GIT: Stomach

Question 1

glands in the ___ and ___ are mucus secreting

Answer 1

glands in the cardia and antrum are mucus secreting

Question 2

glands in the ___ and ___ (____) have chief cells which secrete ___ and parietal cells which secrete ____ and ____

Answer 2

glands in the corpus and fundus (oxyntic) have chief cells which secrete pepsinogen and parietal cells which secrete acid and intrinsic factor

Question 3

congenital hypertrophic pyloric stenosis is associated with ____, ____ and ____

Answer 3

congenital hypertrophic pyloric stenosis is associated with Turner syndrome, trisomy 18 and esophageal atresia

Question 4

congenital hypertrophic pyloric stenosis is caused by concentric ____ of ____

Answer 4

congenital hypertrophic pyloric stenosis is caused by concentric hypertrophy of circular muscular coat

Question 5

congenital hypertrophic pyloric stenosis is treated by ____

Answer 5

congenital hypertrophic pyloric stenosis is treated by surgery (myotomy)

Question 6

acute gastritis affects the ____

full thickness mucosal injury = _____

Answer 6

acute gastritis affects the superficial mucosa (loss of surface epi.)

full thickness mucosal injury = ulcers

Question 7

in acute gastritis, there is edema and congestion of the ____ and ____ are found in the surface epithelium and glands

Answer 7

in acute gastritis, there is edema and congestion of the lamina propria and neutrophils are found in the surface epithelium and glands

Question 8

endoscopy of a patient with chronic gastritis would show ____

Answer 8

endoscopy of a patient with chronic gastritis would show normal to patchy/diffuse erythema +/- hemorrhage to boggy with thick mucosal folds

Question 9

in chronic gastritis, ____ is found in the lamina propria

Answer 9

in chronic gastritis, inflammatory infiltrate (lymphocytes and plasma cells) is found in the lamina propria

Question 10

in chronic gastritis, ____ is found in the surface epithelium and glandular lumen

Answer 10

in chronic gastritis, PMNs is found in the surface epithelium and glandular lumen

Question 11

in chronic gastritis, ____ is found, mainly superficial, which is a maker of H. pylori infection

Answer 11

in chronic gastritis, reactive lymphoid aggregates is found, mainly superficial, which is a maker of H. pylori infection

Question 12

describe what H. pylori infection can lead to

Answer 12

Question 13

describe diagnosis of H. pylori (invasive vs. non-invasive)

Answer 13

Question 14

in autoimmune gastritis, there are autoantibodies to ____

Answer 14

in autoimmune gastritis, there are autoantibodies to parietal cell antigens/intrinsic factor

Question 15

in autoimmune gastritis, there is destruction of ___ glands which leads to ___ and ____

Answer 15

in autoimmune gastritis, there is destruction of oxyntic glands which leads to achlorhydria and increased gastrin levels

Question 16

in autoimmune gastritis, there is an increased risk for ___ and ____

Answer 16

in autoimmune gastritis, there is an increased risk for gastric carcinoma and neuroendocrine tumors (carcinoids)

Question 17

describe the effects of autoimmune gastritis

Answer 17

Question 18

gastric ulcers are caused by a loss of mucosa that extends through ____ or deeper

Answer 18

gastric ulcers are caused by a loss of mucosa that extends through muscularis mucosae or deeper

Question 19

describe acute gastric ulcers

Answer 19

Question 20

the pathogenesis of acute gastric ulcers is related to ____ and ____

Answer 20

the pathogenesis of acute gastric ulcers is related to systemic acidosis and hypoxia (severe trauma and burns) and vagal stimulation (intracranial lesions)

Question 21

list the sites of peptic ulcer disease

Answer 21

Question 22

list clinical features of a peptic ulcer

Answer 22

• clinical features:
  
  • burning epigastric pain 1-3 hours after meals
  • relieved by food and alkali
  • worse at night
  • associated weight loss
  • gastric outlet obstruction

Question 23

list complications of peptic ulcers

Answer 23

• complications:
  
  • bleeding
  • perforation
  • gastric outlet obstruction
  • malignant transformation:
    
    • unknown in duodenal ulcer and exceedingly rare in gastric ulcer

Question 24

a risk factor for ___ gastritis is severe burns, which causes ____

Answer 24

a risk factor for acute gastritis is severe burns, which causes Curling ulcer

caused by hypovolemia → decreased blood flow to stomach → blood can’t “sweep away” the acid or bring nutrients → acute gastritis

Question 25

a risk factor for ___ gastritis is increased intracranial pressure which leads to \_\_\_\_ explain how this occurs

