00:32,8,Feb,2010 | (848/0/0) | Original

pictures of klinefelters syndrome

Styloid process syndrome (styloid syndrome) also known as the styloid process (elongated styloid process), or Eagle syndrome (Eagle syndrome), is due to elongated styloid process or the orientation, morphology abnormal stimulation of adjacent vessels and nerves caused by foreign body in throat flu, sore throat or earache reflex, head and neck pain and increase in the number of salivary gland syndrome. Common in adults with unilateral disease more common.
】 【Etiology and pathogenesis
1, the elongated styloid process:
The average length of the styloid process normally about 2.5cm, than the length that the elongated styloid process. Styloid process of temporal bone from the front under the stylomastoid foramen within the party, was like a thin cylinder, remote stretch, the front bottom, in the carotid artery and external carotid arteries. Styloid process to a remote stretch near the tonsillar fossa or both tonsillectomy or not, foreign body sensation in the throat may occur, such as the oppression of nerve endings, sore throat and other symptoms can occur. Pressure or friction is too long styloid carotid artery, affecting blood circulation, can cause pain in the corresponding region. But there are also styloid process and asymptomatic.
2, position and shape of abnormal styloid process:
Styloid process length of some patients in the normal range, but its position and shape of abnormal, or abnormal carotid artery so that the two offset positions which can cause headaches and other symptoms.
3, tonsillitis and tonsil surgery scars stretch, but also the causes of the disease occurred.
4, glossopharyngeal neuropathy is closely related with the disease.
Clinical manifestations】 【
First, the symptoms
1, pharyngeal pain: slow onset, a history of varying lengths, often tonsillar area, tongue pain, often unilateral, multiple non-violent, may radiate to the ear or neck, sometimes in swallowing, speech, turned around or at night when the increase.
2, pharyngeal obstruction foreign body sensation or feeling: the more common, mostly on one side, such as tingling, tight feeling, pulling flu. Swallowing becomes more apparent.
3, carotid artery symptoms: excessive inward orientation skew styloid process, the more internal carotid artery pressure, pain or discomfort radiation up to the top of the head or eye; and outward deflection who is easy to external carotid artery compression, pain or discomfort more than the equivalent of tonsillar fossa begins at the neck, radiation to the ipsilateral face.
4, other: sometimes may have tinnitus, salivation, insomnia, neurasthenia and other performance. Also can cause coughing,
Second, the signs
Palpation of the tonsil area will be palpable to the hard cord-like or thorn-like protrusions, the patient can appeal here is not the place, and induced sore throat or sore throat worse. Mostly unilateral too long. Styloid process X-ra
y film often shows its length is too long, or deflection, bending and so on.
Diagnosis and differential diagnosis】 【
This disease is often overlooked. Where the age of 20 or more, sore throat, pharyngeal foreign body sensation, both neck pain, earache, headache, should think of the disease, palpation, and taken the styloid process in parallel sheets, if necessary, feasible and tonsil surgical exploration. Disease to be with pharyngitis, glossopharyngeal neuropathy, glossopharyngeal neuralgia, differentiated styloid fractures and other diseases.
Surgical therapy. Based indications should be based on the patient circumstances. Styloid process were asymptomatic or mild symptoms from time to surgery. Symptoms of patients required urgent surgery feasible. More use of transoral surgical approach tonsil surgery, or carotid diameter Surgical chopped styloid.
pictures of klinefelters syndrome

Reye syndrome is an acute encephalopathy and fatty infiltration of the liver syndrome frequently occurs in some acute viral infectious disease later. Significant clinical manifestations of individual differences, the prognosis depends on the severity of coma and the rate of progress, increased intracranial pressure and increased blood ammonia levels. Early diagnosis and supportive care given to strengthening the key to the treatment.
Reye syndrome cause is not yet clear, but generally agreed that the following factors and the pathogenesis of Reye syndrome: virus (eg influenza virus A, B, and varicella-zoster virus), exogenous viruses (such as aflatoxin), salicylates, intrinsic metabolic defects. There may be accompanied by various factors or interactions among various factors caused.
