LINGKOD BAYAN MEDIA MEDICAL CARE ADYENDAS AND YUJ GUANG THERAPYDO ASSN MEDICAL MISSIONARY
by Jesus Ogayre on Thursday, June 16, 2011 at 4:02pm
by Jesus Ogayre on Thursday, June 16, 2011 at 4:02pm
jesoga70therapy service
0916 436 88 75 996 09 04
mrs marina samson . one of kuya elly Ramirez carenoso ,listener was cure for chronic obstructive pulmonary deceased this afternoon 3pm nov 18/010 with her cellphone no.09183073089 from antipolo city.
Chronic obstructive pulmonary disease
Gross pathology of a lung showing centrilobular-type emphysema characteristic of smoking. This close-up of the fixed, cut lung surface shows multiple cavities lined by heavyblack carbon deposits.
Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive lung disease (COLD), chronic obstructive airway disease(COAD), chronic airflow limitation (CAL) and chronic obstructive respiratory disease (CORD), is the co-occurrence of chronic bronchitis andemphysema, a pair of commonly co-existing diseases of the lungs in which the airways become narrowed. This leads to a limitation of the flow of air to and from the lungs, causing shortness of breath. In clinical practice, COPD is defined by its characteristically low airflow on lung function tests. In contrast to asthma, this limitation is poorly reversible and usually gets progressively worse over time. In England, an estimated 842,100 of 50 million people have a diagnosis of COPD; thus, approximately 1 person in 59 is diagnosed with COPD at some point in their lives.
COPD is caused by noxious particles or gas, most commonly from tobacco smoking, which triggers an abnormal inflammatory response in the lung. The inflammatory response in the larger airways is known as chronic bronchitis, which is diagnosed clinically when people regularly cough up sputum. In the alveoli, the inflammatory response causes destruction of the tissues of the lung, a process known as emphysema. The natural course of COPD is characterized by occasional sudden worsenings of symptoms called acute exacerbations, most of which are caused by infections or air pollution.
The diagnosis of COPD requires lung function tests. Important management strategies are smoking cessation, vaccinations, rehabilitation, and drug therapy (often using inhalers). Some patients go on to require long-term oxygen therapy or lung transplantation.
Worldwide, COPD ranked as the sixth leading cause of death in 1990. It is projected to be the fourth leading cause of death worldwide by 2030 due to an increase in smoking rates and demographic changes in many countries.[6] COPD is the fourth leading cause of death in the U.S. and the economic burden of COPD in the U.S. in 2007 was $42.6 billion in health care costs and lost productivity.
Classification
The twofold nature of the pathology has been studied in the past.[9] Furthermore, also in recent studies, many authors found that each patient could be classified as presenting a predominantly bronchial or emphysematous phenotype by simply analyzing clinical, functional, and radiological findings or studying interesting biomarkers.[10][11][12] A statistical model reflecting the specific predominant mechanism of airflow limitation for a specific patient has been developed and trained over a database of hundreds of patients. The model is available here as a free online application.
Chronic bronchitis
Lung damage and inflammation in the large airways results in chronic bronchitis. Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years.[13] In the airways of the lung, the hallmark of chronic bronchitis is an increased number (hyperplasia) and increased size (hypertrophy) of the goblet cells and mucous glandsof the airway. As a result, there is more mucus than usual in the airways, contributing to narrowing of the airways and causing a cough with sputum. Microscopically there is infiltration of the airway walls with inflammatory cells. Inflammation is followed by scarring and remodeling that thickens the walls and also results in narrowing of the airways. As chronic bronchitis progresses, there issquamous metaplasia (an abnormal change in the tissue lining the inside of the airway) and fibrosis (further thickening and scarring of the airway wall). The consequence of these changes is a limitation of airflow.
Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referred to as "Blue Bloaters" because of the bluish color of the skin and lips (cyanosis) seen in them. The hypoxia and fluid retention leads to them being called "Blue Bloaters".
Emphysema
emphysema
Lung damage and inflammation of the air sacs (alveoli) results in emphysema. Emphysema is defined as enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls. The destruction of air space walls reduces the surface area available for the exchange of oxygen and carbon dioxide during breathing. It also reduces the elasticity of the lung itself, which results in a loss of support for the airways that are embedded in the lung. These airways are more likely to collapse causing further limitation to airflow. The effort made by patients suffering from emphysema during exhalation, causes a pink color in their faces, hence the term commonly used to refer to them, "Pink Puffers".
There are two types of emphysema:
1- Centrilobular: focal enlargement of air spaces around the bronchioles
2- Panlobular: enlargement of all air spaces (around bronchioles and in the periphery)
Signs and symptoms
Wheezing
The sound of wheezing as heard with a stethoscope.
Essentials of diagnosis include:
Other symptoms of COPD are a persistent cough, sputum or mucus production, wheezing, chest tightness, and tiredness.
People with advanced (very severe) COPD sometimes develop respiratory failure. When this happens, cyanosis, a bluish discoloration of the lips caused by a lack of oxygen in the blood, can occur. An excess of carbon dioxide in the blood can cause headaches, drowsiness or twitching (asterixis). A complication of advanced COPD is cor pulmonale, a strain on the heart due to the extra work required by the heart to pump blood through the affected lungs. Symptoms of cor pulmonale are peripheral edema, seen as swelling of the ankles, and dyspnea.
There are a few signs of COPD that a healthcare worker may detect although they can be seen in other diseases. Some people have COPD and have none of these signs. Common signs are:
Smoking
The primary risk factor for COPD is chronic tobacco smoking. In the United States, 80 to 90% of cases of COPD are due to smoking. Exposure to cigarette smoke is measured in pack-years, the average number of packages of cigarettes smoked daily multiplied by the number of years of smoking. The likelihood of developing COPD increases with age and cumulative smoke exposure, and almost all life-long smokers will develop COPD, provided that smoking-related, extrapulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand.
Occupational exposures
Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry and chemicals such as cadmium, isocyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in nonsmokers.[24] Workers who smoke and are exposed to these particles and gases are even more likely to develop COPD. Intensesilica dust exposure causes silicosis, a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition.[25] The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking.
Air pollution
Studies in many countries have found people who live in large cities have a higher rate of COPD compared to people who live in rural areas. Urban air pollution may be a contributing factor for COPD, as it is thought to slow the normal growth of the lungs, although the long-term research needed to confirm the link has not been done. Studies of the industrial waste gas and COPD/asthma-aggravating compound, sulfur dioxide, and the inverse relation to the presence of the blue lichen Xanthoria (usually found abundantly in the countryside, but never in towns or cities) have been seen to suggest combustive industrial processes do not aid COPD sufferers. In many developing countries, indoor air pollution from cooking fire smoke (often using biomass fuels such as wood and animal dung) is a common cause of COPD, especially in women.
Genetics
Some factor in addition to heavy smoke exposure is required for a person to develop COPD. This factor is probably a genetic susceptibility. COPD is more common among relatives of COPD patients who smoke than unrelated smokers.[The genetic differences that make some peoples' lungs susceptible to the effects of tobacco smoke are mostly unknown. Alpha 1-antitrypsin deficiency is a genetic condition that is responsible for about 2% of cases of COPD. In this condition, the body does not make enough of a protein, alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke.
Autoimmune disease
Autoimmunity
There is mounting evidence that there may be an autoimmune component to COPD, triggered by lifelong smoking..Many individuals with COPD who have stopped smoking have active inflammation in the lungs.The disease may continue to get worse for many years after stopping smoking due to this ongoing inflammation. This sustained inflammation is thought to be mediated by autoantibodies and autoreactive T cells.
Other risk factors
A tendency to sudden airway constriction in response to inhaled irritants, bronchial hyperresponsiveness, is a characteristic of asthma. Many people with COPD also have this tendency. In COPD, the presence of bronchial hyperresponsiveness predicts a worse course of the disease. It is not known if bronchial hyperresponsiveness is a cause or a consequence of COPD. Other risk factors such as repeated lung infection and possibly a diet high in cured meats (possibly due to the preservative sodium nitrite) may be related to the development of COPD.
how jesoga70therapy helpfully cure and kick off emphysema and asthma.
a couple of minutes of firm concentration letting your knuckles therapy the upper chest can help relieved or cure emphysema and asthma. and letting the motion runs horizontally outer portion of the chest up to the collarbone muscles. jesoga70 therapy also use the Lung associated areas , below the upper tip of the shoulder blade between spine and shoulder blade. as ending therapy treatment jesoga70therapy harmonized the lungs and the solar plexus using the 14 vitality abdominal impulses functioning system to dealing with c.o.p or emphysema including the corresponding touch to the brain , uterus , ovary , testicle , pancreas , and adrenal , pituitary and thyroid gland, respectively.In these disease or sickness such as asthma, bronchitis, emphysema, accessory muscles of respiration are often use , Inspiration is aided by contraction of the sternocleidomastoid and other muscles of the neck , expiration is aided by the use of the internal intercostal and abdominal muscles impulses. The nerves supply to intercostal muscles is from the spinal nerves the thoracic or T1 to T11 (intercostal nerves) now the diaphragm receives its nervous supply from the neck region ( c3 - c5 ) of the spinal cord during the fetal development .A dios amigos, Pls try jesoga70therapyDO cure. acid base balance is the right chi or key energy to cure such ugly diseases like these. PHOTO LATER THANKS
0916 436 88 75 996 09 04
mrs marina samson . one of kuya elly Ramirez carenoso ,listener was cure for chronic obstructive pulmonary deceased this afternoon 3pm nov 18/010 with her cellphone no.09183073089 from antipolo city.
Chronic obstructive pulmonary disease
Gross pathology of a lung showing centrilobular-type emphysema characteristic of smoking. This close-up of the fixed, cut lung surface shows multiple cavities lined by heavyblack carbon deposits.
Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive lung disease (COLD), chronic obstructive airway disease(COAD), chronic airflow limitation (CAL) and chronic obstructive respiratory disease (CORD), is the co-occurrence of chronic bronchitis andemphysema, a pair of commonly co-existing diseases of the lungs in which the airways become narrowed. This leads to a limitation of the flow of air to and from the lungs, causing shortness of breath. In clinical practice, COPD is defined by its characteristically low airflow on lung function tests. In contrast to asthma, this limitation is poorly reversible and usually gets progressively worse over time. In England, an estimated 842,100 of 50 million people have a diagnosis of COPD; thus, approximately 1 person in 59 is diagnosed with COPD at some point in their lives.
COPD is caused by noxious particles or gas, most commonly from tobacco smoking, which triggers an abnormal inflammatory response in the lung. The inflammatory response in the larger airways is known as chronic bronchitis, which is diagnosed clinically when people regularly cough up sputum. In the alveoli, the inflammatory response causes destruction of the tissues of the lung, a process known as emphysema. The natural course of COPD is characterized by occasional sudden worsenings of symptoms called acute exacerbations, most of which are caused by infections or air pollution.
The diagnosis of COPD requires lung function tests. Important management strategies are smoking cessation, vaccinations, rehabilitation, and drug therapy (often using inhalers). Some patients go on to require long-term oxygen therapy or lung transplantation.
Worldwide, COPD ranked as the sixth leading cause of death in 1990. It is projected to be the fourth leading cause of death worldwide by 2030 due to an increase in smoking rates and demographic changes in many countries.[6] COPD is the fourth leading cause of death in the U.S. and the economic burden of COPD in the U.S. in 2007 was $42.6 billion in health care costs and lost productivity.
