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Bronchospasm are caused by a number of reasons. Lower respiratory tract conditions such as asthma, chronic obstructive pulmonary disease (COPD), and emphysema can result in contraction of the airways. Other causes are side effects of topical decongestants such as oxymetazoline and phenylephrine. Both of these medications activate alpha-1 adrenergic receptors that result in smooth muscle constriction. Non-selective beta blockers are known to facilitate bronchospasm as well. Beta blockers bind into the β2 receptors and block the action of epinephrine and norepinephrine from binding to its receptors, causing shortness of breath.
Beta2-adrenergic agonists are recommended for bronchospasm.
- Short acting (SABA)
- Terbutaline
- Salbutamol
- Levosalbutamol
- Long acting (LABA)
- Formoterol
- Salmeterol
- Others
- Dopamine
- Norepinephrine
- Epinephrine
Bronchial hyperresponsiveness (or other combinations with airway or hyperreactivity) is a state characterised by easily triggered bronchospasm (contraction of the bronchioles or small airways).
Bronchial hyperresponsiveness can be assessed with a bronchial challenge test. This most often uses products like methacholine or histamine. These chemicals trigger bronchospasm in normal individuals as well, but people with bronchial hyperresponsiveness have a lower threshold.
Bronchial hyperresponsiveness is a hallmark of asthma but also occurs frequently in people suffering from chronic obstructive pulmonary disease (COPD). In the Lung Health Study, bronchial hyperresponsiveness was present in approximately two-thirds of patients with non-severe COPD, and this predicted lung function decline independently of other factors. In asthma it tends to be reversible with bronchodilator therapy, while this is not the case in COPD.
Bronchial hyperresponsiveness has been associated with gas cooking among subjects with the "GSTM1" null genotype.
Medication challenge tests, such as the methacholine challenge test, have a lower sensitivity for detection of exercise-induced bronchoconstriction in athletes and are also not a recommended first-line approach in the evaluation of exercise-induced asthma.
Mannitol inhalation has been recently approved for use in the United States.
It should be noted, however, that a relatively recent review of the literature has concluded that there is currently insufficient available evidence to conclude that either mannitol inhalation or eucapnic voluntary hyperventilation are suitable alternatives to exercise challenge testing to detect exercise-induced bronchoconstriction and that additional research is required.
While the potential triggering events for E.I.B. are well recognized, the underlying pathogenesis is poorly understood. It usually occurs after at least several minutes of vigorous, aerobic activity, which increases oxygen demand to the point where breathing through the nose (nasal breathing) must be supplemented by mouth breathing. The resultant inhalation of air that has not been warmed and humidified by the nasal passages seems to generate increased blood flow to the linings of the bronchial tree, resulting in edema. Constriction of these small airways then follows, worsening the degree of obstruction to airflow. There is increasing evidence that the smooth muscle that lines the airways becomes progressively more sensitive to changes that occur as a result of injury to the airways from dehydration. The chemical mediators that provoke the muscle spasm appear to arise from mast cells.
Patients, families, and caregivers are encouraged to join the NIH Rare Lung Diseases Consortium Contact Registry. This is a privacy protected site that provides up-to-date information for individuals interested in the latest scientific news, trials, and treatments related to rare lung diseases.
To date, about 420 cases have been reported in the medical literature. Given its unusual nature, the true prevalence of PB is unknown, and it is likely that many patients are undiagnosed. PB does affect patients of all age groups and both genders.
Reactive airways dysfunction syndrome (RADS) is a term proposed by Stuart M. Brooks and colleagues in 1985
It can also manifest in adults with exposure to high levels of chlorine, ammonia, acetic acid or sulphur dioxide, creating symptoms like asthma. These symptoms can vary from mild to fatal, and can even create long-term airway damage depending on the amount of exposure and the concentration of chlorine. Some experts classify RADS as occupational asthma. Those with exposure to highly irritating substances should receive treatment to mitigate harmful effects.
The prevalence of pulmonary interstitial emphysema widely varies with the population studied. In a 1987 study 3% of infants admitted to the neonatal intensive care unit (NICU) developed pulmonary interstitial emphysema.
The morbidity associated with DIPNECH is due to the associated obstructive lung disease. The lung disease tends to be slowly progressive, but given enough time can lead to significant disability and require supplemental oxygen therapy. There have been reports of lung transplantation in the setting of end-stage DIPNECH.
Studies reflecting international frequency demonstrated that 2-3% of all infants in NICUs develop pulmonary interstitial emphysema. When limiting the population studied to premature infants, this frequency increases to 20-30%, with the highest frequencies occurring in infants weighing fewer than 1000 g.
