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Block D - Digestion and Metabolism > Pathology -- Diseases of the Upper GI Tract > Flashcards

Pathology -- Diseases of the Upper GI Tract Flashcards

1
Q

Most common cause of esophagitis

A

Reflux esophagitis – gastroesophageal reflux disease

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2
Q

3 infectious etiologies of esophagitis

A
  • Candida
  • Herpes simplex
  • Cytomegalovirus
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3
Q

3 miscellaneous causes for esophagitis

A
  • Radiation
  • Crohn’s disease
  • Graft-vs-host disease
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4
Q

3 causes of GERD

A
  • Abnormal tonus of lower esophageal sphincter
  • Hiatal hernia
  • Diabetic neuropathy
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5
Q

Symptoms of GERD

A
  • Asymptomatic
  • Heartburns
  • Dysphagia
  • Chest/epigastric pain
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6
Q

What does endoscpoic examination show in the event of GERD?

A

Erythema

In severe cases, erosins/ulcers

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7
Q

What can complicate GERD and what can it lead to?

A

Strictures –> development of Barrett esophagus

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8
Q

Treatment for GERD

A

Proton pump inhibitor treatment

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9
Q

Describe the histology of GERD

A
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10
Q

What leukocyte may appear intraepithelialy in GERD?

A

Eosinophils

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11
Q

Define esinophilic esophagitis

A

Allergic inflammatory disease of the esophagus

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12
Q

3 symptoms of eosinophilic esophagitis

A
  • Dysphagia
  • Food impaction
  • GERD-like symptoms
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13
Q

Describe the histology of esoinophilic esophagitis

A

Numerous intraepithelial eosinophils

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14
Q

What is a differential diagnosis with GERD?

A

Eosinophilic esophagitis

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15
Q

Differentiate between the location of effect of eosinophilic esophagitis vs. GERD

A

EE = entire esophagus

GERD = Distal esophagus

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16
Q

Differentiate between the quantity of intraepithelial esoniphils in EE vs. GERD

A

EE = numerous

GERD = Much fewer than EE

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17
Q

Differentiate between the treatments for EE vs. GERD

A

EE = corticosteroids

GERD = proton pump inhibitors

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18
Q

Who may be affected by herpes esophagitis?

A

May occur in otherwise healthy individuals, but usually seen with immunosuppression:

  • AIDS
  • Transplantation
  • Malignancies
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19
Q

Findings on endoscopy for herpes esophagitis

A

Vesicles followed by ulcers

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20
Q

5 microscopic findings for herpes esophagitis

A
  • Inflammation (neutrophils, histiocytes)
  • Cytopathic effect in epithelial cells
  • Ground glass viral inclusions
  • Multinucleation
  • Nuclear molding
21
Q

Define Barrett esophagus

A

Replacement of the normal squamous mucosa of the lower esophagus with columnar-type epithelium (intestinal metaplasia)

22
Q

Symptoms of Barrett esophagus

A

Since it’s secondary to GERD, clinical symptoms are those of GERD

23
Q

Endoscopic findings of Barrett esophagus

A

Mucosa of the BE is salmon-pink and velvety

24
Q

Potential consequence of Barrett esophagus

A

A minority of patients will develop esophageal adenocarcinoma (BE –> dysplasia –> adenocarcinoma)

25
Q

Describe the histology of Barrett esophagus

A

In this example, intestinal type simple columnar epithelium is present in the middle with frequent goblet cells. Squamous esophageal epithelium present to left and right

26
Q

Describe the histology of Barrett esophagus with low-grade dysplasia

A

In this example, squamous epothelium is to the left and glandular epithelium (adenocarcinoma) to the right. On lower power, the glandular epithelium is much darker than that of the intestinal metaplasia

27
Q

Why is the glandular epithelium of low-grade dysplasia in Barrett esophagus darker than that of regular Barrett esophagus

A
  • Lack of maturation = lesser cytoplasm
  • Nuclear enlargement
  • Nuclear stratification
28
Q

When is H pylori acquired

A

In childhood (causes perisistent infection in most people)

29
Q

Clinical manifestations of H Pylori

A
  • Asymptomatic OR dyspepsia AND/OR epigastric pain
  • May present with peptic ulcer
30
Q

How does H Pylori infect a patient?

