Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

UROGENITAL > [PATHO] ASSESSMENT 1 REVISION > Flashcards

[PATHO] ASSESSMENT 1 REVISION Flashcards

1
Q

Bilateral suppurative inflammation of pelvicalyceal system

A

pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

gross picture of pyelonephritis (4)

A

1-inflamed pelvicalyceal system
2-suppuration foci
3-yellow streaks radiating from papillae
4-abscesses in cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

MICRO picture of pyelonephritis (3)

A

1-parenchyma congested & infilt by neutrophils
2-neutrophils collect in interstitium & tubular lumen forming 3-abscesses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

fever, rigors
frequency, dysuria
loin tenderness
proteinuria
RBCs cast
inflamed pelvicalyceal system
suppuration foci
congested parenchyma
neutrophilic infiltration

A

pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

obstruction leads to recurrent inflammation & scarring of kidneys
can be bilateral/unilateral obstructive lesion

A

chronic obstructive pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

superimposition of UTI
congenital vesicoureteral reflux and intrarenal reflux
unilateral/bilateral
can lead to chronic renal insufficiency

A

chronic reflux associated pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

GROSS picture of chronic pyelonephritis (4)

A

-uneven scarring of kidneys
-scarring of pelvicalyceal system
-papillary blunting
-calyceal deformities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

MICRO picture of chronic pyelonephritis (7)

A

1-uneven interstitial fibrosis
2-lymphocytic, plasma cells, neutrophils
3-tubular dilation
4*Pink PAS +ve casts
*thyroidization of tubules
5-arteriolosclerosis (2ry to HTN)
6-glomerulosclerosis (2ry to nephron loss)
7-inflammation + fibrosis of calyceal wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

CRF
uremia
bacteriuria
polymorphs
casts
proteinuria
hypertension
calyceal destruction & deformities
thyroidization of tubules
Pink PAS+Ve casts

A

pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

-replacement of papillae with caseous material
-caseating granulomatous inflammation
-sterile pyuria
-hematuria
-mild proteinuria

A

TB pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pink PAS +ve casts

A

chronic pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

thyroidization of tubules

A

chronic pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

loins tenderness

A

pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

calyceal destruction & deformities

A

pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

sterile pyuria

A

TB pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

-IgE mediated inflammation
-eosinophilia
-eosinophilic casts
-fever
-skin rash
-follows use of antibiotic, diuretics

A

drug induced interstitial nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

eosinophilic casts

A

drug induced interstitial nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

-papillary coagulative necrosis
-necrotic yellow-brown papillae
-CRF
-HTN
-anemia
-follows use of analgesics

A

analgesic nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

injury caused by covalent binding & oxidative damage

A

analgesic nephropathy & drug-induced interstitial nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

MC cause of acute renal failure

A

acute tubular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

IgE mediated damage

A

drug induced interstitial nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

papillary coagulative necrosis

A

analgesics nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

WBCs cast

A

pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

oliguria
uremia
fluid overload symptoms
patchy all throughout
necrosis of PCT epithelial cells
proteinaceous casts
interstitial edema

A

anoxic acute tubular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

oliguria
uremia
fluid overload symptoms
patchy distally
diffuse proximally
necrosis of PCT epithelial cells
proteinaceous casts
interstitial edema

A

toxic acute tubular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

fluid overload symptoms

A

acute tubular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

symmetrically contracted kidneys
red brown kidneys
diffusely granular
glomeruli scarring
complete glomerulosclerosis
tubular atrophy
proteinuria
HTN
azotemia
nephrotic symptoms
microscopic hematuria
poor prognosis

A

chronic kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

diffuse mesangial matrix increase
GBM thickening
proteinuria
can lt nephrotic $
associated w/ long standing diabetes

A

diffuse diabetic glomerulosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

hyaline nodules in mesangium containing lipid & fibrin
proteinuria
can lt nephrotic $
associated w/ long standing diabetes

A

nodular diabetic glomerulosclerosis
(Kimmelstiel-Wilson lesion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

diabetes mellitus may lead to (4)

A

diabetic glomerulosclerosis
arteriolosclerosis
papillary necrosis
pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

pale eosinophilic deposits detected by congo red
proteinuria
GBM destruction by amyloid fibrils
nephrotic $

A

amyloid nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Dna-anti DNA complexes

A

lupus nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

eosinophilic deposits detected by congo red

A

amyloid nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Kimmelstiel-Wilson lesion

A

nodular diabetic glomerulosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

proliferation of endo,epi & mesangial cells
subendothelial deposits
granular IF
necrosis
hematuria
nephritic + nephrotic $
HTN
CRF
DNA-anti DNA complexes deposits

A

lupus nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

cause of death in lupus nephritis

A

renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

IF of lupus nephritis

A

granular
most Igs
all complements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Class I lupus nephritis

