Pathology-Upper GI Flashcards

1
Q

Congenital abnormality w/rule of 2’s

A

Meckel diverticulum: 2% of population, within 2 feet of ileocecal valve, 2 inches long, 2x more common in males, symptoms by age 2, 2 types of ectopic tissue (gastric or pancreatic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

A 2 week old boy presents with projective vomiting. What congenital abnormality in his stomach could be causing this?

A

Pyloric stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

A Down syndrome child presents with intestinal obstruction. What congenital abnormality happens in 10% of Down syndrome kids that would present this way? What would histology show?

A

Hirschprung disease. This is due to aganglionic megacolon (missing Meissner submucosal and Auerbach myenteric plexuses) from the cecum to the rectum. Histology will show hypertrophy of the nerve bundles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diverticulum above the upper esophageal sphincter that causes food accumulation and regurgitation.

A

Zenker Diverticulum (pharyngoesophageal diverticulum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When are you most likely to see esophageal stenosis?

A

Long standing acid reflux that causes fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Triad of achalasia

A

Incomplete LES relaxation, increased LES tone, aperistalsis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

A patient presents with incomplete LES relaxation, increased LES tone and aperistalsis. What infection could be causing his symptoms?

A

Chagas (trypanosoma cruzi). This causes destruction of the myenteric plexus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Before this patient died, the pathologist received a biopsy from his esophagus. What three things are necessary to diagnose this patient with reflux esophagitis?

A

1) Eosinophils 2) Increasing papillae 3) Expansion of the basilar layer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

A patient presents with GERD and is diagnosed with Barrett esophagus after biopsy. What would you expect to see on biopsy?

A

Metaplasia from squamous to glandular epithelium (specialized columnar epithelium with goblet cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What change comes after Barrett esophagus?

A

High grade dysplasia (top) and adenocarcinoma (bottom). Barrett esophagus is a premalignant lesion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are risk factors for adenocarcinoma in Barrett esophagus?

A

GERD, tobacco, p53, c-ERB B2, cyclin D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why is the 5 year survival rate < 25% in patients with esophageal adenocarcinoma?

A

There is no serosal layer in the esophagus and cancer can spread anywhere in the mediastinum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

A patient presents with dysphagia and no relief with high dose proton pump inhibitors. The patient has a history of allergic rhinitis and asthma. Esophageal biopsy is shown below. How would you treat the patient?

A

This is eosinophilic esophagitis, characterized by high numbers of eosinophils. Treat with dietary restrictions and steroids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Benign smooth muscle tumor of the esophagus

A

Leiomyoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Risk factors for squamous cell carcinoma in the upper esophagus

A

Alcohol, tobacco, poverty, injury, achalasia, Plummer Vinson, loss of p53, p16.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why does this type of esophageal cancer have a 5 year survival rate < 5%?

A

Squamous cell carcinoma is typically caught late and can spread out easily because the esophagus has no serosal layer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cells seen in acute gastritis vs. chronic gastritis

A

Acute: neutrophils. Chronic: plasma cells & lymphocytes. The picture below is chronic active gastritis due to presence of neutrophils in the glands in the setting of lymphocytes and plasma cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What things can initiate acute gastritis?

A

H. pylori, NSAIDs, Aspirin, cigarrettes, alcohol, hyperacidity and duodenal-gastric reflux can all diminish the mucus layer and cause epithelial damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Neutrophils in the epithelium

A

Active acute gastritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

A patient presents with persistent acid reflux. What is likely causing his condition?

A

Note the lymphocyte infiltrate indicating chronic gastritis. The most common cause of this is H. pylori.

21
Q

How do you know if this patient is at risk for a duodenal ulcer, gastric ulcer, intestinal metaplasia or gastric adenocarcinoma?

A

Note the “seagull” appearance in the section indicating H. pylori gastritis. If the H. pylori infection is in the antrum, they are at risk for duodenal ulcer. If the infection is in the body of the stomach they are at risk for gastric ulcer, intestinal metaplasia, dysplasia and gastric adenocarcinoma.

22
Q

What are patients at risk for when they have long standing H. pylori gastritis?

A

Malignant lymphoma. Often, if you treat the H. pylori, the lymphoma regresses.

23
Q

How do you differentiate between autoimmune gastritis and H. pylori gastritis?

A

H. pylori found in the antrum. Autoimmune found in the body. H. pylori infiltrate is mainly neutrophils and subepithelial plasma cells. Autoimmune is lymphocytes and macrophages. H. pylori has increased acid production. Autoimmune has decreased due to atrophy. H. pylori sequelae are peptic ulcers, adenocarcinoma and lymphoma. Autoimmune is atrophy, pernicious anemia, adenocarcinoma and carcinoid tumor.

