Pulmonary pathophysiology

West, J. B. (1982). Pulmonary Pathophysiology—The Essentials. Williams and Wilkins, Baltimore, Maryland. 

Welsh DA, Thomas DA. Obstruotive lung disease. In AM J, Summer WR, Levitzky MG, eds. Pulmonary Pathophysiology. 2nd Ed. New York Lange Medical Books/McGraw-Hill,... 

West JB. Pulmonary pathophysiology the essentials. Baltimore, Maryland William Wilkins, 1982. 

Due to the current limitations in nosology and the paucity of research in the field, 1 will discuss potential mechanisms associated with LTMV based on principles of pulmonary pathophysiology recorded in patients requiring mechanical ventilation for variable periods of time, including those in the acute care setting. Whether it is valid to extrapolate pathophysiological data recorded in the acute care setting to the chronic one is, however, unknown. 

West JB. Pulmonary Pathophysiology The Essentials. 6th ed. Philadelphia Lippincott Williams Wilkins, 2003 68 ... 

FIGURE 7-11. Treatment of venous thromboembolism. LMWH, low-molecular-weight heparin PE, pulmonary embolism SBP, systolic blood pressure UFH, unfractionated heparin VTE, venous thromboembolism. (Reproduced from Haines ST, Zeolla M, Witt DM. Venous thromboembolism. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 398, with permission.)... 

Describe the pathophysiology of chronic obstructive pulmonary disease (COPD). 

Gibson RL, Burns JL, Ramsey BW. State of the art pathophysiology and management of pulmonary infections in cystic fibrosis. Am J Respir Crit Care Med 2003 168 918-951. 

The pathophysiologic mechanisms of portal hypertension and of cirrhosis itself are entwined with the mechanisms of ascites (Fig. 19-3). Cirrhotic changes and the subsequent decrease in synthetic function lead to a decrease in production of albumin (hypoalbuminemia). Albumin is the major intravascular protein involved in maintaining oncotic pressure in the vascular system low serum albumin levels and increased capillary permeability allow fluid to leak from the vascular space into body tissues. This can result in peripheral edema, ascites, and fluid in the pulmonary system. The obstruction of hepatic sinusoids and... 

West, J.B., Pulmonary Physiology and Pathophysiology, an Integrated, Case-Based Approach, Lippincott/Williams Wilkins, Philadelphia, 2001. 

Until now we have been discussing natural product HDAC inhibitors and their benefits for pathophysiological conditions. However, recent research shows that for treatment of a few diseased conditions, it is beneficial to increase HDAC activity. One such example is chronic obstructive pulmonary disease (COPD). 

A common reason for diuretic use is for reduction of peripheral or pulmonary edema that has accumulated as a result of cardiac, renal, or vascular diseases that reduce blood delivery to the kidney. This reduction is sensed as insufficient effective arterial blood volume and leads to salt and water retention and edema formation. Judicious use of diuretics can mobilize this interstitial edema without significant reductions in plasma volume. However, excessive diuretic therapy may lead to further compromise of the effective arterial blood volume with reduction in perfusion of vital organs. Therefore, the use of diuretics to mobilize edema requires careful monitoring of the patient s hemodynamic status and an understanding of the pathophysiology of the underlying illness. 

The pathophysiology of IR injury in the lung involves increased leakage from the pulmonary microvasculature leading to interstitial and alveolar edema, excessive infiltration of polymorphonuclear cells into the lung, tissue inflammation, and apoptosis (de Perrot et al. 2003). 

Cassady SL. Cardiovascular pathophysiology. In DeTurk WE, Cahalin LP, eds. Cardiovascular and Pulmonary Physical Therapy. New York McGraw-Hill 2004. 

Pulmonary Vascular Physiology and Pathophysiology, edited by E. K. Weir and J. T. Reeves... 

Exercise Pulmonary Physiology and Pathophysiology, edited by B. J. Whipp and K. Wasserman... 

Pulmonary hypertension is a devastating, potentially fatal disorder. Recent years have witnessed a great expansion in our understanding of the molecular pathophysiology of this condition. Options for therapy have just become available in recent years, focused either on the prostacyclin pathway or the nitric oxide pathway for pulmonary arteriolar relaxation. Continuous infusion of prostacyclin has been successful, demonstrating the relevance of the former pathway. The efficacy of both inhaled nitric oxide and systemic sildenafil support the latter. In the future, gene transfer could be used for sustained delivery of either of these agents, by means of... 

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