Patients typically have no symptoms until the third or fourth decade of life. In most cases, the disease is discovered incidentally on routine chest Xray. The most common symptoms include the following:

- dyspnea

- dry cough

- chest pain

- sporadic hemoptysis

- asthenia

- pneumothoraces

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.

Idiopathic pulmonary haemosiderosis (or idiopathic pulmonary hemosiderosis; IPH) is a lung disease of unknown cause that is characterized by alveolar capillary bleeding and accumulation of haemosiderin in the lungs. It is rare, with an incidence between 0.24 and 1.23 cases per million people.

Signs that consolidation may have occurred include:

- Expansion of the thorax on inspiration is reduced on the affected side

- Vocal fremitus is increased on the side with consolidation

- Percussion is dull in affected area

- Breath sounds are bronchial

- Possible medium, late, or pan-inspiratory crackles

- Vocal resonance is increased. Here, the patient's voice (or whisper, as in whispered pectoriloquy) can be heard more clearly when there is consolidation, as opposed to in the healthy lung where speech sounds muffled.

- A pleural rub may be present.

- A lower expected Pa02 than calculated in the alveolar gas equation

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.

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.

Pulmonary alveolar microlithiasis (PAM) is a rare, inherited disorder of lung phosphate balance that is associated with small stone formation in the airspaces of the lung. Mutations in the gene "SLC34A2" result in loss of a key sodium, phosphate co-transporter (called Npt2b), known to be expressed in distal airway epithelial alveolar type II cells, as well as in the mammary gland, and to a lesser extent in intestine, kidney, skin, prostate and testes. As the disease progresses, the lung fields become progressively more dense (white) on the chest xray, and low oxygen level, lung inflammation and fibrosis, elevated pressures in the lung blood vessels, and respiratory failure ensue, usually in middle age. The clinical course of PAM can be highly variable, with some patients remaining asymptomatic for decades, and others progressing more rapidly. There is no effective treatment, and the mechanisms of stone formation, inflammation and scarring are not known.

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.

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.

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.

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.

Alveolar capillary dysplasia (ACD, sometimes denoted ACDMPV when including misalignment of the pulmonary veins) is a type of diffuse developmental disorder of the lung. The other two diffuse developmental disorders are congenital acinar dysplasia and congenital alveolar dysplasia (CAD).

ACD or ACDMPV is the best studied diffuse developmental disorder. It is a very rare congenital malformation involving abnormal development of the capillary vascular system around the alveoli of the lungs. It is a rare cause of persistent pulmonary hypertension in infants. It also may be a rare cause of pulmonary hypoplasia.

Babies with ACD may appear normal at birth but within minutes or hours they develop respiratory distress with persistent pulmonary hypertension. ACD does not respond to standard therapies that resolve simple pulmonary hypertension. The lack of response is an important diagnostic clue.

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.

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

- Lymphadenopathy

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

Symptoms of subdural hemorrhage have a slower onset than those of epidural hemorrhages because the lower pressure veins bleed more slowly than arteries. Therefore, signs and symptoms may show up in minutes, if not immediately but can be delayed as much as 2 weeks. If the bleeds are large enough to put pressure on the brain, signs of increased ICP (intracranial pressure) or damage to part of the brain will be present.

Other signs and symptoms of subdural hematoma can include any combination of the following:

- A history of recent head injury

- Loss of consciousness or fluctuating levels of consciousness

- Irritability

- Seizures

- Pain

- Numbness

- Headache (either constant or fluctuating)

- Dizziness

- Disorientation

- Amnesia

- Weakness or lethargy

- Nausea or vomiting

- Loss of appetite

- Personality changes

- Inability to speak or slurred speech

- Ataxia, or difficulty walking

- Loss of muscle control

- Altered breathing patterns

- Hearing loss or hearing ringing (tinnitus)

- Blurred Vision

- Deviated gaze, or abnormal movement of the eyes.

Pneumonia alba (white pneumonia) is often seen in neonates with congenital syphilis. The lung may be firm and pale, owing to the presence of inflammatory cells and fibrosis in the alveolar septa. Spirochetes are readily demonstrable in tissue sections.

Lobar pneumonia usually has an acute progression.

Classically, the disease has four stages:

- Congestion in the first 24 hours: This stage is characterized histologically by vascular engorgement, intra-alveolar fluid, small numbers of neutrophils, often numerous bacteria. Grossly, the lung is heavy and hyperemic

- Red hepatization or consolidation: Vascular congestion persists, with extravasation of red cells into alveolar spaces, along with increased numbers of neutrophils and fibrin. The filling of airspaces by the exudate leads to a gross appearance of solidification, or consolidation, of the alveolar parenchyma. This appearance has been likened to that of the liver, hence the term "hepatization".

- Grey hepatization: Red cells disintegrate, with persistence of the neutrophils and fibrin. The alveoli still appear consolidated, but grossly the color is paler and the cut surface is drier.

