Tractus urinarius

Dr.Resmi Kartini

KERUSAKAN GLOMERULUS

1.Out put urin menurun 2.Proteinuria 3.Hematuria

Swelling of endothel loss of Blood flow epithelium endotel

inflamation altering permeability of layer proteinuria

focal

Urin hematuria

Kerusakan tubulus
1.Loss of mechanisms controlling balance of electrolytes,water 2.upset in acid base balance 3. Loss of substances in urine normally completely or almost completely reabsorbed glucose,potasium,amino acids 4.Proteinuria due to damage to associated capillary

Simple diag.test pada kerusakkan ginjal

1.

2.

Urine : protein,red ceels,hb,pmn Urinary casts : * protein ( hialin / colloid ) * Red cells * Epithelial casts - desquamasi epit.tub * Granular sel tub necrosis * Kristal

B.Kimia darah

Urea ( 2.5 7.0 m mole/ lt ) Creatinin ( 50 100 mole / lt ) C02 ( 22- 28 m mole / lt ) Clearance test

Manifestasi klinik pada ginjal

Azotemia BUN ( blood urea nitrogen ) Creatinin GFR PU Renal Disorder Pre renal ( perdarahan,shock,Vol deplet ion ,congestive heart failure )

- kerusakkan parenkhim ginjal (-) Post renal obstruksi

gejala klinik Biokimia aqbnormal

Uremia

Mayor Renal syndrome

1.Sindr.nefritik akut : sindr.glomerulus hematuria.proteinuria,hipertensi pd glom.is post strept 2.Sindr nefrotik: proteinuria berat(> 3,5 gr/hr) hipo albuminemia edema berat hiperlipidemia / lipiduria 3.Hematuria / proteinuria asimtomatik 4. R F A - oliguria anuria -- azotemia

5. RFC : uremia
5.RFC : uremia chronic renal dis 6. Renal tubuler defect : poliuria Nokturia Elektrolyt disorders (metab acidosis ) 7. Urinary tract infection : bakteriuria,pyuria 8.Nefrolitiasis

Kelainan kongenital

1. AGENESIS 2.HIPOPLASIA 3.ECTOPIC KIDNEYS 4.HORSE SHOE KIDNEYS

Cystic Dis * penting ok : 1. Mrpkan problem diagnostik : Klinisi , radiologis ,patologist 2.Polikistik adult RFC 3.Confuse dg tumor malignant

Klasifikasi :
1.Cystic renal dysplasia 2.Polycystic kidney dis * autosomal dominant ( adult ) * recessive( childhood )
3. Medullary cystic dis : * Med Sponge kidney * Nefronoptisis uremic med.cyst 4. Acquired ( dialysis associated ) cystic dis 5. Localizet (simple ) renal cyst 6. Kista pd malformasi herediter ( tuberous sklerosis) 7. Glomerulo cystic dis. 8. Extraparenkhimal renal cyst

Patogenesis
Genetik Defect Acquire

Altered epithelial cell differentiation

Abnormal EGM matrik

Altered cell growth

Fluid secretion

Cyst

Cystic renal dysplasia Diff metanefrik abnormal

Khas : Struktur ginjal abnormal persisten - Tl rawan, mesenkhim undiff dukt kel imature tbtk lobus abn * Py sporadik Kbnyk kss ~ obstruksi ureteropelvik,agenesis ureter atresi,anomali sal kemih distal Morfologi : Ginjal besar, irreguler, multikistik dilapisi ep flattened Fungsi ginjal lain : N

Autosomal dominant ( adult ) polycystic kidney dis

1 / 1000 org 10 % pd kasus transplantasi ginjal & dialisis khr Morfol : - bilateral - ginjal > 4 kg, 3-4 cm - dari tubulus nepron dilap ep macam 2 Klinik : Asimptomatik insuf renal Nyeri pdrh,kista dil progresif
kolik ekkrei bekuan darah

py ginjal khr prog 40 % ~ polikistik hati, jrg pd limpa, pancr, paru 10 -30 % aneurisma berry : Azotemia spi uremia RF ( 1/3 ) hipertensi (py jant, hemorrag, ruptur aneurisma berry ) unrelated cause

