Lecture 12: Liver Pathology Flashcards

1
Q

define steatosis

A

fatty change within the liver - reversible cell injury
microvesicular - small fat droplets
macrovesicular - big fat droplets

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2
Q

name a common cause of steatosis

A
  • NAFLD –> most common cause of unexplained LFTs; assc. w/ metabolic syndrome; risk factor for sudden cardiac death
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3
Q

define steatohepatitis

A
  • accumulation of fat w/ accompanying inflammatory changes

- more assc. w/ alcohol than NAFDL but can be seen w/ both conditions or medications/drugs

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4
Q

what risk does inflammatory changes in the liver pose

A

smouldering low grade chronic inflammation (most often seen in NAFLD) or repeated bouts of hepatitis (often seen w/ alcohol abuse/addiction) can lead to fibrosis

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5
Q

name a histological feature present in steatosis

A

fatty deposits

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6
Q

name a histological feature present in steatohepatitis

A
  • fatty deposits

- mallory bodies/hyaline

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7
Q

how might a radiologist measure liver stiffness

A

using an ultrasound probe (fibroscan) - elastography

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8
Q

why might a radiologist carry out an elastography

A
  • measure liver stiffness as a surrogate marker of fibrosis

- to estimate degree of steatosis (expressed as CAP score)

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9
Q

define cirrhosis

A
  • diffuse process
  • presence of fibrous septa that subdivide liver parenchyma into structurally abnormal nodules
  • end stage of many different types of progressive liver disease
  • usually a loss of function due to loss of architecture –> scarring + regenerating nodules
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10
Q

what affects healing in the liver

A

nature of insult and amount of damage

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11
Q

name some complications of decompensated liver disease

A
  • jaundice –> bilirubin accumulation
  • coagulopathy –> impaired clotting factor synthesis
  • encephalopathy –> hyperammonaemia
  • ascites –> impaired albumin synthesis, portal hypertension
  • splenomegaly –> portal hypertension
  • GI bleeding –> oesophageal varices
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12
Q

name some signs of chronic liver disease

A
  • Caput Medusa –> distended epigastric veins around umbilicus
  • splenomegaly –> portal hypertension
  • ascites -> low albumin, ^ portal hypertension
  • leukonychia –> white fingernails
  • flapping tremor
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13
Q

what type of virus is hepatitis

A

specific hepatotropic virus

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14
Q

what cell type does hepatitis target and infect

A

specialised parenchymal liver hepatocytes

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15
Q

how does most viral hepatitis present

A

presents as acute

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16
Q

describe some of the dominating clinical features of acute viral hepatitis

A
  • accuse inflammation

- impaired liver function due to liver cell death

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17
Q

what types of hepatitis can present as chronic

A

Hep B and C (also D)

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18
Q

how does Hep A cause liver damage

A

through immune response to virus

19
Q

what type of virus is Hep A specifically

A

RNA virus related to pico virus

20
Q

how might Hep B present

A
  • acute hepatitis w/ recovery
    OR
  • acute fulminant hepatitis w/ massive necrosis
    OR
  • chronic that develops into cirrhosis –> hepatocellular carcinoma
    OR
  • asymptomatic carrier state
21
Q

how is Hep A transmitted

A

faecal oral

22
Q

how is Hep B transmitted

A

parenteral –> blood, sexual transmission

23
Q

in acute hepatitis describe what happens to the level of HBeAg and anti-HBs

A
  • HBeAg levels will rise and peak during active infection before then falling and disappearing entirely
  • anti-has levels will begin to rise once HBeAg has nearly disappeared and then high levels will persist giving immunity
24
Q

in a progression to chronic hepatitis describe what happens to the level of HBeAg and anti-HBs

A
  • HBeAg levels will rise to a peak but then they won’t fall completely but will persist at a mid level
  • anti-HBs won’t be present but instead anti-HBe may be present
25
Q

How is Hep C spread

A

blood products; contamination

26
Q

How might Hep C present

A
  • often asymptomatic and unrecognised initial infection
  • often produce chronic hepatitis –> cirrhosis
  • interface hepatitis that kills hepatocytes
27
Q

How is Hep B prevented

A

screening and vaccination

28
Q

How is Hep C prevented

A
  • prevention of sharing needles
  • screening blood products
  • treated by interferon
29
Q

which Hep virus is most assc w/ fatty change

A

Hep C

30
Q

what type of virus is Hep C specifically

A

RNA virus –> can be measured by PCR

31
Q

what will be seen on the serology of acute Hep C

A
  • rise in HCV to peak then a fall
  • replaced by anti-HCV
  • patient then recovers or is treated by interferon to stimulate immune reaction
32
Q

what will be seen on the serology of chronic Hep C

A
  • HCV remains detectable in bloodstream
  • don’t develop anti-HCV
  • fluctuations of serum transaminases due to ongoing inflammation
33
Q

is autoimmune hepatitis acute or chronic

A

chronic

34
Q

explain the difference in effect between primary biliary cirrhosis/sclerosing cholangitis and autoimmune hepatitis

A

PSC and PBC attack bile ducts while autoimmune attacks hepatocytes

  • PSC both extra and intra hepatic bile ducts
  • PBC intra hepatic bile ducts
35
Q

what sex is most affected by autoimmune hepatitis

A

female

36
Q

describe autoimmune hepatitis

A

a chronic hepatitis which may have an indolent or rapidly progressive course

37
Q

name some features of autoimmune hepatitis

A
  • elevated IgG
  • +ve autoantibodies
  • assc w/ other autoimmune disease e.g. rheumatoid arthritis
38
Q

describe primary biliary cirrhosis (PBC)

A

chronic autoimmune progressive destruction of intrahepatic bile ducts

39
Q

name some features of PBC

A
  • +ve anti-mitochondrial autoantibodies >90%
  • may be ANA or ANCA +ve
  • assc w/ thyroid disease, scleroderma, Sjogren’s syndrome
40
Q

describe primary sclerosis cholangitis (PSC)

A

chronic inflammatory destruction of extrahepatic and larger intrahepatic bile ducts w/ beading of bile ducts on MRI or ERCP

41
Q

what sex does PBC affect more

A

female

42
Q

what sex does PSC affect more

A

male

43
Q

name some features of PSC

A
  • assc w/ CIBD, autoimmune pancreatitis

- up to 2/3 +ve ANCA autoantibodies