[PATHO] ASSESSMENT 1 REVISION Flashcards
Bilateral suppurative inflammation of pelvicalyceal system
pyelonephritis
gross picture of pyelonephritis (4)
1-inflamed pelvicalyceal system
2-suppuration foci
3-yellow streaks radiating from papillae
4-abscesses in cortex
MICRO picture of pyelonephritis (3)
1-parenchyma congested & infilt by neutrophils
2-neutrophils collect in interstitium & tubular lumen forming 3-abscesses
fever, rigors
frequency, dysuria
loin tenderness
proteinuria
RBCs cast
inflamed pelvicalyceal system
suppuration foci
congested parenchyma
neutrophilic infiltration
pyelonephritis
obstruction leads to recurrent inflammation & scarring of kidneys
can be bilateral/unilateral obstructive lesion
chronic obstructive pyelonephritis
superimposition of UTI
congenital vesicoureteral reflux and intrarenal reflux
unilateral/bilateral
can lead to chronic renal insufficiency
chronic reflux associated pyelonephritis
GROSS picture of chronic pyelonephritis (4)
-uneven scarring of kidneys
-scarring of pelvicalyceal system
-papillary blunting
-calyceal deformities
MICRO picture of chronic pyelonephritis (7)
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
CRF
uremia
bacteriuria
polymorphs
casts
proteinuria
hypertension
calyceal destruction & deformities
thyroidization of tubules
Pink PAS+Ve casts
pyelonephritis
-replacement of papillae with caseous material
-caseating granulomatous inflammation
-sterile pyuria
-hematuria
-mild proteinuria
TB pyelonephritis
Pink PAS +ve casts
chronic pyelonephritis
thyroidization of tubules
chronic pyelonephritis
loins tenderness
pyelonephritis
calyceal destruction & deformities
pyelonephritis
sterile pyuria
TB pyelonephritis
-IgE mediated inflammation
-eosinophilia
-eosinophilic casts
-fever
-skin rash
-follows use of antibiotic, diuretics
drug induced interstitial nephritis
eosinophilic casts
drug induced interstitial nephritis
-papillary coagulative necrosis
-necrotic yellow-brown papillae
-CRF
-HTN
-anemia
-follows use of analgesics
analgesic nephropathy
injury caused by covalent binding & oxidative damage
analgesic nephropathy & drug-induced interstitial nephritis
MC cause of acute renal failure
acute tubular necrosis
IgE mediated damage
drug induced interstitial nephritis
papillary coagulative necrosis
analgesics nephropathy
WBCs cast
pyelonephritis
oliguria
uremia
fluid overload symptoms
patchy all throughout
necrosis of PCT epithelial cells
proteinaceous casts
interstitial edema
anoxic acute tubular necrosis
oliguria
uremia
fluid overload symptoms
patchy distally
diffuse proximally
necrosis of PCT epithelial cells
proteinaceous casts
interstitial edema
toxic acute tubular necrosis
fluid overload symptoms
acute tubular necrosis
symmetrically contracted kidneys
red brown kidneys
diffusely granular
glomeruli scarring
complete glomerulosclerosis
tubular atrophy
proteinuria
HTN
azotemia
nephrotic symptoms
microscopic hematuria
poor prognosis
chronic kidney disease
diffuse mesangial matrix increase
GBM thickening
proteinuria
can lt nephrotic $
associated w/ long standing diabetes
diffuse diabetic glomerulosclerosis
hyaline nodules in mesangium containing lipid & fibrin
proteinuria
can lt nephrotic $
associated w/ long standing diabetes
nodular diabetic glomerulosclerosis
(Kimmelstiel-Wilson lesion)
diabetes mellitus may lead to (4)
diabetic glomerulosclerosis
arteriolosclerosis
papillary necrosis
pyelonephritis
pale eosinophilic deposits detected by congo red
proteinuria