Autosomal recessive ( child hood ) poly cystic kidney dis: Perinatal Neonatal Infatil Juvenil Young infant -- R.F Morf : Ginjal .>> Permuk licin Cortek,medula : multiple kista ~ Sponge Like Mikros : Dukt collecting dilatasi - Sakuler / silendris Dilap ep kuboid Kbyk kasus kista liver ( dilapisi Multiple Epithelium line cycts + prol d. bil Portae )

- Cong Hep fibrosis : Fibrosis periportal proli dukt.bil well diff older children hipert portal ,splenomegali
KISTA MEDULA : 1. Medullary sponge kidney : dilat kistik multiple dukt collect pd med. Klinik : Dukt. Dil.hematuria.inf. Batu Morfol : Kista kecil 2 dilap ep kuboid / transtitional

survive infancy ( infatil & juv ) berkemb hepatik fibrosis

2. Nephronophthisis uremic medullary cystic dis (umcd ) complek

Dimulai pada masa anak , progresif Khas : kista multiple insuf renal atropi tubuler --> hereditary fibrosis interts tubulo interst nephitis
1.Sporadic. Non familial ( 2o % ) 2. familial juvenil nephronophthisis (50% )
3. Renal retinal dysplasia ( 15 % ) ~ retinis pigment

Klinik : Poliuria , polidipsia Sodium lossing , tubuler acidosis 5- 10 th RF Mikros : Kista dilat epitel kuboid. Dikelilingi jar fibrosis & inflamasi

GLOMERULAR DISEASES Mrp masalah pd nefrologi ok GNC pybb RF * Primary glomerulopathies Acut diffuse Prol G N
Post Strep Non post Strep

Rapidly Prog. ( crescentic ) G.N

Membr. Glomerulopathy Lipoid neprosis ( minimal change dis )

Focal segmental glom sclerosis Membrano prol.gn IgA Nephropathy,focal prol .g.n; GNC *Systemic dis : SLE,DM,Amiloidosis,Good Pasture
syndr,Wageners granulomatosis,Henoch schohlein purpura.Bact.Endocarditis.

Hereditary Disorders

ALPORTS SYNDR Fabro Syndr

KLINIK :

Glomerular Syndr * Acute nephritic syndr Hematuri Azotemia Proteinuria oligouria Edem Hipertensi

Rapidly prog G.N

* Nefritis akut *Proteinuria * R.F.A

R.F.K

Azotemia --- Uremia prog * Nephrotic Synd : Proteinuria ( > 3,5 gr ) Hipo albuminemia Hiper lipidemia Lipiduria

*ASYMPTOMATIC HEMATURIA / PROTEINURIA

HEMATURIA GLOMERULER SUBNEPHROTIK PROT URIA HISTOLOGIC ALTERATIONS 1.Hipersel Glom : a. Prol sel mesangeal,endotel, atau sel ep
parietal. b. Infiltrasi lekosit 2. Penebalan membr. Basalis

endotel/ epitel

a. Penebalan M. Bas ( D.M ) b.Deposit material amorf ( Protein ) pd

3. Hialinisasi dan sklerosis

( Difus, global, Fokal, segmental , mesangeal

Acute Post Strept ( prol ) G.N

Strep hemol beta tipe A Ag A b glom

complek compl (faring, kulit ) * cytoplasmic AG ( endostreptosin ) * cationik AG *Proteinase ( strep

Planted Ag

circulating
imun

Erythrogenic toxic )

Morfol : A. Glom enlarged, hipersel, blood less relatif

hipersel 1.
/

prol sel endotel,mesangium

2. infiltr sel leukosit,neutropil monosit

Sel endotel bengkak. prol Infiltr sel leukosit obliterasi

lumen kapiler

B. Deposit fibrin C. Edem intersti D. Tubulus --- casts red cell degenerasi

Klinik :
glom capillary obstr
reduce blood flow tub ep damage

damage glom endothel

Stimulation of juxta

diminised filtration

focal increase escape of in permeabilitas red cell

fluid

glom App oliguria

Rise in blood Pressure

retention

rised oedema blood urea

unselektif protein urea Casts

hematuria

epithelial protein red cells *malaise,nausea.edem peri orbital --------- 1- 2 mg post infeksi

