An enthesopathy refers to a disorder involving the attachment of a tendon or ligament to a bone. This site of attachment is known as the enthesis (pl. entheses). If the condition is known to be inflammatory, it can more precisely be called an enthesitis. Forms
Enthesopathy can occur at the shoulder, elbow, wrist, carpus, hip, knee, ankle, tarsus, or heel bone, among other regions. Enthesopathies may take the form of spondyloarthropathies (joint diseases of the spine) such as ankylosing spondylitis, plantar fasciitis, and Achilles tendinitis. Further examples include:
Adhesive capsulitis of shoulder
Rotator cuff syndrome of shoulder and allied disorders
Periarthritis of shoulder
Scapulohumeral fibrositis
Synovitis of hand or wrist
Periarthritis of wrist
Gluteal tendinitis
Iliac crest spur
Psoas tendinitis
Trochanteric tendinitis

Diagnosis
Mainly by clinical examination and provocative tests by counter acting the muscle action. Treatment
The natural history of the two most common enthesopathies (plantar fasciitis and lateral epicondylitis-both mislabeled as inflammatory) is resolution over a period of about 1 year without treatment. There are no known disease-modifying treatments for these enthesopathies. In other words, there is no experimental evidence that any treatment can alter the pathophysiology (mucoid degeneration) or the duration of symptoms. There is no evidence that activity modification alters the natural history of the disease. To date, all treatments are palliative. The evidence suggests that most treatments have non-specific effects (e.g. placebo effect, regression to the mean, self-limiting course of symptoms). Injection of corticosteroid, platelet-rich plasma, or stem cells are examples of treatments that are not supported by experimental evidence and remain open to debate. Extracorporeal shockwave therapy is also in that category.
Lobar pneumonia is a form of pneumonia characterized by inflammatory exudate within the intra-alveolar space resulting in consolidation that affects a large and continuous area of the lobe of a lung.It is one of three anatomic classifications of pneumonia (the other being bronchopneumonia and atypical pneumonia). In children round pneumonia develops instead because the  pores of Kohn which allow the lobar spread of infection are underdeveloped. Mechanism
The invading organism starts multiplying, thereby releasing toxins that cause inflammation and edema of the lung parenchyma. This leads to the accumulation of cellular debris within the lungs. This leads to consolidation or solidification, which is a term that is used for macroscopic or radiologic appearance of the lungs affected by pneumonia. Bacterial pneumonia is mainly classified into lobar and diffuse depending on the degree of lung irritation or damage. Stages
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 blood 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 blood cells disintegrate, with persistence of the neutrophils and fibrin.