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Presentation submitted by:
Abdul Rahman
17-Arid-754
4th Semester (Morning)
Presentation submitted to :
Sir Sohaib Kiyani
PMAS Arid Agriculture University, Rawalpindi
Contents
1. Histology of Esophagus:
Layers of Esophagus:
(i) Tunica Mucosa:
Epithelium, Lamina propria, Lamina muscularis mucosae
(ii) Tunica Submucosa
(iii) Tunica Muscularis
(iv) Tunica Adventitia
2. Histopathology of Esophagus
• Esophagitis
• Megaesophagus
• Esophageal Obstruction
• Cricopharyngeal achalasiais
• Esophageal diverticula
Histology of Esophagus:
 The esophagus connects the oral cavity
with the stomach allowing and aiding in
the movement of food particles to the
stomach.
 It is a muscular tube having the layers
described below for the typical tubular
organ.
 In the esophagus the layers are
specialized for the function of further
fragmenting food particles.
Layers of the esophagus
Tunica mucosa:
a) Lamina epithelialis (Epithelium): consists of stratified
squamous epithelium
Carnivores: Non-Keratinized
Pigs and horses: slightly Keratinized
Herbivores: Highly Keratinized
(b) Lamina propria: consists of loose connective tissue which often
has scattered lymph nodules esp. in pigs and humans
(c) Lamina muscularis mucosae: consists of smooth muscle;
distribution and continuity is highly species variable as follows:
(1) separate muscle bundles that fuse in horses, ruminants and cats,
(2) absent in cervical part in dogs,
(3) absent in pigs in cranial end but complete near the stomach)
Tunica submucosa:
It consists of loose connective tissue that is very elastic allowing for expansion
when food is present; ties the overlying epithelium to the underlying muscle
layers; seromucous glands present in most species and numerous in the dog
but absent in horses and cats. Lymphoid nodules may be present.
Tunica muscularis:
It consists of smooth and/or skeletal muscle; inner circular and outer
longitudinal layers usually begin as skeletal muscle at the cervical end
(voluntary control of swallowing) changing to smooth near the distal end close
to the stomach; skeletal muscle throughout in ruminants and the dog.
Tunica serosa/adventitia:
It consist of typical loose connective tissue that blends into the connective
tissue of surrounding tissues.
Esophagus
Histopathology of Esophagus
Clinically significant esophageal disorders generally manifest themselves as swallowing
dysfunction and regurgitation.
These disorders, found predominantly in small animals, can be classified as congenital
megaesophagus, vascular ring entrapment anomalies, and achalasia.
Esophagitis:
• Inflammation of the esophagus is usually caused by foreign bodies,
gastroesophageal reflux, and occasionally certain drugs (eg, doxycycline)
• Gastroesophageal reflux is usually associated with anesthesia, drugs that decrease
lower esophageal sphincter tone (eg, atropine, acepromazine), and acute or chronic
vomiting. Other causes of esophagitis include ingestion of an irritating or caustic
substance and neoplasia.
• Regurgitation is the classic sign of esophagitis; others include ptyalism, repeated
swallowing attempts, pain, depression, anorexia, dysphagia, and extension of the
head and neck.
• Endoscopy is the diagnostic tool of choice.
Megaesophagus:
 Enlargement and dilation of esophagus.
 Affect various mammalian species including man, dogs and cats.
 Congenital or may be Acquired
 Congenital megaesophagus results from developmental
anomalies in esophageal neuromuscular innervation that controls
dilation and peristalsis.
 Animal may develope Aspiration Pneumonia due to consistant
regurgetation i.e food enters the respiratory pathway.
 Causes of acquired megaesophagus: Myasthenia Gravis,
Esophageal Obstruction, Hypoadrenocorticism
 Symptoms: Halitosis: Extreme bad breath, nasal discharge,
consistant coughing, loss of appetite, fever, anorexia
 Diagnosis: X-rays, TPR (temperature, pulse and respiration),
endoscopy
Esophageal Obstruction
• Malformation in which the esophagus is interrupted and forms a blind ending pouch
rather than connecting to stomach
• Esophageal obstructions may be caused by a primary intraluminal obstruction, or they
may arise secondary to an extraluminal compressive mass or functional problem.
