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Year 3 > Liver and Biliary > Flashcards

Liver and Biliary Flashcards

Liver and Biliary

1
Q

What are the three causes of jaundice?

A

Pre-hepatic
Hepatic
Post-hepatic

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2
Q

What is pre-hepatic jaundice?

A

Excess bilirubin due to excessive haemolysis

liver is fine but can’t conjugate fast enough

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3
Q

What is hepatic jaundice?

A

Impaired hepatocellular uptake, defective conjugation, or abnormal secretion of bilirubin

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4
Q

What is post-hepatic jaundice?

A

Impaired excretion due to a mechanical obstruction of the biliary flow

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5
Q

Which serum markers will be elevated in pre-hepatic jaundice?

A

Unconjugated bilirubin only (normal ALP/AST/ALT)

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6
Q

Which serum markers will be elevated in hepatic jaundice?

A

AST + ALT = sign of hepatocyte damage

Conjugated + unconjugated bilirubin may also be elevated (backlog- impaired metabolism)

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7
Q

Which serum markers will be elevated in post-hepatic jaundice (biliary disease)?

A

ALP + GGT = sign of cholangiocyte damage

Conjugated bilirubin

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8
Q

What are some signs of portal hypertension?

A 
Oesophageal varices
Splenomegaly
Caput medusae
Ascites
Haemorrhoids
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9
Q

What are some signs of liver failure?

A 
Asterixis
Bruising
Clubbing
Dupuytren's contracture
Erythema (palmar)
Fetor hepaticus (breath of the dead)
Gynaecomastia
Hypertension (portal)
Itching
Jaundice
Spider naevi/testicular atrophy
(ABC...)
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10
Q

Which hepatitides are transmitted through the faecal-oral route?

A

Hepatitis A, E (can also spread by sex/contaminated water)

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11
Q

Which hepatitides are transmitted through bodily fluids?

A

Hepatitis B, C, D

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12
Q

What is the incubation period of Hepatitis A?

A

2 weeks

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13
Q

What is the incubation period of Hepatitis B?

A

4-12 weeks

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14
Q

What is the incubation period of Hepatitis C?

A

2 weeks - 6 months

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15
Q

What is the incubation period of Hepatitis D?

A

4-12 weeks

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16
Q

What is the incubation period of Hepatitis E?

A

5-6 weeks

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17
Q

What are the risk factors for Hepatitis A?

A

Poor hygeine

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18
Q

What are the risk factors for Hepatitis B?

A

Health workers
IVDU
M-M sexual relations

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19
Q

What are the risk factors for Hepatitis C?

A

IVDU

M-M sexual relations

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20
Q

What are the risk factors for Hepatitis D?

A

Only co-infects with Hep B

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21
Q

What are the risk factors for Hepatitis E?

A

Immunocompromised Pts

Pregnancy

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22
Q

Which hepatitides are at risk of chronic development?

A 
Hepatitis B (in children)
Hepatitis C (60-80%)
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23
Q

What are some generic symptoms of viral hepatitis?

A 
Reduced appetite
N+V
Abdo pain
Pruritus
Skin rash
Joint pain
Jaundice
Hepatomegaly
Recent travel from Africa/East Mediterranean
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24
Q

What investigations would you do on a Pt with viral hepatitis?

A 
LFTs
FBC
U+Es
Antibodies
NAAT (nucleic acid amplification test can indicate viral load)
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25
Q

What is the interpretation of the following HBV antibodies?

Anti-HBc IgM: -ve
Anti-HBc IgG: -ve
HbSAg: -ve
Anti-HBs: -ve

A

Not infected

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26
Q

What is the interpretation of the following HBV antibodies?

Anti-HBc IgM: -ve
Anti-HBc IgG: -ve
HbSAg: -ve
Anti-HBs: +ve

A

Not infected, with prior vaccination

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27
Q

What is the interpretation of the following HBV antibodies?

Anti-HBc IgM: -ve
Anti-HBc IgG: -ve
HbSAg: +ve
Anti-HBs: -ve

A

Early acute HBV infection

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28
Q

What is the interpretation of the following Hep B antibodies?

Anti-HBc IgM: +ve
Anti-HBc IgG: -ve
HbSAg: +ve
Anti-HBs: -ve

A

Acute HBV infection

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29
Q

What is the interpretation of the following HBV antibodies?

Anti-HBc IgM: -ve
Anti-HBc IgG: +ve
HbSAg: -ve
Anti-HBs: +ve

A

Resolved acute HBV infection

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30
Q

What is the interpretation of the following HBV antibodies?

Anti-HBc IgM: -ve
Anti-HBc IgG: +ve
HbSAg: +ve
Anti-HBs: -ve

A

Chronic HBV infection

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31
Q

Notes for HBV antibody interpretation

A

HBsAg: surface antigens
If these are present, there is an infection

Anti-HBs: surface antigen antibodies
If these are present, body is successfully protected against virus

Anti-HBc IgM/IgG: core antigen antibodies
IgM precedes IgG, hence IgM indicates a more recent infection

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32
Q

What is the management for hepatitis A/E?

A

Supportive care

Avoid alcohol/excess paracetamol

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33
Q

What is the management for hepatitis B?

A

Supportive care if acute

Antivirals and peginterferon if chronic

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34
Q

What is the management for hepatitis C?

A

Supportive care if acute

Antivirals if chronic

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35
Q

What is the prognosis for hepatitis A?

A

Nearly all resolve in 6 months

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36
Q

What is the prognosis for hepatitis B?

A

Viral suppression in 90% of chronic cases

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37
Q

What is the prognosis for hepatitis C?

A

79% mortality at 10 years for chronic cases

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38
Q

What is the cause of NASH/NAFLD?

A

Insulin resistance -> increased triglycerides -> steatosis -> inflammation -> steatohepatitis

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39
Q

What are the risk factors for NASH?

A

No alcohol Hx

Obesity (truncal)
Insulin resistance/diabetes
Hyperlipidaemia
Hypertension
Metabolic syndrome
Short bowel syndrome
TPN.
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40
Q

What is the triad for NASH?

A

RUQ pain
Hepatomegaly
Metabolic syndrome without alcohol

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41
Q

What are the investigations for NASH?

A

Liver function tests

  • AST:ALT elevated <1 (>2 in alcoholic liver disease)
  • FBC- thrombocytopaenia, elevated WCC, deranged clotting
  • Metabolic profile (elevated glucose)
  • Lipid profile- hyperlipidaemia
  • Hepatic ultrasound
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42
Q

What is the management for NASH?

A

Diet and exercise
Correction of glucose and lipid levels (statins, metformin, thiazolidinediones)
Liver transplant if in liver failure

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43
Q

What is the prognosis for NASH?

A

1/3 reverse the condition
1/3 keep the condition
1/3 develops into cirrhosis

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44
Q

What are the complications of NASH?

A 
Cirrhosis
HCC
Ascites
Portosystemic thrombosis
Haemorrhage
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45
Q

What is the cause for ALD?

A

Alcohol metabolism -> XS NADH -> inhibits gluconeogenesis -> increased fatty acid oxidation -> steatosis -> inflammation -> steatohepatitis

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46
Q

What is the triad for ALD?

A

RUQ pain
Hepatomegaly
Associated with a Hx of alcohol consumption

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47
Q

What are the investigations for ALD? What would you see?

A

Liver function tests (AST:ALT >2, raised GGT) = FIRST LINE
FBC- macrocytic anaemia
Clotting screen
Vitamin screen
Hepatic USS (cirrhotic PT to screen for HCC)
Liver biopsy (diagnostic, rarely needed) + histology

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48
Q

What is the management for ALD?

A
  • Alcohol abstinence + withdrawal management (diazepam to prevent seizure)
  • Nutrition (enteral preferred, calories and vitamins)
  • Weight loss/stop smoking
  • Steroids in severe alcoholic hepatitis
  • Liver transplant if in liver failure
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49
Q

What is liver cirrhosis?

A

Scarring of the liver due to hepatocyte damage

Normal liver replaced with fibrosis and nodules of regenerating hepatocytes
Can be stable or decompensated (liver failure)

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50
Q

What are the symptoms of liver cirrhosis?

A

Abdominal distension
Pruritus
Coffee-ground vomit (due to gastro-oesoph varices)

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51
Q

What are the signs of liver cirrhosis?

A 
Jaundice
Ascites
Asterixis
Dupuytren's contracture
Palmar erythema
Caput medusae
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52
Q

What are the investigations for liver cirrhosis?

A 
LFTs
-low albumin
-prolonged PT
U+Es
-hyponatraemia: ascites
US/CT/MRI
can see atrophy/fibrotic nodules
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53
Q

What is the management for liver cirrhosis?

A

Treat underlying cause

Liver transplant if in liver failure

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54
Q

What is Wilson’s disease?

A

Autosomal recessive disease of impaired copper excretion in the bile

ATP7B mutation

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55
Q

What are the signs and symptoms of Wilson’s disease?

A

IN A YOUNG PERSON:

Hepatitis symptoms (liver accumulation):

  • Hepatosplenomegaly
  • RUQ pain
  • jaundice
  • ascites
  • portal HTN

Parkinsonism (basal ganglia accumulation):

  • Ataxia
  • Tremor
  • Dysdiadochokinesia
  • Dementia

Kayser-Fleischer rings

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56
Q

What investigations would you do for Wilson’s disease?

A

FIRST LINE:

  • LFTs (raised transaminases/bilirubin)
  • 24-hr urinary copper
  • slit lamp examination

COPPER STUDIES:

  • ↓ serum ceruloplasmin (copper transport protein)
  • ↑ serum free copper

GOLD STANDARD/DIAGNOSTIC

  • Genetic testing
  • Liver biopsy and measurement of copper content
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57
Q

What is haemochromatosis?

A

Autosomal recessive multisystem disorder of dysregulated dietary iron absorption and increased iron release from macrophages
Commonly C282Y or H63D mutation
Due to HEPCIDIN abnormality so there is no inhibition of Fe uptake

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58
Q

What are the investigations for haemochromatosis?

