W8. glomerulonephritis and interstitial nephritis Flashcards

1
Q

nephrotic syndorme
- charcateristic
-why

A

-MACROPROTEINURIA
-watery, mineral, protien and lipid metabolism
-hypoalbuminemia
-edema-esp preorbital, anasarca
-hyperlipidema
-dysproteinemia
-little/no hematuria
-HYPER coaguable state

-why:dearrangment in glomerular capp walls –>^permeability to plasma proteins

explenation:
1. Hypoalbumin: excessive protein loss in urine
2. Edema: fluid retention bc low albumin lvls reduce plasma oncotic pressure
3. Hyperlipidemia and hyperproteinemia: liver compensation for loss of protein by lipids and proteins–>^chol and protein profile
4. hypercoaguable state: loss of anti coagulated protein in urine

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2
Q

Nephritic syndrome characteristic and why

A

characteristic:
-HEMATURIA
-proteinuria
-hypertension
-oliguria(decreased urine output)
- decresed glomerular filtration
-edema, maybe anasarc

why: infla pf glomeruli

explanation:
Post-strep inf–> decreased filtration=>decresed urine output +fluid retention->fluid overload(retention of Na+H2O->^BV->^BP)–>^BP–>act RAAS–>vasoconstriction+Na retention–>^BP

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3
Q

cystic and developmental diseases classificaiton: in amount of renal tissue

A
  1. uni/bilat hypoplasia
  2. renomegaly
  3. supernumerary kidneys
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4
Q

cystic and developmental diseases classificaiton: in position, form, orientation

A
  1. pelvic kidney
  2. horseshoe
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5
Q

cystic and developmental diseases classificaiton: in differentation

A

cystic disease of kidney

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6
Q

renal aplasia

A

også kalt AGENESIS

  • congenital ABSENCE of kidney/s
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7
Q

renal hypoplasia

A

smaller kidneys, fewer nephrons but normal

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8
Q

renal dysplasia

A

malformed rneal tissue elements

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9
Q

renal hypodysplasia

A

small kidney + displastic

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10
Q

uni or bilat renal hypoplasia: cause

A

-deficit in renal parenchyma(functional part-aka nephrons)
- unilat: maybe asymptomatic
- bilat: renal insuficency/failure

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11
Q

uni or bilat aplasia: who

A

unilat
-1:1000 newborns
-males
-Left kidney
-baby: one umbilical artery

bilat:
- 1:3000 newborns
-oligohydroamnios

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12
Q

bilat agenesis/oligohydramnios/anhydramnios

A

cause:
1.bilat agenesis–>kidney fail to develop in fetis
2. lead to severe oligohydramnios(very low amniotic fluid bc fetal urine is major source of amniotic fluid) (imp bc cushion of fetus, LUNG development, prevent compresison of body
3. decrased fluid–>fetal compression and underdeveloped lungs aka pulmonary hypoplasia–>resp failure

other characteristic:
-low set ears
-broken nose
-epicanthanic folds +downward slant to eyers
-limb deformitis

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13
Q

potter sequences: subtypes

A
  1. associated with AR polycystic kidney
  2. kidney displasia
    -cystic and immature structuren in parenchyma
    -from obst of urinary tract
  3. AD polycystic kidneys
  4. ureter obstruction and hydronephrosis
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14
Q

autosomal recessive polycystic kidney disease- ARPKD /infant PKD(IPKD)
- what
- causes
-clinical
-histo

A

WHAT
-pkhd1 gene mutaiton
-both kidneys-infancy /early childhood

CAUSES what:
-cystic dilation of the collecting ducts
-affectc bile ducts–>congenital hepatic fibrosis

clinical
- oligohydramnios
-potter
- resp distress syndorme(bc underdeveloped lungs)
-RNEAL& PUL faiuler
-heptic fibrosis–>senere hypertension w splenomegaly

Histo:
-radially aranged cysts from dilated collecting ducts/tubules+cuboidal/low columanr epo
-cyst+protal fibrosis in liver
-enlarged kidney w smooth outer surface
-normal number of neprhons
-no normal renal parnechyme

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15
Q

ADPKD-adult /autosmal dom
-what
-clinical
-organs involved

A

what:
-more coomon
-PKD1
- 3rd most common leading to ESRD

clinical:
-cyst in ALL PARTS of nephron,irr, lobulated
-normal renal funciton to 40/50y
-asymp
-kidney enlarge

