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2a mid tier > Liver and friends > Flashcards

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
Q

What is the pathophysiology of hepatitis A?

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
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26
Q

What are the risk factors of hepatitis A?

A
  • Shellfish
  • Travellers
  • Food handlers
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27
Q

What is the presentation of hepatitis A?

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
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28
Q

What are the differential diagnoses of hepatitis A?

A
  • Other causes of jaundice

- Other types of viral and drug-induced hepatitis

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29
Q

How is hepatitis A diagnosed?

A

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
Q

How is hepatitis A managed?

A
  • NOTIFIABLE DISEASE
  • Supportive treatment
  • Avoid alcohol
  • Monitor liver function
  • Manage close contacts
  • Prevention: good hygiene, not resistance to boiling water
31
Q

What is the aetiology of hepatitis B?

A
  • 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
Q

What is the pathophysiology of hepatitis B?

A
  • 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
Q

What are the risk factors for hepatitis B?

A
  • Healthcare personnel
  • Emergency and rescue teams
  • CKD/ dialysis patients
  • Travellers
  • Homosexual men
  • IVDU
34
Q

What is the presentation of hepatitis B?

A
  • 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
Q

How is hepatitis B diagnosed?

A
  • HBsAg is present 1-6m after exposure
  • Presence of >6m implies carrier status
  • Anti-HBs = antibodies to hep B
36
Q

How is hepatitis B managed? (Acute and chronic)

A

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
Q

What is the aetiology of hepatitis C?

A
  • 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
Q

What is the pathophysiology of hepatitis C?

A
  • 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
Q

What are the risk factors of hepatitis C?

A
  • IVDU
  • Men
  • HIV +
  • High viral load
  • Alcohol
  • Receiving blood products before screening
40
Q

What is the presentation of hepatitis C?

A
  • 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
Q

How is hepatitis C diagnosed?

A
  • 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
Q

How is hepatitis C managed?

A
  • 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
Q

What is the aetiology of hepatitis D?

A
  • Incomplete RNA virus
  • Acute and chronic
  • Requires HBV for assembly
  • Blood-borne transmission
44
Q

What is the pathophysiology of hepatitis D?

A
  • 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
Q

What are the risk factors of hepatitis D?

A

Same as Hep B:

  • Healthcare personnel
  • Emergency and rescue teams
  • CKD/ dialysis patients
  • Travellers
  • Homosexual men
  • IVDU
46
Q

What is the presentation of hepatitis D?

A

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
Q

How is hepatitis D diagnosed?

A
  • HBDsAg is present 1-6m after exposure
  • Presence of >6m implies carrier status
  • Anti-HDs = antibodies to hep D
48
Q

How is hepatitis D managed?

A

SC pegylated interferon-alpha 2A

49
Q

What is the aetiology of hepatitis E?

A
  • RNA virus
  • Acute only
  • Spread via faeco-oral route
  • Water or food-bourne
  • Usually spread by contaminated water, rodents, dogs and pigs
50
Q

What is the pathophysiology of hepatitis E?

A
  • Similar to hep A
  • 100% immunity afterwards
  • Can cause chronic disease in immunosupressed
51
Q

What are the risk factors for hepatitis E?

A
  • Older men

- High mortality in pregnancy

52
Q

How is hepatitis E managed?

A
  • Vaccine available

- Prevention by good sanitation and hygiene

53
Q

What is the aetiology of haemochromatosis?

A

Autosomal recessive mutation of C282Y and H63D of the haemochromatosis gene (HFE)

54
Q

What is the pathophysiology of haemochromatosis?

A
  • 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
Q

What are the risk factors of haemochromatosis?

A
  • Middle age
  • Male gender
  • White ancestry
  • Family history
  • Iron supplements
56
Q

What is the presentation of haemochromatosis?

A
  • Fatigue
  • Arthralgias
  • Weakness
  • Lethargy
  • Hepatomegaly
57
Q

What are the differential diagnoses of haemochromatosis?

A
  • Iron overload from chronic transfusion
  • Hep B or C
  • Non-alcoholic fatty liver disease
58
Q

How is haemochromatosis diagnosed?

A
  • Serum transferrin saturation
  • HFE mutation analysis
  • Serum ferritin
  • Liver MRI
  • Liver biopsy
  • LFTs
59
Q

How is haemochromatosis managed?

A
  • Lifestyle modifications
  • Hep A and B vaccinations
  • Iron chelation therapy
  • Phlebotomy
60
Q

What is the aetiology of Wilson’s disease?

A
  • Autosomal recessive disease caused by mutations in the ATP7B gene
61
Q

What is the pathophysiology of Wilson’s disease?

A
  • 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
Q

What are the risk factors of Wilson’s disease?

A
  • Non-vegetarian diet

- Gene mutation (ATP7B)

63
Q

What is the presentation of Wilson’s disease?

A
  • History of hepatitis and behavioural difficulties
  • Tremor
  • Dysarthria (slurred speech)
  • Ascites
  • Jaundice
64
Q

What are the differential diagnoses of Wilson’s disease?

A
  • Viral Hep B and C
  • Haemochromatosis
  • A-1 antitrypsin deficiency
  • Autoimmune hepatitis
  • Alcoholic cirrhosis
  • Haemolytic anaemia
65
Q

How is Wilson’s disease diagnosed?

A
  • Liver function tests
  • 24 hours urine copper
  • FBC
  • Slit-lamp examination
  • Liver biopsy
  • Brain MRI
66
Q

How is Wilson’s disease managed?

A
  • Liver transplantation
  • Zinc monotherapy
  • Dietary restriction
  • Trientine
67
Q

What is the aetiology of alpha-1 antitrypsin deficiency?

A

Decreasing circulating plasma levels of AAT due to autosomal inheritance

68
Q

What is the main risk factor of alpha-1 antitrypsin deficiency?

A

Family history of deficiency

69
Q

What is the presentation of alpha-1 antitrypsin deficiency?

A
  • Productive cough
  • SOBOE
  • Current cigarette smoker
  • Exposure to gas/ fumes/ dust
  • Wheezing
70
Q

What are the differential diagnoses of alpha-1 antitrypsin deficiency?

A
  • Asthma
  • COPD
  • Bronchiectasis
  • Viral hepatitis
  • Alcoholic liver disease
71
Q

How is alpha-1 antitrypsin deficiency diagnosed?

A
  • Plasma AAT level
  • Pulmonary function tests
  • CXR
  • Chest CT
72
Q

How is alpha-1 antitrypsin deficiency managed?

A
  • Smoking cessation

- Supportive treatment for COPD and emphysema

2a mid tier (10 decks)

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