Classification
The twofold nature of the pathology has been studied in the past.[9] Furthermore, also in recent studies, many authors found that each patient could be classified as presenting a predominantly bronchial or emphysematous phenotype by simply analyzing clinical, functional, and radiological findings or studying interesting biomarkers.[10][11][12] A statistical model reflecting the specific predominant mechanism of airflow limitation for a specific patient has been developed and trained over a database of hundreds of patients. The model is available here as a free online application.
Chronic bronchitis
Lung damage and inflammation in the large airways results in chronic bronchitis. Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years.[13] In the airways of the lung, the hallmark of chronic bronchitis is an increased number (hyperplasia) and increased size (hypertrophy) of the goblet cells and mucous glandsof the airway. As a result, there is more mucus than usual in the airways, contributing to narrowing of the airways and causing a cough with sputum. Microscopically there is infiltration of the airway walls with inflammatory cells. Inflammation is followed by scarring and remodeling that thickens the walls and also results in narrowing of the airways. As chronic bronchitis progresses, there issquamous metaplasia (an abnormal change in the tissue lining the inside of the airway) and fibrosis (further thickening and scarring of the airway wall). The consequence of these changes is a limitation of airflow.
Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referred to as "Blue Bloaters" because of the bluish color of the skin and lips (cyanosis) seen in them. The hypoxia and fluid retention leads to them being called "Blue Bloaters".
Emphysema
emphysema
Lung damage and inflammation of the air sacs (alveoli) results in emphysema. Emphysema is defined as enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls. The destruction of air space walls reduces the surface area available for the exchange of oxygen and carbon dioxide during breathing. It also reduces the elasticity of the lung itself, which results in a loss of support for the airways that are embedded in the lung. These airways are more likely to collapse causing further limitation to airflow. The effort made by patients suffering from emphysema during exhalation, causes a pink color in their faces, hence the term commonly used to refer to them, "Pink Puffers".
There are two types of emphysema:
1- Centrilobular: focal enlargement of air spaces around the bronchioles
2- Panlobular: enlargement of all air spaces (around bronchioles and in the periphery)
Signs and symptoms
Wheezing
The sound of wheezing as heard with a stethoscope.
Essentials of diagnosis include:
- History of cigarette smoking.
- Chronic cough and sputum production (in chronic bronchitis)
- Dyspnea
- Rhonchi, decreased intensity of breath sounds, and prolonged expiration on physical examination
- Airflow limitation on pulmonary function testing that is not fully reversible and most often progressive
Other symptoms of COPD are a persistent cough, sputum or mucus production, wheezing, chest tightness, and tiredness.
People with advanced (very severe) COPD sometimes develop respiratory failure. When this happens, cyanosis, a bluish discoloration of the lips caused by a lack of oxygen in the blood, can occur. An excess of carbon dioxide in the blood can cause headaches, drowsiness or twitching (asterixis). A complication of advanced COPD is cor pulmonale, a strain on the heart due to the extra work required by the heart to pump blood through the affected lungs. Symptoms of cor pulmonale are peripheral edema, seen as swelling of the ankles, and dyspnea.
There are a few signs of COPD that a healthcare worker may detect although they can be seen in other diseases. Some people have COPD and have none of these signs. Common signs are:
- tachypnea, a rapid breathing rate
- wheezing sounds or crackles in the lungs heard through a stethoscope
- breathing out taking a longer time than breathing in
- enlargement of the chest, particularly the front-to-back distance (hyperaeration)
- active use of muscles in the neck to help with breathing
- breathing through pursed lips
- increased anteroposterior to lateral ratio of the chest (i.e. barrel chest).
Smoking
The primary risk factor for COPD is chronic tobacco smoking. In the United States, 80 to 90% of cases of COPD are due to smoking. Exposure to cigarette smoke is measured in pack-years, the average number of packages of cigarettes smoked daily multiplied by the number of years of smoking. The likelihood of developing COPD increases with age and cumulative smoke exposure, and almost all life-long smokers will develop COPD, provided that smoking-related, extrapulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand.
Occupational exposures
Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry and chemicals such as cadmium, isocyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in nonsmokers.[24] Workers who smoke and are exposed to these particles and gases are even more likely to develop COPD. Intensesilica dust exposure causes silicosis, a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition.[25] The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking.
Air pollution
Studies in many countries have found people who live in large cities have a higher rate of COPD compared to people who live in rural areas. Urban air pollution may be a contributing factor for COPD, as it is thought to slow the normal growth of the lungs, although the long-term research needed to confirm the link has not been done. Studies of the industrial waste gas and COPD/asthma-aggravating compound, sulfur dioxide, and the inverse relation to the presence of the blue lichen Xanthoria (usually found abundantly in the countryside, but never in towns or cities) have been seen to suggest combustive industrial processes do not aid COPD sufferers. In many developing countries, indoor air pollution from cooking fire smoke (often using biomass fuels such as wood and animal dung) is a common cause of COPD, especially in women.
Genetics
Some factor in addition to heavy smoke exposure is required for a person to develop COPD. This factor is probably a genetic susceptibility. COPD is more common among relatives of COPD patients who smoke than unrelated smokers.[The genetic differences that make some peoples' lungs susceptible to the effects of tobacco smoke are mostly unknown. Alpha 1-antitrypsin deficiency is a genetic condition that is responsible for about 2% of cases of COPD. In this condition, the body does not make enough of a protein, alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke.
Autoimmune disease
Autoimmunity
There is mounting evidence that there may be an autoimmune component to COPD, triggered by lifelong smoking..Many individuals with COPD who have stopped smoking have active inflammation in the lungs.The disease may continue to get worse for many years after stopping smoking due to this ongoing inflammation. This sustained inflammation is thought to be mediated by autoantibodies and autoreactive T cells.
Other risk factors
A tendency to sudden airway constriction in response to inhaled irritants, bronchial hyperresponsiveness, is a characteristic of asthma. Many people with COPD also have this tendency. In COPD, the presence of bronchial hyperresponsiveness predicts a worse course of the disease. It is not known if bronchial hyperresponsiveness is a cause or a consequence of COPD. Other risk factors such as repeated lung infection and possibly a diet high in cured meats (possibly due to the preservative sodium nitrite) may be related to the development of COPD.
how jesoga70therapy helpfully cure and kick off emphysema and asthma.
a couple of minutes of firm concentration letting your knuckles therapy the upper chest can help relieved or cure emphysema and asthma. and letting the motion runs horizontally outer portion of the chest up to the collarbone muscles. jesoga70 therapy also use the Lung associated areas , below the upper tip of the shoulder blade between spine and shoulder blade. as ending therapy treatment jesoga70therapy harmonized the lungs and the solar plexus using the 14 vitality abdominal impulses functioning system to dealing with c.o.p or emphysema including the corresponding touch to the brain , uterus , ovary , testicle , pancreas , and adrenal , pituitary and thyroid gland, respectively.In these disease or sickness such as asthma, bronchitis, emphysema, accessory muscles of respiration are often use , Inspiration is aided by contraction of the sternocleidomastoid and other muscles of the neck , expiration is aided by the use of the internal intercostal and abdominal muscles impulses. The nerves supply to intercostal muscles is from the spinal nerves the thoracic or T1 to T11 (intercostal nerves) now the diaphragm receives its nervous supply from the neck region ( c3 - c5 ) of the spinal cord during the fetal development .A dios amigos, Pls try jesoga70therapyDO cure. acid base balance is the right chi or key energy to cure such ugly diseases like these. PHOTO LATER THANKS
Walang komento:
Mag-post ng isang Komento