PERJALANAN PENYAKIT
ACUTE DIFFUSE ( PROL ) G.N

CARDIAC FAILURE OR UREMIA

MILD PROTEIN PERSISTING PERSISTING FOR PROTEINURIA

MONT OR TWO

RAPIDLY

PROG. G.N AND HEMATURIA

chronic nephritis

DEATH IN ACUTE

RECOVERY

Death years later

Rapidly Prog GN
Khas :
Akumulasi sel pd rongga bowman crescent Klassif & patogenesis 1.Post inf ( post strept ) RPGN 2.GN Py sistemik ------ SLE,Good pastures Syndr
Vasculitis ( poli artritis nodosa ) Wegener granulomatosis Henoch Scholein Purpura

Klinik : ~ APGN --- lebih berat Morfol : Ginjal > >, pucat,hemor.petechiae
Glom : nekrosis focal,prol mesangeal,prol endotel focal/difu prol endotel fokal / difus MIKROS : Ep crescent - prol sel parietal migrasi monosit,makrofag fibrin Perjln Py ~ penyebab . . Hipertensi,uremia super impuse inf perikarditis fibrinosa, Anemia

Nephrotic Syndr.
Cause :
1.Primary glomerular dis * Membr. GN * Lipoid nephrosis Focal seg. GN Membr.Prol.GN Other prol GN ( Focal , pure mesangeal

Ig A nephropathy )
2. Py Sistemik * DM ,Amyloidosis, SLE * Drugs ( penisilin, STREET HEROIN ) * INf ( malaria ,sipilis , hep B, AIDS ) * Malignancy * Miscellaneus ( alergy, nefritis herediter ) Proteinuria >= 3.5 gr Hipo albuminemia, Edem , Hiperlipidemia

Membrano GN / membranous nephropathy

Mrpk penyebab terbnyk pada adult Khas ; deposit imunoglob. Containing , electron. Dence sepanjang epit. ( sub epitel ) membr. Basalis. Penebalan difus dd kap Dpt ~ sebagai Mekanisme sekunder spt : -T. Ep maligna ( dr paru,kolon . Melanoma ) - S.L.E - expore tu inorganic salt ( gold . Mercuri ) - drug ( penisilamine , captopril ) - infeksi ( hep.B kronic, sifilis , schistosomiasis,malaria ) - Metab disorders ( DM ,Tiroiditis ) 85 % kasus idiopatik

ETIOLOGI , PATOGENESIS

DEPOSIT Ig sub epitel -- chronic Ag Ab mediated dis Morfol : Glom : uniform , penebalan dd kap difus deposit ireg dence diantara membr basalis sel epit lost foot prosessus - pros berlanjut glom sklerosis hialinisasi ---hi pertensi mesangium sklerosis Tub --- droplet hialin Respon kortico steroid (+) 10 % 10 % R.F ( 10 thn ); , 40 % renal insuf

Minimal change Dis / lipoid nephrosis :

Terut menyebbkan N.S. pd anak ( 2-6 th ) Khas : Glom. Foot processes menghilang difus
Etiologi 1. Post infeksi resp / imunisasi 2. Respon thdp kortico steroid & terapi imunosupre si 3. ~ Py atopik ( eczema , rinitis ) 4. Minimal change ~ atopi ( genetik ) 5. pd py hodgkin 6. Post transplantasi Morfol : Glom . N. -- Foot processes fusi Tub prox Lipid Respon kortiko steroid ( + )

Focal segmental glomerulo sklerosis

KHAS :Sklerosis bebrapa glom , mengenai sebagian kap Tdd : 1 idiopathic FSG 2.FSG super imposed on another primary glom lesion ( Ig Nephropathy ) 3. FSG loos of renal mass ( renal ablation FSG ) dgn py ginjal stad lanjut ( renal nepropathy , analgetik abuse nephropathy, agenesis ginjal unilat 4. Secondary FSG ( heroin . Inf HIV ) 80 % - NS tetapi beda dgn yg disebabkan minimal change GN - 1. Hematuria , GFR , Hipertensi 2.Prot. Uria non selektif 3.Respon kortico st buruk 4. Progresif - GNC ; 50% end stage ( 10 th ) 5. Deposit Ig.

