viral marker Liverradio isotope scans Liverfunction test: -serum bilirubin -AST -ALT -ALP -Prothrombin time -Serumalbumin
TNM STAGING
SCREENING FOR HCC
Methods: AFP (every 6 month) & Ultrasound Indications Forpatientat risk for HCC:- -Cirrhosis -Hepatitis B,C -Alcohol consumption -Genetic hemachromatosis -Autoimmune hepatitis -Non alcoholic steatohepatitis -Primary biliarycirrhosis -Alpha1antitrypsin deficiency
hcc20-8-15-150824200958-lva1-app6892.pptx
TREATMENT A. Surgical approach B. Non surgical therapy
SURGICAL APPROACH a. Segmental or local resection b. Lobectomy or partial hepatectomy c. Extended lobectomy d. Livertransplantation
IMAGES OF SURGICAL TREATMENT
B.NONSURGICAL THERAPY Majorityof HCC not be amenable tosurgical resection because of :- =Advanced stageof thecarcinoma & =Severity of the underlying liverdisease
CONTD.. Theoptions are: Ablative -Ethanol injection -Aceticacid injection -Thermal(cryotherapy,readiotherapy,microwave) Transarterial -Embolization -Chemoembolization Systemic -Chemotherapy -Radiotherapy -Imunotherapy
RADIOFREQUENC Y ABLATION
TRANSARTERIAL CHEMO EMBOLIZATION
MCQS
PROGNOSIS AFTER TREATMENT: o5 yearsurvival rate:- 30-40% after liver resection o5yearsurvival rate:- 75% in liver transplantation o2 yearsurvival rate :- 60% in transarterial chemoembolization
CONCLUSION In brief ,preventing and treating viral hepatitis may help to reduce the risk of developing liver cancer.Childhood hepatitis vaccinationof hepatitis B may reduce risk of it.Proper nutrition,rest,good habits(avoid alcohol) and safer practises makes a man healthy.
hcc20-8-15-150824200958-lva1-app6892.pptx

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hcc20-8-15-150824200958-lva1-app6892.pptx

Editor's Notes

  • #2: Worthy commandant, respected teachers and fellow colleagues, Asalam-o-Alikum.
  • #7: Her general physical examination revealed a middle aged lady oriented in time, place and person with stable vital signs.
  • #8: On breast examination there was obvious asymmetry of the breast. Right breast was more prominent and had a visible swelling of approximately 6cm x 5cm, which was hard in consistency, present in the outer quadrant of right breast at around 9 oclock position.THE LUMP HAD IRREGULAR MARGINS AND WAS FIXED TO THE CHEST WALL but no fixity to the skin Nipple was retracted.No peau dorange or ulceration was seen. there was no dimpling of skin.There was a mobile, firm pectoral lymph node palpable in the right axilla. Supra clavicular fossa was clear. Contralateral breast, axilla and supraclavicular fossa were normal too
  • #9: There was no evidence of pleural effusion or consolidation No hepatomegaly, ascites or abdominal swelling noticed. PELVIC ,Skull and spine were normal TOO
  • #10: There was no evidence of pleural effusion or consolidation No hepatomegaly, ascites or abdominal swelling noticed. PELVIC ,Skull and spine were normal TOO
  • #11: There was no evidence of pleural effusion or consolidation No hepatomegaly, ascites or abdominal swelling noticed. PELVIC ,Skull and spine were normal TOO
  • #13: There was no evidence of pleural effusion or consolidation No hepatomegaly, ascites or abdominal swelling noticed. PELVIC ,Skull and spine were normal TOO
  • #14: On the basis of the history, examination and investigations a final diagnosis of INVASIVE DUCTAL CARCINOMA of the right breast was made. She was staged as T4aN1M0 (locally advanced) as it was lump more than 5cm, fixed to chest wall with few mobile axillary LN
  • #15: Now the case discussion