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Friday, October 1, 2021

Pathophysiology of Small Intestine

Pathophysiology of Small Intestine

Pathophysiology of Small Intestine

The most important functions of the small intestine are digestion and absorption of nutrients. They are achieved by an interaction between intact small bowel motility and gastrointestinal hormones. Clinically recognizable disturbances of small bowel function arise mainly from alterations in the motor activities or interference with digestion and absorption.

 

Pathophysiology of Small Intestine

ABDOMINAL PAIN

Abdominal pain is a common manifestation of several processes involving the small intestine. The pain is often located in the mid abdomen (periumbilical region) but can also be diffuse across the abdomen. Progressive small bowel distention with or without obstruction causes colicky pain in the early stages, which later becomes constant and unrelenting. Invasive bacteria such as Yersinia can invade the terminal ileum, causing severe pain and tenderness mimicking acute appendicitis. Severe postprandial pain that incites fear of eating (sitophobia) is diagnostic of mesenteric ischemia, especially when it is accompanied by weight loss in an atherosclerotic patient. Crohn disease frequently involves the distal small bowel, with deep transmural ulceration and crampy abdominal pain in the right lower quadrant.

Gastrointestinal Hormones

Gastrointestinal Hormones

Gastrointestinal Hormones

The epithelium of the gastrointestinal tract contains multiple cell types, including specialized cells termed enteroendocrine cells that number less than 1% of the cell population and yet form the largest endocrine system of the body. Enteroendocrine cells synthesize, store, and release chemical transmitters that are involved in gastrointestinal motility, secretion, and absorption and in regulation of appetite. These transmitters are predominantly small polypeptides that are also found in the enteric nervous system and the central nervous system. There are more than 30 gut peptide hormone genes identified, which express more than 100 bioactive peptides. They are grouped into “families” according to their primary structure. In this section, the pancreatic polypeptide family will be discussed.

Gastrointestinal Hormones


Peptide YY is one of the gut peptides that belongs to the pancreatic polypeptide family of peptides, which also includes pancreatic polypeptide and neuropeptide Y. Despite sharing structural similarities and the same 36 amino acid lengths, the gut peptides vary in their biologic functions and locations. Peptide YY, neuropeptide Y, and pancreatic polypeptide bind to a family of G-protein–linked receptors (called Y receptors). At present, five receptor subtypes have been identified.

Thursday, September 30, 2021

CANCER OF CORPUS I—VARIOUS STAGES AND TYPES

CANCER OF CORPUS I—VARIOUS STAGES AND TYPES

CANCER OF CORPUS I—VARIOUS STAGES AND TYPES

Cancer of the uterine corpus usually involves malignant change of the endometrial tissues. These are generally of the adenocarcinoma, adenosquamous, clear cell, or papillary serous cell types. These cancers are the most frequent malignancy of the female reproductive tract, representing the eighth leading site of cancer-related deaths among American women.

CANCER OF CORPUS I—VARIOUS STAGES AND TYPES


Although the possibility of adenocarcinoma must be considered in patients suffering from abnormal bleeding during preclimacteric years, cancer of the uterine body must always be suspected with the appearance of abnormal spotting or staining from the fifth decade on. Any discharge from a normal cervix occurring in the postmenopausal age group should be regarded as highly suspicious of fundal malignancy. The discharge may at times be watery rather than frankly bloody. Pain, except in the presence of pyometrium, is not an early sign. When present, it may signify extension to other organs. Risk factors for the development of endometrial cancer include unopposed (without progestins) estrogen stimulation (such as in polycystic ovary syndrome, obesity, chronic anovulation, and estrogen replacement therapy without concomitant progestin). This may be a factor in up to 90% of cases. Selective estrogen receptor modulators with uterine activity (such as tamoxifen) may also place the patient at increased risk. Oral contraceptives reduce the risk of endometrial cancer.

