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Disease of the urinary
system
Rohadi
Lab PA FK UNRAM
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Kidney Anatomy:
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Kidney Histology :
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Kidney Histology
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Kidney Histology
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Classification of urinary
system disease
Congenital
Infeksi : Parenchim, Interstial Nephritis
Glomerulo Nephritis
Vascular disorder :
Hipertensive Neprosclerosis
-A.C.N.( Acut Cortical Necrosis)
-A.T.N.( Acut Tubular Necrosis )
-Infark Ginjal
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SINDROME PD KELAINAN GINJAL
Neprotic Syndrome
Nepritic Syndrome
A.R.F.( Acut Renal Failure)
C.R.F ( Chronic Renal Failure )
Hidroneprosis +Hidrocalices
Calculi renalis ( Batu Ginjal )
Tumor-tumor ginjal dan kandung kemih
Benign Tumor
Malignant tumor
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Preparat yang ada :
1. TCC
2. TBC Ginjal
3. Pyelonefrosis Khronis
4. PNC
5. Nerfrolitiasis
6. Pyelitis Chronic
7. Nefroblastoma
8. Glomerulonefritis
Kronis
9. Renal Cell Ca
10. Squamous Cell CaGinjal
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TBC Ginjal
Renal tuberculosis. Photograph of a cut gross specimen shows multiple,
predominantly peripheral, white tuberculous granulomas throughout the kidney.
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TBC Ginjal
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Normal
Proliferative
Post strepto
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Chronic glomerulonephritis
Chronic glomerulonephritisrepresents the end-stage of all
glomerulonephritis with unfavorable evolution. This general (glomerular,vascular and interstitial) affection constitutes the so-called "end stage
kidney". In most cases, it is associated with systemic hypertension.
a kidney with chronic glomerulonephritis. The cortex has largely
turned to scar tissue and there is a poor demarcation between
cortex and medulla due to the glomerular scarring.
h l l h
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Chronic glomerulonephritisThe majority of the glomeruli are affected.
Depending on the stage of the disease,
they may present different degrees of
hyalinization (hyalinosclerosis - totalreplacement of glomeruli and Bowmann's
space with hyaline). The hyaline is an
amorphous material, pink, homogenous,
resulted from combination of plasma
proteins, increased mesangial matrix and
collagen. Totally hyalinised glomeruli are
atrophic (smaller), lacking capillaries,
hence these glomeruli are non-functional.
Few glomeruli may still present changes
which permit to discern the etiology of
chronic glomerulonephritis. Obstruction ofblood flow will produce secondary tubular
atrophy, interstitial fibrosis and thickening
of the arterial wall by hyaline deposits. In
the interstitium is present an abundant
inflammatory infiltrate (mostly with
lymphocytes).
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Chronic glomerulonephritis
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Chronic glomerulonephritis
Functional nephrons have dilated tubules, often with hyaline casts in the lumens.
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Pyelonephrosis
An absolute term for any disease of the pelvis
of the kidney. ... Origin: pyelo-+ G. Nephros,
kidney, + -osis,
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Acute pyelonephritis
route of invasion :
via blood stream
ascending route
obstructive
non-obstructive
role of vesicoureteral reflux and infected urine
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PYELONEPHRITIS ACUTA
Makroskopis :
-.Uni/Bilateral
-. Ginjal>> Kapsul meregang
- Abses kecil sub kaps,Pelvis hyperemis
granuler.
-URINE : PURULENT
Mikroskopis :
-Gambaran Abses
Akibat: Resolusi, Chronic Pyel., Supp, Bisa +
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Septicemia-
Microabscess
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Septicemia-Microabscess
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CHRONIC PYELONEPHRITIS
Makroskopis : Ginjal Mengecil
Kapsul melekat, menebal( parut) Cortex tipis
Batas dg medulla kabur,warna pucat
Medulla mengkerut
Pelvis menebal fibrotik,pucat Calyces melebar
Vasculer prominent
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CHRONIC PYELONEPHRITIS
Mikroskopis :
Parenchym : Kelompok jar.parut.
