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.

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 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.

The sinuses similar to other air-filled cavities are susceptible to barotrauma if their openings become obstructed. This can result in pain as well as epistaxis (nosebleed).

Barotrauma can affect the external, middle, or inner ear. Middle ear barotrauma (MEBT) is the most common being experienced by between 10% and 30% of divers and is due to insufficient equilibration of the middle ear. External ear barotrauma may occur on ascent if high pressure air is trapped in the external auditory canal either by tight fitting diving equipment or ear wax. Inner ear barotrauma (IEBT), though much less common than MEBT, shares a similar mechanism. Mechanical trauma to the inner ear can lead to varying degrees of conductive and sensorineural hearing loss as well as vertigo. It is also common for conditions affecting the inner ear to result in auditory hypersensitivity.

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.

PPH presents roughly equally in male and female cirrhotics; 71% female in an American series and 57% male in a larger French series. Typically, patients present in their fifth decade, aged 49 +/- 11 years on average.

In general, PPH is diagnosed 4–7 years after the patient is diagnosed with portal hypertension and in roughly 65% of cases, the diagnosis is actually made at the time of invasive hemodynamic monitoring following anesthesia induction prior to liver transplantation.

Once patients are symptomatic, they present with right heart dysfunction secondary to pulmonary hypertension and its consequent dyspnea, fatigue, chest pain and syncope. Patients tend to have a poor cardiac status, with 60% having stage III-IV NYHA heart failure.

PPH is actually independent of the severity of cirrhosis but may be more common in specific types of cirrhosis, in one series more so in Autoimmune Hepatitis and less in Hepatitis C cirrhosis, while in another it was equally distributed throughout the diagnoses.

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)

Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain–Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation.

Usually the atypical causes also involve atypical symptoms:

- No response to common antibiotics such as sulfonamide and beta-lactams like penicillin.

- No signs and symptoms of lobar consolidation, meaning that the infection is restricted to small areas, rather than involving a whole lobe. As the disease progresses, however, the look can tend to lobar pneumonia.

- Absence of leukocytosis.

- Extrapulmonary symptoms, related to the causing organism.

- Moderate amount of sputum, or no sputum at all (i.e. non-productive).

- Lack of alveolar exudate.

- Despite general symptoms and problems with the upper respiratory tract (such as high fever, headache, a dry irritating cough followed later by a productive cough with radiographs showing consolidation), there are in general few physical signs. The patient looks better than the symptoms suggest.

Respiratory acidosis can be acute or chronic.

- In "acute respiratory acidosis", the "Pa"CO is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.36).

- In "chronic respiratory acidosis", the "Pa"CO is elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (HCO >30 mm Hg).

Obesity hypoventilation syndrome is a form of sleep disordered breathing. Two subtypes are recognized, depending on the nature of disordered breathing detected on further investigations. The first is OHS in the context of obstructive sleep apnea; this is confirmed by the occurrence of 5 or more episodes of apnea, hypopnea or respiratory-related arousals per hour (high apnea-hypopnea index) during sleep. The second is OHS primarily due to "sleep hypoventilation syndrome"; this requires a rise of CO levels by 10 mmHg (1.3 kPa) after sleep compared to awake measurements and overnight drops in oxygen levels without simultaneous apnea or hypopnea. Overall, 90% of all people with OHS fall into the first category, and 10% in the second.

Atypical pneumonia, also known as walking pneumonia, is the type of pneumonia not caused by one of the pathogens most commonly associated with the disease. Its clinical presentation contrasts to that of "typical" pneumonia. A variety of microorganisms can cause it. When it develops independently from another disease it is called primary atypical pneumonia (PAP).

The term was introduced in the 1930s and was contrasted with the bacterial pneumonia caused by "Streptococcus pneumoniae", at that time the best known and most commonly occurring form of pneumonia. The distinction was historically considered important, as it differentiated those more likely to present with "typical" respiratory symptoms and lobar pneumonia from those more likely to present with "atypical" generalized symptoms (such as fever, headache, sweating and myalgia) and bronchopneumonia.

Distinction between atypical and typical pneumonia is, however, medically insufficient. For the treatment of pneumonia, it is important to know the exact causal organism.

Obesity hypoventilation syndrome (also known as Pickwickian syndrome) is a condition in which severely overweight people fail to breathe rapidly enough or deeply enough, resulting in low blood oxygen levels and high blood carbon dioxide (CO) levels. Many people with this condition also frequently stop breathing altogether for short periods of time during sleep (obstructive sleep apnea), resulting in many partial awakenings during the night, which leads to continual sleepiness during the day. The disease puts strain on the heart, which eventually may lead to the symptoms such as heart failure, leg swelling and various other related symptoms. The most effective treatment is weight loss, but it is often possible to relieve the symptoms by nocturnal ventilation with positive airway pressure (CPAP) or related methods.

