Pathology Gi

Front 1

mucosal webs -

Back 1

ledgelike mucosal protursions usually in the upper esophagus,

Front 2

achalasia -

Back 2

failure to relax

Front 3

the constellation of webs, iron deficiency anemia, glossitis, and cheilosis is called

Back 3

the plummer-vinson syndrome

Front 4

a luminal concretion of indigestible ingested material -

Back 4

bezoars

Front 5

diffuse invasion of macroscopic growth of gastric carcinoma throughout the wall creates a rigid thickened stomach,called -

Back 5

linitis plastica

Front 6

inlet patch -

Back 6

ectopic gastric mucosa in the upper third of the esophagus

Front 7

Heterozygous loss-of-function mutations in the receptor tyrosine kinase RET account for the majority of familial cases and approximately 15% of sporadic cases, of??

additional mutations: RET ligand glial-derived neurotrophic factor, endothelin, and the endothelin receptor

Back 7

hirschsprung disease

Front 8

high amplitude esophageal contractions in which the outer longitudinal layer of smooth muscle contracts before hte inner circular layer, diagnosis?

Back 8

nutcracker esophagus - short lived esophageal obstruction

Front 9

dital esophageal rupture and mediastinitis, diagnosis?

Back 9

boerhaave syndrome

Front 10

adherent gray white pseudomembrane composed of densely matted fugal hyphae and inflammatory cells coverring the esophageal mucosa, diagnosis?

Back 10

candidiasis

Front 11

basal epithelial cell apoptosis, mucosal atrophy, and submucosal fibrosis without significant acute inflammatory infiltrates in the esophagus, diagnosis?

Back 11

graft versus host disease

Front 12

a large number of intraepithelial eosinophils, particularly superficially in the esophagus, diagnosis?

Back 12

eosinophilic esophagitis

Front 13

mucosal polyps, composed of firbous and vascular tissue, or adiopose tissue, in the esophagus, diagnosis?

Back 13

fibrovascular polyps or penduculated lipomas respectively

Front 14

sessile lesions with a central core of connective tissue and a hyperplastic papilliform squamous mucosa, diagnosis?

Back 14

squamous paillomas

Front 15

what cells are found in each part of the stomach?

Back 15

The antral glands are similar but also contain endocrine cells, such as G cells, that release gastrin to stimulate luminal acid secretion by parietal cells within the gastric fundus and body.

Front 16

loss of the superficial epithelium, generating a defect in the mucosa that is limited to the lamina propria, in the stomach, diagnosis?

Back 16

erosion

Front 17

individuals with shock, sepsis, or severe trauma, are more likely to get what type of ulcer?

Back 17

stress ulcers

Front 18

ulcer occuring in the proximal duodenum and associated with severe burns or trauma, called?

Back 18

curling ulcers

Front 19

gastric, duodenal, and esophageal ulcers arising in persons with intracranial disease, diagnosis?

Back 19

cushing ulcers

Front 20

ulcer in which there is no scarring and thickening of blood vessels is?

Back 20

acute ulcer, scaring and thickening of blood vessels is a sign of chronic ulcers

Front 21

What are the top three complications of gastric ulcers?

Back 21

bleeding: 20%, 25% of ulcer deaths

perforation: 5%, 2/3 of ulcer deaths

obstruction: mostly in chronic ulcers, most often associated with pyloric channel ulcers, duodenal ulcers, crampy abdominal pain,

Front 22

patient presents with antral gastritis with high acid production but hypogastrinemia, diagnosis?

Back 22

H. Pylori infection

Front 23

what polymorphism is associated with development of pangastritis post h. pylori infection?

Back 23

IL-1beta

Front 24

antral mucosa that is erythematous and has a coarse or even nodular appearance, with intraepithelial neutrophils, pit abscesses, and subepithelial plasma cells, diagnosis?

Back 24

H pylori infection - intraepithelilal neutrophils and subepithelial plasma cells are really characteristic of H. pylori gastritis

Front 25

patient presents with decreased acids production, and hypergastrinemia, with inflammation in the body of the stomach, diagnosis?

Back 25

autoimmune gastritis against parietal cells

Front 26

defective gastric acid secretion -

Back 26

achlorhydria

Front 27

foveolar hyperplasia, glandular regenerative changes, and mucosal edema, post gastric surgery, diagnosis?

Back 27

reactive gastrophathy

Front 28

longitudinal stripes of edematous erythematous mucosa alternating with less severely injured mucosa that is sometimes referred to as watermelon stomach, diagnosis?

