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87 Cards in this Set

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normal cr values`
1.5 men - av. 1.15
1.2 women - av. 0.95
what conditions lead to low cr valuesx
cirhossis
pregnancy
extremes of age/nutrition
what conditions can increase cr wo changing kidney fc
bactrim
cimetidine
rhabdo
if BUN:Cr ratio <10:1 with normal BUN and urine output
Cockroft and Gault depends on
age
weight
sex
the same Cr will be associated w the worst kidney function in a
old skinny woman
echogenicity in chronic v. acute
normal - acute
increased - chronic
granular casts
ARF
waxy casts
CKD
factors that elevate BUN only
corticosteroids
GI bleeding
catabolism
increased protein intake
prerenal v ATN
urine Na
FENA
BUN/Cr
urine specific gravity
urinary sediment
pre v ATN
<20 >40meq/L
<1% >3%
<15:1 normal
>1.015 1.010
none granular
calculated FENA
Clna/Clcr = (Una/Pna)/(Ucre/Pcre)
vasodilates aff a
PGE2
vasoconstricts eff a
ANG II
what drugs contraindicated in prerenal
ANG II, ACEi bc shift autoregulation curve to the right --> fall in GFR
Rx for prerenal azotemia
give volume, manage K (with Ca)
types of ATN
ischemic (80%) in outer medulla PT (pars recta and TALH)
toxic PT (pars convoluta)
common causes of toxic ATN
aminogylcosides, amphotericin, IV contrast, Cis Platinum
criterion for HRS
hepatic failure, portal htn
kidney disease (cr 1.5< or cl<40
no proteinuria
no improvement w volume expansion
2nd hit in hrs
something that causes
most often bacterial peritonitis
pvr in hrs
LOW bc glucagon and NO dilate splanchnic bed
mech of glucagon
inhibits effect of AII and NE to VC splanchnic bed
HRS
why do kidneys fail in HRS
low blood flow (bc of sym activation) and glomeruli shrink (bc mesangial cells contract)
contraindicated in HRS
NSAIDs and ACEi
DX of HRS
Cr hard to interpret bc low baseline with cirrhosis
same Na profile as prerenal BUT wont respond to volume
Rx of HRS
glucagon ANT
TIPs - shunt from portal circulation of systemic--> reduced portal HTN
effect of pregnancy on:
GFR
Cr
tract
size
SVR
Na
acid/base
increases substantially
low
dilates
larger
reduced (relaxin)
hyponatremia
alkalosis (respiratory bc of progesterone)
gestational diabetes inspididus mech:
placenta makes vasopressinase bc destroy ADH --> DI
definition of gestational HTN
AFTER 20 WEEKS, HTN wo Proteinuria
definition of pre-eclampsia
AFTER 20 WEEKS, HTN W PROTEINURIA
mech of pre-eclampsia
cytotrophoblast fails to invade --> failure of development of capacitanc vessles (spiral arteries) and instead become resistance vessels
SS of pre-eclampsia
edema, headaches, visual disturbances, abd/chest pain
labs for pre-eclampsia
increased Cr (>.8), proteinuria, thrombocytopenia (<100,000)
risk factors for pre-eclampsia
1st pregnancy
multiple gestations
hydatiform mole
pre-existing vascular disease
metabolic syndrome
thrombophilia
Path of pre-eclampsia
glomerular endotheliosis
Rx for preeclampsia:
lower bp to <110
NEVER USE ACEi, ARBs (bc teratogenic)
chinese herb nephropathy
agent
mech
loc
effect
aristolochic acid
permanent DNA damage, inhibit tubular protein reabsorption
PT
increased risk for uroepithelial chancer
--> chronic tubulointerstitial fibrosis
St. John's Wart
induced p450 pathway
grapefruit juice
inhibits p450 pathway
star fruit
agent:
effect:
oxalate
stones
ephedra
alpha-adrenergic Ag --> stones
noni juice
lots of K
licorice
inhibits 11-beta hydoxysteroid dehydrogenase pathway
allows cortisol to bind to ALDO receptors --> "aldo-like" effect
lots of Na reabsorption, loss of K
Lead
exposure:
effect:
location:
DX:
RX:
lead-based paints, ammunition, home-brewed ETOH
acute: FANCONI SYNDROME
Chronic: GOUT, HTN, CKD
PT
DX: bones scans, chelation test
RX: chelation if caught early
Cadmium
exposure:
outcome:
Rx:
mining, fish, cigarettes
CKD, HTN, OSTEOPEROSIS
Rx: none
Fanconi's syndrome:
impaired reabsorption at PT -->:
1) type II RTA
2) reduced reabsorption of all major electrolytes at PT
conductive transfer
diffusion, only in dialysis
convective transfer
ultrafiltration, in dialysis and normal pts
hyaline casts
benign finding
hydrophilic drugs have a __ Vd
small
hydrophobic drugs have a ___ Vd
large
drugs with a lot of receptor binding have a ___ Vd
very large
more difficult to dialyze a drug if...
