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265 Cards in this Set

  • Front
  • Back
what is normal GFR? how much is reabsorbed per day?
180L/day or 125ml/min
99% are reabsorbed per day
terms for emptying bladder?
site of filtration?
site of reabsorption/secretion?
glomerulus: filtration
secretion/reasorb: tubules
what pH rang is compatible with survival?
7.8-6.8 or [H] =16=160nEq/L
how is the kidney an endocrine organ?
converts 25OH vit D3 to 1,25-OH2 Vit D3 (calcitriol)
stimulates BM to make RBC
secretes renin to a ctivate RAA
how much of the CO does the kidney need and why?
25% b/c all reabsorption requires lots of energy
what is the renal pyramid? what are the parts of it called?
located in medulla
base adjecent to cortex
apex projects as renal papillae into calyx of renal pelvis
what can cause renal papillary necrosis?
sickle cell
urniary obstruction
non steroidal anti inflam drugs
what is the affect of sickle cell disease concerning vasa recta?
decreased concentrating ability
sickling in vasa recta interferes with countercurrent exchange in inner medulla; impair free water reabsorption
net effect=max urine osmolality at age 10 is only 400mOsm/kg
*will have freq b/c they can't concentrate
osmolarity vs osmolality
osMOLARity: #solute particles/L soln (mOsm/L)
osMOLALity: #solute particles/kg solvent (mOsm/kg H20)
if you have 1mmol/L of NaCl how many mOsm/L do you have?
is osMOLARity or OsMOLALity temp dependent?
osmolarity is temp dependent: vol of 1L will increase with increaseing temp
what must happen for a solute toe exert an osmotic pressure across a membrane?
solute must not permeate the membrane
if crosses the membrane like urea, osmotic pressure = 0 b/c osmotic coefficient =0
if impermeable sucrose osmotic pressure =1
what is urine specific gravity?
weight of solution cmopared with that of an eqal vol of distilled water ~ wt of # of particles in solution therefore MW matters
TBW is what percent of body weight?
ECF and ICF are what percent of TBW?
ICF: 2/3 (42)= 28L
ECF: 1/3 (42) = 14L
what are the components of ECF and what percent of TBW are they?
ECF= interstitium and plasma
plasma: 1/4ECF(3.5L) or 1/12 TBW
interstitium: 3/4 ECF (10.5L)
isotonic saline is what?
NS = 154mM=308mEq/L b/c NaCl
if a RBC is placed in NS what happens?
no change in volume b/c soln is isotonic
waht is Lactated Ringers (LR)?
contains K and Lactate
total of 274 mEq/L
lactate is metabolized to HCO3
why is Lactated Ringers not good for person w/ liver failure?
b/c the lactate will metabolize to HCO3
what happens after IL of NS is added?
NS only distributes in ECF b/c isotonic therfore no fluid shift w/ ICF
ECF expands by 1L thefore plasma expands by 0.25L=250mL
NS only distributes in ECF b/c Na is excluded from cells by action of Na/K pump
what is half NS?
77mM = 0.45% (NS 154mM 0.9%)
HYPOtonic soln therefore cells swell
water rushes into ICF until osmolality are equal
in NS and half NS, where does the NaCl go?
NaCl stays in ECF b/c Na excluded from cells by action of Na/K pump
how many mM/L does hypertonic saline add? mOsm?
what percent is NS? 1/2 NS? Hypertonic saline? D5W?
NS: 0.09%
1/2 NS: 0.45% (hypotonic)
hypertonic: 3%
D5W: 5%
is D5W hyper/hypo/isotonic?
isotonic b/c of presence of glucose
you can't infuse plain water into veins otherwise RBC will lyse therefore give D5W
what intially happens when you give pt D5W?
ECF initially expands by 1L (none enters ICF b/c isotonic)
then dextrose is metabolized and the 1L becomes water
the water then distributes throughout TBW
Pvol will expand by 1/4(0.33)=82.5mL
which is better at restoring volume: NS or D5W?
NS expands vol by 350cc while D5W only expands by 82.5cc
if a pt is dehydrated and volume depleted, what saline do you give them first?
give NS to rstore volume then give D5W to Tx dehydration
which saline will you give GI bleeder?
want to give saline that adds volume
NS expans plasma volme the most
packed red cells are the best but it takes long to get them
renal clearance
what is renal clearance?
volume of plasma that the substance has been removed and excreted in urine/time
does clearance take into account reabsorption and secretion?
no only filtration b/c everything that gets into urine was filtered not reabsorbed
how many mL in 1dL?
