Adenitis is a general term for an inflammation of a gland. Often it is used to refer to lymphadenitis which is the inflammation of a lymph node.

"Lymph adenitis" or "lymph node adenitis" is caused by infection in lymph nodes. The infected lymph nodes typically become enlarged, warm and tender. A swelling of lymph nodes due to growth of lymph cells is called lymphadenopathy. Types include:

- Neck

- Cervical adenitis is an inflammation of a lymph node in the neck.

- Tuberculous adenitis (scrofula) is a tuberculous infection of the skin of the neck caused by "Mycobacterium tuberculosis". Non-tuberculous adenitis can also be caused by "Mycobacterium scrofulaceum" or "Mycobacterium avium".

- Abdomen

- Mesenteric adenitis is an inflammation of the mesenteric lymph nodes in the abdomen. It can be caused by the bacterium "Yersinia enterocolitica". If it occurs in the right lower quadrant, it can be mistaken for acute appendicitis, often preceded by a sore throat.

According to present research, PFAPA does not lead to other diseases and spontaneously resolves as the child gets older, with no long term physical effects.

However, PFAPA has been found in adults and may not spontaneously resolve.

Long-term antibiotics, while they decrease rates of infection during treatment, have an unknown effect on long-term outcomes such as hearing loss. This method of prevention has been associated with emergence of antibiotic-resistant otitic bacteria. They are thus not recommended.

Pneumococcal conjugate vaccines (PCV) in early infancy, decreases the risk of acute otitis media in healthy infants. PCV is recommended for all children, and, if implemented broadly, PCV would have a significant public health benefit. Influenza vaccine is recommended annually for all children. PCV does not appear to decrease the risk of otitis media when given to high-risk infants or for older children who have previously experienced otitis media.

Risk factors such as season, allergy predisposition and presence of older siblings are known to be determinants of recurrent otitis media and persistent middle-ear effusions (MEE). History of recurrence, environmental exposure to tobacco smoke, use of daycare, and lack of breastfeeding have all been associated with increased risk of development, recurrence, and persistent MEE. Thus, cessation of smoking in the home should be encouraged, daycare attendance should be avoided or daycare facilities with the fewest attendees should be recommended, and breastfeeding should be promoted.

There is some evidence that breastfeeding for the first year of life is associated with a reduction in the number and duration of OM infections. Pacifier use, on the other hand, has been associated with more frequent episodes of AOM.

Evidence does not support zinc supplementation as an effort to reduce otitis rates except maybe in those with severe malnutrition such as marasmus.

Tuberculous lymphadenitis (or tuberculous adenitis) is a chronic specific granulomatous inflammation of the lymph node with caseation necrosis, caused by infection with "Mycobacterium tuberculosis" or "Mycobacterium bovis".

The characteristic morphological element is the tuberculous granuloma (caseating tubercule). This consists of giant multinucleated cells and (Langhans cells), surrounded by epithelioid cells aggregates, T cell lymphocytes and fibroblasts. Granulomatous tubercules eventually develop central caseous necrosis and tend to become confluent, replacing the lymphoid tissue.

Incision drainage with proper evacuation of the fluid followed by anti-tubercular medication.

Laryngitis that continues for more than three weeks is considered chronic. If laryngeal symptoms last for more than three weeks, a referral should be made for further examination, including direct laryngoscopy. The prognosis for chronic laryngitis varies depending on the cause of the laryngitis.

Adhesive otitis media occurs when a thin retracted ear drum becomes sucked into the middle-ear space and stuck (i.e., adherent) to the ossicles and other bones of the middle ear.

Several aetiologies are suggested, and any combination of these may be present in any given case.

- Vitamin deficiency (A, B or C)

- Viral infection

- Bacterial infection

- "Leptospira

- "Streptococcus

- "Brucella

- Parasitic infection

- Strongyle

- "Onchocerca cervicalis"

- Autoimmune disease

The disease has been suggested to be primarily autoimmune in nature, being a delayed hypersensitivity reaction to any of the above agents.

Acute prostatitis is a serious bacterial infection of the prostate gland. This infection is a medical emergency. It should be distinguished from other forms of prostatitis such as chronic bacterial prostatitis and chronic pelvic pain syndrome (CPPS).

The Appaloosa has a higher risk of developing ERU than other breeds; this predisposition has a genetic basis. Appaloosas which develop ERU are more likely than other breeds to have ERU in both eyes, and more likely to become blind in one or both eyes.