Cardiac asthma is a medical diagnosis of wheezing, coughing or shortness of breath due to congestive heart failure. It is known as cardiac asthma because the symptoms mimic ordinary asthma (bronchial asthma). One study found that patients with cardiac asthma represented one third of congestive heart failure in elderly patients.
Depending on severity, it may be classified as a medical emergency, as it can be a symptom of acute heart failure leading to the buildup of fluid in the lungs (pulmonary edema) as well as within and around the airways.
The distinction between bronchial asthma and cardiac asthma is especially important because some treatments for bronchial asthma, including inhalers, may worsen cardiac asthma or cause severe heart arrhythmias.
Bronchial asthma, in contrast, is caused by the inflammation and narrowing of pulmonary airways, causing the characteristic breathing difficulties. Bronchial asthma has nothing to do with fluid in the lungs or heart disease, or even the heart failure associated with cardiac asthma.
Sources of such lipids could be either exogenous or endogenous.
Exogenous: from outside the body. For example, inhaled nose drops with an oil base, or accidental inhalation of cosmetic oil. Amiodarone is an anti-arrythmic known to cause this condition. Oil pulling has also been shown to be a cause. At risk populations include the elderly, developmentally delayed or persons with gastroesophageal reflux. Switching to water-soluble alternatives may be helpful in some situations.
Endogenous: from the body itself, for example, when an airway is obstructed, it is often the case that distal to the obstruction, lipid-laden macrophages (foamy macrophages) and giant cells fill the lumen of the disconnected airspace.
Endogenous lipoid pneumonia and non-specific interstitial pneumonitis has been seen prior to the development of pulmonary alveolar proteinosis in a child.
Tuberculosis, pneumonia, inhaled foreign bodies, allergic bronchopulmonary aspergillosis and bronchial tumours are the major acquired causes of bronchiectasis. Infective causes associated with bronchiectasis include infections caused by the Staphylococcus, Klebsiella, or Bordetella pertussis, the causative agent of whooping cough and nontuberculous mycobacteria.
Aspiration of ammonia and other toxic gases, pulmonary aspiration, alcoholism, heroin (drug use), various allergies all appear to be linked to the development of bronchiectasis.
Various immunological and lifestyle factors have also been linked to the development of bronchiectasis:
- Childhood Acquired Immune Deficiency Syndrome (AIDS), which predisposes patients to a variety of pulmonary ailments, such as pneumonia and other opportunistic infections.
- Inflammatory bowel disease, especially ulcerative colitis. It can occur in Crohn's disease as well, but does so less frequently. Bronchiectasis in this situation usually stems from various allergic responses to inhaled fungal spores. A Hiatal hernia can cause Bronchiectasis when the stomach acid that is aspirated into the lungs causes tissue damage.
- People with rheumatoid arthritis who smoke appear to have a tenfold increased rate of the disease. Still, it is unclear as to whether or not cigarette smoke is a specific primary cause of bronchiectasis.
- Case reports of Hashimoto's thyroiditis and bronchiectasis occurring in the same persons have been published.
No cause is identified in up to 50% of non-cystic-fibrosis related bronchiectasis.
Conditions which commonly involve hemoptysis include bronchitis and pneumonia, lung cancers and tuberculosis. Other possible underlying causes include aspergilloma, bronchiectasis, coccidioidomycosis, pulmonary embolism, pneumonic plague, and cystic fibrosis. Rarer causes include hereditary hemorrhagic telangiectasia (HHT or Rendu-Osler-Weber syndrome), Goodpasture's syndrome, and granulomatosis with polyangiitis. In children, hemoptysis is commonly caused by the presence of a foreign body in the airway. The condition can also result from over-anticoagulation from treatment by drugs such as warfarin.
Blood-laced mucus from the sinus or nose area can sometimes be misidentified as symptomatic of hemoptysis (such secretions can be a sign of nasal or sinus cancer, but also a sinus infection). Extensive non-respiratory injury can also cause one to cough up blood. Cardiac causes like congestive heart failure and mitral stenosis should be ruled out.
The origin of blood can be identified by observing its color. Bright-red, foamy blood comes from the respiratory tract, whereas dark-red, coffee-colored blood comes from the gastrointestinal tract. Sometimes hemoptysis may be rust-colored.
The most common cause of minor hemoptysis is bronchitis.
- Lung cancer, including both non-small cell lung carcinoma and small cell lung carcinoma.
