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GI 2 Pathology--Chapt. 18 and 19 > Chapter 18 part 5: Circulatory disorders, pregnancy, tumors > Flashcards

Chapter 18 part 5: Circulatory disorders, pregnancy, tumors Flashcards

1
Q

Circulatory Disorders

A
  • Impaired Blood flow into the Liver
  • Impaired Blood Flow through the Liver
  • Hepatic Venous Outflow obstruction
  • Passive congestion and Centrilobular necrosis
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2
Q

Impaired blood flow into the liver

A
  • Hepatic artery compromise

- Portal vein obstruction and thrombosis

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3
Q

Hepatic artery compromise

A

-infarction is rare bc of dual hepatic blood supply but thrombosis or compression of intrahepatic arterial branches can infrequently result in localized pale infarct, occasionally made hemorrhagic by portal blood suffusion

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4
Q

Portal vein obstruction and thrombosis

A

-Manifestations of extrahepatic protal vein obstruction can range from insiduous and well tolerated to catastrophic and potentially lethal (due to variceal bleeding)

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5
Q

Causes of portal vein obstruction and thrombosis

A
  • neonatal umbilical vein infection or catheterization
  • intraabdominal sepsis causing pyelophlebitis in splanchnic circulation, acquired or heritable coagulopathies, trauma, pancreatic lesions that initiate splenic vein thromboses and cirrhosis
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6
Q

Impaired blood flow through the liver–most important cause is what?

A
  • cirrhosis!!
  • sinusoidal occlusion can also be caused by sickle cell disease, DIC, eclampsia and diffuse intrasinusoidal metastatic tumor
  • Manifestation=Peliosis Hepatitis
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7
Q

Peliosis Hepatitis

A
  • reversible hepatic sinusoid dilation associated with impeded efflux of hepatic blood
  • can occur in setting of malignancy, TB, post-transplantation immunodeficiency and sex hormome administration (anabolic steroids, oral contraceptives, danazol)
  • Bartonella sp seen in sinusoidal endothelial cells in AIDS-associated peliosis
  • unknown etiology; lesions regress after correcting cause
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8
Q

Hepatic Venous Outflow Obstruction caused by:

A
  • Hepatic Vein Thrombosis

- Sinusoidal Obstruction syndrome (Veno-occlusive Disease)

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9
Q

Hepatic Vein Thrombosis–Budd-Chiari syndrome

A
  • occurs when 2 or more major hepatic veins are obstructed

- hepatic damage is a consquence of increased intrahepatic blood pressure

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10
Q

Hepatic vein thrombosis occurs in the setting of?

A

-primary myeloproliferative disorders (polycythemia vera), heritable coagulopathies, pregnancy, anti-phospholipid Ab syndrome, paroxysmal nocturnal hemoglobinuria and intra-abdominal cancers

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11
Q

Prognosis of Hepatic vein thrombosis

A
  • high mortality
  • need prompt surgical portosystemic shunting which improves prognosis
  • subacute or chronic cases are less lethal but can develop superimposed fibrosis
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12
Q

Sinusoidal obstruction syndrome (Veno-Occlusive disease)–SOS

A
  • originally described in Jamaican drinkers of pyrrolizidine alkaloid-containing bush tea–now occurs primarily bc od toxic injury to sinusoidal endothelium by chemotherapy
  • 30% mortality
  • present w: tender hepatomegaly, ascites, weight gain and jaundice
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13
Q

Morphology of SOS

A
  • patchy obliteration of smaller hepatic vein radicles by endothelial swelling and collagen deposition
  • Acute SOS: centrilobular congestion with hepatocellular necrosis, whereas progressive disease shows venule lumen obliteration with dense perivenular fibrosis and hemosiderin deposition
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14
Q

Passive congestion and centrilobular necrosis

A
  • systemic hypoperfusion (shock) leads to hepatocyte necrosis around central vein (centrilobular necrosis)
  • with superimposed passive congestion (right-sided HF or constrictive pericarditis), there is hemorrhage as well producing centrilobular hemorrhagic necrosis with liver taking on variegated mottled appearance (nutmeg liver)
  • Protracted RHF causes chronic passive congestion and pericentral firbosis (cardiac sclerosis), culminating in cirrhosis
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15
Q

Hepatic complications of organ or hematopoeitic stem cell transplantation

A

-Graft vs. Host Disease and Liver Graft Rejection

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16
Q

Graft vs. host disease (GVHD)

A

-occurs in the setting of bone marrow or stem cell transplantation and is characterized by direct lymphocyte attack on liver cells, especially bile duct epithelium

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17
Q

Acute GVHD is characterized by

A

-hepatitis (parenchymal inflammation and hepatocyte necrosis), chronic vascular inflammation and intimal proliferation (endothelialitis) and bile duct destruction

