6. Liver Disease Notes Flashcards

1
Q

Which condition(s) is/are jaundice more common in?
- PBC
- Steatotic cholangitis
- Cirrhosis

A

PBC and Steatotic Cholangitis ( but jaundice may be present in Cirrhosis)

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2
Q

Signs of cirrhosis on the hands and legs

A
  • Clubbing
  • Luekonychia
  • Duputryen’s contracture (ALD in particular)
  • Palmar erythema
  • Flapping tremor ( encephalopathy)
  • Bruising
  • Ankle oedema
  • Leg bruising
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3
Q

What clotting factor does the liver not make?

A

VII

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4
Q

Signs of cirrhosis on the trunk

A
  • Axillary hair loss
  • Gynaecomastia
  • Spider naevi
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5
Q

What drugs can cause gynaecomastia

A

Spironolactone, digoxin, metronidazole

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5
Q

Signs of cirrhosis on the abdomen

A
  • Hepatomegaly
  • Splenomegaly
  • Ascites
  • Dilated veins
  • Testicular atrophy
  • Umbilical hernia
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6
Q

What drug can be used for ascites ( caused by portal hypertension?)

A

Carvedilol

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7
Q

What is the treatment for bleeding oesophageal varices

A
  • Resusc
  • Endoscopic therapy with Band ligation
  • Terlipressin ( vasoconstrictor)
  • Balloon tamponade
  • TIPPS
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8
Q

Primary and Secondary prophylaxis for variceal bleeds

A

Primary - Non selective B blocker and variceal band ligation
Secondary - Band ligation and propanolol/carvedilol

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9
Q

Treatment for ascites

A
  • Sodium restriction
  • Spironolactone (NOT loop diuretics - too strong)
  • Paracentesis (resistant ascites)
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10
Q

When in AST high when ALT may be normal ( ratio >2)

A

Alcoholic liver injury

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11
Q

When does ALT and not AST increase

A

HCV, fatty liver ( unless very serious)

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12
Q

In what non-pathological state is ALP increased

A

Last trimester

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13
Q

In what group of people is GGT increased

A

Heaver drinkers ( esp those with liver disease)
Those on enzyme-inducing meds

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14
Q

How is unconjugated bilirubin transported in blood?
How does it get conjugated and where?
How does bilirubin get into the SI
What does conjugated bilirubin get excreted as?

A
  • With albumin
  • In the liver, with glucronic acid
  • Through the biliary system
  • Urobilinogen, after conversion by bacterial proteases
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15
Q

Which Hep viruses
- are transmitted faeco-orally
- commonly result in chronic infection
- are blood borne
- have vaccine

A
  • A and E
  • B and C
  • B and C
  • A
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16
Q

Sx of HAV and complications

A
  • Jaundice

Complications:
- Fulminant hepatitis
- Cholestatic hepatitis

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17
Q

Incubation period of HAV

A

30 (15-50)

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18
Q

What are HEV epidemics assoc with

A

Contaminated drinking water

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19
Q

How is HEV commonly transmitted

A
  • Foodborne, through uncooked meat such as pork, or molluscs
  • Contaminated water
  • Blood transfusion and transplanted organs
  • Vertical transmission
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20
Q

Most common cause of acute hep in UK

A

HEV

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21
Q

How is HCV commonlly transmitted

A

Blood borne through shared needles

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22
Q

Which Hep Viruses are likely to cause cirrhosis

A

HCV

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23
Q

Can HCV be cured, and if so, with what?

A

Yes, with combination therapies

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24
Q

What can cause HBV to be reactivated

A

Iatrogenic causes
Oncological causes

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25
Q

What defines Hep B as being chronic?

A

HBsAg +ve > 6 mo

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26
Q

Are anti HBe and Hbs present in chronic Hep B

A

No

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27
Q

What is an indicator to acute HBV infection

A

HBsAg main indicator
IgM Anti-HBc- highest in acute infn, and in acute LF HBsAg may be negative but IgM may be present

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28
Q

Is HBe Ag present in chronic HBV infection

A

No,negative in certain infections, HBV DNA usually lower in these pts

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29
Q

Can HBV be cured, and if so, with what?

A

Pegylated interferon
Oral antivirals

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30
Q

Which HEV genotypes are more common in developing countries compared to developed countries? Difference in transmission

A

1 and 2 - Faeco-oral vis infected water
vs 3 and 4 - Faeco-oral via infected pig meat, direct exposure to pigs or infected water`

31
Q

Age at infection of HEV (1,2 vs 3,4)

A

15-30yo vs >50

32
Q

Is HEV self-limiting

A

Yes

33
Q

Does HEV cause chronic hep

A

Yes in genotype 3

34
Q

HEV treatment

A

Ribavarin in immunocompetent, although rarely used.
Interferon a and ribavarin in chronic HEV infxn in immunosuppressed

35
Q

Ribavarin for ?

