Hepatobiliary Diseases Flashcards

1
Q

Liver Anatomy

A
  • weights 1200-1500g , divided into two main lobes (right and left lobes)
  • dual blood supply - 1.) Hepatic artery (ex celiac artery, oxygenated blood from the heart) and 2.) portal vein (deoxygenated blood from GI tract)
  • bile leaves the body via the left and right hepatic ducts that join to form the common hepatic duct. CBD joined by the pancreatic duct just before it enters the duodenum at the ampulla of Vater, which is guarded by the sphincter of Oddi.
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2
Q

Liver Histology

A
  • divided into hexagonal lobules
  • At the center of each lobule is the central vein which joins the hepatic veins
  • portal tracts are at the periphery of the lobules, each containing a hepatic artery, portal vein, and bile duct
  • the parenchyma is comprised of lobules and consists of anastomosing sheets or cords of liver cells (hepatocytes)
  • vascular sinusoids are between the cords
  • arterial and veinous blood enters the liver via the hepatic artery and portal veins through the sinusoids, during which it washes over the hepatocytes and then exits through the central veins to the hepatic veins and vena cava
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3
Q

Liver Function

A

Metabolic
- glucose and lipid physiology
- uses things
- excess blood glucose is stored in the liver as glycogen. Glucose is released into the blood through glycogenolysis, glucose made from AAs - during fasting, the liver converts free fatty acids to triglycerides which is secreted as lipoproteins

Synthetic
- most serum proteins (albumin, clotting factors, complement, iron and copper-binding proteins) made in the liver, with the exception of immunoglobulins

Storage
- liver stores glycogen, triglycerides, irons, copper, and lipid-soluble vitamins

Catabolic
- endogenous (hormones, serum proteins) by the liver to maintain their levels - Exogenous (drugs) substances too

Excretory
- bile (most important for fat absorption in small intestine)

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4
Q

Diagnosis Liver Disease

A

Liver function tests
- bilirubin, albumin, INR (blood clotting test)
- liver clearing toxins, producing proteins, clotting factors
- Not clearing toxins - bilirubin in blood increases
- not producing proteins - albumin in the blood decreases
- not making clotting factors/too long to clot - INR test abnormal (elevated INR)

Liver Enzyme Test
- ALT, AST, GGT, LDH
- when liver cells are inflamed - more enzymes are excreted into the blood, levels increase

Liver Ultrasound
- lesion in liver, screen for cancer

Liver Biopsy

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5
Q

Common Hepatotrophic Viruses

A
  • viral hepatitis is the inflammation of the liver caused by viruses
  • can affect the liver directly (hepatitis viruses) or affect the liver secondary due to a systematic infection (cytomegalovirus or Epstein Barr Virus)
  • Histology - inflamed liver (inflammation amount = grade), dense aggregates of inflamed cells, lymphocyte infiltrate centred on portal tract (chronic appearance), a large quantity of fibrotic tissue (amount determines stage)
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6
Q

Hepatitis A

A
  • causes mild or asymptomatic hepatitis
  • spread via fecal-oral route (food and water contamination)
  • epidemics common, high association with oro-anal sexual practices
  • serology for diagnosis - anti-HAV IgM is indicative of current infection, anti-HAV IgG is indicative of past infection
  • the disease is mild and self-limited, it is protracted and relapsing
  • Few develop fulminant or chronic hepatitis, no carriers of hepatitis A
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7
Q

Hepatitis B

A
  • blood and body fluid-borne disease
  • 400 million, 75% in South-East Asia

High-Risk Individuals
- blood transfusions
- IV drug abusers
- healthcare workers
- hemodialysis patients
- high-risk sex practices

Spread - parenteral (injection), close contact, sexual, vertical

The concentration of body fluids
- high = blood, serum, wound exudates
- Medium = semen, vaginal fluid, saliva
- low = urine, sweat, tears, breastmilk

Serum Antigens and Antibodies
- HBsAg - surface antigen, first appearing marker - >4-6 months = chronic
- HBsAb - normally persists for life and is the protective, the basis of vaccine, which means you have success vaccine or are immune

Infection rates
- 30-40% know they have it
- 5-10% are carriers
- 5-10% chronic, low rate, most clear - 1% recovery, 20% cirrhosis, 2-3% carcinoma
- 25% acute - 99% recover, 1% -> fulminant -> death or transplant
- HCC is 200x risk

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8
Q

Hepatitis C

A

Transmission
- blood transfusion
- parenteral transmission - most common is an IV drug
- sporadic hepatitis
- HBV method higher % than needle

Serological Diagnosis
- Anti-HCV Antibodies or PCR for viral RNA detection

Treatment
- interferon and related drugs, antivirals
- no vaccine

infection
- few have acute hepatitis
- rare fulminant
- chronic is 80% - takes years/decades
- 80% of carrier state
- cirrhosis in 20% of chronic patients

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9
Q

Hepatitis D

A
  • defective virus - HDV can only replicate in the presence of HBV
  • Modifier of acute and chronic hepatitis B
  • presentation depends on the presence of hepatitis B concurrently (co-infection) or after (super-infection)
  • transmitted parenterally
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10
Q