GBM destruction by amyloid fibrils
nephrotic $
amyloid nephropathy
Dna-anti DNA complexes
lupus nephritis
eosinophilic deposits detected by congo red
amyloid nephropathy
Kimmelstiel-Wilson lesion
nodular diabetic glomerulosclerosis
proliferation of endo,epi & mesangial cells
subendothelial deposits
granular IF
necrosis
hematuria
nephritic + nephrotic $
HTN
CRF
DNA-anti DNA complexes deposits
lupus nephritis
cause of death in lupus nephritis
renal failure
IF of lupus nephritis
granular
most Igs
all complements
Class I lupus nephritis
minimal mesangial LN
Class II lupus nephritis
mesangial proliferative LN
Class III lupus nephritis
focal LN
Class IV lupus nephritis
diffuse LN
Class V lupus nephritis
Membranous LN
Class VI lupus nephritis
advanced sclerosing LN
most serious and commonest form of lupus nephritis
Class IV
involves >50% of glomeruli
hypercellularity
capillary wall thickening
leukocytes
crescents
wire loop appearance
DNA-anti DNA complexes
Class IV lupus nephritis
wire loop appearance
Class IV lupus nephritis
basket weave appearance
Alport’s $
Tram Train appearance
Membrano-Proliferative GN
highly selective proteinuria
minimal change GN
non-selective proteinuria
FSGs
MGN
responds to steroids
minimal change GN
resistant to steroids
FSGs
MGN
hemopytsis
Good pasture’s $
fibrinoid necrotizing arteriolitis
malignant nephrosclerosis
fibrinoid necrosis of small BV
intravascular thrombosis
hyperplastic arteriolosclerosis
necrotizing glomerulitis
petechial hemorrhages
malignant nephrosclerosis
flea bitten appearance
malignant nephrosclerosis
onion skin appearance
malignant nephrosclerosis
papilledema
encephalopathy
RF
BP >200/120
uremia
hyperplastic arteriolosclerosis
fibrinoid necrotizing arteriolitis
necrotizing glomerulitis
flea bitten & onion skin appearance
malignant nephrosclerosis
death in malignant nephrosclerosis occurs due to
uremia (90%)
cerebral Hgs/ Heart Failure (10%)
medial & intimal thickening
hyalinization of arteriolar walls
contracted kidneys
finely granular cystic outer surface
irregular cortical atrophy
loss of demarcation b/w cortex & medulla
benign nephrosclerosis
decreased urine conc
decreased GFR
mild proteinuria
hyaline arteriosclerosis
fibroelastic hyperplasia
contracted kidneys
irregular cortical atrophy
thickening +hyalinization
benign nephrosclerosis
supersaturation of urine
changes in pH
bacterial infection
renal colic
hematuria
squamous metaplasia
stricture formation
malignant transformation
urolithiasis
incomplete obstruction in urolithiasis can lead to
hydronephrosis
hydroureter
complete obstruction in urolithiasis can lead to
calculous anuria
chronic irritation of epithelium in urolithiasis can lead to
1-squamous metaplasia
2-malignant transformation
1ry
rough spiky
hard
dark brown-black
radio opaque
oxalate stones
1ry smooth
yellow-brown
stag horn
hard
radio transulcent
urate stones
2ry
radio opaque
smooth
large
stag horn
friable
chalky white
phosphate stones
rare
pale-yellow stones
cystine stones
large lobulated kidney
pelvicalyceal dilation
tubular & glomerular atrophy
fibrosis
may remain silent or lead to CRF
hydronephrosis
polycystin-1 gene defect
ADPKD
fibrocystin gene defect
ARPKD
loin pain
hematuria
HTN
markedly enlarged heavy kidneys
multiple fluid containing cysts
no intervening parenchyma
Circle of Willis aneurysm
ADPKD
liver cysts
multiple small cysts in cortex & medulla
sponge like appearance
death from renal/liver failure
ARPKD
hypercellularity
neutrophils + leukocytes
RBCs cast
