Module 2: GI: Barretts and Esophageal Cancers and Non-Neoplastic Stomach Lesions Flashcards

1
Q

The last non neoplastic condition of the esophagus is Barrett’s Esophagus, what is the etiology for this?

A

Long standing acid reflux esophagitis — GERD

  • -what causes GERD?
    1. obesity
    2. limited scleroderma (CREST syndrome–calcinosis, Raynaud’s phenomenon, esophageal dysmotility (GERD) , sclerodactyly, telangectasia)
    3. Anti-centromere positive
    4. Hiatal Hernia (sliding)
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2
Q

What is the presentation for Barrett’s Esophagus?

A

1.Heart Burn
2. Waterbrush (bad metallic taste of acid in the mouth)
3. Dyspepsia
4. Epigastric pain
5. Substernal discomfort relieved with antacids
(more common in whites)

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3
Q

The definitive diagnosis for Barrett’s Esophagus is an upper GI endoscopy with biopsy, what would the findings be?

A

Normal Epithelium: stratified squamous non-keratinized
Intestinal Metaplasia: Tall columnar with goblet cells as a protective mechanism
Endoscopy: normal pearly white esophageal squamous mucosa — velvety pink columnar mucosa (serpiginuos salmon colored patch)

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4
Q

What is the pathogenesis for Barrett’s Esophagus?

A

Decreased tone in the LES — genetic reprogramming of stem cells in the lower 1/3rd of the esophagus

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5
Q

What are the complications for Barrett’s Esophagus?

A

1 risk factor for intestinal dysplasia —- adenocarcinoma of the esophagus (always due to Barrett’s)

—most common in the US – almost always distal 1/3rd of esophagus and preceded by chronic acid reflux
–globally SCC of esophagus is more common
Progressive dysphagia and odynophagia – difficulty and painful swallowing
Melena — iron deficiency anemia

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6
Q

There are two neoplasms of the esophagus, Squamous Cell Carcinoma (SCC) and Adenocarcinoma. First we will discuss SCC. What is the etiology for SCC?

A

Chronic Alcoholism
Smoking
Plummer-Vinson Syndrome (Patterson Brown Kelly Syndrome)
Achalasia
p16,p53 and Rb mutations (tumor suppressor genes)

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7
Q

What is the pathogenesis for SCC?

A

Usually in upper 2/3rd of esophagus (middle 1/3rd to be specific)
–growth pattern: exophytic, excavated and infiltrative

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8
Q

What is the presentation for SCC?

A

Progressive dysphagia (initially solids than liquids due to gradual luminal narrowing)
Odynophagia
Cachexia
Fatigue (due to melena and iron deficiency anemia)

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9
Q

What demographic of the population presents with SCC?

A

Black and Asian Males greater than 50

–highest incidence in central Asia and Northern China

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10
Q

What are the two investigations done for SCC?

A

Barium Swallow: shows obstruction or narrowing of lumen (however need a Upper GI scope to confirm)
GI endoscopy w/Biopsy: malignant squamous cells invading into the submucosa and muscularis propria

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11
Q

In regards to SCC, explain the two histological slides 5c

A

Pic on left: Malignant squamous cells invading into the submucosa and muscularis propria. without keratin pearls so a worse dx
Pic on right: squamous cell whirls of keratin (Better prognosis because its well differentiated in function)

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12
Q

What is a complication of SCC?

A
  1. Obstruct — regurgitation —- aspiration pneumonia
  2. Bleeding — melena —- iron deficiency anemia
  3. Form a TE fistula (food can get into the lungs –aspiration pneumonia —- lung abscess)
  4. Can spread to cervical, mediastinal, paratracheal, tracheobronchial, gastric and celiac nodes depending on site of tumor
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13
Q

Now moving onto the next malignancy of the esophagus is Adenocarcinoma. What is the etiology for this?

A

Barrett Esophagus (due to chronic GERD) is the precursor lesion

  • -risk varies from 30 fold to 100 fold
  • -more common than SCC
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14
Q

What is the pathogenesis for Adenocarcinoma?