Back 28

gastric antral vascular ectasia

Front 29

thickened folds covered by small nodules with central aphthous ulceration, increase in the number of intraepithelial T lymphocytes, mostly CD8+ cells, in the stomach, diagnosis?

Back 29

lymphocytic gastritis

Front 30

granulomas, narrowing and rigidity of the gastric antrum, and transmural granulomatous inflammation of the stomach with aggregates of epithelioid histiocytes, diagnosis? and possible causes?

Back 30

granulomatous gastritis:
- gastric involvement of crohns disease
-sarcoidosis
-infections: mycobacteria, fungi, CMV, and H. pylori

Front 31

how do chronic renal failure and hyperparathyroidism cause duodenal ulcres?

Back 31

hypercalcemia stimulates gastrin production and therefore increases acid secretion

Front 32

a round to oval, sharply punched out defect in the proximal duodenum, diagnosis?

Back 32

peptic ulcer

-heaped-up margins are more characteristic of cancers

Front 33

patient presents with pain 1-3 hours after meals during the day, gets worse at night, and is releived by alkali or food, sometimes having nausea, vomiting, bloating, belching, diagnosis?

Back 33

peptic ulcers

Front 34

oxyntic atrophy comes with an increased risk of?

Back 34

gastric adenocarcinoma

Front 35

variations in epithelial size, shape, and orientation along with coarse chromatin texture, hyperchromasia, and nuclear enlargement, what are these hallmarks for?

Back 35

morphologic hallmakrs of dysplasia

Front 36

how do you tell the difference between reactive epithelial cells and dysplastic lesions?

Back 36

they both have increased epithelial proliferation and mitotic figures, but dysplastic lesions remain cytologically immature while the epithelial cells mature as they reach the mucosal surface

Front 37

reactive epithelial proliferation associated with entrapment of epithelial lined cysts, in the submucosa -

in the deeper layers of the gastric wall -

Back 37

gastritis cystica profunda gastritis cystica polyposa

Front 38

irregular enlargement of the gastric rugae, hyperplasia of foveolar mucous cells, with glands that are elongated with corkscrew-like appearance and cystic dilation, diagnosis?

Back 38

menetrier disease - caused by excessive secretion of transforming growth factor alpha,

Front 39

within the stomach there is a doubling of oxyntic mucosal thickness due to a fivefold increase in the number of parietal cells, diagnosis?

Back 39

zollinger-ellison syndrome - gastrinoma

Front 40

what polyp is likely to form due to chronic use of PPI's?

Back 40

fundic gland polyp

Front 41

what is the likely polyp to form in an individual with atrophic gastritis?

Back 41

inflammatory or hyperplastic polyps

Front 42

enlargement, elongation, and hyperchromasia of epithelial cell nuclei, epithelial crowding, and pseudostratification occuring in the antrum of the stomach, diagnossi?

Back 42

gastric adenoma -

low grade and high grade which would likely include glandular budding and gland-within gland, or cribiform, structures

Front 43

Germline mutations in CDH1, which encodes E-cadherin, a protein that contributes to epithelial intercellular adhesion, are associated with what cancer?

Back 43

familial gastric cancers, usually the diffuse type

Front 44

what type of gastric cancer predominates in high risk areas?

Back 44

intestinal type, developing from precursor lesions including flat dysplasia and adenomas

Front 45

The t(11;18) --> API2-MLT fusion protein will lead to what cancer?

Back 45

MALToma

although most MALTomas are associatedw with H. pylori, if there is a genetic mutation association with the cancer, this will lead to antibiotic failure in treatment and the cancer will remain

Front 46

reactive appearing b cell follicles may be present and plasmacytic differentiation can be observed in MALTomas, as well as tumor cells accumulating large amounts of pale cytoplasms, called?

Back 46

monocytoid

Front 47

Cancer in the GI with CD19 and CD20, expression, diagnosis?

Back 47

mature b cell tumor: MALTomas

they do not have: CD5 or 10 (immature B cell markers)

Front 48

where is the typically the most dangerous place to find a carcinoid tumor in the GI?

Back 48

the midgut: jejunum and ileum - often multiple and tend to be aggressive, greater depth of local invasion, increased size, and presence of necrosis and mitosis are associated with poor outcomes

Front 49

young female has gastric GIST, paraganglionma, and pulmonary chondroma, diagnosis?

