PATHOLOGICAL

PHYSIOLOGY OF SHIVANI LAL

ESOPHAGUS
ANATOMY ESOPHAGUS
 STRUCTURE

FOOD PIPE
25cm long fibro muscular tube [8 10cm at birth]
Travels behind trachea
Connects pharynx and stomach
Lower border of cricoid cartilage to cardiac orifice of stomach
2 gentle curves
 SPHINCTERS

Upper sphincter/pharyngoesophageal sphincter

Separates pharynx from esophagus
Prevents entry of air into esophagus and stomach during respiration
3cm in length
Circular layer of striated muscle
3 skeletal muscle groups
Lower sphincter/cardiac sphincter/ gastroesophageal
sphincter
Located near hiatus
Prevents regurgitation from stomach
3cm in length
Circular muscle remains tonically contracted: zone of high pressure
External skeletal muscle
Internal smooth muscle
HISTOLOGY ESOPHAGUS
 LAYERS

4 LAYERS
Tunica Mucosa
Stratified squamous non-keratinised
epithelium
Lamina propria
Loose connective tissue
Mucous glands
Small blood vessels
Lymphatic nodules
Muscularis mucosae
Thin layer of smooth muscle
Tunica Submucosa
Thick layer of connective tissue
Mucous [esophageal] glands [branched
tubular]**
Larger branches of blood vessels and nerves
 LAYERS

Tunica Muscularis Externa

Inner circular layers
Outer longitudinal layers
Upper 1/3: striated
Middle 1/3: inner smooth,
outer striated
Lower 1/3: smooth
Tunica Adventitia
layer of connective tissue
merges with surrounding
Blood vessels
Nerves
 CARDIA

Esophago-gastric
junction/cardio-esophageal
junction
Stratified squamous non-
keratinised epithelium -> simple
columnar epithelium
Lamina propria of cardiac mucosa
contains larger accumulation of
lymphoid tissue [lymphatic
follicle]
Cardia
Mucosa forms pits and cardiac
glands
Mucus secreting cells
PHYSIOLOGY ESOPHAGUS
 SWALLOWING

Oropharyngeal phase [voluntary]

Segmentation into bolus [O]
Food moved posteriorly [O]
Superior constrictor muscle contracts [P]
Epiglottis tilts backwards [P]
Respiration is halted
MOTOR IMPULSES: TRIGENMINAL, GLOSSOPHARYNGEAL, VAGUS AND
HYPOGLASSAL NERVE
Esophageal phase [involuntary]
Walls stretch = peristalsis is triggered
Contraction and relaxation pushes bolus
down tube
Lower sphincter relaxes
5 10 seconds
MOTOR IMPULSES: VAGUS NERVE
 PERISTALSIS MOVEMENTS

Swallowing leads to upper esophageal sphincter reflexively

opening
Peristalsis is stimulated when af ferent fibers sense changes
in wall tension caused by stretching
The greater the tension, the grater the intensity of the
esophageal contraction
Intense contractions cause pain similar to heart burn and
angina
 PRIMARY AND SECONDARY

Primary peristalsis
Controlled by swallowing center in brain stem
Continuation of peristaltic reflex wave that begins in pharynx
Spreads into esophagus during pharyngeal stage of swallowing
Secondary peristalsis
Partially mediated by smooth muscle fibres
If bolus/food becomes stuck in lumen [primary is inadequate],
distention of wall stimulates 2ndary peristalsis
Movement continues until all food moves into stomach
 LES

Relaxation of the lower esophageal sphincter is a brain stem

reflex that is mediated by the Vagus nerve
Pressure within sphincter drops from 20 -25mmHg during
relaxation
LES is usually closed: BARRIER AGAINST REFLUX
Harmful gastric juices : pepsin and HCL
Barrier is strengthened when sphincter pressure is increased by
Acetylcholine [from myenteric plexux]
Hormones [gastrin, motilin, somatostatin, substance P]
Protein rich food
Circular muscles of distal esophagus: INTRINSIC FUNCTION
Portion of diaphragm surrounding LES helps maintain zone of
high pressure: EXTRINSIC FUNCTION
Increased parasympathetic stimulation increases constriction of
sphincter
Gastrin also increases constriction of sphincter [stimulus from
gastric acid production therefore protects esophageal mucosa]
PATHOPHYSIOLOGY GERD
 GASTROESOPHAGEAL REFLUX DISEASE
[GERD]
Long term reflux of acid and pepsin from stomach
Causes esophagitis, esophageal strictures and Barretts
esophagus
Risk factors: obesity, hiatal hernia, LES relaxing drugs
[anticholinergics, nitrates, calcium channel blockers, nicotine]
GERD with no symptoms = physiologic reflux
Non-erosive reflux disease [NERD] = Symptoms but no injury
 CAUSES OF GERD

