[PATHO] ASSESSMENT 1 REVISION Flashcards by Aseel Maher

Bilateral suppurative inflammation of pelvicalyceal system

pyelonephritis

How well did you know this?

Not at all

Perfectly

gross picture of pyelonephritis (4)

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

How well did you know this?

Not at all

Perfectly

MICRO picture of pyelonephritis (3)

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

How well did you know this?

Not at all

Perfectly

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

pyelonephritis

How well did you know this?

Not at all

Perfectly

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

chronic obstructive pyelonephritis

How well did you know this?

Not at all

Perfectly

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

chronic reflux associated pyelonephritis

How well did you know this?

Not at all

Perfectly

GROSS picture of chronic pyelonephritis (4)

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

pyelonephritis

How well did you know this?

Not at all

Perfectly

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

TB pyelonephritis

How well did you know this?

Not at all

Perfectly

Pink PAS +ve casts

chronic pyelonephritis

How well did you know this?

Not at all

Perfectly

thyroidization of tubules

chronic pyelonephritis

How well did you know this?

Not at all

Perfectly

loins tenderness

pyelonephritis

How well did you know this?

Not at all

Perfectly

calyceal destruction & deformities

pyelonephritis

How well did you know this?

Not at all

Perfectly

sterile pyuria

TB pyelonephritis

How well did you know this?

Not at all

Perfectly

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

drug induced interstitial nephritis

How well did you know this?

Not at all

Perfectly

eosinophilic casts

drug induced interstitial nephritis

How well did you know this?

Not at all

Perfectly

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

analgesic nephropathy

How well did you know this?

Not at all

Perfectly

injury caused by covalent binding & oxidative damage

analgesic nephropathy & drug-induced interstitial nephritis

How well did you know this?

Not at all

Perfectly

MC cause of acute renal failure

acute tubular necrosis

How well did you know this?

Not at all

Perfectly

IgE mediated damage

drug induced interstitial nephritis

How well did you know this?

Not at all

Perfectly

papillary coagulative necrosis

analgesics nephropathy

How well did you know this?

Not at all

Perfectly

WBCs cast

pyelonephritis

How well did you know this?

Not at all

Perfectly

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

anoxic acute tubular necrosis

How well did you know this?

Not at all

Perfectly

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