Major divisions of the GI system:  PIG BELLY --> P-pancreas, I-intestine, G-gastric, B-bililary system, E-esophagus, L-liver.

·       P  _______________, _______________, _______________, _______________,        _______________, _______________

·       I  _______________, _______________, _______________,  _______________,       _______________, _______________

·       G  _______________, _______________, _______________, ______________,        _______________, ________________

·       B  _______________, _______________, _______________, _______________,      _______________, _______________         

·       E  _______________, _______________, _______________, _______________,       _______________, _______________

·       L  _______________, _______________, _______________, _______________,       _______________, _______________



·      ANATOMY 












ESOPHAGEAL DISEASES:  GERD (face it one cannot talk about the esophagus without thinking of GERD) --> G-GERD (gastroesophageal reflux disease), E-esophagitis, E-esophageal cancer, R-rupture, D-dysphagia.




·       ANATOMY


·       PATHOLOGY:  GASTRIC DISORDERS: Z-zollinger-Ellision syndrome A-affects G-gastric pH = ZAGPH --> Z-zollinger-ellison syndrome, A-adenocarcinoma of the stomach, G-gastritis, PUD, H-hiatal hernia.

1.     MENETRIER’S DISEASE (aka hyperplastic hypersecretory gastropathy):



PUD (Peptic Ulcer Disease):




·       EMBRYOLOGY:. 

·       ANATOMY:  

·       PHYSIOLOGY: 

Small intestine:
Large intestine: 
·       PATHOLOGY:

SMALL INTESTINE:  Diseases of the small intestine SM-small C-colon I-illness = SMCI --> S-SBO (small bowel obstruction), M-malabsorption syndrome, C-carcinoid syndrome, IBS, I-leus.
Ø  SBO (small bowel obstruction):

Ø  MALABSORPTION SYNDROME: TYPES:  WASP DIE --> W-whipple’s disease, A-abetalipoproteinemia, S-sprue, P-pancreatic insufficiency, D-disacharide deficiency, I-infection, E-enteropathy



SPRUE:  Celiac disease and Tropical sprue


INFECTION:  See Infectious Disease section
INFLAMMATORY DISEASE:  See IBD and other rheumatologic conditions

IBS (Irritable Bowel Syndrome): 
LARGE BOWEL:  L-large C-colon I-inflammatory D-disease = LCID (eL CID-the Spanish hero) --> L-LBO (large bowel obstruction),  C-CRC (colorectal cancer), I-IBD (inflammatory bowel disease), D-diverticular disease.
LBO (large bowel obstruction): 


IBD (inflammatory bowel disease): 

Ø  UC (ulcerative colitis): 




·       UGIB (upper gastrointestinal bleeding):

·       LGIB (upper gastrointestinal bleeding): 





·       ANATOMY:


·       PATHOLOGY:  P-portal H-hypertension = PH --> P-portal HTN, H-hepatitis, H-hemochromatosis, H-hepatoma, H-hepatolenticular degeneration (aka Wilson’s disease).

·       PORTAL HTN: 

SBP (spontaneous bacterial peritonitis):
RENAL DYSFUNCTION (HRS-hepatorenal syndrome):
YELLOW (jaundice):

·       CIRRHOSIS:







Ø  ALD (alcoholic liver disease):


Ø  NASH (non-alcoholic steatohepatitis):




·       ANATOMY:


·       PATHOLOGY:





·       ANATOMY:


·       PATHOLOGY: 

BILIARY DISEASE:  4 C’s --> C-choledocholiathiasis --> biliary C-colic, C-cholecystitis, C-choledocholithiasis, C-cholangitis, C-cholangiocarcinoma.
biliary C-COLIC:


o   The gut is an endoderm-derived structure. About the 16th day of human development, the embryo begins to fold ventrally (with the embryo's ventral surface becoming concave) in two directions: the sides of the embryo fold in on each other and the head and tail fold towards one another. The result is that a piece of the yolk sac, an endoderm-lined structure in contact with the ventral aspect of the embryo, begins to be pinched off to become the primitive gut. The yolk sac remains connected to the gut tube via the vitelline duct. Usually this structure regresses during development; in cases where it does not, it is known as Meckel's diverticulum.

o   The epithelial lining and glands of the gut tube mucosa are derived from endoderm, whereas the lamina propria, muscularis muscosae, submucosa, muscularis externa, and adventitia or serossa are derived form mesoderm. 

o   The epithelial lining of the gut tube proliferates rapidly and obliterates the lumen.  Canalization then occurs.

Two of the stages in the development of the digestive tube and its mesentery

By Henry Vandyke Carter - Henry Gray (1918) Anatomy of the Human Body (See "Book" section below) Gray's Anatomy, Plate 987, Public Domain,

Abdominal part of digestive tube and its attachment to the primitive or common mesentery. Human embryo of six weeks.

By Henry Vandyke Carter - Henry Gray (1918) Anatomy of the Human Body (See "Book" section below) Gray's Anatomy, Plate 985, Public Domain,

Schematic figure of the bursa omentalis, etc. Human embryo of eight weeks.

By Henry Vandyke Carter - Henry Gray (1918) Anatomy of the Human Body (See "Book" section below) Gray's Anatomy, Plate 989, Public Domain,

Mesentery in red. Dorsal mesentery is the lower part of the circuit. The upper part is ventral mesentery.

By Own work, Public Domain,

o   The primitive gut can be divided into three segments: foregut, midgut, and hindgut.

o   GI tract has a uniform general histology with some differences which reflect the specialization in functional anatomy.

Layers of the Alimentary Canal. The wall of the alimentary canal has four basic tissue layers: the mucosa, submucosa, muscularis, and serosa.

By Goran tek-en, CC BY-SA 4.0,

MAJOR ARTERIAL SUPPLY OF THE GI TRACT: CELIAC ARTERY, SMA (superior mesenteric artery), and IMA (inferior mesenteric artery)


Ø  The first major branch of the abdominal aorta and branches from the aorta around the level of the T12 vertebra. It is one of three anterior/ midline branches of the abdominal aorta (the others are the superior and inferior mesenteric arteries).

Ø  Supplies oxygenated blood to the liver, stomach, abdominal oesophagus, spleen and the superior half of both the duodenum and the pancreas. These structures correspond to the embryonic foregut.

 VENOUS DRAINAGE:  blood returning from the area of distribution of the celiac artery is diverted to the liver via the portal venous system for further processing and detoxification in the liver before returning to the systemic circulation via the hepatic veins

The celiac artery and its branches

By Henry Vandyke Carter - Henry Gray (1918) Anatomy of the Human Body (See "Book" section below) Gray's Anatomy, Plate 532, Public Domain,

Surface projections of the major organs of the trunk, using the vertebral column and rib cage as main reference points of superficial anatomy. The transpyloric plane and McBurney's point are among the marked locations.

SMA (superior mesenteric artery):

Ø  Arises from the anterior surface of the abdominal aorta, just inferior to the origin of the celiac trunk, and supplies the intestine from the lower part of the duodenum to the left colic flexure and the pancreas.  After passing the neck of the pancreas it starts giving off its branches.

Ø  Supplies oxygenated blood to the lower duodenum, jejunum, ileum, cecum, appendix, ascending colon, and first half of the transverse colon. These structures correspond to the embryonic midgut.

VENOUS DRAINAGE:  SMV (superior mesenteric vein)

By The original uploader was Nephron at English Wikipedia. - Transferred from en.wikipedia to Commons by FSII using CommonsHelper., Public Domain,

Frontal view of the superior mesenteric artery and its branches. The large vessel (blue) beside the SMA is the superior mesenteric vein. A considerable number of different branching patterns exist.

By Mikael Häggström from original image created and uploaded by Dr. I-Chen Tsai (Wikipedia:User:Sillyduck) - LDLT volume measure.jpg., CC BY 3.0,

3D-rendered computed tomography of abdominal aortic branches, showing exit of superior mesenteric artery between the kidneys.

By Mikael Häggström from original image created and uploaded by Dr. I-Chen Tsai (Wikipedia:User:Sillyduck) - LDLT volume measure.jpg., CC BY 3.0,

Superior mesenteric artery

Dissection showing the anatomical relationship between the superior mesenteric artery and surrounding structures

By Anatomist90 - Own work, CC BY-SA 3.0,

IMA (inferior mesenteric artery):

Ø  The IMA branches off the anterior surface of the abdominal aorta below the renal artery branch points, and approximately midway between these and the aortic bifurcation (into the common iliac arteries).

Ø  Supplies the large intestine from the left colic (or splenic) flexure to the upper part of the rectum, which includes the descending colon, the sigmoid colon, and part of the rectum.  The territory of distribution of the IMA is more or less equivalent to the embryonic hindgut.


VENOUS DRAINAGE:   The IMA is accompanied along its course by a similarly named vein, the IMV (inferior mesenteric vein), which drains into the splenic vein.The IMV therefore drains to the portal vein and does not fully mirror the course of the IMA.

The inferior mesenteric artery and its branches.

