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On images, they are visualized as a clearly demarcated cavity with invisible walls, pushing back adjacent structures, with contents characterized by a pattern similar to that of cerebrosinal fluid (hypointense on computed tomography, hyperintense on T2 weighted images, and hypointense on T1WI on magnetic resonance imaging). They can also cause remodeling of Erectile Dysfunction pills bone.
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Work on a specific interpretation of the diagnosis can only be carried out in laboratories specially equipped to work with especially dangerous viruses. It should be borne in mind that antibodies appear no earlier than 10-20 days from the onset of the disease. It is necessary to differentiate from other hemorrhagic fevers. Treatment of Argentine hemorrhagic fever.
Take into account epidemiological data (stay in an endemic area, incidence rate, etc.) and characteristic clinical symptoms.
In more severe forms, pronounced manifestations of thrombohemorrhagic syndrome develop: hematemesis, melena, bleeding gums, nosebleeds, hematuria. Possible changes in the nervous system - excitement, delirious state, stupor. On the 7-10th day, shock, gastrointestinal bleeding may occur. In fatal cases, the cause of death is usually pulmonary edema. Diagnosis of Argentine hemorrhagic fever.
There may be slight enlargement of the lymph nodes. On the 3-5th day of illness, the patient's condition worsens, signs of Erectile Dysfunction pills appear (BP drops to 50-100 mm Hg), oliguria increases.
Symptoms of Argentine hemorrhagic fever. The incubation period lasts from 7 to 16 days. The disease begins gradually. Body temperature rises, sometimes with chills, weakness, headache, muscle pain, nausea, vomiting, anorexia appear. The fever grows and reaches 39-40°C. Examination reveals flushing of the face, neck, injection of scleral vessels.
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At the site of the gate of infection, the primary affect is not observed. The dissemination of the virus and the defeat of a number of organs and systems are characteristic. The development of thrombohemorrhagic syndrome plays an important role in pathogenesis.
- The gates of infection are the mucous membranes of the respiratory organs and the digestive tract, infection through microtrauma of the skin is possible.
- Many issues of pathogenesis are not well understood.
- Pathogenesis (what happens?) during Argentine hemorrhagic fever.
- Epidemic outbreaks were observed annually, the number of cases ranged from 100 to 3500 people.
The reservoir and source of infection are rodents Calomis laucha, Calomis musculinus. Viruses were also isolated from gamasid mites. The incidence is characterized by seasonality - from February to June, the peak incidence in May. Mostly rural residents get sick. Infection occurs by airborne dust, inhaling dust infected by rodents. Infection can also occur through food contaminated with rodent urine.
The causative agent of Argentine hemorrhagic fever - the Junin virus (after the city where the first cases of the disease were registered) belongs to arenaviruses, which include the causative agents of Lassa fever and Bolivian hemorrhagic fever. The virus is pathogenic for newborn white mice and hamsters. Cultivated on chicken embryos and in the culture of transplanted cells.
Argentine hemorrhagic fever. What is ArgentinaArgentine Hemorrhagic Fever What causes Argentine Hemorrhagic Fever Pathogenesis (what happens?) during Argentine Hemorrhagic Fever Symptoms of Argentine Hemorrhagic Fever Diagnosis of Argentine Hemorrhagic Fever Treatment of Argentine Hemorrhagic Fever Prevention of Argentine Hemorrhagic Fever Which doctors should you contact if you have Argentine Hemorrhagic Fever.
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Arachnoid cysts are benign and the vast majority are asymptomatic throughout life. In the presence of symptoms, the following are used: surgical treatment in the form of craniotomy with excision of the cyst walls and its fenestration into the basal cisterns, aspiration through the burr hole, ventriculo-peritoneal shunting.
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Phase-contrast images can be used not only to determine the relationship of the cyst to the subarachnoid space, but also to localize this connection. MR cisternography: high-resolution sequences such as CISS or FIESTA allow determination of walls in relation to adjacent anatomical structures.
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Since their walls are very thin, it is extremely rarely possible to visualize them, and only the displacement of adjacent structures makes it possible to suspect their presence. The absence of a solid component causes the absence of contrast enhancement.
Magnetic resonance imaging. Since arachnoid cysts are filled with cerebrospinal fluid, they have similar signaling characteristics including the FLAIR and DWI sequences, allowing them to be differentiated from epidermoid cysts.
Arachnoid cysts are clearly demarcated formations with non-visualized walls, causing displacement of adjacent structures, with large sizes causing bone tissue remodeling at this level. CT cisternography can help identify the relationship between the subarachnoid space and the cyst.
Most often, arachnoid cysts are located in the middle cranial fossa where they prolapse into the dilated Sylvian fissure, but can occur elsewhere, including: interhemispheric fissure; convexital surface of the cerebral hemispheres.
Arachnoid cysts arise as a result of the formation of a congenital duplication of the arachnoid membrane, followed by its filling with cerebrospinal fluid. The walls of the cyst consist of flat glial cells (meningothelium) forming a translucent membrane. The solid component and epithelial lining are absent.