Symptoms of pulmonary fibrosis are mainly:

- Shortness of breath, particularly with exertion

- Chronic dry, hacking coughing

- Fatigue and weakness

- Chest discomfort including chest pain

- Loss of appetite and rapid weight loss

Pulmonary fibrosis is suggested by a history of progressive shortness of breath (dyspnea) with exertion. Sometimes fine inspiratory crackles can be heard at the lung bases on auscultation. A chest x-ray may or may not be abnormal, but high-resolution CT will frequently demonstrate abnormalities.

Pulmonary fibrosis (literally "scarring of the lungs") is a respiratory disease in which scars are formed in the lung tissues, leading to serious breathing problems. Scar formation, the accumulation of excess fibrous connective tissue (the process called fibrosis), leads to thickening of the walls, and causes reduced oxygen supply in the blood. As a consequence patients suffer from perpetual shortness of breath.

In some patients the specific cause of the disease can be diagnosed, but in others the probable cause cannot be determined, a condition called idiopathic pulmonary fibrosis. There is no known cure for the scars and damage in the lung due to pulmonary fibrosis.

The most common symptom of pulmonary edema is difficulty breathing, but may include other symptoms such as coughing up blood (classically seen as pink, frothy sputum), excessive sweating, anxiety, and pale skin. Shortness of breath can manifest as orthopnea (inability to lie down flat due to breathlessness) and/or paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night). These are common presenting symptoms of chronic pulmonary edema due to left ventricular failure. The development of pulmonary edema may be associated with symptoms and signs of "fluid overload"; this is a non-specific term to describe the manifestations of left ventricular failure on the rest of the body and includes peripheral edema (swelling of the legs, in general, of the "pitting" variety, wherein the skin is slow to return to normal when pressed upon), raised jugular venous pressure and hepatomegaly, where the liver is enlarged and may be tender or even pulsatile. Other signs include end-inspiratory crackles (sounds heard at the end of a deep breath) on auscultation and the presence of a third heart sound.

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.

Restrictive lung diseases (or restrictive ventilatory defects) are a category of extrapulmonary, pleural, or parenchymal respiratory diseases that restrict lung expansion, resulting in a decreased lung volume, an increased work of breathing, and inadequate ventilation and/or oxygenation. Pulmonary function test demonstrates a decrease in the forced vital capacity.

The symptoms for pulmonary veno-occlusive disease are the following:

Interstitial lung disease (ILD), or diffuse parenchymal lung disease (DPLD), is a group of lung diseases affecting the interstitium (the tissue and space around the air sacs of the lungs). It concerns alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues. It may occur when an injury to the lungs triggers an abnormal healing response. Ordinarily, the body generates just the right amount of tissue to repair damage. But in interstitial lung disease, the repair process goes awry and the tissue around the air sacs (alveoli) becomes scarred and thickened. This makes it more difficult for oxygen to pass into the bloodstream. The term ILD is used to distinguish these diseases from obstructive airways diseases.

In children, several unique forms of ILD exist which are specific for the young age groups. The acronym chILD is used for this group of diseases and is derived from the English name, Children’s Interstitial Lung Diseases – chILD.

Prolonged ILD may result in pulmonary fibrosis, but this is not always the case. Idiopathic pulmonary fibrosis is interstitial lung disease for which no obvious cause can be identified (idiopathic), and is associated with typical findings both radiographic (basal and pleural based fibrosis with honeycombing) and pathologic (temporally and spatially heterogeneous fibrosis, histopathologic honeycombing and fibroblastic foci).

In 2013 interstitial lung disease affected 595,000 people globally. This resulted in 471,000 deaths.

Pulmonary edema is fluid accumulation in the tissue and air spaces of the lungs. It leads to impaired gas exchange and may cause respiratory failure. It is due to either failure of the left ventricle of the heart to remove blood adequately from the pulmonary circulation (cardiogenic pulmonary edema), or an injury to the lung parenchyma or vasculature of the lung (noncardiogenic pulmonary edema). Treatment is focused on three aspects: firstly improving respiratory function, secondly, treating the underlying cause, and thirdly avoiding further damage to the lung. Pulmonary edema, especially acute, can lead to fatal respiratory distress or cardiac arrest due to hypoxia. It is a cardinal feature of congestive heart failure. The term is from the Greek (oídēma, "swelling"), from οἰδέω (oidéō, "I swell").

Pulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension caused by progressive blockage of the small veins in the lungs. The blockage leads to high blood pressures in the arteries of the lungs, which, in turn, leads to heart failure. The disease is progressive and fatal, with median survival of about 2 years from the time of diagnosis to death. The definitive therapy is lung transplantation.

The symptoms of pulmonary hypertension include the following:

Less common signs/symptoms include non-productive cough and exercise-induced nausea and vomiting. Coughing up of blood may occur in some patients, particularly those with specific subtypes of pulmonary hypertension such as heritable pulmonary arterial hypertension, Eisenmenger syndrome and chronic thromboembolic pulmonary hypertension. Pulmonary venous hypertension typically presents with shortness of breath while lying flat or sleeping (orthopnea or paroxysmal nocturnal dyspnea), while pulmonary arterial hypertension (PAH) typically does not.

Other typical signs of pulmonary hypertension include an accentuated pulmonary component of the second heart sound, a right ventricular third heart sound, and parasternal heave indicating a hypertrophied right atrium. Signs of systemic congestion resulting from right-sided heart failure include jugular venous distension, ascites, and hepatojugular reflux. Evidence of tricuspid insufficiency and pulmonic regurgitation is also sought and, if present, is consistent with the presence of pulmonary hypertension.

