Upper Gi Path, Exam 3

Front 1

What are most common causes of dental erosions?

Back 1

GERD!
Stages
acute esophagitis
benign structure
columnar metaplasia (Barrett's)
premalignant dysplasia, and adenocarcinoma

Front 2

What do you see in acute esophagitis?

Back 2

Lumen is getting smaller, you see a lot of redness.

Front 3

Barret's mucosa?

Back 3

You see tongue like projections projecting into the lumen that are salmon colored.

You can see white colored goblet cells above the gastroesophageal junction.
typically in normal GI tract, you see columnar epithelium but instead you find intestinal metaplasia.

Front 4

What are the findings of reflux esophagitis in acute, chronic, erosive and stricture stages?

Back 4

Acute: esoinophils, neutrophils
chronic: basal hyperplasia, long rete pegs
erosive: erosions and ulcers
stricture: fibrosis of lamina propria and submucosa

Front 5

Low Grade Dysplasia for Barrett's esophagus

Back 5

-flat or elevated, rarely polypoid
-hyperchromatic ovoid shaped nuclei
-little architectural distortion
-risk of malignant transformation
8-12%

Front 6

What do we find in high grade dysplasia and adenocarcinoma?

Back 6

you see sever cytoloical an architectural abnormality
-adenocarcinoma: same features as HGD but more of a infiltratin pattern.
-aneuploidy, p6 and p53 mutations are more frequent

Front 7

What procedure would you do if the adenocarcinoma extends beyond the submucosa?

Back 7

remove the esophagus
(esophagealectomy..)

Front 8

What are 2 types of carcinomas of the esophagus

Back 8

squamous (50%)
adenocarcinoma (50%)

Front 9

Describe H. pylori infections

Back 9

1. release enzymes such as urease that changes the pH to make it more favorable for the bacteria
2. has flagella
3. tissue specfici adhesins allows it to bind to mucosa easily

Toxic agents: Urea metabolites
Cytotoxins
Cag A related factors
vacuolating cytotoxin (50%)
Cytokines, IL-6,TNF, IL-8
Immune injury

Front 10

Relationship between H pylori and gastritis

Back 10

-causal relationship
-ingestion produces the lesion
-eradiaction imporves the histology

H. pylori gastritis: appears much more heavy. There's a lot of lymphocytic infiltration, multiple neutrophils together distinguishes moderate activity.

You can also see plasma cells

Front 11

Diagnostic tests of H. pylori

Back 11

Non-invasive: Serology, Breath tests
Invasive: urease
Histology: silver stain, giemsa stain, immunohistochemistry

Front 12

Name the patterns of injury and long term sequelae of H pylori infection

Back 12

1. antral gastritis, duodenal ulcer
2. multifocal atrophic gastritis
3. dysplasia and adenocarcinoma
4. malignant lymphoma

Front 13

Describe the stages of antral gastritis and duoedenal cancer

Back 13

H pylori colonization leads to diffuse antral gastritis
then to duodenitis
then to gastric metaplasia

The last 2 stages will result in duodenal ulcer

Front 14

Describe the development of MAG and peptic ulcer

Back 14

H pylori colonization leads to chronic gastritis, leading mostly to multifocal atrophic gastritis.
this can then lead to gastric ulcer

Front 15

Gastric dysplasia and adenocarcinoma

Back 15

intestinal metaplasia leads to low grade dysplasia... eventually to high grade dysplasia and adenocarcinoma

Front 16

Describe what you would see histologically with gastric mucosal dysplasia

Back 16

dysplasia: enlarged glands with enlarged stratified nuclei. This adenomatous appearance is identical to that seen in adenomas of the colon.

Front 17

What are 2 types of gastric carcinoma?

Back 17

Intestinal type: may see ulcerating, fungating, polypoid lesions

molecular genetic markers: MCC, APC, p53, EGFR

E cadherin (diffuse type)

Front 18

Gastric maltoma

Back 18

80% Gastric Lymphomas are Maltomas
B cell lymphomas, negative for CD5, CD 10
T lymphocyte growth factors (in response to HP antigens) dependent
50% respond to antibiotic treatment of HP
Failure to respond linked to Trisomy 3 and t(11;18) translocation

Front 19

Describe the development of gastric maltoma from H pylori infection

Back 19

H plyoria leads to MALT(mucosal associated lymphoid tissue)

H.Pylori infection is associated with lymphoid tissue in the mucosa of the stomach where it is normally absent.

MALT presence will leads to maltoma

Front 20

Name the virus, transmission, carrier stage, chronic stage, and whether or not it will develop hepatocellular carcinoma

1. Hep A
2. Hep B
3. Hep C
4. Hep D

Back 20

1. Hep A: RNA picorna virus, fecal oral, no carrier or chronic stage and will not develop HCC
2. Hep B: DNA hepadna, IV, is carrier stage, 5-10% chronic, HCC
3. Hep C: RNA flavi virus, IV, does have carrier, 70% crhonic and will develop HCC
4. Hep D: RNA, IV, does have carrier, 80% chornic

Front 21

Describe the lab diagnosis of Hepatitis infection

Back 21

Abnormal liver function tests
Serum viral antigens (B)
Serum viral nucleic acid assay(B,C,D,E)
Serum specific antibodies (A, B,C,D,E)
Liver Biopsy - Staging disease

Front 22

What are the histological features of acute viral hepatitis?

Back 22

lymphocytes, monocytes

Front 23

Massive hepatic necrosis

Back 23

Liver cells are destroyed, but liver itself is quite large

Front 24

Chronic viral heaptitis?

Back 24

You see piecemeal necrosis. Due to autoimmune hepatitis

Front 25

Cirrhosis of liver

Back 25

Macronodular. Liver cell plate is surrounded by nodule formation. This is part of the chronic stage that effects mutliple organs and cause hepatic encephalophaty, esophageal varices, splenomegaly,
hemorrhoids

Front 26

Describe hepatocellular carcinoma

Back 26

Males > Females
Single nodule > multinodular
Increasing incidence in US
Trabular-sinusuoidal architecture
No stroma
Angioinvasive
Molecular genetic profile
APC, b-catenin, p53

Especially in those with Hep C infection

Risk factors: viral hepatitis (especially C), aflatoxins, cirrhosis