A

Usually in the lower 1/3rd of the esophagus

–growth pattern: multistep process through dysplasia

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15
Q

What is the presentation for Adenocarcinoma?

A
Progressive Dysphagia 
Odynophagia
Cachexia 
Fatigue (due to melena --- iron deficiency anemia) 
--commonly seen in white males
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16
Q

What investigations are done for Adenocarcinoma?

A

Barium Swallow: shows obstruction of lumen (need to confirm with scope)
GI endoscopy with biopsy: malignant glandular epithelium invading into the submucosa and muscularis propria

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17
Q

What are the complications of Adenocarcinoma?

A
Can obstruct (melena), perforate (mediastinitis) or form a TE fistula (food can get into lungs -- aspiration pneumonia --- lung abscess) 
--can spread to gastric and celiac nodes
18
Q

Now moving onto stomach lesions there are non neoplastic, neoplastic benign and neoplastic malignant. The first condition to discuss is a non neoplastic condition called pyloric stenosis, describe the features of the congenital condition.

A

Congenital: genetic pre-disposition

  • -more common in the first male child
  • -pathology: concentric hypertrophy of the circular muscle layer
  • -clinically: regurgitation, projectile vomiting, palpable epigastric olive like mass, visible peristalsis
  • -tx: myotomy
19
Q

What are some features of acquired pyloric stenosis?

A

Chronic Antral Gastritis
Peptic Ulcers
Malignancy

20
Q

Moving onto the next non-neoplastic lesion of the stomach is gastritis, chronic and acute. First lets start with acute, what is acute gastritis?

A

Acute/transient inflammation and injury of mucosa

21
Q

What are the predisposing factors for acute gastritis?

A
NSAIDS (inhibit PG synthesis) 
Excessive Alcohol 
Heavy smoking (impairs mucosal blood flow) 
Ischemic/shock
Severe stress (burns, surgery) 
Cancer chemotherapy 
Systemic Infections 
Uremia
22
Q

What is the presentation for acute gastritis?

A

May be asymptomatic

-may have epigastric pain, nausea, vomiting, hematemesis and melena

23
Q

What is the pathogenesis for Acute gastritis?

A

Mucosal erosion — loss of surface epithelium
Erosions with hemorrhage — acute erosive gastritis
Edema and congestion of lamina propria
Neutrophils in surface epithelium and glands

24
Q

Before we move onto chronic gastritis, what are diseases caused by H. pylori?

A
  1. Chronic Gastritis
  2. Extranodal Marginal Lymphoma of MALT type (MALToma) —present with abdominal pain, nausea, vomiting and weight loss. tx–with abx if no response tx with chemotherapy/rituximab
  3. Chronic Gastric Ulcer – has malignant potential
  4. Intestinal Gastric Adenocarcinoma
  5. Most common = Duodenal Ulcers (never become malignant and pain is relieved after eating)
  6. Affects the antro–pyloric region at the lesser curvature
25
Q

The next non-neoplastic syndrome we will discuss will be chronic gastritis: What is the etiology for chronic gastritis and most common location?

A

Chronic Gastritis:
Etiology: Chronic infection with H.pylori
Location: at the antro-pyloric region of the lesser curvature.

26
Q

What is the pathogenesis for H.pylori in chronic gastritis?

A

H. pylori produces urease ( cleaves urea and turns into ammonia to neutralize the acid) and phospholipase (destroys the phospholipid bilayer in the mucosa of the stomach)

  • –diffuse effacement of the mucosa by the lymphocytes this gives you chronic gastritis/peptic ulcers
  • -takes place in the antrum and pylorus because G cells are located here and H. pylori loves to destroy the G cells
  • -G cells make gastrin so therefore patients end up with hypogastrinemia (aka low gastrin levels because no G cells)
27
Q

What do you see on histology for chronic gastritis (slide 6a)?

A

Lymphoid Aggregates (can eventually lead to a MALTOMA which is b cell lymphoma in the mucosa)

  • -chronic inflammatory infiltrate (lymphocytes, plasma cells) in the lamina propria
  • -H. pylori is gram negative and non invasive so therefore thats why gastritis stays in the mucosa
  • -Addition of neutrophils when acute on chronic happens
28
Q

What investigations are done for chronic gastritis?

