The document summarizes key aspects of the esophagus anatomy and diseases. It describes that the esophagus transports ingested food through three parts and is lined by stratified squamous epithelium. Common diseases include congenital disorders like atresia, acquired disorders like achalasia and hiatal hernia, inflammations like reflux esophagitis, and tumors. Specific conditions discussed in more detail include achalasia, where the lower esophageal sphincter fails to relax, and varices, which form due to portal hypertension in conditions like liver cirrhosis.

2. THE ESOPHAGUS

6. ‫المريء‬ ‫في‬ ‫أشباح‬

7. • * Esophagus is lined by stratified squamous
epithelial tissue. (Interspersed in between 
Langerhans cells “phagocytes”).
• the role of esophagus is mainly mechanical
transportation of ingested and partially
digested food
• * It’s divided into 3 parts: upper, middle and
lower.
• It is about 25 cm in length .
• C6 – T11

9. • Within the submucosa we can see glands
(esophageal glands)>>> which is mostly
secreting mucus (lubricating) and other
pepsinogen and lysozymes for protection.
• Muscularis externa : inner circular and outer
longitudinal
- Upper third: mostly striated ( 90%)
- Middle third: mixed (50% striated , 50%
smooth )
- Lower third : entirely smooth

10. DISEASES OF
THE ESOPHAGUS
• Congenital anatomic disorders
– Agenesis, atresia, fistula, stenosis
• Acquired anatomic/motor disorders
– Stenosis, webs & rings, HH, achalasia, ...
• Inflammations
– Reflux esophagitis
• Barrett’s esophagus
• Vascular diseases
• Tumors
Most cases occurs at the lower part of the esophagus.
(metaplasia induced by acid exposure) is a
specific disorder that is restricted to the
esophagus

11. • ‐ The lower part of the esophagus is in contact
with the upper part of stomach (cardiac part)
at a junction known as “gastro‐esophageal
junction” which takes a Zigzag form “Z line”

12. 2
Lower part
This angle
Works as anti
reflex ( protect
the esophagus
from gastric
juice)
histological
junction
Lower part of esophagus

13. Clinical Features Of Esophygeal
diseases: terminology
• Dysphagia: difficulty in swallowing
due to mechanical narrowing or obstruction, tumor
• Heartburn ‫:حرقة‬ retrosternal burning pain
regurgitation of gastric contents
• Hematemesis: vomiting of blood
• Melena:caused by excessive upper GIT bleeding,
blood in stools.>>dark
• Hematochezia (fresh blood in the feces) if the
hemorrhage is severe.
• severe inflammation, ulceration or
laceration ‫تمزق‬
• Respiratory symptoms: dyspnea, cough,..
>>aspiration: breathing in a foreign object

14. Congenital disorders of the esophagus:
• Present at birth with vomiting, aspiration
(pneumonia, asphyxia‫)اختناق‬ and gastric
distention.
• 1. Agenesis: Complete Loss
of the esophagus. It’s very rare.

15. • 2. Atresia: Atresia is a condition in which an orifice or passage in the body is
abnormally closed or absent
** Most common
** Part of the esophagus is lost and replaced by
thin non‐canalized cord.
• Most commonly occurs near the tracheal
bifurcation.
• ** Fistula (A connection between the trachea and esophagus due to failure of
separation)might be on the upper or lower part of the
esophageal ligaments though commonly, it occurs
at the lower part.
• ** Gases from the stomach will pass to trachea
then to the LRT leading to pneumonia.

16. vomiting
gastric distention
aspiration

17. To remember

18. • 3. Stenosis:
• ** developmental defect resulting in partial
obstruction or narrowing of the esophageal
lumen.
• **It may be due to neuronal or motor
disorders
Treatment: Urgent medical and
surgical intervention

19. Acquired esophageal disorders
• Stenosis : ( strictures)
Due to: post-surgical ,inflammatory, tumors , chronic
gastroesophageal reflux systemic autoimmune
diseases ( Scleroderma) .
sub‐epithelial deposition
of fibrous connective
tissue, which leads to
narrowing of the esophagus.

20. More illustration

21. • 2.Webs & rings: Mucosal or sub‐mucosal
protrusion in the esophagus in form of
concentric rings, which partially occlude the
esophagus.
• - most often in the upper esophagus.

