Secretion is accomplished by glands located: 1. MUCOSA : 2. SUBMUCOSA : 3. EXTRAMURAL GLANDS :

glands located: 1. MUCOSA (stomach, small + large intestine) 2. SUBMUCOSA (only in esophagus, duodenum) 3. EXTRAMURAL GLANDS (Outside of the tubular gut - e.g., liver, pancreas)

Comprehensive review (1) Flashcards by Meghan May

Secretion is accomplished by glands located:

MUCOSA :
SUBMUCOSA :
EXTRAMURAL GLANDS :

glands located:

MUCOSA (stomach, small + large intestine)
SUBMUCOSA (only in esophagus, duodenum)
EXTRAMURAL GLANDS (Outside of the tubular gut
- e.g., liver, pancreas)

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Glands in esophagus

• Mostly in submucosa
• Primarily mucous secretion
• Note: upper and lower
esophagus also has
MUCOSAL glands (called
“cardiac” due to similarity to
cardiac glands of the
stomach)

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Name of glands located in upper and lower esophagus

cardiac glands

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Function of: Muscularis externa & Myenteric plexus (Auerbach’s plexus)

Controls contraction of muscularis externa; wave-like

contractions that move contents = peristalsis

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heart burn, dysphagia, achalasia, Barrets and esophageal cancer are common place in what region?

the Gastroesophageal junction

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Lack of peristalsis in the lower esophagus due to loss of myenteric neurons
(chalasis = relaxation)

achalasia

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Change in esophageal mucosa from squamous to “intestinal” (i.e. columnar)
Result of prolonged injury: e.g. chronic reflux, noxious agents (smoking, etc.)
“pre-cancerous:” 10% risk of progression to adenocarcinoma

Barrets esophagus

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Esophageal cancer: Squamous cell carcinoma –carcinogenesis of____ cells

basal

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–progression of Barrett’s esophagus into cancer or (rarely)

from submucosal glands

Adenocarcinoma

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inflammation and ulceration of mucosa

odynophagia

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difficulty swallowing) –

obstruction, deranged motor function

dysphagia

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Types of congenital anomailes in espohagus

Ectopic tissue – gastric, pancreatic
Duplication cysts
Atresias and fistulas
aspiration, suffocation from food
fluid and electrolyte imbalance

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Atresia occurs most commonly at or near the tracheal bifurcation and is usually associated with a_____ connecting the upper or lower esophageal pouches to a bronchus or the trachea

fistula

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Esophageal webs are Congenital or acquired
• GERD
• Occur in_____ esophagus
• Produce dysphagia

upper

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• Schatzki ring from esophageal rins:
 A ring____ the GE junction
 B ring ___the GE junction

above

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result of esophageal rings

Produces dysphagia

* Similar to a web but thicker and circumferential

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fibrious thickening of esophageal wall most often due to
inflammation and scarring that may be caused by chronic gastroesophageal reflux, irradiation, scleroderma, or caustic injury

Esophageal stenosis

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Symptoms and features of esophateal stenosis

Symptoms: dysphagia –>total obstruction
Features:
• Inflammatory scarring
• Atrophy and Fibrosis of muscularis propria and secondary epithelial damage

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Incomplete LES relaxation
Increased LES tone
Aperistalsis of the esophagus

features of achalasia

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Primary cause of achalasia

Idiopathic nerve abnormality

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Complications of achalasia

Squamous cell carcinoma (5%)
Candida esophagitis
Diverticula
Aspiration pneumonia

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What cancer can achalasia cause?

squamous cell carcinoma

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The following are all responsible for:
Nerve damage to
1. Trypanosoma cruzi
2. metastatic tumor
3. amyloidosis
4. sarcoidosis

Pseudoacalasia

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MOre common hiatal hernia

symptoms?S

Sliding esophageal, etiology often unknown, often asymptomatic

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Complications of hiatal hernia

* Ulceration * Bleeding * Perforation * Strangulation (paraesophagus)

Diverticulum just above the UES

Zenker diverticulum

etiology of Zenker diverticulum

Motor dysfunction Increased stress on wall GERD

Symptoms of Zenker diverticulm

Dysphagia Regurgitation Mass in neck Aspiration of contents

Diverticulum that occurs near midpoint of esophagus

Traction; scarring from mediastinal lyphadenitis, see motor dysfunx, increased stress on wall and GERD; IG asymptomatic

Diverticulum Occurs just above LES

Epiphrenic diverticulum

Etiology and symptoms of Epiphrenic Diverticulum

``` Etiology – Dyscoordination of peristalsis – LES relaxation • Symptoms – Massive nocturnal regurgitation ```

``` Longitudinal tears at the GE junction from severe wretching and/or vomiting • Seen in alcoholics • Hemorrhage • Accounts for 5-10% of UGI bleeding episodes ```

Mallory Weiss Syndrome

Occur secondary to portal hypertension most often d/t Alcoholism

Esophageal varices

What is the concerning part of esophageal varices?