By Henry Vandyke Carter - Henry Gray (1918) Anatomy of the Human Body (See "Book" section below) Gray's Anatomy, Plate 537, Public Domain,

Sigmoid colon and rectum, showing distribution of branches of inferior mesenteric artery and their anastomoses. (Inferior mesenteric artery labeled at center.)

By Henry Vandyke Carter - Henry Gray (1918) Anatomy of the Human Body (See "Book" section below) Gray's Anatomy, Plate 1121, Public Domain,

Posterior abdominal wall, after removal of the peritoneum, showing kidneys, suprarenal capsules, and great vessels.

Inferior mesenteric artery

By Anatomist90 - Own work, CC BY-SA 3.0,

Lumbar and sacral plexus. Deep dissection.Anterior view.

By Anatomist90 - Own work, CC BY-SA 3.0,

Lumbar and sacral plexus. Deep dissection.Anterior view.

By Anatomist90 - Own work, CC BY-SA 3.0, Text Here...


THE PORTALVENOUS SYSTEM:  drains blood from the digestive system and its associated glands.

Ø  It is formed by the union of the splenic vein and SMV (superior mesenteric vein).

Ø  Divides into a right and a left branch before entering the liver. The portal vein branches into many generation of vessels that open into hepatic sinusoids. Blood is recollected into the hepatic vein and enters the IVC (inferior vena cava).

Ø  Note that the portal vein drains blood into the liver, not from the liver. The blood entering the liver from the portal vein, after being cleaned by the liver, flows into the inferior vena cava via the hepatic veins.

Ø  The IMV (inferior mesenteric vein) usually does not directly connect to the hepatic portal vein; it drains into the splenic vein.

The abdomen viewed from the front, showing the portal venous system, showing the superior mesenteric vein and its tributaries. (Lienal vein is an old term for splenic vein.)

By <a href="" class="extiw" title="w:en:Henry Vandyke 

By &lt;a href=&quot;//; title=&quot;User:Anatomist90&quot;&gt;Anatomist90&lt;/a&gt; - &lt;span class=&quot;int-own-work&quot; lang=&quot;en&quot;&gt;Own work&lt;/span&gt;, <a href="" title="Creative Commons Attribution-Share Alike 3.0">CC BY-SA 3.0</a>, <a href="">Link</a>

Abdominal cavity.Superior mesenteric vein.Deep dissection.


·       EMBRYOLOGY:  The esophagus is a derivative of the foregut.  The tracheoesophageal septum divides the foregut into the esophagus and trachea.  Esophageal atresia occurs when the esophagus ends as a blind tube as a result of malformation of the tracheoseophageal septum.

ESOPHAGEAL ATRESIA:  occurs in approximately 1/4425 live births.  This condition takes several different forms, often involving one or more fistulas connecting the trachea to the esophagus (tracheoesophageal fistula). Approximately 85% of affected babies will have a lower fistula (TYPE C in the picture).

·       Evaluation:  EA & TEF is suggested in a newborn by copious salivation associated with choking, coughing, and cyanosis coincident with the onset of feeding. If above signs & symptoms are noticed, a catheter is passed into the esophagus to check for resistance. If resistance is noted, a catheter can be inserted and will show up as white on a regular x-ray film to demonstrate the blind pouch ending.

Tracheoesophageal Fistula Types

By Jmarchn - Own work and Tracheoesophageal Fistula Types.JPG, CC BY-SA 3.0,

By Kinderradiologie Olgahospital Klinikum Stuttgart - Own work, CC BY-SA 4.0,

Radiograph with oral contrast showing h-type tracheoesophageal fistula in a newborn

·       Treatment: Surgery with resection of any fistula and anastomosis of any discontinuous segments.

o   Congenital TEF with EA is sometimes found in association with VACTERL association and CHARGE syndrome.

Ø  VACTERL ASSOCIATION: Incidence of 1.6 cases per 10,000 live births. Can be seen with some chromosomal defects such as Trisomy 18 and is more frequently seen in babies of diabetic mothers. VACTERL association, however, is most likely caused by multiple factors.

v  V - Vertebral anomalies:  About 70 % of patients with VACTERL association will have vertebral anomalies usually consist of small (hypoplastic) vertebrae or hemivertebra where only one half of the bone is formed.  In early life these rarely cause any difficulties, although later in life these spinal column abnormalities may put the child at risk for developing scoliosis

v  A - Anal atresia  or imperforate anus is seen in about 55 % of patients with VACTERL association. These anomalies are usually noted at birth and often require surgery in the first days of life.

v  C - Cardiovascular anomalies

v  T - Tracheoesophageal fistula:  seen in about 70 % of patients with VACTERL association

v  E - Esophageal atresia

v  R – Renal and/or Radial anomalies:   Renal anomolies is seen in approximately 50 % of patients with VACTERL association and can cause kidney failure early in life and may require kidney transplant.

v  L - Limb anomalies (in front of or above the central axis of the limb):  occur in up to 70 percent of babies with VACTERL association and include absent or displaced thumbs, polydactyly, syndactyly and forearm defects.

Ø  Treatment:  At present this condition is treated after birth with issues being approached one at a time.

v  V  _______________, _______________, _______________, _______________, _______________

v  A  _______________, _______________, _______________, _______________, _______________

v  C  _______________, _______________, _______________, _______________, ________________

v  T  _______________, _______________, _______________, _______________, _______________

v  E  _______________, _______________, _______________, _______________, _______________

v  R  _______________, _______________, _______________, _______________, _______________

v  L  _______________, _______________, _______________, _______________, _______________

Newborn with radial aplasia of the right arm, is displaying a limb anomaly included in VACTERL Association. VACTERL association or a nonrandom association of specific newborn abnormalities include to name a few, vertebral dysgenesis, anal defect, cardiac anomalies, tracheoesophageal fistulae, esophageal atresia, radial limb and renal anomalies.

By CDC/Dr. James W. Hanson - (, Public Domain,

Ø  CHARGE SYNDROME:  Prevalence 1:9000.  A study in the US of 110 individuals with CHARGE syndrome showed that 60% of those tested had a mutation of the CHD7 gene on chromosome 8.

v  C - Coloboma of the eye (term used to describe a hole in one of the structures of the eye, such as the lens, eyelid, iris, retina, choroid or optic disc), central nervous system anomalies

v  H - Heart defects

v  A - Atresia of the choanae

v  R - Retardation of growth and development

v  G - Genital and/or urinary defects (Hypogonadism)

v  E - Ear anomalies and/or deafness

§  C  _______________, _______________, _______________, _______________, _______________

§  H  _______________, _______________, _______________, _______________, ________________

§  A  _______________, _______________, _______________, _______________, _______________

§  R  _______________, _______________, _______________, _______________, _______________

§  G  _______________, _______________, _______________, _______________, _______________

§  E  _______________, _______________, _______________, _______________, _______________

"Lop ear" phenotype characteristic of a person with CHARGE syndrome, along with her cochlear implant.

By Kim D Blake, Chitra Prasad - Kim D Blake, Chitra Prasad. CHARGE syndrome. Orphanet Journal of Rare Diseases. 1, 34. 2006. PMID 16959034., CC BY 2.0,


o   The esophageal wall contains four layers:

Ø  Mucosa -- surface epithelium, lamina propria, and glands.  Mucosa is lined by squamous epithelium that becomes columnar near the GE (gastroesophageal) junction.

Ø  Submucosa -- connective tissue, blood vessels, and glands

Ø  Muscularis (middle layer)

v  Upper third: striated muscle

v  Middle third: striated and smooth

v  Lower third: smooth muscle

Ø  Adventitia/Serosa (connective tissue that merges with connective tissue of surrounding structures): NONE

By Henry Vandyke Carter - Henry Gray (1918) Anatomy of the Human Body (See &quot;Book&quot; section below) Gray&#039;s Anatomy, Plate 1032, Public Domain,

The position and relation of the esophagus in the cervical region and in the posterior mediastinum. Seen from behind.

By -, Public Domain,

1. Mucosa
2. Submucosa (contain Meisner’s plexus)
3. Muscularis
4. Adventitia
5. Circular muscle
6. Auerbach’s plexus
7. Longitudinal muscle
8. Lamina muscularis mucosae
9. Esophageal glands



o   Esophagus is bounded

Ø  Posteriorly by the vertebral column and thoracic duct

Ø  Anteriorly by the trachea

Ø  Laterally by the pleura, and on the left by the aorta.

o   Arterial Supply:

Ø  Superior and Inferior thyroid artery: supply upper esophagus

Ø  Intercostals, left gastric, and phrenic arteries: supply lower esophagus

o   Venous drainage:

Ø  Upper esophagus:  Inferior thyroid and vertebral veins

Ø  Middle and lower esophagus: azygous, hemiazygous, and left gastric veins.

Ø  Submucosal veins become engorged in portal hypertension --> varices and bleeding.

o   Innervation: from the vagus, cervical sympathetic ganglion, splanchnic, and celiac ganglion.  The vagus nerve forms a plexus around the esophagus, which condenses to form 2 trunks on the lateral esophagus.  These in turn rotate so that the left trunk moves anteriorly while the right trunk moves posteriorly.