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18
Q

Chronic GVHD

A

-portal tract inflammation, bile duct obstruction (or complete loss) and fibrosis

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19
Q

Acute rejection of liver allografts

A
  • portal tract inflammation (frequently including eiosinophils), bile duct damage, and endotheliallitis
  • chronic rejection occurs months or years after transplantation and is characterized by bile duct loss and arteriopathy with eventual graft failure
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20
Q

Hepatic Disease Associated with Pregnancy

A
  • -Viral hepatitis is most common cause of jaundice in pregnancy; with exception of HEV (20% mortality) they are not influenced by pregnancy; rarely pregnancy can cause direct hepatic complications (usually nonfatal): acute faty liver of pregnancy (AFLP) and intrahepatic cholestasis of pregnancy (ICP)
  • Preeclampsia and Eclampsia
  • Acute Fatty Liver of Pregnancy
  • Intrahepatic Cholestasis of Pregnancy
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21
Q

Preeclampsia and Eclampsia

A
  • Preeclampsia: HTN, proteinuria, peripheral edema, coagulation abnormalities, and varying DIC
  • with onset of hyperreflexia and convulsion, is called eclapsia and severe cases require termination of pregnancy
  • HEELP syndrome (hemolysis, elevated liver enzymes, and low platelets)=primary manifestations of preeclampsia
22
Q

Morphology of Preeclampsia and Eclampsia

A
  • Gross: small, red, hemorrhagic patches with occasional yellow-white areas of infarction
  • Microscopic: periportal sinusoidal fibrin deposition, periportal necrosis, and hemorrhage
  • Coalescence of bleeding can form hepatic hematomas capable of fatal rupture
23
Q

Acute Fatty Liver of Pregnancy

A
  • rare and has spectrum from subclinical hepatocyte dysfunction to hepatic failure, coma, and death
  • Mitochondrial dysfunction implicated–esp congenital fetal deficiecy in long-chain 3-hydroxyl coenzyme A dehydrogenase results in toxic levels of fetal metabolites that can cause maternal hepatotoxicity
24
Q

Acute Fatty Liver of Pregnancy Morphology

A
  • Microscopic: MICROVESICULAR STEATOSIS!!
  • In severe cases portal inflammation and hepatocyte dropout and lobular disarray can occur
  • Definitive Tx is termination of pregnancy
25
Q

Intrahepatic Cholestasis of Pregnancy

A
  • ICP attributed to altered hormonal state of pregnancy
  • pruritis and jaundice in 3rd trimester with mild cholestasis
  • Although generally benign, pruritis can be severe and maternal gallstones or malabsorption can also occur
26
Q

Nodules and Tumors

A
  • Nodular Hyperplasias
  • Benign Neoplasms
  • Malignant Tumors
27
Q

Nodular hyperplasias

A
  • solitary or multiple benign hepatocellular nodulces in absence of cirrhosis
  • cause= focal hepatic vascular obliteration with compensatory hypertrophy of adjacent well-vascularized lobules
  • Focal nodular hyperplasia or Nodular regenerative hyperplasia
28
Q

Focal nodular hyperplasia

A

-young to middle aged adults and is an irregular, unencapsulated mass containing a central stellate fibrous scar

29
Q

Nodular regenerative hyperplasia

A

-diffuse nodular transformation of liver WITHOUT FIBROSIS occurring as a consequence of conditions affecting intrahepatic blood flow (in solid-organ transplannts (esp kidney), bone marrow transplants and vasculitis)

30
Q

Benign neoplasms

A
  • Cavernous hemangiomas

- Hepatocellular adenomas: HNF1-a inactivated, B-Catenin activated or Inflamatory type!

31
Q

Cavernous hemangiomas

A
  • most common benign tumors

- identical to blood vessel tumors seen in other locations

32
Q

Hepatocellular adenomas

A
  • benign hepatocyte neoplasms up to 30cm in diameter
  • occur in young women, usually associated with OC use
  • 3 subtypes: HNF-1a inactivated, B-Catenin activated, and Inflammatory
33
Q

HNF-1a-inactivated hepatocellular adenomas

A
  • encodes a TF and germline mutations are responsible for autosomal dominant maturity-onset diabetes of the young, type 3
  • most commonly in women
34
Q

B-Catenin-activated hepatocellular adenomas

A
  • Activating mutations of B-catenin are considered at very high risk for malignant transformation and should be resected even when asymptomatic
  • associated with oral contraceptive and anabolic use in both men and women
35
Q

Inflammatory hepatocellular adenomas

A
  • found in both men and women and associated with NAFLD
  • activating mutations in gp130, coreceptor for IL-6 leading to constitutive JAK-STAT signaling and overexpression of acute phase reactants
  • small risk of malignant transformation
36
Q

