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Pathology (Guide) > Histopathology - Liver Pathology > Flashcards

Histopathology - Liver Pathology Flashcards

1
Q

What is the basic structural unit in the liver?

A

Hepatic lobule

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2
Q

How is the hepatic lobule arranged?

A
  • Centre = terminal branches of hepatic vein (=centrilobular vein)
  • Points of hexgon formed by portal tracts containing the portal triad
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3
Q

What components make up the portal triad?

A
  • Branches of bile ducts
  • Hepatic artery
  • Portal vein
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4
Q

What is Zone 1 of the hepatic lobule

A
  • Closest to portal triad
  • Periportal hepatocytes receive more oxygen (best blood supply) + affected first in viral hepatitis
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5
Q

What is Zone 2 of the hepatic lobule?

A

Mid zone

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6
Q

What is Zone 3 of the hepatic lobule?

A
  • Closest to terminal hepatic vein
  • Perivenular hepatocytes are most mature + metabolically active
  • Most liver enzymes (most sensitive to metabolic toxins)
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7
Q

What are the functions of the liver?

A

Metabolism:
- DRUG METABOLISM
- Glycolysis, glycogen storage, glucose synthesis, amino acid synthesis, fatty acid synthesis, lipoprotein metabolism

Protein Synthesis:
- Makes circulating proteins (except gamma globulins)

Storage:
- Glycogen, Vitamins A, D, large amounts of B12 + small amounts of K, folate, iron, copper

Hormone Metabolism:
- Activates Vit D
- Conjugation + excretion of steroid hormones (oestrogen/glucocorticoids)
- Peptide hormone metabolism (insulin, GH, PTH)

Bile Synthesis

Immune Function:
- Antigens from gut reach liver via portal circulation
- Phagocytosed by Kupffer cells

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8
Q

What causes liver injury?

A

Normal Liver:
- Hepatocytes with microvilli
- Stellate cells lie quiescent in Space of Disse (between hepatocytes + sinusoid)

  • Chronic inflammation = loss of microvilli + activation of stellate cells (produce collagen)
  • Become myofibroblasts that initiate fibrosis by depletion of collagen in space of Disse
  • Myofibroblasts contract, constricting sinusoids + increasing vascular resistance
  • Undamaged hepatocytes regnerate in nodules between fibrous septa
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9
Q

What are the causes and histology of acute hepatitis?

A

Causes:
- Viruses (Hep A-E)
- Drugs

Histology:
- SPOTTY NECROSIS: small foci of inflammation + infiltrates

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10
Q

What are the causes of chronic hepatitis?

A
  • Viruses (more often Hep B/C)
  • Drugs
  • PBC/PSC
  • Wilson’s
  • Haemochromatosis
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11
Q

What is the best indicator for portal hypertension (unstable liver disease)?

A

Splenomegaly

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12
Q

What is the histopathology of chronic hepatitis?

A
  1. Portal inflammation
  2. Interface hepatitis (PIECEMEAL NECROSIS) - can’t see border
  3. Lobular inflammation
  4. Bridging fibrosis from portal vein to central vein (critical stage in evolution of hepatitis to cirrhosis) - causes blood to bypass hepatocytes + reduces function of liver (intrahepatic shunting)
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13
Q

What is the stage and grade of chronic hepatitis?

A
  • Grade = Severity of inflammation
  • Stage = Severity of fibrosis
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14
Q

What is cirrhosis?

A

Diffuse abnormality of liver architecture that interferes with blood flow + liver function

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15
Q

What is the histopathology of a cirrhotic liver?

A
  • Hepatocyte necrosis
  • Fibrosis
  • Nodules of regeneration hepatocytes (micro- + macro-)
  • Disturbance of vascular architecture
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16
Q

What are the major causes of cirrhosis?

A
  1. ALCOHOLIC LIVER DISEASE
  2. NON-ALCOHOLIC FATTY LIVER DISEASE
  3. CHRONIC VIRAL HEPATITIS
  4. Autoimmune hepatitis
  5. Biliary causes
  6. Genetic causes
  7. Drugs (e.g. methotrexate)
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17
Q

What are some complications of liver cirrhosis?

A
  • Portal hypertension
  • Hepatic encephalopathy
  • Hepatocellular carcinoma
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18
Q

What is the aetiology of cirrhosis?

A
  • Disruption of liver architecture
  • Causes increased blood flow through liver
  • Leads to portal hypertension
  • FIBROTIC BRIDGES form between portal triad + central vein
  • EXTRAHEPATIC SHUNTING occurs due to portal hypertension
  • Causes congestion of blood = oesophageal varices, anorectal varices, caput medusae
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19
Q

How can cirrhosis be classified?

A

According to size of regenerating nodules (micro + macro)

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20
Q

What are features of micronodular cirrhosis?

A
  • Nodules <3mm
  • Uniform liver involvement
  • Causes: ALCOHOLIC HEPATITIS, Biliary tract disease
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21
Q

What are the features of macronodular cirrhosis?