·       PHYSIOLOGY:  Food is passed through the esophagus by using the process of peristalsis.

·       ESOPHAGEAL DISEASES:  GERD (face it one cannot talk about the esophagus without thinking of GERD) --> G-GERD (gastroesophageal reflux disease), E-esophagitis, E-esophageal cancer, R-rupture, D-dysphagia.

o   G  _______________, _______________, _______________, _______________, _______________

o   E  _______________, _______________, _______________, _______________, ________________

o   R  _______________, _______________, _______________, _______________, _______________

o   D  _______________, _______________, _______________, _______________, _______________

o   G ERD (gastroesophageal reflux disease):  Defined as chronic symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus.  This can be due to incompetence of the LES (lower esophageal sphincter), transient LES relaxation, impaired expulsion of gastric reflux from the esophagus, or a hiatal hernia.  It affects 7% of the population on a daily basis.

A comparison of a healthy condition to GERD

By BruceBlaus - Own work, CC BY-SA 4.0,

Ø  Evaluation: Heartburn (burning pain in the epigastric, sternal, and throat accompanied by a sour taste in the mouth), cough, wheezing, sore throat, laryngitis.  It is aggravated by lying down, EtOH, caffeine, nicotine, chocolate, fatty food, and factors that ↑ intra-abdominal pressure (pregnancy, obesity).  Medication trials.  EGD (if signs of cancer eg, anemia, dysphagia): detect esophagitis, erosions, ulcer, malignancies.  Barium swallow or upper GI series: reveal anatomic abnomalities such as esophageal spasms.  Esophageal pH monitor: for suspected GERD who have normal endoscopy.  Esophageal manometry: for evaluation of motility disorder.  H. pylori test (eg, urea breath test, histologic staining).

By Dr. A. Dickson -, CC BY-SA 4.0,

Severe tooth erosion in GERD.

X-ray showing radiocontrast from the stomach (white material below diaphragm) entering the esophagus (three vertical collections of white material in the mid-line of the chest) due to severe reflux

By Steven Fruitsmaak - Own work, CC BY-SA 3.0,

Endoscopic image of peptic stricture, or narrowing of the esophagus near the junction with the stomach: This is a complication of chronic gastroesophageal reflux disease and can be a cause of dysphagia or difficulty swallowing.

By Samir धर्म - From, Public Domain,

Ø  Treatment:  Lifestyle modification: elevated HOB, avoid triggers, weight loss.  Mediation:  step-down approach advocates initial therapy with a PPI then step-down after 8 weeks of symptom control to a lesser regimen that remains effective such as a lower dose of the PPI, an H2-blocker, antacids, or lifestyle management.  Nissen fundoplication: for refractory or severe disease.  H. pylori:  triple therapy (eg, 2 antibiotic –metronidazole + clarithromycin- and a PPI –omeprazole-) X 7-14 days, then continue PPI for 4-12 weeks. 

o   E SOPHAGITIS: Inflammation of the esophagus.  The most common cause is GERD (reflux esophagitis).  Other causes:   Infections (candida, HSV, CMV; typically seen in immunocompromised people), food allergies, chemical injury by alkaline or acid solutions (usually seen in children or in adults who attempt suicide), physical injury resulting (by radiation therapy or nasogastric tubes).

An esophageal ulcer visualized by esophagoscopy: the reddened area at 10 o'clock on the surface of the mucosa.

By melvil - Own work, CC BY-SA 4.0,

Microscopic Slide of Infectious  HSV Esophagitis

By Nephron - Own work, CC BY-SA 3.0,

H&E stain of a biopsy of the normal esophageal wall, showing the stratified squamous cell epithelium of the esophageal wall

By ​English Wikipedia user Samir, CC BY-SA 3.0,

Histological section of the gastro-esophageal junction, with a black arrow indicating the junction

By Jpogi at en.wikipedia - Transferred from en.wikipedia by Ronhjones, Public Domain,

o   E SOPHAGEAL CANCER:  SqCC (squamous cell carcinoma):  90%, similar to head and neck cancer in their appearance and association with tobacco and alcohol consumption.  Adenocarcinoma: 10%, associated with a history of gastroesophageal reflux disease and Barrett's esophagus.

Ø  Risk:  ♂, EtOH, cigarettes, lye or other caustic substance, dietary nitrosamine, mediastinal radiation therapy.  Barrett's esophagus.  Plummer-Vinson syndrome, Howel-Evans syndrome.

Ø  Evaluation: Dysphagia (first symptom in most patients) and odynophagia. Fluids and soft foods are usually tolerated, while hard or bulky substances (such as bread or meat) cause much more difficulty. Substantial weight loss is characteristic as a result of poor nutrition and the active cancer. Pain, often of a burning nature, may be severe and worsened by swallowing, and can be spasmodic in character. An early sign may be an unusually husky or raspy voice.  The presence of the tumor may disrupt normal peristalsis leading to N/V, regurgitation of food, coughing and an increased risk of aspiration pneumonia. The tumor surface may be fragile and bleed, causing hematemesis.  Compression of local structures occurs in advanced disease, leading to such problems as superior vena cava syndrome. Fistulas may develop between the esophagus and the trachea, increasing the pneumonia risk; this symptom is usually heralded by cough, fever or aspiration.  If the disease has spread elsewhere, this may lead to symptoms related to this: liver metastasis could cause jaundice and ascites, lung metastasis could cause shortness of breath, pleural effusions, etc.  Barium swallow. EGD with biopsy. MRI/CT (evaluatate metastasis).  Esophageal endoscopic ultrasound (provide staging information regarding the level of tumor invasion, and possible spread to regional lymph nodes).

CC BY-SA 3.0,

Endoscopic image of an esophageal adenocarcinoma

By melvil - Own work, CC BY-SA 4.0,

Esophageal cancer (lower part) as a result of Barrettʼs esophagus

Endoscopic image of Barrett esophagus – a frequent precursor of esophageal adenocarcinoma

By Samir धर्म - taken from patient with permission to place in public domain, Copyrighted free use,

Esophageal cancer as shown by a filling defect during an upper GI series

By James Heilman, MD - Own work, CC BY-SA 4.0,

Contrast CT scan showing an esophageal tumor (axial view)

By Tdvorak - Own work, CC BY-SA 3.0,

Contrast CT scan showing an esophageal tumor (coronal view)

By Tdvorak - Own work, CC BY-SA 3.0,

Esophageal cancer

By James Heilman, MD - Own work, CC BY-SA 4.0,

Micrograph showing histopathological appearance of an esophageal adenocarcinoma (dark blue – upper-left of image) and normal squamous epithelium (upper-right of image) at H&E staining

By Nephron - Own work, CC BY-SA 3.0,

T1, T2, and T3 stages of esophageal cancer

By Cancer Research UK - Original email from CRUK, CC BY-SA 4.0,

Stage T4 esophageal cancer

By Cancer Research UK - Original email from CRUK, CC BY-SA 4.0,

Esophageal cancer with spread to lymph nodes

By Cancer Research UK - Original email from CRUK, CC BY-SA 4.0,

Ø  Treatment:  Localized disease (20-30% of all patients): surgery.  All other: Radiotherapy + chemotherapy (cisplatin, epirubicin, 5-FU).  Prognosis: Even in patients who undergo surgery with curative intent, the five year survival rate is only 25%. The prognosis is even more dismal in those who are not fit for surgery.

By Cancer Research UK - Original email from CRUK, CC BY-SA 4.0,

Internal radiotherapy for esophageal cancer

Self-expandable metallic stents are sometimes used for palliative care

By Samir -, CC BY-SA 3.0,

Esophageal stent for esophageal cancer

By James Heilman, MD - Own work, CC BY-SA 4.0,

Esophageal stent for esophageal cancer

By James Heilman, MD - Own work, CC BY-SA 4.0,

By Cancer Research UK - Original email from CRUK, CC BY-SA 4.0,

Before and after a total esophagectomy

Typical scar lines after the two main methods of surgery

By Cancer Research UK - Original email from CRUK, CC BY-SA 4.0,

Ø  BARRETT’S ESOPHAGUS:  Columnar metaplasia of esophageal squamous epithelium.  The metaplasia is often to the intestinal-type columnar epithelium with prominent goblet cells.  The columnar epithelium is better able to withstand the erosive action of the gastric secretions; however, this metaplasia confers an increased cancer risk of the adenocarcinoma type.

v  Evaluation:  History of GERD.  EGD: visualize the metaplasia.  Biopsy specimens must be examined under a microscope to determine whether cells are gastric or colonic in nature. Colonic metaplasia is usually identified by finding goblet cells in the epithelium and is necessary for the true diagnosis of Barrett's. 

Endoscopic image of Barrett's esophagus, which is the area of dark reddish-brown mucosa at the base of the esophagus. (Biopsies showed intestinal metaplasia.)

Add Text Here...

