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Renal Path MC > Renal 7 > Flashcards

Renal 7 Flashcards

1
Q

morphology of ureteropelvic junction obstruction -> boys more common, left side more common

A

abn organization smooth muscle bundles, excess stromal deposition in smooth muscle bundles

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2
Q

associated findings with ureteropelvic junction obstruction

A

agenesis opposite kidney, high ureter insertion

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3
Q

result of ureteropelvic junction obstruction

A

severe vesicoureteral reflux and hydronephrosis

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4
Q

what occurs in diverticula (uncommon in congenital ureters)

A

stasis and infection

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5
Q

obstruction of ureter causes these conditions

A

hydroureters, hydronephrosis, pyelonephritis

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6
Q

intrinsic lesions of ureter obstruction

A

calculi, blood clots, neurogenic, tumorous masses

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7
Q

extrinsic lesions of ureter obstruction

A

periureteral inflammations, endometriosis, pregnancy, tumors

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8
Q

autoimmune reaction occurring in late/middle life -> inflammation encasing retroperitoneal structures and causing ureteral obstruction; what medication might trigger this?

A

sclerosing retroperitoneal fibrosis; ergots, B-blockers

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9
Q

infiltrate/morphology of scerlosing retroperitoneal fibrosis

A

lymphocyte infiltrate, germinal centers and plasma cells

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10
Q

developmental failure of anterior wall of bladder -> causes communication with exterior

A

exstrophy

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11
Q

exposed portion of bladder in exstrophy undergoes this; condition has increased risk of this

A

colonic glandular metaplasia; adenocarcinoma, infection

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12
Q

most common and serious anomaly of urinary bladder -> major contributor to renal infection and scarring

A

vesicoureteral reflex

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13
Q

developmental membrane in male urethra causing congenital outflow obstruction

A

posterior urethral valves

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14
Q

lining of urachal cysts; what does carcinoma of this tissue resemble?

A

transitional or metaplastic epithelium; colonic adenocarcinoms

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15
Q

can cause bladder obstruction in females -> wall between bladder and vagina is torn so bladder can herniate into vagina

A

cystocele

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16
Q

progression of bladder obstruction

A

hypertrophy smooth muscle/wall thickening -> trabeculation (enlarged muscle bundles) -> diverticula formation (crypts…lead to stasis/infection/stones)

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17
Q

morphology of foamy MP found in malacoplakia; what are specific laminated, mineralized concretions bodies found in them

A

granular cytoplasm, PAS positive, phagosomes w/ bacterial debris; Michelis-Gutmann bodies

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18
Q

condition that has Michaelis-Gutman bodies

A

malacoplakia

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19
Q

persistant/chronic cystitis in women -> inflammation and fibrosis of all layers of bladder wall

A

interstitial cystitis

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20
Q

presentation of interstitial cystitis (autoimmune)

A

severe suprapubic pain, urinary frequency, dysuria w/o infection

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21
Q

morphology of interstitial cystitis

A

mucosal ulcer, granulation tissue/mast cells, inflammatory cells

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22
Q

common lesions of bladder inflammation -> nests of transitional epithelium growing inward toward lamina propria

A

cystitis glandularis/cystica

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23
Q

central epithelial cells of bladder transform to these in cystitis glandularis/cystica

A

cuboidal or columnar lining slitlike spaces (glandularis) or cysts (cystica)

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24
Q

intestinal metaplasia in cystitis glandularis/cystica may give rise to these -> more prominent in inflamed/chronically irritated bladder; what does this increase risk for?

A

goblet cells; adenocarcinoma

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25
Q

causes of hemorrhagic cystitis

A

radiation or chemotherapy

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26
Q

immunosuppressed patients and those on long-term antibiotic use may have acute cystitis associated with these organisms

A

candida and cryptococcus

27
Q

common presentation of acute cystitis

A

urgency, frequency, suprapubic pain

28
Q

morphology of chronic cystitis

A

heaping of epithelium, red/friable/granular surface, fibrous wall thickening, could have aggregates of lymphoid follicles (in follicular cystitis)

29
Q

tumor cause by Schistosomiasis hematobium (common in Middle East)

A

squamous cell carcinoma (from metaplasia)

30
Q

conditions that are related to adenocarcinoma cancer of bladder/lower urinary

A

cystitis glandularis/cystica, exstrophy, urachal remnants

31
Q

genetic alteration in small, low grade tumor of transitional cell carcinoma

A

deletion 9p and 9q, loss tumor suppressor gene

32
Q

deletion of tumor suppressor gene on chromosome 9 causes this kind of transitional cell carcinoma