22. • 3. Diverticula: Out pouching of the
esophageal wall outside the esophageal
lining .might be due to tumer or mechanical
traction of the mucosa.
Food will
accumulate
here>>halitosis

23. ACQUIRED ANATOMIC/MOTOR DISORDERS OF THE ESOPHAGUS
4. HIATAL HERNIA
• Protrusion of a dilated sac-like segment of
stomach above the diaphragm
• Separation of the diaphragmatic crura
• Incidence; increase with age
• Mostly asymptomatic
• Some patient have: heartburn & regurgitation of
gastric juices due to LES incompetence; related to
position; symptoms are accentuated by positions
favoring reflux
• Patients with severe reflux esophagitis usually
have HH;.>>>>>why?due to loss of the angle.

24. diaphragmatic crura (two fibromuscular bands that arise from the
lumbar vertebrae and insert into the central tendon of the diaphragm).

25. Types of HH:
1. sliding (axial):
• most common
• Part of the stomach is located
above the diaphragm.
bell‐shaped
dilation(hourglass stomach).
• due to congenital short
esophagus, strictures, spasm
or long‐standing fibrous
scarring of esophagus. predisposing to gastroesophageal reflux
disease (GERD).

26. • 2. paraesophageal (non‐axial or
rolling):
• less common,
• fundus protrudes into the
thorax.
• It’s due to traumatic rupture of
the diaphragm.
• May lead to Strangulation and
infarction of that segment of the
stomach due to the compression
forced by the diaphragm on
stomach.

28. • 5. Achalasia: ** Failure of relaxation

29. • * Normally, when we swallow there will be a
relaxation in the LES. achalasia is a failure of
doing that process which leads to functional
obstruction and subsequent dilation of the
proximal part of esophagus.
• characterized by a triade of (Abnormal
manometric studies): (1) Incomplete
relaxation of LES. (2) Aperistalsis. (3)
Increase basal tone of LES.
https://www.youtube.com/watch?v=KtxuGwIoo5U
procedure for determining how the muscle of
the esophagus and the sphincter (valve) works
by measuring pressures (manometry)
generated by the esophageal muscles and the
sphincter.

30. • ** complications:
• ‐ progressive dysphagia to liquids and solid
foods.
• ‐ nocturnal regurgitation & aspiration of
undigested food, aspiration pneumonia.
“respiratory symptoms”
Achalasia

31. Achalasia
• Pathology: ‫في‬ ‫المشكلة‬innervation
• ‐ Defect in the inhibitory neurons of LES which
results in absence in myenteric ganglia in
esophagus.
• ‐ Muscular tissue: may still normal, or try to
compensate by Hypertrophy , or thin muscle.
• associated mucosal inflammation,ulcers and
fibrosis , or bleeding are common due to the
effect of stucke food.

32. Sphincter
• Sphincter: a cylindrical muscle that normally
maintains constriction of a natural body passage
or orifice which relaxes as required by normal
physiological functioning.
• Anatomical sphincter: has a localized and often
circular muscular thickening to facilitate its action
as a sphincter. So there is a function with an
anatomical structure, so the sphincter is built in.
(a ring of muscle that contracts to close an
opening) .

33. • Physiological sphincter: A sphincter that is not
recognizable at an autopsy because its resting
arrangement cannot be distinguished from
adjacent tissue. Functional sphincters do not
have this localized muscular thickening,
however, they can achieve their action
through muscle contractions around
(extrinsic) the structure. So there is no built in
sphincter (no structure). So in this case
(Cardiac orifice) its function is coming from
the right crus of diaphragm.
If we say anatomical sphincter we mean a structure and function,
while if we say a sphincter is a physiologic sphincter we mean that
it has a function without an intrinsic structure. So it’s redundant to
say a sphincter is anatomic and physiologic sphincter.

35. ** Types of Achalasia
• 1. Primary: Unknown etiology, commoner.
Can be related to autoimmune disease or previous viral
infection.
• 2. Secondary: degeneration in neural plexus
‐Chaga’s disease (mainly): Tryponosoma cruzi infection
causing destruction of myenteric plexus ganglion cells
in the GIT (esophagus, dudenom and colon)& ureters
leads to having: megaduodenum, megacolon,
megaureter.
‐ Diabetes (Autonomic neuropathy); vagus nerve injury

36. ** Patients with a history of having achalasia
are at a higher risk of developing esophageal
Squamous cell carcinoma.

