PATH MIDTERM MASTER
1. Benign No malignant potential Hyperplasia of glands Serrated 2. Benign Premalignant Neoplastic proliferation of glands Progression to adenoma-->carcinoma as related to >2cm, sessile growth, villous histology
For the following polyps: 1. Hyperplastic 2. Adenomatous a. Benign or malignant b. Have malignant potential? c. Caused by: d. How do they look histologically?
Poorly circumscribed, red, velvety eroded area
How does erythroplakia present grossly?
Differentiation: 1: well differentiated (>95% glands) 2: moderate (50-95% glands) 3: poor/undifferentiated (<5% glands) TNM: Tumor (T0-T4), Nodes (0-2), Metastasis (0-1) X: cannot be assessed
How is a cancer graded? Describe the 3 grades. How is it staged?
Celiac disease (celiac sprue) - the characteristic flattened atrophic villi with elongated and hyper plastic crypts. It is the result of T-cell mediated damage HLA-DQ2 & HLA-DQ8
On the left is a histological section of normal small intestines. What condition is seen on the right and what morphological change leads you to this diagnosis? What is this condition caused by? This condition has an HLA association. What is it?
Small, benign, incidental finding
What are carcinoid tumors of the rectum like?
Bleeding Stricture formation ASPIRATION PNEUMONITIS Barrett Esophagus and Adenocarcinoma
What are some complications of reflux esophagitis?
Diverticulosis - picture shows a false diverticula containing only mucosa and submucosa. Sigmoid colon Diverticulitis as a result of fecal contamination and development of an infection
What condition is seen here and what leads you to this conclusion? Where is the most common location of this condition? If obstruction of this diverticula occurs what can develop?
Acute appendicitis Obstruction of the appendiceal lumen by a fecalith or as a result of lymphoid hyperplasia.
What condition is seen here? This condition is usually secondary to what?
The presence of all layers (mucosa, submucosa, serosa/adventitia)
What defines a true diverticulum?
CEA. Follow-up
What is a good tumor marker for colon carcinoma? Is it good for diagnosis or follow-up?
Oral leukoplakia Buccal mucosa, tongue, floor or mouth Men (older)
What is this condition called? Where does it commonly occur? Who does it commonly affect?
1. Chromosomal instability - adenoma-carcinoma sequence starting with APC mutations FAP/Gardner/Turcot Microsatellite instability, may arise from sessile serrated adenomas or hyper plastic polyps Mutations in MLH1, MSH2, MSH6, PMS1 (85% sporadic, 15% familial) HNPCC: Lynch Syndrome 2. Chromosomal instability
1. What are two major pathways for developing colon cancer? -defect -sequence -mutation -diseases? 2. Which pathway is more common?
1. Herniation of stomach through enlarged esophageal hiatus 2. Sliding type (95%), Paraesophageal/rolling type 3. Epigastric pain, heart burn (due to reflux of gastric contents 4. Volvulus strangulation, perforation
1. What is a hiatal hernia? 2. What are the two types? 3. What are the symptoms for the sliding type? 4. What are some complications for the paraesophageal type?
1. Disruption of elongation and separation of esophagus and trachea during embryogenesis 2. Tracheoesophageal fistula, maternal polyhydraminos, single umbilical artery 3. Excessive drooling, choking and cyanosis with first feed
1. What is esophageal atresia? 2. What is it commonly associated with? 3. What are some common symptoms seen in newborns with this condition?
1. Squamous carcinoma of the tongue (whorls, pearls, prickles, bridges) 2. Ventral surface of the tongue, floor of the mouth, lower lip, soft palate, and gingiva
1. What is shown here? 2. Where does it commonly occur?
1. Mallory Weiss Syndrome 2. Alcoholics after a bout of severe retching 3. Inadequate relaxation of LES during vomiting 4. Mucosal or transmural 5.Hematemesis 6. Usually heals, sometimes fatal
1. What is shown here? 2. Who is commonly affected by it? 3. What is the pathogenesis behind it? 4. Where do the tears occur? 5. What clinical symptom is it commonly associated with? 6. What is the prognosis?