A
  1. Endoscopic biopsy with silvers stain: H. pylori appears black (slide 6a) with H and E (6a) cant see H. pylori (best investigation) (mainly see plasma cells, b cells and PMNS)
  2. Urea Breath Test and Stool Antigen: these are the best investigations if H.pylori is causing recurrent infections.
29
Q

What are complications for chronic gastritis?

A
  1. Chronic inflammation – intestinal metaplasia —- dysplasia —- intestinal gastric adenocarcinoma (in antrum and pylorus)
  2. Lymphoid aggregates — uncontrolled proliferation of B cells — MALTOMA (Gastric lymphoma) due to b cell aggregates in the mucosa
30
Q

Now we move onto autoimmune chronic gastritis which is a type II HSR at the fundus and body. What is the pathogenesis?

A

Body and Fundus is the location of parietal cells so damaging the parietal cells means no more negative feedback so constantly in a state of G cell hyperplasia (hypergastrinemia) and enterochromaffin (neuroendocrine) hyperplasia. no parietal cells means no acid which is why G cells are trying to produce more and more gastrin.

  • -no relief with antiacids
  • -etiology is autoimmune destruction by anti-parietal cell Ab
31
Q

What are the complications?

A
  1. Atrophic gastritis: fundus/body becomes antralized (aka no acid)
  2. Intestinal metaplasia – dysplasia —intestinal gastric adenocarcinoma (in fundus and body)
  3. G cell hyperplasia — increased gastrin and enterochromaffin levels – dysplasia — type I gastric carcinoid
  4. Pernicious Anemia (decreased intrinsic factor, decreased vit B12 and increased methylmalonic acid)
32
Q

Next topic are acute gastric ulcers, what is the etiology?

A
  1. Extensive Burns (curling ulcers)
  2. Head Injuries (cushing ulcers)
    (other causes: NSAIDs, alcohol, and stress)
33
Q

What is the pathogenesis for acute gastric ulcers?

A

Systemic acidosis and hypoxia with burns

Vagal stimulation in head injuries

34
Q

What is the histology for acute gastric ulcers?

A

Multiple, small and circular ulcers with no indurated bases

Gastric rugae are normal

35
Q

Now moving onto chronic gastric ulcers (peptic ulcers). What describe the gross image on slide 6b

A

Punched out ulcer with sharp and raised margin
–Rugae radiates like the spokes of the wheel due to fibrosis
(key signs it is chronic)

36
Q

What is the etiology for chronic gastric ulcers (peptic)?

A

H. pylori most common of the lesser curvature

–more common in lesser curvature but if happens in the greater curvature then there is a higher chance of malignancy

37
Q

In a chronic gastric ulcer ,describe the inflammation seen.

A

Inflammation extends beyond the mucosa

38
Q

What is the presentation for gastric ulcer?

A

Epigastric pain that worsens shortly after eating (So therefore these patients have weight loss)

39
Q

The more common location for an ulcer is the duodenal ulcer, what are the signs for duodenal ulcer?

A
  1. Etiology: H. pylori
  2. Pain gets better after eating
    - -dont avoid eating and hence dont lose weight unlike a gastric ulcer
  3. Acid is not entering the duodenum
  4. No risk of malignancy
40
Q

The best investigation for a gastric ulcer is an upper GI scope with biopsy, what would you see on biopsy?

A

Starting from the most superficial down
N: necrotic debris
I: inflammatory cells (lymphocytes, plasma cells, neutrophils if acute on chronic–patients who take NSAIDs)
G: granulation tissue (Angiogenesis + type III collagen)
S: scar (type I collagen)

41
Q

What are complications of chronic gastric ulcer?

A
  1. Bleeding — melena – iron deficiency anemia
  2. Obstruct — pyloric stenosis (projectile vomiting that is non bilious–no bile in the stomach with possible hematemesis)
  3. Perforate — peritonitis — sepsis—DIC
  4. Malignant — intestinal gastric adenocarcinoma