A 3-cm segment in the proximal esophagus at the level of the cricopharyngeus muscle is referred to as the upper esophageal sphincter

(UES). The 2- to 4-cm segment just proximal to the anatomic gastroesophageal junction, at the level of the diaphragm, is referred to as the lower esophageal sphincter (LES). Both "sphincters" are physiologic, in that there are no anatomic landmarks that delineate these higher-pressure regions from the intervening esophageal musculature.

Heartburn (retrosternal burning pain) usually reflects regurgitation of gastric contents into the lower esophagus. Dysphagia (difficulty in swallowing) is encountered both with deranged esophageal motor function and with diseases that narrow or obstruct the lumen. Pain and hematemesis are sometimes evoked by esophageal disease, particularly by those lesions associated with inflammation or ulceration of the esophageal mucosa

Ectopic tissue rests are not uncommon in the esophagus. The most common is ectopic gastric mucosa in the upper third of the esophagus ("inlet patch"), occurring in up to 2% of individuals. Sebaceous glands or ectopic pancreatic tissue are much less frequent. The acid secretions of the ectopic gastric mucosa or pancreatic enzymatic secretions can produce localized inflammation and discomfort. Embryologic formation of the foregut can also give rise to congenital cysts. These are usually duplication cysts, containing double smooth muscle layers and derived from the lower esophagus in 60% of cases. Rarely, bronchial or parenchymal pulmonary tissue may arise from the upper gut and is denoted bronchogenic cyst or pulmonary sequestration, respectively. These lesions usually present as masses. Lastly, impaired formation of the diaphragm may permit herniation of abdominal viscera into the thorax. When severe, this lesion is incompatible with life, since the lungs are severely hypoplastic at the time of birth. This condition is to be distinguished from hiatal hernias, to be discussed presently. Esophageal atresia and tracheoesophageal fistula. A, Blind upper and lower esophageal segments. B, Blind upper segment with fistula between lower segment and trachea. C, Fistula between patent esophagus and trachea. Type B is the most common. Esophageal mucosal webs are uncommon ledgelike protrusions of the mucosa into the esophageal lumen. These are semicircumferential, eccentric, and most common in the upper esophagus. Welldeveloped webs rarely protrude more than 5 mm into the lumen, with a thickness of 2-4 mm. The webs consist of squamous mucosa and a vascularized submucosal core. Webs can be congenital in origin, or they may arise in association with long-standing reflux esophagitis, chronic graft-versus-host disease (GVHD), or blistering skin diseases. When an upper esophageal web is accompanied by an irondeficiency anemia, glossitis, and cheilosis, the condition is referred to as the Paterson-Brown-Kelly or Plummer-Vinson syndrome, with an attendant risk for postcricoid esophageal carcinoma. Esophageal rings are concentric plates of tissue protruding into the lumen of the distal esophagus. One occurring above the squamocolumnar junction of the esophagus and stomach is referred to as an A ring.

One located at the squamocolumnar junction of the lower esophagus is designated a Schatzki ring or a B ring. Histologically, these rings consist of mucosa, submucosa, and sometimes a hypertrophied muscularis propria. Schatzki rings may have columnar gastric epithelium on their undersurface. Esophageal webs and rings are encountered most frequently in women over age 40 and are of uncertain etiology. Episodic dysphagia is the main symptom associated with webs and rings, usually provoked when an individual bolts solid food. Pain is infrequent. Esophageal stenosis consists of fibrous thickening of the esophageal wall, particularly the submucosa, with atrophy of the muscularis propria. The lining epithelium is usually thin and sometimes ulcerated. Although occasionally of congenital origin, stenosis is more frequently the result of severe esophageal injury with inflammatory scarring, as from gastroesophageal reflux, radiation, scleroderma, or caustic injury. Stenosis usually develops in adulthood and becomes manifest by progressive dysphagia, at first to solid foods only but eventually to all foods, which constitutes the major symptom. In severe stenosis, virtually total obstruction may result.

TRUE diverticula usually have all 4 layers in its wall: Muc/Submuc/Musc/Adventitia. Which one of these might result in dysphagia? Ans: Zenkers

LACERATIONS (MALLORY-WEISS SYNDROME) Longitudinal tears in the esophagus at the esophagogastric junction or gastric cardia are termed Mallory-Weiss tears and are believed to be the consequence of severe retching or vomiting.[6] They are encountered most commonly in alcoholics, in whom they are attributed to episodes of excessive vomiting in the setting of an alcoholic stupor. Normally, a reflex relaxation of the musculature of the gastrointestinal tract precedes the antiperistaltic wave of contraction. During episodes of prolonged vomiting, it is speculated that this reflex relaxation fails to occur. The refluxing gastric contents suddenly overwhelm the contraction of the musculature at the gastric inlet, and massive dilation with tearing of the stretched wall ensues. Since these tears may occur in persons who have no history of vomiting or alcoholism, other mechanisms must exist; underlying hiatal hernia is a known predisposing factor.