By Samir धर्म - taken from patient with permission to place in public domain, Copyrighted free use,

By Samir - Own work, CC BY-SA 4.0,

Endoscopic view of Barrett's esophagus showing location of biopsies for screening using the Seattle protocol

Histopathology of Barrett's esophagus, showing intestinalized epithelium with goblet cells, as opposed to normal stratified squamous epithelium of the esophagus, and pseudostratified columnar epithelium of the fundus of the stomach. The submucosa displays an infiltrate including lymphocytes and plasma cells, constituting an underlying chronic inflammation. The area between the stratified and the intestinalized epithelium displays reactive changes, but there is no secondary dysplasia in this case. H&E stain.

By Mikael Häggström, M.D.- Author info- Reusing images- Conflicts of interest:NoneMikael HäggströmConsent note: Consent from the patient or patient&#039;s relatives is regarded as redundant, because of absence of identifiable features (List of HIPAA identifiers) in the media and case information (See also HIPAA case reports guidance). - Own work, CC0,

In incomplete Barrett's esophagus, there are both foveolar cells and goblet cells, the latter (indicated by arrows) usually having a slightly bluish color compared to the apical cytoplasm of foveolar cells on H&E stain. An occasional but specific sign of goblet cells is crescent shaped nuclei (seen in middle one).

By Mikael Häggström, M.D.- Author info- Reusing images- Conflicts of interest:NoneMikael HäggströmConsent note: Consent from the patient or patient&#039;s relatives is regarded as redundant, because of absence of identifiable features (List of HIPAA identifiers) in the media and case information (See also HIPAA case reports guidance). - Own work, CC0,

Micrograph showing Barrett's esophagus - columnar epithelia with goblet cells - on the left side of image; and normal stratified squamous epithelium on the right side of image Alcian blue stain

By Nephron - Own work, CC BY-SA 3.0,

High-magnification micrograph of Barrett's esophagus showing the characteristic goblet cells, Alcian blue stain

By Nephron - Own work, CC BY-SA 3.0,

v  Treatment:  Routine endoscopy and biopsy (looking for dysplastic changes) every 12 months.  PPI: control underlying reflux.  In severe dysplasia, laser treatment is being used, whereas overt malignancy may require surgery, radiation, or systemic chemotherapy.  Nissen fundoplication:   ↓ reflux of acid from the stomach into the esophagus.

Ø  PLUMMER-VINSON SYNDROME (aka Patterson-Brown-Kelly syndrome or sideropenic dysphagia):  a disorder linked to severe, long-term iron deficiency anemia, which dysphagia due to esophageal webs. The cause of Plummer-Vinson syndrome is unknown; however, genetic factors and nutritional deficiencies may play a role. Women are at higher risk than men, particularly in middle age. In these patients, esophageal squamous cell carcinoma risk is increased; therefore, it is considered a premalignant process. 

Evaluation: sufferers often complain of a burning sensation with the tongue and oral mucosa, and atrophy of lingual papillae produces a smooth, shiny red tongue dorsum, dysphagia, odynophagia, pain, weakness , atrophic glossitis.  Also associated with koilonychia, glossitis, angular  cheilitis, esophageal web, and splenomegaly.  Serial contrasted gastrointestinal radiography or upper gastrointestinal endoscopy: reveal the web in the esophagus. CBC:  hypochromic microcytic anemia consistent with iron-deficiency anemia. Biopsy of involved mucosa typically reveals epithelial atrophy and varying amounts of submucosal chronic inflammation. Epithelial atypia or dypslasia may be present. 

Atrophic glossitis:  Patchy depapillation of filiform papillae with prominence of the fungiform papillae.

By Grook Da Oger - Own work, CC BY-SA 3.0,


By CHeitz -, CC BY 2.0,

Angular stomatitis

By Lesion - Own work, CC BY-SA 3.0,

Endoscopic image of esophageal web

By Samir - Own work, CC BY-SA 3.0,

Esophageal web stenosis in barium swallow examination lateral view.

By Hellerhoff - Own work, CC BY-SA 3.0,

Web with "jet-phenomenon". Arrowhead on incomplete opening of the upper esophageal sphincter.

By Hellerhoff - Own work, CC BY-SA 3.0,

By Hellerhoff - Own work, CC BY-SA 3.0,

Esophageal web stenosis in barium swallow examination frontal view.

v  Treatment: Primarily aimed at correcting the iron-deficiency anemia. Iron supplement may improve dysphagia and pain. If not, the web can be dilated during upper endoscopy to allow normal swallowing and passage of food.

v  Plummer-Vinson Syndrome summary:  VINSON --> V-videofluoroscopy to detect esophageal web, I-iron deficiency anemia (weakness, fatigue, pallor, glossitis, angular chelitis, koilonychias), possible I-infilatration of I-inflammatory cell in submucosa on biopsy, mostly in N-northern European/S-scandinavian population, associated with S-sqCC of the O-oesophagus, O-oesophageal web, and O-oral mucosal atrophy/pain, N-nutrition (adequate dietary iron) may prevent this disorder.

§  V  ______________, _______________, _______________, _______________, _______________

§  I  ______________, _______________, _______________, _______________, ________________

§  N  _______________, _______________, _______________, _______________, _______________

§  S  _______________, _______________, _______________, _______________, _______________

§  O _______________, _______________, _______________, _______________, _______________

§  N  _______________, _______________, _______________, _______________, _______________

Ø  Howel-Evans Syndrome:  Extremely rare condition in which the skin of the palms of the hands, and soles of the feet, are affected (hyperkeratosis). The effects on the palms and soles is called tylosis, and in Howel-Evans syndrome, there is a predisposition to oesophageal cancer, particularly squamous cell carcinoma.   The condition is inherited in an autosomal dominant manner, and it has been linked to a mutation in the RHBDF2 gene.

§  Howel-Evans Syndrome summary: HES --> H-hereditary H-hyperkeratosis --> thickening of the skin of the palm & soles (tylosis), E-esophageal cancer especially S-SqCC.

§  H  ______________, _______________, _______________, _______________, _______________

§  E  ______________, _______________, _______________, _______________, ________________

§  S  _______________, _______________, _______________, _______________, _______________

Micrograph showing prominent hyperkeratosis in skin without atypia. H&E stain.

By Mikael Häggström, M.D.- Author info- Reusing images- Conflicts of interest:NoneMikael HäggströmConsent note: Consent from the patient or patient&#039;s relatives is regarded as redundant, because of absence of identifiable features (List of HIPAA identifiers) in the media and case information (See also HIPAA case reports guidance). - Own work, CC0,

Leukoplakia on the inside of the cheek

By Photo uploaded by: dozenist. - Photo taken by Michael Gaither, and he has agreed to release this picture with the following license., CC BY-SA 3.0,

Endoscopy and radial endoscopic ultrasound images of a submucosal tumor in the central portion of the esophagus

By Samir at the English-language Wikipedia, CC BY-SA 3.0,

v  Treatment: The skin is treated with a keratolytic (such as salicylic acid) to dissolve the excess skin, and systemic treatment with retinoids (derivatives of Vitamin A) may be given.

o   R-r UPTURE:

Ø  Iatrogenic (80-95%): typically as a complication of an endoscopic procedure (EGD), feeding tube, or unrelated surgery.

BOERHAAVE SYNDROME: Full thickness/transmural esophageal perforation generally caused by excessive vomiting in eating disorders such as bulimia. Most occur on the posterolateral wall 2-3 cm before the stomach.

Evaluation: Meckler’s triad (present in 50%): Vomiting, cervical subcutaneous Emphysema, and Chest pain after overindulgence of food or EtOH.  CXR: Pleural effusion (91%), Pneumothorax (80%), normal (12%).

v  Treatment:  Antibiotics: to prevent mediastinitis and sepsis.  IVF.  Surgical repair. 

Axial CT image through the upper chest showing extraluminal air (pneumediastinum) surrounding the trachea and esophagus

By Jto410 - Own work, CC BY-SA 3.0,

Sagittal reformatted CT image showing discontinutity in the wall of the posterolateral aspect of the distal esophagus

By Jto410 - Own work, CC BY-SA 3.0,

By Jto410 - In my work as a radiologist, CC BY-SA 3.0,

Upright chest radiography showing mediastinal air adjacent to the aorta and tracking cephalad adjacent to the left common carotid artery. This patient presented to the emergency department with severe chest pain after eating.

Ø  MALLORY-WEISS TEAR:  Mucosal (non-transmural) tear at the GE junction usually occurring after severe retching, vomiting or coughing.

Evaluation: Hematemesis, melana after violent retching or vomiting.  In most cases, the bleeding stops spontaneously after 24-48 hours, but endoscopic or surgical treatment is sometimes required and rarely the condition is fatal.  EGD: definitive diagnosis.

Add TextMallory–Weiss tear affecting the esophageal side of the gastroesophageal junctionHere...

By Samir - Endoscopic photograph of Mallory-Weiss Tear, CC BY-SA 3.0,

Treatment:  IVF.  Treatment is usually supportive as persistent bleeding is uncommon. However cauterization or injection of epinephrine to stop the bleeding may be undertaken during the index endoscopy procedure. Very rarely embolization of the arteries supplying the region may be required to stop the bleeding.

o   D YSPHAGIA: difficulty swallowing. 

