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Gas exchange is the major purpose of the respiratory system. Inhaled air unloads oxygen and picks up carbon dioxide in the alveoli of the lungs, while the blood picks up oxygen and unloads carbon dioxide. The oxygenated blood then travels to body’s tissues, where the reverse process happens.
In the lungs, the gases move across a very thin respiratory membrane which consists of alveolar squamous cells, endothelial cells of blood capillaries, and their fused basement membranes. The exchange of gases occurs due to simple diffusion, as they flow down their concentration gradient, or partial pressure gradient.
Atmospheric air is a mixture of gases, each of which independently contributes to its total pressure. The pressure of each individual gas is known as partial pressure. The atmospheric pressure is the sum of all partial pressures of gases that make up its content. The direction of gas movement from one area to another is determined by the difference in its partial pressure. A gas always moves from higher to lower partial pressure.
Atmospheric air is brought into the lungs through inhalation, but the lungs are not completely emptied and replaced with outside air with each cycle of breathing. In fact, only a relatively small portion of air in the alveoli is refreshed with each breath. This makes the air composition in the alveoli significantly different from that of inhaled air. The gas exchange in the lungs occurs between this alveolar air and the blood in capillaries. Because the volume of blood in pulmonary capillaries at any moment is much smaller than the total volume of air in the alveoli, the gas exchange process essentially brings partial pressures of oxygen and carbon dioxide in the blood to the same levels as those in alveolar air. It is therefore important that the composition of alveolar air is closely monitored and adjusted to maintain the same values. The body does just that: if carbon dioxide levels increase or oxygen levels drop, the airways automatically dilate to bring them back to normal, and vice versa.
Since gas exchange occurs between the air and the liquid of the blood, the movement of individual gases also depends on their solubility in water. This explains why nitrogen, despite being plentiful in atmospheric and alveolar air, does not diffuse much into the blood.
Factors that affect gas exchange include:
– The magnitude of partial pressure gradient: the greater the pressure difference, the more rapid the gas movement. At high altitudes, where partial pressures of all atmospheric gases are lower, the gradient for oxygen is smaller and it needs more time to diffuse into the blood.
– The thickness of the respiratory membrane: the thinner the membrane, the faster the gas diffuses. Diseases that cause pulmonary edema, such as pneumonia or left-sided heart failure, increase the thickness of respiratory membrane and hinder gas exchange.
– The amount of gas exchanged is directly proportional to the contact surface between the blood and the alveolar air. Diseases that affect alveolar surface, such as emphysema, reduce gas exchange efficiency and produce low blood oxygen levels.

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Spirometry is a common test for lung function. It is used to diagnose asthma, COPD, pulmonary fibrosis and other lung diseases. It can also be a helpful tool to monitor disease progression, and evaluate effectiveness of a treatment plan. A tube-like device, called a spirometer, is used to capture and record air volumes and breathing speed.
A spirometry test typically reports 4 respiratory volumes:
– Tidal volume, TV – the amount of air inhaled or exhaled during normal, quiet breathing, without effort.
– Inspiratory reserve volume, IRV – the amount of air that can be inhaled with maximum effort, after a quiet inhalation.
– Expiratory reserve volume, ERV – the amount of air that can be exhaled with maximum effort, after a quiet exhalation.
– Residual volume, RV – the amount of air remaining in the lungs after a maximum exhalation.
These volumes are used to calculate other parameters, called respiratory capacities:
– Inspiratory capacity, IC – the maximum amount of air that can be inhaled after a quiet exhalation.
– Functional residual capacity, FRC, – the amount of air remaining in the lungs after a quiet exhalation.
– Total lung capacity, TLC
– And vital capacity, VC – the amount of air that can be exhaled with maximum effort, after a maximum inhalation. This is basically the volume of the deepest breath the lungs can possibly handle, and is an important indicator of pulmonary function, as well as strength of respiratory muscles.
Vital capacity can be measured as slow vital capacity during slow, relaxed breathing; or as forced vital capacity, FVC, when the patient is asked to breathe out as hard and fast as possible. While there is little or no difference between these two values in healthy individuals, people with difficulty exhaling usually show significantly lower FVC.
Another important parameter obtained during forced spirometry is the forced expiratory volume – FEV1 – the amount of air that is exhaled during the first second of forceful exhalation, after a full inhalation. FEV1 is used to calculate the percentage of air that is expelled during the first second. This FEV1/FVC ratio inversely reflects the resistance to expiratory airflow. In healthy people, it is around 70 to 85%; a smaller number means increased lung resistance.
Spirometry is useful in differentiating between restrictive and obstructive pulmonary diseases. Restrictive lung diseases can be inspiratory or expiratory. Inspiratory restrictive are conditions in which lung compliance is reduced, limiting lung expansion when inhaling. This can happen either because the lungs become “stiff”, as a result of scaring or fibrosis within lung tissues; or the respiratory muscles are too weak to inflate the lungs. Expiratory restrictive is when exhalation volume is limited, due to weakness of accessory muscles involved in deep exhalation. Restrictive lung diseases are associated with decreased lung volumes, or total lung capacity, TLC.
Obstructive lung diseases, such as asthma or COPD, on the other hand, show a normal or somewhat increased total lung capacity, TLC. This is because the obstruction increases lung resistance, making breathing out harder and slower; and this results in increased residual lung volume. Vital capacity remains normal during quiet breathing, but when breathing rapidly, a higher pressure is required to overcome the increased resistance, and forced vital capacity is reduced. A more reliable indicator of obstructive lung disease, however, is the lower percentage of air that is exhaled during the first second of forceful exhalation.

