Urinary tract obstruction

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Urinary tract obstruction Stones
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Loin pain hematuria
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Principal sites of pathology leading to loin pain

• Spinal nerve roots
• Vertebral column
• Paraspinal lumbar muscles
• Kidneys
• Renal pelvis / ureters
• Abdominal aorta
• Pancreas

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• Renal pain arises because of rapid stretching or
  inflammation of renal capsule
• Pain from the renal pelvis / ureter is caused by
  distention excessive peristaltic contractions
• Any back / retroperitoneal structure may give
  rise to back pain

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Macroscopic hematuria

• May arise from lesions anywhere within the
  urinary system, kidney, renal pelvis, ureter,
  bladder, urethra
• As few as 5 x 10 RBC/ml 1ul blood/ml urine can
  be detected visually as red-coloured urine
• Macroscopic hematuria needs to be distinguished
  from
• Red discolouration of urine caused by certain
  dyes some drugs
• Presence of Haem pigment intravascular
  hemolysis (Hb), rhabdomyolysis (myoglobin)
• Bleeding from outside the urinary tract
  perineum, vagina

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• Bleeding from the bladder or above cause uniform
  discoloration of urine
• Bleeding from the urethra may cause bleeding
  separate from the urine or mixed with urine
• Hematuria from the renal parenchyma glomeruli
  or interstitium tends to be accompanied by
  proteinuria, casts, dismorphic RBC (abnormal
  morphology)
• Bleeding from renal tumors or from lesions in the
  renal pelvis or below may be isolated or
  associated with pyuria particularly with
  infections.
• Macroscopic hematuria from tumors are usually
  painless, whereas that from calculi / infection
  is usually associated with pain

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Pyelonephritis/infections
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• The formation of stone is usually the result of
  many metabolic and physiologic disorders
  contributing to stone formation
• Stones in the urinary tract are composed of
  crystals and matrix skeleton.
• Physical factors of stone formation
• Supersaturation of the urine with respect to a
  particular solute, e.g. uric acid, due to
  increase in excretion or decrease in urine
  volume. At some point spontaneous nucleation and
  crystal growth occur homogenous nucleation.
• Urine pH, determines the solubility of ccompounds
  in the urine. Uric acid cystine are poorly
  soluble in acidic media, whereas calcium salts
  are poorly soluble at an alkaline pH.
• Crystalization inhibitors normal urine contain
  factors that inhibit formation growth of
  crystals Mg, citrate, pyrophosphate, TPH,
  glucosamine, nephrocalcin.
• Heterogenous nucleation appears to be a major
  mechanism in stone formation. A small crystal,
  e.g. uric acid, serves as a nidus on which
  another compound, e.g. ca-oxalate, precipitates
• Infection with urea splitting / urease producing
  microorganisms

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Disorders causing stone disease

• Gastrointestinal disorders
• Fat malabsorption, IBD, small bowel resection
  bypass can cause decreased urinery volumes,
  hyperoxaluria, hyperuric-aciduria,
  hypocitrateuria, acidic urine.
• Hyperparathyroidism / hypercalcemia
• Causes of hypercalcemia ( hypercalciuria) are
• Cancer, immobilization, endocrinopathies,
  dietary, granulomatous disease, renal, drugs
• Vit D increases Ca absorption from intestine
• Idiopathic Hypercalciuria.
• 24h urineCa gt 300mg/24h (men), gt250mg/24h
  (women)
• Gout hyperuricosuria.
• May promote Ca-oxalate stones
• Epitaxy, ca-oxalate deposits on uric acid /
  Na-urate crystals as nidus
• Urate in urine binds glycosamineglycans, an
  inhibitor of stone formation
• Uric acid promotes the degree of aggregation of
  precipitated crystals
• Uric acid lithiasis elevated urinary uric acid
  (24h urinary uric acid), acid urine
• Gout, myeloproliferative disorders
• Treatment alkalinization of urine to pH 6-7 ,
  fluids, allopurinol
• Infection with urease producing bacteria? urea
  splitting? struvite stones
• Proteus in majority Klebsiella, Pseudomonas,
  Providencia, Staphylococcus, Ureaplasma
  urealyticum, rarely E. coli.