24
Q

A patient presents with multiple stomach ulcers. Is this likely a stress ulcer or a peptic ulcer?

A

Stress. Peptic ulcers are typically caused by H. pylori and NSAIDs and are single in the antrum, duodenmu or esophagus.

25
Q

Why should you biopsy most ulcers? What are you looking for?

A

Tumors often ulcerate. Tumors will have raised, irregular margins with invasive carcinoma in the pitX. Peptic ulcers will have flattened margins with granulation tissue.

26
Q

Zollinger-Ellison syndrome

A

Uncontrolled gastrin release by tumor, increased acid and multiple peptic ulcers.

27
Q

How would you expect this ulcer to look on biopsy from this patient that died after the ulcer perforated the gastric wall?

A

Ulceration through the mucosa, submucosa and muscularis propria.

28
Q

What accounts for 2/3 of ulcer deaths?

A

Perforation. Bleeding accounts for 25% of deaths.

29
Q

What gastric polyps are benign and what polyps are malignant?

A

Benign: inflammatory polyps (from H. pylori) and fundic gland polyps (from PPI and glandular hypertrophy). Malignant: gastric adenoma

30
Q

What countries have the highest rate of gastric adenocarcinoma?

A

Japan, Chile, Costa Rica and Eastern Europe.

31
Q

What type of gastric adenocarcinoma is rising in the US?

A

Cardia, this is likely due to GERD and obesity. Gastric adenocarcinoma of the antrum of the stomach is low.

32
Q

A biopsy was taken from an ulcer in this patient’s stomach. What are risk factors for this condition?

A

Note the intestinal metaplasia indicating invasive adenocarcinoma. Risks for this include CHD1 (E-cadhedrin), FAP, p53, H. pylori (IL-1).

33
Q

How might you clinically diagnose someone with the stomach condition shown below?

A

Note the invasion of pointy glands indicating gastric adenocarcinoma. Palpation of a supraclavicular node (Virchow’s) or an umbilical node (Sister Mary Joseph node) can clinically indicate cancer.

34
Q

What would you expect to see on higher power of this image below?

A

This patient has diffuse gastric carcinoma called linitis plastica, characterized by signet-ring cells in the muscular layer. Note mucin vacuoles and no glandular formation.

35
Q

Well-differentiated neuroendocrine tumors found in the submucosa of the stomach that forms islets of cells and “salt and pepper” nuclei. What syndrome can this present with?

A

Carcinoid syndrome from carcinoid tumor cells secreting serotonin. This parallels serotonin syndrome with flushing, sweating, diarrhea and bronchospasm.

36
Q

Where would the tumor shown below be most aggressive?

A

Midgut. Carcinoid tumor has a good prognosis in the foregut and hindgut. Note the islets of cells and “salt and pepper” nuclei.

37
Q

What is the most common mesenchymal stomach tumor? How would it look on biopsy?

A

Gastrointestinal Stromal Tumor (GIST). It is a spindle cell tumor.

38
Q

Carney Triad

A

Occurs in children: GIST, paraganglioma and pulmonary chondroma.

39
Q

What increases your risk for GIST?

A

NF-1 and mutated tyrosine kinase (measured with c-kit or CD 117)

40
Q

Treatment for GIST?

A

Imatinib (tyrosine kinase inhibitor)

41
Q

Adenocarcinoma w/ovary involvement

A

Kruckenburg tumor

42
Q

Dry mouth in Sjogren’s

A

Xerostomia

43
Q

Traumatic, viral or bacterial inflammation of salivary glands

A

Sialadenitis

44
Q

Blockade of duct in salivary glands

A

Mucocele

45
Q

Characteristics of the most common salivary gland tumor

A

Pleomorphic adenoma (benign). Encapsulated tumor with mucin, epithelial or mesenchymal proliferation. Most are cured with resection but may recur.

46
Q

Characteristics of other benign salivary gland tumor

A

Warthin (Papillary Cystadenoma Lymphomatosum). Encapsulated epithelial cells on dense lymphoid stroma. Note the nuclei are apically arranged

47
Q

Characteristics of malignant salivary gland tumor

A

Mucoepidermoid carcinoma. Cords and sheets of squamous, mucus and intermediate cells. These are very aggressive tumors when they are high grade tumors.

48
Q

Which salivary gland is more common in men?

A

Warthin

49
Q

Where do most salivary gland tumors occur?

A

Parotid