Histo:
- dilation of renal tubules and bowmans capsule
-large and numerous, randomly distributed
-fluid filled
-ead no pehroclerosis/scarrring,

Når cystene vokser–>ødellegger renal parnechyme–>interstitial fibrosis, tubular atrophy, loss of normal glomeruli

organs:
-cysts in liver, pancrea, spleen, lung, pineal gland
-berry aneurims—>burst–>stroke
-heart issue and hypertension

SÅ HUSK,
AR: in collecting ducts
AD: alle parter an nephrons

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16
Q

aquired cystic kidney disease-ACKD
-who
-hsito

A

who: basically old tired kidneys-funker ikke
-patient with hemo/periotneal dialysis
-long standing uremia’

histo:
-scarring
-hyperplasia(Cells try to repair
- crystals
-cysts

"Worn-out kidneys make cysts"	Long-term damage + dialysis
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17
Q

solitary renal cysts

A

-random cyst in one spot
- helaty people

histo:
-thin wall+flat cells
-clear fluid
-

"One simple water bubble"	Harmless, common, found by chance
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18
Q

kidney insufficency percentage

A

how much nephron is obliterated
50%-decreased kidney capasity
75: kidney insufficienct
90:kindey faukure
95: end stage kidney

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19
Q

cuases of kidney insufficcy

A

hypertension
DM
polycytsic kindey diases
glomerulonephritis
recurrent TIN

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20
Q

manifestation of kindey insufficency

A

urmeic
extrarenal

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21
Q

multicystic dysplastic kindey (MCDK)
-what happens
-uni/bilat
-microscopically

A

-kdiney badly formed of dont work
-irr cysts, diff sizes
-destroyed parnechyma
-urine flow blocled
-

uni–>removed–>good
bilat–>not working–>no urine–>oligohydraminios–>potter, also death/transplant

micro
-undiff mesenchyme
-uvanlig å se: smooth m, cartilage, abnormal collecting ducts
-flattend cuboidal epi
-CT around cysts not nephrons -uvanlig
-glomeruli and yubules missing/underdevelopned

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22
Q

medullary spongy kidney
-what
-causes

A

qhat
-collecting fucts in meddulla are dilated–>tiny cysts
-AD
-enlarged or nomrla, shrunk

causes
-hematuria-bc fragile cysts
-recurrent kidney stones (dilated duct–>collect CA–>stone
-UTI

how it looks
-darkened medullary areas
-cyst trap urine–>stones and inf risk

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23
Q

glomerulonephritis stages

A
  1. glomerulus damage-permebaility increase
  2. infla of mesangium
  3. mesangiail and endotheilial prolif, thickening of BM
  4. hyalinzation and sclerotisation
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24
Q

primary GN: intrinsic to kindey

A

acute gn(post streptococcal, non streptococcal

prolif
- post infection GN
-rapid progressisive gn
-membranoprolif GN
-lgA glomerulopatho

