Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Gastrointestinal Block > L08-Pathology of the oeso and cardia > Flashcards

L08-Pathology of the oeso and cardia Flashcards

1
Q

Oesophagus normal histology

A
  • muscular walls to convey chewed food from pharynx to the stomach
  • stratified squamous nonkeratinizing epithelium to withstand abrasion
  • esophageal cardiac glands (simple tubular, mucous) in lamina propria (near stomach) and submucosal esophageal glands proper eases the passage of ingested food
  • substantial muscularis mucosae
  • muscularis externa:

o striated muscle in the upper third
o smooth muscle in the lower third
o mixed in the middle third

  • physiologic muscular sphincters at two ends of esophagus: pharyngoesophageal and the gastroesophageal sphincters
  • adventitia as the outermost layer (since retroperitoneal)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Esophagus-spectrum of pathologies

A

 Congenital anomalies
 Inflammation (esophagitis)
 Barrett’s esophagus
 Neuromuscular dysfunction
 Neoplasia
 Miscellaneous

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

Esophageal Congenital anomalies

A
  • Atresia
  • tracheo-esophageal fistula
  • stenosis
  • absence
  • duplication

* All congenital anomalies of oesophagus are rare

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

Esophageal atresia and TE Fistula classification

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

Recgnizing esophageal atresia and TE fistula

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

Classes of Esophagitis

A

1) Reflux esophagitis

2) Infective esophagitis

  • Fungal (Candidiasis, mucormycosis, aspergillus)
  • Viral (Herpes simplex virus, cytomegalovirus)

3) Others

  • irritants (alcohol, corrosive acids or alkalis in suicidal attempts), radiation, cytotoxic drugs, prolonged gastric intubation, achalasia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Reflux esophagitis (definition, symptoms, causes, complications)

A

Reflux esophagitis occurs via frequent and protracted reflux of gastric contents in the esophagus.

Symptoms: heartburn and regurgitation

Causes:

  • incompetence of the lower esophageal sphincter
  • Increased intra-abdominal pressure
  • Abnormal upper gastro-intestinal motility
  • often associated with a sliding hiatus hernia

Complications:

  • acute oesophagitis
  • may be complicated by ulceration which, when healed, may lead to circumferential fibrosis and stricture formation
  • may be complicated by Barrett’s esophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Reflux oesphagitis endoscopy and microscopy

A

Endoscopy:

  • Inflammation ->Diffuse reddish mucosal surface

Microscopy:

  • Increased polymorphs
  • Squamous epithelium hyperplasia
  • (above two both as the consequences of inflammation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hiatus Hernia (definition, causes, complications)

A

The protrusion (or herniation) of the upper part (cardia) of the stomach into the thorax through a tear or weakness in the diaphragm.

Causes:

  • Increased intra-abdominal pressure (Obesity, heavy lifting, frequent or hard coughing, etc)
  • incompetence of the lower esophageal sphincter (e.g. loss of diaphragmatic muscular tone with ageing)

Complications:

  • reflux oesophagitis
  • Ulceration at the level of diaphragm as the point is under constant pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Infective esophagitis

A

1) Fungal esophagitis

  • Candida, Aspergillus, Mucor
  • in debilitated / immunocompromised patients

2) Viral esophagitis

  • herpes simplex virus, cytomegalovirus

Biopsies help confirm the diagnosis

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

Fungal oesophagitis (pathogen, endoscopy and microscopy)

A

Candida, Aspergillus, Mucor (usu, in debilitated / immunocompromised patients)

Endoscopy:

  • Inflammation ->Diffuse reddish mucosal surface
  • similar to that of reflux oesophagitis

Microscopy:

  • presence of yeasts and hyphae
  • polymorph aggregation
  • A ‘pseudomembrane’ is present (top) on the surface of the stratified squamous epithelium. It consists of desquamated epithelial cells and thin filament-like fungi.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Herpes oesophagitis (pathogen, microscopy)

A

Caused by Herpes Simplex Virus (HSV)

Microscopy:

  • Aggregates of microphage
  • HSV Viral inclusion bodies
  • multinucleated epithelial cells with ground-glass nuclei and margination of the chromatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cytomegalovirus oesophagitis (Pathogen, microscopy)

A

Caused by cytomegalovirus

Microscopy:

  • Enlarged nucleus
  • large intranuclear inclusion body surrounded by a clear halo
  • Basophilic inclusions are seen also in the cytoplasm.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Other esophagitis (causes)

A

Causes include:

