Lower respiratory tract infection
The lower respiratory tract infection are the infection consisting of
the trachea (wind pipe), bronchial tubes, the bronchioles, and the
lungs, including the bronchitis and pneumonia. According to The World
Health Report 2004 – Changing History(1), in 2002 lower respiratory
track infection were still the leading cause of deaths among all
infectious diseases, and accounted for 3.9 million deaths worldwide and
6.9% of all deaths that year.
Bronchitis is defined as a condition of an inflammation of the
mucous membranes of the bronchi, the larger and medium-sized airways
that carry airflow from the trachea into the lung parenchyma(7). Most
cases of Bronchitis are as a result of recurrent injure to the airways
caused by inhaled irritants and cigarette smoking(6). There are 2 types
of bronchitis
A.1. Causes
A.1.1. Acute bronchitis
The most common causes of acute brochitis are as result of the infection
due to the invasion of Virus, (influenza and cold). Prolonged activity
of the presence of the virus can have many deteriorative effects.Young
adults with underlying medical conditions who are infected with the H1N1
virus are at risk of quickly progressing from mild upper airways
infection to severe ARDS within 4 to 5 days after the onset of the
illness. According to the study by Dr. Homsi S and the research team,
there is a report of a case a 46-year-old morbidly obese and diabetic
woman infected with the H1N1 virus who developed acute bronchitis that
lasted for 4 weeks and then progressed to ARDS. The month-long
persistence of the H1N1 viral bronchitis and its late progression to
ARDS which may reflect prolonged viral activity. Such a prolonged,
rather than quick, course of deterioration can cause clinicians to
misdiagnose the etiology of the ARDS and may cause the patient to
receive a prolonged treatment with steroids to treat bronchitis
symptoms(8).
Other in the reviewed study of reported eight cases of influenza A
(H1N1) 2009 admitted to themedical intensive care with severe
respiratory failure between November and December 2009 and in January
2011. All patients were older than 30 but younger than 50 years, had
clinical and radiological evidence of an Acute Respiratory Distress
Syndrome (ARDS) and needed invasive ventilatory support. The clinical
course of severe cases of influenza A (H1N1) 2009-infection is markedly
different from the disease pattern seen during epidemics of seasonal
influenza. Most of the patients admitted to our intensive care unit due
to influenza A (H1N1) 2009 associated ARDS were previously healthy young
people, according to the University Hospital of Muenster(9).
A.1.2. Chronic bronchitis
Most common causes of chronic bronchitis are as result of chronically smoking cigarettes, air pollution, dust. toxic gases, etc.
1. Smoking
In the case-control study in Beirut in 2009/2010 to evaluate the
relationship: 274 cases of chronic bronchitis and 559 controls without
the condition aged > or = 40 years, conducted by Lebanese University
Beirut, found that current waterpipe dependence was significantly
associated with chronic bronchitis (OR = 3.74, P < 0.001). After
adjustment for covariates/confounders, ever waterpipe smoking > 20
WP-years (P < 0.001) was significantly associated with chronic
bronchitis(10).
Other study indicated that in a retrospective clinical and morphological
study on a group of 17 smoker patients with symptoms of chronic
bronchitis, eight non-smokers diagnosed with chronic bronchitis and five
non-smokers and asymptomatic subjects. CB developed especially in men
of 65-year-old or older, especially in smokers with a median FEV1% at
around 71. Histopathologically, patients with symptoms of CB, regardless
of smoking status, presented on bronchial biopsies with focal squamous
metaplastic change, goblet cell hyperplasia and enlargement of the
bronchial gland mass because of the inflammatory process, consisting
predominantly of mononuclear cells in the bronchial wall. The
statistical testing proved a significant correlation between the
densities of different inflammatory cell classes (with the exception of
mast cells in the bronchial epithelium) and FEV1% values on epithelium
and submucosa regions in all investigated groups(11).
2. Air pollution, dust. toxic gases and other occupational chemical exposures
In the study to ascertain chronic obstructive pulmonary disease (COPD)
prevalence among industrial workers in the Russian Federation and
determine relative contribution of smoking and occupational factors to
COPD of 1,375 workers aged 30 or over, found that those with airfl ow
limitation of FEV1/FVC<0.70 were considered having COPD and those
with presence of cough and sputum production for at least three months
in each of two consecutive years were considered having chronic
bronchitis (CB), with no overlapping between these 2 groups. Data on
occupational history and VGDF levels in the working area were collected
from all participants. In total, 105 cases of COPD and 170 cases of CB
were diagnosed in the cohort of examined workers. Occupational exposure
to VGDF was twice as often present among COPD patients than among both
patients with CB and the control group of healthy workers (p<0.05).
More than 40 % of COPD patients were occupationally exposed to VGDF
above the value of 3.0 of the occupational exposure limit (OEL) and more
than 20 % to 6.0 OEL and higher. Overall odds ratio for COPD
development due to occupational VGDF exposure was 5.9 (95 % CI=3.6 to
9.8, p=0.0001). Both smoking and VGDF seem to be important for the
development of COPD. Analysis of the combined effect of tobacco smoking
and occupational noxious particles and gases on COPD development has
shown the following order of risk factors based on the strength of their
influence: VGDF levels, smoking index, age, and heating
microclimate(12).
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Sources
(1) http://www.who.int/whr/2004/en/
(8) http://www.ncbi.nlm.nih.gov/pubmed/22977983
(9) http://www.ncbi.nlm.nih.gov/pubmed/22075296
(10) http://www.ncbi.nlm.nih.gov/pubmed/23301353
(11) http://www.ncbi.nlm.nih.gov/pubmed/22990540
(12) http://www.ncbi.nlm.nih.gov/pubmed/23152384
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