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PBL SEM 4 > the liver and its lesions > Flashcards

the liver and its lesions Flashcards

1
Q

what are portal tracts like in hepatitis C?

A
  • filled with B lymphocytes and plasma cells (making antibodies against the virus)
  • inflammation at the interface with the lobules - causing loss of hepatocytes (critical in progression from simple inflammation with hepatitis in portal tracts to persistant inflammation in lobules, persistent eroding away of hepatocytes and therefore persistent progression to fibrosis)
  • bile duct damage (not common with viral hepatitis, more seen in autoimmune liver diseases) - which imitates autoimmune liver disease
  • fibrosis
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2
Q

describe the hepatocellular parenchyma in hepatitis C

A
  • inflammatory cells — lymphocytes damage hepatocytes
  • hepatocytes full of fat - steatosis — not sure why this happens
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3
Q

what can cause steatosis?

A

excess alcohol — the combination of alcohol and hepatitis C is really really bad

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4
Q

you get steatosis in what type of hepatitis that you dint get in any other forms of viral hep?

A

C

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5
Q

what is it called when you cant see the boundary between the portal tract and hepatocellular lobule?

A

interface hepatitis

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6
Q

how does fibrosis lead to suboptimal liver function?

A
  • cant see any portal tracts due to progressive fibrosis
  • big thick layer bridging between portal tracts
  • leads to isolation of collections of hepatocytes
  • undergo hyperplasia (re growth/overgrowth of cells)
  • never quite reproduce normal vascular architecture
  • suboptimal liver function
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7
Q

what causes hepatitis and cirrhosis?

A
  • viruses
  • alcohol — hepatitis —> fatty change —> cirrhosis
  • drugs — prescribed and misused
  • autoimmune disease
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8
Q

what autoimmune diseases can cause hepatitis and cirrhosis?

A

primary sclerosing cholangitis, primary biliary cirrhosis, autoimmune hepatitis

—> each have a characteristic set of antibodies and therefore target within the liver

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9
Q

summarise hepatitis A

A
  • infectious
  • endemic
  • oral-faecal transmission — hep A associated with drinking water from unclean sources
  • 2-6 weeks incubation period
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10
Q

summarise hep B

A
  • serum
  • sporadic (small number of cases not spread by serum)
  • blood-borne
  • sexual transmission
  • 6 weeks to 6 months incubation
  • occurs in immunosuppessed
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11
Q

summarise hepatitis C

A
  • transfusion related
  • blood-borne transmission
  • 2 weeks to 6 months incubation period
  • can have it for a very long time without noticing
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12
Q

why is hepatitis delta different?

A

requires hepatitis B

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13
Q

what is hepatitis E similar to?

A

hep A

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14
Q

what is another name for infectious mononucleosis?

A

glandular fever

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15
Q

what virus can infectious mononucleosis be seen with, and may cause acute hepatitis?

A

Epstein-Barr virus

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16
Q

what virus can cause hepatitis and is seen in immunosuppressed pateints?

A

cytomegalovirus

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17
Q

what are the ranging presentations of viral hepatitis?

A
  • asymptomatic subclinical disease
  • acute clinical jaundice
  • acute massive necrosis (<2%)
  • chronic hepatitis > 6 months (esp B and C)
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18
Q

alcohol is absorbed from the ______, then via the _____ to the liver

A
  • upper small intestine
  • portal vein
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19
Q

the varying rate of metabolism of alcohol is linked to what?

A
  • weight, gender and body fat
  • enzymes can be induced (eg previous exposure to alcohol) , so tolerance increases
20
Q

what is 1 unit of alcohol?

A

10ml or 8g of pure ethanol

21
Q

what g/dL is illegal intoxication for driving?

A

0.08 g/dL

22
Q

what g/dL is drunk/smashed/out cold?

A

0.2 g/dL is drunk
0.3 g/dL is smashed
0.4 g/dL is out cold

23
Q

what levels in g/dL is lethal toxicity?