Candida, candida esophagitis in a HIV positive patient often is indicative of full blown AIDS.

Herpes, from the points of view of the endoscopist and the pathologist. Might these large nucleolated cells be exfoliated as Tzanck cells?

Would you call this squamous dysplasia ? Answer: YES Would your fear it would develop into squamous cell carcinoma? Answer: YES Does it always? Answer: NO Does it usually? Answer: With time, YES

If you think of the acid production in the stomach to be ONLY in the mid-BODY, and the proximal and distal ends as chiefly mucous to protect the esophagus and duodenum from the harsh acid, then you will understand the histology.

Somatostatin (also known as growth hormone-inhibiting hormone (GHIH) or somatotropin releaseinhibiting factor (SRIF)) is a polypeptide that regulates the endocrine system and affects neurotransmission and cell proliferation via interaction with G-protein coupled somatostatin receptors and inhibition of the release of numerous secondary hormones. Endothelins are proteins that constrict blood vessels and raise blood pressure

Prostaglandin E both DECREASES acid and INCREASES mucous.

The acute/chronic patterns of gastritis generally conform to the poly/mono principles we so often have referred to. The other category of gastritis are also histologically based.

The concepts and histologic changes in acute and chronic follow the classic histologic principles: Acute polymorphonucleus Chronic mononucleus

ACUTE gastritis Hemorrhage, erosions , neutrophils (i.e., POLYS ) CHRONIC gastritis MONOS, NO hemorrhage, NO erosions And do not forget: CHRONIC of the follows ACUTE

Would an autoimmune gastritis be associated with megaloblastic anemia? Why? Answer: DECREASED intrinsic factor No doubt achlorhydria is the common factor of chronic gastritis and B12 megaloblastic anemias

Please remember acute stress ulcers are highly related to an EXCESS of endogenous or exogenous steroids.

This type of acute stress ulcer is often confused with ulceration from gastric intubation, but intubation ulcers are usually more linear and less diffuse.

A large obstructive bezoar usually takes on the shape and contour of the stomach

HYPERPLASTIC POLYPS are considered to be NON-neoplastic, and therefore NEVER turn into cancers. ADENOMATOUS polyps are true benign neoplasms and MAY turn into carcinomas, particularly if the exhibit DYSPLASIA on biopsy.

The concept of GASTRIC polyps generally follows the concepts of COLONIC polyps, i.e., HYPERPLASTIC are ALL benign with many different types of cells, and ADENOMATOUS are more associated with malignancy, but are NOT NECESSARILLY pre-malignant.

The LINITIS PLASTICA is the most SPECTACULAR, and most FEARED, of all gastric adenocarcinomas. It grows DIFFUSELY through all layers of the stomach, greatly thickening its wall, and giving the stomach a classic LEATHER BOTTLE appearance. It has a horrible prognosis.

If you thought this yucky whitish stuff was mucin, what stain would you order to prove it? Answer: Mucicarmine stain. Is a positive muci-CARMINE stain RED (i.e., carmine colored)? Answer: YES

Signet ring cells are POORLY differentiated adenocarcinoma cells, and are OFTEN seen with linitis plastica. Could those large holes in the cytoplasm possibly be mucicarmine positive Answer: YES

For as notoriously complex as all this sounds, they look like boring leiomyomas, and in the days PREimmunochemistry, they probably WERE called smooth muscle tumors.

Gastroschisis is also called paraomphalocele, laparoschisis, or abdominoschisis. Gastroschisis is a birth defect in which an infant's intestines stick out of the body through a defect on one side of the umbilical cord. Similarly, omphalocoele is a type of abdominal wall defect in which the intestines, liver, and occasionally other organs remain outside of the abdomen in a sac because of a defect in the development of the muscles of the abdominal wall.

Infarcted bowel is usually purple and paper thin

Ileus is a disruption of the normal propulsive gastrointestinal motor activity from NON-mechanical mechanisms. Motility disorders that result from structural abnormalities are termed mechanical bowel obstruction. So if you think of the whole anatomy and physiology of peristalsis, ileus can be defined as any major problem in the whole scheme of things.