Obesity hypoventilation syndrome is defined as the combination of obesity (body mass index above 30 kg/m), hypoxemia (falling oxygen levels in blood) during sleep, and hypercapnia (increased blood carbon dioxide levels) during the day, resulting from hypoventilation (excessively slow or shallow breathing). The disease has been known since the 1950s, initially as "Pickwickian syndrome" in reference to a Dickensian character but currently under a more descriptive name.

Secondary sclerosing cholangitis (SSC) is a chronic cholestatic liver disease. It is an aggressive and rare disease with complex and multiple causes. It is characterized by inflammation, fibrosis, destruction of the biliary tree and biliary cirrhosis. It can be treated with minor interventions, antibiotics, and monitoring, or with more serious cases, surgery, endoscopic intervention, and liver transplantation.

Women with aerobic vaginitis usually present with a thinned reddish vaginal mucosa, sometimes with extensive erosions or ulcerations and abundant yellowish discharge (without the fishy amine odour, typical of bacterial vaginosis). The pH is usually high. Symptoms can include burning, stinging and dyspareunia. The symptoms can last for long periods of time—sometimes even years. Typically, patients have been treated several times with antimycotic and antibiotic drugs without relief. In asymptomatic cases, there is microscopic evidence but no symptoms. The prevalence of asymptomatic cases is unknown.

Aerobic vaginitis (AV) is a form of vaginitis first described by Donders et al. in 2002. It is characterized by a more or less severe disruption of the lactobacillary flora, along with inflammation, atrophy, and the presence of a predominantly aerobic microflora, composed of enteric commensals or pathogens.

It can be considered the aerobic counterpart of bacterial vaginosis. The lack of acknowledgement of the difference between the two conditions might have led to inaccurate conclusions in several studies in the past. The entity that has been described as "desquamative inflammatory vaginitis" probably corresponds to the more severe forms of aerobic vaginitis.

The diagnosis of SSC requires the exclusion of secondary causes of sclerosing cholangitis and recognition of associated conditions that may potentially imitate its classic cholangiographic features. It is morphologically similar to primary sclerosing cholangitis (PSC) but originates from a known pathological process. Its clinical and cholangiographic features may mimic PSC, yet its natural history may be more favorable if recognition is prompt and appropriate therapy is introduced. Sclerosing cholangitis in critically ill patients, however, is associated with rapid disease progression and poor outcome. Serologic testing, radiological imaging and histological analysis can help diagnose SSC.

Toxic oil syndrome or simply toxic syndrome (Spanish: "síndrome del aceite tóxico" or "síndrome tóxico") is a musculoskeletal disease most famous for a 1981 outbreak in Spain which killed over 600 people and was likely caused by contaminated colza oil. Its first appearance was as a lung disease, with unusual features; though the symptoms initially resembled a lung infection, antibiotics were ineffective. The disease appeared to be restricted to certain geographical localities, and several members of a family could be affected, even while their neighbours had no symptoms. Following the acute phase, a range of other chronic symptoms was apparent.

Ulcerative dermatitis is a skin disorder in rodents associated with bacterial growth often initiated by self-trauma due to a possible allergic response. Although other organisms can be involved, bacteria culture frequently shows Staphylococcus aureus. Primarily found on the rib cage, neck, and shoulder, lesions are often irregular, circumscribed, and moist. Intense itching may lead to scratching which may aggravate and perpetuate the lesion. Destruction of the epidermis along with underlying pustules or abscesses, and granulomatous inflammation, may be present.

In cases where topical treatment alone does not resolve the dermatitis and irritants are not known, a secondary bacterial, fungal or yeast infection might be present and may require an anti-fungal or antibiotics to be prescribed by the veterinarian to affect a cure.

In rats, this skin disorder may be observed on the neck and head, often secondary to skin trauma from scratches or fighting.

The condition can cause pain within the affected extremities, discoloration (paleness), and sensations of cold and/or numbness. This can often be distressing to those who are undiagnosed, and sometimes it can be obstructive. If someone with Raynaud's is placed into a cold climate, it could potentially become dangerous.

1. When exposed to cold temperatures, the blood supply to the fingers or toes, and in some cases the nose or earlobes, is markedly reduced; the skin turns pale or white (called pallor) and becomes cold and numb.

2. When the oxygen supply is depleted, the skin color turns blue (called cyanosis).

3. These events are episodic, and when the episode subsides or the area is warmed, the blood flow returns, and the skin color first turns red (rubor), and then back to normal, often accompanied by swelling, tingling, and a painful "pins and needles" sensation.

