Exam 2.2 Flashcards
1
Q
Pre-renal charc.
A
Stenosis cirrhosis NSAIDS heart fail. Vol. depletion
2
Q
Renal artery stenosis-causes
A
MC=Atheroscerlosis
Fibromuscular dysphasia
-incre. sm. wall
-congenital
3
Q
Renal Stenosis-blood flow and kidney P.
A
Narrow lumen=decre. blood flow to kid
-incre. fibrosisi/sm. muscle in T. media
P. in kid. is decre.
4
Q
Which syst. is activated in renal artery stenosis
A
renin angiotensin syst.
-help incre. P. and incre. BF to kid.
5
Q
Renal artery stenosis-s/s
A
Renal HTN
Kid. Injury
6
Q
Renal stenosis-tx
A
Ace inhib. or stunt
7
Q
Juxtaglomerular (JG) app @ vascular ple
A
Spec. cell (modif. sm. muscle)
-produce renin
8
Q
Macula Densa detection and cell type
A
Detect ions
Densly packed cell and alter vessle in DST
9
Q
ID OF Elevated Arteriole P. and correct prob.
A
Incre. GFR=change ionic conce.
-decre Na/Cl resabsop.
-dect. by macula densa
Relase vasoactive compound constrict. arteriole=decre. GFR
10
Q
ID decre. Arteriole P. and correct issue
A
JG cells
corected by renin (aspartyl protease) and +RAA
11
Q
angiotensin I
A
Potent vasoconstric. Stim. adrenal gland=relase aldosteron -Na/H2o absopt. in tubuls and ducts -incre. BV=incre BP Incre. BP=NO renin release
12
Q
Intrarenal
A
Vascular(sclerosis and vasculitis) -Nephrosclerosis Glomerular=membrane damage -nephrotic -nephritic Tubular(cancer, toxic inju, ionic homeos) -acute pyelonephritis -water intoxication -acute/chronic kid. injury
13
Q
Nephortic syndrome-dis.
A
Minimal changes dis.
Membranous nephropathy
14
Q
Nephritic syndrome dis.
A
Post-streptococcal glomerulonephritis(acute porliferative glomerulonephritis)
Goodpasture syndrome
Crescentic glomerulonephritis
15
Q
Nephrosclerosis-BV
A
Sclerosis of arterioles and small arteries w/in kid.
16
Q
Nephrosclerosis can cuase or cuased by AND why
A
HTN
- hyalinzation of vessel walls
- genetics, age, gen. HTN
17
Q
Patchy atrophic ischemia is in?
A
nephorscerlosis-depend on which BV b/c dwnstream affected areas
18
Q
Nephorscerosis-glomerular changes
A
partial or total sclerosis
- GBM damage
- collagen in bowman’s space
- fibrosis around capsule
19
Q
lost of tubules in which dis.
A
nephrosclerosis
20
Q
nephrosclerosis=vessel walls
A
Hyalinization
- fibrin leaks through endoth.–>BV wall
- histologically sm. eosinophilic memb. appearance
21
Q
nephrosclerosis clinical sysmp.
A
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
22
Q
Causes/ immune causes of glomerular damage
A
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.
23
Q
Location of glomerular memb. damage
A
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
24
Q
Minimal-change dis.
A
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
25
Memb. Nephropathy
Diffuse thickening of cap.
-Ig depositis or self-antBD
Ig Activation complement
Attack podocyte allowing protein leakage
26
Memb. Nephrpathy-clinical
Sudden onselt
| and nephrotic
27
Post-streptococcal glomerulonephritis AKA
acute proliferative glomerulonephritis
| ALSO-membranoproliferative glomerulonephritis
28
post-stre. glomerulonephritits antBD recog.
streptococcal protein antBD recog. glomerular proteins
| Complement activation=infiltration of PMN and other leukocytes
29
Post-strep. glomerulonephriits immune response
induce cell proliferation in glomerulus
-incre. glomerulul celularity
deposiit in subendothelial space, memb., subepithelial space
30
GPS need a combo of what
renal fail and pulmonary hem.