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Breathing is mostly an involuntary, automatic process. Because its major function is to supply the body with oxygen and remove carbon dioxide, the rate and depth of breathing is generally regulated by carbon dioxide status or the need for oxygen. For example, breathing automatically accelerates with physical exercise when the body’s need for oxygen is increased.
Basically, various receptors in the body feed information about its metabolic state to the respiratory center in the brainstem, which responds by changing the firing pattern of inspiratory and expiratory neurons. Inspiratory neurons fire during inspiration, while expiratory neurons only fire during deep expiration, since quiet expiration is a passive process. The fibers of these neurons descend to the cervical and thoracic spine where they synapse with motor neurons. Motor neurons then travel in several nerves to respiratory muscles, changing the way these muscles contract, adjusting thereby the rate and depth of breathing to suit the body’s needs. Of most importance are phrenic nerves which control the diaphragm, and intercostal nerves which innervate intercostal muscles.
While the functional anatomy of human respiratory center is complex and not entirely clear, the current consensus is that the primary center is composed of several areas in the medulla: the dorsal respiratory group, DRG, mainly associated with inspiration; the ventral respiratory group, VRG, mostly concerned with expiration; and the pre-Bötzinger complex, possibly coupled with two other oscillators, thought to be the intrinsic rhythm generator, similar to the pacemaker in the heart. The medullar areas also communicate with two other areas in the pons to fine-tune the respiration control: the pneumotaxic center which seems to inhibit inspiration, while the apneustic center stimulates it.
The most important factor regulating breathing rate is the concentration of carbon dioxide. Changes in carbon dioxide leads to changes in pH, and these are detected by chemoreceptors. Central chemoreceptors located on the surface of the medulla monitor pH changes in the cerebrospinal fluid; while peripheral chemoreceptors found in the aortic and carotid bodies respond to fluctuations in pH, carbon dioxide, as well as oxygen levels in the blood. Peripheral receptors transmit signal to the respiratory center via the vagus and glossopharyngeal nerves. An increase in carbon dioxide, such as during exercise, causes a decrease in pH, which is sensed by central or arterial chemoreceptors and leads to deeper, faster breathing; more carbon dioxide is exhaled, and blood pH returns to normal.
The respiratory center also receives input from various mechanoreceptors in the lungs, which transmit information about the mechanical status of the lungs via the vagus nerve. For example, pulmonary stretch receptors present in smooth muscle of the airways are activated when the lungs are excessively inflated, and trigger the inflation reflex, which stops inspiration and prolongs expiration. Other receptors respond to inhaled irritants and are responsible for defensive respiratory reflexes such as bronchoconstriction or coughing.
The limbic system and hypothalamus also send information to the respiratory center and allow pain and emotional state to affect breathing. For example, pain or strong emotion may induce gasping, crying; while anxiety may cause uncontrollable hyperventilation.
While breathing is mostly involuntary, some degree of voluntary control is possible, for example, during singing, playing wind instruments, or holding breath under water. In this case the control originates from the primary motor cortex, which sends signals directly to the spinal cord, bypassing the respiratory center in the brainstem. There are limits, however, to the extent one can control their breath even though it’s possible to increase these limits with training.

