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Liver and friends Flashcards

1
Q

What is the pathophysiology of hepatocellular carcinoma?

A
  • Tumour is either single or occurs as multiple nodules throughout the liver
  • Consists of cells resembling hepatocytes
  • Can metastasise via the hepatic or portal veins to the lymph nodes, bones and lungs
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2
Q

What are the risk factors for hepatocellular carcinoma?

A
  • Carriers of Hep B and C

- Associated with cirrhosis (e.g. alcohol cirrhosis, non-alcoholic fatty liver disease and haemochromatosis)

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3
Q

What is the presentation of hepatocellular carcinoma?

A
  • Weight loss
  • Anorexia
  • Fever
  • Fatigue
  • Jaundice
  • Ache in the right hypochondrium
  • Ascites
  • May have an enlarged, irregular tender liver on examination
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4
Q

How is hepatocellular carcinoma diagnosed?

A
  • Serum alpha-fetoprotein may be raised
  • Ultrasound scan show filling defects in 90% of cases
  • Enhanced CT: identified HCC but can’t diagnose if <1cm
  • Liver biopsy: to confirm diagnosis (used less now due to potential seeding of tumour along biopsy tract)
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5
Q

What is the management of hepatocellular carcinoma?

A
  • Surgical resection of isolate lesion
  • Liver transplant is the only cure
  • Prevention: prevent HBV infection, usually with a vaccine
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6
Q

What are the risk factors for cholangiocarcinoma?

A
  • Associated with parasitic worm infestation (flukes)
  • Biliary cysts
  • IBD e.g. Crohn’s or UC
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7
Q

What is the presentation of cholangiocarcinoma?

A
  • Fever
  • Abdominal pain ± ascites
  • Malaise
  • Jaundice
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8
Q

How is cholangiocarcinoma diagnosed?

A
  • Abdo CT
  • Raised bilirubin
  • Raised alk phos
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9
Q

How is cholangiocarcinoma managed?

A
  • Surgical resection is rarely possible and most patients die in 6m
  • Liver transplant is contraindicated
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10
Q

What is a haemangioma?

A

A benign liver tumour

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11
Q

What are the risk factors for hepatic adenoma?

A

Associated with oral contraceptives, anabolic steroids and pregnancy

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12
Q

What is the presentation of hepatic adenoma?

A

Can present with abdominal pain or intraperitoneal bleeding

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13
Q

How is hepatic adenoma managed?

A

Surgical resection is only required for symptomatic patients with tumours >5cm in diameter

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14
Q

What are the most common primary sites for secondary liver tumours?

A

GI tract, breast and bronchus

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15
Q

What is the presentation of secondary liver tumours?

A
  • Variable
  • Weight loss
  • Malaise
  • Upper abdominal pain
  • Hepatomegaly ± jaundice
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16
Q

How are secondary liver tumours diagnosed?

A
  • USS is primary investigation with CT or MRI to define metastases
  • Raised serum alk phos
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17
Q

Have a secondary liver tumours managed?

A
  • Depends on site of primary tumour and the burden of liver metastases
  • Removal of primary tumour and hepatic resection
  • Chemotherapy is used, particularly with breast cancer
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18
Q

What is the pathophysiology of pancreatic adenocarcinoma?

A
  • Originates in the ductal epithelium and evolves from pre-malignant lesions to full-invasive cancer
  • Most metastasise early so present late
  • 60% arise in the pancreatic head
  • 25% arise in the body
  • 15% arise in the tail
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19
Q

What are the risk factors for pancreatic adenocarcinoma?

A
  • Smoking
  • Excessive coffee or alcohol intake
  • Excessive aspirin use
  • Diabetes
  • Chronic pancreatitis
  • Older age (65-75)
  • FHx of pancreatic cancer
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20
Q

What is the presentation of pancreatic adenocarcinoma?

A
  • Painless jaundice or epigastric pain radiating to the back with progressive weight loss
  • Non-specific upper abdo pain/ discomfort
  • Weight loss and anorexia
  • Diabetes
  • Acute pancreatitis
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21
Q

What are the differential diagnoses of pancreatic adenocarcinoma?

A
  • Chronic pancreatitis
  • Bile duct stones
  • Autoimmune pancreatitis
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22
Q

How is pancreatic adenocarcinoma diagnosed?

A
  • Transabdominal ultrasound and CT to find pancreatic mass ± dilated biliary tree
  • LFTs
  • Biopsy for staging
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23
Q

How is pancreatic adenocarcinoma managed?

A
  • 3% 5 year survival rate
  • Surgical resection
  • Pancreatic enzyme replacement
  • Radio/chemotherapy
  • Palliative care: stenting for jaundice, opiates for pain, nutritional supplementation
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24
Q

What is the aetiology of hepatitis A?

A
  • RNA virus
  • Acute only
  • Ingestion of contaminated food or water
  • Overcrowding and poor sanitation facilitate spread
  • Spread via faeco-oral route
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25
What is the pathophysiology of hepatitis A?
- Type of picornavirus - Replicates in the liver, excreted in bile then excreted in faeces for 2w before clinical illness starts - Disease is most infectious before the onset of jaundice - Incubation period of 2-6w - Usually self-limiting - 100% immunity afterwards
26
What are the risk factors of hepatitis A?
- Shellfish - Travellers - Food handlers
27
What is the presentation of hepatitis A?
- Patient feels unwell with non-specific symptoms like nausea, fever and malaise - Sometimes become jaundiced after 1-2w - Urine gets darker and stool gets paler as jaundice deepens (intrahepatic cholestasis) - Followed by hepatosplenomegaly - Illness is often over within 3-6w after jaundice lessens
28
What are the differential diagnoses of hepatitis A?
- Other causes of jaundice | - Other types of viral and drug-induced hepatitis
29
How is hepatitis A diagnosed?
LIVER BIOCHEM: - Prodromal stage (between initial symptoms and jaundice) = normal bilirubin, raised bilirubinuria and urinary urobilinogen and raised serum AST or ALT - Icteric stage (after jaundice has presented) = serum bilirubin reflects level of jaundice ``` BLOOD TESTS: - Leucopenia (less white cells) and raised ESR Viral markers: - Hep A virus (HAV) antibodies - Anti-HAV IgM = acute infection ```
30
How is hepatitis A managed?
- NOTIFIABLE DISEASE - Supportive treatment - Avoid alcohol - Monitor liver function - Manage close contacts - Prevention: good hygiene, not resistance to boiling water
31
What is the aetiology of hepatitis B?
- DNA virus - Acute and chronic - Bloodborne transmission: needle stick, tattoos, sex, blood products, IVDU, vertical transmission (mother to child in utero or soon after birth) - Horizontal transmission: particularly in children, through minor abrasions or close contact, HBV can survive on household items like toys and toothbrushes
32
What is the pathophysiology of hepatitis B?
- Complete virus comprises of an inner core surrounded by an outer envelope of surface protein (Hep B surface antigen – HBsAg) - HBsAg is produced in excess by infected hepatocytes - Virus loses its coat after penetrating hepatocytes and the virus core is transported into the nucleus without processing - 1-10% of patients will develop chronic Hep B - 1-5% will develop chronic infection which can lead to cirrhosis then liver failure - Chronic Hep B causes continuing hepatocellular damage
33
What are the risk factors for hepatitis B?
- Healthcare personnel - Emergency and rescue teams - CKD/ dialysis patients - Travellers - Homosexual men - IVDU
34
What is the presentation of hepatitis B?
