common - static.s123-cdn-static-c.com
TRANSCRIPT
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• Common clinical problem (5-10% of people) 1% of individuals at autopsy.
• Definition:
“Calculus formation at any level in the urinarycollecting system”.▫ Most often arise in the kidney.
▫ Unilateral in 80% of patients (commonly found at
pelvis, calyx or urinary bladder).
▫ M>F*; peak age of 20-30 yrs.
▫ Has familial tendency**.
Urolithiasis
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Stone Comment
Calcium Oxalate and/or Calcium Phosphate
Idiopathic hypercalciuria (50%)Absorptive hypercalciuria (GI)Renal hypercalciuria
Hypercalcemia and hypercalciuria (10%)Hyperoxaluria (5%)Hyperuricosuria* (20%)No known metabolic abnormality (15-20%)
80%
Alkaline pH**
Struvite(Magnesium, Ammonium, Phosphate)
Due to renal infection by urea splitting bacteria as proteus & staphylococci**
10%
Alkaline pH
Types of Renal Stones
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Stone Comment
Uric Acid
Associated with hyperuricemiaAssociated with hyperuricosuria*Idiopathic (50% of uric acid stones)
6-7%
Acidic pH < 5.5
Cystine
Defect in the renal transport of cystine
1-2% Acidic PH
Types of Renal Stones
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• The most important is ↑ urine concentration of thestone's constituents so that it exceeds their solubilityin urine (supersaturation).
• In all cases, an organic matrix of mucoproteinmakes up 2.5% of the stone (? nidus).
• Predisposing factors:▫ Change of urine pH.
▫ Decreased urine volume.
▫ Presence of bacteria.
▫ Deficiency of inhibitors of crystal formation in the urine
(as Tamm-Horsfall protein).
Pathogenesis(obscure)
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• Number & Size:
▫ Usually multiple.
▫ Tend to be small (smooth or jagged).
• Staghorn calculi:
▫ Progressive accretion of salts leads to the
development of branching structures Lead to
formation of massive stone filling the renal pelvis
and calyceal system (cast of pelvis and calyceal
system).
▫ They are usually composed of struvite.
Morphology
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Nephrolithiasis
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KUB
Kidneys, ureters, bladder (KUB) film showing right staghorn
calculus
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Staghorn stone
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• Large stones are asymptomatic.
• Smaller stones may pass into the ureter,producing renal (or ureteral) colic & grosshematuria.
• Renal stones predispose to bacterial infection,obstruction & UT bleeding.
Clinical Course
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Urianary outflow obstruction
• Importance of UT obstruction:▫ Increases susceptibility to infection & stone formation.
▫ If unrelieved lead to permanent renal atrophy(Hydronephrosis or obstructive uropathy)
▫ Many causes are surgically correctable or medicallytreatable.
• It can occur at any level of urinary tract (intrinsic & extrinsic causes).
• Sudden or insidious, partial or complete, unilateralor bilateral
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Causes
Congenital anomalies: Posterior urethral valves Urethral stricturesMeatal stenosisUreteropelvic junction obstructionSevere vesicoureteral reflux
Inflammation: ProstatitisUreteritis, urethritisRetroperitoneal fibrosis
Sloughed papillae or blood clots
Urinary calculi Pregnancy
Benign prostatic hyperplasia Uterine prolapse & cystocele
Tumors: CA of the prostateBladder tumorsRetroperitoneal tumorsCA of the cervix or uterus
Functional disorders: Neurogenic (spinal cord damage or diabetic nephropathy)
Urinary outflow obstruction
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Urinary outflow
obstruction
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• Definition:
“Dilation of the renal pelvis and calyces, withaccompanying atrophy of the parenchyma, caused byobstruction to the outflow of urine”.
▫ Bilateral: if obstruction is below the ureter.
▫ Unilateral: if obstruction at the level of ureter or above.
Hydronephrosis
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Morphology • Gross:▫ Slight to massive enlargement early features
include simple dilation of the pelvis and calycesand variable interstitial inflammation.
▫ In chronic cases cortical tubular atrophywith marked diffuse interstitial fibrosis.
▫ Advanced cases transformed into thin-walledcystic structure 15-20 cm with striking atrophyand thinning of cortex
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Hydronephrosis
Hydronephrosis of the kidney, with marked dilation of the pelvis and calyces and
thinning of the renal parenchyma
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Clinical features
• Depend on circumstances:
▫ Acute Obstruction: pain.
