Pathophysiological individuals likely

The plasma Hp level rises in disease, like the concentration of fibrinogen and orosomucoid (J8, N5), and this is most likely the result of increased synthesis. The degree of abnormality seems largely to follow the activity of the inflammatory reaction of the disease (infections, tumors, aseptic necrosis). Treatment with cortisol will normalize all three of the above-mentioned plasma proteins. We do not yet know the link between inflammatory reaction and the changed synthesis of Hp and the other plasma proteins. A deeper knowledge of Hp synthesis and the pathophysiology of the inflammatory reaction is necessary for proper utilization in clinical work of the individual Hp values found in diseased subjects. 

Pathophysiology. The etiology of CB is not known. One suspects that there is an individual susceptibility which may predispose to the development of CB which is likely dependent on inherited and acquired host defense capability. A classification of host defense factors would include cellular, immune, non-immune humoral and mucociliary functions (7), Acquired host defense problems may be related to the patient s concomitant disease(s) such as CBA, tuberculosis, sickle cell disease, etc. 

To appreciate the pathophysiology of respiratory failure, and to appropriately tailor therapy to the needs of the individual patient, the different components of the illness must be understood and assessed. The degree to which oxygenation, ventilation, airway protection, and secretion clearance are impaired, and what measures are required to manage each of them, are important determinants of where and by whom a particular patient may be cared for. They determine, for example, whether invasive or noninvasive ventilation will be more appropriate for that patient, how likely it is that the patient can be managed successfully at home, and how much external support in the form of equipment and personnel will be required. 

Animal models have been developed to examine the pathophysiology of auto-immune disease and the putative mechanism of action of new therapies, to assess potential efficacy, and to define an adverse event profile. The particular models utilised in inflammatory/auto-immune diseases mimic only certain aspects of disease. For arthritis, for example, many models are available to help address efficacy and toxicity (Table 1.2), but no model can mimic the anti-inflammatory process in man. However, selected information, based on the accuracy with which individual models mimic the molecular and cellular interactions in man, can be obtained by combining the data obtained from multiple models. Using this composite, it may be possible to predict the likely behaviour of the agent in man. 

---