A

By attaching to the mucosal epithelial cells (stained brown here)

31
Q

5 complications of H Pylori

A
  • Gastric atrophy
  • Intestinal metaplasia
  • Peptic ulcer
  • Gastric cancer (very strong association with the intestinal type of gastric cancer)
  • Lymphoma
32
Q

Describe the histology of chronic active gastritis secondary to H pylori infection

A
  • “Chronic” = plasma cells in lamina propria
  • “Active” = neutrophils infiltrating the lamina propria and glands
33
Q

Define autoimmune gastritis

A

Autoimmune process directed against gastric parietal and chief cells

34
Q

What does autoimmune gastritis lead to?

A

Chronic inflammation of gastric body with loss of parietal and chief cells –> Achlorhydria and megaloblastic anemia (secondary to deficient secretion of intrinsic factor)

35
Q

Define a peptic ulcer

A

Breach in the integrity of the mucosa extending beyond the muscularis mucosae

36
Q

Cause of peptic ulcer

A

Imbalance between the damaging forces and the defense mechanisms of the mucosa

37
Q

Give the 3 locations of peptic ulcer disease in decreasing order of frequency

A
  1. Duodenum
  2. Stomach
  3. Esophagus (in the setting of GERD)
38
Q

Define mucosal erosion

A

Smaller than a peptic ulcer; damage is limited to the mucosa

39
Q

Defense mechanisms to prevent peptic ulcers (4)

A
  • Surface mucus
  • Secretion of bicarbonate which maintains a higher pH within the mucus than in the gastric lumen
  • Epithelial regneration
  • Prostaglandins (reduce acid secretion, arguably cytoprotective)
40
Q

Damaging forces that can lead to peptic ulcer disease (7)

A
  • Gastric acidity
  • Peptic enzymes
  • H pylori infection
  • NSAIDs
  • Bile reflux into the stomach (duodenal-gastric reflux) – for gastric ulcers only
  • GERD – for cardia and lower esophageal ulcers
41
Q

3 macroscopic features of peptic ulcer disease

A
  • Regularly shaped walls, margins at the same level with the surroudning mucosa (“punched out” ulcer)
  • Clean sometimes hemorrhagic base
  • Gastric folds reach the edge of the ulcer
42
Q

Most important differential diagnosis for peptic ulcers

A

Ulcerated tumor (most frequently, an ulcerate adenocarcinoma)

43
Q

Why is the differential diagnosis for peptic ulcers especially important in the stomach?

A

Duodenal neoplasias are very rare and duodenal ulcers are almost always peptic in nature

44
Q

What does the differential diagnosis for peptic ulcer disease depend on?

A

Endoscopic features

Microscopy

45
Q

Differentiate between the size of a peptic ulcer vs. an ulcerated tumor

A

PU = usually small (<2 cm)

UT = usually large (>2 cm)

46
Q

Differentiate between the shape of a peptic ulcer vs. an ulcerated tumor

A

PU = Round to oval, regular “punched out” borders

UT = More irregular in shape

47
Q

Differentiate between the borders of a peptic ulcer vs. an ulcerated tumor

A

PU = edges at the same level with surrounding mucosa or just slightly elevated

UT = elevated, thick borders

48
Q

Differentiate between the base of a peptic ulcer vs. an ulcerated tumor

A

PU = smooth and clean

UT = irregular and necrotic

49
Q

Differentiate between the formation of a peptic ulcer vs. an ulcerated tumor

A

PU = imbalance between defensive and damaging forces

UT = tumor forms in epithelium and grows –> becomes necrotic and the pus drains/pieces break off

Block D - Digestion and Metabolism (29 decks)

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