▫ Unilateral (complete or partial) Obstruction: mayremain silent.
▫ Bilateral partial Obstruction: features of TIN.
▫ Bilateral complete Obstruction: ARF.
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PRIMARY• Benign: Papillary adenoma (in the cortex). Oncocytoma. Medullary fibroma (interstitial cell tumor).
• Malignant: Renal cell carcinoma (most common):• Clear cell renal cell carcinoma.
• Papillary renal cell carcinoma.
• Chromophobe renal cell carcinoma.
Nephroblastoma (Wilms tumor). Urothelial carcinoma of renal pelvis.
SECONDARY
Classification(simplified)
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2. Angiomyolipoma:▫ Consists of vessels,
smooth muscles & fat.
▫ Seen in 25-50% of patientswith (TuberousSclerosis).
Benign renal tumors
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Angiomyolipoma
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1. Renal cell carcinoma (RCC)
• Tumors are derived from the renal tubularepithelium*.
• 2-3% of all visceral cancers. ~85% of all renalcancer.
• M:F = 2:1. commonly 60-70 years.
• Most cases are sporadic.
Malignant renal tumors
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Risk factors
• Smoking (most significant), obesity*, HTN.
• Unopposed estrogen Rx
• Cadmium, petroleum products & heavy metals.
• CRF & acquired cystic disease** (30 folds )
• Familial (4%) most are AD:
▫ Von Hippel-Lindau (VHL) syndrome
▫ Hereditary clear cell carcinoma
▫ Hereditary papillary carcinoma
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Morphology of RCC
• Grossly:▫ Mainly arise in cortex polar & spherical.
▫ Orange – yellow OR tan–brown*, variegated tumor with hemorrhagic, necrotic & cystic areas.
▫ May extend into renal vein.
• Classified according to the histological picture:
▫ Clear cell carcinoma (70-80%).
▫ Papillary carcinoma (10-15%).
▫ Chromophobe renal carcinoma (5%).
▫ Sarcomatoid carcinoma.
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Renal cell carcinoma
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Chromophobe
RCC
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A. Clear cell carcinoma• Most common RCC subtype.
• Arise from proximal convoluted tubules.
• Majority are sporadic & unilateral.
• Familial forms, associated with germ-line mutationof the VHL tumor suppressor gene on 3p:
von Hippel-Lindau: Hemangioblastomas of cerebellum & retina.
Bilateral, multiple renal cysts clear cell carcinomas (40-60%).
Pheochromocytoma.
Familial clear cell carcinoma:• Clear RCC confined to the kidney without other
manifestations of VHL.
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Clear cell carcinoma
Microscopic:
-Vaculated cells with clear or granular cytoplasm.
-Highly vascularized stroma
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B. Papillary RCC
• Arise from distal convoluted tubules.
• Most are sporadic. Frequently multifocal &bilateral.
• Familial forms are associated withactivitating mutation of MET protooncogeneon 7q.
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Papillary RCC
•Microscopic:Papillae with fibrovascular cores
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C. Chromophobe renal cell carcinoma
• Arise from cortical collecting ducts or theirintercalated cells.
• Multiple losses of entire chromosomes(as:1,2,6,10,13,17,21) extreme hypodiploidy
• General good prognosis.
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Chromophobe RCC
•Microscopic:- Tumor cells have clear faint granular cytoplasm with prominent, distinct cell membranes
- The nuclei are surrounded by halos of clear cytoplasm Raisen-like
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• Intra-renal small satellite nodules .
• To pelvicalyceal system & ureter.
• Frequently the tumor invades the renal veinand grows in the IVC to RT side of the heart.
• Direct invasion to perinephric fat, renal sinusfat, regional LNs, or adrenal gland.
Tumor spread
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RCC extending into the renal vein
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Clinical features of RCC• Hematuria is the most frequent symptom (50%).
• Triad of 3 symptoms (in 10%) characteristic:
▫ Flank pain, palpable mass & hematuria.
• Asymptomatic/incidental finding.
• Constitutional symptoms (Fever, wt loss … )
• Present with mets (esp. lungs and bones)*.
• Paraneoplastic syndromes▫ Polycythemia 5-10%.
▫ Hypercalcemia.
▫ HTN.
▫ Cushing’s syndrome.
▫ Feminization or masculinization.
• Prognosis: 5 yr survival is around 70%.