Rogers 12-17-07 Review GI Histopathology

Motor disorders:

The automatic coordination of muscular movement during swallowing is termed a and results in free passage of food through the esophagus
The hallmark of motor disorders is difficulty in swallowing, termed dysphagia
Dysphagia is often an awareness that a bolus of food is not moving downwards, and in itself is not painful
Pain on swallowing is odynophagia

Motor disorders can be caused by:

Dysfunction of striated skeletal muscle in the upper esophagus
Systemic diseases of skeletal muscle such as myasthenia gravis, dermatomyositis, amyloidosis, hyperthyroidism, and myxedema
Neurological diseases that affect nerves to skeletal muscle (e.g., cerebrovascular accidents, amyotrophic lateral sclerosis)
Peripheral neuropathy associated with diabetes or alcoholism

Atrophy - is a reduction in the size and function of the cell e.g. disuse atrophy of skeletal muscle in immobilisation for fracture
Hypertrophy - is the increase in size and function of a cell e.g. physiological (hormonal) or work hypertrophy (left ventricular hypertrophy in hypertension)
Hyperplasia - is the increase in the number of cells in an organ or tissue e.g. hormonal stimulation & increased functional demand - bone marrow in haemolytic anaemia
Metaplasia - is the conversion of one differentiated cell type to another due to alteration in the direction of proliferation and maturation of cells.
Dysplasia - refers to an alteration of size, shape and arrangement of the cellular components of a tissue e.g. in the epidermis in actinic keratosis.

b) Congenital adencarcinoma

Barrett esophagus carries a serious risk of malignant transformation to adenocarcinoma, and the risk correlates with the length of the involved esophagus and the degree of dysplasia
\Virtually all adenocarcinomas arise in the background of the metaplastic epithelium of Barrett esophagus
The symptoms and clinical course of adenocarcinoma of the esophagus are similar to those of squamous cell carcinoma and include dysphagia, pain, and occasionally bleeding.
Diagnosis: Barrett esophagus

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This is Candida esophagitis. Tan-yellow plaques are seen in the lower esophagus, along with mucosal hyperemia. The same lesions are also seen at the upper right in the stomach.

Acute esophagitis is manifested here by increased neutrophils in the submucosa as well as neutrophils infiltrating into the squamous mucosa at the right.
The spaces between cells = inflammatory process = edema

At the upper left is a remnant of squamous esophageal mucosa that has been undermined by an infiltrating squamous cell carcinoma of the mid-esophagus. Solid nests of neoplastic cells are infiltrating down through the submucosa at the right. Esophageal cancers often spread to surrounding structures, making surgical removal difficult.

Anaplasia: Ugly cells. A marker for cancer or pre-cancer
Neoplasia: A new, useless organ produced by cells bearing mutations
Dysplasia: Ugly cells in an epithelium, without invasion. Near-synonyms are "carcinoma in situ", "intraepithelial neoplasia", "incipient neoplasia", and "precancer“
Characteristics of benign tumors - cells resemble normal cells and tumor architecture resembles that of the parent organ ("well-differentiated")

Characteristics of Malignant tumors:

Malignant tumors generally grow more rapidly than benign tumors.
However, no malignant tumor grows as rapidly as an embryo, nor do cancer cells divide nearly as fast as cells in normal bone marrow or intestinal epithelium
Today, anyone who thinks of cancer cells growing "without any control" is guilty of willful ignorance

Characteristics of Malignant tumors:

Cells differ morphologically and functionally from normal cells, and tumor architecture is less organized than that of parent tissue.
Tumor cells are locally invasive - the tumor grows into the surrounding tissue and destroys it.
This feature led Dr. Hippocrates to call such tumors karkinoma after karkinos, Greek for "crab."
Cancer is Latin for "crab"

At high power, these infiltrating nests of neoplastic cells have abundant pink cytoplasm and distinct cell borders typical for squamous cell carcinoma. Esophageal carcinomas are not usually detected early and, therefore, have a very poor prognosis.