A

FIRST LINE = Iron studies:

  • high ferritin (non-specific as acute phase protein)
  • low transferrin
  • high transferrin saturation
Gene typing of HFE 
Liver biopsy (gold standard)
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59
Q

What is cholelithiasis?

A

Presence of solid concentrations in the gall bladder

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60
Q

What is choledocholithiasis?

A

Formation of solid concentrations in the gall bladder which exit the bile duct

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61
Q

What is the anatomy of the biliary tree, starting from the sphincter of Oddi?

A

Sphincter of Oddi -> hepatopancreatic ampulla of Vater
AoV -> common bile duct and pancreatic duct
CBD -> cystic duct and common hepatic duct
CHD -> left and right hepatic duct

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62
Q

What are the risk factors for gallstones?

A 
Fair skinned
Fat
Female
Fertile
Family Hx
Forty+
(6 F's)
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63
Q

What are the symptoms of gallstones?

A

RUQ pain- colicky, post-prandial (fatty meals)
Nausea

NO JAUNDICE- not obstructing biliary flow

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64
Q

What is Murphy’s sign and what pathology does it present in?

A

Palpate the costal margin mid-clavicular plane
Pain/wince upon inspiration
Gallstones

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65
Q

What is Boas’ sign and what pathology does it present in?

A

Pain radiating to below the scapula

Gallstones

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66
Q

What is Kehr’s sign and what pathology does it present in?

A

Pain radiating to the shoulder tip

Gallstones

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67
Q

What investigations would you do for gallstones/cholelithiasis?

A

LFTs (first line)

Abdo US of liver and biliary tree (diagnostic)

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68
Q

What is the management for cholelithiasis?

A

If asymptomatic- nothing

If biliary colic- elective cholecystectomy + analgesia

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69
Q

What is the management for choledocholithiasis?

A

(Analgesia) + ERCP

+ lap chole

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70
Q

What is ascending cholangitis?

A

choledocholithiasis + infection
Bile stasis- bacteria enter the hepatopancreatic duct
Leads to inflammation and infection

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71
Q

What is acute cholecystitis?

A

Gallstone in the gall bladder/cystic duct causing bile stasis, inflammation, and infection

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72
Q

What is Mirizzi syndrome?

A

Blockage of the cystic duct causing inflammation

Inflammation blocks CHD leading to obstructive jaundice

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73
Q

What are the signs and symptoms of acute cholecystitis?

A 
Constant RUQ pain +/- Boas' sign
Fever
N+V
Rebound tenderness
Murphy's sign +ve
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74
Q

What are the signs and symptoms of ascending cholangitis?

A

Charcot’s triad- RUQ pain, fever, jaundice

If septic, Reynold’s pentad

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75
Q

What is Charcot’s triad?

A

RUQ pain
Fever
Jaundice

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76
Q

What is Reynold’s pentad?

A 
RUQ pain
Fever
Jaundice
Hypotension
Confusion
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77
Q

What is primary biliary cirrhosis?

A

Autoimmune damage and destruction of the biliary epithelial cells lining the small intrahepatic bile ducts

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78
Q

What is the epidemiology of PBC?

A

55-65 yrs

F:M 10:1

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79
Q

What are the symptoms of PBC?

A

Pruritus
Fatigue
Sjogren’s (dry mouth and eyes)

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80
Q

What are the investigations of PBC?

A

LFTs
Anti mitochondrial antibodies
Abdo US/MRCP- rule out obstructive duct lesion

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81
Q

What is primary sclerosing cholangitis?

A

Inflammation and fibrosis of the intrahepatic and/or extrahepatic bile ducts, leading to diffuse, multi-focal stricture formation.

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82
Q

What is the epidemiology for PSC?

A

40-50s

Male

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83
Q

What are the symptoms of PSC?

A

RUQ pain
Pruritus
Fatigue

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84
Q

What are the investigations for PSC?

A

LFTs (elevated GGT)
MRCP: beading
AMA: -ve

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85
Q

What are the RF for pancreatic cancer?

A 
65-75 yrs old
Smoking
FHx
Obesity
TD2M
Chronic pancreatitis
86
Q

What are the symptoms for pancreatic cancer?

A

Painless jaundice
Palpable gallbladder
FLAWS

Commonly delayed presentation due to non-specific signs (malaise, weight loss, abdo pain). Jaundice is later sign.
Hepatomegaly if hepatic metastasis

87
Q

What are the investigations for pancreatic cancer?

A

FIRST LINE

  • LFTs
  • Abdominal USS- first line
  • CT pancreas is first line if high suspicion of pancreatic cancer

GOLD STANDARD:

  • Biopsy (via ERCP/EUS)
  • Tumour marker: CA19-9
88
Q

A 26 y/o male returns from holiday in India. He has had diarrhoea after eating at a seafood restaurant on his last night. He is feverish and nauseous. You notice that the whites of his eyes are yellow.

