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1. What is PDC4
2. Desribe intrahepatic choloangiocarcinoma
3. What is in the differential diagnosis of intrahepatic choloangiocarcinoma and how do you differntiate between them?
1. A tumor suppressor gene on long arm of 18. Lost expression in most (55%)pancreatid cancers. Immunostain would be negative.
2. Circumsribed and centrally sclerotic. Can have trabecular growth with some tubule formation. Borders are infiltrative.
3. Epitheliod hemangioendothelioma. IHCC is CK7+ EHE labes with vascular markers. Though it may show central hyalinzation, it looks more blistered and myxoid.
What are some risk factors for intrahepatic cholangiocarcinoma?
Caroli's disease, solitary cysts, recurrent pyogenic cholangitis, intrahepatic lithiasis, parasited (Clonorichis Sinensis)
1. What is Caroli's disease?
2. What are some other associated conditions?
3. True/False, Caroli's disease carries a 100 fold increase in developement of cholangiocarcinoma?
1. Rare inherited disorder characterized by dilation of intrahepatic bile ducts.
2. ARPCKD, cholangitis, gall stones, biliary abcess,septiciemia, liver cirrhosis, renal failure, cholangiocacinoma
3. True
1. describe the simple type of Caroli's disease.
2. Describe the complex form aka Caroli's Syndrome
3. True/False the simple type of Caroli's is the most common
4. True/Fase Caroli's disease is one of the common derivative of choledochal cyst.
5. What gene is mutated in Caroli's disease?
1. The simple form is AD. Bile ducts are ectatic
2. The complex form/Caroli's Syndrome is AR and linked with portal
hypertension, congenital hepatic fibrosis
3. False. It affects 1 in a million, but the complex type is more common.
4. False
5. PKHD1 the same one as in ARPCKD
Rupture of cytstic lesions of the appendix lead to what?
1 rupture of mucinous cystadenomas and mucinous cystadenocarcinomas lead to pseudomyxoma peritonei
2. Rupture of mucinous cystadenoma is termed DPAM diseminated peritoneal adenomucinosis
3. Rupture of mucinous cystadenocarcinoma is termed PCMA peritoneal mucinous carcinomatosis.
1. Describe the life cycle of Schistosoma.
2. How are the eggs of Schistosoma different?
3. What other species has similar morphology (ova) and site of involvement and how do you distinguish between them?
1. Free swimming Cercaria penetrates skin >n on swimming Cercaria blood > intrahepatic portal blood > matures into adult > eggs in urine/feces > Miracidium>penetrates snail> sporocyts> free swimming Cercaria
2. S. Mansoni and S. Japonicum have lateral spine and S. Haematobium has terminal spine
3. Fasciola Hepatica and Fasciolopsis Buski egss are similar size, but they lack a spine
1. What immunostains are useful in differentiating invasive Paget's disease from Malignant melanoma?
1. Paget's stains for CAM5.2, mucicarmen, and CEA while MM is negative for these (+ for S100, HMB45, MART-1/Melan-A)
How do esophageal duplications cysts develope?
It is a congenital anomaly that occurs around wk5to 8 of gestation.
Occurs as a result of failure of tracheal bud from primitive foregut.
commonly results in esophageal atresia
1. This esophageal cyst occurs in the anterior mediastinum.
2. This esophageal cyts occurs in the posterior mediastinum.
3. This espohageal cyst is in close proximity to GI tract
1. Bronchogenic cyst. Composed of ciliated epithelium and fibrous tissue.
2. Enteric/neuroenteric cyst. Composed of ciliated epithelium and discontinuous muscle
3. Duplication cysts. Composed of gastric, intestinal, or nueral tissue. Have a continuous muscle layer.
Describe the types of esophageal fistulas that can develop in atreasia and give their frequencies.
Type A no connection with trachea *%