Non prolif:
-minimal chnage disases
-mebmbranous gn
-focal scelosing gn

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25
acute (post strep k, non strep)
-s.pyogenes, impetigo ==>impetigo, pharyngitis -ASLO deposits in glomeruli-->act of acute infla reaction->prolif of cellular elements -a-hemolytic, hypersens 3 micro: -hypercell+enlarged glomerulus - edema -subepi depocite : starry sky grnular apeare BM +mesanigial skin and throath children
26
lga nephroptahy
-lga AB in glomerulus -henoch schonelin purpura-HSP: skin rash, arthirtis, abd pain, young adults -asym hematuria and proteinura - micro: prolif of mesangium w lga deposits, nephropathy-->is impacted--Zpersistent -->overprod of lga
27
rapid progressive glomerulonephritis: types
-cresent shape in Bowmans space - aggressive Type 1: goodpasture sundrome (anti GBM diseasee) -lgG attack BM of glomeruli -lungs maybe involved ->pulmonary hemorrhae -aka goodpasture=glomeruli+gas exchange Type 2: immune complex mediated -SLE, lga nephropathy, post inf gn -compelx stuck in glomeruli-->infka type 3: pauci immune(no complexes visible -ANCA associated vasculitis: - micro: -focal rupture of glomerular capp walls -fubrin exsudate leak into bowman-->endothelial prolif&mononuclear infiltartion-->cresents(prolif +fibrin) - cresent compress glomerular cpp-->dec filtration, increased pressure, kidney failure
28
membraniprolif glomerulonephritis/membranous nephropathy: primary
-30-50y -idiotpathyc
29
membraniprolif glomerulonephritis/membranous nephropathy:
-immunedeposits in walls of glomerulus ->infla ->structural changes -inlfamed and damaged BM-->^permebility and proteins-->urine-->nephrotic syndrome -nephritic syndrome også micro -increased cellularity->glomerulaus thickened + BM alterations(Also thickened - double contour(tram tarck) -thickened cap loops Type 1: immune complex mediated - in mesangium and subendo -triggere complememnt activation - SLE(lupus), Hepatitis B/C, monoclonal gammopathy type 2:dense deposit disease - abnormal act of alternative complement pathway - dense ribbon like deposits in GBM - c3 glomerulopathy type 3: - subepi and subendo locaiton !MPGN = Proliferative + thick BM + immune complexes Can be both nephritic + nephrotic Seen in infections (HBV, HCV), lupus, and complement disorders!
30
focal segmental glomeruloscelosis
-nephrotic syndrome -heroin abuse, HIV, unknown -certian foci of glomeruli micro: partial sclerotication of glomeruli in varoius extent -hyalination of feeding arterioles but no ^in nr of cells aka non-prolig
31
membranous glomerulonephritis
-patho material/chnages in BM -nephritic /nephrotic syndrome -inlfamed and damaged BM-->^permebility and proteins-->urine-->nephrotic syndrome -damaged from immunecomplexes: auto AB attack GBM hvem :30-50y hsito: -Bm thickening -no prolif=no ^in cellularity -IF: diffuse lgG deposits - subepi immunoglobulin containing deposits -spikey/holey apperance primary: idopathic sec: - autoimmune conditions, infections, drugs, inorganic salts, malignant tumors
32
focal LGN
class 3 <50% of glomeruli
33
thin basement membrane disease
-AD herediatry -thinned glomerular basal memrbane -hematuria and proteinuria
34
hypertension-how it damages the kidney -pressure -injury -ischemia
1. ^pressure in blood vessle - constant pressure-->dmaage small vv-->increase permeability-->firbinogen leak-->trigegr infla and scarring 2. endothelial injury -cells damaged-->microthrombi + fibronoid necrosis 3. ischemia -dmaaged veessles-->porr supply-->RAA trigger-->hypertension worse-->kidney failure
35
secondary gomelerulonephrtiis
lupus nephritis diabetic nephropathy amyloidosis polyarthritis nodosa wegeners granulomatosis
36
lupus nephtritis/SLE
-autoimmuen disease - women, 40y -bytterfly rash -include skin, joints, lungs, cns, indey -interstitial NPHRITIS, nephrotic syndorme and membranous GN
37
diabetic nephropathy
-chronic high blood sugar (hyperglycemia) damage-->progressive protein leakage-->kindey failure -glycemia-->BM thick and dysfunctional-->proteins acc under epi -loss of neg chatrge in bm cant repel the proteins so albumin leak-->microalbunemia and macro - podocyte damage-->BM exposed-->srick to Bowmans-->focal segmental glomeruloscelosis - small vv in kidney damaged-->hyalinosis and arteriosclosis chaaracteristic -kimmel stiel -wilson nodules Mnemonic: "HAG-PK" Hyperglycemia Albuminuria (micro → macro) Glomerulosclerosis Podocyte damage Kimmelstiel-Wilson nodules