Ø  OROPHARYNGEAL DYSPHAGIA:  Arises from abnormalities of the upper esophagus, pharynx, and oral cavity. Involve liquid more than solids and may be accompanied by dysarthria or dysphonia. 

Etiologies:  Neurologic disease: stroke, Parkinson’s disease, ALS (amyotrophic lateral sclerosis), Bell’s palsy, MG (myasthenia gravis).  Muscular disease (MG --> weakness of the muscles of mastication & swallowing). Thyroid disease (mass effect). Sphincter disease.  Zenker’s diverticulum (obstruction).  Neoplasm (mechanical obstruction). Post-surgery: dysphagia is often a side effect of surgeries like anterior cervical spine surgery, carotid endarterectomy, head and neck resection, oral surgeries like removal of the tongue, and parital laryngectomies.  Radiation therapy: cause tissue fibrosis in the irradiated areas.  Medications:  sedative-hypnotic agents, anticonvulsant, antihistamines, neuroleptics, and barbiturates. 

Evaluation:  Symptoms of dysphagia:  inability to recognize food and taste it, difficulty placing food in the mouth, inability to control food or saliva in the mouth, difficulty initiating a swallow, coughing, choking, frequent pneumonia, unexplained weight loss, gurgly or wet voice after swallowing, nasal regurgitation.  When asked where the food is getting stuck patients will often point to the cervical (neck) region.  Speech Language Pathologist to evaluate a patient with suspected dysphagia with MMSE (mini-mental state examination), and oral and facial sensorimotor function, speech, and swallowing are evaluated non-instrumentally. MBS (modified barium swallow): different consistencies of liquid and food mixed with barium sulfate are fed to the patient by spoon, cup or syringe, and x-rayed using videofluoroscopy. FEES (flexible fiberoptic endoscopic examination of swallowing): instrument, is placed into the nose until the clinician can view the pharynx and then he or she examines the pharynx and larynx before and after swallowing. Other less frequently used assessments of swallowing:  ultrasound, scintigraphy,  electromyography, electroglottography, cervical auscultation, and pharyngeal manometry.

Treatment: Speech Language Pathologist will determine the safety of the patient's swallow and recommend treatment accordingly.  Treatment is dependent on etiology and includes postural techniques, swallowing maneuvers (eg, Mendelsohn maneuver), dietary modification (eg, liquid diet), and surgery (eg, tracheostomy).

Ø  ESOPHAGEAL DYSPHASIA:  Arises from the body of the esophagus, lower esophageal sphincter, or cardia of the stomach. Usually due to mechanical causes or motility problems.

v  : Patients usually experience food getting stuck several seconds after swallowing, and will point to the suprasternal notch or behind the sternum as the site of obstruction. If there is dysphagia to both solids and liquids, then it is most likely a motility problem. If there is dysphagia initially to solids but progresses to also involve liquids, then it is most likely a mechanical obstruction. Once a distinction has been made between a motility problem and a mechanical obstruction, it is important to note whether the dysphagia is intermittent or progressive.

Videoesophagography (visualize orpharyngeal).  Barium swallow. EGD.  Manometry.  pH measurement.

Endoscopic image of a non-cancerous peptic stricture, or narrowing of the esophagus, near the junction with the stomach. This is a complication of chronic gastroesophageal reflux disease, and can be a cause of dysphagia. The stricture is about 3 to 5 mm in diameter. The blood that is visible is from the endoscope bumping into the stricture.

By Samir धर्म - From, Public Domain,

v  Treatment:  Etiology dependent.  For example: achalasia is treated with Botox injection, CCB, balloon dilatation, or esophageal myotomy.

Ø  SPECIFIC CAUSES OF ESOPHAGEAL DYSPHAGIA:  All New Severe Dysphagia Requires Proper Workup = ANSDRPW --> A-achalasia, N-nutcracker esphogus, S-scleroderma, D-diffuse esophageal spasm, R-rings, P-pectic stricture, W-webs.

v  A  _______________, _______________, _______________, _______________, _______________

v  N  _______________, _______________, _______________, _______________, _______________

v  S _______________, _______________, _______________, _______________, _______________

v  D  _______________, _______________, _______________, _______________, _______________

v  R  _______________, _______________, _______________, _______________, _______________

v  P  _______________, _______________, _______________, _______________, _______________

v  W  _______________, _______________, _______________, _______________, _______________

v  ACHALASIA:  an idiopathic motility disorder characterized by failure of LES relaxation and loss of peristalsis in the distal esophagus due to the destruction of the myenteric (aka Auerbach’s) plexus. Both of these features impair the ability of the esophagus to empty contents into the stomach. Patients usually complain of dysphagia to both solids and liquids. Dysphagia to liquids, in particular, is a characteristic of achalasia. Other symptoms:  regurgitation, night coughing, chest pain, weight loss, and heartburn. Bariuma swallow: bird’s beak. Manometry, EGD. CT scan.  In most cases the cause is unknown (idiopathic), but in some regions of the world, achalasia can also be caused by Chagas disease due to infection by Trypanosoma cruzi.  Achalasia is also associated with Allgrove syndrome.

A chest X-ray showing achalasia ( arrows point to the outline of the massively dilated esophagus )

By James Heilman, MD - Own work, CC BY-SA 3.0,

An axial CT image showing marked dilatation of the esophagus in a person with achalasia.

By James Heilman, MD - Own work, CC BY-SA 3.0,

"Bird's beak" appearance and "megaesophagus", typical in achalasia.

By Farnoosh Farrokhi, Michael F. Vaezi. - Idiopathic (primary) achalasia. Orphanet Journal of Rare Diseases 2007, 2:38(, CC BY 2.0,

By JC Petit at English Wikipedia, CC BY 3.0,

Schematic of manometry in achalasia showing aperistaltic contractions, increased intraesophageal pressure, and failure of relaxation of the lower esophageal sphincter.

Image of a stomach which has undergone Fundoplomy

By Xopusmagnumx at English Wikipedia - Transferred from en.wikipedia to Commons by Nasiruddin., Public Domain,

§  ALLGROVE SYNDROME (aka the Triple A syndrome):  AAA --> the combination of A-achalasia, A-adrenal insufficiency, A-alacrima in children.

§  A  _____________, _______________, _______________, _______________, _______________

§  A  _____________, _______________, _______________, _______________, _______________

§  A  ______________, _______________, ______________, _______________, _______________

MRI of the brain of 12-year-old boy with triple-A syndrome showing hypoplastic lacrimal glands (yellow arrows)

By Brian P Brooks et al - BMC Ophthalmology 2004, 4:7doi:10.1186/1471-2415-4-7, CC BY 2.0,

v  NUTCRACKER ESOPHAGUS:  Nutcracker esophagus can affect people of any age, but is more common in the 6th and 7th decades of life.  Nutcracker esophagus may also be associated with the metabolic syndrome, obesity, and GERD.

§  Evaluation:  It causes difficulty swallowing, or dysphagia, to both solid and liquid foods, and can cause chest pain; it may also have no symptoms.  The diagnosis is made by an esophageal motility study, which evaluates the pressure of the esophagus at various points along its length, with a diagnosis made when pressures > 180 mmHg; this has been likened to the pressure of a mechanical nutcracker. The disorder does not progress, and is not associated with any complications. Pathology specimens of the esophagus in patients with nutcracker esophagus show no significant abnormality.

Normal peristalsis in time space graph. Nutcracker esophagus shows higher amplitude contractions (Z-axis) that take longer to pass (X-axis)

By Dieter Menne ( - Plotted with JavaView ( by Dieter Menne (, Public Domain,

Diagram of esophageal motility study in nutcracker esophagus: The disorder shows peristalsis with high-pressure esophageal contractions exceeding 180 mmHg and contractile waves with a long duration exceeding 6 sec.

By Samir at the English-language Wikipedia, CC BY-SA 3.0,

Normal esophagus in (A). Nutcracker esophagus in (C): high-pressure waves in blue; cross-sectional areas (CSA) in fucsia.

By Kazumasa Muta, Ravinder K. Mittal, Ali Zifan - Rhythmic contraction but arrhythmic distension of esophageal peristaltic reflex in patients with dysphagia. (2022). PLoS ONE 17(1): e0262948. doi:10.1371/journal.pone.0262948, CC BY 4.0,

§  Treatment:  Symptomatic only.  CCB (diltiazem-Cardizem).  Nitrates (isosorbide dinitrate). PDE inhibitors (sildenafil).  These medications relax the LES and palliate the dysphagia symptoms.  Trazodone-desyrel, an anti-depressant that reduces visceral sensitivity, has also been shown to reduce chest pain symptoms in patients with nutcracker esophagus.  Endoscopic therapy with botulinum toxin (Botox) can also be used to temporarily improve symptoms with the effect lasts for weeks.

