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GI > Focal lesions in the liver > Flashcards

Focal lesions in the liver Flashcards

1
Q

what are solid liver lesions in older patients more likely to be?

A

= malignant with mets more common than primary liver cancer in the absence of liver disease

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2
Q

what are solid liver lesions in chronic liver disease patients more likely to be?

A

= primary liver cancer than mets or benign tumours

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3
Q

in non-cirrhotic patients, what is the most common solid liver tumour?

A

= haemangioma

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4
Q

what are the 2 classification of tumours in liver?

A

1) benign

2) malignant

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5
Q

give examples of benign tumours in the liver?

A
  • haemangioma
  • focal nodular hyperplasia
  • adenoma
  • liver cysts
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6
Q

give examples of malignant tumours in liver?

A

1) primary liver cancers
- hepatocellular carcinoma

  • cholangiocarcinoma
    = fibrolamellar carcinoma
    = hepatobalstoma
    (angiosarcoma and haemangioendothelioma)

2) metastases

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7
Q

who is more likely to acquire haemangioma - males/females?

A

females > males

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8
Q

what type of tumour is haemangioma?

A

= hyper-vascular tumour

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9
Q

describe the usual appearance of haemangioma?

A
  • single small

- well demarcated capsule

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10
Q

describe the clinical features of haemangioma?

A

= asymptomatic

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11
Q

how would you diagnose a haemangioma?

A
  • ultrasound
    = echogenic spot
  • CT
    = venous enhancements from periphery two centre
  • MRI
    = high intensity area
  • no need for FNA
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12
Q

how would you treat hameangioma?

A

= no need for treatment

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13
Q

what is focal nodular hyperplasia (FNH)?

A

= benign nodule formation of normal liver tissue

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14
Q

what is focal nodular hyperplasia associated with?

A

= congenital vascular anomaly: associated with Osler-weber- Rendu and liver haemangioma

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15
Q

describe the classic appearance focal nodular hyperplasia?

A
  • central sac conning large artery, radiating branches to periphery
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16
Q

why does hyperplasia occur in FNH?

A

= occurs in response to abnormal arterial flow

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17
Q

what is present histologically in FNH?

A
  • sinusoids
  • bile ductules
  • Kupffer cells
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18
Q

who is FNH more common in?

A

young, middle aged women

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19
Q

describe the symptoms of FNH?

A
  • asymptotic, may cause minimal pain
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20
Q

how do you diagnose FNH?

A
  • US: Nodule with varying echogenicity
  • CT: Hypervascular mass with central scar
  • MRI: Iso or hypo intense
  • FNA: Normal hepatocytes and Kupffer cells with central core
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21
Q

how do you treat FNH?

A
  • no treat necessary

- pregnancy and hormones no change required

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22
Q

what are hepatic adenomas?

A

= benign neoplasms composed of normal hepatocytes NO portal tract, central veins or bile ducts

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23
Q

who is more likely to get hepatic adenomas?

A

= women

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24
Q

what is hepatic adenoma associated with?

A
  • contraceptive hormones

- anabolic steroids

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25
Q

describe symptoms of hepatic adenoma?

A
  • asymptomatic

- but you can get right upper quadrant pain

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26
Q

what may people with hepatic adenomas present with?

A
  • rupture
  • haemorrhage
  • malignant transformation (risk higher in males)
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27
Q

what life are hepatic adenomas more common in?

A

= right lobe

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28
Q

what is associated with multiple adenomas (adenomatosis)?

A

= glycogen storage disease

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29
Q

how do you diagnose hepatic adenomas?

A
  • US: Filling defect
  • CT: Diffuse arterial enhancement
  • MRI: Hypo or hyper intense lesion
  • FNA: May be needed
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30
Q

how do you treat hepatic adenomas?

A
  • Stop hormones, weight loss
  • Males (irrespective of size) : surgical excision
  • Females : imaging after 6months
    <5cm or reducing in size - annual MRI
    >5cm or increase in size - for surgical excision
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31
Q

describe the difference between adenoma and focal nodular hyperplasia?

A

Adenoma

  • hyper vascular
  • hepatocyte tumour, cold on nuclear sulphur colloid scan
  • maybe pain/bleeding

FNH

  • hyper vascular
  • contains all liver US including RES and bile ductules (isointense on sulfur colloid scan)
  • maybe pain
  • central scar
  • no malignant risk
  • minimal bleeding risk
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32
Q

what is a simple cyst?

A

= liquid collection lined by an epithelium

  • no biliary tree communication
  • solitary and uniloculated
33
Q

are simple cysts symptomatic?

A
  • usually NO
34
Q

if there are symptoms, what are they related to?

A
  • intra- cystic haemorrhage
  • infection
  • rupture
  • compression
35
Q

how do you manage simple cyss?

A
  • no follow up required
  • if doubt = imaging in 3-6months
  • if symptomatic or uncertain diagnosis, then consider surgery
36
Q

what are hydatid cysts?

A

= echinoccoccus granulosus

37
Q

what may patients with hydatid cysts present with?

A
  • disseminated disease

- erosion of cysts into adjacent structures and vessels

38
Q

how is hydatid cysts diagnosed?

A
  • history, appearance and serological testing detection an anti-echinnococcus antibody
39
Q

how do you manage a hydatid cyst?

A
  • Surgery: = Conservative: Open cystectomy, Marsupialization
    = Radical: Pericystectomy, lobectomy

Medical: Albendazole
Percutaneous Drainage: PAIR

40
Q

what are the risks of surgery of hydatid cyst?