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

Pulmonary interstitial emphysema is a concern in any of the following diagnosis:

- Prematurity

- Respiratory distress syndrome (RDS)

- Meconium aspiration syndrome (MAS)

- Amniotic fluid aspiration

- Sepsis, or other infections

- Mechanical ventilation

Pulmonary interstitial emphysema (PIE) is a collection of air outside of the normal air space of the pulmonary alveoli, found instead inside the connective tissue of the peribronchovascular sheaths, interlobular septa, and visceral pleura. (This supportive tissue is called the pulmonary interstitium.) This collection of air develops as a result of alveolar and terminal bronchiolar rupture. Pulmonary interstitial emphysema is more frequent in premature infants who require mechanical ventilation for severe lung disease. Infants suffering from pulmonary interstitial emphysema are typically recommended for admission to a neonatal intensive care unit.

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.

About 20% of DIPNECH patients are symptom free at the time they first present. The most common symptoms include:

- Chronic cough

- Shortness of breath or dyspnea when exercising or exerting one’s self

- Wheezing (less frequent)

- Hemoptysis (Infrequent)

Symptoms may be present for many years prior to diagnosis and are often ascribed to other lung conditions. Erroneous initial diagnoses of asthma or chronic obstructive pulmonary disease often are made in patients with DIPNECH.

Respiratory disease is a medical term that encompasses pathological conditions affecting the organs and tissues that make gas exchange possible in higher organisms, and includes conditions of the upper respiratory tract, trachea, bronchi, bronchioles, alveoli, pleura and pleural cavity, and the nerves and muscles of breathing. Respiratory diseases range from mild and self-limiting, such as the common cold, to life-threatening entities like bacterial pneumonia, pulmonary embolism, acute asthma and lung cancer.

The study of respiratory disease is known as pulmonology. A doctor who specializes in respiratory disease is known as a pulmonologist, a chest medicine specialist, a respiratory medicine specialist, a respirologist or a thoracic medicine specialist.

Respiratory diseases can be classified in many different ways, including by the organ or tissue involved, by the type and pattern of associated signs and symptoms, or by the cause of the disease.

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.

Most common:

- Chest Pain

- Cough

- Fever

- Shortness of breath

- Joint pain, stiffness, swelling

- Skin nodules

People may not present with all these symptoms or non at all.

As with other forms of pulmonary edema, the hallmark of SIPE is a cough which may lead to frothy or blood-tinged sputum. Symptoms include:

- Shortness of breath out of proportion to effort being expended.

- Crackles, rattling or ‘junky’ feelings deep in the chest associated with breathing effort – usually progressively worsening with increasing shortness of breath and may be cause for a panic attack

- Cough, usually distressing and productive or not of a little pink, frothy or blood-tinged sputum (hemoptysis)

The wetsuit may feel as though it is hindering breathing ability.

Chronic respiratory diseases (CRDs) are diseases of the airways and other structures of the lung. This disease could be characterized by a high inflammatory cells recruitment (neutrophil) and/or destructive cycle of infection, (e.g. mediated by "Pseudomonas aeruginosa"). Some of the most common are asthma, chronic obstructive pulmonary disease, or acute respiratory distress syndrome . CRDs are not curable, however, various forms of treatment that help dilate major air passages and improve shortness of breath can help control symptoms and increase the quality of life for people with the disease.

it usually lasts for three months to two years

Portopulmonary hypertension (PPH) is defined by the coexistence of portal and pulmonary hypertension. PPH is a serious complication of liver disease, present in 0.25 to 4% of all patients suffering from cirrhosis. Once an absolute contraindication to liver transplantation, it is no longer, thanks to rapid advances in the treatment of this condition. Today, PPH is comorbid in 4-6% of those referred for a liver transplant.

Clinically, IPH manifests as a triad of haemoptysis, diffuse parenchymal infiltrates on chest radiographs, and iron deficiency anaemia. It is diagnosed at an average age of 4.5 plus or minus 3.5 years, and it is twice as common in females. The clinical course of IPH is exceedingly variable, and most of the patients continue to have episodes of pulmonary haemorrhage despite therapy. Death may occur suddenly from acute pulmonary haemorrhage or after progressive pulmonary insufficiency resulting in chronic respiratory failure.

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.

Aspergillosis is an infection caused by the fungus "Aspergillus". Aspergillosis describes a large number of diseases involving both infection and growth of fungus as well as allergic responses. Aspergillosis can occur in a variety of organs, both in humans and animals.

The most common sites of infection are the respiratory apparatus (lungs, sinuses) and these infections can be:

- Invasive (e.g. – IPA)

- Non-invasive (e.g. Allergic Pulmonary Aspergillosis - ABPA)

- Chronic pulmonary and aspergilloma (e.g. chronic cavitary, semi-invasive)

- Severe asthma with fungal sensitisation (SAFS)

Chronic pulmonary aspergillosis (CPA) is a long-term aspergillus infection of the lung and "Aspergillus fumigatus" is almost always the species responsible for this illness. Patients fall into several groups as listed below.

- Those with an aspergilloma which is a ball of fungus found in a single lung cavity - which may improve or disappear, or change very little over a few years.

- Aspergillus nodule

- Chronic cavitary pulmonary aspergillosis (CCPA) where cavities are present in the lungs, but not necessarily with a fungal ball (aspergilloma).

- Chronic fibrosing pulmonary aspergillosis this may develop where pulmonary aspergillosis remains untreated and chronic scarring of the lungs occurs. Unfortunately scarring of the lungs does not improve.

Most patients with CPA have or have had an underlying lung disease. The most common diseases include tuberculosis, atypical mycobacterium infection, stage III fibrocystic pulmonary sarcoidosis, ABPA, lung cancer, COPD and emphysema, asthma and silicosis.

Symptoms can vary greatly, but they include a persistent dry cough.