- Similar to Hep A - Infection can be subclinical in many cases (little symptoms) - Incubation period of 1-6m - Viremia causes patient to feel unwell, with non-specific symptoms like nausea, fever, malaise, anorexia and arthralgia - May also be rashes affecting small joints - Some patients become jaundiced after 1-2w and symptoms often improve - Urine gets darker and stool gets paler as jaundice deepens (intrahepatic cholestasis) - Followed by hepatosplenomegaly
35
How is hepatitis B diagnosed?
- HBsAg is present 1-6m after exposure - Presence of >6m implies carrier status - Anti-HBs = antibodies to hep B
36
How is hepatitis B managed? (Acute and chronic)
ACUTE: - Supportive - Avoid alcohol - Monitor liver function - Manage close contacts by giving normal immunoglobulin for Hep B and vaccination - Monitor HBsAg at 6m to ensure full clearance and no progression - Primary prev = vaccination - Most = spontaneous resolution CHRONIC: - Sub-cut pegylated interferon-alpha 2a --> weekly injection which stimulates an immune response - Nucleotide analogues e.g. oral tenofovir inhibit viral replication, one tablet a day, may be required long term as they don’t stimulate an immune response
37
What is the aetiology of hepatitis C?
- RNA flavivirus - Acute and chronic - Transmitted by blood and blood products - Was common in haemophiliacs before blood products were screened - Limited sexual transmission - Very high incidence in IVDU - Vertical transmission is rare
38
What is the pathophysiology of hepatitis C?
- 7 genotypes (1a and 1b account for most western cases) - Rapid mutations so envelope proteins change a lot (hard to develop a vaccine) - Can results in chronic hepatitis
39
What are the risk factors of hepatitis C?
- IVDU - Men - HIV + - High viral load - Alcohol - Receiving blood products before screening
40
What is the presentation of hepatitis C?
- Most acute infections are asymptomatic - 10% have mild flu-like illness with jaundice and ALT/AST rise - Most patients present years later with chronic liver disease or abnormal ALT/AST results - Chronic HCV can result in cirrhosis, liver failure and hepatocellular carcinomas
41
How is hepatitis C diagnosed?
- HCV antibodies present within 4-6w (false negative in immunosuppressed and in acute infection) - HCV RNA indicates current infection, so is diagnostic for acute
42
How is hepatitis C managed?
- Acute: no treatment if viral load is falling (observe for months to ensure clearance) - SC pegylated interferon-alpha 2A/B with oral ribavirin if HCV RNA doesn’t decline - Triple therapy with direct acting antivirals - Prevention: no vaccine, can be re-infected, screen blood products, caution when handling body fluids
43
What is the aetiology of hepatitis D?
- Incomplete RNA virus - Acute and chronic - Requires HBV for assembly - Blood-borne transmission
44
What is the pathophysiology of hepatitis D?
- Incomplete RNA particle enclosed in a shell of Hep B surface antigen - Virus is unable to replicate on its own, but is activated by presence of HBV - Increased severity of acute infection if acquired at the same time as HBV - Can either occur as a co-infection or superinfection CO-INFECTION: - Infection of Hep B and D at the same time - Clinically indistinguishable from acute HBV infection SUPERINFECTION: - When a person with chronic HBV gets HDV - Results in secondary acute hepatitis and increased rate of liver fibrosis progression - Rise in serum AST and ALT may be the only indication of a superinfection - Can result in hepatocellular carcinoma
45
What are the risk factors of hepatitis D?
Same as Hep B: - Healthcare personnel - Emergency and rescue teams - CKD/ dialysis patients - Travellers - Homosexual men - IVDU
46
What is the presentation of hepatitis D?