  • ingestion of irritants (alcohol, corrosive acids or alkalis in suicidal attempts)
  • radiation
  • cytotoxic drugs
  • prolonged gastric intubation
  • achalasia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Barrett’s esophagus (Location, Cause, Presentation, Complications, Clinical Considerations)

A

Location: At lower end of esophagus

Cause: A result of prolonged esophageal reflux

Presentation:

  • Barrett’s esophagus appears as a red or pinkish, velvety mucosa. Surface and inner surface of esophagus changed from normal white to pink with white patches
  • The distal esophageal squamous mucosa is replaced by metaplastic glandular columnar epithelium containing goblet cells (which is more resistant to gastric juice)
  • The epithelium could be gastric, intestinal or mixed in composition.
  • Presence of intestinal metaplasia(intestinal epithelium, glandular formation, goblet cells) are regarded as a hallmarks of Barrett’s esophagus.

Complications:

  • dysplasia
  • Peptic ulcer
  • carcinoma (adenocarcinoma at lower 1/3 of esophagus)

Clinical Considerations:

Therefore, critical to the pathologic evaluation of patients with Barrett’s mucosa is the recognition of associated dysplasia, obtained by endoscopy with biopsy and histological examination. High-grade dysplasia demands clinical intervention as it may progress to adenocarcinoma.

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

Pathological relationship between peptic ulcer, gastric reflux & Barrett’s oesophagus

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

Achalasia (Overview, clinical presentation, pathophysiology, epidemiology, complications, etiology)

A

Overview

A neuromuscular dysfunction of Lower esophageal Sphincter, aka cardiospasm; failure to relax

It is characterized by failure of relaxation of the lower esophageal sphincter (LES) during swallowing, resulting in consequent dilation of the esophagus above the level of the LES.

Clinical presentation:

  • Progressive dysphagia
  • Regurgitation
  • Absence of peristalsis (aperistalsis)
  • Incomplete relaxation of the LES

Pathophysiology: decreased number or complete absence of myenteric ganglion cells is observed in the esophagus proximal to the LES. This results in loss of intrinsic inhibitory innervation of the LES and smooth muscle coat of the esophagus. The esophagus becomes dilated, fibrotic and thickened.

Epidemiology:

In middle life, young adulthood, infancy or childhood

Complications:

  • chronic esophagitis
  • aspiration pneumonia
  • predisposition to malignant change

Etiology:

  • Idiopathic primary disorder (most casses)
  • Secondary achalasia are due to damage to neuromuscular system related to:
  • infection (Trypanosoma cruzi [Chagas’ disease])
  • metabolic disease (amyloidosis, diabetes)
  • surgery
  • tumour, etc.
18
Q

Mallory-Weiss Syndrome

A

Lacerations (tears/cuts) at the esophago-gastric junction, leading to bleeding and hematemesis

usually caused by severe alcoholism, eating disorders, coughing, or vomiting

19
Q

Esophageal varices

A

Extremely dilated sub-mucosal veins in the lower third of the esophagus

Occur in patients with portal hypertension (mostly due to liver cirrhosis) at the lower end of the esophagus; give rise to fresh hematemesis when the varices rupture on slight trauma.

20
Q

Diverticulum of the esophagus

A

Diffuse esophageal spasm can cause small pseudo diverticulae (small mucosal outpouchings) to form.

May accumulate significant amounts of food, producing a mass and regurgitation.

21
Q

Neoplasia of esophagus (subtypes)

A

PRIMARY

Benign

  • squamous papilloma
  • lipoma
  • leimyoma

Malignant

  • Squamous cell carcinoma (SCC; commonest)
  • Adenocarcinoma (in lower 1/3; Barrett’s esophagus)
  • Small cell carcinoma

SECONDARY

  • From adjacent structures e.g. larynx, lung
22
Q

Benign esophageal tumour Presentation

A
  • Often small and asymptomatic.
  • The importance lies in their distinction from malignant tumors.
23
Q

Location of benign esophageal tumours

A
24
Q

Benign esophageal tumour gross appearance

A
  • Smooth contour and surface (no mucosa proliferation)
  • Well-defined border
25
Q

Esophageal Cancer epidemiology

A
  • Sex: male predominance
  • Age: peak age at the 6th and 7th decades
  • ranks 8 among the world’s most common cancers
  • relatively uncommon neoplasm in western countries
  • much more prevalent in the Chinese populations(China, Singapore and Hong Kong)
  • The marked differences in epidemiology strongly implicate dietary and environmental factors, with an ill-defined contribution from genetic predisposition.