1. Reflux esophagitis/GERD: most common form of esophagitis 1. Low LES tone (CNS depressants, hypothyroidism, pregnancy, alcohol, tobacco, nasogastric intubation 2. Delayed esophageal clearance 3. Reduced reparative capacity of esophagus 4. Increased gastric volume
1. What is shown here? What is it caused by? (4)
1. Erythroplakia/Erythroplasia 2. Less common 3. Worse prognosis (typically shows marked dysplasia) 4. More than 50% of the cases
1. What is shown here? What is another name for it? 2. Is it more or less common than oral leukoplakia? 3. Does it usually have a better or worse prognosis than oral leukoplakia? Why? 4. How often does a malignant transformation occur?
1. Achalasia: Incomplete relaxation of the LES in response to swallowing - functional obstruction aka Cardiospasm 2. Aperistalsis, partial or incomplete relaxation of LES, increased resting tone of LES
1. What is shown here? What is another name for it? 2. What are the 2 main features?
1. Hyperkeratosis - mucosal acanthosis with underlying keratotic squames 2. No
1. What is the name of the process that leads to oral hairy leukoplakia? 2. Does it have malignant potential?
Pain, usually starting in the periumbilical region, and eventually moving to McBurney's point, nausea, and vomiting. Perforation leading to peritonitis.
Acute appendicitis presents with what symptoms? What is a serious complication of this condition?
Bleeding, lower abdominal pain, constipation, diarrhea, flatulence, and fever. Left lower quadrant (location of the sigmoid colon) Perforation leading to a fistula
Although diverticulitis can be asymptomatic what symptoms can it have? If abdominal pain occurs, where would it likely be? What is a serious complication associated with this condition?
No a. Type I: gastric atrophy and achlorhydria in AI gastritis - hypergastrinemia-->ECL hyperplasia usually benign b. Type II: gastrinoma (Zollinger-Ellison Syndrome, MEN 2 syndrome, hypergastrinemia) c. Type III: sporadic - aggressive with metastasis Type I has the best prognosis
Are carcinoid tumors common in the esophagus? What are the following stomach carcinoid tumors associated with and what are some key features? a. Type I b. Type II c. Type III Which type has the best prognosis?
5% of cases develop into squamous cell carcinoma
Can achalasia progress to carcinoma?
The splenic flexure. Chronic ischemia is a result of chronic inflammation and fibrosis that eventually make the watershed area too far from the blood supply to be adequately oxygenated leading to ischemia of this area.
Chronic ischemic colitis commonly affects what area and why?
Juvenile polyp: lobulated with stalk Lamina propria forms the bulk and encloses abundant cystic dilated glands May or may not have inflammatory cells No
Describe the image. Are sporadic single polyps usually malignant?
Poorer
Do mucinous carcinomas of the colon have a better or poorer prognosis?
Ankylosing spondylitis, migratory polyarthritis, erythema nodosum, sclerosing cholangitis, sacroileitis, and clubbing.
Extraintestinal manifestations can occur even before the onset of GI symptoms in both Ulcerative colitis and Crohn disease. Name some conditions.
Down's syndrome patients Enterocolitis, perforation, and if perforation occurs, peritonitis.
Hirschsprung disease is seen in 10% of what patients? What complications can develop?
Eradicated with antibiotics. 67-90% remission, 10% relapse Grow slowly, stay localized 90% 5Y survival rate, 65-75% 10Y survival rate Rituximab - antiCD20 agent
How are H.Pylori gastric MALT lymphomas treated? What is the prognosis? What are unresponsive cases treated with?
Small, occult primary tumors Carcinoid tumor: when they metastasize to the liver -wheezing, diarrhea, flushing
How do carcinoid tumors of SI and appendix present? What can they lead to? Under what circumstances? -what are the symptoms?
