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                          Myxoid Tumours of Soft Tissue

 
December 2007

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Environmental Pathology- Smoking

 

Cigarette smoking and Cardio vascular Disease 

Cigarette smoking and Cancer

Non-Neoplastic Diseases in Smokers

Cigarette Smoking and diseases in Women

Environmental Pathology- Alcoholism (Mechanism of Tissue Injury)

Complication of Chronic Alcoholism

Environmental Pathology- Drug Abuse

Environmental Pathology - Iatrogenic Drug Injury:

Iatrogenic Drug Injury - Oral contraceptives

Environmental Pathology - Effect of Chemicals

Toxic effect of volatile organic solvents and vapors

Toxic effect of agricultural chemicals

Environmental Pathology - Toxic effect of Metal

Lead Intoxication

Mercury Exposure

Arsenic  

Iron

Environmental Pathology - Physical Agents  

Environmental Pathology-Thermal Regulatory Dysfunction

Environmental Pathology - Hypothermia

Environmental Pathology - Hyperthermia

Environmental Pathology- Electrical Burns

Environmental Pathology- Altitude Related Illnesses

Environmental Pathology - Physical Injuries

                         

CLICK ON THE IMAGE (Acute Radiation Syndromes).

There have been few instances of human disease caused by whole-body irradiation, and most of our information has been derived from studies of Japanese atom bomb casualties.

Further information have been obtained from study of the survivors of the much smaller sample of people exposed in the accident at the Chernobyl nuclear power plant in the USSR in 1986.

Since by definition the same dose of radiant energy is transmitted to all organs in whole-body irradiation, the development of the different acute radiation syndromes clearly reflects only the dissimilarities in the vulnerbility of the target tissues.

At a dose of approximately 300 rads, a syndrome characterized by hematopoietic failure develops within 2 weeks.  Since all hematopoietic precursor elements are highly sensitive to radiant energy, a pancytopenia typically characterizes the hematopoietic whole-body irradiation syndrome. Following an initial depression of  circulating lymphocytes, a progressive decrease in formed elements of the blood eventually leads to bleeding, anemia and infection. The last is often the cause of death.

With more intense radiation, about 1000 rads, the principal cause of death is related to the gastrointestinal system. While gastrointestinal symptoms characterizes the entire dose range of whole-body exposure, at higher levels severe destruction of the entire epithelium of the gastrointestinal tracts occur within 3 days, the time that corresponds to the normal life span of the villous and crypt cells. As a result the fluid homeostasis of the bowel is disrupted and severe diarrhea and dehydration ensue. Moreover, the epithelial barrier to intestinal bacteria is breached, and bacteria invade and disseminate throughout the body. Shock and septicemia kill the victim.

With exposure to whole-body doses of 2000 rads and greater, central nervous system damage causes death within hours. In most cases, endothelial injury resulting in cerebral edema and loss of the integrity of the blood-brain barrier predominates, but with extreme doses radiation necrosis of neurons can be expected. Convulsions, coma, and death follow.

The effects of whole-body irradiation on the human fetus have been documented in studies of the survivors of the atom bomb explosions in Japan.

Pregnant women exposed to doses of 25 rads or greater gave birth to infants with reduced head size, diminished overall growth , and mental retardation. [ Intrauterine exposure to radiation at Nagasaki was significantly less teratogenic than at Hiroshima. This disparity has been attributed to a difference in the quality of the radiation in the two cities. The bomb dropped on Hiroshima produced far greater fast-neutron radiation (20% as opposed to 1% of the total energy released), which is lower in energy than comparable doses of gamma rays and, therefore, produce greater biologic damage.]

In studies of the clinical status of children who were exposed to therapeutic doses of radiation in utero, the most likely time for the production of growth retardation and microcephaly was between third and twentieth week of gestation.

Other effects of irradiation in utero include hydrocephaly, microphthalmia, chorioretinitis , blindness, spina bifida, cleft palate, club feet, and genital abnormalities.

Data derived from experimental and human studies strongly support the conclusion that major congenital malformations are highly unlikely with doses less than 20 rads after 14 days of pregnancy.

This does not mean that lower doses cannot produce subtle effects, but these have not been documented.

To protect against such a possibility, the established maximum permissible dose to the fetus from exposure of the expectant mother is far below the known teratogenic dose.

The potential genetic effects of radiation have been the source of considerable public concern.

After long-term follow-up, even the survivors of Hiroshima and Nagasaki have failed to manifest evidence of genetic damage in the form of either congenital abnormalities or hereditary diseases in subsequent offspring or their descendants.

The finding that rodents exposed to whole-body radiation have a shortened life span led to the suggestion that radiation accelerates the aging process.

The effects or ionizing radiation on mortality are specific and focal, and there is no reason to believe that premature aging in humans or radiation-induced carcinogenesis is due to a general acceleration of aging.

Environmental Pathology - Radiation : click here

Localized Radiation Injury Associated with Radiotherapy: click here

Radiation and Cancer: click here

Cutaneous lesions after exposure to Radiation: click here

                         

Acute radiation colitis in patients treated with short-term preoperative radiotherapy for rectal cancer.Am J Surg Pathol 2002 Apr;26(4):498-504.

The histopathologic features of acute radiation-induced colitis in humans have been described in occasional, >20-year-old studies, but they have not been analyzed in detail.

We characterize such findings in 34 patients with rectal cancer who underwent surgery a few days after preoperative irradiation with 25 Gy given over 5-7 days, and we compare the results to the histopathologic features detected in 18 patients treated by a conventional preoperative irradiation protocol consisting of 45 Gy during 5 weeks followed by surgery after a time interval of at least 3 weeks. Short-term preoperative irradiation therapy generally induced severe mucosal inflammation characterized by increased cellularity of the lamina propria, prominent eosinophilic infiltrates, crypt disarray, surface and crypt epithelial damage, nuclear abnormalities, and presence of apoptotic bodies in the crypt epithelium. These histopathologic features were absent or detected only occasionally in the patient group treated according to the long-term preoperative irradiation protocol. Despite acute severe inflammation, none of the patients treated by short-term irradiation developed perioperative complications. These observations indicate that acute radiation colitis may remain clinically silent and resolve spontaneously within a few weeks after irradiation.

Given the widening acceptance of short-term preoperative irradiation protocols for rectal cancer, pathologists should be aware of the rather characteristic histologic findings of acute radiation colitis and avoid unnecessary concern of clinicians. The differential diagnosis includes infectious colitis, collagenous and ischemic colitis, nonsteroidal anti-inflammatory drug-associated colitis, and chronic idiopathic inflammatory bowel disease.