SCLERODERMA:  disease characterized by atrophy and sclerosis of the gut wall, most commonly of the distal esophagus (~90%). Consequently, the LES cannot close and this can lead to severe GERD. Patients typically present with progressive dysphagia to both solids and liquids secondary to motility problems or peptic stricture from acid reflux.

DIFFUSE ESOPHAGEAL SPASM (aka corkscrew esophagus):  uncoordinated contractions of the esophagus thought to result from motility disorders of the esophagus. These spasms do not propel food effectively to the stomach.

§  Evaluation:  Dysphagia, regurgitation and chest pain. It's been reported that very cold or hot beverages can trigger an esophageal spasm. Contrary, rapid swallowing of a liquid often provides immediate relief.  The condition is sometimes referred to as corkscrew esophagus, due to a characteristic appearance of the esophagus as a corkscrew on barium swallow x-rays.

§  Treatment:  Nitroglycerins and CCB.

Corkscrew appearance of the esophagus due to Diffuse esophageal spasm. (DES) is a condition in which uncoordinated contractions of the esophagus occur.

By © Nevit Dilmen, CC BY-SA 3.0,

Corkscrew appearance of the esophagus.

By Hellerhoff - Own work, CC BY-SA 3.0,

ESOPHAGEAL RING (aka Schatzki’s ring):  A ring found in the lower part of the esophagus that can cause difficulty swallowing.  These rings are usually mucosal rings rather than muscular rings, and are located near the gastroesophageal junction at the squamo-columnar junction. Presence of multiple rings may suggest eosinophilic esophagitis.

§  Evaluation:  Intermittent mechanical dysphagia, while swallowing solids and then liquids, depending on the constriction of the ring.  EGD or Barium swallow to visualize the ring.

§  Treatment:  Esophageal balloon dilatation.

Endoscopic image of esophageal web

By Samir - Own work, CC BY-SA 3.0,

Esophageal web stenosis in barium swallow examination lateral view.

By Hellerhoff - Own work, CC BY-SA 3.0,

Web with "jet-phenomenon". Arrowhead on incomplete opening of the upper esophageal sphincter.

By Hellerhoff - Own work, CC BY-SA 3.0,

Esophageal web stenosis in barium swallow examination frontal view.

By Hellerhoff - Own work, CC BY-SA 3.0,

PEPTIC STRICTURE:  Most commonly due to long-standing GERD. Acid reflux can also be due to other causes, such as Zollinger-Ellison syndrome, NG tube placement, and scleroderma. Other non-acid related causes of peptic strictures include infectious esophagitis, ingestion of chemical irritant, pill irritation, and radiation.

o   Evaluation: Progressive mechanical dysphagia (initial intolerance to solids followed by inability to tolerate liquids).

o   Treatment:  Treat underlying disorder.  Balloon dilatation of stricture.

Endoscopic image of a benign peptic stricture

By Samir धर्म - From, Public Domain,

ESOPHAGEAL WEB:  Squamous mucosal protrusion into the esophageal lumen, especially anterior cervical esophagus behind the cricoid area. Patients are usually asymptomatic or have intermittent dysphagia. An important association of esophageal webs is to the Plummer-Vinson syndrome in iron deficiency Esophageal webs are associated with bullous diseases (such as epidermolysis bullosa, pemphigus, and bullous pemphigoid), with GVHD involving the esophagus, and with celiac disease.

§  Evaluation:  Usually asymptomatic.  Symptoms: Dysphagia (solid more than liquids), thoracic pain, nasopharyngeal reflux, aspiration, perforation and food impaction (the last two are very rare).

§  Treatment:  Esophageal webs can be ruptured during upper endoscopy.


·       EMBRYOLOGY:  The stomach develops from a dilatiation arising from the foregut during week 4.  The primitive stomach rotates 90° clockwise & then twists distal end up during its formation.  The ventral mesentery rotates and twists along with the stomach, causing the formation of the bursa omentalis (aka the less sac)


The stomach lies between the esophagus and the duodenum (the first part of the small intestine). It is on the left side of the abdominal cavity. The top of the stomach lies against the diaphragm. Lying beneath the stomach is the pancreas, and the greater omentum which hangs from the greater curvature.

In humans, the stomach has a volume of about 50 mL when empty. After a meal, it generally expands to hold about 1 litre of food, but it can actually expand to hold as much as 4 litres. When drinking milk it can expand to just under 6 pints, or 3.4 litres.

Schematic drawing of the digestive system.

By Indolences created it on the English Wikipedia.This SVG image was created by Medium69.Cette image SVG a été créée par Medium69.Please credit this : William Crochot - US PD picture., Public Domain,

Sections of the human stomach

By Henry Vandyke Carter - Henry Gray (1918) Anatomy of the Human Body (See &quot;Book&quot; section below) Gray&#039;s Anatomy, Plate 1046, Public Domain,

o The stomach is divided into four sections, each of which has different cells and functions.


Ø  The lesser curvature of the stomach:  supplied by the right gastric artery (a branch of the hepatic artery proper) inferiorly, and the left gastric artery (a branch of the celiac trunk) superiorly, which also supplies the cardiac region.

Ø  The greater curvature: supplied by the right gastroepiploic artery (a branch of the gastroduodenal artery) inferiorly and the left gastroepiploic artery (a branch of the splenic artery) superiorly.

Ø  The fundus of the stomach, and also the upper portion of the greater curvature: supplied by the short gastric artery (a branch of the splenic artery).

Ø  The pylorus: supplied by the gastroduodenal artery.

Schematic image of the blood supply to the human stomach: left and right gastric artery, left and right gastroepiploic artery and short gastric artery.

By Mikael Häggström.When using this image in external works, it may be cited as:Häggström, Mikael (2014). &quot;Medical gallery of Mikael Häggström 2014&quot;. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.008. ISSN 2002-4436. Public Domain.orBy Mikael Häggström, used with permission. - Essential Clinical Anatomy. K.L. Moore &amp; A.M. Agur. Lippincott, 2 ed. 2002. Page 150, Public Domain,

o INNERVATION: The vagus nerve supplies parasympathetic signals via the anterior left and posterior right trunks. These nerves stimulate gastric motility and the secretion of pepsinogen and HCl.


The stomach is a highly acidic environment due to gastric acid production and secretion which produces a luminal pH between 2-3 depending on food intake, time of the day, drug use, and other factors. Such an environment is able to break down large molecules to smaller ones so that they can eventually be absorbed from the small intestine. The stomach can produce and secrete about 2 to 3 liters of gastric acid per day.  Pepsinogen is secreted by chief cells and turns into pepsin under low pH conditions and is a necessity in protein digestion.  Absorption of vitamin B12 from the small intestine is dependent on conjugation to a glycoprotein called intrinsic factor which is produced by parietal cells of the stomach.


1. Body of stomach 2. Fundus 3. Anterior wall 4. Greater curvature 5. Lesser curvature 6. Cardia 9. Pyloric sphincter 10. Pyloric antrum 11. Pyloric canal 12. Angular incisure 13. Gastric canal 14. Rugae

By -, Public Domain,

The gastrointestinal wall of the human stomach.

By NIH / National Cancer Institute -, Public Domain,

By Carrasco G, Corvalan AH - Carrasco G, Corvalan AH (2013). &quot;Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer.&quot;. Gastroenterol Res Pract 2013: 393015. DOI:10.1155/2013/393015. PMID 23983680. PMC: 3745848.Figures - available via license: Creative Commons Attribution 3.0 Unported, CC BY 3.0,

Histology of normal fundic mucosa. Fundic glands are simple, branched tubular glands that extend from the bottom of the gastric pits to the muscularis mucosae; the more distinctive cells are parietal cells. H&E stain.

Histology of normal antral mucosa. Antral mucosa is formed by branched coiled tubular glands lined by secretory cells similar in appearance to the surface mucus cells. H&E stain.

By Carrasco G, Corvalan AH - Carrasco G, Corvalan AH (2013). &quot;Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer.&quot;. Gastroenterol Res Pract 2013: 393015. DOI:10.1155/2013/393015. PMID 23983680. PMC: 3745848.Figures - available via license: Creative Commons Attribution 3.0 Unported, CC BY 3.0,

o CONTROL OF SECRETION & MOTILITY: The movement and the flow of chemicals into the stomach are controlled by both the autonomic nervous system and by the various digestive system hormones. Other than gastrin, these hormones all act to turn off the stomach action.

·       PATHOLOGY:  GASTRIC DISORDERS: Z-zollinger-Ellision syndrome A-affects G-gastric pH = ZAGPH --> Z-zollinger-ellison syndrome, A-adenocarcinoma of the stomach, G-gastritis, PUD, H-hiatal hernia.


o ADENOCARCINOMA & OTHER CANCERS OF THE STOMACH: Develop in any part of the stomach and may spread throughout the stomach and to other organs; particularly the esophagus and the small intestine. Stomach cancer causes nearly one million deaths worldwide per year.

