Exam 2.2 Flashcards

1
Q

Pre-renal charc.

A
Stenosis 
cirrhosis
NSAIDS 
heart fail. 
Vol. depletion
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2
Q

Renal artery stenosis-causes

A

MC=Atheroscerlosis
Fibromuscular dysphasia
-incre. sm. wall
-congenital

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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.

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4
Q

Which syst. is activated in renal artery stenosis

A

renin angiotensin syst.

-help incre. P. and incre. BF to kid.

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5
Q

Renal artery stenosis-s/s

A

Renal HTN

Kid. Injury

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6
Q

Renal stenosis-tx

A

Ace inhib. or stunt

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7
Q

Juxtaglomerular (JG) app @ vascular ple

A

Spec. cell (modif. sm. muscle)

-produce renin

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8
Q

Macula Densa detection and cell type

A

Detect ions

Densly packed cell and alter vessle in DST

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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

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10
Q

ID decre. Arteriole P. and correct issue

A

JG cells

corected by renin (aspartyl protease) and +RAA

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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
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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
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13
Q

Nephortic syndrome-dis.

A

Minimal changes dis.

Membranous nephropathy

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14
Q

Nephritic syndrome dis.

A

Post-streptococcal glomerulonephritis(acute porliferative glomerulonephritis)
Goodpasture syndrome
Crescentic glomerulonephritis

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15
Q

Nephrosclerosis-BV

A

Sclerosis of arterioles and small arteries w/in kid.

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16
Q

Nephrosclerosis can cuase or cuased by AND why

A

HTN

  • hyalinzation of vessel walls
  • genetics, age, gen. HTN
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17
Q

Patchy atrophic ischemia is in?

A

nephorscerlosis-depend on which BV b/c dwnstream affected areas

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18
Q

Nephorscerosis-glomerular changes

A

partial or total sclerosis

  • GBM damage
  • collagen in bowman’s space
  • fibrosis around capsule
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19
Q

lost of tubules in which dis.

A

nephrosclerosis

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20
Q

nephrosclerosis=vessel walls

A

Hyalinization

  • fibrin leaks through endoth.–>BV wall
  • histologically sm. eosinophilic memb. appearance
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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

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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.
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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
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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
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25
Q

Memb. Nephropathy

A

Diffuse thickening of cap.
-Ig depositis or self-antBD
Ig Activation complement
Attack podocyte allowing protein leakage

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26
Q

Memb. Nephrpathy-clinical

A

Sudden onselt

and nephrotic

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27
Q

Post-streptococcal glomerulonephritis AKA

A

acute proliferative glomerulonephritis

ALSO-membranoproliferative glomerulonephritis

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28
Q

post-stre. glomerulonephritits antBD recog.

A

streptococcal protein antBD recog. glomerular proteins

Complement activation=infiltration of PMN and other leukocytes

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29
Q

Post-strep. glomerulonephriits immune response

A

induce cell proliferation in glomerulus
-incre. glomerulul celularity
deposiit in subendothelial space, memb., subepithelial space

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30
Q

GPS need a combo of what

A

renal fail and pulmonary hem.

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31
Q

GPS-antiBD against

A
BsM component 
-anti-GBM in kid.=sever glomerular injury 
-anti-GBM recog. alveolar BsM
  :antGN in collagen IV 
  :source of pulmonary hemorrhage
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32
Q

GPS-pareital epith. cell

A

Transdiff. producing replace. of podocyte

-immune reposne=necrosis in glomerulus

33
Q

GPS-clinical

A

Hemoptysis
Hematuria
Nephrotic synd.

34
Q

GSP-TX

A

Plasmapheresis removing antBD and immune suppression

35
Q

Crescentic Glomerulonephritis AKA

A

Rapidly progresive glomerulonephriits (RPGN)

36
Q

Crescentic Glomerulonephritis-clinic

A

Rapid loss of renal function
Porlif. of parietal cells of bowman’s memb.
-induce by MAC (monocyte chemotaxis)

37
Q

Crescents glomerulonephritis-3 types based on immunological mech.