Acute laryngitis may persist, but will typically resolve on its own within two weeks. Recovery is likely to be quick if the patient follows the treatment plan. In viral laryngitis, symptoms can persist for an extended amount of time, even when upper respiratory tract inflammation has been resolved.

The cause of PFAPA is unknown. It is frequently discussed together with other periodic fever syndromes.

Possible causes include primarily genetic or due to an initial infection.

The condition appears to be the result of a disturbance of innate immunity. The changes in the immune system are complex and include increased expression of complement related genes (C1QB, C2, SERPING1), interleulkin-1-related genes (interleukin-1B, interleukin 1 RN, CASP1, interleukin 18 RAP) and interferon induced (AIM2, IP-10/CXCL10) genes. T cell associated genes (CD3, CD8B) are down regulated. Flares are accompanied by increased serum levels of activated T lymphocyte chemokines (IP-10/CXCL10, MIG/CXCL9), G-CSF and proinflammatory cytokines (interleukin 6, interleukin 18). Flares also manifest with a relative lymphopenia. Activated CD4(+)/CD25(+) T-lymphocyte counts correlated negatively with serum concentrations of IP-10/CXCL10, whereas CD4(+)/HLA-DR(+) T lymphocyte counts correlated positively with serum concentrations of the counterregulatory IL-1 receptor antagonist.

The etiology of the condition is unknown. Possible but unproven infectious causes are "Klebsiella", polyomaviridae, Epstein–Barr virus, parvovirus B19, and human herpesvirus 6. Jilin University researchers suggested in 2017 that monocytes recruited to inflammatory lesions could produce macrophage colony-stimulating factor, which leads to a complex signal transduction, which leads to the histiocytosis characteristic of Rosai–Dorfman disease.

In 2016 the Histiocyte Society proposed a classification of histiocytoses into five groups designated by letters: "C," "H," "L," "M," and "R." Group "R" included Rosai–Dorfman disease and "miscellaneous noncutaneous, non-Langerhans cell histiocytoses." Rosai–Dorfman disease itself was classified into "Familial," "Classical (nodal)," "Extranodal," "Neoplasia-associated," and "Immune disease-associated" subtypes.

Men with acute prostatitis often have chills, fever, pain in the lower back, perineum, or genital area, urinary frequency and urgency often at night, burning or painful urination, body aches, and a demonstrable infection of the urinary tract, as evidenced by white blood cells and bacteria in the urine. Acute prostatitis may be a complication of prostate biopsy. Often, the prostate gland is very tender to palpation through the rectum.

There are several causes of acute pericarditis. In developed nations, the cause of most (80–90%) cases of acute pericarditis is unknown but a viral cause is suspected in the majority of such cases. The other 10–20% of acute pericarditis cases have various causes including connective tissue diseases (e.g., systemic lupus erythematosus), cancer, or involve an inflammatory reaction of the pericardium following trauma to the heart such as after a heart attack such as Dressler's syndrome. Familial mediterranean fever and TNF receptor associated periodic syndrome are rare inherited autoimmune diseases capable of causing recurring episodes of acute pericarditis.

Before the development of modern cardiovascular surgery, cases of acute mediastinitis usually arose from either perforation of the esophagus or from contiguous spread of odontogenic or retropharyngeal infections. However, in modern practice, most cases of acute mediastinitis result from complications of cardiovascular or endoscopic surgical procedures.

Treatment usually involves aggressive intravenous antibiotic therapy and hydration. If discrete fluid collections or grossly infected tissue have formed (such as abscesses), they may have to be surgically drained or debrided.

Chronic mediastinitis is usually a radiologic diagnosis manifested by diffuse fibrosis of the soft tissues of the mediastinum. This is sometimes the consequence of prior granulomatous disease, most commonly histoplasmosis. Other identifiable causes include tuberculosis, IgG4-related disease and radiation therapy. Fibrosing mediastinitis most frequently causes problems by constricting blood vessels or airways in the mediastinum. This may result in such complications as superior vena cava syndrome or pulmonary edema from compression of pulmonary veins.

Treatment for chronic fibrosing mediastinitis is somewhat controversial, and may include steroids or surgical decompression of affected vessels.

