Renal 7 Flashcards
morphology of ureteropelvic junction obstruction -> boys more common, left side more common
abn organization smooth muscle bundles, excess stromal deposition in smooth muscle bundles
associated findings with ureteropelvic junction obstruction
agenesis opposite kidney, high ureter insertion
result of ureteropelvic junction obstruction
severe vesicoureteral reflux and hydronephrosis
what occurs in diverticula (uncommon in congenital ureters)
stasis and infection
obstruction of ureter causes these conditions
hydroureters, hydronephrosis, pyelonephritis
intrinsic lesions of ureter obstruction
calculi, blood clots, neurogenic, tumorous masses
extrinsic lesions of ureter obstruction
periureteral inflammations, endometriosis, pregnancy, tumors
autoimmune reaction occurring in late/middle life -> inflammation encasing retroperitoneal structures and causing ureteral obstruction; what medication might trigger this?
sclerosing retroperitoneal fibrosis; ergots, B-blockers
infiltrate/morphology of scerlosing retroperitoneal fibrosis
lymphocyte infiltrate, germinal centers and plasma cells
developmental failure of anterior wall of bladder -> causes communication with exterior
exstrophy
exposed portion of bladder in exstrophy undergoes this; condition has increased risk of this
colonic glandular metaplasia; adenocarcinoma, infection
most common and serious anomaly of urinary bladder -> major contributor to renal infection and scarring
vesicoureteral reflex
developmental membrane in male urethra causing congenital outflow obstruction
posterior urethral valves
lining of urachal cysts; what does carcinoma of this tissue resemble?
transitional or metaplastic epithelium; colonic adenocarcinoms
can cause bladder obstruction in females -> wall between bladder and vagina is torn so bladder can herniate into vagina
cystocele
progression of bladder obstruction
hypertrophy smooth muscle/wall thickening -> trabeculation (enlarged muscle bundles) -> diverticula formation (crypts…lead to stasis/infection/stones)
morphology of foamy MP found in malacoplakia; what are specific laminated, mineralized concretions bodies found in them
granular cytoplasm, PAS positive, phagosomes w/ bacterial debris; Michelis-Gutmann bodies
condition that has Michaelis-Gutman bodies
malacoplakia
persistant/chronic cystitis in women -> inflammation and fibrosis of all layers of bladder wall
interstitial cystitis
presentation of interstitial cystitis (autoimmune)
severe suprapubic pain, urinary frequency, dysuria w/o infection
morphology of interstitial cystitis
mucosal ulcer, granulation tissue/mast cells, inflammatory cells
common lesions of bladder inflammation -> nests of transitional epithelium growing inward toward lamina propria
cystitis glandularis/cystica
central epithelial cells of bladder transform to these in cystitis glandularis/cystica
cuboidal or columnar lining slitlike spaces (glandularis) or cysts (cystica)
intestinal metaplasia in cystitis glandularis/cystica may give rise to these -> more prominent in inflamed/chronically irritated bladder; what does this increase risk for?
goblet cells; adenocarcinoma
causes of hemorrhagic cystitis
radiation or chemotherapy
immunosuppressed patients and those on long-term antibiotic use may have acute cystitis associated with these organisms
candida and cryptococcus
common presentation of acute cystitis
urgency, frequency, suprapubic pain
morphology of chronic cystitis
heaping of epithelium, red/friable/granular surface, fibrous wall thickening, could have aggregates of lymphoid follicles (in follicular cystitis)
tumor cause by Schistosomiasis hematobium (common in Middle East)
squamous cell carcinoma (from metaplasia)
conditions that are related to adenocarcinoma cancer of bladder/lower urinary
cystitis glandularis/cystica, exstrophy, urachal remnants
genetic alteration in small, low grade tumor of transitional cell carcinoma
deletion 9p and 9q, loss tumor suppressor gene
deletion of tumor suppressor gene on chromosome 9 causes this kind of transitional cell carcinoma
papillary or flat tumors
genetic alterations in high grade, aggressive tumors -> multiple alterations with aneuploid DNA, loss blood group antigens
deletion 17p and loss p53
most common etiology of transitional cell cancer
male, 50-80, industrialized/urban nations
morphology of low grade lesions of transitional cell carcinoma
papillary w/ limited cellular and nuclear pleomorphism
morphology of high grade lesions of transitional cell carcinoma -> 60% mortality in 10 years
papillary or nodular (or both), pleomorphism, anaplasia, loss blood group antigens
most common presentation of transitional cell carcinoma
painless hematuria
transitional cell carcinoma may invade these areas
prostate, seminal vesicles, retroperitoneum
grade of bladder cancer: papillary or flat (both), more extensive growth and invasion of the muscularis -> HIGH risk of invasive disease
3
grade of bladder cancer: papillary and have increased number of TC layers with loss of polarity
2
grade of bladder cancer: similar to solitary papillomas, but have some minor atypic -> low malignant potential
1
result of persistent urinary obstruction
renal atrophy and hydronephrosis
most common causes of urinary obstruction
posterior urethral valves, ureteropelvic junction narrowing, vesicuoreteral reflux
causes of extrinsic urinary obstruction
BPH, normal pregnancy, uterine prolapse and cystocele, tumors
morphology of medullary dysfunction in hydronephrosis (due to protract obstruction)
interstitial fibrosis, distal tubular acidosis, renal salt wasting, loss GFR (LATE)
morphology of chronic hydronephrosis -> due to cortical tubular atrophy
blunting pyramidal apices
morphology of advanced cases of hydronephrosis -> due to striking parenchymal atrophy
obliteration pyramids, thinning of cortex
complete bilateral obstruction of urinary system causes this -> incompatible with long survival
oliguria or anuria
organic matrix of this material makes up 1-2% of all stones by weight
mucoprotein matrix
calcium oxalate stones are associated with this condition
calciuria (not necessarily hypercalcemia)
enteric hyperoxaluria occurs in these individuals -> leads to urolithiasis
vegetarians
condition with calcium oxalate stones in the presence of increased uric acid secretion -> uric acid crystals cause nucleation of calcium oxalate
hyperuricosuric calcium nephrolithiasis
staghorn calculi typically create cast of these; what is the formation of these associated with?
renal calyces; chronic pyelonephritis
cause of ascending infection leading to pyelonephritis in women
Strep faecalis
conditions that can lead to hematogenous route of spread causing pyelonephritis -> non enteric organisms (Staph, TB)
ureteral obstruction, debilitated patients, immunosuppressive thearpy
associated condition with ascending infection leading to pyelonephritis
vesicoureteral reflux
morphology of acute pyelonephritis
patchy interstitial suppurative inflammation, tubular necrosis, abscess with destruction engulfed tubules (glomeruli resistant to infection) -> scarring, cortical depression
complications of acute pyelonephritis
papillary necrosis and pyonephrosis
complication of acute pyelonephritis -> obstruction where suppurative exudate can’t drain
pyonephrosis
area involved in papillary necrosis -> coagulative necrosis
tips or distal 2/3 pyramids
chronic inflammation of tubules and interstitium
chronic pyelonephritis
morphology of chronic pyelonephritis
tubular hypertrophy, dilated tubules with colloid casts (thyroidization), chronic interstitial inflammation/fibrosis -> irregular scarring
infection commonly associated with xanthogranulomatous pyelonephritis -> foamy MP and plasma cells, staghorn calculi formation
Proteus
possible presentations of xanthogranulomatous pyelonephritis
renal insufficiency and HTN, FSGN w/ proteinuria (poor prognostic indicator)