subepithelial humps
granular IF
child
following skin infection
acute post infectious GN
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
acute post infectious GN
MC cause of recurrent hematuria
IgA nephropathy (Berger’s)
MC glomerular disease
IgA nephropathy (Berger’s)
male
10-29 yo
hematuria
following URT
genetic susceptibility
(+) alternative complement system
IgA aggregates in mesangium
granular IF
IgA nephropathy (Berger’s)
IF: IgA, IgG, IgM, C3
IgA nephropathy (Berger’s)
IF: IgG & C3
Cresentric GN
IF: IgG & complement
acute post infectious GN
Membranous GN
IF: IgG, C3, C1q, C4
Type II MPGN (C3GN & DDD)
Foamy MQs
FSGs
SYSTEMIC
purpuric rash
abdominal pain
arthritis
hematuria
IgA deposition in mesangium
HSP: Henoch-Schonlein Purpura
sensorineural HL
lens dislocation
posterior cataract
corneal dystrophy
IV collagen mutations
alternating thin & thick areas of GBM
Basket weave appearance
Alport’s $
MC cause of familial hematuria
Thin BM disease
X linked or AD IV collagen mutation disease
Alport’s $
AR IV collagen mutation disase
Thin BM disease
Males
5-20 yo
persistent hematuria
proteinuria
progress to RF
tubular atrophy
glomerulosclerosis
interstitial fibrosis
Hereditary nephritis
severe GBM destruction
escape of fibrin into Bowman’s space
parietal epithelial cells proliferation
Cresentric GN
associated w/ lung affection
immune mediated
normocellular tufts
linear deposits
cross reaction w/ alveolar BM
Type I crescentric GN (anti GBM)
associated w/ post-streptococcal infection, SLE etc.
immune mediated
hypercellularity
leukocytic infiltration
linear deposits
Type II crescentric GN
component of ANCA associated vasculitis
normocellular tufts
interstitial granulomas
necrotizing vasculitis
NO deposits
Type III crescentric GN (Pauci-immune)
enlarged kidneys
petechial Hgs
proteins in tubules
RBCs cast
severe HTN
proteinuria
increased BUN
rapidly progressive azotemia
abrupt anuria
oliguria
Crescentric GN
fibrin deposits in Bowman’s space
Crescentric GN
petechial Hgs seen in
Malignant nephrosclerosis
Crescentric GN
Type I crescentric GN IF
LINEAR
IgG, C3
Type II crescentic GN IF
granular
IgG, C3
Type III crescentic GN IF
NEGATIVE
edematous interstitium
capsular epithelium proliferation
parietal cells proliferation
breaks in GBM
segmental capillary necrosis
fibrin deposits in bowman’s space
Crescentric GN
hemoptysis in crescentric GN is seen in
Type I (anti-GBM/Good pasture’s $)
hematuria
dysmorphic RBCs
RBCs cast
oliguria
azotemia
HTN
mild periorbital edema
Nephritic $
Heavy proteinuria
Hypoalbuminemia
Generalized edema
Hyperlipidemia
Lipiduria
Nephrotic $
enlarged pale yellow tinged kidneys
hyaline droplet degeneration
vacuolar degeneration
Protein casts
interstitial edema
fusion, effacement of foot processes
Nephrotic $
kids
benign
autoimmune
hyaline tubular degeneration
vacuolar tubular degeneration
interstitial edema
effacement
highly selective proteinuria
responds to steroids
-ve IF
minimal change GN
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
FSGs
Adults
slowly progressive
isolated proteinuria
resistant to steroids
non-selective proteinuria
PLA2R autoantibodies
(+) C5b-9 MAC & (+) TGF
subepithelial SPIKES
diffused foot fusion
MGN
IgM & C3 IF
FSGs
MC cause of nephrotic $ in nondiabetics
MGN
subepithelial humps
post infectious GN
subepithelial spikes
MGN
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
Type I MPGN
intramembranous IC depostis
C3GN
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
C3GN & DDD