In Hong Kong:

  • ranks 8th for all cancer deaths (5th in men and 13th in women)
26
Q

Esophageal cancer etiology

A

Risk Factors include:

  1. Diet - MAIN FACTOR; Restricted diet of cornmeal and pickled vegetable, nitrosamine, trace elements deficiency, fungal contaminants
  2. Chronic alcoholism and tobacco smoking
  3. Esophageal disorder: e.g. achalasia
  4. Genetic predisposition
    (5. Barrett’s esophagus - for adenocarcinoma not SCC)
27
Q

Esophageal cancer gross appearance

A

- Polypoid or fungating

- Ulcerative - everted/heaped up edges(commonest)

- Sclerosing or constrictive

* In some of the cases, the edges of ulcer will appear black indicating necrosis

28
Q

Spread of CA esophagus

A

1) Direct - to lungs, trachea and aorta

2) Lymphatic spread

  • spread to regional lymph nodes
  • submucosal spread, forming submucosal and intramuscular satellite nodules

3) Hematogenous spread

  • to lungs, liver, brain, etc
29
Q

SCC as a subtype

A
  • Squamous cell carcinoma is the commonest tumor of the esophagus.
  • It accounts for approximately 90% of malignant tumors.
  • This histological subtype is more common in Chinese populations.
30
Q

SCC location

A

Upper esophagus: 17%

Middle esophagus: 50% (most common)

Lower esophagus: 33%

31
Q

SCC (and esophageal cancer in general) Clinical Features (symptoms)

A
  • It invades locally, causing obstruction.
  • The most common symptoms are **progressing dysphagia **caused by constriction and obstruction
  • May infiltrate into the trachea to form fistula, with subsequent aspiration pneumonia
  • May infiltrate the aorta causing massive bleeding
32
Q

SCC Etiology

A
  1. Diet - MAIN FACTOR; Restricted diet of cornmeal and pickled vegetable, nitrosamine, trace elements deficiency, fungal contaminants
  2. Chronic alcoholism and tobacco smoking
  3. Esophageal disorder: e.g. achalasia
  4. Genetic predisposition
33
Q

SCC Staging

A

clinicopathological staging of the tumors is the most important prognosis determinant

Classified into Stage 1 to 5 based on:

  • lymphatic infiltration
  • hyperaemia
  • fibrosis
34
Q

SCC microscopy

A
  • nests of malignant cells that partially recapitulate the organization of squamous epithelium.
  • Subtyped into well, moderately and poorly differentiated squamous cell carcinoma depending on histological parameters like presence of intercellular bridges, keratin pearls and differentiation of cells in the tumor cells.
35
Q

SCC Characteristic features

A

1) Lymphatic Spread

  • has a particular tendency to spread by lymphatics in the submucosa and muscles of the esophagus and forms multiple tumor nodules in the esophagus.

2) Multiple tumours

  • 10%
  • multiple neoplastic lesions are common in the esophagus as well as other parts of the upper aerodigestive tract
  • e.g. tongue, hypopharynx, larynx and esophagus.
  • Synchronous (same time) and metachronous (different times)
36
Q

esophageal adenocarcinoma

A

Epidemiology:

  • rare in Hong Kong.
  • continuing rise in the prevalence of this cancer in the western populations

Etiology:

There is a link between Barrett’s esophagus and adenocarcinoma as a complication of gastroesophageal reflux disease.

37
Q

Small cell carcinoma of esophagus

A
  • A neuroendocrine tumour
38
Q

Secondary tumours of esophagus

A

The esophagus may be infiltrated by tumors in the adjacent structures like the larynx and lung.

39
Q

Carcinoma of the gastroesophageal junction

A
  • Adenocarcinoma is the most common tumor in this region.
  • center within 5 cm proximal and distal to the anatomical gastroesophageal junction
  • may be adenocarcinomas of distal esophagus, adenocarcinoma of the cardia or subcardial adenocarcinoma that infiltrates to this region
  • Histologically divided into well, moderately and poorly differentiated depending on histological features such as the degree of glandular differentiation.
  • There is a link between Barrett’s esophagus and adenocarcinoma as a complication of gastroesophageal reflux disease.
40
Q

Clinical significance of cardia

A

Cardia is the narrow portion of the stomach immediately distal to the gastroesophageal junction. Because of the borderline location between the esophagus and stomach, the lesions here include both lower esophageal (e.g. adenocarcinoma) and gastric (e.g. tumors, gastritis and peptic ulceration) pathologies

Gastrointestinal Block (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions