FISIOPATOLOGIA DE LA UROPATIA OBSTRUCTIVA PDF

Seifter J.L. Seifter, Julian cción de vías urinarias. INTRODUCCIÓN; ETIOLOGÍA; MANIFESTACIONES CLÍNICAS Y FISIOPATOLOGÍA; DIAGNÓSTICO Asimismo, la uropatía obstructiva quizá sea resultado de una neoplasia. Existen pocos datos o signos clinicos que puedan orientar al diagnostico de RVU. Este se basa en la frecuencia de los hallazgos de este. Pérdida del funcionamiento normal de la vejiga provocada por alteración de la inervación vesical que origina un trastorno en el fenómeno de.

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Hospital Italiano de Buenos Aires. Universidad Peruana Cayetano Heredia. There are many renal dysfunction inducing mechanisms involved in this entity: Obstructive nephropathy can also lead to hypertension vasoconstriction-hypervolemiahyperkalemia, metabolic acidosis aldosterone resistancediabetes insipidus vasopressine resistance. In conclusion, since obstructive nephropathy is a potentially reversible cause of renal dysfunction, it should always be taken into account among the differential diagnosis of renal failure inducing mechanisms.

In the same way, when such obstruction is located in any point between the renal pelvis and the distal end of the urethra, it receives the more specific name of obstructive uropathy. It is worth mentioning that hydronephrosis is the expansion of the pelvis and renal calyces proximal to the obstruction point; and that expansion is not always synonym of obstruction, since there are non-obstructive types of expansion known as ectasias 1 Tabla 1.

It is worth mentioning that hydronephrosis is the expansion of the pelvis and renal calyces proximal to the obstruction point; and that expansion is not always synonym of obstruction, since there are non-obstructive types of expansion known as ectasias 1 Tabla 1 Physiopatology The obstruction of the urinary flow can take place inside the renal tubules as well as in any other segment of the urinary tract renal pelvis, ureter, bladder and urethra.

Independently of the place where the urinary obstruction happens, and from this moment, a series of events start to happen, which if they are not corrected can lead, in time, to irreversible renal damage obstructiv tubular atrophy. After an obstruction has settled, there is an increase in the pressure corresponding to its proximal section, due to the effect of the net glomerular filtration pressure, which leads to an increase in intraluminal pressure, that carries a progressive expansion of the ureter as a compensating mechanism ley de la Lapacethus the fisiopatokogia difference of pressure between the ureter in a state of contraction and at rest is reduced, resulting in fisippatologia ineffective ureteral peristalsis.

Sometimes there is a rapture of the renal calices with the subsequent formation of urinomas. On the other hand, such pressure is transmitted to the tubular sectors proximal to the obstruction causing a reduction of the glomerular filtration since it counteracts to the glomerular filtration net pressure.

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In this sense, it should be taken into consideration that the glomerular filtration is the result obstructuva a game of pressures which are established in the glomerular capillaries and the Bowman capsule, where in favor of the filtration we find the hydrostatic pressure of the capillary very important and the oncotic pressure of the Bowman ee minimumwhile against it we find the oncotic pressure of the capillary considerable and the hydrostatic pressure of the Bowman capsule minimum.

Usually glomerular hydrostatic pressure is largely predominant, on whom the net ultrafiltration pressure depends almost completely. What happens during a complete and bilateral uro-obstruction is that the hydrostatic pressure of the Bowman capsule increases greatly, and it can even override the net ultrafiltration pressure and lead to obstructive renal failure.

Nevertheless, if the obstruction is sustained in time, it leads to intrarenal vasoconstriction with the subsequent reduction in the glomerular blood flow. This uroopatia could be mediated by the release of angiotensin II and tromboxane by the obstructed nephrons. The consequence of this obsructiva phenomenon is that it avoids the perfusion of the non-functioning nephrones by fisiopatologiw of the redistribution of flow towards those who are functioning.

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In the case of severe and prolonged urinary obstructions, the renal parenchyma is reduced to a thin ring of atrophic tissue mainly as a consequence of the ischemia suffered by its continuous hyperfusion. It is also stated that the damaged tubules release a chemotactic substance which would attract monocytes and macrophagues, which would infiltrate the renal parenchyma, damaging it by means of the local release of proteases and free radicals. An uro-obstruction can also cause hypertension which at its first fisiopatllogia in general is mediated by the activation of the renine-angiotensin-aldosterone system vasoconstriction and later, if a total obstruction occurs it is mainly due to water and salt retention hypervolemia.

Likewise, the urinary obstruction can lead to a dysfunction of the distal nephron sectors resistance to aldosterone and vasopresinmaking it difficult for the local secretion of potassium and protons, as well as reducing the water reabsorption, thus facilitating the development of hyperkalemia, hyperchloremic metabolic acidosis and nephrogenic diabetes utopatia, respectively.

The latter causes polyuria which is characteristic of partial obstructive uropathy. In the case of intratubular fiskopatologia uric acid, pigments, etc. Regarding the urinary obstruction mechanisms, it is possible to divide them laa those which are intra-renal intratubular and those which are extra-renal.

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The latter can be subdivided obstructivx those which have intrinsic and extrinsic causes to the urinary tract Data obtained from tests performed in animal models and information obtained from obstructivs evolution of clinical cases, suggest that the resolution of a complete obstruction before 8 weeks after it has settled can achieve a total recovery of the glomerular filtration. A later resolution can mean partial or nule recovery, depending on the evolution time of the obstruction, the age of the patient and the degree of damage to the renal function previous to the obstruction.

After the resolution uropatai a bilateral obstruction or a unilateral one in a patient with only one kidney, it is normal to find elevated serum levels of atrial factors, tubular resistance to vasopressin reduction of the expression of aquaporin 2 channels in the collecting tubules and compromise of the medullar tonicitydecrease in the tubular reabsorption capacity of sodium and urea uroatia presence of a free urinary tract, so the osmotic diuretic effect of the not reabsorbed urea and sodium starts to act, which increment diuresis finally leading to potassium, calcium, magnesium and phosphorus expoliation, which puts the patient at risk of having severe hydroelectrolytic depletion if these losses are not adequately monitored and treated.

Uropatia obstructiva by Paula Tamara Mohamad on Prezi

In general, this condition known as post desobstructive poliuria, usually self-constraints in three days and does not extend for longer than a week. Obstructive uropathy is a mechanism of renal insufficiency, which since it is relatively simple to solve, should always be taken into consideration as one of the differential diagnosis of renal failure.

Obstructive uropathy and benign prostatic hyperplasia. The aging kidney in health and disease. In Schrier R Ed.

Chevalier RL and Cachat F. Role of angiotensin II in chronic ureteral obstruction. Klahr S, Morrissey J.: Obstructive nephropathy and renal fibrosis: The role of bone morphogenic protein-7 and hepatocyte growth factor. J Clin Invest ; Nephron Exp Nephrol ; Am J Physiol Renal Physiol ; Rohatgi R, Flores D: Intratubular hydrodynamic forces influence tubulointerstitial fibrosis in the kidney.

Curr Opin Nephrol Hypertens ; Comment of the reviewer Jesus Garrido MD. Received, October 3, Published, October 8,

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