Back 49

Carney triad (GIST- GI stromal tumor)

Front 50

c-KIT is associated with what GI tumor?

Back 50

GIST - gain of function mutations

Front 51

the sigmoid colon and rectum get supplied with blood from?

Back 51

inferior mesenteric, pudendal, and iliac arterial circulations

Front 52

patient presents with suface epithelial atrophy, some necrosis and sloughing, with normal or hyperproliferative crypts in the splenic flexure, diagnosis?

Back 52

ischemic bowel disease - the surface epithelium is the most vulnerable to ischemic damage

Front 53

what are the four phases of nutrient absorption?

Back 53

(1) intraluminal digestion, in which proteins, carbohydrates, and fats are broken down into forms suitable for absorption; (2) terminal digestion, which involves the hydrolysis of carbohydrates and peptides by disaccharidases and peptidases, respectively, in the brush border of the small intestinal mucosa; (3) transepithelial transport, in which nutrients, fluid, and electrolytes are transported across and processed within the small intestinal epithelium; and (4) lymphatic transport of absorbed lipids.

Front 54

patient presents with increased numbers of intraepithelial CD8+ T cells, intraepithelial lymphocytosis, crypt hyperplasia, and villous atrophy, diagnosis?

Back 54

celiac disease

Front 55

FOXP3 gene mutation leads to what disorder?

Back 55

autoimmune enteropathy - IPEX: immune dysregulation, polyendocrinopathy, enteropathy, and X linkage,

Front 56

mutation in MTP leads to?

Back 56

*microsomal triglyceride transfer protein), enterocytes are unable to export lipoproteins and ffa's, then malabsorption of abetalipoproteinemia --> this leads to defects in lipid membranes causing burr cells

Front 57

what are the diagnostic criteria for irritable bowel syndrome?

Back 57

occurrence of abdominal pain or discomfort at least 3 days per month over 3 months, improvement with defectation, and a change in stool frequency or form

Front 58

NOD2 mutations lead to susceptibility to what disease?

Back 58

Crohn's disease

Front 59

a UC patient undergoes surgery to have their colon removed, now the distal segment of colon is erythematous, friabile, and has developed numerous mucosal lymphoid follicles, diagnosis?

Back 59

diversion colitis

Front 60

patient presents with rectal bleeding, mucus discharge, and an inflammatory lesion of the anterior rectal wall, diagnosis?

Back 60

solitary rectal ulcer syndrome --> with an inflammatory polyps


An inflammatory polyp may ultimately form as a result of chronic cycles of injury and healing. Entrapment of this polyp in the fecal stream leads to mucosal prolapse. Thus, the distinctive histologic features are those of a typical inflammatory polyp with superimposed mucosal prolapse and include lamina propria fibromuscular hyperplasia, mixed inflammatory infiltrates, erosion, and epithelial hyperplasia

Front 61

macrocephaly, intestinal hamartomatous polyps, and benign skin tumors, typically trichilemmomas, papillomatous papules, and acral keratoses. A variety of other lesions derived from all three embryologic layers, including subcutaneous lipomas, leiomyomas, and hemangiomas, also occur, diagnosis?

Back 61

cowden syndrome

Front 62

harmartomatous polyposis with nail atrophy and splitting, hair loss, and areas of cutaneous hyperpigmentation and hypopigmentation, diagnosis?

Back 62

cronkhite-candada syndrome

Front 63

serrated architecture throughout the full length of the glands, including the crypt base, associated with lateral growth and crypt dilation, found in the right colon, diagnosis?

Back 63

sessile serrated adenoma - seperate from hyperplastic polyps (more commonly found in the left colon)

Front 64

How do tumors differ in their growth patterns from the proximal colon to the distal colon?

Back 64

Tumors in the proximal colon often grow as polypoid, exophytic masses that extend along one wall of the large-caliber cecum and ascending colon; these tumors rarely cause obstruction. In contrast, carcinomas in the distal colon tend to be annular lesions that produce “napkin-ring” constrictions and luminal narrowing

Front 65

tumor populated by immature cells derived from the basal layers of transitional epithelium

Back 65

basaloid - tumor populated by immature cells derived from the basal layers of transitional epithelium

Front 66

child has fusion of genes associated with ewing sarcoma and wilms tumor (EWS-WT1) --> t(11;22), what cancer will this cause?

Back 66

desmoplastic small round cell tumor of the peritoneum - aggressive tumor