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URINARY OBSTRUCTION & STASIS

URINARY OBSTRUCTION & STASIS. 동국대학교 의과대학 비뇨기과학 교실 부교수 하 달 봉. Obstructive Uropathy. 학 습 목 표 I. 1. 방광이하 폐색시 일어나는 방광의 변화를 단계적으로 기술하고 , 이때 나타날 수 있는 증상을 기술한다 . 2. 하부요로 폐색시 일어나는 집뇨계 ( 신배 , 신우 , 요관 ) 의 변화를 설명한다 . 3. 요로폐색으로 인한 신실질의 위축성 변화의 기전을 기술한다.

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URINARY OBSTRUCTION & STASIS

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  1. URINARY OBSTRUCTION & STASIS 동국대학교 의과대학 비뇨기과학 교실 부교수 하 달 봉

  2. Obstructive Uropathy 학 습 목 표 I 1. 방광이하 폐색시 일어나는 방광의 변화를 단계적으로 기술하고, 이때 나타날 수 있는 증상을 기술한다. 2. 하부요로 폐색시 일어나는 집뇨계 (신배, 신우, 요관) 의 변화를 설명한다. 3. 요로폐색으로 인한 신실질의 위축성 변화의 기전을 기술한다.

  3. Obstructive Uropathy 학 습 목 표 II 4. 완전폐색된 신장에서 지속적인 요의 생성 과정이 일어나는 기전을 설명한다. 5. 요로폐색의 치료원칙을 설명한다. 6. 요로폐색 교정 후 나타나는 이뇨현상을 설명한다.

  4. Etiology Obstructive Uropathy

  5. 1. Etiology Functional obstruction 1> loss of ureteral peristalsis 2> vesicoureteral reflux 3> neurogenic bladder with detrusor-sphincter dyssynergia

  6. 1. Etiology Mechanical obstruction 1. Congenital 1> intrinsic: UPJ obstruction, UVJ obstruction, ureterocele, ectopic ureter, phimosis posterior urethral valve, meatal stenosis, 2> extrinsic: UPJ obstruction, retrocaval ureter 2. Acquired 1> intrinsic: stone, bladder tumor, BPH, urethral stricture 2> extrinsic: retroperitoneal fibrosis, pregnancy, metastasis (cervix ca., colon ca.)

  7. Pathogenesis Obstructive Uropathy

  8. 2. Pathogenesis 1. Lower tract - dilatation of the urethra proximal to obstruction 2. Mid tract (bladder) - stage of compensation: detrusor hypertrophy - stage of decompensation: dilatation & atony 3. Upper tract 1> Ureter - compensation : thickening, tortuosity, elongation - decompensation: dilatation 2> Kidney - convex(clubbed) calyx → compression & ischemic - pyelointerstitial reflux - contralateral compensatory hypertrophy

  9. 2. Pathogenesis Renal counterbalance : functional impairment in unilateral hydronephrosis will be greater and will increase faster than that seen in bilateral hydronephrosis.

  10. Pathology Obstructive Uropathy

  11. 3. Pathology 1. kidney weight - increase initially (edema) - after 4 to 8 wks, decrease (atrophy) 2. first few days: flattening of the papilla 1 wk : dilated collecting tubules show some atrophy 2 wk : atrophy of proximal tubules 4 wk : 50 % decrease in medullary thickness pathologic changes in glomerulus 8 wk : 1cm parenchyme 3. Tamm-Horsfall protein casts in Bowman's space : pathognomonic of obstruction or VUR.

  12. Pathophysiology Obstructive Uropathy

  13. 4. Pathophysiology Functional changes 1> concentrating ability : the first parameter of renal function to be impaired and is the last to return 2> GFR ↓, RBF ↓ 3> sodium reabsorption ↓, urine acidification ↓ 4> urea : Cr ratio ↓ (in urine) 5> urine dilution is not affected.

  14. 4. Pathophysiology Turnover of renal pelvis urine in hydronephrosis 1> extravasation into the perirenal space ------ high pr. 2> pyelovenous backflow ------------------------ high pr. 3> pyelolymphatic backflow --------------------- low pr.

  15. 4. Pathophysiology Acute obstruction (Triphasic response) -------------------------------------------------------------- RBF ureteral pr. -------------------------------------------------------------- Phase I (0 - 1.5 hr.) ↑* ↑ Phase II (1.5 - 5 hr.) ↓** ↑ Phase III (5 - 18 hr.) ↓ ↓ -------------------------------------------------------------- * prostaglandins (vasodilatation) ** thromboxane (vasoconstriction)

  16. 4. Pathophysiology Chronic obstruction Ureteral pressure : 15 mmHg (6-8 wk) RBF : 18 % (6 wk) GFR : 0.4 ml/min (5 wk) - 6 weeks of complete obstruction in the dog → no return of function

  17. 4. Pathophysiology Unilateral vs. bilateral obstruction 1. Mechanism of decreased GFR Unilateral Bilateral tubular pressure ↓, N ↑↑ afferent arteriolar pr. ↓↓ ↑ 2. Filtration fraction (GFR/RPF) unilateral ↓ (GFR ↓↓ / RPF ↓) bilateral ↑ (GFR ↓ / RPF ↓↓)

  18. 4. Pathophysiology Postobstructive diuresis in bilateral obstruction - massive diuresis after relief of chronic obstruction - mechanism: 1. impaired sodium reabsorption 2. impaired urine concentrating ability 3. solute diuresis (retained urea) 4. decreased responsiveness to ADH

  19. 4. Pathophysiology Recoverability of renal function (1) Duration of obstruction (acute, chronic) (2) Severity of obstruction (partial, complete) (3) Magnitude of intrapelvic pressure (4) Infection (5) Age (6) Status of contralateral kidney (abnormal, normal) (7) Bilateral or unilateral obstruction

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