Exam 2.2 Flashcards
Pre-renal charc.
Stenosis cirrhosis NSAIDS heart fail. Vol. depletion
Renal artery stenosis-causes
MC=Atheroscerlosis
Fibromuscular dysphasia
-incre. sm. wall
-congenital
Renal Stenosis-blood flow and kidney P.
Narrow lumen=decre. blood flow to kid
-incre. fibrosisi/sm. muscle in T. media
P. in kid. is decre.
Which syst. is activated in renal artery stenosis
renin angiotensin syst.
-help incre. P. and incre. BF to kid.
Renal artery stenosis-s/s
Renal HTN
Kid. Injury
Renal stenosis-tx
Ace inhib. or stunt
Juxtaglomerular (JG) app @ vascular ple
Spec. cell (modif. sm. muscle)
-produce renin
Macula Densa detection and cell type
Detect ions
Densly packed cell and alter vessle in DST
ID OF Elevated Arteriole P. and correct prob.
Incre. GFR=change ionic conce.
-decre Na/Cl resabsop.
-dect. by macula densa
Relase vasoactive compound constrict. arteriole=decre. GFR
ID decre. Arteriole P. and correct issue
JG cells
corected by renin (aspartyl protease) and +RAA
angiotensin I
Potent vasoconstric. Stim. adrenal gland=relase aldosteron -Na/H2o absopt. in tubuls and ducts -incre. BV=incre BP Incre. BP=NO renin release
Intrarenal
Vascular(sclerosis and vasculitis) -Nephrosclerosis Glomerular=membrane damage -nephrotic -nephritic Tubular(cancer, toxic inju, ionic homeos) -acute pyelonephritis -water intoxication -acute/chronic kid. injury
Nephortic syndrome-dis.
Minimal changes dis.
Membranous nephropathy
Nephritic syndrome dis.
Post-streptococcal glomerulonephritis(acute porliferative glomerulonephritis)
Goodpasture syndrome
Crescentic glomerulonephritis
Nephrosclerosis-BV
Sclerosis of arterioles and small arteries w/in kid.
Nephrosclerosis can cuase or cuased by AND why
HTN
- hyalinzation of vessel walls
- genetics, age, gen. HTN
Patchy atrophic ischemia is in?
nephorscerlosis-depend on which BV b/c dwnstream affected areas
Nephorscerosis-glomerular changes
partial or total sclerosis
- GBM damage
- collagen in bowman’s space
- fibrosis around capsule
lost of tubules in which dis.
nephrosclerosis
nephrosclerosis=vessel walls
Hyalinization
- fibrin leaks through endoth.–>BV wall
- histologically sm. eosinophilic memb. appearance
nephrosclerosis clinical sysmp.
ONLY nephrosclerosis=rare for renal fialure
Unresolved HTN=malignant HTN
-w/ diabe. or syst. sclerosis=incre. risk of renal failure
Endoth. damage=prot. leakage/develop clots
-lead to renal ischemia
Aff. arteriol for renin elevation
-fibrionid necorsis and hyperplastic arteriollitis
Causes/ immune causes of glomerular damage
Secondary effects systemic dis. -lupus -DM -amyloidosis -GPS Primary starts in kid. -most primary r immunde dis. Immune causes -Circulating antGN:antBD complexes deposit in filtration memb. -antiBD reacting agaisnt components of the filtration memb.
Location of glomerular memb. damage
Podocyte effacement(podocyte partially sep. from theri BSM but still attached) -minimal change dis. Subepithelial deposits -membranous nephropathy Subendothelial depositis -membranoproliferative glomerulonephritis -GPS -Centric glomerulonephitis Mesangial deposits -IgA nephropathy
Minimal-change dis.
MC w/in children Nephrotic synd. Only visible by TEM Cause=glomerular damage, leakage across filtration memb. Lipoprotein Accum. in PCT -visible lipid droplet -visible prot. accum. w/in tubule
Memb. Nephropathy
Diffuse thickening of cap.
-Ig depositis or self-antBD
Ig Activation complement
Attack podocyte allowing protein leakage
Memb. Nephrpathy-clinical
Sudden onselt
and nephrotic
Post-streptococcal glomerulonephritis AKA
acute proliferative glomerulonephritis
ALSO-membranoproliferative glomerulonephritis
post-stre. glomerulonephritits antBD recog.
streptococcal protein antBD recog. glomerular proteins
Complement activation=infiltration of PMN and other leukocytes
Post-strep. glomerulonephriits immune response
induce cell proliferation in glomerulus
-incre. glomerulul celularity
deposiit in subendothelial space, memb., subepithelial space
GPS need a combo of what
renal fail and pulmonary hem.
