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Pathology Term 2 > Week 3 - HEPATOBILIARY > Flashcards

Week 3 - HEPATOBILIARY Flashcards

Viral Hepatitis, Hepatitis (Alcohol), Cirrhosis, Others

1
Q

Which hepatitis viruses are serum based and which are water-borne?

A 
Serum = B, C, D
Water-borne = A, E
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2
Q

Which type(s) of hepatitis is vertical transmission more common in?

A

B + C

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3
Q

Outline modes of transmission for hepatitis?

A

Horizontal

  • body fluids; sex –> B, C, D
  • faeco-oral; food/water –> A, E

Vertical
-Mother to fetus –> increase in B, C

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4
Q

What is the pathogenesis of viral hepatitis?

A

Immune-mediated hepatocyte damage

  • hepatocytes display viral Ag (HBsAg) on surface
  • exposes them to immune attack + apoptosis

Inflammation
-fever, anorexia, indigestion, lack of fat absorption

Loss of liver function
-indigestion, jaundice

Increased liver enzymes
-AST, ALT, GGT (ALP –> biliary duct obstruction)

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5
Q

What LFTs rise in hepatocyte damage and biliary duct damage/obstruction?

A

Hepatocyes
-AST, ALT, GGT

Biliary ducts
-ALP

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6
Q

What is meant by carrier states in viral hepatitis?

A

ASYMPTOMATIC

  • dormant viral genome within hepatocyte
  • NO hepatocyte damage –> normal clinically + normal LFTs
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7
Q

Which type(s) of viral hepatitis can cause chronic hepatitis? And what can chronic hepatitis lead to?

A 
Serum hepatitis (B, C, D) 
-chronic hepatitis --> cirrhosis --> heptocellular carcinoma
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8
Q

Which hepatitis virus is the only non-RNA virus?

A

Hep B (Hepadnavirus)

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9
Q

Which hepatitis virus has the longest IP?

A 
Hep B (4-26wks)
-the rest are roughly 2-6wks
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10
Q

Which is the only hepatitis virus that can cause a carrier status in a pt.?

A

Hep B (5-10%)

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11
Q

Which hepatitis virus most commonly causes chronic hepatitis and liver cirrhosis?

A

Hep C

  • chronic hepatitis (80%)
  • cirrhosis (50%)
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12
Q

What pattern of liver damage causes cirrhosis?

A 
Bridging necrosis (viral hepatitis)
-increase septa between hepatocytes with nodules
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13
Q

What are the gross and microscopic features of acute hepatitis?

A

Gross:

  • slightly swollen
  • inflamed
  • patchy, muddy-red areas of necrosis
  • oedematous

Micro: –> “acute war”

  • intact architecture
  • marked swelling of cells (due to Na/K pump damage)
  • ballooning degeneration of hepatocytes –> enlarged, swollen, cytoplasmic oedema
  • some dead hepatocytes (bright pink, dark pyknotic nuclei) –> apototic hepatocytes (“councilman bodies”)
  • inflammatory cell infiltration
  • diffuse inflammation
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14
Q

What are the clinical features of acute hepatitis?

A
  • fever
  • jaundice
  • indigestion
  • RUQ tenderness
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15
Q

Why is there RUQ tenderness in acute hepatitis?

A
  • swelling of the liver in acute hepatitis causes stretching of the liver capsule
  • this stimulates pain receptors resulting in the clinical tenderness experienced by patients
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16
Q

What are the laboratory findings in acute hepatitis?

A
  • markedly increased ALT/AST
  • mildly increased ALP (swelling of hepatocytes can cause bile canaliculi –> block)
  • mixed hyperbilirubinemia (jaundice)
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17
Q

True or False?

There is necrosis of hepatocytes in chronic hepatitis

A

False

-no diffuse inflammation or hepatocyte necrosis

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18
Q

What are the microscopic features of chronic hepatitis?

A
  1. limited portal + bridging inflammation (hepatocytes normal elsewhere)
  2. NO diffuse inflammation or hepatocyte necrosis
  3. increased fibrous tissue –> cirrhosis
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19
Q

What are laboratory findings in chronic hepatitis?

