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Pathology > Liver > Flashcards

Liver Flashcards

1
Q

Explain the blood supply to the liver

A

2 Blood supplies

  • Hepatic arterial- direct blood supply and portal venous- indirect blood supply from the gut
  • This is important in metastatic liver disease
  • Hepatic venous drainage of blood and bile drainage via biliary tract
  • Blood drains into sinusoids then into central veins (terminal hepatic venulels) - in hexagon shape blood travels from outside to inside (from portal tracts to centre)
  • Bile calculi drain into bile ducts
  • Portal tracts- contain a branch of the hepatic artery, portal vein and a bile duct
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2
Q

What is the difference between the lobule and acinus anatomy of the liver

A
  • Lobule= structural unit centered on the central hepatic vein (hexagonal) and portal tracts are at the periphery
  • Acinus= functional, defined by dual blood supply and divided into zones 1-3 with central veins at the periphery. Zone 1- hepatocytes closest to hepatic arteries (blood supply) so o2 is highest. Zone 2- in between. Zone 3- around central veins where oxygen is poor
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3
Q

What does an elevated bilirubin, ALP, and GGT

A

-A secretory/ cholestatic picture indicates bile stasis

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4
Q

What does elevated AST and ALT indicate

A

A hepatic picture

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5
Q

What are albumin and coagulation factor problems indicative of

A
  • Albumin- only diminished in setting of chronic liver disease
  • Coagulation factors- can be depleated in acute and severe liver disease leading to coagulopathy- good marker for acute injury
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6
Q

Discuss the various types of liver enzymes

A
  • AST, ALT, GGT- intracellular enzymes which leak into blood on injury to the cell- eg acute hepatitis
  • ALP- usually in bile- so indicates biliary obstruction
  • ALP is not exclusive to liver- bone damage can cause serum elevation
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7
Q

What are the various studies that can be conducted in liver disease

A
  • Immunology- autoantibodies
  • Virology- hep, EBV and CMV
  • Haemochromatosis (iron studies), Wilson’s disease (copper studies) , Alpha 1 anti-trypsin deficiency
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8
Q

What imaging can be conducted in the investigation of liver disease

A
  • USS/CT to look for bile duct dilation
  • Cholangiography (MRCP/ERCP) to assess biliary tract if duct dilation
  • Endoluminal USS - mass at the head of the pancreas
  • CT/MRI liver- liver mass
  • CT/Ultrasound can perform a percutaneous needle biopsy liver
  • Liver biopsy needed when there is no explanation for liver disease or to grade disease staging in viral hepatitis*
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9
Q

What are the common causes of acute liver injury

A
  • Viral hepatitis
  • Alcoholic hepatitis
  • Drugs
  • Biliary disease
  • Autoimmune hepatitis
  • Can present with acute jaundice or abnormal LFTS
  • Coag disturbance
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10
Q

What are the causes of jaundice

A

Pre-hepatic- haemolytic anaemia, drugs, gilberts syndrome

Hepatic- acute hepatitis, drug induced liver disease, alcoholic hepatitis, Intrahepatic biliary hepatitis, autoimmune hepatitis, end stage cirrhosis

Post-hepatic- gallstones, surgical strictures, extra-hepatic malignancy

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11
Q

What are the 2 types of patterns of liver cell injury

A

-Reversible change- fatty change and feathery degeneration
-Irreversible (necrosis)- individual cells (apoptotic bodies)
Groups of cells at edge of portal tract
Death of large groups of cells around central veins

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12
Q

What are the causes of chronic liver disease

A
  • Chronic liver disease- viral hep, autoimmune hep, drugs
  • Alcoholic liver disease
  • Metabolic liver disease- haemochromatosis and Wilson’s
  • Biliary disease- primary biliary cirrhosis and primary sclerosis cholangitis
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13
Q

What are the main causes of biliary disease

A
  1. Extrahepatic biliary obstruction
  2. Primary biliary sclerosis
  3. Primary sclerosis cholangitis
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14
Q

What are the causes of Extrahepatic biliary obstruction

A
  • Stones
  • Benign stricture (including PSC)
  • Tumour
  • Superimposed secondary infection (ascending cholangitis) - biliary obstruction can lead to bacterial infection causing ascending cholangitis
  • If uncorrected can lead to secondary biliary cirrhosis
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15
Q

