What are the causes of muscular dystrophy, what are the causes of muscular dystrophy?

The focus is on hereditary diseases. According to the genetic mode, pseudohypertrophic muscular dystrophy, Becker guanidine dystrophy, and Emery-Drcifuss muscular dystrophy were X-linked recessive inheritance, while facioscapulohumeral muscular dystrophy and myotonic muscular dystrophy were autosomal dominant inheritance. Limb-girdle muscular dystrophy is inherited in an autosomal recessive manner.

1 Myasthenic crisis: neostigmine deficiency crisis, precipitated by various triggers and drug tasins. Weak breathing, cyanosis, irritability to bathe, difficulty swallowing and nuclear phlegm, low speech until no one can speak, and finally complete cessation of breathing. It can be reversed or prolonged into chronic.

2 Cholinergic crisis: that is, neostigmine overdose crisis, which mostly occurs after a temporary overdose, in addition to the above-mentioned symptoms such as dyspnea, there are also symptoms of excessive acetylcholine accumulation: including symptoms of toxogenic poisoning (vomiting, abdominal pain, diarrhea, miosis, excessive sweating, salivation, increased tracheal secretions, slow heart rate, etc.), symptoms of nicotinic poisoning (muscle tremors, spasms and tightness, etc.) and central nervous system symptoms (anxiety, insomnia, confusion, confusion, convulsions, coma, etc.).

3. Repulsive crisis: It is difficult to distinguish the nature of the crisis and the symptoms cannot be improved by stopping the drug or increasing the dosage. It mostly occurs after long-term use of larger doses.

The three types of crises can be identified by the following methods: Tensilon test. Atropine test. Electromyography.

The disease** is a genetic abnormality that can be carried out in different ways in different types, but it is still unclear how genetic factors ultimately cause muscle degeneration. At present, it is believed that the morphological structure of muscle cell membrane may be abnormal due to genetic defects, and the permeability and transport function of muscle membrane may be changed, so that a large amount of muscle enzymes leak out of the cytoplasm through the muscle membrane and increase the relevant enzymes in the serum. The spillover of muscle enzymes leads to the compensatory synthesis of more muscle enzymes by ribosomes, and because this compensatory effect is quite limited, after a certain period of time, muscle cells are destroyed and replaced by proliferative connective tissue.

Since the introduction of DNA recombinant technology into the research in the early 80s, breakthroughs have been made in the genetic research of pseudohypertrophic muscular dystrophy, in addition to affirming that it is an X-linked recessive genetic disease, it has also been found that the DMD locus is on XP21 (i.e., the X chromosome history of the short arm 2 region 1 band), it is likely that the two subtypes of DMD and BMD are allele XP21 gene defects resulting in the lack of a specific dystrophin in skeletal muscle. As a result, the development of myotubes is hindered and the regeneration ability of muscle cells is poor, resulting in obvious abnormalities in the morphology and function of myotubes.

Muscular dystrophy is mainly a muscle degenerative disease caused by genetic factors, and in addition to genetic factors, the patient's own genetic mutations can also cause the disease. Progressive muscle atrophy and weakness are the main clinical manifestations. At present, although many scholars have explored the pathogenesis of muscular dystrophy, it is still unclear.

The specific ** of this disease is unknown, and there are currently three main theories, namely the vascular theory, which believes that blood circulation disorders cause muscle tissue infarction; The second is the neurogenic theory, which holds that abnormal motor neuron function causes muscle degeneration; The third is the genetic theory, the hereditary abnormality of the cell membrane is slippery, resulting in the overflow of muscle enzymes, so that the body can metabolize and synthesize more muscle enzymes. I don't know the specifics, I'm sorry. Tell you about some daily care:

Muscular dystrophy care 1 Keep the environment clean and quiet, pay attention to moisture and cold, and actively prevent complications such as respiratory tract infection. Care for muscular dystrophy 2 Adhere to physical exercise, self-massage to increase activity, promote blood circulation, and prevent muscle atrophy, but it should be moderate and not overworked. Care of muscular dystrophy 3 The diet should be light and nutritious, avoid eating or eating less greasy and thick food, excessive heat, injury and fluid consumption and damage to the spleen and stomach, you can eat more fish, eggs, chicken, lean pork, etc., but not too much, so as not to damage the spleen and stomach.

Muscular dystrophy care4 Actively fights the disease, insists on appropriate recreational activities, promotes the patient's optimistic and cheerful mood, and builds the confidence to overcome the disease with strong perseverance. Vegetables and fruits such as cabbage, bean sprouts, tomatoes, hawthorn, mandarin oranges, and dates can be eaten more appropriately. While ensuring nutrition, weight should be properly controlled.

Oh, take good care of it...

