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Y3 CBLs > CBL 6 Fatty liver (2) > Flashcards

CBL 6 Fatty liver (2) Flashcards

1
Q

Reversible complications of haemochromatosis?

A
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2
Q

Irreversible complications of haemochromatosis

A
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5
Q

(2) modes of screening for haemochromatosis

A
  • general population: transferrin saturation, ferritin

​*ferritin should also be measured but is not usually abnormal in the early stages of iron accumulation

  • testing family members: genetic testing for HFE mutation
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6
Q

(2) specific diagnostic tests for haemochromatosis

A
  • molecular genetic testing for the C282Y and H63D mutations
  • liver biopsy: Perl’s stain
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7
Q

Haemochromatosis

  • management
  • monitoring
A
  • Venesection is the first-line treatment
  • monitoring adequacy of venesection: transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l
  • 2nd line (chelating agent) Deferoxamine -> binds to iron so it can be excreted in the urine
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8
Q

What may be seen on joint x ray of a person with haemochromatosis?

A

chondrocalcinosis

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9
Q

What’s haemosiderosis?

A

Process of depositing of extra iron in the organs

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10
Q

What happens (pathophysiology) in HFE mutation?

A

ENterocytes absorb iron from the intestine (from food) but are not good at regulating its release into bloodstream (they release too much)

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11
Q

Type I autoimmune hepatitis

  • circulating antibodies
  • affected population
A
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12
Q

Type II autoimmune hepatitis

  • circulating antibodies
  • affected population
A
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13
Q

Type III autoimmune hepatitis

  • circulating antibodies
  • affected population
A
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14
Q

Difference between primary and secondary haemochromatosis

A
  • Primary - genetic mutation (HFE)
  • Secondary - acquired (e.g. frequent blodo transfusion)
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15
Q

What type of population is autoimmune hepatitis more commonly seen in?

A

Young females

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19
Q

Clinical features of autoimmune hepatitis

A
  • may present with signs of chronic liver disease
  • acute hepatitis: fever, jaundice etc (only 25% present in this way)
  • amenorrhoea (common)
  • ANA/SMA/LKM1 antibodies, raised IgG levels
  • liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis
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20
Q

Management of autoimmune hepatitis

A
  • steroids, other immunosuppressants e.g. azathioprine
  • liver transplantation
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21
Q

What genes are associated with autoimmune hepatitis

A

Chromosome 6

  • HLA - DR3
  • HLA - DR4
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22
Q

Another name for Primary biliary cholangitis (PBC)

A

aka (old name: Primary Biliary Cirrhosis)

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23
Q

Typical population profile of PBC

A

middle-aged females (female:male ratio of 9:1)

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24
Q

Causes of extrahepatic cholestasis

A
  • gallstones,
  • pancreatic cancer
  • stricture,
  • cholangiocarcinoma
  • primary sclerosing cholangitis
25
Q

Causes of intrahepatic cholestasis

A
  • Liver cirrhosis
  • primary biliary cirrhosis
  • malignancy
26
Q

What to do when there is evidence of biliary dilatation on CT or USS?

A

Urgent referral

27
Q

Pathophysiology of PBC

A
  • not fully understood
  • thought to be: an autoimmune condition
  • Interlobular bile ducts become damaged by a chronic inflammatory process -> progressive cholestasis -> eventually progress to cirrhosis
28
Q

A classic presentation of PBC

A

Itching in middle-aged woman

29
Q

Associations of PBC with different diseases

A
  • Sjogren’s syndrome (seen in up to 80% of patients)
  • rheumatoid arthritis
  • systemic sclerosis
  • thyroid disease
30
Q

Diagnosis of PBC

A
  • anti-mitochondrial antibodies (AMA) M2

​ (present in 98% of patients and are highly specific)

  • smooth muscle antibodies in 30% of patients
  • raised serum IgM
31
Q

Management of PBC

A
  • pruritus: cholestyramine (limits reabsorption of bile acids in GI tract)
  • fat-soluble vitamin supplementation
  • ursodeoxycholic acid
  • liver transplantation
32
Q

What’s the major indication for liver transplant in PBC?

A

bilirubin > 100

33
Q

Possible complications of PBC

A
  • cirrhosis
  • osteomalacia and osteoporosis
  • significantly increased risk of hepatocellular carcinoma
34
Q

What (2) enzymes are increased in the blood tests for PBC?

A

ALP and GGT -> they are normally found in bile duct cells

*when cell is damaged or dies -> enzymes released into blood stream

35
Q

What does the investigation for viral hepatitis involve?

A

Hepatitis serology:

  • hepatitis A IgM antibodies
  • hepatitis B surface antigen
  • hepatitis C antibodies
36
Q

What bloods to do when starting statins?

A

ALT & AST

(re-check after 3 months; if x3 than normal limit -> stop statins)

37
Q

(2) markers of liver synthetic function

A
  • albumin
  • PT (clotting)
38
Q
A
39
Q

Increased Fib4 - what does it mean?

A

Poorer prognosis - need to be more pro-active with lifestyle changes

40
Q

Which antibiotic commonly causes liver damage?

A

Co-amoxiclav

*damage will heal on its own after stopping co-amoxiclav (may take few months)

41
Q

Hepatocellular carcinoma

  • do we do a biopsy?
  • other options of investigations
A
  • we don’t do biopsy if liver is the original ca site - as we may spread it
  • biopsy possible if metastatic ca on the liver
  • do imaging and alpha -fetoprotein
42
Q

What tests to do if we suspect hemochromatosis?

A
  • fasting transferrin
  • HFE gene
43
Q

Diagnostic marker for Primary Sclerosing Cholangitis

A

pANCA and imaging

44
Q

What to do if a pregnant woman is positive for Hep B?

A
  • refer for specialist assessment within 6 weeks
  • check HBV DNA

*if high, give anti-viral Tenofovir disoproxil

  • When child is born: HBV immunogobulin in 12 h, vaccine in 24h, then 1 month, then 6-12 months)

*90% risk of transmission from positive mum to a child

* increased risk of premature labour (obstetric input + monitoring)

* if infant is immunised -> safe to breastfeed

45
Q

What infections do we screen for in antenatal/early pregnancy?

A
  • hepatitis
  • HIV
  • rubella
  • syphilis
46
Q

RA drugs that may induce liver damage

A
  • methotrexate
  • biologics
  • sulfasalazine
47
Q

Which enzyme is specific for the liver damage?

A

ALT

48
Q

Which enzyme is used to confirm that ALP increase is due to liver?

A

Ganna - glutamyltransferase -> it mirrors ALP

*gammaGT is also raised with: enzyme-inducing drugs, alcohol abuse

49
Q

How much of the raise in ALT/AST do we see in:

a) acute hepatitis
b) chornic hepatitis

A

A. Acute - ALT/AST raised in 1000s

B. Chronic - ALT/AST raised in 100s

50
Q

Cholestatic (obstructive) picture on blood tests (LFTs)

A
  • ALP raised significantly
  • ALT/AST raised mildly (AST>ALT)
  • bilirubin increased

Y3 CBLs (13 decks)

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