Answer 25

a cause of **acute** gastritis is increased intracranial pressure which leads to **Cushing ulcer** increased intracranial pressure → increased vagal stimulation → increased ACh → binds to parietal cell and increases acid production

Question 26

describe the mechanism of NSAID injury

Answer 26

* inhibition of enzyme COX * rate limiting step in converting arachidonic acid to PGs * PGs protect gastric mucosa * maintain blood flow, increase mucus and bicarb. secretion and augment epithelial defenses * direct irritant * denudation of surface epi., increased mucosal permeability to ions

Question 27

intestinal gastric adenocarcinoma is associated with \_\_\_\_

Answer 27

intestinal gastric adenocarcinoma is associated with **H. pylori**

Question 28

diffuse gastric adenocarcinoma is caused by a mutation in \_\_\_\_

Answer 28

diffuse gastric adenocarcinoma is caused by a mutation in **E-cadherin**

Question 29

in diffuse gastric adenocarcinoma, ____ cells can be seen when the single cells proliferate (since they are detached from one another because of the mutation in E-cadherin)

Answer 29

in diffuse gastric adenocarcinoma, **signet ring** cells can be seen when the single cells proliferate (since they are detached from one another because of the mutation in E-cadherin)

Question 30

in diffuse gastric adenocarcinoma, there is a _____ appearance

Answer 30

in diffuse gastric adenocarcinoma, there is a **linitis plastica** appearance

Question 31

describe what is seen in the image

Answer 31

intestinal gastric adenocarcinoma

Question 32

describe what is seen in the image

Answer 32

diffuse gastric adenocarcinoma

Question 33

describe what is seen in the image

Answer 33

signet ring cells (diffuse gastric adenocarcinoma)

Question 34

early gastric carcinoma is confined to ___ and ___ regardless of \_\_\_\_

Answer 34

early gastric carcinoma is confined to **mucosa** and **submucosa** regardless of **involvement of regional lymph nodes**

Question 35

list clinical features of gastric adencarcinoma

Answer 35

* mostly asymptomatic in early stages * non-specific weight loss, anorexia, abdominal pain * pyloric outlet obstruction * prognosis depends upon depth of invasion and nodal status * **Krukenberg tumor**: bilateral ovarian spread * **Virchow node**: left supraclavicular lymph node

Question 36

gastrointestinal stromal tumors are derived from \_\_\_\_

Answer 36

gastrointestinal stromal tumors are derived from **cells of Cajal (the pacemaker cells)**

Question 37

describe the appearance of GIST

Answer 37

whorls and bundles of spindle-shaped or epithelioid cells

Question 38

\_\_\_\_ mutations are present in most GIST tumors

Answer 38

**Kit** mutations are present in most GIST tumors

Question 39

\_\_\_, a KIT inhibitor, is used for malignant GIST

Answer 39

**imatinib (Gleevec)**, a KIT inhibitor, is used for malignant GIST

Question 40

describe oral leukoplakia

Answer 40

* well-defined white patch or plaque caused by **epidermal thickening** or **hyperkeratosis**

Question 41

oral leukoplakia is associated with.... (3 things)

Answer 41

oral leukoplakia is associated with: * tobacco use * chronic friction (ill-fitting dentures) * HPV infection

Question 42

oral leukoplakia are (removed or not removed?) with scraping

Answer 42

oral leukoplakia are **not removed** with scraping

Question 43

oral leukoplakia range from ___ to \_\_\_\_

Answer 43

oral leukoplakia range from **benign epithelial lesions** to **highly dysplastic lesions**

Question 44

oral hairy leukoplakia is seen in patients with ___ and is caused by \_\_\_\_

Answer 44

oral hairy leukoplakia is seen in patients with **HIV** and is caused by **EBV**

Question 45

what words are used to describe oral hairy leukoplakia?

Answer 45

white, confluent, fluffy hyperkeratotic thickenings

Question 46

there (is or is no) malignant potential in oral hairy leukoplakia how does this differ from oral leukoplakia?

Answer 46

there **IS NO** malignant potential in oral hairy leukoplakia **oral leukoplakia has** **small** **chance of malignancy (there is dysplasia!)**

Question 47

describe erythroplakia aka erythroplasia

Answer 47

* red, velvety eroded area * poorly circumscribed * more atypical epithelial changes * typically marked dysplasia * malignant transformation in more than 50%

Question 48

what words are used to describe erythroplakia?

Answer 48

red, velvety, eroded area

Question 49

list the order of malignant potential seen in oral epithelial changes (oral leukoplakia, oral hairy leukoplakia, erythroplakia)

Answer 49

erythroplakia/erythroplasia \>\> oral leukoplakia NO malignant potential in oral hairy leukoplakia