Liver, Pancreas And Gallbladder Flashcards
(21 cards)
What is the blood supply of the liver?
•Dual blood supply: Hepatic Artery (30%) and Portal Vein (70%)
•Blood flows from the portal tracts to terminal hepatic -> venules/central venules -> segmental and lobar hepatic veins -> hepatic vein -> inferior vena cava
What are the functional units of the liver?
•Lobule– terminal hepatic venule at the centre and periphery delineated by portal tracts
•Zone 1 (periportal) and zone 3 (peri-central)
•Blood flows from portal vasculature to terminal hepatic venule – decreasing nutrient and oxygen gradient
•Acinus– functional unit with a portal tract in centre and terminal hepatic venules at the periphery
What are hepatocytes?
Hepatocytes: one cell thick plates separated by sinusoids (fenestrated endothelium)
–Free exchange of molecules at the cell surface, sinusoidal blood drains into central veins
–Bile drained into canaliculi between hepatocyte
What is hepatitis A?
•RNA virus
•Transmission- fecal-oral route (person to person or contaminated food and drink)
• Symptoms-nausea, anorexia, fever, malaise, and abdominal pain,dark urine, pale stools jaundice
• Diagnosis- detection of serum immunoglobulin (Ig)M anti-HAV antibodies
•Self limited course with fulminant hepatic failure in less than 1%
•Does NOT cause chronic hepatitis
•Lifelong immunity once infected
What is hepatitis B?
•DNA virus with 8 genotypes
•High infection rates in China, Southeast Asia and sub-Saharan Africa (15% of population)
•Transmission– Horizontal transmission - Sexually transmitted, iv drug abusers ( needles and syringes) and vertical transmission - perinatal transmission
•Symptoms- Acute HBV infection – 70% have no symptoms, 30% symptomatic with mild flu-like symptoms to nausea, vomitting and jaundice
•Diagnosis– serum markers including Hepatitis B surface antigen
•Risk of chronic infection in less than 5% of those with acute infection
•Treatment- acute infection – supportive
•Chronic infection – antiviral agents – pegylated interferon, Entacavir, Tenofovir
•Integration of HBV DNA into the human genome – pro-carcinogenic pathways – strong risk factor for hepatocellular carcinoma
What is hepatitis D?
•RNA virus of Deltaviridae family
•Dependent of hepatitis B for it’s life cycle – coinfection (acquired simultaneously with Hep B) or superinfection in a person who already has hepatitis B
•Infects about 5% of hepatitis B infected persons
•acute hepatitis D has an increased risk of a fulminant course when compared to acute hepatitis B
•exacerbates the preexisting liver disease due to HBV
•Highest fatality rate of all hepatitis infections (~20%
What is hepatitis C?
•RNA virus
•Transmission- Blood borne transmission – iv drug abuse, needle stick injury, blood products. Sexual transmission infrequently
•Progression to chronic disease occurs in a majority of HCV infected individuals (upto 80-90%)– asymptomatic or mild non-specific symptoms such as fatigue
•Cirrhosis in 20-30% and risk of hepatocellular carcinoma (25% of all HCCs due to HCV)
•Commonest cause for liver transplantation worldwide, but virus will recur
•Now 90% cure with new antiviral (Sufosbuvir)
What is hepatitis E?
•Single stranded RNA virus
•Transmission – faeco-oral transmission
•Animal reservoir – monkeys, cats, pigs and dogs
•Spectrum – from mild symptoms to fulminant hepatic failure
•High mortality rate among pregnant women – approaching 20%
What are the types of autoimmune hepatitis?
•Type-1 autoimmune hepatitis-positive ANA, anti-smooth muscle (SMA) and anti-soluble liver, antigen. Predominantly involving adults
•Type 2 autoimmune hepatitis-anti-liver, kidney microsomal antibodies. Disease occurs predominantly in children
What are the main morphological features of cirrhosis?
•Bridging fibrous septa
•Parenchymal nodule formation
•Disruption of the architecture of the entire liver – diffuse changes involving the whole liver
What are the causes of cirrhosis?