Vomiting, coughing, lifting, bending or obesity

increases abdominal pressure, contributing to
development of reflux esophagitis
LES failure and hiatal hernia
Zollinger-Ellison syndrome: gastrin secreting
tumor of pancreas
Increased blood calcium levels = increased
gastrin production
Systemic scleroderma: AI disease of C.T. =
thickening of skin caused by accumulation of
collagen
Delayed gastric emptying:
Lengthens period during which reflux is possible
Increases acid content of chyme
Disorders that delay emptying
Gastric ulcers or duodenal ulcers = pyloric edemas
Strictures = narrow pylorus
Hiatal hernia = weakens LES
 GERD CAN LEAD TO

GERD leads to inflammatory responses

in esophageal wall resulting in
Hyperemia
Edema
Tissue fragility
Erosion
Ulceration
Severity of inflammation depends on
Composition of gastric contents
Length of exposure
Fibrosis, basal cell hyperplasia and
elongation of papillae are common
Precancerous lesions with progression
to adenocarcinoma [long term
consequence]
Barretts esophagus
 SYMPTOMS & CLINICAL MANIFESTATIONS
Acid taste in mouth and bad breathe
Heart burn from acid regurgitation
Vomiting [sometimes blood]
Wearing away of teeth
Chronic cough
Asthma attacks and other breathing problems
Laryngitis
Upper abdominal pain within 1 hour of eating [relapsing and
remitting]
Heartburn experienced as chest pain
Edema
Fibrosis and esophageal bleeding
Esophageal spasms or decreased esophageal motility may result
in dysphagia
Alcohol or acid containing foods cause discomfort during
swallowing
 DIAGNOSIS

10 20% af fected in west

Esophageal endoscopy:
Hyperemia: excess of blood
Edema: accumulation of fluid in interstitium
Erosion
Strictures: narrowing of esophagus
Dysplastic changes [Barrett esophagus] confirmed in tissue biopsy
Ulceration
Impedance/pH monitoring measures movement of gastric
juices upwards, and acidity of refluxuate
Esophageal manometry:
Measures pressures and pattern of muscle contraction in esophagus
 TREATMENT

Medication
Proton pump inhibitors: decrease gastric acid production [kids,
persistent reflux]
Histamine-2 receptor antagonists: block histamine at histamine H2
receptors of parietal cells of stomach = decrease acid production
[kids, persistent reflux]
Prokinetics: enhance GI motility = increase frequency of small
intestine contraction [not recommended in kids, side effects]
Antacids: neutralize stomach acidity to relieve heartburn and
indigestion [commonly used for kids, over the counter]
Elavation of head of bed 6 inches
Weight reduction
Cessation of smoking
Laparoscopic fundoplication: surgical intervention
No lying down for up to 3hrs after meal
PATHOPHYSIOLOGY BARRETTS
ESOPHAGUS
 BARRETT ESOPHAGUS

Metaplasia: change in stress = change in cell type to better

handle altered conditions
Esophagus: stratified squamous non -keratinized
Stomach: simple columnar
Acid reflux [stress] = metaplasia = non -ciliated columnar
Mechanism: reprogramming of stem cells
Lower 1/3 rd of esophagus contains stem cells able to produce
new squamous cells
Reversible with removal of stress
Chronic acid exposure leads to reflux esophagitis
Therapeutics can be used to cease acid reflux
 GERD AND CANCER

GERD can lead to Barretts esophagus

GERD leads to chronic inflammation
Barretts is more likely in suf fers of GERD
Dysplasia [precancerous change in tissue] can develop in
Barrett tissue
Metaplasia > dysplasia > cancer
Risk of development of adenocarcinoma of esophagus
[malignant tumor formed from glandular structures of
epithelial tissue]
PATHOLOGICAL SLIDE

This biopsy of the lower

esophagus in a patient with
chronic gastroesophageal
reflux disease (GERD)
shows columnar
metaplasia [BE]. Squamous
epithelium typical of
normal esophagus appears
on the right.
 SIGNS, SYMPTOMS AND PROGNOSIS