SARCOMA

SARCOMA

SARCOMA

Sarcomatous change can occur in the tissues of the müllerian system, including the endometrial stroma and myometrium. Mixed müllerian sarcomas may include elements not native to the genital tract such as cartilage or bone (heterologous type). Sarcoma of the uterus, whether primary or occurring secondary to a preexisting fibroid, is a relatively rare disease. Of all malignancies of the female genital tract, sarcomas represent less than 5% of uterine malignancies, or roughly 1 of 800 smooth muscle tumors, with a prevalence of 0.67 per 100,000 women older than 20 years. The incidence of sarcomatous degeneration of a myoma is less than 1%. It has been found in ages from childhood to many years after menopause. There appear to be no genetic pattern, and though sarcomas are reported more often in black women, there is no racial predisposition. Leiomyomas have been proposed as risk factors for these tumors as have estrogen and obesity, though evidence is lacking. The use of oral contraceptives is associated with a reduced risk.

SARCOM


These tumors grow with surprising rapidity. Even in children, tumors have been observed that were larger than a pregnant uterus at term. The grave prognosis of such a tumor, even when treated with radical surgery, makes it advisable to cut open all leiomyomas at the time of their removal and submit all surgical specimens for histologic evaluation. A sarcoma is most apt to appear at the center of the larger tumors. It is easily recognized on cross sections, as it is soft and meaty and lacks the firm, characteristic whorled appearance of a myoma. Inadequate blood supply is often responsible for a central necrosis or hemorrhage.

MYOMA (FIBROID) III—DEGENERATION, OBSTRUCTION

MYOMA (FIBROID) III—DEGENERATION, OBSTRUCTION

MYOMA (FIBROID) III—DEGENERATION, OBSTRUCTION

Although the diagnosis of fibroids is generally a clinical one, it must be remembered that it is impossible to prove, without surgery, either the suspected diagnosis of a fibroid uterus or the assumption that such a tumor may be the cause for symptoms; ovarian neoplasms occasionally adhere to and invade the fundus posteriorly and present a mass with misleading characteristics; and bleeding may be caused by an endocrine dysfunction. After the menopause, such bleeding from a benign endometrial hyperplasia may be a telltale sign of a functioning ovarian tumor that might be overlooked unless it is recalled that fibroids almost never initiate bleeding in the postmenopausal period and certainly never cause endometrial proliferation.

MYOMA (FIBROID) III—DEGENERATION, OBSTRUCTION


Many factors play a role in each patient’s decision of management. Justification for multiple myomectomy is found in those desiring to preserve the chance of pregnancy. In those with abnormal bleeding and small fibroids at the climacteric, after the possibility of cancer has been investigated by endometrial biopsy or curettage, the diagnosis of anovulatory cycles may suggest hormonal therapy, with the hope that the complaint may be controlled until ovarian function ceases. Uterine artery embolization may be used for patients who are not surgical candidates or those who wish to preserve fertility. (Successful pregnancy is possible, but because uterine embolization has been associated with a number of both short- and long-term complications, it is considered experimental in women who desire fertility.) If the cervix has been the site of persistent atypia, or if cystocele or rectocele or uterine prolapse is present, then in those women beyond an interest in childbearing, it is wise to remove a fibroid uterus as a part of the reconstruction of a firm pelvic floor. Occasionally and unfortunately, a patient may be told that she has a tumor, and she may become so concerned with undue anxiety with regard to cancer that no choice is left in order to set her mind at rest but operative removal of the fibroids.

MYOMA (FIBROID) II—SECONDARY CHANGES

MYOMA (FIBROID) II—SECONDARY CHANGES

MYOMA (FIBROID) II—SECONDARY CHANGES

Fibroids vary greatly in size and position. Proper management, therefore, demands a consideration of the biologic life cycle of such tumors and an individual evaluation of each patient’s age, physiologic status, and procreative ambitions.

MYOMA (FIBROID) II—SECONDARY CHANGES


The diagnosis of a fibroid uterus is not in itself a justification for either myomectomy or hysterectomy. Historically, the indications for surgery were undue bleeding, increasing pressure on bladder or bowel, a rapid increase in size or change in consistency of the tumor, or some degenerative change causing pain. With improved imaging and more effective medical therapies available, the need for surgical intervention has been more limited: symptoms unresponsive to therapy and acute pain. There has also been a limited role for myomectomy when a few large fibroids are present and there has been recurrent pregnancy loss.

