W8. glomerulonephritis and interstitial nephritis Flashcards
nephrotic syndorme
- charcateristic
-why
-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
Nephritic syndrome characteristic and why
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
cystic and developmental diseases classificaiton: in amount of renal tissue
- uni/bilat hypoplasia
- renomegaly
- supernumerary kidneys
cystic and developmental diseases classificaiton: in position, form, orientation
- pelvic kidney
- horseshoe
cystic and developmental diseases classificaiton: in differentation
cystic disease of kidney
renal aplasia
også kalt AGENESIS
- congenital ABSENCE of kidney/s
renal hypoplasia
smaller kidneys, fewer nephrons but normal
renal dysplasia
malformed rneal tissue elements
renal hypodysplasia
small kidney + displastic
uni or bilat renal hypoplasia: cause
-deficit in renal parenchyma(functional part-aka nephrons)
- unilat: maybe asymptomatic
- bilat: renal insuficency/failure
uni or bilat aplasia: who
unilat
-1:1000 newborns
-males
-Left kidney
-baby: one umbilical artery
bilat:
- 1:3000 newborns
-oligohydroamnios
bilat agenesis/oligohydramnios/anhydramnios
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
potter sequences: subtypes
- associated with AR polycystic kidney
- kidney displasia
-cystic and immature structuren in parenchyma
-from obst of urinary tract - AD polycystic kidneys
- ureter obstruction and hydronephrosis
autosomal recessive polycystic kidney disease- ARPKD /infant PKD(IPKD)
- what
- causes
-clinical
-histo
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
ADPKD-adult /autosmal dom
-what
-clinical
-organs involved
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
aquired cystic kidney disease-ACKD
-who
-hsito
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
solitary renal cysts
-random cyst in one spot
- helaty people
histo:
-thin wall+flat cells
-clear fluid
-
"One simple water bubble" Harmless, common, found by chance
kidney insufficency percentage
how much nephron is obliterated
50%-decreased kidney capasity
75: kidney insufficienct
90:kindey faukure
95: end stage kidney
cuases of kidney insufficcy
hypertension
DM
polycytsic kindey diases
glomerulonephritis
recurrent TIN
manifestation of kindey insufficency
urmeic
extrarenal
multicystic dysplastic kindey (MCDK)
-what happens
-uni/bilat
-microscopically
-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
medullary spongy kidney
-what
-causes
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
glomerulonephritis stages
- glomerulus damage-permebaility increase
- infla of mesangium
- mesangiail and endotheilial prolif, thickening of BM
- hyalinzation and sclerotisation
primary GN: intrinsic to kindey
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