38. 6. LACERATIONS
Mallory‐Weiss syndrome whiskey ;)
• ‐Longitudinal tears at the esophago‐gastric
junction.
• ‐Encountered in alcoholics due to repetitive
vomiting and bulimics [ who force themselves to
vomit after eating in order to lose weight !. But
may occur in patients without history of
repetitive vomiting.
• Pathogenesis: inadequate
relaxation of LES muscle
during vomiting.

39. LACERATIONS
• HH is found in 75% of patients with MWS
• Linear irregular lacerations, few mm-cm in
length
• Involve mucosa or deeply penetrate &
perforate wall
• 5-10% of all cases of massive
hemetemesis; however, the majority do
not cause profuse bleeding

40. LACERATIONS

41. • the postmortem ‫التشريح‬ examination is of 2 types:
• 1- forensic postmortem : by forensic pathologists
,, for medico legal purposes.
• 2- hospital postmortem : to know the exact cause
of death in hospitalized patients ,,
- EX: if our patient was alcoholic we are concerned
with specific findings
- [ look for bleeding due to MWS , CNS damage ,
esophageal varices (EV) and liver cirrhosis (LC) as
they are the main complications in alcoholics

42. DISEASES OF
THE ESOPHAGUS
• Congenital anatomic disorders
– Agenesis, atresia, fistula, stenosis
• Acquired anatomic/motor disorders
– Stenosis, webs & rings, HH, achalasia, ...
• Inflammations
– Reflux esophagitis
• Barrett’s esophagus
• Vascular diseases
• Tumors

43. • Due to portal hypertension, which leads to
formation of portal-systemic collateral
bypass channels.
VASCULAR LESIONS OF THE ESOPHAGUS
VARICES
as the veins in the systemic part of this
anastomosis are not designed to handle this
increased amount of blood , increased
pressure will induce their diltation

44. https://www.youtube.com/watch?v=Cox6Z5pqMBo
1;30
the sinusoids are
compressed

46. 1) Splenic vein.
drains blood from
spleen, pancreas and
two stomach veins "Left
gastroepiploic vein &
Short gastric
vein“(fundic v)..
2) Inferior mesentric
vein.
Drains blood from the
hindgut (distal 1/3 of the
transverse colon “left
colic vein “until the upper
2/3 of the anal canal).”
superior rectal vein”.

47. • 1) Venous blood from GIT goes to liver
through the portal vein before going to the
IVC. when there is a defect in the portal
vein>>>>>>>>>>the blood can’t go to the liver
• Collateral veins will develop in the region
of lower esophagus when portal flow is
diverted through the coronary veins of
stomach into the plexus of esophageal
submucosal veins into azygous veins

48. • Most common cause of portal
hypertension is liver cirrhosis
• Rare causes: portal vein thrombosis,
hepatic vein thrombosis (Budd-Chiari
syndrome), pylephlebitis, tumor
compression or invasion into major portal
radicals
*Develops in 2/3 of
cirrhotic patients;
accounts for 50%
of deaths in liver
cirrhosis
Irreversible End
stage of chronic
liver disease.
hepatitis C is
the most
common cause
of cirrhosis.

49. chronic hepatitis
• is graded according to degree of fibrosis into :
1. Portal (mild ) 2. Periportal 3. Bridging
(cirrhosis ).
• Initially, the liver is yellow tan,fatty & enlarged
• Eventually, it becomes brown, shrunken & non
fatty

50. • With excessive intake of alcohol, the liver
switches over from the use of fats and
carbohydrates as its primary "fuel" to the use of
alcohol as its primary fuel.
• As alcohol-induced hepatitis progresses, the
unused fat accumulates in the liver, causing the
organ to change in color from a dark, reddish
brown to a yellowish color that resembles
nutmeg (hence the terms "nutmeg liver" or "fatty
liver").
chronic hepatitis

52. Consequences of liver cirrhosis :
• Portal hypertension which leads to :
hemorrhoids, esophageal varices, capot
medusa ( all are at the portosystemic
anastomosis)
• Splenomegaly
• Charachtarised histologically by :
1. Bridging fibrous septa ( delicate fibers
between two portal tracts and between portal
tracts and central veins)
2. Paranchymal nodules ( which are regeneretive
hepatocytes encircled by fibrous tissue )