Morfol
Mengenai sebagian glom Pd segmen sklerotik , membr bas kolaps matrix mesangeal , hialinosis PD : tebal ( hialin ) Glom sklerosis atropi tubuler- fibrosis interst Patogenenesis : Hipert glom , kap hipert Perub sel epit dipus - deg dan kerusakan fokal sel epit visera - khas med - FSG Deposit prot fibrin reaksi sel mesangeal

Fokus 2 permeabilitas

- hialinosis sklerosis

Perjalanan penyakit

Idiopathic FSG ----Remisi spontan Anak prog > baik dari adult 20% malignant fokal sclerosis - prot uria masif -- RF kronik ( 2 tahun) 25-50% rekuren pada alograf HIV associated nephropathy 5 10 %

Membrano prol GN
Khas : lesi pada membrana basalis Prol sel glom > mesangeal - masangio capillary Primer MPGN - idiopatik Sekunder MPGN -- sistemik disorder Secara Mikros elektron : dibagi tipe I & II Morfol : Glom : Bsr , Hipersel- Prol sel mesangium : Lobular Appearance GBM : Tebal tu pd kapiler loop membr Basal splitting - inklusi sel pros mesang ke kap loop perifer - : mesangeal interposition TIPE I : 2/3 Kss Deposit elektron dense sub epitel ; Ig G ( + ) II : Deposit dence material posisi tdk dike -- dsbt DENCE DEPOSIT DIS Ig G ( - )

IgA nephropathy ( BergerS Dis )

Khas : Deposit IgA pd mesangium
Plg banyak menyebabkan hematuria rekuren Frek Morfol : FPGN Diffuse mesangeal prol -- sklerosis fokal Deposit Ig A mesangium Perjalanan peny Anak inf : resp mukosa git -- 1-2 hr urin tract Dewasa

IgA nephropathy ( BergerS Dis )

Klinik : Py heterogenous Biasa benign- slowly progresif 50% RF ( 20 thn ) Terut : Prot urin brt Hipert ditemukan
sklerosis vasc -- Progresif

Fokal prol dan necrotizing GN

Fokal GN : Prol glom tbts segmen glom dan bg glom

Nekr .Focal Deposit fibrin Fokal GN : <---1. Manifest dini ( RGN py sist : SLE , PAN , Henoc Schonlein pur, Good Pasture synd , Subacut bact .endoc, Wegener S Granulomatosis 2. IgA 3. Primary idiopathic focal GN

CHRONIC GN

End state GN Post strep GN 1-2% RPGN 40% MGN 50% F.G sklerosis 50-80% MPGN 50% IgA 30-50% others

CGN

Morfol :
Ginjal kontraksi simetris , granular difus Korteks tipis , lemak peripelvic Early : glom etiol obliterasi hialin prot plasma trapped , matrik mesangeal kolagen arteriosklerosis tub atropi, intersti fibrosis - dialysis changes

- disertai CRF uremic pericarditis uremic Gastroenteropathy Hiperparatiroid ---- Nefrocalcinosis Uremic pneumonitis

__

Lesi glom akibat py sistemik SLE

klinik : hematuria , nefritis akut
NS , CRF , Hipertensi HIST: Mesangeal lupus nephritis Focal GN Diffuse Prol GN Diffuse Membr GN

Henoch Schonlein Purpura

Tdr : lesi kulit khas : daerah extensor lengan ,kaki , bokong ( Hemorr necrotizing vasculitis ) manifes abdomen : nyeri , V. intestinal bleeding Arthralgia non migratory , abn ginjal hematuria,proturia NS, rapidly prog GN - RF atopi post inf resp Morfol : Prol. mesang. Fokal / difus, crescentic GN Deposit Ig A

Endokarditis bakterialis
- immune complex GN hematuria, prot. Uri fokal / segmental necrotizing GN diffus prol GN, RPGN DIABETIC GLOMERULO SCLEROSIS
cause 30 % end stage py ginjal 20 % ---- < 40 th

Klinik :