Describe the causes and effects of primary biliary cirrhosis/ cholangitis

A
  • Autoimmune destruction of bile ducts
  • Common in middle aged females- itch and jaundice
  • Serum alk phos (ALP) and cholesterol raised
  • Anti-microbial antibodies positive *** most important for diagnosis
  • histology: Portal tract lymphocytic infiltrate which destroys bile ducts and causes granulomatous destruction of bile ducts
  • At advanced stage bile ducts are lost and portal tracts replaced with fibrous scars forming bridges between portal regions
  • Eventually will lead to cirrhosis
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16
Q

What does primary biliary cirrhosis look like histologically

A
  • Early - Portal duct targeted by inflam cells with lymphoid cells - bile duct shows degenerative change
  • Later- Later stage when bile ducts are lost and portal tracts are replaced - fibrous scars link portal regions - minimal inflam at this stage
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17
Q

Describe the causes and features of primary sclerosis cholangitis

A
  • Chronic inflam that Involves intra and extra hepatic ducts
  • Associated with chronic idiopathic inflammatory bowel disease (mainly UC)
  • Diagnosis by cholangiogram - MRI Cholangiography
  • Histology shows: onion skinning fibrosis (when there is intra and extra hepatic disease), ductopenia (eventually cirrhosis)- will lead to a smaller bile duct
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18
Q

Describe the features of hepatitis A

A
  • ssRNA entervirus
  • Faecal-oral spread, endemic in countries with poor sanitation
  • Acute disease and asymptomatic infection , self limiting in children
  • Protective antibodies and no chronic infection - there is no carrier state so no risk of chronic hepatitis or hepatocellular carcinoma
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19
Q

Describe the features of Hepatitis B

A
  • dsDNA hepadnavrisu
  • Paraenteral transmission- IV drug abuse
  • Sexually transmitted
  • Liver damage caused by immune reaction (to HBsAg)- hep B surface antigen
  • Long incubation period
  • Carrier state
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20
Q

Describe the two phases of viral growth in Hepatitis B

List the 3 patterns of disease

A
  • Proliferative- episcopal viral DNA and formation of complete visions
  • Integrative- viral DNA incorporated into host genome

3 patterns of disease

  • Acute hepatitis and recovery
  • Asymptomatic carrier state - only 5-10%
  • Chronic hepatitis and progression to cirrhosis and or hepatocellular carcinoma
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21
Q

Describe the features of hepatitis C

A
  • ssRNA flavivirus
  • Multiple genotyypes or varying pathology
  • Paraenteral transmission (blood donors screened for HCV)
  • Shorter incubation period
  • Much less severe illness at time of infection
  • Carrier state
  • 75% asymptomatic on infection (seroconversion)
  • 75% develop persistent infection with a degree of chronic hepatitis- cirrhosis and risk of hepatocellular carcinoma
22
Q

What is the definition of chronic hepatitis

A

-Symptomatic, biochemical or serological evidence of continuing or relapsing hepatic disease> 6 months and histologically documented inflam and necrosis

Causes: Viral Hep C and B, drugs (methotrexate), autoimmune hepatitis (positive for ASMA/ANA antibodies)

Clinical signs: Disturbed LFTs

Needle core biopsy: Necroinflammatory disease activity
-Degree of fibrosis and nodularity staged 0-6

23
Q

What are the 3 characteristics of liver cirrhosis

A
  1. Diffuse, irreversible disruption of the entire liver architecture
  2. Structurally abnormal regenerative nodules of hepatocytes
  3. Separated by interconnecting bridging fibrous bands

small shrunken nodular surfaces

24
Q

What are the main complications of cirrhosis

A

-Liver failure - jaundice, coagulopathy, hepatic encephalopathy (failure to break down toxic blood substances) , hypoproteinaemia (inadequate serum albumin) this can precipitate hypoaldosteronism

  • Portal hypertension (>7mmhg in portal vein)
    • Increased portal blood flow, hepatic vascular resistance, and AV shunting
    • Causes ascites, splenomegaly, oesophageal varicies, haemorrhoids, caput Medusa

-Hepatocellular carcinoma

Cirrhosis can be triggered by other insults to the liver- sepsis or drugs

25
Q

What are the main causes of liver cirrhosis

A
  • Alcoholic liver disease (most common)
  • Viral hepatitis (B and C)
  • Biliary disease
  • Hereditary haemochromatosis
  • Autoimmune hepatitis
  • Wilsons disease, alpha 1 anti-trypsin deficiency
  • Unknown cause
26
Q