Asymptomatic Occult blood loss Hypoproteinemia, Hypokalemia due to loss of fluid, proteins, electrolytes
How do most adenomas present clinically? How do villous adenomas present clinically?
It drives the proliferation of the B cells No. T cells, specific strain of H-pylori even if it is heat-killed No, only the proliferative response is strain specific Dietary mutagens
How is H.Pylori associated with MALT Lymphoma? Does H. Pylori infect the B cells? What else do the B cells need in order to proliferate? Are the B cells H.pylori specific? What other factors may be involved?
1. PUD (peptic ulcer disease) 2. Salmonellosis and typoid fever (S. typhi) 3. CMV (usually seen in immunosuppressed patients) 4. NSAIDs 5. Necrotizing tumors leading to ulceration 6. Crohns disease and ulcerative colitis
Intestinal ulcers have a variety of causes. Name some examples for each of the following: 1. Seen in the duodenum 2. Bacterial enterocolitis 3. Viral infection 4. Drugs 5. Tumors 6. IBD
1. UC 2. CD 3. UC 4. Both 5. UC 6. CD Ulcerative colitis
Is the following characteristic of Ulcerative colitis or Crohn disease? 1. Presents as mucosal and submucosal ulcerations 2. Cobblestone mucosal appearance 3. Associated with primary sclerosing cholangitis 4. Increased risk of developing colonic malignancy 5. Formation of pseudopolyps 6. Presents with characteristic "creeping fat" Which has a higher risk of developing malignancy?
1. CD 2. UC 3. CD (string sign) 4. CD 5. UC 6. CD Healing by fibrosis in the bowel which causes eventual stricture of the bowel.
Is the following characteristic of Ulcerative colitis or Crohn disease? 1. Transmural involvement of an inflammatory process 2. Starts in the rectum and moves proximally 3. Characteristic radiographic appearance seen here (name the appearance) 4. Can lead to fistula formation 5. Can lead to backwash ileitis in 10% of patients 6. Can lead to fat and vitamin malabsorption What causes the radiographic appearance?
1. Non-occlusive 2. Occlusive 3. Miscellaneous 4. Non-occlusive The amount of wall involvement. If only the mucosa is involved the symptoms will typically be minor but if it is transmural it will be more serious leading to potential of gangrene, perforation, peritonitis, shock, and vascular collapse.
Ischemic bowel disease can be occlusive, non-occlusive or miscellaneous. Below is a list of causes, what category does each fall into? 1. Shock 2. Arterial or venous thrombosis 3. Volvulus 4. Dehydration What determines whether an ischemic bowel disease is mild or more serious?
Chronic diarrhea that typically contains fatty feces. Digestion of the nutrients, absorption of nutrients, or delivery of nutrients to tissues.
Malabsorption syndromes typically present with what symptom? Impairment of what can cause a malabsorption syndrome?
Hamartomatous polyp: Arborizing network of smooth muscle extends into polyp and surrounds the glands and lamina propria Non-dysplastic epithelium lining the glands; rich in goblet cells No Carcinomas of the pancreas, breast, lung, ovary, uterus
Name the disease and describe the image. What is the nature of the epithelium? Do these polyps have malignant potential? What are these patients at risk of developing?
1. Intramural 2. Luminal 3. Luminal 4. Extramural
Small intestinal obstruction can be luminal, intramural (within the bowel wall), or extramural. Identify which the following causes: 1. Crohn's disease 2. Therapeutic agents like barium sulphate and antacid gels 3. Mass of roundworms (Anscaris lumbricoides) 4. Intussuscception
1. Intramural 2. Luminal 3. Extramural 4. Luminal
Small intestinal obstruction can be luminal, intramural (within the bowel wall), or extramural. Identify which the following causes: 1. TB 2. Swallowed foreign bodies 3. Hernia 4. Food bolus like persimmon, macaroni, and sauerkraut
1. Luminal and extramural 2. Extramural 3. Intramural 4. Luminal A gallstone that lodges in the terminal ileum that enters the small bowel through a cholecytoduodenal fistula. Adhesions
Small intestinal obstruction can be luminal, intramural (within the bowel wall), or extramural. Identify which the following causes: 1. Tumors 2. Volvulus 3. Drug induced stenosis (NSAIDS) 4. Gallstone ileus What is gallstone ileus? What is the most common cause of extramural obstruction?