Non nephrotic prot uri NS,CRF,Arterioler Sclerosis, Pielo nefritis, Necrosis papiler, Lesi tubulerp - Nefropati Diabetik 50 % insulin dependent Insulin independent ( tipe II ) Nefrotik 12 -22 thn - CRF 4-5 th

MORFOL :
1.Penebalan Membr. Basalis & P..
2. Glom. Sklerosis difus - 3.Glom Sklerosis Noduler intercapillary Glom SKLe. Kimmelstiel Wilson Dis. Glom Hialin - Ginjal Ischemia Arteriol Atropi Tub Fibrosis interst Kontraksi

Perjalan Py :

GFR -- Micro albuminuria 20 -200 gr / menit Prot. Uri GFR PROG.Loss RF ( 5 TH ) Hipert -- Prot uri insuf renal

NEFRITIS HEREDITER

Alport S Synd : Nefritis

tuli (saraf )

lensa ,katarak post, distropi kornea berat Hematuria, NS, Timbul pd usia 5-20 th RF 20 th 50 th Morf: Glom prol Segmental & sklerosis Matrik mesangial Foam cells - glom sklerosis, pd sempit , tub atropi fibrosis interst

ggn mata ( dislokasi

PENYAKIT TUBULUS dan interstitium

1. Ischemik / toxic tubuler injury

- ATN dan RFA 2. Inflamasi tub dan interstitium - Nefritis tubulointersti

ATN

Khas : destruksi ep tubulus fg ginjal akut - RFA ( 24 jam - urin , 400 cc ----------

1. Organic vascular obstruktion - Pd intra renal difus ( Poli artritis N,

Hipert malignant,Hemolytic uremic syndr) 2. Severe Glom. Dis ( RPGN ) 3. Acute Tubulo intersti. Nephritis ( Hipersensitif drug )

4. Massive infection ( Pielonef ) Nekr.Papil 5. DIC ( pd ginjal ) 6.Urinary obstruction ( Hipertr Prostat ; Blood clot - Post renal ARF ) 7. ATN

Patogenesis
Ischemic ATN - KRSK tubulus Nefrotoxic Ep tubulus sensitif thdp anoxia, toxin
injury

Faktor predisposisi 1. Gg sensorik - reabsorbsi tub 2. Sist Transport ion dan organi acids 3.Kesanggupan - konsentrasi efektif

Sel epitel : Struktur }

} terganggu -- loss of polarity

Fungsi }

Sekali terjadi injuri tub - ARF progresif

1.Kerusakan tubulus vasokonstruksi arteriol preglom GFR 2.Kerusakan tubulus oliguria tubulus debris blok uriner flow, intratubulus GFR 3.Cairan dari tubulus rusak jaringan intersti tekanan intersti tubulus kollaps 4.Efek langsung toxin pada ultra filtration glomerulus

MORFOLOGI
ATN Ischemic khas : nekrosis tubulus fokal, multipel point sepanjang nefron, skip area, membrane basale ruptur (tubulo rehexis) lumen oklusi oleh cats Terdapat pula: kristal hialin eosinofilik tamm horsfall protein. Jaringan intersti odem Regenerasi epitel Toxic Atn: terutama tub.proximal tersering MgCl2

Perjalanan Penyakit
Akut Tubuler Nekrosis : 1. Initiating:36 jam urine rendah sedikit (oliguria) 2. Maintenance stage:oliguria 40-400ml Garam Air

Tubulo interstitial nephrosis

Krsk TUB

Intersti

Pielonefritis Akut

Inflam supuratif akut Inf bakt

Hematogen Penyebaran septikemi Ascending vesico uretral reflux.- kerusakkan pada upper /

lower Morfol : inflam supp interst pathy - abses pada 1 /2 ginjal Nekrosis tub. Infitr neutro jar intertsitiel - tub Khas : Glom resisten thdp infeksi Bl nekrosis luas dpt - Glom Komplikasi :1. Nekro. Papil , dgn obstr urin tract Mikros : Infark nekro koagulatif 2. Pioneprosis #. Abses perinefrik sembuh Fibros Interst,atropi tub ,infiltrasi limposit