A

minimal mesangial LN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Class II lupus nephritis

A

mesangial proliferative LN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Class III lupus nephritis

A

focal LN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Class IV lupus nephritis

A

diffuse LN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Class V lupus nephritis

A

Membranous LN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Class VI lupus nephritis

A

advanced sclerosing LN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

most serious and commonest form of lupus nephritis

A

Class IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

involves >50% of glomeruli
hypercellularity
capillary wall thickening
leukocytes
crescents
wire loop appearance
DNA-anti DNA complexes

A

Class IV lupus nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

wire loop appearance

A

Class IV lupus nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

basket weave appearance

A

Alport’s $

48
Q

Tram Train appearance

A

Membrano-Proliferative GN

49
Q

highly selective proteinuria

A

minimal change GN

50
Q

non-selective proteinuria

A

FSGs
MGN

51
Q

responds to steroids

A

minimal change GN

52
Q

resistant to steroids

A

FSGs
MGN

53
Q

hemopytsis

A

Good pasture’s $

54
Q

fibrinoid necrotizing arteriolitis

A

malignant nephrosclerosis

55
Q

fibrinoid necrosis of small BV
intravascular thrombosis
hyperplastic arteriolosclerosis
necrotizing glomerulitis
petechial hemorrhages

A

malignant nephrosclerosis

56
Q

flea bitten appearance

A

malignant nephrosclerosis

57
Q

onion skin appearance

A

malignant nephrosclerosis

58
Q

papilledema
encephalopathy
RF
BP >200/120
uremia
hyperplastic arteriolosclerosis
fibrinoid necrotizing arteriolitis
necrotizing glomerulitis
flea bitten & onion skin appearance

A

malignant nephrosclerosis

59
Q

death in malignant nephrosclerosis occurs due to

A

uremia (90%)
cerebral Hgs/ Heart Failure (10%)

60
Q

medial & intimal thickening
hyalinization of arteriolar walls
contracted kidneys
finely granular cystic outer surface
irregular cortical atrophy
loss of demarcation b/w cortex & medulla

A

benign nephrosclerosis

61
Q

decreased urine conc
decreased GFR
mild proteinuria
hyaline arteriosclerosis
fibroelastic hyperplasia
contracted kidneys
irregular cortical atrophy
thickening +hyalinization

A

benign nephrosclerosis

62
Q

supersaturation of urine
changes in pH
bacterial infection
renal colic
hematuria
squamous metaplasia
stricture formation
malignant transformation

A

urolithiasis

63
Q

incomplete obstruction in urolithiasis can lead to

A

hydronephrosis
hydroureter

64
Q

complete obstruction in urolithiasis can lead to

A

calculous anuria

65
Q

chronic irritation of epithelium in urolithiasis can lead to

A

1-squamous metaplasia
2-malignant transformation

66
Q

1ry
rough spiky
hard
dark brown-black
radio opaque

A

oxalate stones

67
Q

1ry smooth
yellow-brown
stag horn
hard
radio transulcent

A

urate stones

68
Q

2ry
radio opaque
smooth
large
stag horn
friable
chalky white

A

phosphate stones

69
Q

rare
pale-yellow stones

A

cystine stones

70
Q

large lobulated kidney
pelvicalyceal dilation
tubular & glomerular atrophy
fibrosis
may remain silent or lead to CRF

A

hydronephrosis

71
Q

polycystin-1 gene defect

A

ADPKD

72
Q

fibrocystin gene defect

A

ARPKD

73
Q

loin pain
hematuria
HTN
markedly enlarged heavy kidneys
multiple fluid containing cysts
no intervening parenchyma
Circle of Willis aneurysm

A

ADPKD

74
Q

liver cysts
multiple small cysts in cortex & medulla
sponge like appearance
death from renal/liver failure

A

ARPKD

75
Q

hypercellularity
neutrophils + leukocytes

RBCs cast
subepithelial humps
granular IF
child
following skin infection

A

acute post infectious GN

76
Q

fever malaise
hematuria
oliguria
HTN
mild edema
mild azotemia
mild periorbital edema
mild BUN increase
smoky urine
increased urine specific gravity
increased ASO
low serum complements
child
following skin infection

A

acute post infectious GN

77
Q

MC cause of recurrent hematuria

A

IgA nephropathy (Berger’s)

78
Q

MC glomerular disease

A

IgA nephropathy (Berger’s)

79
Q

male
10-29 yo
hematuria
following URT
genetic susceptibility
(+) alternative complement system
IgA aggregates in mesangium
granular IF

A

IgA nephropathy (Berger’s)

80
Q

IF: IgA, IgG, IgM, C3

A

IgA nephropathy (Berger’s)