Whipple disease Tropheryma whippelii. The bacteria are engulfed by macrophages which are only able to partially destroy the bacteria leading to their accumulation and swelling in the small bowels lamina propria causing compression of the lacteals and inability of chylomicrons to move from the enterocytes to the lymphatics. This results in fat malabsorption and steatorrhea. With antibiotics
The following photo shows a PAS stain indicating what disease? This disease is the result of infection with what bacteria? What occurs in this disease leading to this characteristic appearance? How is this condition treated?
Amebic colitis - Flask shaped ulcers Entamoeba histolytica Fecal-oral route Anti-parasitic agents
The following was taken from a patient with chronic destructive colitis. What is a likely diagnosis and how did you come to this conclusion? What is the causative agent of this condition? How is this agent transferred? How is this treated?
Anti-tissue transglutaminase Ab (tTG), anti-gliadin Ab, and anti-endomysial Ab. Iron deficiency anemia because this condition commonly affects the proximal intestine (duodenum). The symptoms are usually resolved when the patient maintains a gluten free diet Intestinal T-cell lymphoma
What antibodies can be identified to aid in diagnosis of celiac disease? Suspecting celiac disease should be the result of a presenting history showing malabsorption. Name a condition that can help us suspect celiac disease and why? How is this condition treated? What long term risk should you be aware of for this condition?
Epithelial proliferative dysplasia Tubular, villous, tubulovillous - they are DYSPLASTIC by definition and are preneoplastic Carcinoma Polyp size if the most imp criteria, and severity of dysplasia No polyps, screen in 10 years Remove polyps, screen in 5 years 4cm polyp villous/tubular/tubulovillous: screen sooner!
What are adenomas? What are 3 histological descriptions of adenomas? What do they have in common? What can they lead to? What increases the risk of them becoming malignant? What should the follow up be for absence/presence/size of these polyps?
MALTOMA, DLBL (high grade) Mantle cell, Burkitt and Burkitt-like, Follicular lymphomas, Immunodeficiency related
What are the 2 most common B-cell lymphomas of the GI tract? What are some other types?
dysphagia, odynophagia (pain swallowing), reflex, vomiting, aspiration pneumonia
What are the clinical features for achalasia?
a. fatigue, weakness, iron deficiency anemia due to exophytic polyploidal lesions. No. b. altered bowel habits, decreased stool caliber due to napkin-ring lesions, left lower quadrant pain, blood-streaked stool
What are the clinical features of: a. Right sided (proximal) colon carcinoma? Are obstructions common? b. Left sided colon carcinoma?
Dyspepsia, burning, water brash, nocturnal cough a. After a large meal or lying down
What are the clinical signs of reflux esophagitis? a. When do symptoms increase?
Chromogranin (slide) Synaptophysin
What are two histological markers used to stain neuroendocrine cells? Which one is this?
Dilation of the lumen due to mucinous secretion from a benign or malignant tumor. It is the result of the appendiceal mucocele rupturing leading to what is referred to as "jelly belly."
What causes appendiceal mucocele? What is pseudomyxoma peritonei?
Physical and mental stress. CD: Right lower quadrant pain because it most commonly affects the ileum UC: Left lower quadrant pain because it most commonly affects the rectum and progresses proximally
What causes flare-ups of inflammatory bowel disease? It can present with bloody and mucoid diarrhea, fever, weight loss, and lower abdominal pain. Where would the abdominal pain most likely be in each disease?
