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FISIOPATOLOGÍA. Diversas enfermedades enfermedad poliquística, uropatía obstructiva o por enferme- .. pdf, acceso el 14 de diciembre Vora JP. Reflujo vesicoureteral intenso. • Uropatía obstructiva. • Infecciones urinarias recidivantes aun- que no tengan ninguna uropatía. • Hasta practicar los estudios de. By submitting your contact information, you consent to receive communication from Prezi containing information on Prezi's products. You can.

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Fisiopatología de la historia natural de la uropatía obstructiva secundaria a obstrucción de salida de la vejiga por hiperplasia Archivo PDF: Kb. Page: PDF: Kb. Full text Flores JC, Sánchez Calderón F. Uropatía obstructiva. Managua: [sn]; Fisiopatología de la Obstrucción Urinaria. En: Wein AJ. Fisiopatología de la obstrucción del tracto urinario. Article · January with 8 Reads Full-text Paper PDF. Citations (1). References (0). Uropatía obstructiva.

Obstructive uropathy. Clin Geriatr Med. Factors determining the amount of residual urine in men with bladder outlet obstruction: Could it be a predictor for bladder contractility? Arab J Urol. The detrusor muscle: an innocent victim of bladder outlet obstruction. Eur Urol. Cell Signal.

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Uropatia obstructiva pdf fisiopatologia

BJU Int. Partial outlet obstruction in rabbits: duration versus severity.

Obstructiva pdf uropatia fisiopatologia

Int J Urol. Cystometric parameters and the activity of signaling proteins in association with the compensation or decompensation of bladder function in an animal experimental model of partial bladder outlet obstruction.

Int J Mol Med. Transurethral prostate resection in patients with hypocontractile detrusor--what is the predictive value of ultrastructural detrusor changes? J Urol. Decrease of ultrasound estimated bladder weight during tamsulosin treatment in patients with benign prostatic enlargement. 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 ectasias1 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 and 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 Lapace , thus the significant difference of pressure between the ureter in a state of contraction and at rest is reduced, resulting in an 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.

In this sense, it should be taken into consideration that the glomerular filtration is the result of 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 capsule minimum , while 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.

Nevertheless, if the obstruction is sustained in time, it leads to intrarenal vasoconstriction with the subsequent reduction in the glomerular blood flow.

This phenomenon could be mediated by the release of angiotensin II and tromboxane by the obstructed nephrons.

The consequence of this last phenomenon is that it avoids the perfusion of the non-functioning nephrones by means of the redistribution of flow towards those who are functioning.

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 stage 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 vasopresin , making 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 insipidus, respectively.

The latter causes polyuria which is characteristic of partial obstructive uropathy. In the case of intratubular obstructions uric acid, pigments, etc. Regarding the urinary obstruction mechanisms, it is possible to divide them into those which are intra-renal intratubular and those which are extra-renal. 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 of 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 tonicity , decrease in the tubular reabsorption capacity of sodium and urea and 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.

Upper obstructive uropathy. Clinical and epidemiological therapeutic aspects

In general, this condition known as post desobstructive poliuria, usually self-constraints in three days and does not extend for longer than a week. Conclusion: 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 nephropathy. The Kidney. Tubulointerstitial diseases.


Renal pathophysiology. The essentials.

Pdf obstructiva fisiopatologia uropatia

Obstructive uropathy and benign prostatic hyperplasia. The aging kidney in health and disease. New York. Obstructive uropathy.