A
  • asymptomatic pt./mild jaundice
  • normal/mildly increased AST/ALT/ALP –> NO liver damage
  • “war truce”
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20
Q

What is the progression of chronic hepatitis?

A
  • lasts many years
  • chronic persistent hepatitis (CPH - stable) –> chronic active hepatitis (CAH - reactivation of virus) –> cirrhosis –> cancer
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21
Q

What are groundglass hepatocytes?

A
  • cells loaded with hep B virus

- no damage being caused

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22
Q

What are some complications of chronic hep B?

A
  • cirrhosis
  • cancer
  • membranous glomerulonephritis
  • polyarteritis nodosa
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23
Q

What are these markers for:

  • Anti-HBs?
  • Anti-HBc?
  • HBeAg?
  • Anti-HBe?
  • HBsAg?
A

Anti-HBs
-marker of recovery and immunity

Anti-HBc
-marker of prior or current infection

HBeAg
-marker of viral replication and infectivity

Anti-HBe
-marker of reduced viraemia

HBsAg
-marker of infection

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24
Q

What is HBV-X protein?

A
  • oncogene
  • required for viral infectivity of Hep B
  • may have a role in development of hepatocellular carcinoma by regulating p53 degradation + expression
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25
Q

What is fulminant hepatitis?

A
  • acute massive necrosis
  • hepatic failure from onset within 2-3 wks
  • reactivation of chronic (CAH) or acute hepatitis (de novo)
  • shrinkage of whole liver –> wrinkled + small
  • massive hepatocyte necrosis
  • collapsed lobules with only portal tracts
  • little inflammation
  • if pt. survives (>1 wk) –> complete recovery OR cirrhosis if fibrosis
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26
Q

True or False?

Acute hepatitis can progress to chronic, but chronic cannot regress to acute

A

False

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27
Q

When is Hep A infective?

A

BEFORE the Sx. (i.e. jaundice)

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28
Q

What is the most common outcome for Hep B infection?

A
  • 90% recovery

- 10% complications (–> chronic –> cirrhosis –> cancer)

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29
Q

True or False?

Carriers for hepatitis will have HBeAg + and anti-HBe -

A

False

  • HBeAg -
  • anti-HBe +
30
Q

What are quasispecies?

A
  • HCV variants due to many viral mutations

- therefore difficult to develop HCV vaccine

31
Q

What is hepatitis D virus?

A

-defective virus “deltavirus”
-circular ssRNA virus
-infects ONLY in presence of HBsAg
-70% = superinfection of chronic HBV
Dx. by IgM anti-HDV Ab

32
Q

What is the most common early clinical presentation of pts. infected by HCV?

A

asymptomatic

33
Q

What are the 5 patterns of change in alcoholic liver disease?

A
  1. steatosis (fatty change) - 90%
  2. steatohepatitis (fatty change + inflamm.) - 25%
  3. chronic hepatitis
  4. cirrhosis - 10% –> IRREVERSIBLE HERE
  5. carcinoma - 1%
34
Q

What is the pathway pf metabolism of alcohol?

A

Ethanol —alcohol deH—> acetaldehyde —acetaldehyde deH—> acetate –> CO2 + H2O

35
Q

What is the pathogenesis of alcoholic liver injury?

A
  • decreased acetaldehyde dehydrogenase (congenital) + increased alcohol –> increased actaldehyde :(
  • acetaldehyde –> lipid peroxidation + disrupts cytoskeleton
  • alcohol –> damages cytoskeleton + mitochondria –> mallory bodies (irregular clumps of protein)
  • ROS –> generated during ethanol ketabolism
36
Q

What are Ito cells?

A

collagen-producing fibroblasts present in the walls of the sinusoids

37
Q

What are the 3 major features of alcoholic liver injury?

A
  1. Fatty change (steatosis)
  2. Collagen synthesis via Ito cells (fibrosis)
  3. Inflammation
38
Q

What are the gross and microscopic features of alcoholic steatosis?