What are the 3 patters of disease in alcohol related cirrhosis

A
  1. Simple steatosis or fatty change- reversible no fibrosis yet
  2. Steatohepatitis 10-20% - Fibrosis

1 & 2 both occur before cirrhosis and can be seen in conditions not related to alcohol

  1. Cirrhosis

Fatty change is reversible until the onset of fibrosis

27
Q

What 3 factors contribute to the pathogenesis of alcohol related liver disease
And what is the histological appearance

A
  1. Cellular energy diverted from fat metabolism to alcohol metabolism
  2. Toxic acetaldehyde accumulation in liver
  3. Direct stimulation of collagen synthesis by alcohol

Histologically

  1. Steatosis, hepatocyte swelling and degeneration
  2. Mallory bodies
  3. Neutrophillic reaction
  4. Fibrosis
28
Q

List the 3 main metabolic causes of chronic liver disease

A
  • Haemochromatosis -common
  • Wilson’s disease
  • Alpha 1 antitrypsin deficiency

-All caused by single gene mutations with autosomal recessive inheritance

29
Q

Describe the features of primary and secondary haemochromatosis

A
  • Primary- Genetic - autosomal recessive inheritancee (iron stored mainly in hepatocytes)
  • Secondary - (Haemosiderosis) - excess iron intake or absorption - blood transfusions usually the cause (iron mainly stored in macrophages)
30
Q

Describe the genetic features of haemochromatosis

A

Pathogenesis: Mutation in HFE gene - excessive iron absorption in small intestine, leading to accumulation in liver heart and pancreas

  • Homozygous C282Y mutation accounts for 90% typical causes
  • Diagnosis : Elevated serum transferrin, ferritin and hepatic iron index= all iron studies
  • Histology and genetic testing
31
Q

Describe the complications of genetic haemochromatosis

A
  • Bronze pigmentation of skin
  • Diabetes mellitus
  • Cardiac arrhythmia
  • Infertility
  • High risk liver cirrhosis and carcinoma

Treatment = phlebotomy or chelating agents - remove iron from system and reduce complications

32
Q

Describe the features of Wilson’s disease

A
  • Autosomal recessive inheritance
  • Accumulation of copper in hepatocytes due to mutation in copper transporting ATPase
  • Eye and brain involvement usually - copper deposition in peripheral iris
  • Non-specific histology - hard to diagnose - Distribution of copper in liver can be patchy
  • Diagnosis confirmed by biochemistry- serum/ urine/ liver tissue
  • treatment: Penicillamine (chelating agent)
33
Q

Describe the features of Alpha 1 anti-trypsin deficiency

A
  • a1AT is a serum protease inhibitor produced in the liver
  • Normal phenotype PiMM - abnormal phenotype PiZZ produce abnormal a1AT which is not released by the liver accumulates
  • Serum deficiency causes emphysema esp in smokers and cirrhosis

Emphysema due to increased elastase activity

34
Q

List the various types of benign liver mass

A
  • Cysts- simple or hydatid
  • Haemangioma - benign vascular tumour
  • Focal nodular hyperplasia -benign neoplastic growth of hepatocytes
  • Hepatocellular adenoma -benign neoplastic growth of hepatocytes
35
Q

List the primary malignant tumours of the liver

A
  • Hepatocellular carcinoma- from hepatocellular tissue
  • Cholangiocarcinoma- comes from bike ductular epithelium
  • Angiosarcoma- quite rate
36
Q

List the common secondary/ metastatic tumours that cause liver cancer

A
  • Colorectal carcinoma
  • Lung carcinoma
  • Breast carcinoma
  • Gastric carcinoma
  • Pancreatic carcinoma
  • Malignant melanoma
  • Carcinoid tumours
37
Q

What are the features and risk factors associated with hepatocellular carcinoma

A
  • Common in developing world with high rates of hep B
  • Can also be due to Hep C
  • Integration of viral genome into hepatocyte
  • Rapid increase in liver size, worsening blood staining ascites, fever and pain
  • Usually incurable survival approx 7 months

Risks

  • Hep B and C
  • Cirrhosis of any kind - alcohol, haemochromatosis
  • Aspergillus flavus infection due to it’s associateion with carcinogenic aflatoxins
38
Q