81
Q

IF: IgG & C3

A

Cresentric GN

82
Q

IF: IgG & complement

A

acute post infectious GN
Membranous GN

83
Q

IF: IgG, C3, C1q, C4

A

Type II MPGN (C3GN & DDD)

84
Q

Foamy MQs

A

FSGs

85
Q

SYSTEMIC
purpuric rash
abdominal pain
arthritis
hematuria
IgA deposition in mesangium

A

HSP: Henoch-Schonlein Purpura

86
Q

sensorineural HL
lens dislocation
posterior cataract
corneal dystrophy
IV collagen mutations
alternating thin & thick areas of GBM
Basket weave appearance

A

Alport’s $

87
Q

MC cause of familial hematuria

A

Thin BM disease

88
Q

X linked or AD IV collagen mutation disease

A

Alport’s $

89
Q

AR IV collagen mutation disase

A

Thin BM disease

90
Q

Males
5-20 yo
persistent hematuria
proteinuria
progress to RF
tubular atrophy
glomerulosclerosis
interstitial fibrosis

A

Hereditary nephritis

91
Q

severe GBM destruction
escape of fibrin into Bowman’s space
parietal epithelial cells proliferation

A

Cresentric GN

92
Q

associated w/ lung affection
immune mediated
normocellular tufts
linear deposits
cross reaction w/ alveolar BM

A

Type I crescentric GN (anti GBM)

93
Q

associated w/ post-streptococcal infection, SLE etc.
immune mediated
hypercellularity
leukocytic infiltration
linear deposits

A

Type II crescentric GN

94
Q

component of ANCA associated vasculitis
normocellular tufts
interstitial granulomas
necrotizing vasculitis
NO deposits

A

Type III crescentric GN (Pauci-immune)

95
Q

enlarged kidneys
petechial Hgs
proteins in tubules
RBCs cast
severe HTN
proteinuria
increased BUN
rapidly progressive azotemia
abrupt anuria
oliguria

A

Crescentric GN

96
Q

fibrin deposits in Bowman’s space

A

Crescentric GN

97
Q

petechial Hgs seen in

A

Malignant nephrosclerosis
Crescentric GN

98
Q

Type I crescentric GN IF

A

LINEAR
IgG, C3

99
Q

Type II crescentic GN IF

A

granular
IgG, C3

100
Q

Type III crescentic GN IF

A

NEGATIVE

101
Q

edematous interstitium
capsular epithelium proliferation
parietal cells proliferation
breaks in GBM
segmental capillary necrosis
fibrin deposits in bowman’s space

A

Crescentric GN

102
Q

hemoptysis in crescentric GN is seen in

A

Type I (anti-GBM/Good pasture’s $)

103
Q

hematuria
dysmorphic RBCs
RBCs cast
oliguria
azotemia
HTN
mild periorbital edema

A

Nephritic $

104
Q

Heavy proteinuria
Hypoalbuminemia
Generalized edema
Hyperlipidemia
Lipiduria

A

Nephrotic $

105
Q

enlarged pale yellow tinged kidneys
hyaline droplet degeneration
vacuolar degeneration
Protein casts
interstitial edema
fusion, effacement of foot processes

A

Nephrotic $

106
Q

kids
benign
autoimmune
hyaline tubular degeneration
vacuolar tubular degeneration
interstitial edema
effacement
highly selective proteinuria
responds to steroids
-ve IF

A

minimal change GN

107
Q

any age
HTN
hematuria
non-selective proteinuria
resistant to steroids
poor prognosis
podocyte injury & effacement
hyaline masses in glomeruli
glomerular sclerosis
tubular atrophy
interstitial fibrosis
foamy MQs

A

FSGs

108
Q

Adults
slowly progressive
isolated proteinuria
resistant to steroids
non-selective proteinuria
PLA2R autoantibodies
(+) C5b-9 MAC & (+) TGF
subepithelial SPIKES
diffused foot fusion

A

MGN

109
Q

IgM & C3 IF

A

FSGs

110
Q

MC cause of nephrotic $ in nondiabetics

A

MGN

111
Q

subepithelial humps

A

post infectious GN

112
Q

subepithelial spikes

A

MGN

113
Q

late childhood
poor prognosis
progress to endstage RF
proteinuria
hematuria
combo of nephritic & nephrotic
immune mediated
hypercellularity
increased mesangial matrix
*accentuated lobulation
GBM thickening
Tram track appearance
subendothelial deposits

A

Type I MPGN

114
Q

intramembranous IC depostis

A

C3GN

115
Q

late childhood
rare
poor prognosis
mild proteinuria
hematuria
nephritic OR nephrotic symptoms
complement dysregulation
complement regulatory proteins mutation
*C3Nef autoantibodies
hypercellularity
*accentuated lobulation
*Tram track appearance
*intramembranous deposits

A

C3GN & DDD

UROGENITAL (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions