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

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.

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.

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 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.

Clinical symptoms and signs are often non-specific or absent in early CTEPH, with signs of right heart failure only in advanced disease. The main symptom of CTEPH is exertional breathlessness (shortness of breath during exertion such as exercise), which is unspecific and may often be attributed to other, more common, diseases by physicians. When present, the clinical symptoms of CTEPH may resemble those of acute PE, or of idiopathic pulmonary arterial hypertension (iPAH). Leg oedema (swelling) and haemoptysis (blood in mucus) occur more often in CTEPH, while syncope (fainting) is more common in iPAH.

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.

According to WHO classification there are 5 groups of PH, where Group I (pulmonary arterial hypertension) is further subdivided into Group I' and Group I" classes. The most recent WHO classification system (with adaptations from the more recent ESC/ERS guidelines shown in italics) can be summarized as follows:

WHO Group I – Pulmonary arterial hypertension (PAH)

- Idiopathic

- Heritable (BMPR2, ALK1, SMAD9, caveolin 1, KCNK3 mutations)

- Drug- and toxin-induced (e.g., methamphetamine use)

- Associated conditions:Connective tissue disease, HIV infection, Portal hypertension, Congenital heart diseases, Schistosomiasis

WHO Group I' – Pulmonary veno-occlusive disease (PVOD), pulmonary capillary hemangiomatosis (PCH)

- Idiopathic

- Heritable (EIF2AK4 mutations)

- Drugs, toxins and radiation-induced

- Associated conditions:connective tissue disease, HIV infection

WHO Group I" – Persistent pulmonary hypertension of the newborn

WHO Group II – Pulmonary hypertension secondary to left heart disease

- Left ventricular Systolic dysfunction

- Left ventricular Diastolic dysfunction

- Valvular heart disease

- Congenital/acquired left heart inflow/outflow tract obstruction and congenital cardiomyopathy

- Congenital/acquired pulmonary venous stenosis

WHO Group III – Pulmonary hypertension due to lung disease, chronic hypoxia

- Chronic obstructive pulmonary disease (COPD)

- Interstitial lung disease

- Mixed restrictive and obstructive pattern pulmonary diseases

- Sleep-disordered breathing

- Alveolar hypoventilation disorders

- Chronic exposure to high altitude

- Developmental abnormalities

WHO Group IV – chronic arterial obstruction

- Chronic thromboembolic pulmonary hypertension (CTEPH)

- Other pulmonary artery obstructions

- Angiosarcoma or other tumor within the blood vessels

- Arteritis

- Congenital pulmonary artery stenosis

- Parasitic infection (hydatidosis)

WHO Group V – Pulmonary hypertension with unclear or multifactorial mechanisms

- Hematologic diseases: chronic hemolytic anemia (including sickle cell disease)

- Systemic diseases: sarcoidosis, pulmonary Langerhans cell histiocytosis: lymphangioleiomyomatosis, neurofibromatosis, vasculitis

- Metabolic disorders: glycogen storage disease, Gaucher disease, thyroid diseases

- Others: pulmonary tumoral thrombotic microangiopathy, fibrosing mediastinitis, chronic kidney failure, segmental pulmonary hypertension (pulmonary hypertension restricted to one or more lobes of the lungs)

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

- Lymphadenopathy

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

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.

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

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.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a long-term disease caused by a blockage in the blood vessels that deliver blood from the heart to the lungs (pulmonary arteries), resulting in increased pressure in these arteries (pulmonary hypertension). The blockage either results from a hardened blood clot that is thought to originate from the deep veins of the body (thromboembolism) and remains in the arteries, or from a scar that forms at the site where the clot has damaged the arteries, causing permanent fibrous obstruction (blood flow blockage). Most patients have a combination of microvascular (small vessel) and macrovascular (large vessel) obstruction. Some patients may present with normal or near-normal pulmonary pressures at rest despite symptomatic disease. These patients are labelled as having chronic thromboembolic disease (CTED).

Diagnosis is based on findings obtained after at least 3 months of effective anticoagulation therapy (blood thinners) in order to discriminate this condition from ‘subacute’ pulmonary embolism (blood clot in the lungs, PE). Diagnostic findings for CTEPH are:

1. Invasively (i.e., in the blood) measured mean pulmonary arterial pressure (mPAP) ≥25 mmHg;

2. Mismatched perfusion defects on lung ventilation/perfusion (V/Q) scan and specific diagnostic signs for CTEPH seen by multidetector computed tomography angiography (MDCT), magnetic resonance imaging (MRI) or conventional pulmonary cineangiography (PAG), such as ring-like stenoses, webs/slits, chronic total occlusions (pouch lesions, or tapered lesions) and tortuous lesions.

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.

Shortness of breath is often the symptom that most bothers people. It is commonly described as: "my breathing requires effort," "I feel out of breath," or "I can't get enough air in". Different terms, however, may be used in different cultures. Typically the shortness of breath is worse on exertion of a prolonged duration and worsens over time. In the advanced stages, or end stage pulmonary disease it occurs during rest and may be always present. It is a source of both anxiety and a poor quality of life in those with COPD. Many people with more advanced COPD breathe through pursed lips and this action can improve shortness of breath in some.

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.

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.

Diagnosis of obstructive disease requires several factors depending on the exact disease being diagnosed. However one commonalty between them is an FEV1/FVC ratio less than 0.7, i.e. the inability to exhale 70% of their breath within one second.

Following is an overview of the main obstructive lung diseases. "Chronic obstructive pulmonary disease" is mainly a combination of chronic bronchitis and emphysema, but may be more or less overlapping with all conditions.

In COPD, breathing out may take longer to than breathing in. Chest tightness may occur, but is not common and may be caused by another problem. Those with obstructed airflow may have wheezing or decreased sounds with air entry on examination of the chest with a stethoscope. A barrel chest is a characteristic sign of COPD, but is relatively uncommon. Tripod positioning may occur as the disease worsens.

Advanced COPD leads to high pressure on the lung arteries, which strains the right ventricle of the heart. This situation is referred to as cor pulmonale, and leads to symptoms of leg swelling and bulging neck veins. COPD is more common than any other lung disease as a cause of cor pulmonale. Cor pulmonale has become less common since the use of supplemental oxygen.

COPD often occurs along with a number of other conditions, due in part to shared risk factors. These conditions include ischemic heart disease, high blood pressure, diabetes mellitus, muscle wasting, osteoporosis, lung cancer, anxiety disorder, sexual dysfunction, and depression. In those with severe disease, a feeling of always being tired is common. Fingernail clubbing is not specific to COPD and should prompt investigations for an underlying lung cancer.

Obstructive lung disease is a category of respiratory disease characterized by airway obstruction. Many obstructive diseases of the lung result from narrowing (obstruction) of the smaller bronchi and larger bronchioles, often because of excessive contraction of the smooth muscle itself. It is generally characterized by inflamed and easily collapsible airways, obstruction to airflow, problems exhaling and frequent medical clinic visits and hospitalizations. Types of obstructive lung disease include; asthma, bronchiectasis, bronchitis and chronic obstructive pulmonary disease (COPD). Although COPD shares similar characteristics with all other obstructive lung diseases, such as the signs of coughing and wheezing, they are distinct conditions in terms of disease onset, frequency of symptoms and reversibility of airway obstruction. Cystic fibrosis is also sometimes included in obstructive pulmonary disease.

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.

From most to lest common:

- Pleural involvement (pleurisy, effusions)

- Pulmonary parenchymal nodules, more common in men than in women

- Rheumatoid-associated interstitial lung disease

- Bronchiolitis obliterans organizing pneumonia

- Obliterative bronchiolitis (obstructive lung disease/bronchiectasis)

- Rheumatoid-associated pulmonary hypertension

- Pulmonary vasculitis/arteritis

- Shrinking lung syndrome

- Miscellaneous: MTX, cricoarytenoid arthritis, infection, cancer

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.

The average age of onset is the early to mid 30s. Exertional dyspnea and spontaneous pneumothorax have been reported as the initial presentation of the disease in 49% and 46% of patients, respectively.

Diagnosis is typically delayed 5 to 6 years. The condition is often misdiagnosed as asthma or chronic obstructive pulmonary disease. The first pneumothorax precedes the diagnosis of LAM in 82% of patients. The consensus clinical definition of LAM includes multiple symptoms:

- Fatigue

- Cough

- Hemoptysis (rarely massive)

- Chest pain

- Chylous complications arising from lymphatic obstruction, including

- Chylothorax

- Chylous ascites

- Chylopericaridium

- Chyloptysis

- Chyluria

- Chyle in vaginal discharge

- Chyle in stool.

- Angiomyolipomas (fatty kidney tumors) are present in about 30% of patients with sporadic LAM and up to 90% of patients with TSC-LAM. Angiomyolipomas can sometimes spontaneously bleed, causing pain or hypotension.

- Cystic lymphangiomas or lymph nodes with hypodense centers, which mimic necrotizing lymphomas, ovarian or renal cancers, or other malignancies can occur in the retroperitoneum, pelvis or mediastinum.

Lung destruction in LAM is a consequence of diffuse infiltration by neoplastic smooth muscle-like cells that invade all lung structures including the lymphatics, airway walls, blood vessels and interstitial spaces. The consequences of vessel and airway obstruction include chylous fluid accumulations, hemoptysis, airflow obstruction and pneumothorax. The typical disease course displays progressive dyspnea on exertion, spaced by recurrent pneumothoraces and in some patients, chylous pleural effusions or ascites.

Most people have dyspnea on exertion with daily activities by 10 years after symptom onset. Many patients require supplemental oxygen over that interval.

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