38
amyloidosos
-abnormal deposits of protiens -feet, ankles, calves swell -kidney smalla nd hard -cholestrol elevation and proteiunuria congored, thioflavin, schema
39
polyarthitis nodosa
-40-50 -men - hepatitis b , unkoen renal a vasculitis-->proteinuria, imparied kidney function and hypertension - polymorphonuclear leukocytes
40
wegeners grnaulomatosis
-nose, lungs, kidneys, and others -micro hematuria and proteiuria -kindey failure if not trated
41
diffuse process
whole kidney oarenchyme
42
partial/focal process
part pf parenchyme but involve all structural components
43
concrete indicidual parts
44
acute tubular necrosis -ATN
-tubule and surroindign interstitial tissue become inflamed or damaged from toxins or low BF cause 1.ischemia(low BF) -hypovolemia -low perfusion-->tubules dont get enough oxy-->cell death -get shock kidney: aka enlarged, odematous kidney, pale corte and dark medulla, focal tubuular necoriss, 2. toxic damage -antibiotis, antiviral, NSAIDS, chemo drugs, heavy metals, endogenous substnced - get toxic kidney: tubular vacuolization and dilation mciro: -abnormal tubule strucyrie->flattened, ruptures, missing nuclei -necrosis -
45
acute tin chaarcteristics
interstitial edema, neutrophils, focal tubular necorsis, hyepremaia, leukocyte
46
chronic tin
mononuclear infla, interstitial fibrosis, tubualr atrophy
47
infectionus tin
-most common -bacteria, viruses, parasites ASCENDING ROUTE: common -vesicouretral reflux, obstructive nephropathy HEMATOGENOUS: - bacteria to kidney-sepsis
48
acute infectious tin/acute pyelonephritis -what -route -signs and synptoms
suppurative/pus formin infection f kidney in collecting system and interstitium - ascending UTI, catetrization, hydronephrosis, pregnancy, hematogenous -e.coli - nephritis, necrosis, absess -recurrent attacks of acute IN-->chornic signs and symptoms -costovertebral angle pain and fever -symptoms of systemic infection or UTI -pyuria, WBC in urine
49
acuyt inf TIN -macro -complications -micro
-enlargment fo kidney - focal abscessin og bilat kidney and renal cortex -wedge shaped area of suppuration, radial yellow stripes complications -mucosa inflamed and edomatous -abscesses overlalt micro: -pathy, diffuse suppurativ einfka -intersitital ededma -neutrophils -tubular necrosis -abscess -normal glomeruli and vv -paipllary coagulative necorsis
50
chronic infectionus tin/chronic pyelonephritis -what -cause
-infka w renal scarring -calyces and pelvis-deformation , scarrring an datrophy -recurrent attack of IN cause: 1. refluc: childhood, uni/bilat, infection: calcyecael dilation (functional changes-->urine flow stopped+^pressure-->dilation of calcyeal and pelvis 2. obstruction: hydronephrosis signs: -in apparent -advace
51
micro of chronic inf tin
-destroyed parenchyme w fibrosis -tubular dialtion and atrophy - tubular thyroidization -interstitial inflamamation -obliterative endarteritis -later glomeruli hyalinization(aka thickened capsul and periglomerular fibrosis)
52
xanthogranulomatous tin
normal chronic tin w ^macrophages macro - multiple yellow nodules around calyces-->tumorus mass and maybe infiltartice micro: - foamy macrophages-hsitiocytes -multinuclear giant cells -lymphoplasmatic infilatraiton -some neutro
53
sepcific (TB) tin
primary and secondary macro: -multiple yellow nodues - isolaated noduel-aka granuloma: casefication, colliquation micro: -caseous necrosis + giant langerhans cells
54
toxic tin
durgs, poisons, heavy metals
55
abakfetuc induced tin: phenacetin kdiney
-80% women -kidney dont concenrate urine, renal stones -anaemia UTI, HT -necrosis of papils -chronic TIN
56
ACUTE DRUG INDIUCED INTERSTITIAL NEPHRITIS
hypersens 4 RASH, FEVER, ESOSINOPHULIA, HEMATURIA, MILD PROTEINUNARIA, RISING CREATINE
57
acute toxic tubular necroris
-procimal concoluted tubule morphology: -enlarged and edomatous kidney -extensive necrosis of tubular cells -fatty chnage, balloning, hydropic chnages, calcium oxolate cyrstals
58
metabolic tin causes
urate nephropathy hyeprcalcemia nephropathy plasmatic myeloma
59
cause sof obstructive uropathy w hydronephrosis
stones prostatic hypertrophy tumors infla normal pregnancy uterine prolapse pain due to distention of collecting system or renal capsuel
60
bstructive uropathy-urolithiases -who -what happens - uni or lat