Asymptomatic until they bleed – | massive hemorrhage

Veins involved in esophageal varices and mortality rate

Lower esophageal veins, mortality is 40-50%

Inflammation of the esophageal mucosa

Esophagitis

Etiology of esophagitis

 Reflux (GERD)  Mucosal irritants, alcohol, acid, alkalis  Infections, especially in immunosuppressed patients  Post radiation therapy  GVHD  Allergies (eosinophilic esophagitis)

``` All of the following can lead to: • Decrease LES tone • Sliding hiatal hernia • Delayed gastric emptying • Decreased reparative capacity ofesophageal mucosa ```

Gastroesophageal Reflux | Disease (GERD)

What are the sypmtoms of GERD

* Heartburn * Dysphagia * Regurgitation * Hematemesis or melana

What do we see with the lamina propria papillae in reflux

elongation of lamina propria papillae

What happens to the basal and supra-basal cells in reflux esophagiits

hyperplasia; shouldn't extend more then 15% of mucosa

What kind of chages do we see in the cells in reflux esophatitis?

reactive epithelial changes and mixed acute and chronic inflammatory cells in epithelium and lamina propria

Consequences of reflux

* Bleeding * Ulceration – perforation * Stricture development * Barrett’s esophagus

Pt presents with all the symptoms of GERD but don't respond to GERG therapy. ON endoscopy, you see rings in the esophgus.

Eosinophilic Esophagitis

If you see basal cell hyperplasia with over 20 eosinophils per field dx is

eosinophilic esophagitis

``` scattered intraepithelial eosinophils. Although mild basal zone expansion can be appreciated, squamous cell maturation is relatively normal. ```

reflux esophagits

``` Endoscopic evidence (velvet mucosa) at GE junction • “Intestinal metaplasia” of mucosa Single most important risk factor for esophageal adenocarcinoma ```

Barrets Esophagus

What type of cells are seen in intestinal metaplasia of Barrets

Goblet cells ~ should only be in intestine!!

Syptoms of esophageal carcinoma and prognostic factors

• Symptoms include dysphagia, weight loss • Prognostic factors – Depth of tumor – Nodal metastasis

Adenocarcinoma of esophagus are located near: | mean age?

arise near GE junction in Barrett’s esophagus | occurs after age 40, mean age 60

progression from normal esophagus to adenocarcinoma (w/ BE)

normal--> esophagitis--> Barrets--> Dysplasia in Barrets--> adenocarcinoma

Age and gender of sq cell carcinoma of esophagus

after 50 and male predominance from (2:1 to 20:1)

Histologic features of sq.cell carcinoma

keritanized nests!

FActors associated with devo os sq cell carcinoma

* Dietary * Lifestyle * Predisposing esophageal disorder * Genetics

Fundus has what cell types that secreate what?

Cheif cells--> pepsin | parietal cells--> acid

The cardia of the stomach secreaetes?

mucous via mucous cells

The antrum of stomach has what type of cells?

Mucous cells and G cells--> gastrin

Progressive hypertrophy of pyloric sphincter Presentation at 2-4 weeks of age male predominant and seen in 1:500 live births

Congenital Hypertrophic Pyloric | Stenosis

baby born with regurg and projective vomiting and dx with Congenital Hypertrophic Pyloric Stenosis. What would this look like grossly and what is in the vomit?

vomit has NO bile | grossly there would be a palpable mass and there would be visible peristalsis

Symptoms of gastritis

epigastric pain nausea vomiting hemorrhage

Hemorrage from gastritis could result in

- chronic anemia - melana - massive life threatening

Inflammation of the gastric mucosa

gastritis

What is responsible for acute gastritis?

```  NSAIDS  Excessive ethanol  Heavy smoking  Cancer chemotherapy agents  Ischemia and shock  Stress (severe, e.g. trauma, burns, surgery)  Uremia  Systemic infections  Suicide attempts (acid, alkali)  Mechanical trauma (NG tube “hickeys ```

Cell type seen in acute gastritis?

neutrophils

Stomach has Punctate erosions with dark adherent blood (acid | exposure); this is seen with

acute gastritis

What do we see on low power micrograph with acute gastritis?

– focal mucosal disruption with | hemorrhage

What happens with chronic gastritis, what can happen eventually?

mucosal inflammatory changes leading to atrophy and metaplasia • A set-up for dysplasia and neoplasia

Cell type seen in chronic gastritis?

Lymphocytes

Causes of Chronic gastritis

* Chronic infection (Helicobacter pylori) – most important (Type B) * Immunologic (in association with pernicious anemia) (Type A) * Toxic (ethanol, tobacco) * Post-surgery (e.g., partial gastrectomy)

Morphology of chronic gastritis

``` • Lymphocytic mucosal infiltrate  Neutrophils in epithelium, and gastric pits • Regenerative change • Metaplasia (intestinal) • Atrophy • Dysplasia ```

* Accounts for < 10% of chronic gastritis * Occurs in pernicious anemia * Autoantibodies

Autoimmune gastritis

AutoantiB in autoimmune gastritis are made against what?

 Parietal cells  Achlorhydria, hypergastrinemia  Intrinsic factor (pernicious anemia develops due to lack of absorption of vitamin B12)

Where in the stomach do we see autoimmune gastritis?

In the body-fundic mucosa, not antrum

What factors in H.Pylori set it to cause chronic gastritis?

urease, toxins, gastric acidity, peptic enZ d/t infection

What happens overtime with chrnoic gastritis from H.pylori

intestinal metaplasia, lymphoid aggregates, neurtophil infiltratres

How can we Dx H.Pylori infection?

* Detect urease in gastric biopsy * Radiolabeled urea breath test * Store antigen * Serologic tests * Demonstrate organism in gastricmucosa

Diseases associated with H.pylori

• Gastric MALT lymphoma: Definite etiologic role • Chronic gastritis:Strong causal association • Peptic ulcer disease: Strong causal association • Gastric carcinoma: Strong causal association

Comprehensive review (1) Flashcards

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