NOTE the various types of epithelial cells .this is the reason it is benign, i.e., NON monoclonal.

Villous adenomas behave more aggressively than tubular adenomas. They have a HIGHER rate of developing into frank adenocarcinomas than the tubular patterns.

The liver is nothing more than an array of cells between the portal and caval venous systems. This shows the direction of flow. The liver gets about 80% of its blood supply fron the portal veins and 20% from the hepatic arterial system.

Recognizing those little holes grossly, is the same as recognizing them microscopically. If they seem to have connective tissue or bile around them, they are PORTAL veins. If they seem to have NO connective tissue or bile around them, they are central or hepatic veins.

The FIRST part of the lobule, i.e., portal triad is the FIRST to get blood flow, so it is also the FIRST to get the brunt of general toxic effects, and the LAST to get the brunt of ischemic effects.

Heatocyte cytoplasm is balooned This is nothing more than the swelling we learned of in chapter 1

Hepatocytes have feathery cytoplasm This is nothing more than the swelling we learned of in chapter 1

You must always know the THREE common causes of fatty liver, also called fatty metamorphosis, also called fatty change, also called steatosis: 1) Obesity 2) Alcoholism 3) Diabetes

Fat vacoules are small enough to lie completely WITHIN the hepatocte cytoplasm are termed MICROvesicular

Fat vacuoles which are LARGER than hepatocytes is termed MACRO-vesicular. Why is the differential diagnosis of MACRO vesicular steatosis the same as MICRO vesicular steatosis? Answer: It is just a matter of severity.

Crucially important concept worth repeating. KNOW the difference between an acinus and a lobule. The best tip to understanding liver disease is to understand the direction of blood flow. TOXIC injuries generally do more damage in the part of the liver closest to the PORTAL vein, and HYPOXIC injuries generally do more damage in the parts of the liver around the CENTRAL vein, i.e., centrolobular necrosis.

The hyalinized appearing round structures are cells dying from a NORMAL replacement process called apoptosis. Where should we put the 2 arrows to demonstrate two apoptotic cells? If this was hepatitis, we might call them Councilman bodies.

Triads are involved with hepatitis earlier than general sinusoids. Why?

Is this type of hepatitis likely to be SUB-clinical? Answer: YES Is most hepatitis SUB-clinical? Answer: YES

The hepatoma/cirrosis cycle: Hepatomas often, perhaps usually, arise in a cirrhosis background, and can be thought of as regenerating nodules that have lost growth control, ususlly NOT metastasizing, the hepatoma itself causing FURTHER functional liver disease.

How can a blind man differentiate cirrhosis from metastatic disease? Answer: In cirrhosis there are no SMOOTH areas between nodules.

Why are TRICHROME stains recommended for every liver biopsy?

Almost all primarilly INTRACELLULAR liver pathologies result in MEMBRANE elevations too, and VICE VERSA!

A normal liver should NOT have this much bile pigment, in fact bile pigment in a normal liver biopsy should be scarce!

The inflammation of hepatitis starts in the portal triad areas, with increasing severity it extends to the sinusoids.

Fulminant hepatitis is associated with massive hepatic necrosis and often (usually) results in death. If you think this liver is abnormally SMALL, you are correct

Note complete COLLAPSE of lobules, and only remnants of biliary epithelium.

It would be VERY nice to see Councilman bodies on a liver biopsy to enable the diagnosis of Hepatitis B. Unfortunately, you may not be lucky enough to find them. Does this remind you of the apoptosis image? Each Councilman body represents apoptotic death of a single liver cell.

The MAIN differential of NON viral hepatitis : 1) TOXIC (alcohol the most common), 2) autoimmune, and 3) non-viral infectious!

Alpha-1-antitrypsin PROTECTS tissues, especially lung, liver, from HARMFUL NATURAL PROTEASE. Lack of this enzyme, due to a genetic defect, would then be expected to cause destructive changes in these areas.

Individually, hepatoma cells usually very closely resemble normal hepatocytes! The toxin AFLATOXIN from certain ASPERGILLIS species of fungus is a carcinogen and aids carcinogenesis of hepatocellular cancer by building up in the liver. The combined high prevalence of rates of aflatoxin and hepatitis B in settings like China and West Africa has led to relatively high rates of heptatocellular carcinoma in these regions.

Cholangiocarcinoma is ALWAYS confused with liver metastases. Why? What feature of this picture would NOT suggest metastases?

Is a gallbladder coated with cholesterol, like this one, associated with arteries coated with cholesterol? Ans: YES