A. Hepatitis A
B. Hepatitis B
C. Hepatitis C
D. Hepatitis D
E. Hepatitis E
A

A. Hepatitis A

89
Q

A 64 y/o male with thalassaemia is investigated under the two-week wait for jaundice and weight loss. His blood tests show a raised αFP. Which chronic infection is he most likely to have?

A. Hepatitis A
B. Hepatitis B
C. Hepatitis C
D. Hepatitis D
E. Hepatitis E
A

C. Hepatitis C

aFP is raised in cancer. Hep C chronicity has a high risk of HCC.

90
Q

A 32 y/o male returns from holiday in Thailand, feeling ‘under the weather’ with RUQ pain, fevers and nausea. He is jaundiced. He reveals he has used IV drugs and had unprotected sex with a stranger while on holiday. Which test is most likely to give the correct diagnosis?

A. Liver function tests
B. HIV serology
C. Hepatitis B serology
D. Hepatitis C PCR
E. CXR
A

C. Hepatitis B serology

91
Q

A 43 y/o confused man is brought to A&E by police after being found wandering the streets. He is disorientated and unable to give a clear history. You notice brown rings in his eyes. What is he likely to have?

A. Alcohol intoxication
B. Wilson’s disease
C. Opiate overdose
D. Haemochromatosis
E. Hypoglycaemia
A

B. Wilson’s disease

92
Q

72 y/o man with cirrhosis presents to A&E with diffuse abdominal pain and fever. He is nauseous and has vomited. His abdomen is distended and there is shifting dullness on examination. Which investigation would be most urgent?

A. Paracentesis
B. Stool sample MC&S
C. Abdominal USS
D. LFTs
E. Blood cultures
A

A. Paracentesis

Has signs of bacterial peritonitis, which needs to be treated more urgently than the cirrhosis

93
Q

A 41 y/o female presents with a history of colicky, right sided abdominal pain. She states the pain is worse after eating fish and chips and Indian takeaways. On examination her abdomen is soft and non-tender. Which is the best investigation to confirm her diagnosis?

A. Abdominal X-ray
B. ERCP
C. Liver biopsy
D. USS of biliary tree
E. CT-KUB
A

D. USS of biliary tree

94
Q

A 41 y/o female presents to A&E with a history of severe, continuous, RUQ pain. She feels feverish and complains of an occasional pain in her right shoulder. On examination she displays RUQ tenderness and a positive Murphy’s sign. What is the most likely diagnosis?

A. Biliary colic
B. Ascending cholangitis
C. Acute cholecystitis
D. Primary biliary cirrhosis
E. Cholangiocarcinoma
A

C. Acute cholecystitis

95
Q

A 41 y/o female presents to A&E with a history of severe, continuous, RUQ pain. She feels feverish and complains of an occasional pain in her right shoulder. On examination she displays RUQ tenderness and a positive Murphy’s sign. While waiting to be admitted, her RUQ pain becomes worse and she starts shaking uncontrollably. You notice she now looks jaundiced. What is the most likely diagnosis?

A. Biliary colic
B. Ascending cholangitis
C. Acute cholecystitis
D. Primary biliary cirrhosis
E. Cholangiocarcinoma
A

B. Ascending cholangitis

96
Q

A 35 y/o man presents with a two week history of jaundice and RUQ pain. He is taking mesalazine for a “bowel condition”. What is the most likely cause of his jaundice?

A. Autoimmune hepatitis
B. Haemochromatosis
C. Primary sclerosing cholangitis
D. Primary biliary cirrhosis
E. Drug side effect
A

C. Primary sclerosing cholangitis

97
Q

A 39 year old female attends her GP for a routine check-up. She is obese and has type II diabetes, and been taking metformin and simvastatin for around 2 years. She complains of mild fatigue but has otherwise been well. She says she drinks around 8 units of alcohol per week. On examination there are no signs of chronic liver disease.

Investigations
Albumin		38 g/L (35-51)
ALT		178 IU/L (<40)
AST 		154 U/L (<40)
ALP 		57 U/L (35-51)
GGT		19 U/L (11-42)
Bilirubin 		12 umol/L (<17)
What is the most likely diagnosis? 
Drug-induced hepatitis
Non-alcoholic steatohepatitis
Alcoholic hepatitis
Viral hepatitis
Cirrhosis
A

Non-alcoholic steatohepatitis

98
Q

A 21 year old male student in London was well until 4 days ago when he developed diarrhoea, vomiting and RUQ pain. Yesterday morning, his flatmates noticed that his eyes had turned yellow. He has not lost any weight in the past few months and his stools are brown. LFTs revealed high transaminases, and a viral screen was ordered.

Viral screen
Anti-HepA IgM/IgG			Negative
Hep C Virus RNA			Undetectable 
HBsAg (HepB surface antigen) 	Positive
Anti-HBcAg IgM 			Positive 
Anti-HBcAg IgG			Negative
Anti-HBsAg IgG			Negative

Given the diagnosis, what is the most likely prognosis for this patient?