GPS-antiBD against
BsM component -anti-GBM in kid.=sever glomerular injury -anti-GBM recog. alveolar BsM :antGN in collagen IV :source of pulmonary hemorrhage
GPS-pareital epith. cell
Transdiff. producing replace. of podocyte
-immune reposne=necrosis in glomerulus
GPS-clinical
Hemoptysis
Hematuria
Nephrotic synd.
GSP-TX
Plasmapheresis removing antBD and immune suppression
Crescentic Glomerulonephritis AKA
Rapidly progresive glomerulonephriits (RPGN)
Crescentic Glomerulonephritis-clinic
Rapid loss of renal function
Porlif. of parietal cells of bowman’s memb.
-induce by MAC (monocyte chemotaxis)
Crescents glomerulonephritis-3 types based on immunological mech.
Anti-GBM antBD mediated si. (GPS) Immune complex deposition (lupus) Anti-PMN cytoplasmic antBD (ANCAs) -idiopathic (limited to kid.) -systemic vasculitis
Nephritic-charact.
Glom. inflam.
Prolif. change and leakage infiltration
Proteinuria and edema (less severe)
Nephritic clinic
Hematuria
Oliguria(decre. urin production) w/ azotemia (incr. N w/in blood)
Proteinuria
HTN
Nephritic-MC
immunological-mediated glom. injury
- acute postinfect. glomulonephritis
- Rapid progressive glomerunephritis (RPGEN)=cresecentric lesion
Neprotic-charct.
Podocyte injury
Immune/not immune causes
Structural/or phyhscicochem changes
Glom. memb. damage incre. perm=plasma prot. leakage
-Massive proteinuria=deplete serum albumin
-Hypoalbminemia=decre. albumin
:decre. osmoP.
:incre. plasma flow into tissue=edema
:edema=decre. osmo P. and compensate w/ aldosteron secretion hypovol.
-hyperlipediemia and lipiduria
Tubulointerstitial nephritis is what type of infection
renal infection
types of inflammation in tubular interstitium and tubules
Acute pyelonephritis -bact. infection -due to UTI Chronic pyelonephritis -hist. of UTI -fibrosis of pelvis and caylx Drug induced -Edema and mononuclear infiltrate into inerstitium -penicillin dervatives other antBT, NSAIDs and among others
ionic homeostasis is balance b/w what
cation and anions
what does balancing cation and anions in ionic homeostasis
Maintain pH
Ion conc. maintain osmolarity
-necessary for function maintained @ correct conc.
Excretion match intake
Body H2O distributed
Total wt=60%
ECF=20%
-plasma/interstial (filtrate plasma and no cell/lrg prot.)
-Na+ and Cl/HCO3
ICF=40%
-K+/mg2+ and prot./organic P(ATP, ADP, AMP)
H2O intoxication aka
H2O poisonings/fatal hyponatermia
Max of H2O the body can hold
16ml
when does hypotonic ECF
cont’/cell swell due to H2O uptake coping w/
s/s of H2O intox.
incre. H2O in cell
CNS N. swell=convulsion, coma and die
AKI MC
acute renal failure
does AKI of tubular injury
yes–>acute tubular injury
Result from glomerular, interstitial or vascular injury
AKI cuases
Ischemia -intrarenal B malfunction -Thromboses -decre. -BV (hemorrhage/sclerosis vasculitis) Direct toxic Injury=antBT, anesthetic, heavy metal, organic solv. Inflam (drug hypersensitivity) Urinary obstruction=tumor, prostatic hypertrophy, blood clot
AKI-pathogenesis
Tubular cell Injruy
-toxic injury=cell incere. sensitivity b/c incre. metabolic req., incre. reab. rate
:incre. absorp rate and conc. capacity
-Ischemic injury
:ischemia=vasoconcstricion in kid.
:incre. sensitivity to lack Nutrients/O2
Disturbed blood flow
-hemodynamic alteration affect GFR
AKI-tx
Address cause to stop futher damage
AntBT=not 2ry infection
Diuretics=flush out kid.
Dialysis
Chronic Kid. Injury-MC
DM
Other
-HTN
-glomerulonephritis (endpt. of all chronic renal pranchymal dis.)