A
  • Nodules >3mm
  • Variable nodule size
  • Causes: viral hepatitis, Wilson’s disease, α1-antitrypsin deficiency
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22
Q

What is the purpose of the modified Child’s Pugh Score (ABCDE)?

A

Indicates prognosis in liver cirrhosis + takes into account albuin, bilirubin, prothrombin times, presence of ascites + encephalopathy

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23
Q

What are the different prognoses from the different Child’s Pugh Scores?

A
  • A = score <7 = 45% 5yr survival
  • B = Score 7-9 = 20% 5yr survival
  • C = Score 10+ = <20% 5yr survival
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24
Q

What are the three different types of alcoholic liver disease?

A
  • Hepatic Steatosis (Fatty Liver)
  • Alcoholic Hepatitis
  • Alcoholic Cirrhosis
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25
Q

What are the macro- + microscopic features of hepatic steatosis (fatty liver)?

A

Macro:
- Large, pale, yellow + greasy liver

Micro:
- Accumulation of fat droplets in hepatocytes (steatosis)
- Chronic exposure leads to fibrosis (late stage)
- Fully reversible if alcohol avoided

26
Q

What are the macro- and microscropic features of alcoholic hepatitis?

A

Macro:
- Large, fibrotic liver

Micro:
- Hepatocyte BALLOONING + necrosis (due to accumulation of fat, water + proteins)
- MALLORY DENK BODIES
- Fibrosis
- Mainly zone 3 damage + neutrophil polymorphs

27
Q

What are the amcro- and microscopic features of alcoholic cirrhosis?

A

Macro:
- Yellow-tan, fatty, enlarged
- Transforms into shrunken, non-fatty, brown organ

Micro:
- Micronodular cirrhosis (small nodules + bands of fibrous tissue)

28
Q

What are some basic features of non-alcholic fatty liver disease (NAFLD)?

A
  • Hepatic Steatosis in non-alcoholics
  • Histology looks similar to alcoholic hepatitis
  • Most common cause of chronic liver disease in West + worldwide
29
Q

What are some RFs for NAFLD?

A
  • Obese individuals with hyperlipidaemia/metabolic syndrome
  • Diabetes
30
Q

What are the types of NAFLD + their features?

A

Simple Steatosis:
- Fatty infiltration
- Relatively benign

Non-alcoholic steatohepatitis (NASH):
- Steatosis + hepatitis (fatty infiltration + inflammation)
- Can progress to cirrhosis

31
Q

What are some features of autoimmune hepatitis?

A
  • Common with other autoimmune diseases
  • 78% female = young + postmenopausal
  • A/w HLA-DR3
32
Q

What are the different types of autoimmune hepatitis and how are they different?

A

Type 1:
- More common in postmenopausal women
- ANA (anti-nuclear Ig)
- Anti-SMA Ig
- Anti-Actin Ig
- Anti-soluble liver Ag Ig

Type 2:
- More common in younger women
- Anti-LKM Ig (anti-liver kidney microsomal Ig)

33
Q

What is the treatment for autoimmune hepatitis?

A

Immune suppression until liver transplant
- Disease returns in <40%

34
Q

What are some biliary causes of cirrhosis?

A
  • Primary Biliary Cholangitis
  • Primary Sclerosing Cholangitis
35
Q

How is primary biliary cholangitis caused and what is its epidemiology?

A
  • Autoimmune inflammatory destruction of small/medium sized intrahepatic bile ducts leads to cholestasis and eventually slow development of cirrhosis (years)

Epi:
- F>M 10:1
- Associated with other AI conditions
- Peak incidence = 40-50yrs

36
Q

What are some investigative findings of primary biliary cholangitis?

A

Bloods:
- Increased serum ALP
- Increased cholesterol
- Increased IgM
- Hyperbilirubinaemia (late disease)

  • ANTI-MITOCHONDRIAL ABS IN >90%

US Scan:
- No bile duct dilatation

37
Q

What is the histology of primary biliary cholangitis?

A

Bile duct loss with granulomas

38
Q

How does primary biliary cholangitis present?

A

Initially:
- Fatigue
- Pruritis
- Abdominal discomfort

Secondary:
- Skin pigmentation
- Xanthelasma
- Steatorrhoea
- Vitamin D malabsorption
- Inflammatory arthropathy

39
Q

What is the treatment + prognosis for primary biliary cholangitis?

A
  • Ursodexoycholic acid in early phase
  • Remission in 25%
40
Q

What is primary sclerosing cholangitis and its epidemiology?

A
  • Inflammation + obliterative fibrosis of extrahepatic + intrahepatic bile ducts leading to multi-focal stricture formation with dilatoin of preserved segments

Epi:
- M > F
- Peak incidence = 40-50yrs
- A/w IBD (especially UC)

41
Q

What investigative findings are seen for primary sclerosing cholangitis?

A

Bloods:
- Increased serum ALP
- Several associated auto-Ig
- p-ANCA

US Scan:
- Bile duct dilatation

ERCP:
- Beading of bile ducts (due to strictures)

42
Q

What is seen on histology for primary sclerosing cholangitis?

