The classic presentation of COP is the development of nonspecific systemic (e.g., fevers, chills, night sweats, fatigue, weight loss) and respiratory (e.g. difficulty breathing, cough) symptoms in association with filling of the lung alveoli that is visible on chest x-ray. This presentation is usually so suggestive of an infection that the majority of patients with COP have been treated with at least one failed course of antibiotics by the time the true diagnosis is made.

"Organizing" refers to unresolved pneumonia (in which the alveolar exudate persists and eventually undergoes fibrosis) in which fibrous tissue forms in the alveoli. The phase of resolution and/or remodeling following bacterial infections is commonly referred to as organizing pneumonia, both clinically and pathologically.

Most types of eosinophilic pneumonia have similar signs and symptoms. Prominent and nearly universal signs and symptoms include cough, fever, difficulty breathing, and night sweats. Acute eosinophilic pneumonia typically follows a rapid course. Fever and cough may develop only one or two weeks before breathing difficulties progress to the point of respiratory failure requiring mechanical ventilation. Chronic eosinophilic pneumonia usually follows a slower course. Symptoms accumulate over several months and include fever, cough, difficulty breathing, wheezing, and weight loss. Individuals with CEP are often misdiagnosed with asthma before CEP is finally recognized.

EP due to medications or environmental exposures is similar and occurs after an exposure to a known offending agent. EP due to parasitic infections has a similar prodrome in addition to a host of different symptoms related to the variety of underlying parasites. EP in the setting of cancer often develops in the context of a known diagnosis of lung cancer, cervical cancer, etc.

The typical symptoms of UIP are progressive shortness of breath and cough for a period of months. In some patients, UIP is diagnosed only when a more acute disease supervenes and brings the patient to medical attention.

The signs and symptoms of PAP include shortness of breath, a cough, low grade fever, and weight loss.

The clinical course of PAP is unpredictable. Spontaneous remission is recognized, and some patients have stable symptoms. Death may occur due to the progression of PAP or of any underlying associated disease. Individuals with PAP are more vulnerable to lung infections such as bacterial pneumonia, mycobacterium avium-intracellulare infection, or a fungal infection.

Eosinophilic pneumonia is divided into different categories depending upon whether a cause can be determined or not. Known causes include certain medications or environmental triggers, parasitic infections, and cancer. EP can also occur when the immune system attacks the lungs, a disease called eosinophilic granulomatosis with polyangiitis. When a cause cannot be found, the EP is labeled "idiopathic." Idiopathic EP can be divided into "acute eosinophilic pneumonia" (AEP) and "chronic eosinophilic pneumonia" (CEP) depending on the symptoms a person is experiencing.

Alveolar disease is visible on chest radiography as small, ill-defined nodules of homogeneous density centered on the acini or bronchioles. The nodules coalesce early in the course of disease, such that the nodules may only be seen as soft fluffy edges in the periphery.

When the nodules are centered on the hilar regions, the chest x-ray may develop what is called the "butterfly," or "batwing" appearance. The nodules may also have a segmental or lobar distribution. Air alveolograms and air bronchograms can also be seen.

These findings appear soon after the onset of symptoms and change rapidly thereafter.

A segmental or lobar pattern may be apparent after aspiration pneumonia, atelectasis, lung contusion, localized pulmonary edema, obstructive pneumonia, pneumonia, pulmonary embolism with infarction, or tuberculosis.

Non-specific interstitial pneumonia (NSIP) is a form of idiopathic interstitial pneumonia.

The cause of the scarring in UIP may be known (less commonly) or unknown (more commonly). Since the medical term for conditions of unknown cause is "idiopathic", the clinical term for UIP of unknown cause is idiopathic pulmonary fibrosis (IPF). Examples of known causes of UIP include systemic sclerosis/scleroderma, rheumatoid arthritis, asbestosis, and prolonged use of medications such as nitrofurantoin or amiodarone.

The fibrosing pattern of NSIP has a five year survival rate of 86% to 92%, while the cellular pattern of NSIP has a 100% five year survival rate. Patients with NSIP(whether cellular or fibrosing), have a better prognosis than those with usual interstitial pneumonia (UIP).

Patients with subacute HP gradually develop a productive cough, dyspnea, fatigue, anorexia, weight loss, and pleurisy. Symptoms are similar to the acute form of the disease, but are less severe and last longer. On chest radiographs, micronodular or reticular opacities are most prominent in mid-to-lower lung zones. Findings may be present in patients who have experienced repeated acute attacks.

The subacute, or intermittent, form produces more well-formed noncaseating granulomas, bronchiolitis with or without organizing pneumonia, and interstitial fibrosis.

