Obstructive Uropathy and Myocardial Infarction Essay

Obstructive Uropathy and Myocardial Infarction - Essay Example Obstruction to urine flow can result from intrinsic or extrinsic mechanical blockade as well as from functional defects not associated with fixed occlusion of the urinary drainage system. Mechanical obstruction can occur at any level of the urinary tract, from the renal calyces to the external urethral meatus. Normal points of narrowing, such as the ureteropelvic and ureterovesical junctions, bladder neck, and urethral meatus, are common sites of obstruction. When blockage is above the level of the urinary bladder, unilateral dilatation of the ureter or hydroureter and renal pyelocalyceal system or hydronephrosis, occur; whereas, lesions at or below the level of the bladder cause bilateral involvement. While obstructive uropathy can occur in all age groups, in relation to the following case study that is about a 77-year-old patient, not all the causes are relevant. Bladder dysfunction may be secondary to bladder neck obstruction. In adults, urinary tract obstruction is due mainly to acquired defects; pelvic tumors, calculi, and urethral stricture predominate. Schistosoma haematobium and genitourinary tuberculosis are infectious causes of ureteral obstruction. Obstructive uropathy may also result from extrinsic neoplastic or inflmmatory disorder (Goldfarb, S., 2008). Pathophysiology: Myocardial infarction generally occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis. Slowly developing, high-grade coronary artery stenoses do not usually precipitate myocardial infarction (MI) because of the development of a rich collateral network over time. Instead, MI occurs when a coronary artery thrombus develops rapidly at a site of vascular injury. This injury is produced or facilitated by factors such as cigarette smoking, hypertension, and lipid accumulation. In most cases, infarction occurs when an atherosclerotic plaque fissures, ruptures, or ulcerates and when conditions favor thrombogenesis, so that a mural thrombus forms at the site of rupture and leads to coronary artery occlusion. Histologic studies indicate that the coronary plaques prone to rupture are those with a rich lipid core and a thin fibrous cap. Myocardial infarction is defined as the death of heart mu scle resulting from severe, prolonged ischemia. It usually involves the left ventricle. Most MIs are confined to the distribution of a single coronary artery and are designated as anterior, anteroseptal, lateral, and posteroinferior. Multiregional infarcts also occur. Myocardial infarctions are designated as subendocardial or non-Q-wave when the necrosis is limited to the inner half of the ventricular wall or transmural or Q-wave when the necrosis involves not only the inner half but significant amounts of the outer half of the ventricular wall. The electrocardiographic (ECG) correlates are the ST segment elevation with Q-wave pattern for transmural infarcts and the ST segment depression without Q-wave pattern for subendocardial infarcts. If it is a thrombus, the thrombus typically involves the major coronary artery in the distribution of the infarcted myocardium (K/DOQI, 2004). Subendocardial MI without occlusive thrombosis is related to the influence of other factors,