In the United States, the annual incidence is 18 cases of acute pancreatitis per 100,000 population, and it accounts for 220,000 hospitalizations in the US. In a European cross-sectional study, incidence of acute pancreatitis increased from 12.4 to 15.9 per 100,000 annually from 1985 to 1995; however, mortality remained stable as a result of better outcomes. Another study showed a lower incidence of 9.8 per 100,000 but a similar worsening trend (increasing from 4.9 in 1963-74) over time.

In Western countries, the most common cause is alcohol, accounting for 65 percent of acute pancreatitis cases in the US, 20 percent of cases in Sweden, and 5 percent of those in the United Kingdom. In Eastern countries, gallstones are the most common cause of acute pancreatitis. The causes of acute pancreatitis also varies across age groups, with trauma and systemic disease (such as infection) being more common in children. Mumps is a more common cause in adolescents and young adults than in other age groups.

Clinical presentation of diseases of pericardium may vary between:

- Acute and recurrent pericarditis

- Pericardial effusion without major hemodynamic compromise

- Cardiac tamponade

- Constrictive pericarditis

- Effusive-constrictive pericarditis

The reason for its occurrence is unknown. Investigations have suspected that obesity and preceding psoriatic lesions cause local lymphatic disturbances, followed by the development of stasis papillomatosis. On the other hand, genetic or environmental factors may play a role. Some investigators have speculated that it represents an allergic response to an epidermal protein antigen created through increased hydrostatic pressure, whereas others believe that the skin has been compromised and is more susceptible to irritation and trauma.

The age is an important factor, because as some people get older the veins which carry blood from the legs back to the heart do not work as well as they use to. This causes fluid to settle in the lower legs.

The most important cause of this condition is insufficient lymphatic drainage, causing soft tissue swelling due to fluid accumulation. Obstruction of lymphatic tissue causes increased intravascular tissue protein; this will increase the production of fibroblasts and mast cells. Lymphatic obstruction due to any cause can increase the amount of proteins in the intravascular tissue, either by root osmotic pressure, or because it absorbs a little liquid. The further roteins increase the vascular fluid, fibroblasts and promote the ploriferation of mast cells which produce the clinical symptoms of nonpitting edema. The epidermis may be hyperkeratotic and warty and this predisposes to tissue cracks and allows secondary infection.

A number of infectious agents have been recognized as causes of pancreatitis including:

- Viruses

- Coxsackie virus

- Cytomegalovirus

- Hepatitis B

- Herpes simplex virus

- Mumps

- Varicella-zoster virus

- Bacteria

- Legionella

- Leptospira

- Mycoplasma

- Salmonella

- Fungi

- Aspergillus

- Parasites

- Ascaris

- Cryptosporidium

- Toxoplasma

The signs of sebaceous adenitis are caused by an inflammatory disease process which affects the sebaceous glands of the skin. The cause of the inflammatory disease is unknown. Different breeds of dogs may have different underlying causes of the disease.

Research is currently underway to find if there is a genetic predisposition for sebaceous adenitis; the exact mode of inheritance remains unknown.

In Standard Poodles, sebaceous adenitis is most likely an autosomal recessive inherited disease, with variable expression.

There are seven classes of medications associated with acute pancreatitis: statins, ACE inhibitors, oral contraceptives/hormone replacement therapy (HRT), diuretics, antiretroviral therapy, valproic acid, and oral hypoglycemic agents. Mechanisms of these drugs causing panreatitis are not known exactly; but it is possible that statins has direct toxic effect on the pancreas or through the long term accumulation of toxic metabolites. Meanwhile, ACE inhibitors causes angioedema of the pancreas through the accumulation of bradykinin. Oral contraceptives/HRT causes arterial thrombosis of the pancreas through the accumulation of fat (hypertriglyceridemia). Diuretics such as furosemide has direct toxic effect on the pancreas. Meanwhile, thiazide diuretics causes hypertriglyceridemia and hypercalcemia, where the latter is the risk factor for pancreatic stones. HIV infection itself can cause a person to more likely to get pancreatitis. Meanwhile, antiretroviral drugs may cause metabolic disturbances such as hyperglycemia and hypercholesterolemia, which predisposes to pancreatitis. Valproic acid may have direct toxic effect on the pancreas. There are various oral hypoglycemic agents that contributes to pancreatitis including metformin. But, glucagon-like peptide-1 (GLP-1) is more strongly associated with pancreatits by promoting inflammation.

Atypical antipsychotics such as clozapine, risperidone, and olanzapine can also cause pancreatitis.