EPIDEMIOLOGY:  Stomach cancer represents roughly 2% (25,500) cases of all new cancer cases yearly in the US, but it is much more common in Korea, Japan, Great Britain, South America, and Iceland. Infection with H. pylori is the main risk factor in about 80% or more of gastric cancers. It is more common in men.  It is suspected several risk factors are involved including diet (high salt, and low intake of fruits and vegetables), smoking, gastritis, intestinal metaplasia.  In Japan and other countries bracken consumption and spores are correlated to stomach cancer incidence. Ten percent of cases show a genetic component.  A very small percentage of diffuse-type gastric cancers are thought to be genetic (Hereditary Diffuse Gastric Cancer-HDGC).   

Stomach cancer types by relative incidence

By Mikael Häggström, M.D.- Author info- Reusing images- Conflicts of interest:NoneMikael Häggström - Own work, CC0,

PRESENTATION:  In early stages, stomach cancer is often asymptomatic or causes only nonspecific symptoms. By the time symptoms occur, the cancer has generally metastasized to other parts of the body, one of the main reasons for its poor prognosis. Possible signs and symptoms:  1) Early:  Indigestion or heartburn, loss of appetite (especially for meat).  2) Late:  Abdominal pain/discomfort in the upper abdomen, N/V, diarrhea or constipation, bloating after meals, weight loss, weakness and fatigue, bleeding (hemoptysis or melana), which can lead to anemia, These can be symptoms of other health problems, such as a stomach virus or gastric ulcer, and diagnosis should be done by a gastroenterologist or an oncologist.

DIAGNOSTIC EVALUATION:  Upper GI series (aka barium roentgenogram).  FOBT:   Obsolete except possibly as a screening test; a negative test proves nothing and a positive result may result from a large number of other conditions beside gastric carcinoma. Gastroscopic exam:  Diagnostic method of choice.  Abnormal tissue seen in a gastroscope examination will be biopsied by the surgeon or gastroenterologist.

Endoscopic images of the stomach cancer in early stage. Its histology was poorly differentiated adenocarcinoma with signet ring cells. Left above: normal, right above: FICE, left low: acetate stained, right low: AIM stained

By Med Chaos - Own work, CC BY-SA 3.0,

A stomach ulcer that was diagnosed as cancer on biopsy and surgically removed

By, Public Domain,

Endoscopic image of linitis plastica, a type of stomach cancer where the entire stomach is invaded, leading to a leather bottle-like appearance with blood coming out of it

By This work has been released into the public domain by its author, Samir. This applies worldwide.In some countries this may not be legally possible; if so:Samir grants anyone the right to use this work for any purpose, without any conditions, unless such conditions are required by law. - Transferred from en.wikipedia to Commons., Public Domain,

Sequence of 123-iodine human scintiscans after an intravenous injection: (from left) after 30 minutes, 20 hours, and 48 hours - a high and rapid concentration of radio-iodine is evident in gastric mucosa of the stomach, in salivary glands, oral mucosa, and the periencephalic and cerebrospinal fluid (left). In the thyroid gland, I-concentration is more progressive, also in the reservoir (from 1% after 30 minutes to 5.8% after 48 hours, of the total injected dose).

By Venturi Sebastiano - Own work, CC BY-SA 3.0,

T stages of stomach cancer

By Cancer Research UK - Original email from CRUK, CC BY-SA 4.0,

By Cancer Research UK - Original email from CRUK, CC BY-SA 4.0,

Stomach cancer metastasized to the lungs

TYPES OF STOMACH CANCER:  Gastric adenocarcinoma originates from glandular epithelium of the gastric mucosa.  Histologically, there are two major types of gastric cancer (Lauren classification): intestinal type and diffuse type.

1.     Intestinal type adenocarcinoma: Irregular tubular structures, harboring pluristratification, multiple lumens, reduced stroma ("back to back" aspect). Often, it associates intestinal metaplasia in neighboring mucosa. Depending on glandular architecture, cellular pleomorphism and mucosecretion, adenocarcinoma may present 3 degrees of differentiation: well, moderate and poorly differentiate.

2.     Diffuse type adenocarcinoma (mucinous, colloid): Tumor cells are discohesive and secrete mucus which is delivered in the interstitium producing large pools of mucus/colloid (optically "empty" spaces). It is poorly differentiated. If the mucus remains inside the tumor cell, it pushes the nucleus at the periphery - "signet-ring cell".

Poor to moderately differentiated adenocarcinoma of the stomach. H&E stain.

Public Domain,

Adenocarcinoma of the stomach and intestinal metaplasia. H&E stain.

By Nephron - Own work, CC BY-SA 3.0,

Gastric signet ring cell carcinoma. H&E stain.

By No machine-readable author provided. KGH assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0,

TREATMENT:  Cancer of the stomach is difficult to cure unless it is found in an early stage (before it has begun to spread). Unfortunately, because early stomach cancer causes few symptoms, the disease is usually advanced when the diagnosis is made. Treatment for stomach cancer may include

1.     Surgery:  Most common treatment for stomach cancer. Procedure includes subtotal (partial gastrectomy) or total gastrectomy.  Depending on the extent of invasion and the location of the tumor, surgery may also include removal of part of the esophagus, spleen, ovaries, intestine or pancreas . Tumors in the lower parts of the stomach may call for a Billroth I or Billroth II procedure. Surgical interventions are currently curative in less than 40% of cases, and, in cases of metastasis, may only be palliative.

2.     Chemotherapy:  Gastric cancer has not been especially sensitive to these drugs until recently, and historically served to palliatively reduce the size of the tumor and increase survival time. Some drugs used include: 5-FU, carmustine, Semustine, doxorubicin, Mitomycin C, cisplatin, and taxotere. The benefits of giving chemotherapy before surgery to shrink the tumor, or as adjuvant therapy after surgery to destroy remaining cancer cells are being explored. Intraperitoneal hyperthermic chemoperfusion (cancer drugs are put directly into the abdomen) is being trialed. Chemotherapy also is being studied as a treatment for cancer that has spread, and as a way to relieve symptoms of the disease.

3.     Radiation therapy:  Generally in combination with surgery and chemotherapy, or used only with chemotherapy in cases where the individual is unable to undergo surgery. Radiation therapy may be used to relieve pain or blockage by shrinking the tumor for palliation of incurable disease

4.     Multimodality Therapy (combinations of surgery, chemotherapy and radiation therapy):  Study showed a survival benefit to the combination of chemotherapy and radiation therapy in patients with nonmetastatic, completely resected gastric cancer. Patients were randomized after surgery to the standard group of observation alone, or the study arm of combination chemotherapy and radiation therapy. Those in the study arm receiving chemotherapy and radiation therapy survived on average 36 months, compared to 27 months with observation.

5.     Biological therapy:  PD-L1 inhibitors (nivolumab, pembrolizumab). Some cause flu-like symptoms, such as chills, fever, weakness, nausea, vomiting, and diarrhea. Patients sometimes get a rash, and they may bruise or bleed easily. These problems may be severe, and patients may need to stay in the hospital during treatment.

PROGNOSIS:  Metastasis occurs in 80-90% of individuals with stomach cancer, with a five year survival rate of 75% in those diagnosed in early stages and less than 30% of those diagnosed in late stages. The death rate is 12,400 a year in the United States.

SUMMARY OF ADENOCARCINOMA OF STOMACH:  ADENOCARCS --> A-adenocarcinoma, A-achlorhydia, D-diffuse type (linitis plastica), E-early metastasis to lymph N-nodes (Virchow’s node = supraclavicular node), O-ovaries metastasis is known as C-crukenberg’s tumor; stomach cancer is A-associated with R-reduced fiber/fresh fruits & vegetables, and C-chronic gastritis; see S-signet ring cells in linitis plastica type.

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o GASTRITIS: Inflammation limited to the gastric mucosa. Depending on the cause, it may persist acutely or chronically and may coincide with more serious conditions such as atrophy of the stomach. Causes of gastritis include:

ACUTE GASTRITIS: BAN CIGaretteS = BAN CIGS (because cigs cause gastritis) --> B-burn injury (Curling’s ulcer), B-brain injury (Cushing’s ulcer), B-bile injury, A-alcohol, A-allergens, NSAIDs, C-cigarettes, C-caffeine, I-infection (bacterial-H. pylori, viral, and fungal), G-gastrinoma, S-stress.

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1.     TYPE A (10%)Occur in the fundus and is due to autoantibodies to parietal cells.  Associated with other autoimmune disorders (eg, pernicious anemia, thyroiditis).  Type A: 4 A’s --> A-autoimmune dz, A-autoantibodies to parietal cell --> A-achlorhydia and pernicious A-anemia.

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2.     TYPE B (90%): Occur in the antrum and is due to B-bug H. pylori is most cases.

PRESENTATION:  Upper abdominal pain or discomfort, gastric hemorrhage, hypochlorhydria, appetite loss, belching, N/V, fever, lethargy

DIAGNOSTIC EVALUATION:  Obtain history regarding medications, alcohol intake, smoking, and other factors that can be associated with gastritis. Barium meal test and gastroscopy:  Determine gastritis and related conditions such as peptic ulcers and gastric cancer.  The most reliable method for determining gastritis is doing a biopsy during gastroscopy and checking for histological characteristics of gastritis and infection. Urea breath test, stool antigen test, or blood antibody test: For Helicobacter infection (the most common cause).