Alveolar lung disease may be divided into acute or chronic. Causes of acute alveolar lung disease include pulmonary edema (cardiogenic or neurogenic), pneumonia (bacterial or viral), pulmonary embolism, systemic lupus erythematosus, bleeding in the lungs (e.g., Goodpasture syndrome), idiopathic pulmonary hemosiderosis, and granulomatosis with polyangiitis.

Chronic alveolar lung disease can be caused by pulmonary alveolar proteinosis, alveolar cell carcinoma, mineral oil pneumonia, sarcoidosis (alveolar form), lymphoma, tuberculosis, metastases, or desquamative interstitial pneumonia.

Pulmonary Langerhans cell histiocytosis, silicosis, coal workers pneumoconiosis, carmustine related pulmonary fibrosis, respiratory broncholitis associated with interstitial lung disease.

- Lower lung predominance

Idiopathic pulmonary fibrosis, pulmonary fibrosis associated with connective tissue diseases, asbestosis, chronic aspiration

- Central predominance (perihilar)

Sarcoidosis, berylliosis

- Peripheral predominance

Idiopathic pulmonary fibrosis, chronic eosinophilic pneumonia, cryptogenic organizing pneumonia

Acute:

- Cough

- Difficulty Breathing

- Abnormal lung sounds (wet, gurgling sounding breaths)

- Chest pain, tightness or burning

Chronic:

- Persistent cough

- Shortness of breath

- Increased susceptibility to respiratory illness

Symptoms of chronic chemical pneumonitis may or may not be present, and can take months or years to develop to the point of noticeability.

Pulmonary edema, connective tissue diseases, asbestosis, lymphangitic carcinomatosis, lymphoma, lymphangioleiomyomatosis, drug-induced lung diseases

- Lymphadenopathy

Sarcoidosis, silicosis, berylliosis, lymphangitic carcinomatosis, lymphoma, lymphocytic interstitial pneumonia

In the acute form of HP, symptoms may develop 4–6 hours following heavy exposure to the provoking antigen. Symptoms include fever, chills, malaise, cough, chest tightness, dyspnea, rash, swelling and headache. Symptoms resolve within 12 hours to several days upon cessation of exposure.

Acute HP is characterized by poorly formed noncaseating interstitial granulomas and mononuclear cell infiltration in a peribronchial distribution with prominent giant cells.

On chest radiographs, a diffuse micronodular interstitial pattern (at times with ground-glass density in the lower and middle lung zones) may be observed. Findings are normal in approximately 10% of patients." In high-resolution CT scans, ground-glass opacities or diffusely increased radiodensities are present. Pulmonary function tests show reduced diffusion capacity of lungs for carbon monoxide (DLCO). Many patients have hypoxemia at rest, and all patients desaturate with exercise. Extrinsic allergic alveolitis may eventually lead to Interstitial lung disease.

In many patients, symptoms are present for a considerable time before diagnosis. The most common clinical features of IPF include the following:

- Age over 50 years

- Dry, non-productive cough on exertion

- Progressive exertional dyspnea (shortness of breath with exercise)

- Dry, inspiratory bibasilar "velcro-like" crackles on auscultation (a crackling sound in the lungs during inhalation similar to Velcro being torn apart slowly, heard with a stethoscope).

- Clubbing of the digits, a disfigurement of the finger tips or toes (see image)

- Abnormal pulmonary function test results, with evidence of restriction and impaired gas exchange.

Some of these features are due to chronic hypoxemia (oxygen deficiency in the blood), are not specific for IPF, and can occur in other pulmonary disorders. IPF should be considered in all patients with unexplained chronic exertional dyspnea who present with cough, inspiratory bibasilar crackles, or finger clubbing.

Assessment of "velcro" crackles on lung auscultation is a practical way to improve the earlier diagnosis of IPF. Fine crackles are easily recognized by clinicians and are characteristic of IPF.

If bilateral fine crackles are present throughout the inspiratory time and are persisting after several deep breaths, and if remaining present on several occasions several weeks apart in a subject aged ≥60 years, this should raise the suspicion of IPF and lead to consideration of an HRCT scan of the chest which is more sensitive than a chest X-ray. As crackles are not specific for IPF, they must prompt a thorough diagnostic process.

Pulmonary alveolar proteinosis (PAP) is a rare lung disease in which an abnormal accumulation of pulmonary surfactant occurs within the alveoli (microscopic air sacs in the lung), interfering with the lungs' ability to exchange oxygen from the air, and carbon dioxide from the blood. PAP can occur in a primary form or secondarily in the settings of certain cancers (such as myeloid leukemia), lung infections, or environmental exposure to dusts or chemicals. Rare familial forms have also been recognized, suggesting a genetic component in those cases.