100 mL = 1 dL
how do you determine the removal rate of a substance from the plasma?
(Px)(Cx) mg/min
P=concentration of x in plama
C=cleareance of x from plasma
how do you determine the excretion rate of a substance from the urine?
UxV mg/min
Ux=conc of x in urine
V=urine flow rate
units of Ux? units of V?
therfore excretion rate units: mg/min
how do removal rate from plasma and excretion rate give you clearance?
removal rate = excretion rate
C=UV/P mL/min
units of clearance/
what does freely filtered mean?
filtered plasma has same concentration as unfiltered plasma
afferent conc = efferent conc
what is the ultrafiltrate?
plasma ultrafiltrate that is filtered through glomerulus into bowman's capsule
free of cellular elements and large proteins
(water, glucose, salt, amino acids, and urea pass freely into bowman's space)
what are some examples of freely filtered substances?
Na, K, Cl
NOT albumin
if freely filtered, what will GFR =?
normal GFR in mL/min and L/day?
filtration fraction =
FF=GFR/RPF = 0.2 most of the time
meaning only 20% of the plasma that is enters the glomerulus is actually filtered
what is filtred load?
amt removed from plasma by filtration
what is the filtered load in idealized substance like inulin?
the removal rate from plasma will = FL
b/c it isn't reabsorbed or secreted
what is the clearance of glucose?
b/c glucose normally doesnt appear in urine, FL must be reabsorbed by tubules therefore C=0
what is fractional excretion?
percent of FL that is excreted in urine
Fractional excretion = excretion rate/FL
what is the fractional excretion of inuline?
fractional excretino = excretion rate/FL
all inuline is excreted therefore = 1
what is the fractional excretion of glucose?
fractional excretion=excretion rate/FL
no glucose is excreted therefore = 0
eqn for FeNa?
FeNa= excretion rate / FL
= Na clearance/Cr clearance *100
when is FeNa impt?
in pts with oliguria
if Fena is <1%=low vascular volume
if FeNa is >2%=ATN
what is the problem in Acute Tubular Necrosis?
tubular cells are deprived of O2 therefore not reabsorbing
why is FeNa low in GI bleeder? compare with ATN
person is volume depleted..cells aren't damaged like in ATN so they reabsorbe Na and H2O leaving a low FeNa
in ATN : FeNa is high b/c tubular cells are damaged and they can't reabsorb Na
GFR ~ ?
GfR ~ Cr clearance
are the following mostly reabsorbed or non reabsorbed?
glucose and amino acids
glucose and amino acids: all or most
inuine: none
creatinine: none (but some secreted)
HCO3: most
CL: most
is PAH completely filtered?
wahtever PAH is not filtered is completely secreted
RPF for PAH is = to?
PAH = RPF b/c PAH delivery to kidney=PAH excretion
what does RBF=
waht is Tm? Tmglucose=
Tm: max reabosortpive capacity/unit time
Tmglucose = 375mg/min (largest FL w/o having glucose spill into urine) but b/c of splay, glucose apppars in urine when plasma glucose exceeds 180-200mg/dL
when does splay change?
when GFR is increased, Increased GFR means increased FL
if you have glucose showing up in the urine, how high is your blood glucose?
must have FL higher than the Tm which is 375
your plasma glucose must be higher than 300mg/dl
what is splay and why does it occur?
premature spilling due to heterogenity of nephrons
*not all nephrons have same Tm b/c not all have the same GFR, If incresaed GFR, more glucose being filtered which means more chance of splay
is BUN a good measure of GFR?
no b/c approx 40-50% of filtered urea is normally reabsorbed by the tubules
what increases Urea prodxn?
when more amino acids are metabolized in teh liver
high protein diet
enhanced tissue breakedown due to trauma
decreased tissue anabolism
what decrease urea prodxn?
severe liver disase
low protein intake
what percent of filtered urea is reabsorbed by tubules?
drived by urea concentration in tubules which is drived by Na/water reabsorption
what happesn to BUN in hypovolemic states?
BUN increases b/c Na and Water reabosorption increases
waht is the normal BUN:plasma creatine ration?
if greater than >20:1 consider enhanced urea prodxn or volume depletion
how do you convert mg/dL to mmol/L?
divide mg/dL by 1/10 MW
to convert mmol/L to mg/dL multiply 1/10 by Mw then multiply that by mmol/L
what are the units of BUN?
how do you estimate the plasma osmolality?