A

Full recovery

This patient currently has acute hepatitis B infection (evidenced by presence of Hep B surface antigen, and IgM antibodies against Hep B core antigen, but no IgG). The most common outcome of an acute hep B infection in adults is natural clearance of the virus and full recovery. For this reason there is no need to treat acute hep B patients with antivirals

99
Q

A 59 year old man with a history of long-standing alcoholism and previous episodes of hepatic encephalopathy presents to ED with altered mental status, fever and worsening abdominal distension and tenderness. An ascitic tap shows neutrophil concentration of 345 cells/mm3

Given the most likely diagnosis, how would you manage this patient?

Reassure and discharge
IM chlordiazepoxide and IV rifaximin
Large volume paracentesis
IV Cefotaxime and oral lactulose
IV vancomycin and IV albumin
A

Both SBP and HE require treatment so this is not a suitable option

Chlordiazepoxide is a sedative, and sedatives should generally be avoided in hepatic encephalopathy

Paracentesis can be used as an adjunct in uncomplicated SBP, although IV antibiotics are first line. However, this patient clearly has SBP complicated by HE so this may not be appropriate

This option provides broad spectrum antibiotics to treat the SBP empirically. Furthermore, the oral lactulose would aid to reduce ammonia production in the gut. IV fluids along with short-term protein restriction are likely to be indicated in this patient

IV vancomycin is typically used for hospital acquired SBP (whereas this patient has been brought into ED without mention of another recent hospital stay) due to a wider range of potential causative agents. IV albumin is indicated in SPB only when there is concurrent renal dysfunction, of which there is no sign here.

100
Q

Briefly explain bilirubin metabolism

A
  1. reticuloendothelial cells in spleen break down RBCs into haem and globin
  2. haem oxygenase breaks down haem into iron and biliverdin
  3. bilviderin –> unconjugated bilirubin
  4. In blood, unconjugated bilirubin binds to albumin and travels to liver
  5. glucuronyl transferase conjugates bilirubin (soluble)
    bilirubin excreted into the duodenum in bile
  6. in colon, bacteria deconjugate bilirubin into urobilinogen
    -20% –> absorbed and excreted in kidneys
    - 80% further oxidised to stercobilin + excreted in faeces
101
Q

Causes of pre-hepatic jaundice

A
  • Haemolysis

- Gilbert’s

102
Q

Causes of post-hepatic jaundice

A

Anything blocking the bile duct:

  • Gallstone
  • Pancreatic cancer/(bile duct cancer)
  • PSC/PBS
  • Drugs
103
Q

Causes of hepatic jaundice

A

Hepatitis
Cirrhosis
Liver mass
Haemochromatosis

Usually issues with

104
Q

Compare urine and stools for the different types of jaundice

A 
pre-hepatic = normal urine
hepatic = dark urine (conjugated bilirubin absorbed into blood)
post-hepatic = dark urine, light stools (no stercobilin)
105
Q

Cause of pruritis

A

excess bile acids in blood due to blockage of the bile ducts
Think POST-HEPATIC causes of jaundice`

106
Q

Causes of hepatitis

A
  • Autoimmune
  • Viral
  • Alcoholic
  • Non-alcoholic Steatohepatitis (NASH)
  • Drugs
107
Q

Hepatitis signs and symptoms

A
  • RUQ pain
  • Jaundice
  • Hepatomegaly
  • Joint pain
  • Nausea
  • Fatigue
  • Dark urine

Can’t differentiate causes based on symptoms as these are generally similar

108
Q

Stages of progression of alcoholic liver disease

A
  1. Steatosis (fatty)- after a few days of heavy drinking
  2. Alcoholic Hepatitis (inflammation)- due to chronic alcohol abuse
  3. Cirrhosis- irreversable scarring
109
Q

LFTs in alcoholic hepatitis

A 
AST/ALT ratio >2
↑bilirubin
-/↑ALP
↑GGT
↓ albumin
110
Q

Which 2 markers represent the functional capacity of the liver?

A

CLOTTING FACTORS- INR: ↑ prothrombin time = sensitive marker of significant liver damage
ALBUMIN: ↓ albumin

111
Q

What would liver biopsy show in ALD?

A

Ballooning

Mallory bodies indicates hepatitis

112
Q

When can Hep E cause chronic hepatitis?

A

Immunosuppressed (post-transplant, HIV)

113
Q

When can Hep E cause liver failure?

114
Q

What serology would you do for HEV/HAV? How would they differ?

A

IgM and IgG antibodies

HEV: IgM lasts 6 weeks + IgG persist for LIFE
HAV: IgM lasts 2 months + IgG last a few YEARS

115
Q

What is the commonest cause of HCC ?

A 
UK = HCV
Worldwide = HBV (less carcinogenic BUT much more common)
116
Q

What percentage of HBV becomes chronic?

A

B usually stays acute (10% chronic)

117
Q

Which hepatitis most commonly becomes chronic?

A

HCV

As can be chronic, risk of cirrhosis/HCC

118
Q

What increases risk of liver failure in HBV?

A

hepatitis D coinfection/superinfection

119
Q

How does ACUTE management of HBV and HCV differ?