Damage to the small intestinal villi from an unknown organism that results in malabsorption. Seen in patients living in or visiting endemic areas like the Caribbean. Months or years after the visit to the endemic area. Treated with antibiotics
What causes tropical sprue? What patients is this condition seen in? When do the symptoms appear? How is it treated?
Ischemic bowel disease 1. Occlusive 2. Non-occlusive 3. Miscellaneous 4. Miscellaneous A small herniation as it is more likely to cause strangulation of the bowel when it herniates through the space.
What condition is being illustrated in this photo? It can be occlusive, non-occlusive or miscellaneous. Below is a list of causes, what category does each fall into? 1. Arterial embolism 2. Cardiac failure 3. Radiation 4. Herniation Is a large herniation defect or small herniation defect more likely to cause this condition?
Pseudomembranous colitis Use of broad spectrum antibiotics Clostridium difficile C. diff toxin mediated damage leading to formation of fibrinopurulent-necrotic debris (pseudomembranes).
What condition is seen grossly and microscopically? What causes this condition? What bacteria causes this condition? What leads to the formation of the pseudomembranes in this condition?
Crohn disease - characteristic lymphoid aggregates with non-caseating granulomatous inflammation
What condition is seen here and what about the histology is characteristic of this condition leading you to this conclusion?
Ulcerative colitis - characteristic crypt abscesses with neutrophil infiltration
What condition is seen here and what about the histology is characteristic of this condition leading you to this conclusion?
Hirschsprung disease A defect of migration and survival of intestinal ganglion cells leading to an absence of Auerbach's and Meissner's plexus in a section of the LI. Resection of the affected area. The left side is the affected side as the dilation occurs proximal to the affected area. Rectal biopsy that must include the submucosa and muscularis.
What condition is seen here? What causes this condition? What is the treatment for this condition? Which side is the affected side? How do you diagnose this condition?
Meckle's Diverticulum It is the result of the failure of involution of the vitelline duct. True because it involves all three layers of the bowel.
What condition is seen here? What is it the result of? Is it a true diverticula or a false diverticula and why?
Ulcerative colitis - red, granular, and friable mucosa that is progressing proximally as opposed to Crohn disease which is seen as skip lesions throughout the GI tract.
What inflammatory bowel disease is seen here and what about its gross morphology leads you to this conclusion?
FAP with: Multiple osteomas, Desmoid tumors, Epidermal cysts
What is Gardner Syndrome characterized by?
Dysphagia due to esophageal webs, glossitis and iron deficiency anemia. More common in M than F, associated with Koilonychia and Splenomegaly. Increases risk for SCC of Esophagus Tx: Iron, endoscopic dilatation Genetic
What is Plummer Vinson Syndrome? What causes it, is it more common in M or F? What are the complications?
FAP with: With CNS tumors (medulloblastoma and glial tumors)
What is Turcot Syndrome?
HNPCC a. Defective DNA repair genes, MLH1, MSH2, MSH6, PMS1 --> microsatellite instability b. multiple from none to sessile serrated adenomas or large hyperplastic polyps Can go from nothing to malignant polyps c. Right side (proximal colon) d. Mucinous, with many tumor infiltrating lymphocytes e. Less e. Endometrial, ovarian, stomach, small intestine, biliary tract
What is Warthin-Lynch Syndrome? a. Mutations, inheritance pattern? b. Tumors? What is special about them? c. Which part of the colon are polyps commonly found? d. What is the histology of the polyps? e. More or less polyps than FAP? e. Associated with what other carcinomas?
When a lymphoma presents with the main bulk of disease in the GI tract with or without contiguous lymph nodes No Stomach > SI > Colon and rectum
What is a PRIMARY GI lymphoma? Is there any liver, spleen or bone marrow involvement at the time of diagnosis? Where are they most commonly seen?
EATL: enteropathy associated, including ulcerative jejunitis Refractory/Collagenous sprue
What is a T-cell lymphoma seen in the GI tract? What predisposes patients to this type of lymphoma?