Tubulus : Delatasi,epit.atrofi : berisi bahan albominus (koloid/ Tiroidisasi)
Asal : Dr.proses inf ringan,lama,berkelanj.
-Pyelo.Acut Berulang
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PNC
You can see the stones, dark red and rough. They have plugged the renal
collecting system and dilated the calyces. Stasis of urine and the presence of the
inert stones themselves both promote infection. This in turn can make the stones
grow larger.
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Microscopic View of PNC
1. scarring and shrinking of the renal tubules, with the glomerulus spared.In contrast to rapidly progressive glomerulonephritis, the scar is outside
Bowman's capsule.
2. a group of tubules filled with cast protein and distended from scar
contraction. The unwary may mistake this for thyroid.
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Urolithiasis :
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Urolithiasis:
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NEPHROLITHIASIS
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Staghorn Calculus:
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NEPHROLITHIASIS
Top left: Retention of calcium oxalate crystals in the renal tubules after kidney
transplantation. Top right: Close-up image of calcium oxalate crystals plugging the renal
tubules of a primary hyperoxaluria patient with end-stage renal failure. Obstruction of the
renal tubules leads to tubular necrosis and loss of the total nephron mass. In preterm
infants, tubular nephrocalcinosis may lead to reduced renal function in adulthood, while in
renal transplant patients it may have a negative impact on long-term graft survival.
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Hidronefrosis
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Urolithiasis with hydronephrosis:
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Hidronefrosis
Obstructive uropathy; form a continuousspectrum from minor changes of blunting
of the renal papillae to severe from where
kidney converted into a multiseptate sac
with paper-thin walls.
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Hidronefrosis
1. Thinning renal parenchyma with residual large renal vessels in the hilum;
note dilated renal pelvis with flattened epithelia.
2. Sclerosis of glomeruli with atrophic tubules; note renal pelvis with flattened
epithelia.
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TUMOR GINJAL
Benigna : Adenoma
Hamartoma
Haemangioma
Lipoma,Angiomio lipoma,Fibro
ma, liomyoma.
Maligna : Adeno Ca, Grawits tu, Willm Tu,Sarcoma
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Renal carcinoma(renal cell carcinoma, clear cell carcinoma,
grawit tumor )
Definition:
Renal carcinoma is a malignant tumor, it
is originate from renal tubule
epithelium . 80
90 %. Age : 60
70 th.
Risk Factor : Smoking
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RCC
This renal cell
carcinoma is very large,
as indicated by the 15
cm ruler. A portion ofnormal kidney
protrudes at the lower
center. This patient was
a physician himself andjust didn't have any
early symptoms.
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RCC (GRAWITS TUMOR)
Morfologi : Makros
Tumor besar 3-15 cm
Pd irisan : Kuningabu2 dg area kis
tik & perdrhn prominent
Ada satelit nodul
Bisa meluas : Ke Collect Tub---Calyces-------Pelvis--- Ureter
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Pathology
Grossly :
Nodular, might have a pseudo
capsula, usually on the upperpole of the kidney; yellowcolored, hemorrhagic andnecrotic
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Slide 21.72
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Microscopic View :The cancer cells are clear (lipid and
glycogen deposition), nuclei notbig, nucleus-cytoplasm ratio not
large. Cancer cells arrange nest-
like or gland-like. Stroma is scanty.
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Slide 21.73
Renal Cell Carcinoma
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Renal Cell Carcinoma:
Incidence:
Etiology:
Clinical
Features:
Lab:
Path:
Clinical
Course:
Cells of proximal convoluted tubule. Risk
factors are smoking, obesity, analgesic
abuse.
Hematuria*, flank pain, palpable mass.
Frequently metastasize (lungs, bone, skin,
liver, brain).Gross or microscopic hematuria.
Specific Dx by radiographic techniques.