Predisposisi
Predisposisi : 1. Obstruksi Uriner 2. Instrumentasi 3. Vesicoureteric reflux 4. Pregnancy 5. Sex & age Thn2 pertama laki 2 - meninggi 40 th - wanita usia ---BPH 6. Lesi primer - Jar parut intra renal obstruksi 7. DM tindakan kateter 8. Imunosupresi & imunodefisiensi

Klinik :
Akut : nyeri kostovertebral demam, malaise disuria Urine : Pus . Bakteri(E. Coli .Pseudomonas. Strep. Faecalis ) , RBC, protein , darah

Pielonefritis chronik

CPN : merupakan inflamasi tubulo interstitial chr Jar parut kel calykes dan pelvis TDD : 1. Chronic Obstruksi PN Dpt bilat anomali OBSTR Urin Tract Unilat Calculi __ Obstruksi unilat 2. Refluk Nefropati VUR ,intra renal reflux kerusakkan ginjal, atropi, insuf renal chr

Recurrent Infection

Chr . Intersti Inflamasi Urinary obt End Arteritis

Fibrosis
Stagnation of urine Scarring of cortex Back Pressure

Atropi Parenkhim

Distort of med Prog. Obstr Of Nephron Tu TUBULUS

MORFOL

Jar parut ireg , asimetris Atropi tub , Hipertr , Dil - tiroidization Colloud ( protein ) Inflam intersti . CHR End arteritis obliterasi T sebar arteriosclerosis hialin tapi glom normal - sp Focal segmental glomeruloscle Klinik :1. FG konsentrasi ginjal m hil prog 2. Acidosis 3. RF 4. Hipertensi

Analgetic Abuse Nefropathy

Py Ginj kronik - intake analgetik Khas : . Nefritis tubulo interstitial chr Nekrosis papil Phenacetin , Asoirin - 2 kg > 3 thn , Kafein, Acetaminophen , Codein Patogenesis : mula 2 nekrosis papil nefritis tubulo interstinal cortical Aspirin Menghambat kerja prostaglandin ischaemi papil Klinik : Haedeche , anemi, GIT symptome ,HT pelvis renalis Pap. Trans .Ca

Urate Nephropathy
Pada Hiperurecemia 1. Acute uric acid Nephropathy Presipitasi kristal urat pada tub ( Collecting tub ) Obstr nefron ARF Tu Pada pendrt luekemia, limfoma chemoterapi INTI SEL HANCUR As urat 2. Chronic uric acid nephropathy / gouty nephropathy Hiper urecemia Arteri ,Arteriol dd nya tebal tophus - Hipertensi

Nephrolithiasis

Hipercalcemia > Hiperparatir * MM VIT D intoxikasi Metastatic bone DIS

Disease of blood vessles

Nefrosklerosis benigna istilah nyg dipakai pada hpt benigna hialin arteriosclerosis ischemia fokal parenkhim penyempitan arteriol Mrpkan kead khronik 20- 30 thn

Patchy vasc occlution

Stimulation & tr of Prog Sclerosis -------- un affected glom Of Glom supplied Increase filtration Atropi tub Tub Dilat Replacement fibrosis
Cortical Scars Un affected area cortex swelling Granularity of surface

Morfol
Ginjal sdkt mengecil Cortex sempit Mikros : Arteri / arteriol lumen sempit -DD tebal & hialinisasi ( prot. Plasma, lipoid, pd membr basalis Atropi ischemik pathy 1. Atropi tub, fibr interst
2.

Kerusakk glom Jrg- insuf ginjal / uremia GFR N Prot uri RGN

hiperplasia fibroelastis

Malignant Nephrosclerosis
Malignant / allelarated HT <-- normotensi benign HT sekunder form of ht Py ginjal lain(glomis /Reflux Nefropati ) Morfol : ukuran ginjal lama py Hemor kecil - Ruptur arteriol / glom kap - flea buten

Mikros :
1. Arteriol nekrosis fibrinoid Arteriolitis Necrotizing 2. Arteri interlobuler Intima tebal lum Arteriol en sempit - Prol elongated sel konsentrik ( sel otot polos ) kolagen konsentrik arteriolitis hiperplastik onion skinning renal failure in hioert malig Kdg Glom nekro infilt PMN Kap Trombus ( Necrotizing glomerulitis )