• The most common presenting signs are acute onset of excessive salivation, retching
(repeated flexion and extension of the neck), coughing, and copious discharge of
saliva from the nostrils.
• Affected horses often sweat excessively and appear distressed, but the body
temperature is usually normal.
• There may be a palpable swelling in neck in the jugular groove or over the trachea (if
the obstruction is in the cervical region). If the obstruction is in the cervical part of the
esophagus, most affected horses will retch immediately after attempting to swallow.
(There is often a 10- to 12-second delay between the swallow and the onset of
retching if the obstruction is in the distal esophagus.)
• The obstructing mass is usually food, especially dry pelleted food or dry sugar beet
pulp. The dry, fibrous material swells with the absorption of saliva, and an expanding
bolus occludes the esophageal lumen. Subsequent boluses compound the obstruction.
• Occasionally, foals and young horses may eat foreign bodies that lodge in the
esophagus and initiate an obstruction
Esophageal diverticula
• Outpouching comprised of all visceral layers
• Sites: Hypopharynx, Thoracic, Epinephrenic
• Congenital/ Embryological defect
• Small diverticula may not cause any clinical signs.
• In more severe cases, clinical signs may include impaction,
esophagitis, and rarely rupture and pyothorax.
• Treatment (if necessary) is by surgical resection.
• Esophageal diverticulae just cranial to the thoracic inlet may be
seen in English Bulldogs due to thoracic shortening and external
compression of the esophagus by other thoracic structures.
Pharyngeoesophageal
Diverticulum
Cricopharyngeal achalasiais:
• It is a failure of the upper esophageal sphincter (specifically,
the cricopharyngeal muscle) to relax during swallowing,
thereby preventing the normal passage of a food bolus from
the caudal pharynx to the cranial esophagus.
• Congenital or Acquired neuromuscular disorder
• Cocker and Springer Spaniels Dogs appear to be at increased
risk.
• Treatment of congenital achalasia is cricopharyngeal myotomy.
• Acquired achalasia is treated by addressing the inciting cause
and implementing dietary management.
• Lower esophageal sphincter achalasia is considered to be a
component of a more generalized esophageal motor
disturbance (ie, megaesophagus) and no longer a distinct
entity.
References:
• MERCK Mannual
Comparative histology and histopathology of ruminant esophagus

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Comparative histology and histopathology of ruminant esophagus

  • 1.
  • 2. Presentation submitted by: Abdul Rahman 17-Arid-754 4th Semester (Morning) Presentation submitted to : Sir Sohaib Kiyani PMAS Arid Agriculture University, Rawalpindi
  • 3. Contents 1. Histology of Esophagus: Layers of Esophagus: (i) Tunica Mucosa: Epithelium, Lamina propria, Lamina muscularis mucosae (ii) Tunica Submucosa (iii) Tunica Muscularis (iv) Tunica Adventitia 2. Histopathology of Esophagus • Esophagitis • Megaesophagus • Esophageal Obstruction • Cricopharyngeal achalasiais • Esophageal diverticula
  • 4. Histology of Esophagus:  The esophagus connects the oral cavity with the stomach allowing and aiding in the movement of food particles to the stomach.  It is a muscular tube having the layers described below for the typical tubular organ.  In the esophagus the layers are specialized for the function of further fragmenting food particles.
  • 5. Layers of the esophagus Tunica mucosa: a) Lamina epithelialis (Epithelium): consists of stratified squamous epithelium Carnivores: Non-Keratinized Pigs and horses: slightly Keratinized Herbivores: Highly Keratinized (b) Lamina propria: consists of loose connective tissue which often has scattered lymph nodules esp. in pigs and humans (c) Lamina muscularis mucosae: consists of smooth muscle; distribution and continuity is highly species variable as follows: (1) separate muscle bundles that fuse in horses, ruminants and cats, (2) absent in cervical part in dogs, (3) absent in pigs in cranial end but complete near the stomach)
  • 6. Tunica submucosa: It consists of loose connective tissue that is very elastic allowing for expansion when food is present; ties the overlying epithelium to the underlying muscle layers; seromucous glands present in most species and numerous in the dog but absent in horses and cats. Lymphoid nodules may be present. Tunica muscularis: It consists of smooth and/or skeletal muscle; inner circular and outer longitudinal layers usually begin as skeletal muscle at the cervical end (voluntary control of swallowing) changing to smooth near the distal end close to the stomach; skeletal muscle throughout in ruminants and the dog. Tunica serosa/adventitia: It consist of typical loose connective tissue that blends into the connective tissue of surrounding tissues.