A

Gross:

  • enlarged liver (tender on palpation)
  • yellowish appearance (patchy)

Micro:

  • cell swelling
  • steatosis (fat accumulation)
  • nuclei pushed to peripheries
  • NO significant inflammation/fibrosis
39
Q

What is the microscopy of alcoholic hepatitis?

A
  • cell swelling
  • steatosis
  • inflammatory cells
  • fibrosis (mild)
  • MALLORY BODIES –> dark pink clumps of protein within hepatocytes (mallory hyaline) –> form due to alcohol damaging the cytoskeleton and mitochondria
40
Q

What are the 2 microscopic features of alcoholic cirrhosis?

A
  1. regenerating nodules

2. marked fibrosis

41
Q

What are the complications of alcoholic liver disease?

A
  • hepatic failure
  • GIT bleeding
  • infections
  • hepatorenal syndrome
  • hepatocellular carcinoma (1%)
42
Q

What are the gross features of cirrhosis? And what are the common causes?

A

Gross:
-shrunken + nodular liver

Causes:

  • ALCOHOL (60-70%)
  • viral hepatitis (10%)
  • cryptogenic (10-15%)
  • biliary dysfunction (5-10%)
  • hemochromatosis (5%)
43
Q

What are Kupffer cells?

A

Liver macrophages

44
Q

What are stellate cells and how do they play a role in cirrhosis?

A
  • myofibroblasts in ‘Space of Disse’
  • normally quiescent
  • ANY liver damage activates stellate cells and kupffer cells –> rellease of Growth factors (increased stellate cells)
  • stellate cells secrete collagen fibres –> FIBROSIS/SCARRING
45
Q

Why are LFTs normal in cirrhosis?

A
  • typically normal as there is NO necrosis (only marked fibrosis + regenerating nodules)
  • BUT –> there is a drastic loss of liver function
46
Q

What is the reason for hepatic failure in the case of cirrhosis?

A

loss of architecture

47
Q

What is the cause of portal hypertension in cirrhosis?

A
  • obstruction to portal circulation by marked fibrosis
  • chronic hepatocyte injury –> chronic inflammation –> fibrosis –> regenerating hepatocytes –> isolation of hepatocytes from portal circulation –> portal HTN + liver failure
48
Q

What are the clinical findings and their pathogenesis in liver cirrhosis?

A
  • hypoalbuminemia/oedema –> decreased synthesis
  • hyperammonemia –> hepatorenal failure
  • hypoglycemia –> decreased glycogen metabolism
  • palmer erythema/spider angiomas –> increased oestrogens
  • hypogonadism/gynecomastia –> increased oestrogens
  • wt. loss/muscle atrophy –> decreased metabolism
  • ascites/splenomegaly/porta-sys-varices –> portal HTN
  • coagulopathy –> lack of synthesis of coag. factors
  • hepatic encephalopathy –> lac of detoxification
  • hepatorenal syndrome –> renal ischaemia
  • pulmonary HTN/pulmonary failure –> hepatopulmonary syndrome
49
Q

What is the pathogenesis of ascites and splenomegaly in cirrhosis?

A
  1. obstruction to portal circulation
  2. portal HTN
  3. increased HP/decreased OP from backflow + hypoalbuminemia (decreased OP) –> ascites
  4. backflow through portal circulation –> splenomegaly
50
Q

What is the cause of hepatic encephalopathy?

A

CIRRHOSIS

  • hyperammonemia (+toxins/gut bacteria)
  • due to decreased liver function and shunt from portal circulation –> systemic –> CNS

*asterixis –> flapping tremor (CNS oedema)

51
Q

What is the cause of hepatopulmonary syndrome?

A
  • decreased alpha1 anti-trypsin due to liver failure
  • idiopathic –> portopulmonary HTN
  • R –> L shunt (CLUBBING)
52
Q

What is Non-Alcoholic Fatty Liver Disease (NAFLD)? and what is it AKA?

A
  • AKA: - NASH (Non-Alcoholic Steatohepatitis)
  • common cause of increased AST
  • v. similar to alcoholic steatohepatitis BUT very rarely progresses to cirrhosis
  • causes:
  • T2DM, obesity, metabolic syndrome X, dyslipidaemia, HTN

*impaired oxidation + decreased hepatic secretion –> FAT RETENTION!