All three color changes are observed in classic Raynaud's. However, not all patients see all of the aforementioned color changes in all episodes, especially in milder cases of the condition. Symptoms are thought to be due to reactive hyperemias of the areas deprived of blood flow.

In pregnancy, this sign normally disappears owing to increased surface blood flow. Raynaud's has also occurred in breastfeeding mothers, causing nipples to turn white and become extremely painful. Nifedipine, a calcium channel blocker and vasodilator, was recommended to increase blood flow to the extremities and noticeably relieved pain in the breast in an extremely small study group.

Signs/symptoms of humoral immune deficiency depend on the cause, but generally include signs of infection such as:

- Sinusitis

- Sepsis

- Skin infection

- Pneumonia

Cryofibrinogenmic disease commonly begins in adults aged 40–50 years old with symptoms of the diseases occurring in the almost always affected organ, skin. Cutaneous symptoms include on or more of the following: cold contact-induced urticarial (which may be the first sign of the disease); painful episodes of finger and/or toe arterial spasms termed Ranaud phenomena; cyanosis, s palpable purpura termed Cryofibrinogenemic purpura), and a lace-like purplish discoloration termed livedo reticularis all of which occur primarily in the lower extremities but some of which may occur in the nose, ears, and buttocks; non-healing painful ulcerations and gangrene of the areas impacted by the cited symptoms. Patients also have a history of cold sensitivity (~25% of cases), arthralgia (14-58%), neuritis (7-19%), myalgia (0-14%); and overt thrombosis of arteries and veins (25-40%) which may on rare occasions involve major arteries such of those of the brain and kidney. Signs of renal involvement (proteinuria, hematuria, decreased glomerular filtration rate, and/or, rarely, renal failure) occur in 4-25% of cases. Compared to secondary cryofibrinogemia, primary crygofibrinogenemia has a higher incidence of cutaneous lesions, arthralgia, and cold sensitivity while having a far lower incidence of renal involvement. Patients with secondary cryofibrinogenemia also exhibit signs and symptoms specific to the infectious, malignant, premalignant vasculitis, and autoimmune disorders associated with their disease. While rare, individuals with cryofibrinogemic disease may experience pathological bleeding due to the consumption of blood clotting factors consequential to the formation of cryofibrinogen precipitates.

Livedo reticularis is a common skin finding consisting of a mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin. The discoloration is caused by swelling of the venules owing to obstruction of capillaries by small blood clots. The blood clots in the small blood vessels can be a secondary effect of a condition that increases a person's risk of forming blood clots, including a wide array of pathological and nonpathological conditions . Examples include hyperlipidemia, microvascular hematological or anemia states, nutritional deficiencies, hyper- and autoimmune diseases, and drugs/toxins.

The condition may be normal or related to more severe underlying pathology. Its differential diagnosis is broadly divided into possible blood diseases, autoimmune (rheumatologic) diseases, cardiovascular diseases, cancers, and endocrine disorders. It can usually (in 80% of cases) be diagnosed by biopsy.

It may be aggravated by exposure to cold, and occurs most often in the lower extremities.

The condition's name derives from the Latin "livere" meaning bluish and "reticular" which refers to the net-like appearance.

Raynaud syndrome, also known as Raynaud's phenomenon, is a medical condition in which spasm of arteries cause episodes of reduced blood flow. Typically the fingers, and less commonly the toes, are involved. Rarely, the nose, ears, or lips are affected. The episodes result in the affected part turning white and then blue. Often, there is numbness or pain. As blood flow returns, the area turns red and burns. The episodes typically last minutes, but can last up to several hours.

Episodes are often triggered by cold or emotional stress. There are two main types: primary Raynaud's, when the cause is unknown, and secondary Raynaud's, which occurs as a result of another condition. Secondary Raynaud's can occur due to a connective tissue disorder, such as scleroderma or lupus, injuries to the hands, smoking, thyroid problems, and certain medications, such as birth control pills. Diagnosis is typically based on the symptoms.

The primary treatment is avoiding the cold. Other measures include the discontinuation of nicotine or stimulants use. Medications for treatment of cases that do not improve include calcium channel blockers and iloprost. Little evidence supports alternative medicine. Severe disease may rarely be complicated by skin sores or gangrene.

About 4% of people have the condition. Onset of the primary form is typically between ages 15 and 30 and occurs more frequently in females. The secondary form usually affects older people. Both forms are more common in cold climates. It is named after the French physician Maurice Raynaud, who described the condition in 1862.