What are some of the main complications of gall stones

A
  • Cholescystitis (acute or chronic) - thickening of glands, chronic inflam and cell infiltrate
  • Mucocele - accumulation of mucus and distension
  • Obstruction and biliary colic pain associated with this
  • Obstructive jaundice - failure to secrete bilirubin into intestine
  • Infection causing ascending cholangitis
  • Pancreatitis- when inflam spreads to liver
  • Gall bladder carcinoma (rare)

-Gall stones cause pain when impacted in Hartmann’s pouch of the gall bladder- leads to cholelithiasis

39
Q

Describe the features of gall bladder carcinoma

A
  • Usually adenocarcinoma
  • Associated with gall stones
  • Uncommon
  • Elderly females
  • Advanced stage at presentation
  • Poor prognosis
40
Q

What are the clinical features of biliary obstruction

A
  • Obstructive jaundice- raised bilirubin, pale stools, dark urine
  • Raised ALP
  • Complications: Cholangitis, abscess
41
Q

What radiological investigations can be done for biliary tract obstruction

A
  • Percutaneous transhepatic cholangiogram - needle through skin and liver into biliary tract
  • ERCP-
  • Ultrasound
  • Cytology of bile duct brushings usually during ERCP
  • CT/MRI for definitive mass lesion
42
Q

Describe the features of cholangiocarcinoma

A
  • Adenocarcinoma of bile structures
  • Intrahepatic or extrahepatic
  • Presents at early stage with obstructive jaundice - causes obstruction early due to narrow lumen of bile duct
  • Risk factors- sclerosis cholangitis/ ulcerative cholangitis , liver infection, congenital biliary tree abnormality
  • Often it is a diagnosis of exclusion
43
Q

Describe the features of an ampullarf carcinoma

A
  • Malignant epithelial tumour
  • Carcinoma that involves the ampulla of vader - can originate from common bile duct,, duodenum, pancreas, or in ampulla
  • An advanced tumour here may obliterate it’s origin then you can’t tell where its from
  • Need to distinguish it from a peri-ampullary carcinoma or mets
44
Q

Describe the features of acute pancreatitis

A
  • Acinar cell injury/ necrosis and inflammation
  • Autodigestion of pancreatic substance by activated enzymes- trypsin, lipase and elastase with inflammatory response mediated by cytokines
  • This leads to necrosis of pancreatic substance, fat necrosis and haemorrhage
45
Q

Describe the features of chronic pancreatitis

A
  • Repeated episodes of pancreatic inflammation with loss of pancreatic parenchyma and fibrosis
  • Characterised by inspissation of secretions within ductal system forming ductal plugs
  • Dystrophic calcification results in formation of calcified debris or stones
46
Q

What are the causes of pancreatitis

A

I GET SMASHED

Metabolic - ALCOHOL, hyperlipidaemia, hypercalcaemia, drugs (thiazides, cyclosporin)
Genetic- cystic fibrosis

Mechanical- Gall stones, traumatic injury , preoperative and post ERCP

Vascular- shock, atheroembolism, vasculitis

Infection- Mumps, mycoplasma

47
Q

What are the clinical features of acute pancreatic

A
  • Epigastric abdo pain - radiating to back
  • Acute abdomen
  • Shock
  • Adult resp distress syndrome, multi organ failure
  • Biochemical abnormalities - RAISED SERUM AMYLASE
48
Q

What are the features of chronic pancreatitis

A
  • Relasping episode of abdominal
  • Malabsorption due to enzyme insuffiency
  • Exocrine affected more than endocrine
  • Diabetes mellitus (Late)
  • Pseudocyst formation- accumulation of fluid around the gland
  • Calcification of gland - CT/ X-ray
  • ERCP shows distorted ducts
49
Q

What are the risk factors for chronic pancreatitis

A
  • Cigarette smoking
  • Chronic pancreatitis
  • Genetics
50
Q

Describe the features of pancreatic carcinoma

A
  • Head is most likely location - cause painless jaundice
  • Tumours of tail and body present much later

Signs

  • Obstructive jaundice
  • Abdo pain
  • Cachexia
  • Mets to liver and lymph node s
  • Thombophelbitis
  • Raised CA19.9 , CEA and CA125

Diagnosis
Via- CT guided FNA or fine needle core biopsy

51
Q

What surgical intervention is used in pancreatic adenocarcinoma

A
  • Whipple procedure - pancreaticodueodenectomy - resection of all duodenum, part of stomach, proximal 1/3 pancreas, biliary tract and gall bladder
  • If patient not fit for this surgery then place a stent

Pathology (12 decks)

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