has a high Vd
lots of protein binding
large
water soluble
effect of CKD on protein binding
reduced (ex of dilantin)
effect of CKD on p450
slows it down
effect of 50% saline
--> ECFV expansion and reduced Na
calculate osmolarity/tonicity
osm = 2*na+glu/18+BUN/3
ton+ same-BUN (bc exerts no force)
Causes of hyponatremia
increased water intake or impaired exretion
reduced GFR
CHF
nephritic syndrome
cirrhosis
adrenal insufficiency or hypothroidism
thiazides
SIADH (CNS, pulmonary, nausea and pain, nicotine, drugs)
effect of rapid Na correction in chronic hyponatremia
osmotic demyelination syndrome
for every 100mg/dl increase in glucose, Na changes...
decreased by 1.6
in correcting Na, never exceed
12meq/24hrs
important pharmalogical cause of nephrogenic diabetes insipidus
Li
in assessing hypernatremia, low urine osmolarity suggests
water diuresis (central or nephrogenic --- central responds to ADH given to pt)
which types of stones are radio-opaque
calcium oxalate
cystine
triple phospahte
ca-phosphate
which stones are radio-lucent
uric acid, xanthine, ephedrine
which stones are in acidic urine
calcium oxalate, uric acid, cystine
which stones are in basic urine
the phosphates, triple and ca
crystal of ca oxalate
envelopes/dumbbells
crystals of uric acid stones
rhomboids/stellate
crystals of cystine stones
benzene rings
crystals of triple phosphate stones
coffins
epitaxy
growth of one crytsal over another type of core
% of ppl w ca-oxalate stones who have high Ca
1/3
how to reduce Ca levels in ppl with Ca-oxalate stones
reduced Na intake
how to avoid excess oxalate
avoid things with Vit C and oxalate
high uric acid most often -->?
ca-oxalate (epitaxy)
to rx cystine stones
alkanalize the urine
triple phosphate stones associated with
urease producing infections
AG =
Na - Cl - HCO3
causes of AG acidosis
A MUD PIES

ASA
methanol
uremia
diabetic ketoacidosis,
phenformin or paraldehyde
idiopathic
lactic acidosis
ethanol or ethylene glycol
causes of non-AG acidosis
RTA (II-PT, I-DT)
severe diarrhea
early renal failure
causes of metabolic alkalosis
vomiting
diuretics
primary or secondary hyperaldosteronism
microalbuminuria important bc tells
early kidney damage in DM
risk factor bc of endothelial dysfunction
confounders for dipstick
concentrated urine
infection
hematuria
fatty casts
glomerular disease
oval fat bodies
glomerular disease
kidney responsible for following as endocrine orgin
reinin
ANG II
EPO
1,24 (OH)2 D3
which 3 secondary GNs have low complement?
PSGN
MPGN
Lupus