~2*plasma[Na] + glucose/18 + BUN/2.8
when is estimating plasma osmolality useful?
if >25
if diagnosiing suspected methanol and ethylene glucol ingestion in a pt with an unxplanined high anion gap metabolic acidosis
high anion gap with ketoacidosis also
where is creatinine from? what are the normal values for men and women?
men: 0.8-1.3 mg/dL
women: 0.6-1.0mg/dL
creatinine comes from metabolism of creatine in sk muslce
when does plasma creatinine reflect GFR?
only in steady state
if kidney fxn is decreasing, creatine will change
if you have a small change in Pcr what hapens to kidney fxn?
small change in Pcr = big change in kidney fxn (large change in GFR)
if you have a large change in Pcr, what happens to kidney fxn?
large change in Pcr=small change in kidney fxn( small change GFR)
how will the Pcr vs GFR curve shift as muscle mass decreases?
Pcr: y
GFR: x
curve shifts L as muscle mass decreases (elderly)
what is Cr an imprecise measure of GFR?
b/c only works when in steady state
on graph, if small change in Pcr from 1-1.5, large change in kidney fxn
if large change in Pcr from 6-10, small change in kidney fxn
what is the Cockcroft-gault formula used for and what is ti?
estimation of Ccr from Pcr
Ccr = 140-age/Pcr * lean body wt/72 *0.85(if female)
what is the Ccr of 72kg 40 yr man? what will his GFR be if he has bilatereal nephrectomy?
use cockcroft gault formula
Ccr = 100/Pcr
eqn will tell you 100, but b/c he is no longer in steady state the eqn can't be used b/c GFR=0
what is a better estimate of GFR than Pcr?
Cr cleareance: Ccr=UV/Pcr
why can't you use cockcroft -gault formula or any other eqn using Pcr to find Ccr when pt is GI bleeder?
the pt is no longer in steady state
can only determine GFR form Pcr if pt in steady state
if the state they are in their GFR will contine to decrease every day and the plasma Cr will increase b/c no Cr is leaving the body. this will make you change the Tx daily
waht are the limitations to Ccr in estimating GFR?
incomplete urine colections: 24hr urine
if GFR decreases, creatinine secretion increases by 50%
non-Cr chomagens that are measured give rise to falsely high Pcr (acetoacetate in diabetic ketoacidosis)
why do acetone, ascorbic acid or pyruvate not have any affect on Ccr?
b/c even though they increase Pcr by 10-20%, at the same time Cr is secreted normally 10-20% so they counterbalance
what must you normalize GFR to?
BSA by multiplying by 1.73m2
how does filtration occur from the blood pace to the urinary space?
moves b/n endothelial cells w/ fenestrations
across glomerular BM (type IV collagen with high negative charge)
b/n podocytes into urine
waht is Alport's syndrome? inheritance
x linked R
defects in type IV collagen
neural hearing loss
what happens when you lose the negtive charge of the glomerular bM?
albumin cna leadk out
how does ultrafiltation occur?
occurs b/c of starling forces
GFR: kf[(Pgc-Pbs)-(oncoticGC-oncoticBS)}
what does it mean if relfection coeeficient is 0? 1?
o- compltely permeable
1=completely impermeable
waht is the oncotic pressure of Bowmans'?
0 b/c no protein is filtered into BS
how does the oncotic pressure of GC change from afferent to efferent?
increases b/c the ultrafiltrate is protein free which means proteins in GC increase
how does net hydrostatic pressure change?
how does Pgc change from afferent to efferet?
decreases b/c of resistance to flow
what are the 2 ways in which RBF is autoregulated?
myogenic mxn:intrinsic tendency of vascular smoooth mucle to contract when stretched to decrease bld Q
Tubuloglomerular feedback: macula desnsa sense Na load: if Na high then trys to decrease GFR by adenosine which contricts the aff arteriole
what is the action of adenosine?
contricts the aff artertiole to decrease GFR
waht is the JG complex?
consits of macula densa clls in the TAL that stiulate release of renin from JG cells when Na is low
JG cells are modificed smooth muscle cell in aff arteriole that moniter change in BP
result of constricting afferent arteriole?
decrease GFR, decrease RBF, decrease Pgc to oppose filtration and thus reabsorption
action of Pgc?