A

papillary or flat tumors

33
Q

genetic alterations in high grade, aggressive tumors -> multiple alterations with aneuploid DNA, loss blood group antigens

A

deletion 17p and loss p53

34
Q

most common etiology of transitional cell cancer

A

male, 50-80, industrialized/urban nations

35
Q

morphology of low grade lesions of transitional cell carcinoma

A

papillary w/ limited cellular and nuclear pleomorphism

36
Q

morphology of high grade lesions of transitional cell carcinoma -> 60% mortality in 10 years

A

papillary or nodular (or both), pleomorphism, anaplasia, loss blood group antigens

37
Q

most common presentation of transitional cell carcinoma

A

painless hematuria

38
Q

transitional cell carcinoma may invade these areas

A

prostate, seminal vesicles, retroperitoneum

39
Q

grade of bladder cancer: papillary or flat (both), more extensive growth and invasion of the muscularis -> HIGH risk of invasive disease

A

3

40
Q

grade of bladder cancer: papillary and have increased number of TC layers with loss of polarity

A

2

41
Q

grade of bladder cancer: similar to solitary papillomas, but have some minor atypic -> low malignant potential

A

1

42
Q

result of persistent urinary obstruction

A

renal atrophy and hydronephrosis

43
Q

most common causes of urinary obstruction

A

posterior urethral valves, ureteropelvic junction narrowing, vesicuoreteral reflux

44
Q

causes of extrinsic urinary obstruction

A

BPH, normal pregnancy, uterine prolapse and cystocele, tumors

45
Q

morphology of medullary dysfunction in hydronephrosis (due to protract obstruction)

A

interstitial fibrosis, distal tubular acidosis, renal salt wasting, loss GFR (LATE)

46
Q

morphology of chronic hydronephrosis -> due to cortical tubular atrophy

A

blunting pyramidal apices

47
Q

morphology of advanced cases of hydronephrosis -> due to striking parenchymal atrophy

A

obliteration pyramids, thinning of cortex

48
Q

complete bilateral obstruction of urinary system causes this -> incompatible with long survival

A

oliguria or anuria

49
Q

organic matrix of this material makes up 1-2% of all stones by weight

A

mucoprotein matrix

50
Q

calcium oxalate stones are associated with this condition

A

calciuria (not necessarily hypercalcemia)

51
Q

enteric hyperoxaluria occurs in these individuals -> leads to urolithiasis

A

vegetarians

52
Q

condition with calcium oxalate stones in the presence of increased uric acid secretion -> uric acid crystals cause nucleation of calcium oxalate

A

hyperuricosuric calcium nephrolithiasis

53
Q

staghorn calculi typically create cast of these; what is the formation of these associated with?

A

renal calyces; chronic pyelonephritis

54
Q

cause of ascending infection leading to pyelonephritis in women

A

Strep faecalis

55
Q

conditions that can lead to hematogenous route of spread causing pyelonephritis -> non enteric organisms (Staph, TB)

A

ureteral obstruction, debilitated patients, immunosuppressive thearpy

56
Q

associated condition with ascending infection leading to pyelonephritis

A

vesicoureteral reflux

57
Q

morphology of acute pyelonephritis

A

patchy interstitial suppurative inflammation, tubular necrosis, abscess with destruction engulfed tubules (glomeruli resistant to infection) -> scarring, cortical depression

58
Q

complications of acute pyelonephritis

A

papillary necrosis and pyonephrosis

59
Q

complication of acute pyelonephritis -> obstruction where suppurative exudate can’t drain

A

pyonephrosis

60
Q

area involved in papillary necrosis -> coagulative necrosis

A

tips or distal 2/3 pyramids

61
Q

chronic inflammation of tubules and interstitium

A

chronic pyelonephritis

62
Q

morphology of chronic pyelonephritis

A

tubular hypertrophy, dilated tubules with colloid casts (thyroidization), chronic interstitial inflammation/fibrosis -> irregular scarring

63
Q

infection commonly associated with xanthogranulomatous pyelonephritis -> foamy MP and plasma cells, staghorn calculi formation

A

Proteus

64
Q

possible presentations of xanthogranulomatous pyelonephritis

A

renal insufficiency and HTN, FSGN w/ proteinuria (poor prognostic indicator)

Renal Path MC (5 decks)

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