Q. 404. What is normal urine flow?

 

Urinary Tract Obstruction

Q. 404. What is normal urine flow?

A. N. urine flow = 1.5-2  L/d.                         

Q.405. Define hydronephrosis?   

         

A. = Renal pelvic (collecting system) dilatation proximal to a point of obstruction.

Q.406.What is obstructive uropathy?

A. Ob. uropathy = Block of urine flow due to functional & structural derangement anywhere from (tip of urethra) back to (R. pelvis) 🠞🠝pressure proximal to the site of obstruction.

Q.407 What is the congenital causes of obstructive uropathy?

A. Three groups:  👌

1)   Ureteropelvic junction: the most common cause of hydronephrosis é fetus & young children us. é Lt. side. The presenting C/O: flank pain & abdominal mass.

2)   Ureterovesical junction: Second most common site of congenital ureteric obstruction.

3)   Abn. development of the venous system: Rt. ureter located behind I.V.C. a ureteric ob. a Fish hook or Reversed “j” Sn deformity in I.V.P.

Q.408 Can drugs induce obstructive uropathy?

A. Yes, drug-induced crystaluria & ob. uropathy include the foll. :

1)   Sulphonamide, esp. s. diazine (ttt. of toxoplasmosis in AIDS.)⮞Crystaluria.

2)   Acyclovir⮞Crystalluria.

3)   Indinavir⮞ Crystalluria.

4)   Ciprofluxacin⮞ Crystalluria + Stone formation ⮞Ob. uropathy.

5)    Anticholinergic ⮞ intraluminal obstruction by s. m. disruption ⮞🠝intraluminal pressure.

6)    Levodopa ⮞ a-adrenergic a urethral sphincter tone⮞🠝U.B. outlet resistance.

7)   Tiaprofenic ⮞ (surgam)a severe cystitis é subsequent ureteric ob. & R. dge.

Q.409 What is “medical hydronephrosis”?

A. It includes {the aforementioned drug list + Multiple myeloma}. M.M. a Hypercalcemia a Crystalluria + stone formationa hydronephrosis.

Q.410. Enumerate the possible causes of “papillary necrosis”?   

A. Causes of “papillary necrosis”:    

1)   D.M.

2)   Amyloidosis.

3)   Analgesic abuse.

4)   Allograft Rj.: surgical interference.

5)   Ac. Pyelonephritis.

6)   Sickle cell disease or trait.

Q.411. What is the most common site of obstruction in males?

A. B.P.H. 8 is the most common site of U.T. Ob. in ♂.

Q.412. When does U/S fail to diagnose obstruction?   

      

A. U/S may fail to diagnose obstruction in two ✌ situations: 

      Early é 1^st 48 h.

      When hydronephrosis is absent despite obstruction (false –ve).

Q.413. What is false –ve hydronephrosis?

A. False –ve hydronephrosis:

1)   Dehydration.

2)   Staghorn stone.

3)   Nephrocalcinosis.

4)   Retroperitoneal fibrosis.

5)   Cortical cysts.

Every experienced nephrologist hs sn a case of ob. uropathy é negative U/S results, therefore diagnosis of obstruction , must still be considered é any patient é worsening renal function, chronic azotemia, acute changes in renogram or urine output even é absence of hydronephrosis in U/S. 💢

Q.414. Then, what is the false +ve hydronephrosis?

A.  False +ve hydronephrosis:

1)   Large extrarenal pelvis.

2)   Parapelvic cyst.

3)   Vesicoureteric reflux.

4)   High urinary flow rate.

Q.415 How can u differentiate (dilatation + obstruction) fr. dilatation alone?

A. Color dopler study:

      Resistance Index (R.I.) 🠞🠝0.7 = Obstruction & intrarenal V.C.

      Resistance Index (R.I.) 🠊🠟0.7 = Dilatation only, No Ob. No V.C.

Q.416 What is the role of MRI in diagnosis of obstructive nephropathy? What are its main drawbacks?

A. MRI is a useful tool for children, women é child-bearing period, R.I. ptn. & allograft evaluation, as no ionizing radiation & because “Gadolinium” is non-nephrotoxic”. However, certain gadolinium namely🠊”Gadodiamide”, in R.I. ptn. can induce a serious dis., Nephrogenic systemic fibrosis, a non-treatable , fatal condition 🠊 fibrosis of the skin, lung, etc..  💀💀

** Recently, BOLD (blood oxygenation level dependent) imaging has been introduced for safe evaluation of renal function.   

Q.417. How can obstruction affect the GFR?

A. Obstruction & inflammatory cells 🠞🠝Angio.II. & T.X.A2 a sharp reduction of the perfused glomeruli &🠟 SNGFR 🠊🠟 total GFR profoundly dur. & immed-iately after release of obstruction.

Q.418 So, when this obstructed kidney expected to be completely recovered?