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The major function of the respiratory system is to exchange oxygen and carbon dioxide between the body and the environment. The gas exchange process itself takes place in the respiratory division within the lungs. The rest of the respiratory tract – the nose, pharynx, larynx, trachea, bronchi and bronchioles – essentially serve as passageways for air to flow in and out of the lungs, and constitute the conducting division.
The nasal cavity is lined with a ciliated mucus membrane. The sticky mucus traps inhaled particles, while the beating of cilia drives debris-laden mucus toward the throat to be swallowed. Inhaled bacteria are destroyed by lysozyme in the mucus. Additional protection against potential pathogens is provided by lymphocytes and antibodies.
There are three folds of tissue arising from the wall of the nasal cavity, called nasal conchae, or turbinates. These structures serve to increase the contact surface with inhaled air, enabling the nose to RAPIDLY warm, moisten and cleanse it. The roof of the nasal cavity has olfactory nerve cells in its lining and is responsible for the sense of smell.
From the nose, inhaled air turns 90 degrees downward as it reaches the pharynx. This turn is another trap for large dust particles, which, because of their inertia, crash into the posterior wall of the throat, and stick to the mucosa.
The pharynx houses several tonsils. These immunocompetent tissues of the immune system are well positioned to respond to inhaled pathogens.
In addition to inhaled air, which is on its way to the lungs, the pharynx also passes food and drink from the mouth to the esophagus. Because aspiration of food or drink into the lungs may potentially be life threatening, there are mechanisms in place to prevent this from happening. The larynx is most critical in this regard. The opening of the larynx is guarded by a tissue flap called the epiglottis. During swallowing, the larynx is pulled up and the epiglottis flips over, directing food and drink to the esophagus. More importantly, the vocal folds also close to protect the airway.
From the larynx, air passes to the trachea, the windpipe, which then splits into two primary bronchi, supplying the two lungs. In the lungs, primary bronchi branch into smaller and smaller bronchi and bronchioles, forming the bronchial tree with millions of air tubes, or airways. The airways have a layer of smooth muscle in their wall which enables them to constrict or dilate. In response to the body’s higher demand for air, such as during exercise, the airways dilate to increase air flow. On the other hand, in the presence of pollutants in the air, the airways constrict to minimize their entry to the lungs.
The larynx, trachea and bronchial tree are lined with ciliated columnar epithelium, which produces mucus and functions as a mucociliary escalator: the mucus traps inhaled particles, while the cilia beating moves the mucus up toward the throat, where it is swallowed.
The last component of the conducting division, the terminal bronchioles, branch into several respiratory bronchioles which mark the beginning of the respiratory division. The respiratory bronchioles end with microscopic air sacs called the alveoli, each of which is surrounded by blood capillaries. This is where the gas exchange process takes place. The alveolar wall is composed mainly of type I – thin squamous cells which allow rapid gas diffusion. Inhaled oxygen moves from the alveoli into the blood in the capillaries, while carbon dioxide relocates from the blood to the alveoli to be exhaled out of the body. There is also a small number of type II cuboidal cells secreting a surfactant, whose function is to lower the surface tension at the air-liquid interface and prevent the alveolus from collapsing at the end of each exhalation. The alveoli also house a large number of macrophages, ready to engulf any inhaled particles that managed to get past previous barriers to the lungs. The debris-laden macrophages then ride the mucociliary escalator up to the throat to be swallowed and digested.

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Pulmonary ventilation, commonly referred to as breathing, is the process of air flowing IN and OUT of the lungs during inspiration and expiration. The air movements are governed by the principles of gas laws. Basically:
– air flows from HIGHER to LOWER pressure;
– pressure within a cavity increases when its volume decreases, and vice versa;
– volume of a given amount of gas increases with increased temperature.

