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?
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 1st 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.
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