PATOGENESIS
HT malignant : Renin vasokonstriksi Angiotensin HT nekrosis Aldosteron vasc (injury endotel,Tr . Nekr fibrinoid. Coagulasi intravasc ) HT Malig : Diast 130 mmHg Papil edem Retinopati Ensefalopati CVS. RF

Morfol
i

Tiba 2 + komplit GFR sdg Pelvik + calices dilat Atropi parenchym kadang 2 Sub total / intermiten GFR tdk Dil progresif ( tergantung lokalisasi obstr ) Makr : Ginjal > > >, Pelvic + calyc dilatasi Histol : Atropi tubulus intersti fibrosis kista 2 ( 15 20 cm ) kortek tipis , piramid obliterasi Obstruksi : Akut Unilat , komplit / partial Bilat partial poliuria , nokturia Bilat , komplit oliguria , anuria

OBSTRUKSI

UROLITHIASIS

> 20 30 thn Familial Herediter ( inborn error of metab ) Gout , sistinuria , hiper okaluria primer ETIOL Patogen : Tipe 1. Ca ( 75 % ) oxalat fosfat 2., Triple stone ( 15 % ) / Struvite stones Mg amonium phosphat 3.Uric acid ( 3 % ) 4. Cystene ( 2 % )

 Konsentrasi uriner ( vol urin )

Morfol : Renal- Calyc + pelvis

staghorn stone

Perjalanan PY
Ptg obstruksi uriner / ulcerasi bleeding Batu kecil - Ureter Besar ----- silent Excess excretion of stone + Ca Substance ( oxalate ) lack of urinary super saturation fibrinolysis solution of salt lack of subtsan keeping Prot nidus ---------Ca salt in solution (Mg.P) -------- \ Presipition and \ Stone formation \-- lack of inhib of cyistal formation

Type of renal stone

*Ca ( oxalat , fosfat )

75%

hipercalcemia ,hipercalciuria ( 5% ) hipercalciuria tanpa hipercalcemia ( 15 % ) Absorptive , renal , idiopatik hiperuricosuria ( 20 % ) hiper oxaluria ( 5 % ) enteric primary * Mg ++ , NH3 , Ca , PO4 renal infektion

10 15 %

* Uric acid ~~ hiperuresemia hiper uricosuria idiopatik * Cystine

6%

12%

Benig : ditemukan pada autopsi jarang menyebabkan gej klinik Malignan : pada klinik T. JInak : Adenoma korteks : kecil, discrete dari tub ginjal 7-22 % autopsi Morfol : < 2 cm , kuning abu 2 pucat discrete , encapsul , nodule Mikros : Kista papilomatous , sel kuboid / poligonal tubuler , glanduler , cords , massa undiff

TUMOR

RENAL FIBROMA / HAMARTOMA

< 1 cm , pd autopsi sel ~ fibroblas Jar kolagen ANGIOMIOLIPOMA ONCOCYTOMA MALIGNANT TUMOR : RENAL CELL Ca / HIPERNEFROMA / ADENO Ca 1- 3% T. Ganas viscera 85- 90% dari T.Ganas pd dewasa T dekade 5 6 : = 3 : 1 Dari Ep Tub ; ~ sigaret Genetik pd VON HIPPEL LINDAU SYNDR (VHL ) Ditandai ( Hemangioblastoma ssp & Retina ) berkembang Multiple renal cell Ca

Morfol :
Timbul , dimana saja dr ginjal p.U nya POOL ATAS Soliter , unilat , 3 15 cm Ischemik, nekrosis, fokus hemorragic Batas tegas, Dgn kapsul renalis Satelit nodul - agresif Khas : invasi V. ren ( nod solid ) - V. C. Inf - jantung

Mikros :
Papiler - solid clear cell 70 % Granuler cell ; sarcomatoid pattern --. Prog buruk well diff ( GRAD I & II ) grade I V Perjln Py : Klinik nyeri costo vert .masa palpable , hematuria ( 90 % ) : demam, malaise, weak ness , BB menurun Para Noe plastik syndr ( polisitemia, hiper calcemia , Hipertensi dis fingsi hati , feminisasi / maskulin , sindr cushing, eosinopilia , Rx lekemoid , amiloidosis