The ** of muscular dystrophy is now basically clear, it is caused by mutations in the hereditary antecedents of base failure, there are many types, and the location, mutation type and inheritance mode of various types of muscular dystrophy genes are different. The mechanism of pathogenesis is also different, in fact, each type is an independent genetic disease, which is caused by genetic mutations or mutations. The consequences are weakness and atrophy of the limbs, as in the case of the most common pseudohypertrophic muscular dystrophy of the muscular dystrophy, where the main lead withering gene mutation is located at the 21st position of chromosome.

Muscular dystrophy is due to a genetic defect that causes abnormalities in a group of proteins that maintain the structural and functional stability of skeletal muscle cells.

If the chickens are malnourished, the main reason is that the feed you are not feeding is good, or that you are feeding too much feed, what's wrong?

Muscular dystrophy syndrome includes congenital muscular dystrophy syndrome, other Becker MD and other types.

The cause of muscular dystrophy is related to genetic factors and gene mutations, and it is a degenerative disease of muscle, and it may also be related to chronic gastrointestinal diseases and malabsorption. Usually patients have varying degrees of abdominal distention, diarrhea, and irregular diet. Patients with muscular dystrophy may also have other chronic diseases, such as chronic blood loss and anemia.

For muscular dystrophy caused by different causes, the program is also different, if it is caused by genetic factors and gene mutations, it is mainly functional exercise, training, symptomatic treatment, to prevent some complications. In terms of diet, it is necessary to have a high-protein, high-nutrition, and high-vitamin diet. In life, acupuncture, physiotherapy, massage, and hot compresses should be used to prevent progressive aggravation of muscles.

The occurrence of the disease is often a combination of causes, or a prominent factor plays a role in the case of a combination of causes. In general, muscular dystrophy is related to the following factors, such as hereditary diseases, autoimmune diseases, and acute infectious diseases, which can lead to muscular dystrophy.

After the occurrence of the disease, you should go to the hospital in time to clarify the severity of the disease, and prevent and slow down the aggravating factors that can be controlled. However, there is no need to investigate too many uncontrollable factors, because such genetic factors are difficult to change under the current medical science conditions. Malnutrition is classified as primary and secondary.

Primary is mostly caused by genetic factors, and the parents can have no matching symptoms, and most of them are in the offspring, and most of these diseases have no effective effect. Secondary can be secondary to muscle atrophy caused by myositis, etc., and requires hormone shocks or other symptomatic **.

In addition to genetic factors, malnutrition can also lead to the occurrence of the disease due to genetic mutations, and muscle atrophy and weakness are the main clinical manifestations. The main symptoms of malnutrition are falling when walking on flat ground, walking swaying from side to side like a duck's step, difficulty climbing and descending stairs without balance, difficulty squatting and standing up, and pseudohypertrophy of the muscles.

The pathogenesis of muscular dystrophy is complex and has not been fully elucidated. Different types are different, and there is heterogeneity even within the same type. In conclusion, genetic factors are important factors in its pathogenesis.

The genetic location, mutation type, and inheritance mode of each type of muscular dystrophy are different, and their pathogenic mechanisms are also different.

1. Pseudohypertrophic muscular dystrophy: DMD patients lack dystrophic protein in muscle cells due to gene defects, resulting in unstable muscle cell membranes and leading to muscle cell necrosis and loss of function. The deficiency of dystrophin in the synaptic region of the cerebral cortex nerve rush in patients with DMD may be the cause of mental retardation.

2. Facicoscapulohumeral muscular dystrophy: the gene is located at the end of the long arm of chromosome 4 (4q35), and there is a repeat fragment associated with the KPN enzyme cleavage site in this region. The fragment is repeated 10 100 times in normal people, but less than 8 times in patients with facicoscapulohumeral muscular dystrophy, so the genetic diagnosis can be made by measuring the number of fragment repeats.

3. Limb-girdle muscular dystrophy: It is an autosomal hereditary myopathy with a high degree of genetic heterogeneity and phenotypic heterogeneity, and limb-girdle dystrophin and dystrophin-glycoprotein complex constitute a myofibrin complex. Within the complex, proteins are tightly bound to each other and are related to each other.

The loss of any one protein will affect the stability of the entire membrane structure, leading to the necrosis of muscle cells.

4. Oculopharyngeal muscular dystrophy: the gene is located on the chromosome, and the increase of GCG repeat mutation on exon 1 of PABPA gene is the cause of the disease; Normal people have only 6 repetitions, while patients with oculopharyngeal muscular dystrophy have GCG 8 13 repetitions, and the more repetitions, the more severe the symptoms.

5. Emery-Dreifuss muscular dystrophy: the gene is located on chromosome XQ28, and the mutation of this gene causes the loss of the Emerin protein located in the nuclear lining of skeletal muscle and cardiomyocytes, and its deletion can cause damage to skeletal muscle and myocardium.