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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
What is fulminant hepatitis?
- 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
26
True or False? | Acute hepatitis can progress to chronic, but chronic cannot regress to acute
False
27
When is Hep A infective?
BEFORE the Sx. (i.e. jaundice)
28
What is the most common outcome for Hep B infection?
- 90% recovery | - 10% complications (--> chronic --> cirrhosis --> cancer)
29
True or False? | Carriers for hepatitis will have HBeAg + and anti-HBe -
False - HBeAg - - anti-HBe +
30
What are quasispecies?
- HCV variants due to many viral mutations | - therefore difficult to develop HCV vaccine
31
What is hepatitis D virus?
-defective virus "deltavirus" -circular ssRNA virus -infects ONLY in presence of HBsAg -70% = superinfection of chronic HBV Dx. by IgM anti-HDV Ab
32
What is the most common early clinical presentation of pts. infected by HCV?
asymptomatic
33
What are the 5 patterns of change in alcoholic liver disease?
1. steatosis (fatty change) - 90% 2. steatohepatitis (fatty change + inflamm.) - 25% 3. chronic hepatitis 4. cirrhosis - 10% --> IRREVERSIBLE HERE 5. carcinoma - 1%
34
What is the pathway pf metabolism of alcohol?
Ethanol ---alcohol deH---> acetaldehyde ---acetaldehyde deH---> acetate --> CO2 + H2O
35
What is the pathogenesis of alcoholic liver injury?
- 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
What are Ito cells?
collagen-producing fibroblasts present in the walls of the sinusoids
37
What are the 3 major features of alcoholic liver injury?
1. Fatty change (steatosis) 2. Collagen synthesis via Ito cells (fibrosis) 3. Inflammation
38
What are the gross and microscopic features of alcoholic steatosis?
Gross: - enlarged liver (tender on palpation) - yellowish appearance (patchy) Micro: - cell swelling - steatosis (fat accumulation) - nuclei pushed to peripheries - NO significant inflammation/fibrosis
39
What is the microscopy of alcoholic hepatitis?
- 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
What are the 2 microscopic features of alcoholic cirrhosis?
1. regenerating nodules | 2. marked fibrosis
41
What are the complications of alcoholic liver disease?
- hepatic failure - GIT bleeding - infections - hepatorenal syndrome - hepatocellular carcinoma (1%)
42
What are the gross features of cirrhosis? And what are the common causes?
Gross: -shrunken + nodular liver Causes: - ALCOHOL (60-70%) - viral hepatitis (10%) - cryptogenic (10-15%) - biliary dysfunction (5-10%) - hemochromatosis (5%)
43
What are Kupffer cells?
Liver macrophages
44
What are stellate cells and how do they play a role in cirrhosis?
- 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
Why are LFTs normal in cirrhosis?
- typically normal as there is NO necrosis (only marked fibrosis + regenerating nodules) - BUT --> there is a drastic loss of liver function
46
What is the reason for hepatic failure in the case of cirrhosis?
loss of architecture
47
What is the cause of portal hypertension in cirrhosis?
- 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
What are the clinical findings and their pathogenesis in liver cirrhosis?
- 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
What is the pathogenesis of ascites and splenomegaly in cirrhosis?
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
What is the cause of hepatic encephalopathy?
CIRRHOSIS - hyperammonemia (+toxins/gut bacteria) - due to decreased liver function and shunt from portal circulation --> systemic --> CNS *asterixis --> flapping tremor (CNS oedema)
51
What is the cause of hepatopulmonary syndrome?
- decreased alpha1 anti-trypsin due to liver failure - idiopathic --> portopulmonary HTN - R --> L shunt (CLUBBING)
52
What is Non-Alcoholic Fatty Liver Disease (NAFLD)? and what is it AKA?
- 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
What is primary biliary cirrhosis?
autoimmune destruction of intra-hepatic bile ducts
54
What are the features of primary biliary cirrhosis?
* CHOLESTASIS --> main - liver appears "greenish-brown" due to bile accumulation others: -insidious onset of pruritis + cholestatic jaundice
55
What is the microscopy and LFTs of primary biliary cirrhosis?
- marked inflammation around bile ducts | - markedly increased ALP
56
What antibody is responsible/diagnostic for primary biliary cirrhosis?
Antimitochondrial Ab
57
What is the commonest cause of drug-induced zonal hepatitis and why does it affect centrilobular zones over portal triad?
- paracetamol/acetaminophen (NSAID) overdose - haemorrhagic necrosis of centrilobular zones (around central veins) --> as these regions have a greater activity of drug-metabolising enzymes
58
How is autoimmune hepatitis diagnosed?
increased serum IgG (autoantibody)
59
What is Reye syndrome and what are the clinical features?
- acute, sudden fatty liver and brain following a febrile illness + aspirin Tx. in children - mitochondrial injury Clinical features: - microvesicular steatosis - hepatic failure - encephalopathy
60
What is hemachromatosis and what are the clinical features?
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
What is Wilson's disease and what are the clinical features?
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
What is Dubin Johnson syndrome?
- congenital disorder of impaired biliary excretion - very dark black pigmented liver - asymptomatic
63
What is Gilbert's syndrome?
- congenital disorder of a genetic deficiency of bilirubin conjugation --> unconjugated hyperbilirubinemia (jaundice) - NO liver necrosis (normal LFTs)
64
What is Criggler-Najjar syndrome?
- congenital disorder of a severe defiiency of bilirubin conjugation resulting in neonatal death/jaundice * severe form of Gilbert's syndrome
65
What is the primary liver cancer and what tumour marker can be used for it?
hepatocellular carcinoma --> tumour marker = alpha fetoprotein
66
What is the morphology of liver metastases?
- multiple - clear demarcation - haemorrhage/central necrosis (+/-)
67
What does dog tapeworm cause?
Hydatid cyst of Liver - echinococcus granulosus - multiple large cysts
68
What can entamoeba histolytica cause in the liver?
Amoebic liver abscess - large shaggy abscess - 'muddy' pus production --> ANCHOVY SAUCE - spreads from colon
69
What is the characteristic feature of schistomiasis when it affects the liver?
Granulomas in liver - fibrotic reaction around worm eggs - pipe stem portal fibrosis (fibrous tissue around bile ducts)
70
What is HELLP syndrome and when is it seen clinically?
Hemolysis, Elevated Liver enzymes + Low Platelets | -seen in pregnancy
71
What are pre-eclampsia and eclampsia comprised of?
Pre-eclampsia: - HTN - proteinuria - oedema - coagulopathy Eclampsia: -pre-eclampsia features + CONVULSIONS
72
What are the laboratory tests used to asses the liver's synthetic function?
- albumin | - Prothrombin Time (PT) --> !

Pathology Term 2 (6 decks)

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