A

> 0.4g/dL in alcohol naive (drink regularly)
0.5 g/dL in anyone

but it is very variable

24
Q

what is death by alcohol intoxication due to?

A

respiratory depression

25
Q

what is the average rate of elimination of alcohol?

A

0.015 g/dL/hr

26
Q

from legal intoxication to undetectable levels of alcohol takes how long?

A

5 hours

27
Q

what is post mortem production of alcohol up to?

A

0.05 g/dL/hr
(body generates alcohol as it decays)

28
Q

what are the stages of alcoholic liver disease and are they reversible or irreversible?

A
  • fatty change = reversible
  • alcoholic hepatitis = reversible
  • pericellular fibrosis = reversible, up to a point
  • cirrhosis = irreversible
29
Q

what is Mallory’s hyaline?

A

very characteristic of alcoholic liver disease — cytoskeletal particles which have aggregated in severely damaged hepatocytes

30
Q

pericellular fibrosis in alcoholic liver disease is normally where?

A

around centra vein in each lobule

31
Q

how does fibrosis cause damage?

A
  • each hepatocyte is surrounded by fibrous tissue, instead of vascular structures
  • function individually but they are separated from the bloodstream with the toxic substances that cant be removed
32
Q

what limits regeneration potential in the fibrosed hepatocytes?

A

disturbance to vascular architecture

33
Q

what are the stages in non-alcoholic fatty liver disease?

A
  • fatty change eg. from metabolic syndrome, obesity, type 2 diabetes - non-alcoholic steatohepatitis (NASH)
  • fibrosis
  • cirrhosis

—> changes near identical to alcohol
—> associated with obesity, diabetes, hyperlipidaemia, some drugs

34
Q

what is cirrhosis?

A

disease of ALL of the liver with parenchymal nodules and surrounding fibrosis (separating them from the blood that carries toxic substances for metabolising)

35
Q

what are the 2 types of cirrhosis?

A
  1. micronodular
    - <_ 0.3cm
    - typically alcohol
  2. macronodular
    - >_ 0.3cm
    - typically viral
36
Q

what types of hepatitis is cirrhosis especially associated with?

A

HBV and HCV

37
Q

what metabolic diseases is cirrhosis associated with?

A
  • iron, copper (Wilsons disease), glycogen storage disease, lipid disorders, a-1 antitrypsin deficiency

excess Fe in liver tissue — haemachromatosis (inherited), lots of transfusions

38
Q

what autoimmune diseases are associated with cirrhosis?

A
  • “lupoid” - young women : anti-nuclear and anti-smooth muscle antibodies
  • primary biliary cirrhosis : middle aged women, anti-mitochondrial antibodies
39
Q

what are the effects of cirrhosis?

A
  • liver failure
  • portal hypertension
  • hepatocellular carcinoma
40
Q

describe the effects of liver failure in cirrhosis

A
  • protein synthesis — low albumin —> peripheral oedema, ascites
  • coagulation factors — bleeding
  • jaundice
  • encephalopathy — confusion
41
Q

why does encephalopathy occur in liver failure?

A

if the liver doesn’t process the toxic substances, they bypass hepatocellular nodules and enter the systemic bloodstream

42
Q

what is the liver flap a sign of?

A

hepatic encephalopathy

43
Q

what are the effects of portal hypertension in cirrhosis?

A
  • ascites
  • varices = dilated venous channels
  • splenomegaly
44
Q

why does portal hypertension develop in cirrhosis?

A

nodules distort blood flow through adjacent blood vessels — increases pressure in portal vein and branches due to back pressure

45
Q

describe varies in portal hypertension

A
  • increased pressure in portal vein
  • blood bypasses liver — lower oesophageal / periumbilcial / perianal veins
  • very dilated veins — rupture easily
46
Q

describe hepatocellular carcinoma due to cirrhosis

A
  • more common carcinoma where HBV endemic (SE asia, africa)
  • very poor prognosis
  • raised serum alpha-fetoprotein levels (not sufficient alone for diagnosis. need imaging and biopsy)

hep B has its own oncogenic potential

PBL SEM 4 (50 decks)

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