Type B upper connection with trachea 1%

Type C lower connection with trachea 87%

Type D both separately connect with trachea 1%

Type E the segments are connected to one another and also connect with trachea 4% aka H-type
1. What are the the causes of primary and secondary achalasia?
2. What are possible complications of Chagas dz?
3. How is Chagas treated?
1. Primary is due to chronic ganlionitis or aganglionosis. Can see Wallerian degeneration and Lewy bodies. Secondary causes include scleroderma, Chagas dz (trypanosoma cruzi) amyloidosis, pneumonia...
2. Problem is decreased peristalsis and failure of LES to relax. can get aspiration pneumonia, 30x incereae in SQCC
3. Balloon dilation, botulinum toxin, myotomy
1. What drugs are commonly associated with pill esophagitis?
2. What histologic findings are clues to pill esophagitis?
1. Iron, potasium chloride, doxycycline, tetracycline, quinidine, gluconate, ferous sulfate, vitamin C, Aspirin, ocp, alendronate(fosamax)
2. May see polarizable material in necroinflammatory debris. Iron associated frequently see pigment that is positive on iron stain.
1. What types of dermatologic conditions are associated with esophagitis?
2. What types of esophageal infections and or inflammatory conditions occur in immunocompitent individuals?
3. What types of iesophageal nfections occur in immunocompromised individuals?
1. Pemphigus vulgaris, recessive dystrophic form of epidermolysis bullosa, Stephen-Johnson syndrome, GVHD in pts with bone marrow transplant.
2. Rarely any, but may see HSV in children and adults, eosinophilic gastroenteritis, Crohns.
3. Candida, CMV, HSV, HIV related ulcers
1. What is the incidence of esophageal cancer in the US?
2. What is the most commen type of esophageal cancer world wide and in the US?
3. T/F esophageal ADCA and SQCC affects AA and C similarly
1. 5/100,000
2. WW its SQCC in the US it's adenocarcinoma.
3. False. ADCA is more common in C and SQCC affects AA 5x more frequently than C
1. T/F a common mutations in esophageal SQCC involve K-ras, and APC.
2. T/F p53 point mutations and or mutations in p16 are commonly seen in esophageal SQCC.
1. False. loss of heterozygosisty of K-ras and APC is absent.
2. True
1 What isthe most Commons cause of malabsorption syndrome?
2. Exposure to which fractions of gluten induce celiac dz?
3. Which HLA types are most common in celiac dz?
1. Celiac Disease
2. The gliadin or prolaminin fractions.
3. HLA-DQ2 and HLA-DQ8
1. What is another possible etiology for celiac disease?
2. What other diseases are associated with celiac dz?
1. The E1b protein od type 12 adenoviris has homology with alpha gliadin.
2. Dermatitis herpetiformis, type 1 DM, Down syndrome, autoimmune thyroid disease, osteoporosis, selective IgA deficiency,
1. What are some possible complications of celiac disease?
2. T/F ATTG is highly sensitive and specific for celiac dz?
1. EATL, small intestinal adenocacinoma.
2. False. ATTG is sensitive, but not specific. Can see increase in HP. Most specific finding is villous atrophy on biopsy
1. In what regions is tropical sprue most common?
2. What is the causative agent in tropical sprue and how is it diagnosed?
1. South Asia, Philippines, West Indies, Africa (parts), Middle East, Central America
2. Tropheryma whipelii. Affects intestines and mesenteric LN (also CNS, eye, heart, skin, bone...)
Dx by PCR. Bx with villous atrophy and foamy macrophases with PAS + rods is suggestive.
1. How is amyloid differentiated from Waldenstorms macroglobulinemia?
2. How does abetalipoproteinemia and hypolipoproteinemia look microscopically?
3. How is the above entitiy diagnosed?
1. WMG has dilated lateals with delicate eosiophilic material versus the homogenous appearing amyloid. WMG has IgM by IHC and is PASD +. Amyloid of course is congo red +.
2. Vacuolated enterocytes doue to entraped lipids.
3. Need clinical correlation. It is caused by autosomal codominant mutation of apolipoprotein B gene
1. How is amyloid differentiated from Waldenstorms macroglobulinemia?
2. How does abetalipoproteinemia and hypolipoproteinemia look microscopically?
3. How is the above entitiy diagnosed?
1. WMG has dilated lateals with delicate eosiophilic material versus the homogenous appearing amyloid. WMG has IgM by IHC and is PASD +. Amyloid of course is congo red +.
2. Vacuolated enterocytes due to entraped lipids.
3. Need clinical correlation. It is caused by autosomal codominant mutation of apolipoprotein B gene. neurologic defects due to vit E deficiency, see acanthocytes in blood. Mutation in microsomal triglyceride transfer protein.
1. Name some diseases of the small bowel that histologically look similar.
2. What small bowell entities show villous atrophy, but not necessarily inflammation?
1. Celiac, collagenous sprue(+ collagen in lp), tropical sprue, familial enteropathy(EM shows microvillous inclusions), giardiasis(+trophozoites)
2. Folate deficiency (+ crypt atrophy, megalocytosis), B12 deficiency (similar to folate +hyalinized mucosal vessels), radiation enteritis (similar to B12 w/o megalocytosis)
True/False Merkel cell carcinoma of the gyn tract may be associated with Bowens disease.
True
How is the morphology of rhabdomyoma in the gyn tract different from that found in the head and neck?
Gyn is more spindle and haphazard in morphology vs head and neck being more polygonal
Name some high risk HPV types.
HPV's 16, 18, 31, 33, 35
True/False HPV types 6 and 11 are never seen in high grade lesions.
False. They are rarely seen in high grade lesions, but that is not synonymous with never.
HPV DNA is detected in what percent of cancers and SILs
Greater than 90%
Cervical cancer is the __th leading cause of death in women and accounts for__% of all cancer deaths in women.
Cx CA is the 6th leading cause of death and accounts for 5% of all CA deaths.
Compare and contrast low risk and high risk HPV ifections
Low Risk
1. productive infection
2. express early and late genes (E4, L)
3. non integration of viral DNA
4. euploid or polyploid
High Risk
1. nonproductive infection
2. express only early genes (E6, E7)
3. integration of viral DNA
4. aneuploid
What is the significance of E4 protein?
non integration leads to accumilation in cytoplasm with disruption in cytoplasmic keratin matrix. organelles get pushed to the side ergo koilocytic change.
What is the significance of E6 gene?
Binds to p53 the regular of cell death/apapotosis which promotes degredation of p53 and therefore infected cells don't die.
What is the significance of E7 gene?
Binds Rb protein a tumor supressor that prevents excessive cells growth by inhibiting cell cycle progression.
1. What are some primary causes of motility disorders?
2. What are some secondary cuases of motility disorders?
1. muscular, myenteric plexus (Hirshprungs)
2. Diabetic neuropathy, systemic sclerosis, amyloidosis, hypothyroidism
Which form of pneumatosis intestinalis is associated with necrotizing enterocolitis?
Diffuse form.
The other forms are microvesicular, and cystic
Which type of carcinoid is liked to peritoneal mucinosis?
Goblet cell carcinoid
A mother brings herson in for a well check visit. Per the mother, the child has been developing normally, but has mild difficulty keeping up in school. The physician notices a few brown patches on the skin and a few sub cutaneous nodules. Please answer the following questions
1. What gastrointestinal tumor can be seen in this entity?
2. What are some other defining characteristics?
3. What genes are involved
.1 Gangliocytic paraganglioma
2.
3. 17q nerofibromin which