MYOMA (FIBROID) I—LOCATIONS

MYOMA (FIBROID) I—LOCATIONS

MYOMA (FIBROID) I—LOCATIONS

MYOMA (FIBROID) I—LOCATIONS


Uterine myomata are the most frequent tumors found in the female pelvis, with a reported incidence of from 4% to 11%. Fibroids are found in 30% of all women, and 40% to 50% of women older than 50 (one study has demonstrated a rate of more than 80% in African Americans older than 50). Leiomyomata account for approximately 30% of all hysterectomies. They are a benign connective tissue tumor found in or around the uterus, which may be disseminated in rare cases. They are commonly called “fibroids,” although these tumors derive not from fibrous tissue components but from vascular smooth muscle cells. From the point of view of the pathologist, the tumors under discussion should be classified as leiomyomata (from leios, meaning smooth).

ENDOMETRIAL HYPERPLASIA, POLYPS

ENDOMETRIAL HYPERPLASIA, POLYPS

ENDOMETRIAL HYPERPLASIA, POLYPS

ENDOMETRIAL HYPERPLASIA, POLYPS


Under the prolonged influence of estrogen, the endometrial tissues become thickened and edematous. The characteristic microscopic changes of such endometrial hyperplasia are recognizable in the epithelial glands, the endometrial stroma, and the vascular architecture. The glands often show irregular cystic dilation and are lined with low cuboidal epithelium. In long-standing cases, the size of the glands and their lumina varies to a great extent. This causes a characteristic pattern of tissue and holes, which has been called “Swiss cheese” type. In other regions or cases, adenomatous buds or pockets with heaped-up epithelial lining may appear. The over-growth in both glands and stroma and the mitotic activity in the hyperplastic endometrium are explainable by persistent estrogen stimulation. The capillary network is prominent; venous lakes are evident and spiral arterioles are thick-walled and numerous. These adenomatous changes may, at times, be so extensive and may differ from the normal or hyperplastic endometrium by such enormous proliferation that it becomes difficult, if not impossible, to exclude the presence of an early adenocarcinoma. When nuclear atypia is present, more than 40% of patients will have a coexisting endometrial cancer.

Monday, September 27, 2021

ASHERMAN SYNDROME (UTERINE SYNECHIA)

ASHERMAN SYNDROME (UTERINE SYNECHIA)

ASHERMAN SYNDROME (UTERINE SYNECHIA)

ASHERMAN SYNDROME (UTERINE SYNECHIA)


Asherman syndrome (uterine synechia) is scarring or occlusion of the uterine cavity after curettage, especially when surgery is performed after septic abortion or in the immediate postpartum period. (Though the same changes occur following therapeutic endometrial ablation, the term is generally not applied in that setting.) This scarring generally results from endometrial damage involving the basal layers (normal curettage, excessive curettage, curettage when infection is present or in the immediate postpartum period—some intra-uterine adhesions form in 30% of patients treated by curettage for missed abortion), or endometrial infection (tuberculosis or schistosomiasis). More than 90% of the cases occur following pregnancy-related curettage. A severe pelvic infection unrelated to surgery, including endometrial tuberculosis infections, may also lead to Asherman syndrome. (Chronic endometritis from genital tuberculosis is a significant cause of severe intra-uterine scarring in the developing world, often resulting in total obliteration of the uterine cavity.) A less common cause of IUA is severe endometritis or fibrosis following a myomectomy, metroplasty, or cesarean delivery. In some cases, the whole cavity may be scarred and occluded, resulting in secondary amenorrhea. Even with relatively few scars, the endometrium may fail to respond to estrogens, which means that there is a poor correlation between symptoms and the severity of scarring found.

ADENOMYOSIS

ADENOMYOSIS

ADENOMYOSIS

ADENOMYOSIS


Adenomyosis is a condition where endometrial glands and stroma are found within the uterine wall (myometrium). This is the intramural equivalent of extrauterine endometriosis. This is somewhat misleading because endometriosis and adenomyosis coexist in the same patient in about 15% of women while they are clinically different diseases. The only common feature is the presence of ectopic endometrial glands and stroma. Adenomyosis is thought to affect 10% to 15% of all women and may be as high as 60% in women 40 to 50 years old. The predominant age of patients with adenomyosis is between 35 and 50 years, and there appears to be a mild familial predisposition (polygenic or multifactorial inheritance) pattern.

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