●Alcoholic liver disease
●Non-alcoholic fatty liver disease
●Chronic viral hepatitis (hepatitis C)
What is steatohepatitis?
Steatohepatitis-constellation of findings with evidence of cell injury/cytoskeletal disruption, cell death and accompanying inflammation
•Histologically ballooned hepatocytes- essential finding-indicative of microtubular disruption
•Ballooned hepatocytes may contain Mallory-Denk bodies (cytoskeletal aggregates composed predominantly of protein) – p62, anti-ubiquitin immunohistochemistry
•Necroinflammation-Lobular inflammation-lymphocytes, macrophages and neutrophils
•Hepatic fibrosis-characteristic early fibrosis that is perivenular/pericellular which may be accompanied by portal and periportal fibrosis
What is PSC histology?
What is hereditary haemochromatosis?
•Autosomal recessive pattern of inheritance (HFE C282Y homozygosity)
•Iron deposition in liver (hepatomegaly), pancreas and skin (bronze diabetes), heart (cardiomyopathy), joints (arthritis) etc
•Biochemical findings – raised transferrin saturation
•MRI –estimation of iron overload
•Liver biopsy
•Liver biops
What is Alpha-1 antitrypsin deficiency?
•Autosomal recessive disorder
•Glycoprotein synthesized by hepatocytes (Protease inhibitor (Pi) family)
•Genotypes PiMM (most common 90%)
•Deficiency variant PiS (moderate reductions), PiZ (most common clinically significant variant)
•Homozygotes – PiZZ– very low circulating alpha-1 antitrypsin levels
•Protein is synthesised and secreted normally but defect in migration from endoplasmic reticulum (ER) to Golgi apparatus – mutant polypeptide (abnormal) accumulates in ER
of hepatocytes
•Clinically – pulmonary emphysema and liver disease (neonatal hepatitis, fibrosis,
cirrhosis)
Primary vs secondary liver tumours
• Primary: Neoplastic transformation of normal cells within the liver. Benign= hepatocellular adenoma, intraductal papillary neoplasm, haemangioma. Malignant= angiosarcoma, hepatocellular carcinoma and cholangiocarcinoma
• Secondary: Haematogenous (via blood) metastases from other primary malignant tumours
What is Wilson’s?
What is Hepatocellular adenoma?
• Clinical importance: distinction from malignancy and focal nodular hyperplasia (FNH)
• FNH = non-neoplastic nodular overgrowth of liver tissue
• Pathology:
• Soft, well circumscribed, tan coloured tumour
• Histology: Sheets of bland hepatocytic cells without normal portal triads/tract
What is Cholangiocarcinoma (CCA) ?
Clinical presentation:
• Intrahepatic: vague and insidious, late presentation
• Perihilar and distal: jaundice, itch, abdominal pain, weight loss, fever
• Pathology:
• Intrahepatic: majority expansile, firm, white tumours with scalloped margin
• Perihilar and distal: infiltrating, ill-defined, fibrous tumour
• Histology: Abnormal glands/tubules with mucin production associated with stroma (fibrous tissue)
What is Pancreatic ductal adenocarcinoma?
Clinical presentation:
• Late symptoms – 85% inoperable at presentation
• Abdominal or back pain, jaundice, weight loss
• Diabetes mellitus, nausea/vomiting, poor appetite, thromboses (Trousseau’s sign)
• Pathology:
• Ill-defined, infiltrative, firm, fibrous tumour, commonest in head of pancreas
• Histology: Abnormal glands associated with prominent stroma (fibrous tissue)
What are Pancreatic Neuroendocrine Neoplasms?
• Pancreatic Neuroendocrine neoplasms are rare tumours arising from (neuro)endocrine cells
• Mostly well differentiated, potentially malignant, slow progression
= well differentiated neuroendocrine tumours (NETs)
• Poorly differentiated are rare and highly aggressive
= Neuroendocrine carcinomas (NECs)
