T10 Liver, biliary, pancreatic diseases II Flashcards
MOCK:
85/M identified RUQ tenderness and prescribed antibiotics.
+ve Murphy sign, high fever.
With old stroke, on clopidogrel (anti-platelet).
Working diagnosis and supporting evidence? (1)
Acute cholecystitis (0.5) Murphy sign + typical // high fever indicated sepsis (0.5)
MOCK:
85/M identified RUQ tenderness and prescribed antibiotics.
+ve Murphy sign, high fever.
With old stroke, on clopidogrel (anti-platelet).
Gross features of specimen:
- Multiple pigmented gallstones
What other gross features expected? (1.5)
- Thickened wall (0.5)
- Hepatitis/ liver abscess (0.5)
- Crohn’s colitis/ RLL pneumonia (0.5)
MOCK:
85/M identified RUQ tenderness and prescribed antibiotics.
+ve Murphy sign, high fever.
With old stroke, on clopidogrel (anti-platelet).
What are the typical histological features of this condition (acute and chronic) and underlying mechanism? (2)
Acute
- Mucosal erosion/ulceration (0.5)
- Transmural neutrophilic exudate (0.5)
Chronic
- Rokitansky-Aschoff sinuses (0.5)
- Outpouching of gallbladder mucosa in response to repeated inflammation/increased intraluminal pressure (0.5)
Potential complications of acute cholecystitis? (4)
- Empyema
- Ruptured GB wall
- Acute cholangitis
- Liver abscess
MOCK:
85/M identified RUQ tenderness and prescribed antibiotics.
+ve Murphy sign, high fever.
With old stroke, on clopidogrel (anti-platelet).
Why did surgeon wait one week before performing an operation (2)?
- Clopidogrel > low platelet, high risk of bleeding
- Stopped clopidogrel + infuse platelet, allow time for patient to rise to an acceptable platelet level
- need to to monitor the RUQ mass to secure diagnosis
- need time to perform investigations/imaging to confirm diagnosis
64/M with chronic viral hep B and cirrhosis admitted for anorexia, progressive weight loss, and RUQ pain for 2 months. The patient passed away despite the use of Sorafenib. (for renal/liver cancer).
Gross: multiple hepatic tumoral masses in cirrhotic background.
Describe the histological feature of the specimen.
(architecturally + cytologically) (7)
Architecturally,
- it is composed of a proliferation of tumor cells
- with hepatocellular differentiation in thickened trabeculae
Cytologically,
- tumor cells show malignancy cytology with nuclear enlargement
- pleomorphism
- increase N:C ratio
- frequent mitosis
- hyperchromasia
In contrast to other organs, why the histological confirmation of liver cancer is not always required? (4)
- Should be based on radiological/pathological examination.
- Hallmark: Contrast enhancement of the arterial phase, washout during the venous phase
Liver biopsy
- invasive procedure with bleeding, puncture risk
- tumor seedling along needle track is possible
64/M with chronic viral hep B and cirrhosis admitted for anorexia, progressive weight loss, and RUQ pain for 2 months. The patient passed away despite the use of Sorafenib. (for renal/liver cancer).
There is a portal vein tumor thrombus in the hilar region. One week before his death, he developed massive ascites and his serum creatinine was abnormally elevated to 4 times of upper limit of normal.
Diagnosis of his rapidly deteriorating renal function?
Explain.
Hepatorenal syndrome.
- Newly formed portal vein thrombus in porta hepatis worsened portal hypertension, induced ascites
- Massive ascites decreased ECV, thus induced RAAS > pre-renal renal failure - hepatorenal syndrome
70/M with chronic HepB, Child-Pugh C cirrhosis, found to have elevated serum alpha-fetoprotein.
Presence of solitary liver cancer in multiphase CT.
Diagnosis?
Child-Pugh C meaning?
Hepatocellular carcinoma;
Child-Pugh score 10-15 with 50% 1-5 year survival rate
What is the use of serum alpha-fetoprotein in patients with chronic liver disease and liver cancer? (3)
- Diagnosis
- Prognosis
- Disease monitoring (for treatment response and recurrence)
What are the major components of BCLC (Barcelona Clinic Liver Cancer) staging system? (3)
- Tumor burden (size and nodules)
- Performance status
- Liver function (Child-Pugh grade)
60/M with chronic viral HepB had a previous operation for lung adenocarcinoma 3 years ago. Now revealed multiple tumoral masses in non-cirrhotic liver.
How to differentiate between primary and secondary liver tumors? (Grossly, histologically, immunohistochemically) (3)
- Grossly, non-cirrhotic liver is in favor of metastasis
- Histologically, HCC is composed of a proliferation of tumor cells with hepatocellular differentiation in thickened trabeculae;
whereas adenocarcinomas are composed of a proliferation of tumor cells with glandular differentiation in irregular angulated and complex glands, - immunohistochemically, HCC expresses hepatic markers, e.g. HepPar-1/ Arginase-1;
whereas metastatic pulmonary adenocarcinoma expresses pulmonary markers e.g. TTF-1, Napsin-A
Pulmonary primary adenocarcinoma metastasized to the liver. Describe features of liver biopsy.
Architecturally, is composed of a proliferation of tumor cells with glandular differentiation in irregular angulated and complex glands.
Cytologically, tumor cells shows malignant cytology with increased N:C ratio, hyperchromasia, pleomorphism, nuclear enlargement, and frequent mitosis.
60/M with chronic viral HepB had a previous operation for lung adenocarcinoma 3 years ago. Now revealed multiple tumoral masses in non-cirrhotic liver.
The clinical oncologist requested EGFR mutation test and ALK translocation test.
Clinical significance of these tests?
Activated EGFR mutation and ALK translocation indicate eligibility for EGFR tyrosine kinase inhibitor (TKI) and ALK inhibitor, respectively.
Anti-EGFR targeted therapies are used in both advanced lung and colorectal cancer patients. Compare and contrast target therapies and molecular tests for these 2 cancers. (4)
Colorectal adenocarcinoma
- targeted therapy: anti-EGRF antibody
- molecular test (predictive biomarker): KRAS/NRAS mutation +ve - no response
Lung adenocarcinoma
- targeted therapy: EGFR tyrosine kinase inhibitor (TKI)
- molecular test (predictive biomarker): EGFR mutation +ve - responsive