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• Obstruction anatomic abnormalities
• Drugs.
• Acetazolamide causes hyperchloremic metabolic
  acidosis, transiently elevates urine pH, and
  reduces citrate excretion
• Allopurinol increases xanthine excretion and may
  produce xanthine stones
• Several drugs have limited urine solubility,
• May promote stone formation or are absorbed into
  the crystal matrix of other stone
• Triamterene, ceftriaxone, sulfonamides, bactrim,
  sulindac, phenazopyridine
• Other laxatives, vit D, calcium,
• Renal tubular disorders.
• Cystinuria,
• Inherited disorder of amino acid transport,
• associated with increased urinary excretion of
  cystine, ornithine, lysine, arginine (COLA)
• Limited soloubility of cystine promotes recurrent
  stones, which are radioopaque, homogeneous, may
  assume staghorn form
• Therapy high fluid intake, alkalinization of
  urine to pH 7.5 or more reduce cystine excretion
  by low Na diet, D-penicillamine, trioponine,
  captopril (drugs with sulfhydryl)
• Distal RTA
• Alkaline urine, hypocitrateuria,hypercalciuria
• Hyperphosphaturia, causing hypophosphatemia
  elevated 1,25-(OH)2D3, hypercalcemia
• Idiopathic hypercalciuria reduced tubular
  reabsorption of Ca

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• Enzymatic defects
• Xanthinuria. Deficiency xanthine oxidase
• Radiolucent xanthine stones
• 2,8-dihydroxyadenine.
• Deficiency adeninephosphoribosyl transferase
  (APRT)
• Radiolucent stones, requires infrared /
  crystallographic analysis
• Treatment with allopurinol
• Primary hyperoxaluria,
• Idiopathic Urolithiasis
• Majority of patients
• Risk factor profile
• Abnormally high excretion of Ca (gt4mg/kg/d), uric
  acid, oxalate, Na
• Decrease in several inhibitory solutes
• Decreased urine volume!
• Ability of urine to inhibit agglomeration
  improves after treatment with alkali, which
  increase urinary citrate
• Excretion of citrate is decreased by systemic
  acidosis, depletion of kalium magnesium,
  starvation acetazolamide,
• Most patients with low urinary citate have RTA,
  chronic diarrhea, hypokalemia, malabsorption, or
  high intake of animal protein

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First stone episode
Dietary advice meat, dairy, salt Fluids f/u
6-12 months
No growth
Metabolically active
Monitor 1-2 years
Urinary risk assessment
Dietary/fluid hypercalciuria
hyperuricosuria hypocitric
aciduria hyperoxaluria Factors
persist
Evaluate diet
Evaluate for
Evaluate for Meat, Ca, Na
acidosis, RTA
dietary excess

GI
malabsorption
Dietary,
meat GI disorders


measure oxalate/


glycoliate
Treatment options
Repeat specific
Reduce meat
dietary fat
/ Dietary advice dietary Rx /
excess
oxalate



restriction
Thiazides
allopurinol
K-Citrate B6, PO4



?thiazides
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Asymptomatic ? No Rx Symptomatic
Acute colic analgetics, fluids
Calcium stones Mg/NH4/PO4
Cystine (cannot Uric acid
stones
dissolve, or
(cannot dissolve/

obstructive obstructive)
Symptomatic obstructive
Percutaneous extraction ESWL
Small lt2cm gt2cm New stones old stones
ESWL Perc
ESWL Often requires Urography Usg
lt2cm gt3cm ureteric
stones
ESWL Perc upper1/3 lower1/3
ESWL
ESWL Extraction laser Rx
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7-dehydrocholesterol Diet
Skin UV
Cholecalciferol
liver
Metabolic activation of vit.D The result is an
increase in Ca PO4 concentration
25-hydroxycholecalciferol
kidney
PTH Hypophosphatemia
Calcitriol 24,25 D
Small intestine Bone
Kidney
PTH
Increase Increase
Decrease CaHPO4
Ca Po4
Ca PO4 absorption
release excretion
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Plasma Ca PTH
Bone
Kidney
Vit.D
Reabsorption
Phosphate Ca
Calcitriol
Excretion reabsorption
formation
Release of Calcium phosphate
Intestinal CaHPO4 absorption
Effect of PTH on Ca phosphate metabolism. Net
effect is increase in plasma Ca, with no change
or decrease in plasma phosphate concentration
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Plasma Ca 2 PTH Cacitriol
Increased Ca increased Ca
increased phosphate increased
phosphate From bone
from intestine
from bone intestine excretion in
urine
Plasma Ca
Plasma Phosphate increase

unchanged
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Plasma phosphate Calcitriol
PTH
Ca from intestine
Decreased decrease
increase phosphate Ca from bone
phosphate from intestine
excretion in
urine
Plasma Ca
Plasma
PO4 Slight increased

increased
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Increased systemic disease
Serum calcium
normal
Normal Hyperuricosuria Hyperoxaluria No
abnormality
Urinary calcium
idiopathic hypercalciuria RTA
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Laboratory investigation

• Serum electrolytes, BUN, Cr, Ca, PO4, Uric acid
• Urinalysis microscopic exam of fresh specimen
• Urine culture
• Nitroprusside test for cystine
• Urine pH, first AM urine, under oil
• Stone analysis
• 24h urine for Cr, Ca, PO4, uric acid, Cystine,
  oxalate
• Radiologic studies, USG, BNO, IVP
• Special test as indicated PTH, Thyroid,
  Cortisol, etc