From 1974-1984, the 200 in the United States each year 550 children suffering from Reye syndrome, but has been rare in recent years, less than 20 cases per year, more than the general age of onset of 18 years of age. In the U.S., most cases have occurred in the late fall and winter. It is reported that there are regional and short-term popularity of small and sporadic cases. Outbreaks of influenza and chicken pox with the local outbreak, but even during the outbreak, Reye syndrome is still rare. In Thailand and Jamaica, the syndrome with the consumption of food containing aflatoxin and other toxins. It has been noted a high incidence of compatriots, but whether the environmental factors (such as exposure to exogenous toxins or the same virus) or genetic factors (such as hereditary enzyme deficiency) affect, or because of increased awareness of the disease that causes the disease The family cluster phenomenon is unclear.
Influenza patients taking salicylates cause Reye syndrome increased the risk 35 times. In fact, in addition to rare special diseases such as juvenile rheumatoid arthritis, Kawasaki disease, etc., "18-year-old patient with Reye syndrome after salicylate potentially dangerous. In recent years, a significant reduction in this disease, I do not know whether the salicylic acid was significantly less on drugs.
Frozen sections of liver tissue by oil - red-O (a Sudan dye) staining was seen under the light microscope was uniform throughout the hepatic lobule foamy cytoplasm of fatty infiltration. Mitochondrial electron microscope specimens of liver damage can be seen, the degree varies according to clinical condition, but generally have glycogen consumption, proliferation of smooth endoplasmic reticulum, peroxisome damage and mitochondrial matrix swelling. Abnormal liver histology generally takes 8 to 12 weeks to recover.
No specific changes in the central nervous system, often cerebral edema, brain back to the flattened, white matter edema, intraventricular pressure. Microscope, the surrounding nerves and blood vessels accompanied by a clear gap astrocytic swelling.
Symptoms, signs and complications
The severity of the disease obvious individual differences, but the general performance of the two phases: the beginning often viral infections, usually upper respiratory tract infection (and occasionally a rash appears), then, about 6 days intractable nausea and vomiting and the sudden disturbance of consciousness. Those caused by the varicella-zoster virus, usually after the eruption of the rash appears 4 to 5 days encephalopathy symptoms. Changes in consciousness can range from mild forgetfulness, drowsiness, to the intermittent disorientation, anxiety, and quickly into a deep coma, showing the low response to the brain cortex and rigidity to the state, convulsions, muscle relaxation, fixed and dilated pupils respiratory arrest. Often without focal neurological signs. 40% Reye syndrome, enlargement of the liver of sick children, but no jaundice.
Reye syndrome, complications of water and electrolyte balance disorders, diabetes insipidus, syndrome of inappropriate antidiuretic hormone secretion, hypotension, arrhythmia, bleeding tendency (especially gastrointestinal bleeding), pancreatitis, respiratory failure, and aspiration pneumonia.
Any manifestations of acute encephalopathy and intractable vomiting in children with abnormal liver function (in the removal of heavy metals and toxins poisoning outside) should be suspected to Reye syndrome. Liver biopsy can confirm the diagnosis, and thus sporadic cases and the pediatric patient particularly useful. Based on the typical history, clinical manifestations, laboratory findings and corresponding clinical diagnosis can be made. Laboratory tests have elevated liver transaminase (serum aspartate aminotransferase and alanine aminotransferase more than 3 times above normal), normal serum bilirubin, blood ammonia concentration, prothrombin time prolonged. CSF examination showed increased intracranial pressure, WBC <8 ~ 10X106 / L (8 ~ 10/μl), normal protein, glutamine concentration. About 15% of patients, especially children under 4 years old hypoglycemia and reduced sugar content in cerebrospinal fluid.
Patients may have signs of metabolic disorders, including serum amino acid concentration; acid-base imbalance (often accompanied by hyperventilation and respiratory alkalosis and metabolic acidosis), other electrolyte disturbances such as increased or decreased plasma osmotic pressure , hypernatremia, hypokalemia, and hypophosphatemia.
Differential diagnosis includes other causes coma and abnormal liver function, such as sepsis, high fever (especially infants); treatable congenital abnormalities of urea synthesis (ornithine carbamoyl transfer enzyme deficiency) and fatty acid oxidation disorders [ systemic carnitine deficiency, or medium chain fatty acyl coenzyme A dehydrogenase deficiency (MCAD)]; phosphorus or carbon tetrachloride poisoning, salicylic acid or other drugs or poisons induced acute encephalopathy, viral encephalitis or meningitis encephalitis and acute hepatitis. Liver biopsy in the light microscope and found to have pathological changes similar to Reye syndrome, a pregnancy of idiopathic fatty liver degeneration and tetracycline poisoning.
