Pathophysiology for G,L
ESRD: renal failure is progressive, from acute to chronic, then end stage. In ESRD, the kidneys fail to function. Once in chronic renal failure, damage to kidneys is progressive and irreversible. The nephrons are damaged, can't function and don't recover. Surviving nephrons then hypertrophy and increase their rate of filtration, reabsorption, and secretion. Compensatory excretion continues as GFR decreases. This leads to retention of water, waste products, oliguria, and even hypertension because the kidneys cannot excrete. Also due to ESRD, BUN, creatinine, are high, GFR decreases, resulting anemia, metabolic acidosis.
Hypertension: progressive damage to major organs like the kidneys, brain or heart, lead to hypertension. The kidneys, through the renin-angiotensin system help control blood pressure, by releasing angiotensin II a vasoconstrictor, and aldosterone, which leads to sodium and water retention. Impairment in this system affects blood pressure. Also changes in blood vessels cause hypertension, if their force of contractility is increased due to blockage or structural changes.
Diabetes mellitus: it is known as type 2 diabetes mellitus, and is as a result of relative insulin deficiency. The pancreas produces either normal or excessive amounts of insulin but the body s unable to use it effectively, so glucose levels remain elevated, thus know as insulin resistance. Also, failure of the pancreas to produce enough insulin to overcome this insulin resistance precipitates clinical type 2 diabetes in predisposed individuals. One of the complications of diabetes is hypertension, which could eventually lead to CAD, and eventually heart failure.
Chronic obstructive pulmonary disease: COPD is a mixture of separate disease processes that together form the complete clinical and pathophysiological picture. These processes are chronic bronchitis, emphysema. In COPD, there is the destruction of the lung parenchyma, and inflammation of the central airways, resulting in expiratory airflow limitation. Progression of COPD is characterized by the accumulation of inflammatory mucous exudates in the lumens of small airways and the thickening of their walls. These walls become infiltrated by adaptive and innate inflammatory immune cells.