A
  • Operative morbidity
  • anaphylaxis
  • disseminaion of infection
41
Q

what is polycystic liver disease?

A

= embryonic ductal plate malformation of intra-hepatic biliary tree

  • numerous cysts through liver parenchyma
42
Q

what are the 3 types if polycystic liver disease?

A
  • Von Meyenburg complexes (VMC)
  • Polycystic Liver disease (PCLD)
  • Autosomal dominant Polycystic Kidney disease
    (ADPKD)
43
Q

what are VMC?

A

= benign cystic nodules through liver

  • cystic bile duct malformations, origination from peripheral biliary tree
  • remnants develop into small hepatic cysts and remain silent during life
44
Q

describe PCLD?

A
  • liver function preserved, renal failure rare
  • symptoms depend on size of cyst
  • PCLD gene = PRKCSH and SEC63
45
Q

describe ADPKD?

A

= renal failure due to polycystic kidneys and non-renal extra hepatic features
- potential massive hepatic enlargement

  • ADPKD genes - PKD1 and PKD2
46
Q

how do you manage polycystic liver disease?

A

In advanced PCLD, ADPKD or liver failure;
= defenestration/aspiration
= liver transplantation

47
Q

what pharmacological therapy is used for polycystic liver disease?

A

= somastatin analogues

  • symptom relief and liver volume reduction
48
Q

what are features that come along with liver abscess?

A
  • high fever
  • leukocytosis
  • complex liver lesions
49
Q

what are 2 key things to gleam in a history of liver abscess?

A
  • abdominal or biliary infection

- dental procedure

50
Q

how do you manage liver abscess?

A
  • empiric broad spectrum antibiotics
    (4 weeks of therapy)
  • aspiration /drainage percutaneously
  • echocardiogram
  • operation if no clinical improvement;
    = open drainage
    = resection
51
Q

what is the most common primary liver cancer (malignant) and who is more likely to get it?

A

hepato-cellular carcinoma (HCC)

= men

52
Q

what are risk factors for developing HCC?

A

= cirrhosis from any cause;

  • hep B
  • hep C
  • alcohol
  • aflatoxin
53
Q

what are clinical features of HCC?

A
  • weight loss
  • right upper quadrant pain
  • asymptomatic
  • worsening pre-existing chronic liver disease
  • acute liver failure
  • signs of cirrhosis
  • hard enlarged RUQ mass
  • liver bruit
54
Q

where can HCC metastasise?

A
  • rest of liver
  • portal vein
  • lymph nodes
  • brain
  • bone
  • lung
55
Q

describe the lab tests of HCC?

A
  • AFP (alfa fetoprotein) is a HCC tumour marker

values >100ng/ml suggestive of HCC

56
Q

how do you diagnose HCC?

A
  • presentation
  • elevated AFP
  • US
  • triphasic CT scan: early arterial perfusion
  • MRI
  • biopsy
57
Q

if HCC is stage O how would you treat it?

A

= resection

58
Q

if HCC is early stage A, single tumour or 3nodules how would you treat it?

A
  • liver transplantation

- percutaneous ethanol injection or radio-frequuency ablation

59
Q

if HCC is intermediate sage , multi-lobular, PST O, how would you treat it?

A

= trans-arterial chemoembolisation

60
Q

if HCC is advanced Stage C, portal invasion, N1, M1, PST 1-2, how would you treat it?

A

= sorafenib

61
Q

how would you treat end stag D HCC?

A

= symptomatic treatment

- mean survival is < 3months

62
Q

what is the best available treatment for HCC?

A

=liver transplant
- removes liver and liver

  • can only be done if tumour is < 5cm or less than 3 tumours less than 3cm each
63
Q

when is HCC resection feasible?

A

= for small tumours With preserved liver function (no jaundice or portal HTN)

64
Q

when is HCC local ablation used?

A
  • for non resectable patients
  • for patients with advanced liver cirrhosis
  • alcohol injection
65
Q

what is TACE?

A

= trans-arterial chemo embolisation

66
Q

what happens in TACE of HCC?

A

= chemo is injected selectively into hepatic artery

- then inject an embolism agent

67
Q

who is allowed to receive TACE?

A

= only in patients with early cirrhosis

68
Q

when are systemic therapies like sorafenib used?

A

= for advanced HCC thats is evolving

69
Q

what is sorafenib?

A

= a multi-kinase inhibitor of vascular endothelial growth factor receptor, platelet derived growth receptor and Raf

70
Q

who presents with fribo-lamellar carcinoma?

A

= young patients

- not related to cirrhosis

71
Q

is AFP normal or raised in fibro-lamellar carcinoma?

A

= normal

72
Q

what would a CT of fibro-lamellar carcinoma show?

A

= stellate scar with radial septa showing persistent. enhancement

73
Q

how do you treat fibro-lamellar carcinoma?

A

= surgical resection or transplantation

74
Q

how would you treat unresectable fibre-lamellar carcinomas?

A

= TACE

75
Q

what are common sites of secondary liver mets?

A
  • colon
  • breast
  • lung
  • stomach
  • pancreas
  • melanoma
76
Q

describe the ALP and live function in liver mets?

A

= mild cholestatic picture (ALP) with preserved liver function

77
Q

how do you diagnose secondary liver mets?

A
  • Dx imaging

- FNA

78
Q

what is treatment of secondary liver mets dependent on?

A

= primary cancer

79
Q

what could be possible in some cases with secondary liver mets?

A
  • resection

- chemo-embolisation

GI (43 decks)

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