A

Hep B: Acute = supportive

Hep C: Acute = antiviral

120
Q

State some antiviral treatments for HCV

A

Sofosbuvir (NS5B inhibitors)
Ledipasvir (NS5A inhibitors)
Grazoprevir (NS3/4 protease)

121
Q

Prognosis HCV

A

80% progresses to chronic if left untreated

Directly-acting antivirals mean that HCV can be cured in nearly 100% of cases, with short treatment regimens and minimal side effects

122
Q

Management of HBV

A

ACUTE = supportive
CHRONIC = antivirals:
- if no decompensated cirrhosis = peginterferon-a-2a
- if poor liver function = tenofovir / entecavir

123
Q

Management of HBV with HDV coinfection

A

peginterferon-a-2a
AND
tenofovir/entecavir

124
Q

if HBV surface antigen is present, what does this mean?

A

the patient is currently infected with HBV (active infection)

NOT PRESENT IN CLEARED INFECTION

125
Q

What does it mean is someone has antibodies to HBsAg?

A

either:

  • vaccinated (if nothing else)
  • cleared infection

NOT PRESENT IN ACTIVE INFECTION

126
Q

What does it mean is someone has antibodies to HBcAg?

A

SIGN OF PAST OR ONGOING INFECTION

Means that patient has either:

  • acute (IgM)
  • chronic (IgG)
127
Q

Serological markers- vaccinated against HBV

A

HBcAg IgM: -ve
HBcAg IgG: -ve
Hb S antigen: -ve
anti-HBs: +ve

128
Q

Serological markers- past HBV infection

A

HBcAg IgM: -ve
HBcAg IgG: +ve
Hb S antigen: -ve
anti-HBs: +ve

129
Q

Serological markers- acute HBV infection

A

HBcAg IgM: +ve
HBcAg IgG: -ve
Hb S antigen: +ve
anti-HBs: -ve

130
Q

Serological markers- chronic HBV infection

A

HBcAg IgM: -ve
HBcAg IgG: +ve
Hb S antigen: +ve
anti-HBs: -ve

131
Q

Which serological marker is positive in both cleared and current HCV infection?

A

anti-HCV antibodies

132
Q

Which serological marker is positive in current HCV infection only?

A

HCV RNA

if very high for >6 months = chronic

133
Q

Serological markers for acute and chronic HDV

A

if acute:

  • positive HDV RNA
  • positive HDV IgM
  • positive HDV antigen
  • negative IgG

if chronic:

  • positive HDV RNA
  • positive HDV IgG
  • negative HDV antigen + IgM
134
Q

RF for Hep A

A

Asia and Africa travel
MSM
Shellfish- improperly cleaned shellfish from contaminated water

135
Q

Symptoms of HAV/HEV

A 
Acute onset, lasts 8 weeks max:
Nausea
Vomiting (+ Diarrhoea)
Fever
Jaundice
Abdominal pain (particularly RUQ)
136
Q

What type of virus is HCV

A

RNA flavivirus

137
Q

HEV treatment in immunocompromised

138
Q

Predominant mode of transmission HCV

A

Blood product spread (IVDU/transfusion)

139
Q

Predominant mode of transmission HBV

A

Sexually transmitted; IVDU; vertical

140
Q

What are the symptoms of HCV?

A

most commonly ASYMPTOMATIC

implications for chronic disease progression

141
Q

In terms of blood investigations, compare the 5 main causes of hepatitis

A

ALCOHOLIC

  • AST:ALT >2
  • ↑GGT

NASH
- AST:ALT <1

VIRAL

  • AST + ALT in 1000s
  • serology

DRUG

  • AST + ALT in 1000s
  • serum drug conc

AUTOIMMUNE

  • AST + ALT in 1000s
  • ANA / ASMA / AMA positive
142
Q

Tx paracetamol overdose

A

N-acetyl cysteine

143
Q

Define haemochromatosis

A

condition leading to abnormal iron deposition in certain organs
(liver, pancreas, skin, pituitary, heart, joints)

144
Q

How can haemachromatosis be classified?

A

PRIMARY
Hereditary- autosomal recessive- defect in the HFE gene
Cannot stop iron absorption from GI tract

SECONDARY
Iron overload e.g., multiple transfusions

145
Q

Pathophysiology primary haemachromatosis

A

Defect in the HFE gene
Transferrin binds poorly to its receptor, causing the liver to reduce hepcidin production.
Hepcidin usually inhibits ferroportin (the enterocyte iron transporter).
With reduced hepcidin production, ferroportin activity in the enterocytes is unregulated
More iron is transported across the enterocytes, and
Results in iron accumulation and damage to the affected organs.

146
Q

Clinical features of haemachromatosis

A

75% asymptomatic- takes years for iron to accumulate

  • hepatomegaly
  • diabetes mellitus onset
  • bronze skin
  • arthralgia
  • male impotence

M experience before F
May progress to cirrhosis and HCC

147
Q

Why do females experience haemachromatosis later than males?