Khas :
Metastase luas sebelum gejala klinik paru ( . 50 % ) , tulang ( 33 % ) K G B regional , hati , adrenal , 0tak 5 th survival rate 45 % 75 % ( tanpa metastase jauh ) perinefrik . 15 % - 20 % ( V. Ren ) Th / Nefrektomi

URETER
Kel kongenital :
Double / bifid ; uretero pelvic juntion obstruksi ; divertikel ; hidro ureter ; megalo ureter Inflamasi : Pada urinary tract infeksi : * Ureteritis folikulris * Ureteritis cystica Tumor / tumor like : Benig T jar mesenchimal Polip fibro epitelial Malignan tumor

OBSTRUKSI
INTRINSIK : calculi Strikctura Tumor Blood Clot Neurogenic EXTRINSIK : Hamil Peri ureteral inflam Endometriosis Tumor

VESICA URINARIA
Divertikel : kongenital Accuired EXSTROPHY : -- Gangguan perkembangan dinding ant dan V. URINARIA Inflamasi : Cystitis acut & chronis Pielonef bakterial Etiologi : E. Coli ; Proteus ; Klebsiella , entero bacter TBC, Kandida , Schistosomiasis , Chlamidia , miko plasma

Morfol :
Hiperemi mukosa , Exudat Hemor. Cystitis Suppurasi Ulcerasi - CHR Folikularis Eosinofilik KLINIK : 1. Polalisiria 15 20 % 2. Lower Abdomen pain 3. Disuria

*Sistitis INTERSTITIAL ( Hummers

Cyctitis )
inflam + Fibrosis Mast Cell Ulcus Unknown - Autoimun * Malakoplakia - Reaksi inflamasi ---- plak mukosa 3-4 cm * Metaplasia : Glanduler ( BRONN S Nest ) - infeksi Nefrogenik ? Skuamous Nonspesific inflam : Batu : RD

NEOPLASIA
Bladder Epithelial Tumor Benigna Transtitional cell papilloma Inverted papilloma Malignant Transti . Ca Grade I 20 % II , III 60 % CIS 5- 10 % Squamous cell ca Mixed Undiff . Small cell Ca Adeno Ca 2-3% rare 40 %

37%

GRADING TUMOR TGTG DARI ATIPIA TUMOR

( I ) Some atipia , diff baik Mitosis jarang > 7 lapis sel , slight loss of polarity ( II ) Sel tumor msh dikenal dari sel transitional > 10 lapis sel Mitosis > , Greater loss of polarity Pleomorfik Bbrp dif skuamosa ( III ) > > ( II )

Keditak teratur nya sus sel Kehilangan & fragmentasion permukaan sel

Giant cells sel tent - Flatten , Fokus dif . Glanduler

Ca sel skuamosa

Staging : Description Marshall stage ------------------------------------------------------non invasive Papillary 0 CIS 0 Invasive L. propria A Superfis muscle B1 Deep muscle B2

Description

Marshall stage
D1 D2

---------------------------------------------------Metastatic Regional KGB Distant site

Epidemiologi , Patogenesis : >3:1 50 -80 thn ( 80 % ) Di lokasi industri , urban ? 1.Industri exposure td arylamines ( 2 naftil amine ) - stlh 15 40 thn 2. Cigarette smoking 3. S. Haematobium 70 % ca squamosa 4. Long time Fenasetin 5. Cyclofosfamide , imunosupresi agent -- sistitis hemoragik Ca ( 10 x , set 12 thn )

KLINIK : Hematuria
Prognose : TGTG STAD , GRADE Grade I : 10 thn survival rate 98 % II 30 % -- 68 % Agresif 70 % Ca Squamosa T. C. C Papillary Flat lesion Non invasive invasive

Grading I papiler

II papiler / flat III papiler , flat , fungating. nekrosis , ulserasi invasi ---- otot Mesenchimal tumor & sekundary tumor

Uretra :

Inflamasi Tumor Caruncle - inflamasi Papilloma Carsinoma