At rest, in between breaths, the pressure inside the lungs, or intrapulmonary pressure, EQUALS the pressure outside the body, or atmospheric pressure. When discussing respiratory pressures, this is generally referred to as a RELATIVE pressure of ZERO. This is because what matters is the DIFFERENCE between the two pressures, NOT their absolute values. Thus, a NEGATIVE pressure is a pressure BELOW atmospheric, while a POSITIVE pressure is ABOVE atmospheric.
The lungs are covered in a double-layer membrane, which forms a THIN space surrounding the lungs, called the PLEURAL cavity. The pressure within the pleural cavity, or intrapleural pressure, is normally negative. This negative pressure acts like a SUCTION to keep the lungs inflated. If this becomes zero, such as in the case of pneumothorax, when the chest wall is punctured and the pleural cavity has the same pressure as the outside air, the lung would COLLAPSE.
Pulmonary ventilation is achieved by rhythmically changing the volume of the thoracic cavity. During inspiration, the diaphragm and the external intercostal muscles contract, expanding the thoracic cavity and the lungs. This increase in volume results in a decrease in pressure, causing outside air to flow IN. Another factor that helps to inflate the lungs is the warming of the inhaled air. This effect is most notable on a cool day, when the temperature outside is significantly lower, the inhaled air increases in volume as it warms up inside the body and inflates the lungs, FURTHER facilitating inhalation.
While inspiration requires muscular contraction and hence energy expenditure, expiration during quiet breathing is a PASSIVE process. As the diaphragm returns to its original position and the muscles relax, thoracic and lung volumes decrease and pressures increase, pushing air OUT of the lungs. Quiet expiration relies therefore on the ELASTICITY of the lungs and rib cage – their ability to SPRING BACK to the original dimensions. Conditions that REDUCE pulmonary elasticity, such as emphysema, can cause difficulty exhaling.
Deep breathing requires more forceful contractions of the diaphragm, intercostal muscles, and involves ADDITIONAL muscles to produce LARGER changes in the thoracic volume. DEEP expiration, unlike quiet expiration, is an active process.
Another factor that affects ventilation is the RESISTANCE to airflow, which exists within the lung tissues and in the airways. Lung COMPLIANCE refers to the EASE with which the lungs EXPAND. Healthy lungs normally have HIGH compliance, LOW resistance, like a THIN balloon, easy to inflate. Lung compliance is REDUCED when the lungs become “STIFF”, in conditions that cause scarring of lung tissues, or fibrosis. In this case the lung turns into a THICK balloon, harder to inflate.
Diseases that NARROW the airways, such as asthma, INcrease resistance, making it harder to breathe. The airways may also DILATE or CONSTRICT in response to various factors. For example, parasympathetic stimulation and histamine typically narrow the bronchioles, increase resistance and decrease airflow; while epinephrine, a hormone released during exercises, dilates bronchioles and thereby increases airflow.

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La neumonía es una infección común de los pulmones que afecta en su mayoría a los sacos de aire microscópicos – los alvéolos. La función del sistema respiratorio es intercambiar oxígeno y dióxido de carbono entre el cuerpo y el medio ambiente. Este proceso ocurre en los alvéolos de los pulmones. El oxígeno inhalado pasa de los alveolos a la sangre de los capilares mientras el dióxido de carbono se traslada desde la sangre hasta los alvéolos para ser exhalado fuera del cuerpo. En las personas con neumonía, estos sacos de aire están llenos de líquido o pus, lo que dificulta el proceso de intercambio gaseoso, resultando en dificultad respiratoria y un reflejo de toser. Otros síntomas pueden incluir dolor de pecho, fiebre, escalofríos y confusión.

La neumonía no es una sola enfermedad. Un gran número de diversos organismos pueden causar neumonía. La neumonía bacteriana es la más común, siendo el Streptococcus pneumoniae el principal culpable. La neumonía viral es más común en los niños pequeños. Una variedad de virus están implicados, cada uno de ellos predominando en diferentes épocas del año.

La neumonía por lo general empieza como una infección del tracto respiratorio superior – un resfriado o gripe, que luego se disemina hacia los pulmones. Las vías más comunes de transmisión son a través de la inhalación de gotitas de aerosol contaminadas y por la aspiración de las bacterias orales hacia los pulmones.

El escenario en el cual se desarrolla la neumonía es una información importante en la medida en que ayuda a identificar la fuente del agente causante y por lo tanto el enfoque del tratamiento. Generalmente, la neumonía adquirida en la comunidad es menos peligrosa que la neumonía asociada al cuidado de la salud, nosocomial o asociada a ventilación mecánica. Esto es por qué una infección contraída por fuera de los centros de salud tiene menor probabilidad de involucrar bacterias multirresistentes. Los pacientes intrahospitalarios son también más propensos a tener otros problemas de salud y un sistema inmunológico debilitado y por lo tanto están en menor capacidad de combatir la enfermedad.