57. Due to
scratchy
food :nuts ,…
• Asymptomatic until they rupture when
massive hematemesis results; rupture may
be spontaneous or secondary to vomiting;
hemorrhage rarely subsides spontaneously;
40% die after 1st episode
• 70% of survivors will re-bleed within 1 year;
mortality rate 40%
• *It’s very emergent case and should be treated
even though the prognosis is very .
• bad balloon temponade is the way by which we
can stop the bleeding in order to be able to
perform the endoscopy
VASCULAR LESIONS OF THE ESOPHAGUS
VARICES

62. INFLAMMATIONS OF THE ESOPHAGUS
ESOPHAGITIS
• Caused by multiple factors:
– 1. Reflux of gastric contents (reflux esophagitis)
– 2. Ingestion of irritants (alcohol, corrosive acids, alkali,
excessive hot fluids like tea, heavy smoking).
- Infective eosphagitis:measles, scarlet fever, diphtheria, typhoid
– 3. Bacteremia & viremia with direct infection of
esophageal wall or contiguous structures (HSV, CMV)
– 4. Fungal infections in immunocompromised patients
(Candidiasis, mucormycosis, aspergillosis)
– 5. because the esophagus lining is squamous epithelium .>> Systemic
desquamative skin diseases (pemphigoid)
– 6. Graft-versus-host disease
– 7. Radiation; cytotoxic therapy; uremia

64. Oesophageal candidiasis Herpes simplex oesophagitis
characterized by multiple ulcers

66. Oesophagitis: Morson & Dawson, 5th ed, 2012
• Reflux
• Infective oesophagitis
herpes simplex
CMV
candidiasis
immunocompetent: measles, scarlet fever, diphtheria &
typhoid
immunoparetic: HIV, HZV, HPV, HHV6, varied bacteria
& fungi
• Pill oesophagitis: ferrus sulfate, (tetracyclines), NSAIDs, drugs used
for osteoporosis]
-- risk factors includes [elderly, diabetes, women (M:F = 1:2) ]
• Sloughing oesophagitis
• Eosinophilic oesophagitis
• Radiation oesophagitis
• Chagas disease

68. 1. Reflux of gastric contents (reflux esophagitis)
• including some refluxed contents from the
intestines (bile, bile salts, bile acids).
• Predisposing factors:
– Fat, chocolate, alcohol, smoking
– Hiatal hernia
– Pregnancy (increases the abdominal pressure)
– Drugs

69. • the main pathological/histological finding for
Reflux Esophagitis is: basal zone hyperplasia
and the presence of intra-epithelial
eosinophils&/or PMNs.

72. ESOPHAGEAL TUMORS
• Benign tumors are rare: leiomyoma is the
most common, and is usually ,asymptomatic
and discovered incidentally.
• Malignant tumors
- More common in males (M:F=3:1).

73. SQUAMOUS CELL CARCINOMA
• The most common malignant tumor of
esophagus.
• has a higher contribution to mortality, why?
(asymptomatic with late diagnosis).
• Patients: most patients are adults >50 years.
• Higher incidence in blacks than whites.

75. Esophageal cancers often spread
to surrounding structures, making surgical
removal difficult.
infiltrating nests of neoplastic cells
have abundant pink cytoplasm and distinct
cell borders typical for squamous cell
carcinoma.

76. • Associated factors/Risk factors:
- 1) Dietary:- Fungal contamination of food by
Aspergillus, High content of nitrites/ nitrosamines,
Deficiency of vitamins (A, C, riboflavin, thiamin),
Deficiency of trace metals (zinc, molybdenum).
- 2) Esophageal disease: achalasia, reflux
esophagitis , strictures, Plummer-Vinson
syndrome.
- 4) genetic predisposition: celiac disease,Tylosis.

77. • Pathology:
- 50% of the cases happen in middle third of the
esophagus, 30% in lower third and 20% in
upper third.
• Prognosis: 70% die within 1 year, 5 years
survival 5-10% (poor prognosis).
full thickness
dysplasia and
invasion of the
sub mucosa

78. SQUAMOUS CELL CARCINOMA

79. ADENOCARCINOMA
• Middle or lower third; may extend to stomach

80. • Most are adults >40 yrs; M:F=5:1; v. rare in
blacks.(has a rising incidence especially in
western countries).
The background is Barrett’s esophagus and its
composed of glandular epithelium.