Reye syndrome prognosis depends on the severity of coma and the rate of progress, increased intracranial pressure and increased blood ammonia levels. In the blood ammonia concentration> 100μg/dl (60μmol / L) and prothrombin time greater than 3 seconds were the case, the disease will progress to a higher stage of stage Ⅰ. The death of the patient, from admission to death, the average time was 4 days. Reye syndrome mortality in stage Ⅰ <2%, Ⅳ and Ⅴ> 80%, the average fatality rate was 21%. Fortunately, most of the sick child can be diagnosed in stage Ⅰ, the disease through early treatment can improve or prevent further deterioration. If convulsions, flaccid paralysis, respiratory pause, the mortality is extremely high. Good survival prognosis, recurrence is rare. Neurological sequelae (such as mental retardation, epilepsy, cranial nerve paralysis, movement disorders) during hospitalization in those brain tonic spasm or the incidence of patients up to 30%.
Because the cause of Reye syndrome has not yet understood, in addition to a variety of metabolic disorders associated with, so there is no generally acceptable method of treatment. Early diagnosis and supportive care given to strengthening the key to the treatment of terminally ill patients with rapid or active support of the more important. Carefully observe the sick child nervous, electrolyte, metabolic, cardiovascular, respiratory, and changes in fluid balance is essential for timely processing. The monitoring of arterial blood gas, blood pH and blood pressure. Tracheal intubation and controlled ventilation are commonly used measures. Treatment including intravenous electrolyte solution containing glucose infusion to prevent dehydration and lack of glycogen. Appropriate guidance given laxatives and intestinal absorption of antibiotics is not (for example, oral administration of neomycin to prevent hepatic coma), vitamin K if necessary, can be used fresh plasma to prevent clotting disorder. Increased intracranial pressure must be controlled with mannitol. Also dexamethasone or glycerol, by gastric tube injection. Close monitoring to help guide treatment of intracranial pressure. Other treatments, such as exchange transfusion therapy, hemodialysis, in order to induce deep coma phenobarbital (to reduce intracranial pressure), etc., efficacy has not yet confirmed, but sometimes has been used.
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Down syndrome, also known as 21 - trisomy syndrome, congenital mental retardation or Down syndrome is an autosomal aberration, is the most common chromosomal disorder in children a kind of live births, an incidence of about 1 / (600 ~ 800), the older the mother, the higher the incidence of this disease. 60% of the children that died in the early fetal abortion. Down syndrome includes a series of genetic diseases, the most representative of chromosome 21 trisomy phenomenon causes, including learning disabilities, mental retardation, a high degree of deformity and disability. As maternal age increases the risk of babies with Down syndrome rate of Down syndrome children compared with children without the disease in direct disadvantage. That sick children often mental retardation, IQ of less than 60, the brain is usually too small, too light. Cerebellum, brain stem and the former will be surprisingly small brain. Educational progress of disease and disability due to the destruction, such as infectious diseases continue to relapse, heart disease, low vision, hearing and so on. Other physiological characteristics of illness caused by wrinkles, including apes and other facial features distorted, and some young adult patients with Down syndrome after the pressure will lead to depression. But in general showed a tendency cheerful. After 40 years of age suffer from high rates of Alzheimer's disease, prone to memory loss, poor knowledge and skills continuously, personality changes and other symptoms. In 1866, British doctors Tangyuehanlang Dayton was first published in the Society of this disease. It was originally called mongolism (Mongolism) or dementia Mongolia (mongolian idiocy), as Dr. Tang found that his patient's face wider than normal, small eyes and on the pick, it seems a resemblance with the Mongols. This name is now considered offensive and not the medical profession without the widespread use of medical significance. In 1959, French geneticist
       (Jerome LeJeune) found that Down syndrome is the human chromosome 21 the variability caused by three phenomena. This is the first discovered human disease caused by chromosomal defects. 1961, "Down Syndrome" is the editorial in The Lancet from the first use. In 1965, WHO will be officially named the disorder "Down Syndrome." Down syndrome features: short stature, low muscle tone, strength is low, cervical vulnerable. He walks very short length of the head, face less ups and downs, nose, eyes, parts between the lower corner on the pick, deep double eyelids. Bending toward the top of the inside of the ear, ears, and the whole place look less rounded. Tongue is relatively large. Thick neck. Hand is wide, fingers shorter interval between the thumb and index finger far, the lack of a little finger joint, curved inwards. Horizontal lines only one hand, the fingerprint for the bow. The first toe and second toe toe the interval between the relatively large.
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