The signs and symptoms of ARDS often begin within two hours of an inciting event, but can occur after 1–3 days. Signs and symptoms may include shortness of breath, fast breathing, and a low oxygen level in the blood due to abnormal ventilation.

Acute eosinophilic pneumonia is the acute-onset form of eosinophilic pneumonia, a lung disease caused by the buildup of eosinophils, a type of white blood cell, in the lungs. It is characterized by a rapid onset of shortness of breath, cough, fatigue, night sweats, and weight loss. Though the underlying cause is unknown, it can be triggered by a change in medication or tobacco smoking. It is treated with corticosteroids and has a favorable prognosis.

Acute respiratory distress syndrome (ARDS) is a medical condition occurring in critically ill patients characterized by widespread inflammation in the lungs. ARDS is not a particular disease; rather, it is a clinical phenotype which may be triggered by various pathologies such as trauma, pneumonia and sepsis.

The hallmark of ARDS is diffuse injury to cells which form the barrier of the microscopic air sacs of the lungs, surfactant dysfunction, activation of the innate immune system response, and dysfunction of the body's regulation of clotting and bleeding. In effect, ARDS impairs the lungs' ability to exchange oxygen and carbon dioxide with the blood across a thin layer of the lungs' microscopic air sacs known as alveoli.

The syndrome is associated with a death rate between 20 and 50%. The risk of death varies based on severity, the person's age, and the presence of other underlying medical conditions.

Although the terminology of "adult respiratory distress syndrome" has at times been used to differentiate ARDS from "infant respiratory distress syndrome" in newborns, the international consensus is that "acute respiratory distress syndrome" is the best term because ARDS can affect people of all ages.

In disorders that are intrinsic to the lung parenchyma, the underlying process is usually pulmonary fibrosis (scarring of the lung). As the disease progresses, the normal lung tissue is gradually replaced by scar tissue interspersed with pockets of air. This can lead to parts of the lung having a honeycomb-like appearance.

Idiopathic pulmonary fibrosis (IPF) is a chronic irreversible and ultimately fatal disease characterized by a progressive decline in lung function. American Thoracic Society/European Respiratory Society International Multidisciplinary Consensus Classification of the Idiopathic Interstitial Pneumonias. This official statement of the American Thoracic Society (ATS), and the European Respiratory Society (ERS) was approved by the ATS board of directors, June 2013 and by the ERS Steering Committee, March 2013. "Am Respir Crit Care Med." 188 (6): 733–748. September 15, 2013. The term pulmonary fibrosis means scarring of lung tissue and is the cause of worsening dyspnea (shortness of breath). Fibrosis is usually associated with a poor prognosis.

IPF belongs to a large group of more than 200 lung diseases known as interstitial lung diseases (ILDs), characterized by the involvement of lung interstitium. The interstitium, the tissue between the air sacs in the lung, is the primary site of injury in ILDs. However, these disorders frequently affect not only the interstitium, but also the airspaces, peripheral airways, and vessels. Lung tissue from people with IPF shows a characteristic histopathologic pattern known as usual interstitial pneumonia (UIP). UIP is therefore the pathologic counterpart of IPF. The term 'idiopathic' is used because the cause of pulmonary fibrosis is still unknown. IPF usually occurs in adults of between 50 and 70 years of age, particularly those with a history of cigarette smoking, and affects more men than women. The diagnosis of IPF requires exclusion of other known causes of ILDs and the presence of a typical radiological pattern identified through high resolution computed tomography (HRCT). In the right clinical setting, it is possible to make the diagnosis of IPF by HRCT alone, obviating the need for surgical lung biopsy.

Treatment to slow down the progression of the disease may include nintedanib or pirfenidone.

Chemical pneumonitis is inflammation of the lung caused by aspirating or inhaling irritants. It is sometimes called a "chemical pneumonia", though it is not infectious. There are two general types of chemical pneumonitis: acute and chronic.

Irritants capable of causing chemical pneumonitis include vomitus, barium used in gastro-intestinal imaging, chlorine gas (among other pulmonary agents), ingested gasoline or other petroleum distillates, ingested or skin absorbed pesticides, gases from electroplating, smoke and others. It may also be caused by the use of inhalants.

Mendelson's syndrome is a type of chemical pneumonitis.

Mineral oil should not be given internally to young children, pets, or anyone with a cough, hiatus hernia, or nocturnal reflux, because it can cause complications such as lipoid pneumonia. Due to its low density, it is easily aspirated into the lungs, where it cannot be removed by the body. In children, if aspirated, the oil can work to prevent normal breathing, resulting in death of brain cells and permanent paralysis and/or retardation

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