Eosinophilic esophagitis Hyperemia Inflammatory cells: eosinophils and neutrophils Elongation of lamina propria papillae (>2/3 thickness of epithelium) Basal zone hyperplasia Usually bilobed and the pink granules in the cytoplasm are much more dense
What is another name for allergic esophagitis? Describe the image. -what cells do you see -lamina propria -basal zone How can the eosinophils be distinguished from neutrophils in histological section?
Elderly Young with ulcerative colitis Polyposis syndromes Obesity, physical inactivity, not enough dietary indigestible fiber, rich in animal fat Antioxidants
What is colorectal carcinoma associated with? What are the risk factors? What can protect from this?
Infections with HSV, CMV, Candidiasis Moulding, Margination, Multinucleation No
What is infectious esophagitis? What is it characterized by? Do you have to be immunocompromised to get it?
Tobacco use Chronic friction (ill-fitting dentures) HPV infection
What is oral leukoplakia associated with?
Loss or absence of ganglion cells in myenteric plexus i.e. loss of inhibitory innervation of LES and smooth muscle
What is primary achalasia caused by?
Impaired function due to other causes: -Chagas (Trypanosoma cruzi) -Polio -Paraneoplastic syndrome -Sarcoidosis
What is secondary achalasia caused by? Give some examples of what causes secondary achalasia.
Barrett's esophagus Salmon-pink patch extending up at the gastroesophageal junction (and tongue)
What is shown here?
Carcinoid tumor of GI tract -small nests of cells in submucosa Small intestine and appendix
What is shown here? (Describe image) What is the most common location?
APC gene defect (5q1) - 2 hits Young individuals Tubular polyps Colon, sometimes SI and stomach 500-2500 mucosal adenomas >100 for diagnosis Prophylactic colectomy
What is shown here? What are the characteristics of this syndrome? a. gene defect b. who does it affect? c. how does it look histologically? d. where are the polyps usually seen? How many adenomas are usually seen? How is FAP diagnosed? How is it treated?
Juvenile polyps aka retention polyps. Rectum. Children and adults
What is shown here? Where is it commonly found? Who does it commonly affect?
Painful defecation Abdominal pain, bloody and/or mucoid diarrhea, abdominal cramps, etc.
What is tenesmus? Colitis can be associated with tenesmus. What other symptoms are associated with colitis?
CD: HLA-DR7 & HLA-DQ4 UC: HLA-DRB1 CD: Transmural UC: Mucosa and submucosa CD: Ileum (can involve any area of the GIT) UC: Always starts at the rectum and moves proximally
What is the HLA association of Crohn disease and Ulcerative colitis? What area of the GI wall does each affect? What area is most often affected by these conditions?
APC mutation (2-hits): inc risk of polyp formation K-ras mutation: polyp formation p53 mutation, increased COX: progress to carcinoma
What is the adenoma-carcinoma sequence?
Biopsy and histological examination
What is the best way to confirm whether or not oral leukoplakia is dysplastic?
Celiac sprue - most comon in the proximal intestines (duodenum) Tropical sprue - occurs in all parts of the intestine (but can predominate in the jejunum and ileum)
What is the difference between the area affected by celiac sprue and tropical sprue?
Mostly erythroplakias and some leukoplakias Tobacco use, HPV 16/18
What is the etiology of squamous carcinoma of the tongue? What is is associated with?
GI malignancy
What is the first thing that should come to mind when an elderly man presents with Fe deficiency anemia?
Inflammatory bowel disease Ulcerative colitis and Crohn disease
What is the following: Chronic, relapsing, inflammatory disorder of the bowel. What are the two inflammatory bowel disease?
