Please enable JavaScript.
Coggle requires JavaScript to display documents.
UROPATHOLOGY, Urinary Tract Tumor, Glomerulopathies, kidney tumors,…
UROPATHOLOGY
congenital defect of renal pelvic and ureter
duplication of Ureter
VUR
III - ureter and renal pelvis are dilated, the contours of the calces are perserved
IV - significant dilation, contour of the calyx dull
II - reflux to renal pelvis, which is not dilated
V - massive dilation of the hollow system, the calyces are convex
I - reflux to lower part of unexpanded ureter
Uretero-cele
Bladder Extrophy: bladder is open to abdo surface (failure of ant wall closure) , boys, ass w/ epispadias, ↑ risk of adenocarcinoma of the bladder
Megalo-Ureter
Hydro-Nephrosis
secondary: obstruction BELLOW PyeloUreteral Transition(eg. dolich-mega--ureter oe post urethral valve in boys)
primary : obstruction in PyeloUreteral Transition (congenital fibrous tissue, aberrant vessels, ... )
U/L , Obst of the urine outflow from the renal pelvis → accumulation in calyceopelvic system → pressure atrophy of the kidney + destruction by inflam → sac-like kidney
posterior Urethral Valve
Bladder Diverticulum
Bladder Agenesis : very rare, girls
Urachal: urine flows out of the umbilical cord, possibly umbilical diverticulum (incomplete involution of the urachus), risk of adenocarcinomas, stones, infections
Malformation of kidney
dysplasia = Multi-cystic Dysplasia
loc abnormality = ectopic kidney
congenital
UPJO (utero-pelvic junction obstruction)
VUR (vesicular urethral reflux)
Cystic Kidney
ADPKD: adult, B/L, >1kg, +liver
ARPKD: infante, rare
double ureter > Weigert-Myeer ryle
Bypo-Plastic
Multi-cystic Dysplasia : U/L , non-communicating cysts, palpable abdo mass
Agensis: unilat / bilat (Potter Sy) > oligo-hydr-aminos > fetal compression
renal fusion = horseshoe (ren arcuatus): obst by inf mesenteric a.
Hypo-plasia
OligoMegaNephornia
Segmental hypoplasia
Mlaformation of testes
Ectopic testicles
Absence of testicle
Slippery testes
Retractile testes
CryptorChidism: undescended , (should desced by 4m), ↑ Risk of germ cell tumors, Orchidopexy surgery
Ascendant Testicle
Malformation of urethra, penis
HypoSpadia
EpiSpadia
Tumor
Sex Cord-Stromal Tumors (Germline Tumors)
Leydig Cell Tumor
Sertoli Cell Tumor
Non-Germ Cell > Lymphomas : in old man, Especially Diffuse Large B-Cell Lymphoma (DLBCL)
Germ Cell Tumor
GCT
GNCIS — Aggressive
Embryonal Carcinoma
Yolk Sac Tumor : produce AFP
Seminoma
Choriocarcinoma: Highly Malig, Hemorrhagic Mts (Lung, Brain), produce hCG
Teratoma
Mixed Germ Cell Tumors
Non GCNIS — Usually Benign
Prepubertal Type Teratoma or Yolk Sac Tumor
Spermatocytic Tumor
Orchitis, Epididymitis
Bac
younger : N. gon, Ch. trachomatis
older : E. coli, Kleb, Pseudomo, H. inf
Viruses
mumps, Coxsackie
Urinary Tract Tumor
Urothelial Tumors
Papillary Lesions : LG (recurs often but rarely invades / HG
Invasive Urothelial Carcinoma : stages dep on depth - invasion into lamina propria or m. propria - may spread to pelvic LU ,
Flat Lesions (CIS) : a serious dg (unlike othe CIS)Severe dysplasia of entire urothelium thickness - HG lesion with rapid prog to invasion
Non-Urothelial Malignancies of the Bladder
SCC : Originates from squa cell metaplasia of the urothelium - rare, ass w/ bloodstream infection (developing countries) / histo: keratinize squa epthe , no glandularor or urothelial differentiation
Primary Adenocarcinoma: are, arising in the urachus or in rare Glandular metaplasia of the urothelium / histo: Enteric (colonic-like) , mucinous , Signet ring cell (Aggre)
bladder is normally lined by urothelium, chronic irritation or other triggers can lead to metaplasia (the tumor is not of urothelial origin, but from transformed/metaplastic epithelium.) 1.Urothelium → squamous epithelium → SCC / 2.Urothelium → glandular epithelium → adenocarcinoma
🧬 Pathogenesis: Two Molecular Pathways
Papillary Pathway (≈80%) : CDKN2A (p16) del > hyperplasia - exophytic (growth outward) , LG , recurrent , low Aggre, rarely invasive
Non-papillary (Flat) Pathway : TP53 mut - benign as CIS → invasive carcinoma - HG , Aggre, invasive, poor prog
from the Urothelium - Common in developed countries - More in men - > 60 yo - early in non-invasive stages (good for treatment) - RF: smikonig, aniline
later stages, they can grow into the uterus/rectum - Metastases in small pelvic nodes and to unusual localisations
Clinically: hematuria to blood coagula with obstruction, dysuria
Therapy: resection, cystectomy
Glomerulopathies