A peptic ulcer may accompany gastritis. Endoscopic image.

By User:Samir -, CC BY-SA 3.0,

Updated Sydney System for visual classification of gastritis on histopathology.

By Carrasco G, Corvalan AH - Carrasco G, Corvalan AH (2013). &quot;Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer.&quot;. Gastroenterol Res Pract 2013: 393015. DOI:10.1155/2013/393015. PMID 23983680. PMC: 3745848.Figures - available via license: Creative Commons Attribution 3.0 Unported, CC BY 3.0,

Micrograph showing gastritis. H&E stain.

By Nephron - Own work, CC BY-SA 3.0,

Early acute superficial gastritis: Marked neutrophilic infiltrates appear in the mucous neck region and lamina with a pit microabscess. This case was caused by Helicobacter pylori.

By Carrasco G, Corvalan AH - Carrasco G, Corvalan AH (2013). &quot;Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer.&quot;. Gastroenterol Res Pract 2013: 393015. DOI:10.1155/2013/393015. PMID 23983680. PMC: 3745848.Figures - available via license: Creative Commons Attribution 3.0 Unported, CC BY 3.0,

TREATMENT:  Etiology dependent.  Removing the irritant or the infection; antacids, sucralfate, H2 blockers, and/or PPI may help. Helicobacter infection typically responds well to the triple therapy protocol (consisting of two antibiotics, and a proton pump inhibitor).  Give prophylactic H2 blocker or PPI for patients at risk for stress ulcers (i.e. burn injury, brain injury, and patient on mechanical ventilation).


1.     MENETRIER’S DISEASE (aka hyperplastic hypersecretory gastropathy):  A disorder in which the gastric mucosal folds (rugae) are enlarged, making the surface of the stomach look a bit like the brain gyri. The total weight of the stomach is increased.  The altered gastric mucosa secretes massive amounts of mucus, resulting in low plasma protein levels (mostly albumin). The tissue may be inflamed and may contain ulcers.  Two forms of the disease:   A) Childhood form:   It affects boys and girls equally, most often after they have a viral illness caused by CMV or a bacterial infection caused by Helicobacter pylori. Has a better prognosis.  B) Adult form:  Associated with overexpression of TGF-α. It is four times more common in men, primarily affecting men between 30-60 y/o.  Ménétrier's disease increases risk of stomach cancer.

PRESENTATION:  Postprandial pain relieved by antacids, weight loss, cachexia, peripheral edema, ascites, anemia symptoms secondary to blood loss

DIAGNOSTIC EVALUATION:  Diagnosed by x-ray (rare) or endoscopy and biopsy of the stomach. Microscopically, the disease is characterized by hyperplasia of the crypts, which are elongated and may appear cystic or corkscrew-like.

CT abdomen, coronal section, showing characteristic large rugal folds in the stomach. A cyst is also seen in the liver.

By Hellerhoff - Own work, CC BY-SA 3.0,

Biopsy of the stomach in Ménétrier disease showing the substantial pit hyperplasia makes the large rugal folds appear to be covered by myriad polyps resembling hyperplastic polyps. The muscularis propria is the folded structure at the bottom center.

By AFIP Atlas of Tumor Pathology - [1], Public Domain,

TREATMENT:  Pediatric cases (CMV-related Ménétrier):  Often self-limited, and are normally treated for symptoms with the disease clearing up in weeks to months.  Adult cases:  Medications to relieve ulcer symptoms and treat inflammation, and a high-protein diet. Part or all of the stomach may need to be removed if the disease is severe. Since it predisposes to stomach cancer, periodic endoscopic surveillance is mandated. 


PORTAL HYPERTENSIVE GASTROPATHY:  Changes in the mucosa of the stomach in patients with portal hypertension; most common cause of this is liver cirrhosis. These changes in the mucosa include friability of the mucosa and the presence of ectatic blood vessels at the surface.

PATHOPHYSIOLOGY: Patients with portal hypertension develop increased blood flow to the stomach secondary to backflow from decreased hepatic blood flow.

PRESENTATION:  Most patients with portal hypertensive gastropathy have either a stable or improving course in the appearance of the gastropathy on endoscopy. Patients with chronic bleeding will usually come to the attention of the medical system because of anemia.  It uncommonly manifest itself in vomiting blood or melena

DIAGNOSTIC EVALUATION:  EGD:  Diagnosis is usually made on endoscopy. The usual appearance is a mosaic-like or reticular (snake skin) pattern in the mucosa seen throughout the stomach. A similar pattern can be seen with a related condition called gastric antral vascular ectasia (GAVE), or watermelon stomach. However, in GAVE, the ectatic blood vessels are more commonly found in the antrum or lower part of the stomach.   Biospy:  Ectatic (or dilated) blood vessels, evidence of bleeding by means of RBCs in the lamina propria, and edema in the stomach wall.

Image of portal hypertensive gastropathy seen on endoscopy of the stomach. The normally smooth mucosa of the stomach has developed a mosaic like appearance, that resembles snake-skin.

By Original uploader was Samir at en.wikipedia - Transfered from en.wikipedia, CC BY-SA 3.0,

Argon plasma coagulation, seen here to treat gastric antral vascular ectasia, has also been used to treat bleeding from portal hypertensive gastropathy

By The original uploader was Samir at English Wikipedia. - Transferred from en.wikipedia to Commons., CC BY-SA 3.0,

TREATMENT:  Medications:  Non-selective beta blockers (such propranolol and nadolol):  Have been shown to regress portal hypertensive gastropathy.  Anti-fibrinolytic medications (eg, tranexamic acid):  Work by stabilizing deposits of fibrin at sites that ordinarily would bleed.  Octreotide (somatostatin analogue):   For active bleeding due to portal hypertensive gastropathy.  It causes vasoconstriction of the portal circulation.   Procedural:  Endoscopic treatment:  Argon plasma coagulation, cryotherapy and electrocautery have both been used to stop bleeding from ectatic vessels, and to attempt to obliterate the vessels, but have limited utility if the disease is diffuse.  TIPS (transcutaneous intrahepatic portosystemic shunt): Decompressing the portal vein by shunting a portal venule to a lower pressure systemic venule, under guidance with fluoroscopy.

o PUD (Peptic Ulcer Disease): SUBMUCOSAL LESION (vs. MUCOSAL in gastritis)

EPIDEMIOLOGY:  Risk factors: Corticosteroids, EtOH, Cigarettes, NSAIDs, hyperCa++, Zollinger-Ellison syndrome, MEN Type I.  Lifetime prevalence: 5-10% of population.  Peak in the 5th decade; M > F

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1.     GASTRIC ULCER (70% associated with H. pylori): In these patient, the parietal cell gastric acid production is normal or ↓.  Pain is G-greater with meal (              ).  G-greater risk (vs. duodenal ulcer) of progressing to stomach adenocarcinoma (up to 10%).

2.     DUODENAL ULCER (90% associated with H. pylori): In these patient, ↑ gastric acid production is necessary for its development.  Pain is D-decreased with meal. 

DIAGNOSTIC EVALUATION:  CBC (anemia from bleeding); AXR ( rule out perforation-upright XR see free AIR under the diaphragm); EGD with biopsy (confirm diagnosis by visualizing the ulcer); Barium swallow (alternative to EGD); H. pylori test; Serum gastrin (Zollinger-Ellison syndrome screening); DRE (check for melena).  In patient with presenting with a typical history and without evidence of complication or malignancy, a successful therapeutic med trial can be diagnostic.

Deep gastric ulcer

By User:Samir -, CC BY-SA 3.0,

Duodenal ulcer A2 stage, acute duodenal mucosal lesion(ADML)

By melvil - Own work, CC BY-SA 4.0,

Endoscopic image of gastric ulcer, biopsy proven to be gastric cancer.

By Samir (The Scope) at the English Wikipedia, CC BY-SA 3.0,

A benign gastric ulcer (from the antrum) of a gastrectomy specimen.

By Ed Uthman, MD -, Public Domain,

Micrograph showing erosive gastric ulcer. (H&E stain)

By Department of Pathology, Calicut Medical College - Calicut Medical College, CC BY-SA 4.0,


1.     If perforated: Emergent surgery

2.     If bleeding: Inpatient treatment with serial CBC (HCTs); DRE; FOBT; NGT; IVF and PRBCs as needed.

3.     Outpatient: Pharmacotherapy S-should B-block H-HCl P-pump = SBHP -->  S-sucralfate/B-bismuth, H-H2-blocker, P-PPI, P-PGs (misoprostol).  Triple therapy for H-pylori.

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4.     Surgery: Parietal cell vagotomy with gastrectomy &/or pyloroplasty.  For IHOP --> I-intractable pain, H-hemorrhage, O-obstruction, P-perforation.

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Peptic ulcer treatment: pharmacology of drugs

By Karen Dilbaryan PHD - Own work, CC BY-SA 4.0,