T0: none Tis: in situ T1: invades submucosa T2: invades muscularis propria T3: invades past muscularis propria T4: invades other organs/perforates visceral peritoneum N=0: none N=1: 1-3 positive nodes N=2: 4 or more positive nodes M=0: none M=1: any distant metastases
What is the meaning of: T0 Tis T1 T2 T3 T4 What is the meaning of: N = 0, 1, 2 What is the meaning of: M = 0,1
Esophageal squamous mucosa--> metaplastic columnar epithelium Prolonged injury such as long standing GERD Progenitor/stem cells proliferate attempting to heal --> columnar cells are more resistant to acid peptic injury Men, whites ADENOCARCINOMA (30-40X inc) Serial endoscopic biopsies (look for dysplasia)
What is the pathogenesis behind Barrett's esophagus? What causes the change? How does it occur? Who does it commonly effect? What does it increased the risk for? How do you screen for it?
Entirely mucinous: No epithelium Abundant mucin: Scant low grade neoplastic epithelium Abundant malignant epithelial cells: Signet ring cells, infiltrating columnar epithelium • d/d mucinous cystadenocarcinoma ovary
What is the range for pseudomyxoma peritonei?
Rule of 2s: In 2% of the population, ~2 inches, is 2 feet from the ileocecal valve, usually presents in the first 2 years of life, and is sometimes lined by two types of tissue, gastric and/or pancreatic. Appendicitis
What is the rule associated with Meckle's Diverticulum? Although it is commonly asymptomatic, what condition can it mimic?
Gastric MALTOMA a. 60, males more than females b. dyspepsia, abdominal pain, nausea, vomiting, weight loss, abdominal mass, blood loss
What is this and how does it present? a. mean age of occurrence, gender b. symptoms
Pedunculated adenoma
What is this?
Sessile serrated adenoma Sessile: forms a mat along the wall (**** malignant potential) Serrated: surface of the polyp has a saw-tooth appearance
What is this? What particular feature is associated with malignancy?
Uremia Anticancer therapy, Bisphosphonates, Tetracycline antibiotics like Doxycycline
What pre-existing condition can cause esophagitis? What drugs can cause esophagitis?
Hamartomatous polyp: Peutz Jegher Polyp Autosomal dominant, multiple polyps in whole GIT, melanotic pigmentation in mucocutaneous areas, lips, perioral areas, face, genitalia, palms
What syndrome are the following associated with? Describe the manifestation of this syndrome.
In juvenile polyposis syndrome where there are multiple polyps in stomach and colon. SMAD4 mutation Cowden and Bannayan-Ruvacalba-Riley syndromes. PTEN mutations
When are juvenile polyps malignant? What mutation are they associated with? In what other syndromes are juvenile polyps common? What mutation do these syndromes have in common?
90% are in the colon and usually solitary Tall, hyperchromatic, disordered epithelium lining glands Invasion of the submucosal stalk (past the muscularis mucosa) --> invasive carcinoma Sessile
Where are most adenomas found? How do they usually look? What constitutes progression to invasive carcinoma? Do sessile or pedunculated adenomas have a greater risk of malignancy?
Regional lymph nodes, liver, lung, bones T1 (submucosa): 97% M1 (metastasis): 4%
Where can colon carcinomas spread? What are 2 stages and what is the prognosis?
Crohn disease: Non-caseating granulomas TB: Caseating, necrotizing granulomatous inflammation with samples staining positive for M. tuberculosis.
Which infectious colitis, amebic colitis, typhoid fever, or TB, is associated with the following: 1. Necrotizing granulomatous inflammation 2. Flask shaped ulcers with organisms engulfing RBCs 3. Longitudinal ulcers, typically over Peyer's patches How can we determine whether a colitis is the result of Crohn disease or TB?
1. Oral hairy leukoplakia (white, confluent, fluffy or hairy hyperkeratotic thickenings) 2. Almost always in HIV patients, majority have EBV infection
1. What is shown here? 2. What patients is it usually seen in?
1. Hyperkeratosis i.e. epidermal thickening 2. No 3. Range between both; 3-7% undergo malignant transformation
1. What process causes oral leukoplakia? 2. Can it be removed by scraping? 3. Are they benign or dysplastic lesions?