53
Q

What is primary biliary cirrhosis?

A

autoimmune destruction of intra-hepatic bile ducts

54
Q

What are the features of primary biliary cirrhosis?

A
  • CHOLESTASIS –> main
  • liver appears “greenish-brown” due to bile accumulation

others: -insidious onset of pruritis + cholestatic jaundice

55
Q

What is the microscopy and LFTs of primary biliary cirrhosis?

A
  • marked inflammation around bile ducts

- markedly increased ALP

56
Q

What antibody is responsible/diagnostic for primary biliary cirrhosis?

A

Antimitochondrial Ab

57
Q

What is the commonest cause of drug-induced zonal hepatitis and why does it affect centrilobular zones over portal triad?

A
  • paracetamol/acetaminophen (NSAID) overdose
  • haemorrhagic necrosis of centrilobular zones (around central veins) –> as these regions have a greater activity of drug-metabolising enzymes
58
Q

How is autoimmune hepatitis diagnosed?

A

increased serum IgG (autoantibody)

59
Q

What is Reye syndrome and what are the clinical features?

A
  • acute, sudden fatty liver and brain following a febrile illness + aspirin Tx. in children
  • mitochondrial injury

Clinical features:

  • microvesicular steatosis
  • hepatic failure
  • encephalopathy
60
Q

What is hemachromatosis and what are the clinical features?

A

HFE gene mutation causing excess iron absorption (>20g) –> causes oxidation and hepatocyte damage –> hepatitis + cirrhosis

  • also causes damage to spleen + pancreas –> diabetes
  • bronze skin pigmentation
61
Q

What is Wilson’s disease and what are the clinical features?

A

ATP7B gene mutation causing lack of copper excretion into bile –> hepatocyte damage + steatosis –> fatty liver –> acute steatohepatitis –> chronic hepatitis –> cirrhosis

  • brain + kidney damage
  • cornea –> Kayser-Fleischer rings
62
Q

What is Dubin Johnson syndrome?

A
  • congenital disorder of impaired biliary excretion
  • very dark black pigmented liver
  • asymptomatic
63
Q

What is Gilbert’s syndrome?

A
  • congenital disorder of a genetic deficiency of bilirubin conjugation –> unconjugated hyperbilirubinemia (jaundice)
  • NO liver necrosis (normal LFTs)
64
Q

What is Criggler-Najjar syndrome?

A
  • congenital disorder of a severe defiiency of bilirubin conjugation resulting in neonatal death/jaundice
  • severe form of Gilbert’s syndrome
65
Q

What is the primary liver cancer and what tumour marker can be used for it?

A

hepatocellular carcinoma –> tumour marker = alpha fetoprotein

66
Q

What is the morphology of liver metastases?

A
  • multiple
  • clear demarcation
  • haemorrhage/central necrosis (+/-)
67
Q

What does dog tapeworm cause?

A

Hydatid cyst of Liver

  • echinococcus granulosus
  • multiple large cysts
68
Q

What can entamoeba histolytica cause in the liver?

A

Amoebic liver abscess

  • large shaggy abscess
  • ‘muddy’ pus production –> ANCHOVY SAUCE
  • spreads from colon
69
Q

What is the characteristic feature of schistomiasis when it affects the liver?

A

Granulomas in liver

  • fibrotic reaction around worm eggs
  • pipe stem portal fibrosis (fibrous tissue around bile ducts)
70
Q

What is HELLP syndrome and when is it seen clinically?

A

Hemolysis, Elevated Liver enzymes + Low Platelets

-seen in pregnancy

71
Q

What are pre-eclampsia and eclampsia comprised of?

A

Pre-eclampsia:

  • HTN
  • proteinuria
  • oedema
  • coagulopathy

Eclampsia:
-pre-eclampsia features + CONVULSIONS

72
Q

What are the laboratory tests used to asses the liver’s synthetic function?

A
  • albumin

- Prothrombin Time (PT) –> !

Pathology Term 2 (6 decks)

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