A

females have an additional method of excreting iron through menstruation, whereas this is not possible in males so iron accumulates more quickly

148
Q

Investigations for haemachromatosis

A

FIRST LINE: Transferrin saturation (raised) and serum ferritin (raised, non-specific as acute phase protein)

Gene typing of HFE

Liver biopsy (gold standard)

149
Q

Epidemiology of Wilsons

A

Autosomal recessive genetic disorder

Age of onset 5-35 years

150
Q

Causes of cirrhosis

A 
Alcohol misuse
viral hepatitis (B/C)
autoimmune hepatitis
haemochromatosis
NASH
chronic biliary disease
151
Q

causes of macro/micro nodular cirrhosis

A 
MACRO = viral
MICRO= alcoholic
152
Q

signs of of chronic stable liver disease

A 
clubbing
spider naevi 
dupuytren’s contracture
palmar erythema
gynaecomastia 
bruising
153
Q

Define portal hypertension

A

↑ pressure in portal vein due to cirrhosis (of any cause)

Blood flows from portal to systemic circulation (porto-systemic anastamosis)

154
Q

sites of porto-systemic anastamosies

A

Lower eosophagus
Anal canal
Umbilicus
Splenorenal

leads to varices

155
Q

Signs of portal hypertension

A

caput medusae
ascites
oesophageal varices

156
Q

What causes hepatic encephalopathy?

A

Impaired liver function in decomponesated cirrhosis means that ammonia is not metabolised in liver

Toxins + ammonia make their way into the systemic circulation (intrahepatic shunting + extrahepatic via anastamoses)

Travels to brain impacting neurotransmission and causing confusion

157
Q

Precipitating factors for hepatic encephalopathy

A
  • high protein diet
  • GI bleed
  • Infection
  • Benzodiazepines

protein –> ammonia (gut flora)

158
Q

Management of cirrhosis

A

Treat cause + avoid hepatotoxic drugs (alcohol, sedative, opiates, NSAIDs etc.)

Monitor risk of complications (MELD score, 6-monthly
USS, endoscopy upon diagnosis and every 3 years)

Manage complications- ascites, encephalopathy, SBP, varices

159
Q

Management of hepatic encephalopathy

A

Treat precipitating event (GI bleed, infection etc.) + short term protein restriction

Oral lactulose, phosphate enema

Avoid sedatives

160
Q

Management of ascites

A

Sodium restriction ±
Diuretics (furesomide + spironolactone) ±
Large volume paracentesis

161
Q

Management of SBP

A

Abx (cefuroxime + metronidazole)

162
Q

Define SBP

A

On ascitic drain:
>250 neutrophils per mm3ascitic fluid

….with no obvious cause of infection

163
Q

Commonest pathogen causing SBP

164
Q

Management of varices

A

Non-selective β-blocker (if small) = propanolol

Endoscopic variceal band ligation (if large)

If this doesn’t work:
Transjugular intrahepatic portosystemic shunt (TIPS)

165
Q

Management of bleeding varices

A

A-E, IV fluids + blood (when Hb<7g/dL)

Terlipressin (reduce blood flow to gut, reduce pressure on portal system)
Antibiotics
Uncontrollable bleeding use balloon tamponade/metal mesh stent

When stable: endoscopic variceal band ligation

166
Q

Define liver failure

A

severe liver dysfunction leading to jaundice, encephalopathy and coagulopathy

167
Q

most common causes of ALF

A 
paracetamol overdose (transaminitis +++) (50% of ALF)
viral hepatitis

acute on chronic: acute decompensation in patients with chronic liver disease

168
Q

How can liver failure be categorised?

A

Hyperacute: Encephalopathy <7 days after onset of jaundice
Acute: Encephalopathy 1-4 weeks after onset of jaundice
Subacute: Encephalopathy 4-12 weeks after onset of jaundice
Acute on chronic: acute decompensation in patients with chronic liver disease

169
Q

Treatment for ALF

A

treat cause

liver transplant

170
Q

Define liver abscess + give 4 main types

A

Liver infection –> walled off collection pus/cyst fluid

  • Pyogenic
  • Amoebic
  • Hydatid cyst
  • TB
171
Q

most common pathogen in pyogenic abscess

A

most polymicrobial

  • S. Aureus (kids)
  • E. Coli (adults)
172
Q

most common pathogen in amoebic abscess

A

Entamoeba histolytica infection (faeco-oral spread)

Associated with amoebic dysentery (profuse bloody diarrhoea)

173
Q

most common pathogen in hydatid cyst

A

Tapeworm Echinococcus granulosis infection

174
Q

Commonest causes of pyogenic abscess

A

60% related to biliary disease

e.g., gallstones, strictures

175
Q

symptoms of liver abscess

A 
Fever
malaise
weight loss
RUQ pain (referred shoulder pain)
jaundice
Foreign travel.
176
Q

signs of liver abscess

A

Jaunice
tender hepatomegaly
dullness to percussion/↓ breath sounds at right
lung base

177
Q

Investigations for liver abscess

A

Bloods (FBC- mild anaemia, leukocytosis, eosinophilia for hydatid cyst

Liver USS- hyperechoic

Stool microscopy: For Entamoeba histolytica or Echinococcus granulosis

Aspiration and culture of abscess: pyogenic (most polymicrobial), amoebic (anchovy sauce with necrotic hepatocytes/trophozoites)

178
Q

2 associations of raised GGT

A

bile duct damage

chronic alcohol abuse

179
Q

Name some common drugs that cause drug induced cholestasis

A

Co-amoxiclav
Nitrofurantoin
OCP

cause a paralysis of the biliary system (ileus).

