pathology Flashcards
what is the type of mutation causes cholangiocarcinoma?
KRAS, BRAF, P53
why extrahepatic cholangiocarcinoma has a better prognosis than intrahepatic?
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
which of the following routes of the spread of cholangiocarcinoma will spread to the abdomen?
by peribiliary nerve
which of the following gall bladder tumors have a better prognosis and why?
papillary type because
1- it has less tendency to spread
2- formed of well-differentiated adenocarcinoma
morphology of chronic cholecystitis?
1- contracted, thick, atrophied gall bladder 2-cholestrolosis 3- porcelain gall bladder 4- aschoff - rokitansky sinusis 5- xanthogranulumatous cholecystitis
what are the associations of carcinoid tumor?
1- endocrine cell hyperplasia
2- chronic atrophic gastritis
3- ZE syndrome
4- MEN syndrome
how carcinoid tumor can lead to bowel obstruction?
1- metastasis to the mesentery 2- release vasoactive material 3- stimulation of fibroblast and collagen 4- desmoplastic reaction 5-kinking 6-obstriction
that characteristic histochemical stains found in the carcinoid tumor is?
1- chromogranin A
2- synaptophysin
characteristic morphology of carcinoid tumor?
sal and paper appearance
what is the problem in Lynch syndrome?
defect in mismatched repair system (MSH2 , MLH1)
What are the genetic mutations in colonic adenocarcinoma?
1- APC gene 2- DNA mismatch repair system 3- KRAS and P53 4- reactivation of telomerase 5- SMAD mutation
numerate the pediatrics childhood lymphoma?
1- HL
2-NHL (lymphoblastoma , follicular, Burkitt’s, DLBCL, Anaplastic T cell)
what are the complications of a patient with long-term HL treated with chemotherapy and radiotherapy?
1- development of 2nd hematologic cancer
2- solid cancers (lung, skin, stomach, breast, soft tissue
what are the non-neoplastic complication of radiotherapy
1- pulmonary fibrosis
2- accelerated AS
when do the fibrous septa in liver cirrhosis will be reversible or irreversible?
it will be reversible if the underlying disease is treated
irreversible if the underlying disease no treated or treated but associated with vascular shunt
discuss the “ductular reactions” found in the periphery of most of the cirrhotic nodules?
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
mention the 3 causes of Portal hypertension in cirrhosis
1/ fast flowing, narrow vascular channel
2/ shunt btw portal and hepatic artery
3/ hepatic nodules that compress the sinusoid => ↑the resistance.
which of the following liver tumers maybe associated with fibropolycystic liver disease ?
when multiple von myenburg complexes present
which of the following liver tumor have no risk of malignancy ?
focal nodular hyperplasia
what are the clinical significance of hepatic adenoma?
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
write the microscopic picture of hepatic adenoma?
1- hepatocyte resemble the normal with few variations
2- absent portal tracts
3- prominent hepatic veins and arteries
what are the microscopical features of nodular dysplasia in HCC?
1- large size
2- dysplastic hepatocyte
3- contain overly malignant submodules
mention the etiologies associated with HCC?
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
explain how aflatoxin comes and causes HCC?
fungus aspergillus => aflatoxins => bind covalently to cellular DNA => gene mutation as P53, found in moldy grains and peanuts
what are the main 3 causes of hepatic adenoma?
1- biallelic inactivation
2- gain of function mutation
3- inflammation
what are the prucesure lesions for HCC
1- hepatic adenoma (b-catenin)
2- chronic liver disease (cellular dysplasia + nodular dysplasia)
3- liver cirhosis
write the gross picture of HCC
- 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.
pseudocanaliculi present in which of the following diseases?
HCC
explain why alpha-fetoprotein is not diagnostic in HCC?
- 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
how can we don the Clinical assessment of chronic hepatitis ?
by clinical data, serologic data, and histologic data :
1- grading: the degree of inflammation, and extent of hepatocyte injury
2- staging: progression of scarring
what re the clinical feature of autoimmune hepatitis?
1- predominance in female
2- the absence of viral evidence
3- high IgG
4- the presence of other autoimmune diseases
what are the genetic associations of autoimmune hepatitis?
HLADR3, HLADR4
numerate the pathological classification of granulomatous diseases?
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
what is the microscopic picture of bilharzial granuloma?
1- ova in the center 2- epithelioid cell 3- multinucleated giant cell 4- eosinophils 5- lymphocytes
discuss the fate of primary biliary cirrhosis
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).
