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GI > Esoph and Gastric Pathophys > Flashcards

Esoph and Gastric Pathophys Flashcards

1
Q

Esophageal Atresia

A

Esophagus closes before reachign stomach

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2
Q

Treacheal-esophageal fistula

A

Hole between the two structures

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3
Q

Duplication cyst

A

Embryologic abnormality where you have a pouch that is a duplication of the esophagus where food can get stuck, give bad breath, regurgitation

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4
Q

Duplication cyst increases your risk for…?

A

Increased risk for squamous cell carcinoma of the esoph due to stasis of food

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5
Q

Inlet patch

A

Patches of ciliated or gastric type epithelium in the esophagus of embryologic origin (since fetal esophagus is initially ciliated since its is derived from same embryonic origin as trachea)

-no consequences for pt

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6
Q

Esophagitis

A

Inflammatory injury to mucosal lining of the esophagus causing inflammation–neutrophils and eosinophils are never normal while lymphocytes are sometimes normal

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7
Q

Reflux esophagitis

A

Failure of LES causing gastric contents to come into the esophageal lumen. Often causes linear ulcerations

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8
Q

Herpes esophagitis

A

Ulcers caused by herpetic infection, generally only in immunocompromised people

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9
Q

Candida esophagitis

A

fungal infection that often causes white, cheesy plaques

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10
Q

Eosinophilic esophagitis

A

Allergic reaction that can be caused by food or seasonal allergies causing infiltration or eosinophils that can lead to rings and fibrosis of esophagus

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11
Q

Schatzki ring

A
  • Muscular ring covered by squamous epithelium

- One of the most common causes of dysphagia

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12
Q

Achalasia

A
  • Initially a hypermotility disorder where LES does not relax thereby impeding on the progression of food bolus into stomach.
  • Over time, esophagus dilates to accommodate inc pressure and food
  • This leads to food stasis, increasing risk of squamous dysplasia and squamous cell carcinoma progression
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13
Q

Scleroderma

A

Causes selective atrophy of inner circular muscle layer of muscularis propria (smooth muscle so it is just the distal part)

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14
Q

Mallory Weiss Tear

A

A rip in distal esophagus causing massive bleeding due to repeated wrenching vomiting

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15
Q

List the benign tumors

A
  • Papilloma
  • Granular cell
  • Mixed
  • Lieyomyoma
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16
Q

List the malignant tumors

A
  • Squamous and adenomcarcinoma
  • Malignant nerve sheath
  • ADenoid cystic
  • Lieyomyo-sarcoma
17
Q

Most common tumor worldwide vs US?

A

World: squamous cell carcinoma
USA: adenocarcinoma

18
Q

Risk factors for adenocarcinoma?

A
  • *obesity
  • reflux
  • diet
  • male
  • microbiome
19
Q

Precursor lesion for adenocarcinoma?

A

Barrett’s esophagus (intestinal metaplasia in esophagus)

20
Q

Long vs short segment of intestinal metaplasia

A
  • Short segments do not convert to long segments (ie length of metaplasia is static)
  • Risk of cancer is greater in long segment than in short segment Barett
21
Q

Risk factors for squamous cell carcinoma

A

Drinking, smoking, moldy foods, geography, achalasia, lye ingestion, NOT HPV

22
Q

Gastritis

A
  • Inflammatory disorder of stomach that can be acute (iron pills, NSAIDs etc) or chronic (h pylori, autoimmune)
  • Ulcers can bleed or completely perforate the stomach
  • With or without “Activity” means with or without neutrophils.
23
Q

What does atrophic gastritis mean?

A

Atrophic means loss of parietal and chief cells in the oxyntic mucosa.

Can lead to carcinoma/lymphoma

Most commonly caused by autoimmune disease

24
Q

Acute gastritis leads to…

A

Barrier/epithelial breakdown/bleeding and inflammation allowing HCL to back diffuse into the lamina propria

25
Q

Where does h pylori preferentially infect?

A

Antrum

  • binds to surface cells by receptors so need biopsy to see organism
  • with prolonged infection and injury, epithelium may undergo intestinal metaplasia and h pylori will migrate up
  • some inject toxic Cag A, which injures the cell
26
Q

Describe long term injury associated with atrophic gastritis

A
  • pH increases due so G cells produce more gastrin
  • Gastrin levels get too high trying to stimulate parietal cells, but there are none to stimulate
  • ECLs are still stimulated, so histamine is released and ECL cells proliferate causing carcinoid tumors
  • Also have decreased intrinsic factor (as well as acid) which leads to bacterial overgrowth and vitamin B12 deficiency, cancer and pernicious anemia
27
Q

Fundic gland polyps

A

Benign protrusions, no proliferation involved

28
Q

Hyperplastic gastric polyp

A
  • Benign, must define the underlying gastric pathology
  • Can be a source of bleeding, arise in gastritis setting
  • USually in antrum, but can be anywhere
  • Little neoplastic risk
  • Composed of inflamed and proliferating mucosa
29
Q

Why may gastric folds become enlarged?

A
  1. Lymphoma
  2. Gastric cancer
  3. MEtastatic breast lobular carcinoma
  4. Diffuse gastritis
  5. hypertrophic gastrophathies (true increase in gastric epith)
30
Q

Zollinger Ellison Syndrome

A
  • Gastrin secreting tumor causes expansion of parietal cell compartment and hypertrophy or folds
  • Increased acid production leads to gastric ulcers (not stomach ulcers since there is no perforation of epithelium)
  • Low pH inactivated pancreatic enzymes
31
Q

Extra nodal marginal zone b cell lymphoma

A
  • Most common lymphoma in the stomach

- H pylori causes lymphocytic response and these can transform

32
Q

Two types of gastric cancer

A
  1. Intestinal (Gland formation)

2. Signet rings (single cells)

33
Q

Pathogenesis of intestinal gastric cancer

A
  • Repeated injury/chronic gastritis (can be due to h py) leads to intestinal metaplasia, dysplasia, adenocarcinoma
  • Vit C protective as is vegetable consumption
  • No inc risk with alcohol use
  • Inc risk with processed meat due to N-nitroso compounds
  • Can present as a non-healing ulcer
34
Q

PAthogenesis of signet ring intestinal gastric cancer

A
  • No injury/gastritis, need two hit E cadherin mutation.
  • Associated with lobular breast cancer
  • Presents as giant folds or leather bottle stomach

GI (12 decks)

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