180
Q

common characteristic of pancreatic cancer

A

painless palpable gallbladder (Courvoisier’s law) and jaundice

181
Q

typical presentation of acute cholangitis

A

RUQ pain, fever and jaundice.

Acute cholangitis is typically extremely painful

182
Q

typical presentation of cholangiocarcioma

A

Gradual onset obstructive pattern

183
Q

UC is associated with which bile duct disease?

A

PBC

Primary Biliary Cholangitis

184
Q

Management of acute cholangitis

A

Clear fluids only. Analgesics, fluid resus, broad IV Abx if infection.
Definitive: Lap cholecystectomy (within 1 week if uncomplicated)

185
Q

what is ascending cholangitis

A

Choledocholithiasis + infection

186
Q

Difference between ascending cholangitis and acute cholecystitis

A

Ascending cholangitis: may be jaundice/raised ALP/GGT- obstruction to biliary flow

acute cholecystitis = no obstruction

187
Q

management of abscess in gall bladder

A

cholecystostomy

188
Q

What are the 2 key complications of choledocolithiasis?

A

Ascending cholangitis

Pancreatitis

189
Q

Management of ascending cholangitis

A

Clear fluids only. Analgesics, fluid resus, broad IV Abx

+ ERCP

Lap cholecystectomy

190
Q

What are most gallstones formed from?

A

Mostly mixed (20–80% cholesterol, calcium carbonate, bile salts, bilirubin)

191
Q

What causes pigment stones?

A

Haemolysis

Calcium bilirubinate

192
Q

Severe RUQ pain, +ve murphy’s sign without jaundice strongly points to what?

A

acute cholecystitis

193
Q

compare definitions/location of PBC and PSC

A

Both inflammatory conditions of the bile ducts causing cholestasis

PBC = intrahepatic ducts, F>M
PSC = intra and extra hepatic ducts, M>F

Think PSC-ary- generally worse condition

194
Q

What are the associations of PBC and PSC?

A

PBC: Sjorgen’s, RA
PSC: associated with IBD (esp UC)

195
Q

compare complications of PSC and PBC

A

PBC: granulomas
PSC: cirrhosis, cholangiocarcinoma

Both can increase risk of HCC

196
Q

compare histology of PSC and PBC

A

PBC: florid ductal lesions
PSC: concentric onion skin fibrosis

197
Q

compare diagnosis of PSC and PBC

A

PBC: presence of AMA antibodies

PSC: MRCP shows beaded appearance- segmental fibrosis with saccular dilation.
Most prevalent serum antibodies= p-ANCA, then ANA

198
Q

What is the tumour marker for pancreatic cancer?

A

CA19-9

CEA (les common)

199
Q

What is the most common cause of liver tumours?

A 
SECONDARY TUMOURS 
Metastasised commonly from: 
bowel
breast
oesophagus
stomach
pancreas
200
Q

What are the 2 main types of primary liver tumour?

A 
Hepatocellular carcinoma (90%)
Cholangiocarcinoma
201
Q

RF for HCC

A 
HBV- commonest worldwide
HCV- commonest in europe
ALD
AIH
haemochromatosis
NAFLD
aflatoxin
PBC
Smoking
Obesity
202
Q

Signs and symptoms of HCC

A 
Malaise, FLAWS
RUQ pain
Jaundice
scites (due to chronic liver disease) 
Cachexia
Hepatomegaly
203
Q

Investigations for HCC

A

FIRST LINE:

  • Liver USS (6 monthly USS for high risk PTs)
  • LFTs
  • Tumour markers - AFP
  • Viral serology

GOLD STANDARD

  • Liver CT
  • Liver biopsy
204
Q

Most common type + location of pancreatic cancer

A

Mostly adenocarcinoma from exocrine tissue

75% in head of pancreas

205
Q

Define cholangiocarcinoma

A

adenocarcinomas of bile duct epithelium

206
Q

RF cholangiocarcinoma

A

PSC, worm infections and cirrhosis

207
Q

Investigations for cholangiocarcinoma

A 
Abdo USS (dilated intrahepatic ducts, mass lesion)
Gold standard- biopsy (using ERCP)
208
Q

signs and symptoms cholangiocarcinoma

A

same as pancreatic cancer
-distinguished by imaging/histology
Pancreatic cancer more common

209
Q

Presence of anti-smooth muscle antibodies is a feature of which disease?

A

autoimmune hepatitis

210
Q

appearance of PSC on MRCP

A

BEADS ON A STRING

segments of fibrotic bile duct, followed by dilated bile duct

Year 3 (38 decks)

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