-males, 20-49y -^conc of metabolitc substarte, decreses urine volume or deficit of crystal inhibitors in urine -80% uni -pain and hematuria -mocturia, polyuria->after relief -hydronephrosis=cystic dialtion f renal pelvis and calyces associated with progressive atrophy of kidney bc of obstructive uropathy
61
hydronephrosis: sign and symtoms
flank pain palpable mas nause and vomiting UTI fever painful urination ^urinary frequency and urgency
62
mciro hydronephrosis
early -dilated tubules -atrophy and firbous replacement of epi later: -atrophy an disappering of glomeruli -thin , fibrous shell remains of parenchyme
63
bilateral hydronephrosis
-obst below ureter -complete obs: anuria, bladde robstruciton -incompleted: fysfunctionaø tubular -no treat: uremia and renal failure
64
unilat:
obstru above bladder - incomplete: enlargement, atrophy and compression of parenchyme. papilla diminshes and flattened pyramids -complete: glomerular filtartion and decreased renal function. hydroureter complication: coagulative necosis of papillae and pyelonephritis
65
arterioscleotic nephroscleosis-beining
-red GFR or proteinuria macro: -little shrunken kindyes -grnaular cortical surface +smal cysts micro: - ats plaques -initmal and medial dystrophic hcnages -intimal prolif w fibroplasia, irr thickening of intima -chirnic infla reactions
66
pediatric tumors:
-nrphroblastoma-wilsm tumors 99% -congenitalmesoblastic nephroma -neuroblastoma -metnephric stromal tumors -clear cell sarcoma -ossifying renalt umor of infancy -renal cell carcinoma -rhabdoid tumor
66
malignant nephroscleosis
-young people-malignant hypertension -^permeability of vascular wall for fibrinogen -damage of endo micro: fibrinoid necrosis -hemorrhages
67
nephroblastoma-wilms tumors
-most common in children -on of most common tumor in infancy -90% bfore 6y -large abd mass, -MTS to lung or traumatic ruoture -spred into perrenal soft tissue -from nephrogenic blastoam cells-small blue cell triphasic tumor: 1-undiff blastema 2. fibroblast like stroma 3. eoi
68
epi tumors-bening
rare 1. papillary cortical adneoma 2. oncocytoma-peculiar
69
epi tumors-malingnat
1.clear cell carcinoma-renal cell carcinoma . MOST common and malingnant 2.papillary carincoma -intermediate malingnacy 3. chromophobe carcinoma- highest risk of recurrency 4. sacromatoid carcinoma
70
mesenchymal and mixed tumors
1. angiomyolipoma-most common, mixed 2.leiomyoma 3.lipoma 4. mixed epi and stromal 4. primitive neuroepi tumors (PNET)|
71
childhood tumors
nephroblastoma-wilsms clear cells sarcoma anaplsatic sarcoma
72
secondary malignnat
mts of lungs, thyroid, breast carcinoma, CRC
73
Renal cell cardinoma -who -why dangerous -symptoms
who: adult over 50y, males more dangerous - detected incidentally(bc it doesnt innercate kidney parenchyme -shen it invade UT: hematuria -when renal capsule: discomfort clincial -costrovertebral oain -palpamble mass hematuria mTS: lungs, bones, LN, adrenals , liver, bra
74
sarcomatoid (renal cell)carcinoma
1% of renal tumors in adults -act of MET gene -age 60y -MTS ti lungs -poor prognosis -spindle girantl cells, resemble sarcoma
75
angiomyolipoma-
-peculiar macro: -red, gray-white, yellow -may inavede LN and renal vain -capsular invasion 25% micro -triphasic tumors
76
clear cell renal cells carcinoma/grawits -risk factor -why the name clear cell -mciro -MTS -symotoms
risk: smokin, obesity, hypertension -others: APKD, renla cystic dissde WHY called: -high glycogen and lipid content-->yellowish-orange appearnce mcrio: -weel circusided, yellow -show hemmprhage, necrosis, calcification, cystic degeneration, renal vein thrombosis mts: lung, LN, liver, bone, adrenal gland, colat kidney, brian, heart, spleen , intesitne , skin symptoms -hematuria -flank pain -night swats -weight loss
77
papillary (renal cell) carcinoma -macro -mciro -mTS
macro: -red brown color-hemoorahe -multifocal -well circumscribed micro: -papillary/tubulopapillary pattern - foamy macrophage -psammoma bodies -adneomatous chnges in adjacent kindey mts: regional LN
78
chromophobe (renal cell) carcinoma
-cells of this cancer are afriad to be stained by histological staining -good prognnosnis -but high recurrency macro: -weel circumscribed -tan brown -necrosis -small cyst mciro: -nests/broaf alveoli and trabeculae -large polygonal cells with cytopllams and siticnt cell borders -perinuclaer halo -calcification