La neumonía se diagnostica a menudo sobre la base de exámenes físicos y una radiografía de tórax. La evaluación clínica para los niños se basa principalmente en una alta frecuencia respiratoria, tos, presencia de retracción de la pared torácica inferior, y el nivel de consciencia. Los adultos suelen ser examinados en busca de signos vitales y presencia de crepitaciones en el pecho – el sonido estrepitoso proveniente de un pulmón enfermo.

La neumonía bacteriana es tratada con antibióticos. La elección de los antibióticos depende de la edad, las condiciones de salud del paciente y de cómo fue adquirida la infección. La neumonía viral causada por virus de la gripe puede ser tratada con medicamentos antivirales. La hospitalización puede ser necesaria para los casos graves con dificultad respiratoria, especialmente en los niños pequeños, los ancianos, y aquellos con otros problemas de salud.

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Chronic obstructive pulmonary disease, or COPD, is a PROGRESSIVE inflammatory lung disease characterized by INCREASING breathing difficulty. Other symptoms include cough, most commonly with mucus, chest tightness and wheezing. COPD develops as a result of LONG-TERM exposure to irritants such as smoke, chemical fumes or dusts, and may go UNNOTICED for years. Most people show symptoms after the age of 40 when the disease is already in its advanced stage.
Pathology

The lungs consist of millions of air tubes or airways, called bronchi and bronchioles, which bring air in and out of the body. These airways end with tiny air sacs – the alveoli – where the gas exchange process takes place. REPEATED inhalation of irritants results in a CHRONIC inflammatory response which brings in a large amount of defensive cells along with inflammatory chemicals from the immune system. Inflammation of the airways causes them to thicken and produce mucus, NARROWING the air passage – this is known as CHRONIC BRONCHITIS. Inflammatory chemicals also dissolve alveolar walls, resulting in DESTRUCTION of the air sacs – this is EMPHYSEMA. COPD is, basically, a COMBINATION of these two conditions.
Causes

Tobacco smoking is accountable for about 90% of COPD cases. These include current, former smokers and people frequently exposed to second-hand smoke.
Extended contact with harmful chemicals such as fumes from burning fuel or dusts, at home or workplace, may also cause COPD.
Genetics has been implicated in a small number of cases. Notably, a condition known as alpha-1 antitrypsin deficiency, or AAT deficiency, has been shown to increase risks for COPD and other lung diseases. AAT protein protects the lungs from damaging effects of enzymes released during inflammation. Low levels of AAT make lung tissues more vulnerable to destruction when inflamed. While people with AAT deficiency may develop COPD even WITHOUT smoking or exposure to harmful irritants, AAT deficient smokers are at MUCH greater risks.

Diagnosis

COPD is diagnosed based on symptoms, history of exposure to irritants and lung function tests. The major test for COPD is SPIROMETRY, in which the patient is asked to blow into a tube connected to a machine – a spirometer. Spirometry evaluates pulmonary functions by measuring the volume and the speed of air flow during inhalation and exhalation.

Treatments

There is no cure for COPD but treatments can relieve symptoms, prevent complications and slow down progression of the disease. The first and most essential step to treatment is to stop smoking and/or improve air quality at home and workplace. These are also the most effective measures in preventing the disease.
Other treatments include:
-Medication: bronchodilators are used to widen the airways; steroids to relieve inflammation.
-Vaccination against flu and pneumococcal pneumonia: this is to prevent serious complications COPD patients may have with these respiratory infections.
-Supplemental oxygen: this can improve quality of life provided that the patient no longer smokes.
-Breathing exercises and other therapies as part of a pulmonary rehabilitation program.
-Finally, surgery may be performed for severe cases when other methods fail. Surgical procedures include bullectomy, lung volume reduction surgery, where damaged parts of the lung are removed; and lung transplant, where the entire diseased lung is replaced with a healthy lung from a deceased donor.