Similar to Hep B: - Infection can be subclinical in many cases (little symptoms) - Incubation period of 1-6m - Viremia causes patient to feel unwell, with non-specific symptoms like nausea, fever, malaise, anorexia and arthralgia - May also be rashes affecting small joints - Some patients become jaundiced after 1-2w and symptoms often improve - Urine gets darker and stool gets paler as jaundice deepens (intrahepatic cholestasis) - Followed by hepatosplenomegaly
47
How is hepatitis D diagnosed?
- HBDsAg is present 1-6m after exposure - Presence of >6m implies carrier status - Anti-HDs = antibodies to hep D
48
How is hepatitis D managed?
SC pegylated interferon-alpha 2A
49
What is the aetiology of hepatitis E?
- RNA virus - Acute only - Spread via faeco-oral route - Water or food-bourne - Usually spread by contaminated water, rodents, dogs and pigs
50
What is the pathophysiology of hepatitis E?
- Similar to hep A - 100% immunity afterwards - Can cause chronic disease in immunosupressed
51
What are the risk factors for hepatitis E?
- Older men | - High mortality in pregnancy
52
How is hepatitis E managed?
- Vaccine available | - Prevention by good sanitation and hygiene
53
What is the aetiology of haemochromatosis?
Autosomal recessive mutation of C282Y and H63D of the haemochromatosis gene (HFE)
54
What is the pathophysiology of haemochromatosis?
- HFE gene is involved in iron regulation - A lack of regulation causes iron accumulation in multiple organs including liver, heart, anterior pituitary, joints, pancreas
55
What are the risk factors of haemochromatosis?
- Middle age - Male gender - White ancestry - Family history - Iron supplements
56
What is the presentation of haemochromatosis?
- Fatigue - Arthralgias - Weakness - Lethargy - Hepatomegaly
57
What are the differential diagnoses of haemochromatosis?
- Iron overload from chronic transfusion - Hep B or C - Non-alcoholic fatty liver disease
58
How is haemochromatosis diagnosed?
- Serum transferrin saturation - HFE mutation analysis - Serum ferritin - Liver MRI - Liver biopsy - LFTs
59
How is haemochromatosis managed?
- Lifestyle modifications - Hep A and B vaccinations - Iron chelation therapy - Phlebotomy
60
What is the aetiology of Wilson's disease?
- Autosomal recessive disease caused by mutations in the ATP7B gene
61
What is the pathophysiology of Wilson's disease?
- ATP7B gene is involved in the excretion of excess copper in bile, so copper accumulates, causing toxicity by oxidant damage - Excess copper results in cell injury, inflammation and death
62
What are the risk factors of Wilson's disease?
- Non-vegetarian diet | - Gene mutation (ATP7B)
63
What is the presentation of Wilson's disease?
- History of hepatitis and behavioural difficulties - Tremor - Dysarthria (slurred speech) - Ascites - Jaundice
64
What are the differential diagnoses of Wilson's disease?
- Viral Hep B and C - Haemochromatosis - A-1 antitrypsin deficiency - Autoimmune hepatitis - Alcoholic cirrhosis - Haemolytic anaemia
65
How is Wilson's disease diagnosed?
- Liver function tests - 24 hours urine copper - FBC - Slit-lamp examination - Liver biopsy - Brain MRI
66
How is Wilson's disease managed?
- Liver transplantation - Zinc monotherapy - Dietary restriction - Trientine
67
What is the aetiology of alpha-1 antitrypsin deficiency?
Decreasing circulating plasma levels of AAT due to autosomal inheritance
68
What is the main risk factor of alpha-1 antitrypsin deficiency?
Family history of deficiency
69
What is the presentation of alpha-1 antitrypsin deficiency?
- Productive cough - SOBOE - Current cigarette smoker - Exposure to gas/ fumes/ dust - Wheezing
70
What are the differential diagnoses of alpha-1 antitrypsin deficiency?
- Asthma - COPD - Bronchiectasis - Viral hepatitis - Alcoholic liver disease
71
How is alpha-1 antitrypsin deficiency diagnosed?
- Plasma AAT level - Pulmonary function tests - CXR - Chest CT
72
How is alpha-1 antitrypsin deficiency managed?
- Smoking cessation | - Supportive treatment for COPD and emphysema

2a mid tier (10 decks)

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