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SYSTEMIC PATHOLOGY > Hepatobiliary - biliary tract diseases + neoplastic conditions > Flashcards

Hepatobiliary - biliary tract diseases + neoplastic conditions Flashcards

1
Q

cause of pre-hepatic jaundice

A

excess production of bilirubin:

  • haemolysis (breakdown of RBC)
  • ineffective erythropoiesis
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2
Q

cause of hepatic jaundice (3)

A
  • reduced hepatic uptake e.g. drugs
  • impaired bilirubin conjugation:
    physiologic/ neonatal jaundice
    genetic deficiency
    diffuse hepatocellular disease
  • impaired bile flow
    AI (autoimmune) cholangiopathies
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3
Q

cause of post-hepatic jaundice

A
  • impaired bile flow

- large duct obstruction

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4
Q

what causes bile duct obstruction (5)

A
  • Gallstones (extrahepatic cholelithiasis)
  • Malignancies of biliary tree / head of pancreas
  • Inflammatory bile duct strictures
  • Porta hepatis lymphadenopathy
  • Bile duct malformations/ loss (children)
    choledochal cysts, biliary atresia (EHBA), Fibropolycystic disease
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5
Q

bile duct obstruction

  • complications
  • presentation
A

intrahepatic cholangitic abscesses/ sepsis

chronic obstruction: Biliary cirrhosis

jaundice, pale stools, tea-coloured urine

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6
Q

hepatholithiasis

A

intrahepatic biliary stone formation

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7
Q

primary hepatholithiasis complications

A

recurrent ascending cholangitis, progressive inflammatory destruction / collapse and scarring of hepatic parenchyma

progress to form Biliary Intraepithelial Neoplasia (BilIN) and cholangiocarcinoma (bile duct cancer)

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8
Q

causes of neonatal (14-21 days) cholestasis (5) **

A
  • Cholangiopathies: Extrahepatic biliary atresia (atresia = blocked passageway like a dead end)
  • EHBA (Extrahepatic biliary atresia)
  • Toxic: Drugs, parenteral nutrition
  • Metabolic disease: Tyrosinemia (cannot breakdown tyrosine)
  • Infections: CMV, bacterial sepsis
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9
Q

EHBA (Extrahepatic biliary atresia)

  • definition
  • caution
  • presentation
A

Complete/ partial obstruction of the lumen of the extrahepatic biliary tree within the first 3 months of life

  • needs to be identified early and corrected by surgery

jaundice, pale stools, tea-coloured urine (high conjugated bilirubin)

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10
Q

Choledochal cyst

  • definition
  • complications
A

Developmental malformation of biliary tree, usually CBD (common bile duct)

stones
stenosis
strictures
pancreatitis
risk of bile duct carcinoma
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11
Q

Fibropolycystic disease

  • definition
  • complications
A

lesions causing congenital malformations of the biliary tree

  • Von Meyenburg complex (small bile duct hamartomas/tumours)
  • extra hepatic biliary cysts
  • Caroli disease (dilation of bile ducts -> formation of stones
  • Congenital hepatic fibrosis
  • polycytic renal disease
  • cholangiocarcinoma
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12
Q

benign lesions of the liver

A

HF-BBC
affecting hepatocytes:
- Hepatocellular adenoma
- Focal nodular hyperplasia

affecting bile duct:

  • Bile duct hamartoma
  • Bile duct adenoma

Cavernous hemangioma**

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13
Q

malignant lesions of the liver

A

affecting hepatocytes:

  • Hepatocellular carcinoma (HCC)**
  • Hepatoblastoma

affecting bile duct:
- Cholangiocarcinoma (CC)**

adenocarcinoma - metastasis from the colon/lung/breast -> identify primray site

Angiosarcoma

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14
Q

Focal nodular hyperplasia

  • cause
  • gross/micro features
A
  • caused by focal alterations in hepatic blood supply

gross:
- well-demarcated but poorly encapsulated
pale nodule with central fibrous scar
non-cirrhotic liver