Needle stick Injury

A

Risk of transmission after needle prick
- Hepatitis B - 30%
- Hepatitis - 3% (0-10)
- HIV - 0.3%

Follow up after needle
- HBV - vaccine if unvaccinated
- post-exposure prophylaxis with HBV immunoglobulin (HBIg) considered

HCV - baseline, follow up testing for anti-HCV antibodies and ALT activity (inflamed hepatocytes)

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11
Q

Cirrhosis

A
  • end-stage in the evolution of many chronic liver diseases - includes viral hepatitis

The diffuse process involves:
- deposition of fibrous tissue (fibrosis)
- conversion of moral architecture into regenerative nodules

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12
Q

Etiology of Cirrhosis

A
  • infections - HBV, HCB, schistosomiasis
  • drugs/toxins - alcohol, methotrexate, amiodarone
  • Metabolic - NAFLD/NASH, hemochromatosis, Wilson’s disease, alpha-1-antitrypsin deficiency
  • autoimmune - primary biliary cirrhosis
  • biliary obstruction - calculi, sclerosing cholangitis
  • venous - veno-occlusion disease, Budd-chiari syndrome
  • Miscellaneous - neonatal hepatitis syndromes
  • cryptogenic
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13
Q

3 Major Causes of Cirrhosis

A

1.) Cell death
- initiating factors occurs continuously over a long period of time
- mild = can recover, cirrhosis does not occur
- MUST be recurrent to be cirrhosis

2.) Regeneration
- Completes the reparative process
- Hepatocytes will try to regenerate to restore normal function
- End up with Regenerative nodules - due to fibrous tissue present

3.) Fibrosis
- Repair mechanism that follows cell death
- When cells cannot repair quickly enough to repair damaged tissue
- Lay down fibrous tissue - provides structure and stability

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14
Q

Complications of Cirrhosis

A

abnormal blood flow - Problematic
- leads to portal hypertension
- portal vein drains blood from the entire GI tract through the liver - back pressure = problems
- esophageal varices (rupture -> hematemesis) - vomit blood, vital
- splenomegaly (enlargement of spleen) and ascites (build-up of fluid in the abdominal cavity that leaked out of the vascular system)

Parenchymal Insufficiency
- impaired protein synthesis - decrease in albumin (keep blood plasma in the vascular system, clotting factors)
- inadequate deactivation of drugs and hormones
- jaundice
- Clotting abnormalities
- Hepatic encephalopathy - altered mental state

Hepatocellular carcinoma
- can be a late complication

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15
Q

Stages of Alcoholic Liver Disease

A

Steatosis (fat)
- earliest manifestations - least serious
- fat in the liver
- few symptoms or signs
- usually disappears in 4-6 weeks of abstinence
- pink hepatocytes, purple nuclei, large white fat droplets in cytoplasm, no inflammation

Alcoholic Hepatitis (steatohepatitis)
- elevated liver enzymes
- Triad (inflammation, steatosis, liver cell damage)
- elevated aminotransferase, alkaline phosphatase, and jaundice
- fat droplets, small purple dots (inflammation cells), Mallory bodies (damaged hepatocytes, a marker)

Cirrhosis
- often due to alcohol - 80 g (8 beers) is mild and reversible,
- hepatitis Cellular Cirrhosis (HCC) - 5-15%, may act as a promoter or co-carcinogen related to the induction of microsomal enzymes.

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16
Q

Fatty Liver Disease

A
  • most common liver abnormality disease in NA
  • the hepatic expression of the metabolic syndrome - increased associated with obesity

Two main morphological Types
- Non-alcoholic fatty liver
- Non-alcoholic Steatohepatitis

17
Q

Non-alcoholic Fatty Liver

A

steatosis
- usually macrovascular (admixed with micro)
- Zone 3 or diffuse
- Quantified as <5%, 5-33%, 33%-65%, >66%

No hepatocellular injury
NAFL does not always -> NASH

–> Steatosis without hepatobiliary injury - just fat in liver

18
Q

Non-alcoholic Steatohepatitis

A

Steatohepatitis
- steatosis
- hepatocyte ballooning
- inflammation (lobular +/- portal) - +/- Mallory Denk bodies (Mallory bodies, Mallory hyaline) - +/- fibrosis

Grading
- depends on inflammation and cellular damage

Staging
- quantity of fibrosis

20-25% get cirrhosis, risk increase with more liver diseases

–> steatosis with inflammation and hepatic injury - +/- fibrosis
CANNOT tell if fatty liver cause by NASH or alcohol

19
Q

Metabolic Diseases

A

Most important (excluding NASH):
- Hemochromatosis
- Wilson’s Disease
- Alpha-1-antitrypsin (ATT) deficiency
- maybe non-inherited iron overload

20
Q

Hemochromatosis

A
  • one of the most common hereditary/genetic diseases in the West
  • individuals homozygous for C282Y mutation for the HFE gene (chromosome 6)
  • life long excess iron absorption (duodenum)
  • deposition of iron cells and tissues - liver (cirrhosis), heart (cardiac failure), pancreas (diabetes mellitus), joints (arthropathy), bronze skin
  • increased risk of HCC - abnormal iron in hepatocytes, brown pigment

