pathology Flashcards

1
Q

what is the type of mutation causes cholangiocarcinoma?

A

KRAS, BRAF, P53

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2
Q

why extrahepatic cholangiocarcinoma has a better prognosis than intrahepatic?

A

because extrahepatic form jaundice which will appear early with other symptoms ut intrahepatic will. no cause symptoms until a large mass of the liver replaced by tumor

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3
Q

which of the following routes of the spread of cholangiocarcinoma will spread to the abdomen?

A

by peribiliary nerve

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4
Q

which of the following gall bladder tumors have a better prognosis and why?

A

papillary type because
1- it has less tendency to spread
2- formed of well-differentiated adenocarcinoma

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5
Q

morphology of chronic cholecystitis?

A
1- contracted, thick, atrophied gall bladder 
2-cholestrolosis 
3- porcelain gall bladder 
4- aschoff - rokitansky sinusis 
5- xanthogranulumatous cholecystitis
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6
Q

what are the associations of carcinoid tumor?

A

1- endocrine cell hyperplasia
2- chronic atrophic gastritis
3- ZE syndrome
4- MEN syndrome

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7
Q

how carcinoid tumor can lead to bowel obstruction?

A
1- metastasis to the mesentery 
2- release vasoactive material  
3- stimulation of fibroblast and collagen 
4- desmoplastic reaction 
5-kinking 
6-obstriction
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8
Q

that characteristic histochemical stains found in the carcinoid tumor is?

A

1- chromogranin A

2- synaptophysin

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9
Q

characteristic morphology of carcinoid tumor?

A

sal and paper appearance

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10
Q

what is the problem in Lynch syndrome?

A

defect in mismatched repair system (MSH2 , MLH1)

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11
Q

What are the genetic mutations in colonic adenocarcinoma?

A
1- APC gene 
2- DNA mismatch repair system 
3- KRAS and P53
4- reactivation of telomerase
5- SMAD mutation
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12
Q

numerate the pediatrics childhood lymphoma?

A

1- HL

2-NHL (lymphoblastoma , follicular, Burkitt’s, DLBCL, Anaplastic T cell)

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13
Q

what are the complications of a patient with long-term HL treated with chemotherapy and radiotherapy?

A

1- development of 2nd hematologic cancer

2- solid cancers (lung, skin, stomach, breast, soft tissue

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14
Q

what are the non-neoplastic complication of radiotherapy

A

1- pulmonary fibrosis

2- accelerated AS

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15
Q

when do the fibrous septa in liver cirrhosis will be reversible or irreversible?

A

it will be reversible if the underlying disease is treated

irreversible if the underlying disease no treated or treated but associated with vascular shunt

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16
Q

discuss the “ductular reactions” found in the periphery of most of the cirrhotic nodules?

A

source: stem cells adjacent to bile ductules and canal of herrings
mechanism:
when parenchyma meets damaged stroma
proliferation of endothelial cells and the presence of myofibroblast and inflammatory cells

17
Q

mention the 3 causes of Portal hypertension in cirrhosis

A

1/ fast flowing, narrow vascular channel
2/ shunt btw portal and hepatic artery
3/ hepatic nodules that compress the sinusoid => ↑the resistance.

18
Q

which of the following liver tumers maybe associated with fibropolycystic liver disease ?

A

when multiple von myenburg complexes present

19
Q

which of the following liver tumor have no risk of malignancy ?

A

focal nodular hyperplasia

20
Q

what are the clinical significance of hepatic adenoma?

A

1- may be mistaken by sever HCC
2- maybe rupture in pregnant women causing intraabdominal hemorrhage
3- may lead to HCC if b-catenin mutation involved

21
Q

write the microscopic picture of hepatic adenoma?

A

1- hepatocyte resemble the normal with few variations
2- absent portal tracts
3- prominent hepatic veins and arteries

22
Q

what are the microscopical features of nodular dysplasia in HCC?

A

1- large size
2- dysplastic hepatocyte
3- contain overly malignant submodules

23
Q

mention the etiologies associated with HCC?

A
1- HBV (Asian countries)
2- HCV (japan, central europ, western)
3- aflatoxin exposure 
4- alcoholic cirrhosis
5- NAFLD 
6- hemochromatosis 
7- alpha 1 antitrypsin deficiency, and tyrosinemia
24
Q

explain how aflatoxin comes and causes HCC?

A

fungus aspergillus => aflatoxins => bind covalently to cellular DNA => gene mutation as P53, found in moldy grains and peanuts

25
Q

what are the main 3 causes of hepatic adenoma?

A

1- biallelic inactivation
2- gain of function mutation
3- inflammation

26
Q

what are the prucesure lesions for HCC

A

1- hepatic adenoma (b-catenin)
2- chronic liver disease (cellular dysplasia + nodular dysplasia)
3- liver cirhosis

27
Q

write the gross picture of HCC

A
- patterns
1- unifocal 
2- multifocal 
3- diffuse
color
- white - yellow, some bile stain, may hemorrhage and necrosis
risks
 - may metastasize to the heart by vascular invasion invading portal vein to IVC => reaching the right heart.
28
Q

pseudocanaliculi present in which of the following diseases?

A

HCC

29
Q

explain why alpha-fetoprotein is not diagnostic in HCC?

A
  • only useful in advanced cases in 50% of patients
  • because it may be mistaken with yolk sac tumor, normal pregnancy, liver cirrhosis, massive liver disease, or chronic hepatitis
30
Q

how can we don the Clinical assessment of chronic hepatitis ?

A

by clinical data, serologic data, and histologic data :
1- grading: the degree of inflammation, and extent of hepatocyte injury
2- staging: progression of scarring

31
Q

what re the clinical feature of autoimmune hepatitis?

A

1- predominance in female
2- the absence of viral evidence
3- high IgG
4- the presence of other autoimmune diseases

32
Q

what are the genetic associations of autoimmune hepatitis?

A

HLADR3, HLADR4

33
Q

numerate the pathological classification of granulomatous diseases?

A

1- granuloma with cassation: TB
2-granuloma without cassation: IBD, BILH, sarcoidosis
3- suppurative granuloma: cat scratch, lymphogranuloma
4- foreign body granuloma: thread and silicone implant

34
Q

what is the microscopic picture of bilharzial granuloma?

A
1- ova in the center
2- epithelioid cell
3- multinucleated giant cell 
4- eosinophils 
5- lymphocytes
35
Q

discuss the fate of primary biliary cirrhosis

A

1- Patients develop prominent H.T, and nodular regenerative hyperplasia (nodularity with no scar)
2- Patient develop duct loss leading to cirrhosis and profound cholestasis (periportal/periseptal, associated with degeneration, marked by ballooned bile stained hepatocyte with Mallory denk bodies).