Micro:
- Fibrous scar with radiating fibrous septa
large misshapen arterial vessels and accompanying ductular reaction, separating hyperplastic hepatocytes No normal bile ducts

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15
Q

Cavernous hemangioma**

  • gross/micro features
  • complications
A

most common benign liver tumour

gross:
Subcapsular, discrete, red-blue, soft
spongy appearance

Micro:
- Large vascular channels separated by thin fibrous connective tissue

Complications: **
rupture -> intraperitoneal bleeding, thrombosis, DIVC (Disseminated intravascular coagulation)
is a blood forming tumour - will bleed a lot. DO NOT BIOPSY

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16
Q

Hepatocellular adenoma

  • clinical presentation
  • risk factor
A
  • incidental, abdominal pain from rapid growth or haemorrhage
  • intraabdominal bleeding due to rupture

risk factors: oral contraceptive pill, anabolic steroids

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17
Q

hepato-carcinogenesis

hepatocellular adenoma -> hepatocellular carcinoma

A

due to mutations:

  • beta-catenin activation causing genetic instability
  • p53 inactivation
18
Q

HCC clinical presentation

A
  • Asymptomatic
  • Ill-defined upper abdominal pain, malaise, fatigue, weight loss
  • Hepatomegaly, abdominal mass or fullness
  • distended abdomen
  • hematemesis (vomiting of blood)/ black tarry stools
19
Q

HCC diagnosis

A
  • Serum alpha-fetoprotein (AFP) (insensitive as screening test)
  • imaging to detect tumours (taken w/ contrast)
    [dont need biopsy to diagnose HCC]
20
Q

HCC gross features

A
  • Unifocal (usually large) mass
  • Multifocal, widely distributed nodules of variable size
  • Diffusely infiltrative cancer

apeears pale/ varied (depends on bile production, fatty change, stroma)

21
Q

HCC micro features

A
  • poorly differentiated
  • Trabecular-sinusoidal, pseudoacinar and compact growth patterns
  • Polygonal cells with eosinophilic cytoplasm and central round nucleolus with distinct nucleolus
  • Pleomorphism
  • Bile production
22
Q

spread of HCC

A
  • vascular (intrahepatic metastasis) forming satellite lesions
  • through portal/hepatic vein
23
Q

prognosis of HCC

A 
factors determining prognosis: 
Stage, number and size of tumour nodules (tumour burden)
vascular spread
histologic grade
presence of cirrhosis

most die within 2 yrs via

  • cachexia (muscle/fat wasting)
  • variceal bleeding
  • liver failure or hepatic coma
  • tumour rupture with fatal haemorrhage
24
Q

treatment of HCC

A
  • Surgical resection
  • Locoregional ablation
  • Immunotherapy
  • Liver transplantation
25
Q

hepatoblastoma

  • who does it affect
  • 2 types
  • treatment
A
  • early childhood (<3yrs)
  • epithelial
  • Mixed epithelial and mesenchymal

Surgical resection and chemotherapy
(fatal if untreated)

26
Q

cholangiocarcinoma

  • causes
  • pathogenesis
A

Carcinoma of bile duct

  • Liver fluke infestation** (Opisthorchis, Clonorchis sp. in Thailand, Laos)
  • Primary sclerosing cholangitis
  • Hepatolithiasis
  • Fibropolycystic liver disease
  • HBV, HCV infection
  • NAFLD

premalignant lesions that progress to form CC:

  • Biliary intraepithelial neoplasia (BilIN) 1-3
  • intraductal papillary biliary neoplasia
  • mucinous cystic neoplasms

chronic inflammation and cholestasis -> promotes somatic mutations or epigenetic alterations

27
Q

cholangiocarcinoma

  • clinical presentation
  • prognosis
A

Extrahepatic tumours:
- present earlier and smaller with biliary obstruction, cholangitis and RUQ pain