A

HCV in decompensated cirrhosis, HEV in immunosuppressed and sometimes in immunocompetent

36
Q

which group is more liely to get chronic HEV infxn?

A

Solid organ transplant individuals

37
Q

Main serology when acute hepatitis has resolved?

A

HBsAg negative

38
Q

Risk of reactivation is HBsAg positive compared to HBsAg negative but core Ab positive

A

Higher if HBsAg +ve

39
Q

What to treat HBV in pregnancy

A

Tenovir if viral load>200000 IU in third trimester

40
Q
A
41
Q

Sexually transmitted Hep Viruses

A

B and D mainly

42
Q

Features of viral hep

A

headache, myalgia, arthralgia, nausea and anorexia usually precedes the development of jaundice by a few days to 2 weeks.

43
Q

Which viral heps are more likely to cause cirrhosis

A

B and C

44
Q

ALT in Viral Hep

A

200-2000

45
Q

Vehicles of transmission of HAV in occassional outbreaks

A

Shellfish and water

46
Q

What is diagnostic of HAV infxn

A

HAV IgM

47
Q

How to provide immediate protection soon after exposure to HBV

A

Give IMMUNISATION or immune serum globulin ( esp in >60yo or immunocompromised indiv)

48
Q

If vaccination to HBV is given, will anti HBc and HBs present?

A

HBs yes, HBc no

49
Q

What does seroconversion to e ag in HBV suggest

A

Seroconversion to e antigen (i.e. loss of HBeAg and development of anti-HBe antibody) indicates a partial immune control of the virus and is associated with a significant drop in viral load

50
Q

Is chronic HBV infxn more common in children or adults

A

children

51
Q

What does HBeAg negativity in chronic hep mean

A

HBV mutants that escape from immune regulation

52
Q

Who gets antiviral therapy for Hep B

A

Those with sever liver injury and INR >1.5, or protracted course with persistent sx >4 weeks

53
Q

LFT in HCV

A

LFTs may be normal or show fluctuating serum transaminases between 50 and 200 U/L

54
Q

Diagnosis of acute HEV infection

A

Diagnosis of acute infection is usually based on detection of anti-HEV IgM antibodies

55
Q

In which groups can HEV be more serious

A

nfection with genotype 1 or 2 virus during pregnancy carries a high risk of acute liver failure, which has a high mortality. Hepatitis E also causes more severe disease in those with underlying cirrhosis, resulting in decompensation or acute-on-chronic liver failure.

56
Q

Which patiens are at higher risk of HCC

A

Viral Hep and Haemachromatosis patients

57
Q

NASH CRN Scoring System for fibrosis stages:

A

Centrilobular peri-sinusoidal fibrosis
+ Periportal fibrosis
+ bridging fibrosis
cirrhosis

58
Q

What inherited metabolic disorders can cause fibrosis

A

Hemachromatosis, wilsons, a1-antitrypsin

59
Q

What drug can cause liver fibrosis

A

Methothrexate

60
Q

Liver enzymes in MASLD

A

AST and GGT elevated, ALT normal , ferritin slightly elevated

61
Q

What is MetALD

A

MASLD + Increased alcohol intake

62
Q

How to risk stratify pt with MASLD/MASH?

A

FIB-4

63
Q

Ix for NAFLD

A
  • USS
  • FIB-4
  • Fibroscan
  • Liver Biopsy : Can give NAS score and fibrosis stage
64
Q

Possible surgical tx for NAFLD and side effects

A

Laparoscopic sleeve gastroscopy, chronic diarrheoa

65
Q

Blood Tests for ALD

A

Elevated AST, ferritin and GGT ( higher than for NAFLD)

66
Q

Ferritin and transferrin level in haemachromatosis

A

Ferritin and transferrin both high

67
Q

Investigations in cirrhosis of the liver

A
  • USS (fat) , Fibroscan (stiffness) - esp for those with indeterminate firbosis scores, Fib4, biopsy - GOLD STANDARD
  • Ascitic tap if ascites present, to culture fluid
  • UGIE for varices
68
Q

Clinical features of NAFLD

A

Often aSx but may have assoc RUQ discomfort

69
Q

What drugs cause fatty liver

A

tamoxifen, amiodarone and corticosteroids.

70
Q

Is ALT or AST higher in advanced NAFLD

A

AST

71
Q

Expected liver biopsy obs for NAFLD

A
  • steatosis, hepatocellular injury and inflammationwith mainly centrilobular, acinar zone 3 distribution
  • perisinusoidal fibrosis is characteristic feature of NAFLD
72
Q

How to determine Tx for NAFLD

A

Based on FIB-4, and TE if indeterminate risk
- Low risk, lifestyle advice (GP)
- High risk, address CV risks and assess for portal HT and HCC (hep clinic)

73
Q
A
74
Q

How to differentiate cholecystitis from cholangitis

A

Murphy’s sign positive for cholecystitis and fever and raided inflammatory markers

Charcot’s triad for cholangitis - RUQ pain, jaundice and fever