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Pneumonia is a common infection of the lungs affecting mostly the microscopic air sacs – the alveoli. The function of the respiratory system is to exchange oxygen and carbon dioxide between the body and the environment. This process takes place in the alveoli of the lungs.  Inhaled oxygen moves from the alveoli into the blood in the capillaries while carbon dioxide relocates from the blood to the alveoli to be exhaled out of the body. In people with pneumonia, these air sacs are filled with fluid or pus, hindering the gas exchange process, resulting in difficulty breathing and a cough reflex. Other symptoms may include chest pain, fever, chills and confusion.

Pneumonia is not a single disease.  A large number of various organisms can cause pneumonia. Bacterial pneumonia is the most common, with Streptococcus pneumoniae being the main culprit. Viral pneumonia is more common in young children. A variety of viruses are implicated with each of them predominating in different times of the year.

Pneumonia commonly starts as an infection of the upper respiratory tract – a cold or flu, which then spreads to the lungs. The most common routes of transmission are through inhalation of contaminated aerosol droplets and aspiration of oral bacteria into the lungs.

The setting in which pneumonia develops is an important information as it helps to identify the source of the causative agent and hence the treatment approach. Generally, community-acquired pneumonia is less dangerous than health care-associated, hospital-acquired, or ventilator-associated pneumonia. This is because an infection contracted outside health care facilities is less likely to involve multidrug-resistant bacteria. Patients who are already in hospitals are also most likely to have other health problems and weakened immune system and are thus less able to fight the disease.

Pneumonia is often diagnosed based on physical exams and a chest X-ray. Clinical assessment for children is primarily based on a rapid respiratory rate, a cough, presence of lower chest wall indrawing, and the level of consciousness. Adults are usually checked for vital signs and presence of chest crackles – the rattling noise coming from a diseased lung.

Bacterial pneumonia is treated with antibiotics. The choice of antibiotics depends on the patient’s age, health conditions and how the infection was acquired. Viral pneumonia caused by influenza viruses may be treated with antiviral drugs. Hospitalization may be required for severe cases with breathing difficulty, especially for young children, the elderly, and those with other health problems.

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Sinusite, também conhecida como rinossinusite, é uma condição muito comum onde os seios paranasais estão inflamados, causando congestão nasal, dor de cabeça e dor facial.

Os seios paranasais são cavidades dos ossos do crânio. Existem quatro pares de cavidades localizadas em ambos os lados da cabeça. Eles são os seios maxilar, frontal, etmoidal e esfenoidal.

Os seios são revestidos por epitélio respiratório que produz muco. A drenagem do muco para a cavidade nasal ocorre através de pequenas aberturas. A drenagem prejudicada tem sido associada com a inflamação dos seios. Quando um seio é bloqueado, o fluido se acumula, tornando esse ambiente favorável para o crescimento de bactérias ou vírus, podendo causar infecção.

Um sintoma típico da sinusite é descrito como uma dor ou pressão constante, geralmente, localizada no seio afetado. A dor pode piorar quando a pessoa se inclina ou enquanto está deitada. Os sintomas geralmente começam em um lado da cabeça e se espalham para o outro lado. A sinusite aguda pode também ser acompanhada de secreção nasal espessa de cor amarelo esverdeado.

A sinusite pode ter diferentes causas, que incluem:

– Alergia (rinite alérgica): alérgenos, como o pólen, pelos de animais … pode desencadear uma resposta inflamatória na mucosa do nariz e seios paranasais, resultando na produção excessiva de muco, congestão nasal, espirros e coceira.

– Infecção: geralmente ocorre como uma complicação de um resfriado comum. A drenagem do seio prejudicada, devido à inflamação da mucosa nasal durante um resfriado, muitas vezes leva à infecção do próprio seio. Sintomas gripais, além de dor de cabeça e dor ou pressão facial são queixas comuns.

– Outras condições que causam bloqueio de drenagem do seio incluem: anormalidades estruturais, tais como desvio de septo nasal; formação de pólipos nasais.

Os tratamentos variam de acordo com a causa da sinusite:

– Para alergia: corticosteróides intranasais são comumente usados.

– Para infecção viral: medicamentos para alívio de sintomas, tais como spray nasal para irrigação e descongestionante; outros tratamentos para resfriado comum, como repouso e beber bastante líquido.

– Para infecção bacteriana: antibióticos podem ser prescritos.

– Para sinusite recorrente ou crônica devido a anormalidades estruturais ou pólipos nasais, a cirurgia nasal pode ser recomendada para desobstruir o canal de drenagem.