  • poor prognosis
    extrahepatic: 15% at 2 yrs
    intrahepatic: 6 mths
28
Q

gallbladder diseases

A
  • cholelithiasis (gallstones)

- cholecystitis (inflammation)

29
Q

types of gallstones

- risk factors + pathogenesis

A
  • cholesterol: made of cholesterol, phospholipids, bile salts
    caused by supersaturation of bile -> bile stones
    gallbladder hypomotility/
    mucus hypersecretion
  • pigmented:
    black: caused by increase in secretion of conjugated bilirubin -> hydrolysis

brown: hydrolysed bilirubin glucronides

30
Q

cholecystitis

  • definition
  • 3 types
A
  • gallbladder inflammation

- acute/ chronic/ acute on chronic

31
Q

acute cholecystitis

  • clinical presentation
  • 2 types
A
  • progressive RUQ pain >6 hrs
  • mild fever, tachycardia, sweating, nausea and vomiting
    may also progress to be more severe or recur

usually not presented w/ jaundice unless there is CBD obstruction

  • Calculous (more common) / acalculous [involvement of gallstones}
32
Q

Calculous acute cholecystitis (more common) pathogenesis

A

caused by gallstones obstructing the cystic duct
-> Mucosal phospholipases hydrolyze some toxic product
-> Disruption of normal protective glycoprotein mucus layer
-> mucosal epithelium gets
exposed to direct detergent action of bile salts
-> release of prostaglandins
-> mucosal and mural inflammation
-> Distension and increased intraluminal pressure compromise blood flow to mucosa
-> bacterial contamination

33
Q

acalculous acute cholecystitis pathogenesis

A

cause by ischemia - decrease in blood flow from cystic artery

ischemia causes the inflammation -> Inflammation and oedema of wall further compromises blood flow, with gallbladder stasis, biliary sludge and gallbladder mucus causing cystic duct obstruction in the absence of stones
(vicious cycle)

34
Q

gross features of acute cholecystitis

A
  • Enlarged, tense edematous and congested
  • Violaceous to green-black
  • Fibrinous/ fibrinopurulent serosal exudates
  • GB mucosa ulcerated
  • calculous AC will present w/ gallstones
35
Q

acute cholecystitis complications (5)

A
  • Gangrene (with perforation and peritonitis) or empyema (pus in pleural cavity)
  • Pericholecystic and subdiaphragmatic abscesses
  • Ascending cholangitis
  • liver abscesses
  • Septicaemia
36
Q

chronic cholecystitis

gross and micro features

A
  • caused by progression of acute cholecystitis
  • Contracted, thickened wall, smooth mucosa +/-calculi
  • Chronic inflammatory infiltrates
  • Fibromuscular hypertrophy
  • Rokitansky-Aschoff sinuses
  • Subserosal fibrosis
37
Q

gallbladder carcinoma

  • males/females more affected
  • risk factors
A
  • affects females more

risk factors

  • gallstones
  • chronic infections: bacterial/parasitic
38
Q

gallbladder carcinoma

  • metastasis
  • prognosis
A

Direct invasion: liver, stomach and duodenum (surrounding organs)

Metastases: liver, regional lymph nodes, lungs

Prognosis is poor

39
Q

gallbladder carcinoma

- gross and micro features

A

Diffuse (70%) / infiltrating
Polypoid (30%) / exophytic

micro: usually adenocarcinoma (glandular)

40
Q

most common cause of HCC

A

hep C viral infection

41
Q

acute cholecystitis pathogenesis

A
  • mucosal phospholipases hydrolyse luminal lecithins, forming toxic lysolecithins
  • disruption of normal protective glycogen mucus layer:
    mucosal epithelium exposed to direct detergent action of bile salts
  • prostaglandins released within the wall of distended gallbladder causes mucosal and mural inflammation
  • distension and increased intraluminal pressure compromise blood flow to mucosa
  • risk of bacterial contamination

SYSTEMIC PATHOLOGY (27 decks)

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