hemorrhagic necrosis
Introduction
Introduction The pathological anatomy of aflatoxin poisoning showed diffuse hyperemia and hemorrhagic necrosis of the liver. Aflatoxin is a molecular mycotoxin. In China, the allowable amount of aflatoxin in rice and edible oil is 10ug/Kg, and other foods, beans and fermented foods are 5ug/Kg. Baby milk substitute foods should not be detected. The World Health Organization recommends a maximum allowable amount of aflatoxin in food and feed of 15 ng/kg. 30 ~ 50ug / kg for low toxicity, 50 ~ 100ug / kg for poisoning, 100 ~ 1000ug / kg for high toxicity, 1000ug / kg or more for extreme toxicity. Its toxicity is 10 times that of potassium cyanide and 68 times that of arsenic. In addition, aflatoxin is highly carcinogenic.
Cause
Cause
It is mainly produced by Aspergillus flavus and Aspergillus parasiticus. Its basic structure contains difuran ring and dicoumarin. According to its fine structure, it can be divided into B1, B2, G1, G2, M1, M2 and so on. B2 is blue under ultraviolet light, and G1 and G2 are green fluorescence. Among them, aflatoxin B1 is the most toxic and has strong carcinogenicity. Aflatoxin mainly damages the liver, manifested as hepatocyte nuclear swelling, steatosis, hemorrhage, necrosis and bile duct epithelium, fibrous tissue hyperplasia. At the same time, the kidney can also be damaged, mainly characterized by degeneration, necrosis of the renal tubular epithelial cells, and tubular formation.
Examine
an examination
(1) A history of eating food contaminated with aflatoxin.
(2) All seasons can occur, but often after the rainy season.
(3) Children are more susceptible to aflatoxin poisoning. According to historical data analysis, the most dangerous age for human poisoning is 1 to 3 years old.
(4) The precursor of poisoning is fever, abdominal pain, vomiting, loss of appetite, etc.
(5) toxic liver disease occurs very quickly after 2 to 3 weeks: liver enlargement, pain in the liver area, jaundice, splenomegaly. Ascites, lower extremity edema and abnormal liver function.
(6) may have heart enlargement, pulmonary edema, and even convulsions, coma, etc., most patients may have gastrointestinal bleeding before death.
(7) Clinical toxicity studies of experimental animals showed that after feeding the aflatoxin-containing feed to the animals, the performance was asexual loss of appetite, thirst, blood in the stool, slow growth, weight loss, skin bleeding, excessive excitement, yellow colonization, convulsions. , angle bow reversal, etc. Pathological anatomy showed diffuse hyperemia of the liver, hemorrhagic necrosis and other manifestations.
Diagnosis
Differential diagnosis
Ischemic necrosis of the appendix wall: the intracavitary pressure continues to increase, the appendix wall is also compressed, the venous return is blocked, the appendix wall edema and ischemia, bacteria can penetrate into the abdominal cavity. In severe cases, the arteries are also blocked, causing necrosis of the appendix. The location of the luminal obstruction is mostly at the base of the appendix, but also in the middle and distal segments of the appendix.
Small vessel fibrotic necrosis: common in Fibrinous inflammation. Celluloid inflammation, which is dominated by fibrinogen exudation, which in turn forms fibrin, or cellulose. In HE sections, cellulose is red-dyed interlaced in a network, strip or granule, often mixed with fragments of neutrophils and necrotic cells. Necrosis is the death of local tissue cells in vivo characterized by changes in enzyme solubility. Necrosis can be directly caused by strong pathogenic factors, but most of them are developed from reversible damage. The basic manifestations are cell swelling, organelle disintegration and protein denaturation.
Tissue necrosis: After local tissue and cell metabolism stop, its function is completely lost. The cells may undergo changes such as nuclear condensation, nuclear fragmentation, and nuclear dissolution. The organization that truly loses its ability to live is called inactivation tissue. Generally, the inactivated tissue has a dull appearance and is relatively turbid (matte). Loss of normal tissue elasticity (inelasticity). Because of the lack of normal blood supply, the temperature is low, and the pulsation of the blood vessels is not felt. When the inactivated tissue is removed during debridement, no fresh blood flows out from the blood vessels (no blood supply). Inactivated tissue loses normal sensation (skin pain, tenderness) and motor function (intestinal peristalsis) (no sensory and motor function).