31
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
```
32
GPS-pareital epith. cell
Transdiff. producing replace. of podocyte
| -immune reposne=necrosis in glomerulus
33
GPS-clinical
Hemoptysis
Hematuria
Nephrotic synd.
34
GSP-TX
Plasmapheresis removing antBD and immune suppression
35
Crescentic Glomerulonephritis AKA
Rapidly progresive glomerulonephriits (RPGN)
36
Crescentic Glomerulonephritis-clinic
Rapid loss of renal function
Porlif. of parietal cells of bowman's memb.
-induce by MAC (monocyte chemotaxis)
37
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
```
38
Nephritic-charact.
Glom. inflam.
Prolif. change and leakage infiltration
Proteinuria and edema (less severe)
39
Nephritic clinic
Hematuria
Oliguria(decre. urin production) w/ azotemia (incr. N w/in blood)
Proteinuria
HTN
40
Nephritic-MC
immunological-mediated glom. injury
- acute postinfect. glomulonephritis
- Rapid progressive glomerunephritis (RPGEN)=cresecentric lesion
41
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
42
Tubulointerstitial nephritis is what type of infection
renal infection
43
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
```
44
ionic homeostasis is balance b/w what
cation and anions
45
what does balancing cation and anions in ionic homeostasis
Maintain pH
Ion conc. maintain osmolarity
-necessary for function maintained @ correct conc.
Excretion match intake
46
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)
47
H2O intoxication aka
H2O poisonings/fatal hyponatermia
48
Max of H2O the body can hold
16ml
49
when does hypotonic ECF
cont'/cell swell due to H2O uptake coping w/
50
s/s of H2O intox.
incre. H2O in cell
| CNS N. swell=convulsion, coma and die
51
AKI MC
acute renal failure
52
does AKI of tubular injury
yes-->acute tubular injury
| Result from glomerular, interstitial or vascular injury
53
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
```
54
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
55
AKI-tx
Address cause to stop futher damage
AntBT=not 2ry infection
Diuretics=flush out kid.
Dialysis
56
Chronic Kid. Injury-MC
DM
Other
-HTN
-glomerulonephritis (endpt. of all chronic renal pranchymal dis.)
57
Chronic kid. injury-seen in
Sig. decre. GFR/albuminuria for 3 mo.
- irreversible tubular cell lost
- AKI resolve via region
58
chronic kid. injury -tx
Changes in diet, lifestyle to prevent damage
| Serious=dialysis or transplant
59
Chronic kid. injury-path.
biochem marker or changes blood/urine composition
60
aki-damage distribution
```
Ischemic
-Necrotic is Patchy=PCT/PST and little w/in distal
-Cast-distal
Necrotic
-Necrotic all over PCT/PST
-Cast=distal
```
61
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
62
incre. necrosis in PCT than distal
Incre. mitochondial for E needs
| Incre. microvillie b/c incre. SA
63
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
```
64
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
65
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)
66
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
67
Obstructive uropathy and type
post renal
| Kid. stone
68
Kid. stone MC site and cause
```
MCsite=collecting system
-renal pelvis and calyces
Causes
-genetics
-dehydration
-dietary intake
-Hormonal imbalance (parathyroid tumor)
```
69
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
```
70
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)
71
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
```
72
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)
```
73
types of cystitis
acute=pmn infiltrate
| chronic cystitis
74
bladder infection is known as
cystitis
75
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
```
76
Cystitis triad s/s
freq. (15-20 min.)
lower abdo pain
dysuria(pain/burining upon urination_
77
cystitis-bact.
MC=E.coli
Proteus
Klebsiella
Enterobacter
78
cystitis predisposing factors
Bladder stones
Obstruction(uremia)
DM
Immune def.
79
can pyelonephritis precede cystitis
infect. w/in bladder-->ureter=infect kid.