- Sarcoidosis
- Aspergilloma
- Tuberculosis
- Histoplasmosis
- Pneumonia
- Pulmonary edema
- Pulmonary embolism
- Foreign body aspiration and aspiration pneumonia
- Goodpasture's syndrome
- Granulomatosis with polyangiitis
- Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
- Bronchitis
- Bronchiectasis
- Pulmonary embolism
- Anticoagulant use
- Trauma
- Lung abscess
- Mitral stenosis
- Tropical eosinophilia
- Bleeding disorders
- Hughes-Stovin Syndrome and other variants of Behçet's disease
- Squamous Cell Carcinoma Of Esophagus
Hemoptysis is the coughing up of blood or blood-stained mucus from the bronchi, larynx, trachea, or lungs. This can occur with lung cancer, infections such as tuberculosis, bronchitis, or pneumonia, and certain cardiovascular conditions. Hemoptysis is considered massive at . In such cases, there are always severe injuries. The primary danger comes from choking, rather than blood loss.
Anaphylaxis can occur in response to almost any foreign substance. Common triggers include venom from insect bites or stings, foods, and medication. Foods are the most common trigger in children and young adults while medications and insect bites and stings are more common in older adults. Less common causes include: physical factors, biological agents such as semen, latex, hormonal changes, food additives such as monosodium glutamate and food colors, and topical medications. Physical factors such as exercise (known as exercise-induced anaphylaxis) or temperature (either hot or cold) may also act as triggers through their direct effects on mast cells. Events caused by exercise are frequently associated with the ingestion of certain foods. During anesthesia, neuromuscular blocking agents, antibiotics, and latex are the most common causes. The cause remains unknown in 32–50% of cases, referred to as "idiopathic anaphylaxis." Six vaccines (MMR, varicella, influenza, hepatitis B, tetanus, meningococcal) are recognized as a cause for anaphylaxis, and HPV may cause anaphylaxis as well. Physical exercise is an uncommon cause of anaphylaxis; in about a third of such cases there is a co-factor like taking an NSAID or eating a specific food prior to exercising.
Reactive airway disease is a group of conditions that include reversible airway narrowing due to an external stimulation. These conditions generally result in wheezing.
Conditions within this group include asthma, chronic obstructive pulmonary disease, and viral upper respiratory infections.
The term reactive airway disease may be used in pediatrics to describe an asthma-like syndrome in infants too young for diagnostic testing such as the bronchial challenge test. These infants may later be confirmed to have asthma following testing. The term is sometimes misused as a synonym for asthma.
Venom from stinging or biting insects such as Hymenoptera (ants, bees, and wasps) or Triatominae (kissing bugs) may cause anaphylaxis in susceptible people. Previous systemic reactions, which are anything more than a local reaction around the site of the sting, are a risk factor for future anaphylaxis; however, half of fatalities have had no previous systemic reaction.
The disease affects between 1 per 1000 and 1 per 250,000 adults. The disease is more common in women and increases as people age. It became less common since the 1950s, with the introduction of antibiotics. It is more common among certain ethnic groups such as indigenous people.
The exact rates of bronchiectasis are often unclear as the symptoms are variable. Rates of disease appeared to have increased in the United States between 2000 and 2007.
Bronchomalacia can best be described as a birth defect of the bronchus in the respiratory tract. Congenital malacia of the large airways is one of the few causes of irreversible airways obstruction in children, with symptoms varying from recurrent wheeze and recurrent lower airways infections to severe dyspnea and respiratory insufficiency. It may also be acquired later in life due to chronic or recurring inflammation resulting from infection or other airway disease.
A pulmonary consolidation is a region of (normally compressible) lung tissue that has filled with liquid, a condition marked by induration (swelling or hardening of normally soft tissue) of a normally aerated lung. It is considered a radiologic sign. Consolidation occurs through accumulation of inflammatory cellular exudate in the alveoli and adjoining ducts. Simply, it is defined as alveolar space that contains liquid instead of gas. The liquid can be pulmonary edema, inflammatory exudate, pus, inhaled water, or blood (from bronchial tree or hemorrhage from a pulmonary artery). It must be present to diagnose pneumonia: the signs of lobar pneumonia are characteristic and clinically referred to as consolidation.
Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) is a diffuse parenchymal lung disease which often presents with symptoms of cough and shortness of breath. The pathological definition published by the World Health Organization is “a generalized proliferation of scattered single cells, small nodules (neuroendocrine bodies), or linear proliferations of pulmonary neuroendocrine (PNE) cells that may be confined to the bronchial and bronchiolar epithelium.” The true prevalence of this disease is not known. To date, just under 200 cases have been reported in the literature. However, with an increase in recognition of this disease by radiologists and pulmonologists, the number of cases has been increasing. DIPNECH predominantly affects middle-aged women with slowly progressive lung obstruction. DIPNECH is usually discovered in one of two ways: 1) as an unexpected finding following a lung surgery; or 2) by evaluation of a patient in a pulmonary clinic with longstanding, unexplained symptoms.
To help the bronchial tree heal faster and not make bronchitis worse, smokers should quit smoking completely.