  • 8. Histopathology of Esophagus Clinically significant esophageal disorders generally manifest themselves as swallowing dysfunction and regurgitation. These disorders, found predominantly in small animals, can be classified as congenital megaesophagus, vascular ring entrapment anomalies, and achalasia. Esophagitis: • Inflammation of the esophagus is usually caused by foreign bodies, gastroesophageal reflux, and occasionally certain drugs (eg, doxycycline) • Gastroesophageal reflux is usually associated with anesthesia, drugs that decrease lower esophageal sphincter tone (eg, atropine, acepromazine), and acute or chronic vomiting. Other causes of esophagitis include ingestion of an irritating or caustic substance and neoplasia. • Regurgitation is the classic sign of esophagitis; others include ptyalism, repeated swallowing attempts, pain, depression, anorexia, dysphagia, and extension of the head and neck. • Endoscopy is the diagnostic tool of choice.
  • 9.
  • 10. Megaesophagus:  Enlargement and dilation of esophagus.  Affect various mammalian species including man, dogs and cats.  Congenital or may be Acquired  Congenital megaesophagus results from developmental anomalies in esophageal neuromuscular innervation that controls dilation and peristalsis.  Animal may develope Aspiration Pneumonia due to consistant regurgetation i.e food enters the respiratory pathway.  Causes of acquired megaesophagus: Myasthenia Gravis, Esophageal Obstruction, Hypoadrenocorticism  Symptoms: Halitosis: Extreme bad breath, nasal discharge, consistant coughing, loss of appetite, fever, anorexia  Diagnosis: X-rays, TPR (temperature, pulse and respiration), endoscopy
  • 11.
  • 12. Esophageal Obstruction • Malformation in which the esophagus is interrupted and forms a blind ending pouch rather than connecting to stomach • Esophageal obstructions may be caused by a primary intraluminal obstruction, or they may arise secondary to an extraluminal compressive mass or functional problem. • The most common presenting signs are acute onset of excessive salivation, retching (repeated flexion and extension of the neck), coughing, and copious discharge of saliva from the nostrils. • Affected horses often sweat excessively and appear distressed, but the body temperature is usually normal. • There may be a palpable swelling in neck in the jugular groove or over the trachea (if the obstruction is in the cervical region). If the obstruction is in the cervical part of the esophagus, most affected horses will retch immediately after attempting to swallow. (There is often a 10- to 12-second delay between the swallow and the onset of retching if the obstruction is in the distal esophagus.) • The obstructing mass is usually food, especially dry pelleted food or dry sugar beet pulp. The dry, fibrous material swells with the absorption of saliva, and an expanding bolus occludes the esophageal lumen. Subsequent boluses compound the obstruction. • Occasionally, foals and young horses may eat foreign bodies that lodge in the esophagus and initiate an obstruction
  • 13. Esophageal diverticula • Outpouching comprised of all visceral layers • Sites: Hypopharynx, Thoracic, Epinephrenic • Congenital/ Embryological defect • Small diverticula may not cause any clinical signs. • In more severe cases, clinical signs may include impaction, esophagitis, and rarely rupture and pyothorax. • Treatment (if necessary) is by surgical resection. • Esophageal diverticulae just cranial to the thoracic inlet may be seen in English Bulldogs due to thoracic shortening and external compression of the esophagus by other thoracic structures.
  • 15. Cricopharyngeal achalasiais: • It is a failure of the upper esophageal sphincter (specifically, the cricopharyngeal muscle) to relax during swallowing, thereby preventing the normal passage of a food bolus from the caudal pharynx to the cranial esophagus. • Congenital or Acquired neuromuscular disorder • Cocker and Springer Spaniels Dogs appear to be at increased risk. • Treatment of congenital achalasia is cricopharyngeal myotomy. • Acquired achalasia is treated by addressing the inciting cause and implementing dietary management. • Lower esophageal sphincter achalasia is considered to be a component of a more generalized esophageal motor disturbance (ie, megaesophagus) and no longer a distinct entity.