A. Recovery of complete ureteric obstruction needs: 14- 60 d. من أسبوعين لشهرين

 - Two important factors affecting complete recovery: 

1.    Duration.      &

2.    Severity of obstruction, e.g. complete obstruction for 🠝 4 w. ⮞No recovery at all.  ⚫

Q.419 How can obstruction affect Na+ homeostasis?

A. Obstruction c Reduces the net reabsorption of Salt by incr. level of Nat-ruretic substances e.g. PGE2 & by infiltration of the kidney by mononuclear cells. 🠝 ANP & 🠟aldosterone c Salt wasting.  

      After release of bilateral obstruction c Salt & water excretion jumps 💣5-9 times normal, so, fluid compensation is mandatory to guard against dehydration-induced deterioration of renal function.

      The inability to concentrate urine results fr. failure of TALLH to generate concentrated interstitium as well as inability of collecting ducts to synthetize & traffic [aquaporin-2] in response to ADH.

Q.420 What about other electrolytes?

A. Obstruction 🠞🠝 ANP.🠞Kaliuresis  fr. “distal” tubules.

    Obstruction  🠞🠝 Po4 & Mg. wasting.

  *** Summery: Post Ob. wasting of 🠞{Na, K, Mg & Po4 }🠞 Multi-hypo.s.

Q.421 How can the fibrosis cascade (due to odstruction) proceed?

A. Ob. 🠞🠝 Hydrostatic pressure 🠞 V.C. 🠞K tub. Epithelial cell perfusion🠞Release of cytokines [Angio.II.-TGFB -TNF] + Adhesive f. 🠞 inflmmation cell infilt-ration (including macrophage) 🠞 more Cytokine release.

** Combination of R. & inflmmation cell cytokines 🠞 accelerates Apoptosis of tubuler cells & interstitial fibrosis.

Q.422 How can this cascade affect renal function?

A. ** 

 I. N.F.k.B.: &

1)   Tub. cell 🠞Chemoattract inflmm., apoptosis & fibrosis.

2)   Fibroblasts 🠞Proliferation & differentiation 🠞fibrosis.

II. Pro-fibrotic cytokines 🠞Cytokine release 🠞 Fibrosis.

*** So, fibrosis is a summation of:  👌

(1)    Pro-fibrotic cytokines.

(2)   Tub. cell inflmm. & Apoptosis. (N.F. k.B.)

(3)   Fibroblast proliferation & differentiation. (N.F. k.B.)

Q.423. What are the proinflammatory cytokines?    

A. The proinflammatory cytokines 🠞👌

 

1)   TGF.B.

2)   Osteopontin.

3)   V.A.M. (Vascular cell adhesion molecule).

Q.424 Is there any role for ACEI in this surgical (urological) problem?

A. Fortunately, Yes, see next question. 👉

Q.425. What are the possible tools to prevent & stop this cascade?

A. Medical ttt. of “Obstructive uropathy” (O.U.):         

1)   ACEI 🠞🠝Kinin🠞🠝L-arginine🠞NOS 

🠞N.O. (ACEI is a vital N.O.👆generator).

2)   Dietary L-arginine🠞Attenuate renal damage.

3)   a -MSH. (a-melanocyte-stimulating hormone)= a potent anti-inflammatory.

Q.426. Mention some “surgical” ttt. options for O.U. ?

A. Surgical” options for O.U.:

1)   Ob. below U.B.🠞Catheter or “suprabubic cystostomy”.

2)   Ob. above U.B. 🠞“Ureteral stent” or “Nephrostomy tube”.

3)   Stone 🠟½ cm.🠞Passes spontaneously.  😊

4)   If 🠝½ cm.🠞EXSWEL (Extracorporeal short wave Lithotripsy) + Stent placement.

5)   Recently, Laser EXSWEL is available.       

Q.427. How to monitor recovery of obstructive uropathy?

A. Recovery is a matter of severity, dose & duration dependent. A period of 69 d., hs bn recorded. So,     

🠞Isotopic Renography, shd be performed repeatedly.   Even;

🠞R. biopsy, can be performed to ensure complete recovery.

- Many factors affect the process: 

1)   R.V.C.🠞e.g. {Renin, Angio.II. & T.X.A2 }.

2)   Growth f.🠞Enhance fibrosis.

3)   Ammonia genesis 🠞🠟 Cell growth.

   …. So, ACEI/ARBs 🠞Ameliorate this greatly (e.g. captopril).

Q.428. How to monitor post-obstruction diuresis?

A. Release of obstruction 🠞Natriuresis & diuresis é wasting of K+, Po4 & divalent cation.                 *** Mechanism: 🠞Intrinsic dge of tub. cells 🠞Salt & solvent & ureteric reabsorption + vol. expansion 🠞🠝 ANP 🠞Natriuresis🠞Multi-hypo.s (Na+, K+, Mg+, Cl -, Hco3-).

v It is a self-limited condition, but may persist for months.  So,

v Start é ½ N.S. (0.45%) saline, at a rate slightly slower than “urine output”.

v A 4 time/24 h. monitoring of electrolytes, may be warranted.