A

ONION SKINNING FIBROSIS (concentric fibrosis)

43
Q

What are some benign liver tumours and their clinical features?

A

Hepatic (+bile duct) Adenoma:
- Associated with OCP
- Presents with abdo pain / intraperitoneal bleeding
- Resection IF: symptomatic, >5cm, no shrinkage when OCP stopped

Haemangioma:
- Most common benign lesion (tumour of blood vessels)
- No Tx

44
Q

What are some malignant liver cancers and which is most common?

A
  • Hepatocellular carcinoma
  • Cholangiocarcinoma
  • Haemangiosarcoma
  • Hepatoblastoma
  • Secondary tumours (most common)
45
Q

What are the causes and investigations for hepatocellular carcinoma?

A

Causes:
- In pts with chronic liver disease
- Viral hepatitis
- Alcoholic cirrhosis
- Haemochromatosis
- NAFLD
- Aflatoxin (mouldy grain)
- Androgenic steroids

Ix:
- Screening in cirrhotic pts with 6-mthly USS
- Α-FETOPROTEIN (AFP)
- USS

46
Q

What are the causes, clinical features and histological findings of cholangiocarcinoma?

A

Causes:
- PRIMARY SCLEROSING CHOLANGITIS
- Parasitic liver disease
- Chronic liver disease
- Congential liver abnormalities
- Lynch syndrome Type II

Features:
- Adenocarcinomas arising from bile ducts
- 10% of liver tumours
- Intra/Extrahepatic
- Poor prognosis
- 90% A/w Gallstones

Histology:
- Capillary ingrowth

47
Q

What is haemangiosarcoma?

A

Cancer of the vascular epithelium - highly invasive

48
Q

What are the clinical features of hepatoblastoma?

A
  • Occurs in children/infants
  • Presents with abdominal mass
  • Originate from immature liver precursor cells
49
Q

What are the clinical features of secondary tumours?

A
  • Usually from GI tract, breast or bronchus
  • Often multiple
  • MOST COMMON
50
Q

What is the epidemiology and pathophysiology of haemochromatosis?

A

Epi:
- Caucasian
- Homozygote = 1/400
- Heterozygote = 1 in 10 (carriers)
- Incidence = 40-50yrs

Pathophysiology:
- Autosomal recessive
- Mutation of HFE gene increases gut iron absorption deposits in liver (+ other organs) leading to fibrosis

51
Q

What is found on histology of haemochromatosis?

A
  • Iron deposits in hepatocytes
  • Stain with PRUSSIAN BLUE STAIN
52
Q

What are the signs and symptoms of haemochromatosis?

A
  • Skin bronzing (melanin deposition)
  • Diabetes
  • Hepatomegaly with micronodular cirrhosis
  • Cardiomyopathy
  • Hypogonadism
  • Pseudogout
53
Q

What are the investigations and treatment for haemochromatosis?

A

Ix:
- Increased Iron
- Increased Ferritin
- Transferrin Saturation >45%
- Decreased TIBC

Tx:
- VENESECTION
- DESFERRIOXAMINE

54
Q

What is the epidemiology + pathophysiology of Wilson’s Disease?

A

Epi:
- Rare
- Incidence = 11-14yrs

Patho:
- Autosomal recessive
- Mutated gene ATP7B causes decreased biliary copper excretion, causing deposition and accumulation in liver (+ other organs)

55
Q

What is seen on histology for Wilson’s Disease?

A
  • Copper stains with RHODAINE STAIN
  • Microscopy: Mallory bodies + fibrosis
56
Q

What are the signs and symptoms of Wilson’s Disease?

A
  • Liver disease: acute hepatitis, fulminant liver failure/cirrhosis
  • Neuro disease: parkinsonism, psychosis, dementia
  • Kayser Fleischer rings: copper deposits in Descemet’s membrane in cornea
57
Q

What are the investigations and treatment for Wilson’s disease?

A

Ix:
- Decreased serum caeruloplasmin
- Decreased serum copper
- Increased urinary copper

Mx:
- Lifelong PENICILLAMINE
- Good Px with early Tx, neurodamage = permanent
- ?liver transplant

58
Q

What is the pathophysiology of α1-antitrypsin deficiency?

A
  • Autosomal Dominant
  • Failure to secrete A1AT in blood causes accumulation in hepatocytes and can lead to hepatitis
  • Lack of A1AT in lungs = emphysema
59
Q

What is seen on histology for α1-antitrypsin deficiency?

A

Intracytoplasmic globules of A1AT (in hepatocytes) which stain with PERIODIC ACID SCHIFF (periportal red hyaline globules)

60
Q

What are the signs + symptoms and investigations for α1-antitrypsin deficiency?

A

Kids:
- Neonatal Jaundice

Adults:
- Emphysema
- Chronic liver disease

Ix:
- Decreased serum A1AT
- Absent α-globulin band on electrophoresis

Pathology (Guide) (84 decks)

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