A
Anti-GBM antBD mediated si. (GPS) 
Immune complex deposition (lupus)
Anti-PMN cytoplasmic antBD (ANCAs)
-idiopathic (limited to kid.) 
-systemic vasculitis
38
Q

Nephritic-charact.

A

Glom. inflam.
Prolif. change and leakage infiltration
Proteinuria and edema (less severe)

39
Q

Nephritic clinic

A

Hematuria
Oliguria(decre. urin production) w/ azotemia (incr. N w/in blood)
Proteinuria
HTN

40
Q

Nephritic-MC

A

immunological-mediated glom. injury

  • acute postinfect. glomulonephritis
  • Rapid progressive glomerunephritis (RPGEN)=cresecentric lesion
41
Q

Neprotic-charct.

A

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
Q

Tubulointerstitial nephritis is what type of infection

A

renal infection

43
Q

types of inflammation in tubular interstitium and tubules

A
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
Q

ionic homeostasis is balance b/w what

A

cation and anions

45
Q

what does balancing cation and anions in ionic homeostasis

A

Maintain pH
Ion conc. maintain osmolarity
-necessary for function maintained @ correct conc.
Excretion match intake

46
Q

Body H2O distributed

A

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
Q

H2O intoxication aka

A

H2O poisonings/fatal hyponatermia

48
Q

Max of H2O the body can hold

A

16ml

49
Q

when does hypotonic ECF

A

cont’/cell swell due to H2O uptake coping w/

50
Q

s/s of H2O intox.

A

incre. H2O in cell

CNS N. swell=convulsion, coma and die

51
Q

AKI MC

A

acute renal failure

52
Q

does AKI of tubular injury

A

yes–>acute tubular injury

Result from glomerular, interstitial or vascular injury

53
Q

AKI cuases

A
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
Q

AKI-pathogenesis

A

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
Q

AKI-tx

A

Address cause to stop futher damage
AntBT=not 2ry infection
Diuretics=flush out kid.
Dialysis

56
Q

Chronic Kid. Injury-MC

A

DM
Other
-HTN
-glomerulonephritis (endpt. of all chronic renal pranchymal dis.)

57
Q

Chronic kid. injury-seen in

A

Sig. decre. GFR/albuminuria for 3 mo.

  • irreversible tubular cell lost
  • AKI resolve via region
58
Q

chronic kid. injury -tx

A

Changes in diet, lifestyle to prevent damage

Serious=dialysis or transplant

59
Q

Chronic kid. injury-path.

A

biochem marker or changes blood/urine composition

60
Q

aki-damage distribution

A
Ischemic
-Necrotic is Patchy=PCT/PST and little w/in distal  
-Cast-distal 
Necrotic 
-Necrotic  all over PCT/PST
-Cast=distal
61
Q

What causes cast in damage distribution in AKI

A

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
Q

incre. necrosis in PCT than distal

A

Incre. mitochondial for E needs

Incre. microvillie b/c incre. SA

63
Q

Kid. damage clinical manifestation

A
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
Q

S/S kid. damage

A

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
Q

Kid. damage-uremia

A

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
Q

Renal osteodystorphy in kid. damage

A

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
Q

Obstructive uropathy and type

A

post renal

Kid. stone

68
Q

Kid. stone MC site and cause

A
MCsite=collecting system 
-renal pelvis and calyces 
Causes 
-genetics
-dehydration
-dietary intake 
-Hormonal imbalance (parathyroid tumor)
69
Q

types of Kid. Stones

A
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
Q

Kid. stone-consequences

A

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
Q

kid. stones=Hydroenphrosis

A
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
Q

Kid. stones-tx

A
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
Q

types of cystitis

A

acute=pmn infiltrate

chronic cystitis

74
Q

bladder infection is known as

A

cystitis

75
Q

types of cystitis

A
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
Q

Cystitis triad s/s

A

freq. (15-20 min.)
lower abdo pain
dysuria(pain/burining upon urination_

77
Q

cystitis-bact.

A

MC=E.coli
Proteus
Klebsiella
Enterobacter

78
Q

cystitis predisposing factors

A

Bladder stones
Obstruction(uremia)
DM
Immune def.

79
Q

can pyelonephritis precede cystitis

A

infect. w/in bladder–>ureter=infect kid.