Malignant rumors

A
  • In US, most liver tumors are metastatic
  • HCC=most common primary liver cancer; CCAs much less common
  • Types: Hepatoblastomas, HCC, Cholangiocarcinoma
37
Q

Hepatoblastoma

A
  • most common liver tumor of early childhood
  • characteristic=activation of Wnt-B-catenin signaling pathway
  • hepatoblastomas also associated with familial polyposis syndrome and Beckwith-Weideman syndrome
  • 2 types: epithelial type and mixed epithelial and mesenchymal type
38
Q

epithelial type hepatoblastoma

A

-vaguely recapitulates liver development

39
Q

Mixed epithelial and mesenchymal type hepatoblastoma

A

-contains foci of mesenchymal differentiation including osteoid, cartilage or striated muscle

40
Q

Hepatoblastoma prognosis

A

-fatal if untreated but resection and chemotherapy yield 80% 5-yr survival

41
Q

Hepatocellular carcinoma

A
  • 3 to 8:1 male predominance!
  • most common in developing countries with high rates of HBV infection, esp where infection starts in infancy and there is high associated carrier rate
  • Half cases=no cirrhosis but may be associated with exposure to aflatoxin (mycotoxin produced by Aspergillus species that contaminates staple food crops)
  • In western world, increased hepC infection also give rise to HCC
42
Q

Pathogenesis of HCC–causes

A
  • in background of chronic liver disease
  • Major etiologic factors= chronic viral infection (HBV, HCV), chronic alcholism, NASH, and food contaminants (aflatoxins)
  • lesser causes: hemochromatosis, tyrosinemia, and a1-AT deficiency
43
Q

HCC associated genetics

A
  • Activating mutations of B-catenin occur in 40% of HCC, and p53 inactivation in 60% of HCC
  • Chronic inflamation associated with genotoxic products, cytokine production and hepatocyte regeneration–these changes along with genetic susceptibility lead to tumorigenesis
  • IL-6 can suppress hepatocyte differentiation and promote hepatocyte proliferation by regulating function of transcription factor HNF4-a
44
Q

Morphology of HCC

A
  • can present as solitary mass, multifocal nodules or diffusely infiltrative cancer with massive liver enlargement, often (although not necessarily) in bacground of cirrhosis; intrahepatic spread and vascular invasion are common
  • Histo: range from well differentiated to highly anaplastic and undifferentiated
45
Q

Fibrolamellar carcinoma

A
  • variant of HCC
  • presents as single scirrhous, hard tumor in 20-40 year olds in absence of chronic liver disease
  • cells are well differentiated cells in cords or nests separated by dense lamellar collagen bundles
46
Q

Clinical features of HCC

A
  • hepatomegaly, RUQ pain, weight loss, and elevated serum a-fetoprotein
  • Prognosis depens on resectability of tumor
  • mortality secondary to cachexia, GI or esophageal variceal bleeding, liver failure with hepatic coma or tumor rupture and fatal hemorrhage
47
Q

Cholangiocarcinoma

A
  • arises from elements of intrahepatic and extrahepatic biliary tree
  • most are perihilar (KLASTKIN tumors); others are distal and intrahepatic
  • dismal outlook bc CCA is rarely resectable at Dx
48
Q

Cholangiocarcinoma–what increases risk?

A
  • most have no apparent preceding conditions but chronic inflamation and cholestasis increase risk
  • also associated with PSC, congenital fibropolycystic lesions, hepatolithiasis, NAFLD and HBV or HCV
  • In Southeast Asia, protracted biliary tree parasitic infection by Opisthorchis sinensis is major risk factor
49
Q

Cholangiocarcinoma–morphology

A
  • can manifest as a single large mass, as multifocal nodules or can be diffusely infiltrative
  • In contrast to HCC, CAA is typically pale bc biliary epithelium does not secrete bilirubin pigment
  • Microscopic: variably differentiated bile duct elements that resemble adenocarcinomas elsewhere in alimentary tract; most CAA are markedly desmoplastic with dense collagenous stroma
50
Q

Other primary hepatic malignant tumors

A
  • some show combined HCC and CCA–suggesting origin from multipotent stem cell
  • Angiosarcomas of liver resemble those occurring elsewhere and are associated with exposures to vinyl chloride, arsenic or Thortrast
  • Hepatic lymphomas (mostly diffuse large B-cell lymphomas) occur primarily in middle-aged men and can occur in association with hepatitis B and C, and PBC
51
Q

Metastasis

A
  • any cancer can spread to liver
  • colon, breast, lung, pancreas primaris are most common
  • Typically multiple implants are present with massive hepatic enlargement
  • Large implants have defective vascular supplies and become centrally necrotic
  • Massive involvement of liver present before hepatic failure develops

GI 2 Pathology--Chapt. 18 and 19 (8 decks)

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