EVs are dilated veins located immediately below the mucosa that prone to rupture and hemorrhage
They arise in the lower third of the esophagus, virtually always in patients with cirrhosis and portal hypertension
The lower esophageal veins are linked to the portal system through gastroesophageal anastomoses
If portal system pressure exceeds a critical level, these anastomoses become prominent in the upper stomach and lower esophagus
When varices are greater than 5 mm in diameter, they are prone to rupture, leading to life-threatening hemorrhage
Reflux injury or infective esophagitis can contribute to variceal bleeding

Numerous prominent blue venous channels are seen beneath the mucosa of the everted esophagus, particularly above the gastroesophageal junction. Section of the esophagus reveals numerous dilated submucosal veins.

The mucosa has three components: a lining epithelium, an underlying lamina propria consisting of a vascularized loose connective tissue, and a thin layer of smooth muscle, the muscularis mucosae
Lymphatic nodules and scattered immunocompetent cells (lymphocytes, plasma cells, and macrophages) are present in the lamina propria (the lamina propria of the small and large intestines is a relevant site of immune response)
The lining epithelium invaginates to form glands, extending into the lamina propria (mucosal glands) or submucosa (submucosal glands), or ducts, transporting secretions from the liver and pancreas through the wall of the digestive tube (duodenum) into its lumen.

The muscularis contains two layers of smooth muscle: the smooth muscle fibers of the inner layer are arranged around the tube lumen (circular layer); fibers of the outer layer are disposed along the tube (longitudinal layer)
Contraction of the smooth fibers of the circular layer reduces the lumen; contraction of the fibers of the longitudinal layer shortens the tube
Skeletal muscle fibers are present in the upper esophagus and the anal sphincter

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The submucosa contains a network of collagen and elastic fibers and many small blood vessels
At the lower end of the esophagus, submucosal venous plexuses drain into both the systemic venous system and the portal venous system
An increase in pressure in the portal venous system, caused by chronic liver disease, results in dilation of the submucosal venous sinuses and the formation of esophageal varices
Rupture of the varices or ulceration of the overlying mucosa can produce hemorrhage into the esophagus and stomach, often causing vomiting (hematemesis)

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The two most common types of esophageal cancer are squamous cell carcinoma, which originates in the squamous cells lining the esophagus, and adenocarcinoma, which develops in the glandular cells lining the organ
Esophageal cancer is notorious for its aggressive behavior, local infiltration, involvement of the adjacent lymph nodes, and a wide metastasis through the hematogenous spread
Tumors of the upper and mid-thirds infiltrate the loop around the aortic arch, whereas lower third tumors may invade the diaphragm, pericardium, or stomach
The extensive mediastinal lymphatic drainage, which communicates with cervical and abdominal collateral vessels, is responsible for the finding of mediastinal, supraclavicular, or celiaclymph node metastases in at least 75% of patients with esophageal carcinoma

Stage I. The cancer is found only in the top layers of cells lining the esophagus.
Stage II. The cancer involves deeper layers of the lining of the esophagus, or it has spread to nearby lymph nodes. The cancer has not spread to other parts of the body.
Stage III. The cancer has invaded more deeply into the wall of the esophagus or has spread to tissues or lymph nodes near the esophagus. It has not spread to other parts of the body.
Stage IV. The cancer has spread to other parts of the body. Esophageal cancer can spread almost anywhere in the body, including the liver, lungs, brain, and bones

As its incidence has recently increased, adenocarcinoma of the esophagus is now more common (60%) in the United States than squamous carcinoma
Virtually all adenocarcinomas arise in the background of Barrett esophagus, although a rare case originates in submucosal mucous glands
Endoscopic surveillance for adenocarcinoma is now commonly done in patients with Barrett esophagus, particularly in those with dysplasia
The symptoms and clinical course of esophageal adenocarcinoma are similar to those of squamous cell carcinoma

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