Chronic kid. injury-seen in
Sig. decre. GFR/albuminuria for 3 mo.
- irreversible tubular cell lost
- AKI resolve via region
chronic kid. injury -tx
Changes in diet, lifestyle to prevent damage
Serious=dialysis or transplant
Chronic kid. injury-path.
biochem marker or changes blood/urine composition
aki-damage distribution
Ischemic -Necrotic is Patchy=PCT/PST and little w/in distal -Cast-distal Necrotic -Necrotic all over PCT/PST -Cast=distal
What causes cast in damage distribution in AKI
Prox. tubule damage cell flush down distal tub
- Prot./lipid and lbood cn brk off and seen in necrosis
- judge lumen in distal tube
incre. necrosis in PCT than distal
Incre. mitochondial for E needs
Incre. microvillie b/c incre. SA
Kid. damage clinical manifestation
Na/K homeost. -excess Na+ expand intravascular vol. H2O and A/B balance Urea excretion -decre. excretion=incre. BUN and serum creatinine, producing uremia
S/S kid. damage
Dehydration, edema, hyperKemia
HyperPhosemia, hypoCa2emia, bone/PTH effects
Anemia
HTN, cong. heart failure, cardiac myopathy, pulm. edema, uremic pericarditis
Nasea/vomiting, GI bleeding, stomac/eosphagus/colon inflam
Skin=shallow/prutic dermatitis
-lost color/more flushed
Kid. damage-uremia
Kid failure=accum. of N. waste products due to kid. failure
-der. appetite
-fatique
-neurological/sysmp. (confusion, coma)
-Skin excretion
:uremic frost=white crystal
-Results in hypotension, dehydration or trauma (incre. port. catabolism)
Renal osteodystorphy in kid. damage
kid. dnt activate vit. D w/in skin
-needed for Ca2+/Phosphate absorp
:decre. vit D=no absorb of Ca2+
Decre. Ca2+ plasma=parathryroid hyperplsai
-PTH incre. osteoclast activity
-2ndry hyperparathyroid for bone Ca2+ depletion
Obstructive uropathy and type
post renal
Kid. stone
Kid. stone MC site and cause
MCsite=collecting system -renal pelvis and calyces Causes -genetics -dehydration -dietary intake -Hormonal imbalance (parathyroid tumor)
types of Kid. Stones
MC=Ca2+ -oxalate and/or phosphate salte -benign PTH tumor Uric acid -25% of gout/hyperuricemia pt. -mostly idiopathic Cysteine=children w/ hereditary cystinuria Infection -bacteria cleave urea :proteus or providencia species :produce ammonia -alkaline urine :favors salt despostion :struvite :apatite
Kid. stone-consequences
Obstruction=damage w/in tubules b/c cause incre. intrarenal P.
-damage tissue
-infection or abcess behind stones
:stone press against tissue
pain
-b/c distension of renal capsule, renal pelvis or ureters
-damage to these structure cn cause hematuria (w/in kid. caylx and urters)
kid. stones=Hydroenphrosis
Incre renal P. Expansion of pelvis and caylces b/c ureters or father out -urine cnt expel ourt=back up fluid Calculus cn block ureters -uinlateral block(ureter) -bilateral blockage(bladder/urethra) Cn compress parenchyma and damage it -tubule 1st-->medlaris-->glomeruli -atrophy fibrosisi or scar tissue
Kid. stones-tx
Pain maage Prevent dehydration Shock waves to brkup stones Stent in ureter maintaining patency Prevent new stones from forming -depend on stone type -tx w/ allopurinaol (inhib. purine catabo. to reduce uric acid production)
types of cystitis
acute=pmn infiltrate
chronic cystitis
bladder infection is known as
cystitis
types of cystitis
Bact. infection Hemorrhagic -side effect of cytotoxic chemo. -cn be b/c adenovirus infection Interstitial -Pain when bladder fills -S/S=urgency, hematuria, dysuria Malakoplakia=detects in phagocytic cell (undigested bact. components accum.) Polypoid=look like papillomatous cancer but due to submucosal edema
Cystitis triad s/s
freq. (15-20 min.)
lower abdo pain
dysuria(pain/burining upon urination_
cystitis-bact.
MC=E.coli
Proteus
Klebsiella
Enterobacter
cystitis predisposing factors
Bladder stones
Obstruction(uremia)
DM
Immune def.
can pyelonephritis precede cystitis
infect. w/in bladder–>ureter=infect kid.