5-yr. survival 40%. Poor prognosis with
metastases.
Gross: Large yellow mass with hemorrhage
and necrosis. Invade renal vein.
Micro: Usually clear or granular cells with
little anaplasia. Other histologic variants
(great mimicker).
5th
and 6th
decades, most commonprimary renal malignancy.
Treatment: Chemotherapy, surgery, immunotherapy.
Synonyms: Hypernephroma, clear cell carcinoma.
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Squamous Cell Carcinoma Ginjal
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Squamous Cell Carcinoma Ginjal
The tumor is moderately differentiated with
formation of abundant keratin pearls
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Nephroblastoma(embryonal adenosarcoma, wilmstumor)
Nephroblastoma is a malignant
tumor, it originate fromembryonal cell (Nephroblast).
Usually is seen in the children,
very common.
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WILMS TUMOR("nephroblastoma"): One of thecommonest pediatric solidtumors (peak age 1-4 years).Wilms tumor microscopicallyresembles the primitive
nephrogenic zone of the fetalkidney, with primitiveglomeruloid structures and acellular stroma. Wilms tumor isassociated with mutationsinvolving the WT1 tumorsuppressor gene on chromosome
11. This neoplasm is verytreatable with an excellentprognosis and >80% cure rateoverall.
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WILMS TUMOR
Makroskopis :
Tumor berukuran bbrp Cmsangat
besar
Warna putih abu2
Homogen dlm kapsel ginjal
Tampak area nekrosis & perdrhn
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WILMS TUMOR
Mikroskopis :
1. Jaringan ikat
2. Blastema
3. Komp.Epit.yg dpt membent.strt.Tub,
Glomerulus ( Abortive Glom. )
Salah satu komponen bisa dominant
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Microscopic View :
Two components:adenocarcinoma
fibrosarcoma
Sometime tumor cell would formglomerulus-like or tubule-like structures.
Sometime having some well differentiated
cartilage
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WILM TUMOR
Wil T
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Wilms Tumor
Incidence:
Etiology:
Clinical
Features:
Lab:
Path:
Clinical
Course:
Embryonic renal tissue (metanephric
blastema). Genetic abnormalities.
Palpable abdominal mass. Abdominal
pain, fever, anorexia, nausea/vomiting.
Hematuria.
No specific clinical laboratory findings.Diagnosis by radiographic techniques.
5-yr. Survival 80%. Metastases to lung,
liver, bone, brain.
Gross: Solitary/multiple cystic mass,
sharply delineated. Soft, bulging, gray-
white with focal hemorrhage and necrosis.
Micro: Triphasic mesenchymal stroma,
tubules, and solid areas (blastema).
Primitive glomeruli, skeletal muscle,cartilage, bone, etc. (embryonic tissues)
Most common renal tumor of
childhood. Peak age - 2.5 - 3.5 years.
Treatment: Prompt resection with chemotherapy
radiotherapy.
Synonyms: Nephroblastoma.
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Carcinoma of Bladder
Transitional cell carcinoma of bladder
Definition
Transitional cell carcinoma of
bladder is a malignant tumor. It
originate from transitional cell ofbladder. It occupy 90% of cases in
carcinoma of bladder.
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Pathology
. Grossly:
Usually it is a papillary tumor with
slender or broad pedicle,
sometime it show cauliflower-likeor polypous, sometime it is flat.
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TCC Bladder
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TCC Bladder
These tumors showmore architectural
disorder and nuclear
atypia than Grade 1
tumors. The nuclear
size, shape, polarity,
and chromatin show
greater variability.Mitoses are still
infrequent.
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TCC Bladder
Another look at grade 1 papillaryurothelial carcinoma. These
patients are at risk of developing
recurrent tumors which may be
of higher grade. This entity is
considered synonymous withpapillary urothelial neoplasm of
low malignant potentialin the
1998 WHO/ISUP Classification of
papillary urothelial neoplasms.
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