Frequent and long lasting heart burn

Trouble swallowing [dysphagia]
Vomiting blood [hematemesis]
Pain under sternum [meeting point of esophagus and
stomach]
Unintentional loss of weight due too painful eating
[odynophagia]
Prognosis:
Premalignant condition
Can lead to gastro-esophageal junction adenocarcinoma
85% mortality rate
Survival <1year
6-7/1000 Barretts esophagus patients have esophageal adenocarcinoma
 TE AND
PATHOPHYSIOLOGY ATRESIA
 TRACHEOESOPHAGEAL FISTULA AND
ATRESIA
What is a fistula? Abnormal connection between 2 body parts
Tracheoesophageal type: congenital detect of septation of
trachea and esophagus at 4-5th week of development
What is atresia? Absence or abnormal narrowing of opening in
a passage in body
1/45,000 neonates are ef fected
Most common variant: upper esophagus ends in blind pouch
and TEF is connected to trachea 85%
Survival rate: 90% [with early detection and correction]
Presentation: vomiting, frothing and bubbling at mouth and
nose, abdominal distention, coughing episodes, cyanosis,
respiratory distress, copious salivation
Feeding exacerbates these manifestations, causes
regurgitation and precipitates aspiration of feed
 TREATMENT

Surgical
Ligation and end-to-end anastomosis
Temporary ligation and insertion of gastrostomy tube
Preoperative management:
Maintain airway
Prevent lung damage from aspiration of gastric contents
Position adjustments to prevent gastric secretion entering distal
fistula
Esophageal suction
 OTHER ESOPHAGEAL DISEASES

Erosive esophagitis
Esophageal carcinoma
Cancer arising in the esophagus with symptoms of dysphagia and weight
loss
Hiatal hernia
the protrusion of stomach through the esophageal opening in the
diaphragm
Esophageal diverticulum
out pouching of mucosa through the muscular layer which can be
asymptomatic or cause dysphagia and regurgitation
Mallory -Weiss syndrome
bleeding from a laceration in the mucosa at the junction of the stomach
and esophagus
Achalasia
rare disease of the muscle of the lower esophageal body and the lower
esophageal sphincter that prevents relaxation of the sphincter and an
absence of contractions, or peristalsis, of the esophagus
Dysphagia
difficulty or discomfort in swallowing, as a symptom of disease
 CASE STUDY

A 40-year-old man reports to his health care provider

complaining of heartburn and chest pain that occurs after
eating and also wakes him up at night. He is overweight,
admits to enjoying fatty foods, and usually lies down on the
sofa and watches T V after dinner. He also complains that
lately he has been having a cough. He has been smoking for
20 years and takes Nifedipine [CCB] for hypertension. What is
he suf fering from?
Depression
GERD
Atresia
Physiological GERD
 ANALYSIS

Heartburn
DUE TO ACID REFLUX
Chest pain
NON-CARDIAC
After eating
STOMACH IS ACTIVE AND PRODUCING GASTRIC JUICE
Overweight
INCREASES ABDOMINAL PRESSURE
Lies down on the sofa and watches T V after dinner
GASTRIC JUICE MORE ABLE TO TRAVEL INTO ESOPHAGUS
Smoking
NICTONIE IS AN LES RELAXER
Takes Nifedipine [CCB] for hypertension
DECREASES LES PRESSURE
 CASE STUDY

A 6 year old boy comes to the clinic and his mum has
observed that he has vomited blood on may occasions,
experienced pain while eating, is irritable has dif ficultly
feeding. He suf fers from asthma and a recent blood test
shows that he suf fers from anemia. What are your clinical
recommendations and what is the most likely cause of his
problems?
Atresia with distal fistula [most common form]
Atresia with proximal fistula
GERD
ADHD
 ANALYSIS

6 year old
TEF OR ATRESIA WOULD NOT GO UNDIAGNOSED FROM BIRTH
Pain while eating
SYMPTOMATIC INDICATION OF INJURY
Irritability and dif ficultly feeding
BEHAVIOURAL INDICATION OF DISCOMFORT
Asthma
WHEN ACID ENTERS ESOPHAGUS, NERVE REFLEX IS TRIGGERED =
AIRWAYS NARROW TO PREVENT ACID ENTERING, LES RELAXING BY
BRONCHODIALATORS
Vomited blood and anemia
DUE TO ESOPHAGEAL BLEEDING
Thank you

THE END
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