Pr-uria / NephrOtic sy
MGN : adult, AI, diffuse glomerular damage w/ deposition in capillaries > thick GBM, unchanged mesangium, not inflammatory - first = segmental later = global - may ass w/ tumor, SLE - can progress to failure
Amyloidosis: AL, AA, hereditary - deposits in GBM, blood vessels
FSGS: idio, here, congestion(hyperten, obesity), HIV, drugs -- detachment of podocytes , obesit
Diabetic
MCD * : children, idio, podocytes distruption, well resp to steroids in children - not progress to failure
Lupus 1 (minimal mesangial GN): detectable by IF
rapid proressing RF *
GN in systemic vasculitis
MPA: less acure, p-acna
E-GPA (Churg-Strauss sy)> rare in kidney
GPA; aggre, c-ANCA Ab, cause ARF & MODS, skin manifes, pulmonary infec, abnorm urine finding
Anti-GBM disease : AI w/ Ab ti Goodpasture Ag in GBM , smoking & infec - Micro: IgG and C3 positive deposits → linear positivity, sickles
Goodpasteur syndrome - kidney and lung involvement
Crescentic IgA nephropathy
Lupus 6 (Advanced sclerosis) : 90% of the glomeruli in global sclerosis
Acute Nephritic sy *
post infec: strep-cocc, children, sever > ARF - nowaday more in elderly, polymorbis alcoholic staph, manifes w/ HF - micro> inflam infiltration of glomerular capillaries
Mem-Proliferative-GN : imm complex deposits, C3 disorders, densa deposit disease - similar morphology to post infec
Lupus 3,4,5 (focal, diffuse, membranous) : 3 < 50% - 4 >50% of all glumeruli
HEAM-uria
IgA nehropathy
Alport sy ; mut in coll 4 , affects eye and ear as well
Lupus 2 (mesanial proliferative GN) : mesangial matrix expansion w/ imm deposits, detec by LM
kidney tumors
RCC
Papillary RCC: often MultiFocal, DCT, less Aggre than clear cell , fewer mts, -------------------- Type 1 : small Baso , Foamy Mf, Cholestrol crystal -------------------- Type 2: Eosino, more Aggre
Chromophobe RCC: intercalated cells of CT - Solid Brown No Hemorrhage Nor Necrosis - micro = pale cells w/ Wrinkles Ncl + large light cells & small dark cells - best prognosis
Clear Cell RCC (most common subtype) : PCT - Yellow Nodular Hemorrhagic CAP - can Invade to pelvises and vessels of hilum . - Delicate vasculature ("chicken-wire") - poor prognosis ------------------------------------------------------- mts to lungs, lymph nodes, skin, neck, face , More organelles → worse differentiation → worse prognosis
☠️ Sarcomatoid Dedifferentiation : Any RCC subtype can undergo this transformation, becomes HG Aggre asso w/ poor prognosis
mostly from tubular epithelial cells, Czech highest incidence globally, always sporac, no causitive gene known - RF> obesity, lifestyle, hyperten, chronic dialysis
Benign
Renal Oncocytoma: Brown tumor w/ a central stellate scar - oncocytes (eosin cytoplasm, many mitocho, small roud ncl), surgery
Papillary Adenoma : Small (≤1.5 cm), multiple, non-sheathed often found in end stage kidneys
Angiomyolipoma: PEComa (tumour arising from perivascular epithelioid cells) , can be within tuberous sclerosis , Benign but tends to spread renal v. → heart - risk of hemorrhage
Wilms Tumor (Nephroblastoma): <5yo, mut in WT1, large abdo mass, good prognosis (chemo, surgery),
-------------------------------------------- Triphasic histology: blastema, epithelial, and stromal components
Tubulointerstitial diseases
Acute tubular necrosis (shock kidney) : caused by ischemia or nephrotoxins > Leads to tubular cell death, especially in PCT and thick ascending limb
Infectious nephritis: ascending infections, possibly septic embolization in IE, E. coli, Enterobac, Kleb, Proteus, staphcocc, pseudomo
Non-infectious nephritis (IgG4, Sjorgen's sy, sarcoidosis) : AI or inflammmatory > Leads to chronic inflammation and tubule damage
Obstruction - postrenal/intrarenal (cast in myeloma) > tubular cast obst > hydronephrosis, interstitial inflammation, fibrosis
Metabolic disorders - Urate nephropathy : Acute = in tumor lysis sy - chronic = part of gout ,, deposition of tophi (nodular urate) in intersti of medulla, fibrosis
Toxic damage - chemotherapy, lead, ethylene glycol
Drugs: ATB, NSAR, diuretics
Analgesic nephropathy: Chronic NSAID , phenacetin , paracetamol > hyali of vessels > necrotic papillae > obstruction > hydronephrosis - risk of urothelial carcinoma
Herbal / Balkan nephropathy ; Aristolochic acid - Cortical fibrosis, atrophy - alkaloid in slimming teas
Increased glomerular cellularity,
mesangial expansion,
endocapillary proliferation,
sickle formation
hematuria, pr uria, hyperten
Micro: fibrinoid necrosis
→ GBM ruptures → sickles