- Resolution (complete recovery): The exudate is digested by enzymatic activity, and cleared by macrophages or by cough mechanism. Enzymes produced by neutrophils will liquify exudates, and this will either be coughed up in sputum or be drained via lymph.

Lobar pneumonia is a form of pneumonia that affects a large and continuous area of the lobe of a lung.

It is one of the two anatomic classifications of pneumonia (the other being bronchopneumonia).

The newer National Institute of Health (US) criteria for BPD (for neonates treated with more than 21% oxygen for at least 28 days) is as follows:,

- Mild

- Breathing room air at 36 weeks post-menstrual age or discharge (whichever comes first) for babies born before 32 weeks, or

- breathing room air by 56 days postnatal age, or discharge (whichever comes first) for babies born after 32 weeks gestation.

- Moderate

- Need for <30% oxygen at 36 weeks postmenstrual age, or discharge (whichever comes first) for babies born before 32 weeks, or

- need for <30% oxygen to 56 days postnatal age, or discharge (whichever comes first) for babies born after 32 weeks gestation.

- Severe

- Need for >30% oxygen, with or without positive pressure ventilation or continuous positive pressure at 36 weeks postmenstrual age, or discharge (whichever comes first) for babies born before 32 weeks, or

- need for >30% oxygen with or without positive pressure ventilation or continuous positive pressure at 56 days postnatal age, or discharge (whichever comes first) for babies born after 32 weeks' gestation.

The most common symptoms of acute interstitial pneumonitis are highly productive cough with expectoration of thick mucus, fever, and difficulties breathing. These often occur over a period of one to two weeks before medical attention is sought. The presence of fluid means the person experiences a feeling similar to 'drowning'. Difficulties breathing can quickly progress to an inability to breathe without support (respiratory failure).

Acute interstitial pneumonitis typically progresses rapidly, with hospitalization and mechanical ventilation often required only days to weeks after initial symptoms of cough, fever, and difficulties breathing develop.

The classic diagnosis of BPD may be assigned at 28 days of life if the following criteria are met:

1. Positive pressure ventilation during the first 2 weeks of life for a minimum of 3 days.

2. Clinical signs of abnormal respiratory function.

3. Requirements for supplemental oxygen for longer than 28 days of age to maintain PaO2 above 50 mm Hg.

4. Chest radiograph with diffuse abnormal findings characteristic of BPD.

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.

Multifocal micronodular pneumocyte hyperplasia (MMPH) is a subtype of pneumocytic hyperplasia (hyperplasia of pneumocytes lining pulmonary alveoli).

Several synonymous terms have been done for this entity: adenomatoid proliferation of alveolar epithelium, papillary alveolar hamartoma, multifocal alveolar hyperplasia, multinodular pneumocyte hyperplasia.

These multifocal lesions are observed in tuberous sclerosis, and can be associated with lymphangioleiomyomatosis and perivascular epithelioid cell tumour (PEComa or clear cell "sugar tumor")).

It can be diagnosed through lung biopsy using thoracoscopy.

The symptoms of a cerebral contusion (bruising on the brain) depend on the severity of the injury, ranging from minor to severe. Individuals may experience a headache; confusion; sleepiness; dizziness; loss of consciousness; nausea and vomiting; seizures; and difficulty with coordination and movement. They may also have difficulty with memory, vision, speech, hearing, managing emotions, and thinking. Signs depend on the contusion's location in the brain.

Subdural hematomas are divided into acute, subacute, and chronic, depending on the speed of their onset. Acute subdural hematomas that are due to trauma are the most lethal of all head injuries and have a high mortality rate if they are not rapidly treated with surgical decompression.

Acute bleeds often develop after high speed acceleration or deceleration injuries and are increasingly severe with larger hematomas. They are most severe if associated with cerebral contusions. Though much faster than chronic subdural bleeds, acute subdural bleeding is usually venous and therefore slower than the typically arterial bleeding of an epidural hemorrhage. Acute subdural bleeds have a high mortality rate, higher even than epidural hematomas and diffuse brain injuries, because the force (acceleration/deceleration) required to cause them causes other severe injuries as well. The mortality rate associated with acute subdural hematoma is around 60 to 80%.

Chronic subdural bleeds develop over a period of days to weeks, often after minor head trauma, though such a cause is not identifiable in 50% of patients. They may not be discovered until they present clinically months or years after a head injury. The bleeding from a chronic bleed is slow, probably from repeated minor bleeds, and usually stops by itself. Since these bleeds progress slowly, they present the chance of being stopped before they cause significant damage. Small chronic subdural hematomas, those less than a centimeter wide, have much better outcomes than acute subdural bleeds: in one study, only 22% of patients with chronic subdural bleeds had outcomes worse than "good" or "complete recovery". Chronic subdural hematomas are common in the elderly.