Treatment
- removal of iron from phlebotomy - remove blood and iron at regular intervals

21
Q

Wilson’s Disease

A
  • copper accumulation in the liver and multiple other organs
  • patients develop hepatitis and cirrhosis
  • degenerative neurological disease from brain involvement - neuropsychiatric symptoms
22
Q

Alpha-1-Antitrypsin Deficiency

A
  • A1AT is a protein which inhibits proteinase digestion, synthesized in the liver
  • deficiency = abnormal proteins produced and accumulated in the liver - > difficulty excreting hepatocytes
  • main consequences to liver and lungs - chronic hepatitis and cirrhosis (children), emphysema (adults, alveolar membranes broken down by proteinases)
23
Q

Metabolic Syndrome X

A
  • increased in obesity and in metabolic syndromes
  • a cluster of metabolic abnormalities that are risk factors for cardiovascular disease
  • insulin resistance, diabetes mellitus, obesity, dyslipidemia, and systemic hypertension
  • NAFLD is considered a hepatic expression of metabolic syndromes
24
Q

Cholestasis

A
  • impaired excretion of bile -> hyperbilirubinemia -> manifests as jaundice (+/-) prurtis
25
Q

Extrahepatic Cholestasis

A
  • obstruction of large bile ducts OUTSIDE of the liver

Etiology
- Gallstones
- Tumours - around bile ducts
- Congenital abnormalities - Astrea, choledochal cyst
- strictures -following surgery, sclerosing Cholangitis

Gall stones
- Cholelithiasis = gall bladder stones
- choledocholithiasis = bile duct stones
- 10-20% adults, >80% asymptomatic
- 3 types: Cholesterol (80%), black pigment, brown pigment

Complications of Cholelithiasis
- Swelling
- Acute inflammation (acute cholecystitis) - Red, inflamed
- Fibrosis (chronic cholecystitis) - Thicken and fibrotic tissue
- Stone may move down to -> bile duct (choledocholithiasis)
- Ball-valve obstruction
- Fibrotic Stricture
- Ascending bacterial cholangitis
- Eventually prolonged obstruction -> secondary cirrhosis

26
Q

Intrahepatic Cholestasis

A
  • a failure for bile secretion within the liver or obstruction of intrahepatic biliary passages

Etiology
- congenital/familial
- acquired - hepatitis, drugs/toxins, sepsis, primary biliary cholangitis, primary sclerosing cholangitis, liver tumours

Primary Biliary Cholangitis - PBC
- peak age 40-60
- Autoimmune disorder -> inflammation of intrahepatic bile ducts
- appearance - florid duct lesion (inflammation and damage at bile duct) and Granulomas portal/ bile duct inflammation

Primary Sclerosing Cholangitis
- Blood test - Antimitochondrial antibodies >95%
- Treatment is with immunosuppression/transplantation
- 30-40 year age group
- 2/3 of patients have ulcerative colitis
- Fibrosing process that causes narrowing and obstruction of intra and extrahepatic bile ducts
- Appearance - Stricturing and beading, Onion Skinning fibrosis
- Increased incidence of cholangiocarcinoma
- Treatment is with transplantation

27
Q

Neoplasms of Liver

A

Primary Tumors
- epithelial (Bening, metastatic) - major cells (hepatocytes, bile ducts)
– Hepatocytes - Benign: Hepatic Adenoma, Malignant: HCC
– bile ducts - Benign: Bile duct adenoma, Malignant: cholangiocarcinoma

  • Nonepithelial - Benign: Hemangioma (most common benign tumor), Malignant: Angiosarcoma, Rhabdomyosarcoma (muscle cell)

Secondary
- Metastases that have come from somewhere else
- Common in the liver because it receives a large blood supply - specifically GI tract portal vein
- Usually non-cirrhotic liver
- Metastases come from:
Colon, pancreas, lung, breast, melanoma

28
Q

Calculous and Acalculous Cholecystitis

A

-Cholecystitis (inflammation of the gallbladder) may be:
- Calculous = with stones - Most common
- Acalculous = without stones - Most Dangerous
- acute or chronic

Acute Calculous
- 90% of cases
- cystic duct obstructions - chemical irritation, inflammation, increased pressure, infection, decreased blood flow (ischemia)
- complications - perforation, gangrenous, gallstone ileus (rare, gallbladder wall so inflamed it sticks to the duodenum and a fistulas tract develops between them where a gallstone can directly pass through into small bowel)
chronic

Acute Acalculous
- 10% of acute cholecystitis
- Major surgery, critically ill patients
- Multifactorial: bile stasis, increased bile viscosity, decreased blood flow - Dehydration, vascularly compromised
- Increased gangrene, perforation %
Increased morbidity, mortality %

29
Q

Nonneoplastic lesions

A
  • cysts (infectious etiology or widespread disorder)
  • Focal nodule hyperplasia
  • Nodular regenerative hyperplasia
  • Hematomas