promote the mvmt of fluid from the glomerular capillary into Bowman's space
*favors filtration
waht are the 2 forces that oppose filtration?
hydrostatic pressure in bowman's capusle
oncotic pressure in GC
when you have high BP what happens to the arterioles?
constrict afferent to decrease GFR, Pgc and RBF
what is the result of constriction of eff areterole?
increase GFR
decrease RBF
increase Pgc
what is the result of dilation of eff?
decrease Pgc
decrease GFR
increase RBF
what is the result of dilation of aff?
increase Pgc
increase GFR
increase RBF
actoin of sym nn on arteroles
releaes NE which causes vasocontrxn of afferent arterioles
decrease GFR
decreae RBF
what is the action of prostaglandins? when do they act?
act only when pt and kideny are severely stressed
oppose systemic vasconstrictors of sym thus prevent harmful renal ischemia
stimulated by low ECF, stress, Ang II
they increase RBF w/o changing GFR
action of NSAIDS as opposed to prostaglandins
ex: ibuprofen
interfere with protective mxn of prostagladns and further decrease RBF
thererfore stop NSAIDS if have severe kidney disease
fxn of NO/
vasodilation of aff and eff
fxn of endothelin?
potent vasoconstrictor of aff and eff in response to Ang II, bradykinin
wht factors can cuase the releaes of NO to cuase vasodilation?
Ach, histamine, bradykinin, ATP, sheer stress
where does the largest pressure drop occur?
aff aterole (#2=efferent)
if eff > aff P GFR increaes
what is occuring in in hemorrhage?
decreased BP stimulates sympathetics
sym cause constxn of renal arterioles
decrease GFR, decrease RBF
decrease renal excretion of Na and H20
decrease Pgc to increase reabsorption
if you increase Pgc what does this mean?
decrease reabsorption
how are proteins reabsorbed and where?
in PT by endocytosis
then metabolized to amino acids, which are then taken up into capillary
what is considred microalbuminuria?
persistant albumin excretion b/n 30-300mg/day
waht is macroalbuminuria?
albumin above 300mg/day
micro: 30-300
nl: <30
at what level does the standard dipstick bcome postive for albumin?
macroalbuminuria levels: above 300mg/day
at this level practically all protein in urine=albumin
what are some limits to standard dipstick detection of proteinuria?
reacts primarily wi/ albumin
does not detect Ig light chains
dipstick will miss microalbuminuria
dipstick measures a CONC of protein not an amt/ day
waht does a dipstick measure?
a concentration of protein, not an amt/day
how will dipstick measuremnt change?
if the urine flow rate changes
increase urine flow rate then protein concentration=mgprotein/urine vol
what is the gold standard for measurement of proteinuria? but what is more convenient than this?
24hr urine but protein:creatinine ratio obtained from random urine is more convenient
what is the avg creatinine excretion?
what is the formula for protein: creatinine ratio to measure proteinuira?
24hr protein excretion/24hr creatine excretion (1g/day) =
random urine protein/randome creatine in urine
what is the difference b/c focal and diffuse nephritic disease
focal: less than 1/2 glomeruli involved,see red cell casts and MILD proteinuria
diffuse: heavy proteinuria, all glomeruli involved
*both active urine sediment: lots of cells in urine and RBC casts
what is the diff b/n Nephritic and Nephrotic glomerulare disease?
Nephritic: red cell casts, mild protienuria (less than 1.5g/day), lots of cells in urine
Nephrotic: heavy protienuria (>3g/day), few cells or casts, lipiduria causing lipids to show up in urine "maltese cross"
where is 2/3 of water, Na and HCO reabsorbed?
PT: isotonic
what is imperm to Na and reabsorbs water alone?
thin descedn limb
what is imperm to water and reabsorbes Na?
thin ascend limb
where are there active transporters for Na?
all energy for reabsorpiton comes from where?
Na/K ATPase on BL membrane
in the 1st 1/2 of PCT, how does Na move across a pical membrane?
through Na channel down gradient
via Na/H antiporter
via Na/glucose symporter
via Na/amino acid, phosphorous, lactate
H secretion =?
HCO reaborption
need to reabsorb HCO to control pH
where is ALL glucose reabsorbed?
in PT via Na/glucose symmporter
what type of exchange occurs in 2nd 1/2 of PT?
Cl reabsorption down gradient via Cl/anion exchanger
anions can be OH, HCO2, HCO3
excreted anion needs to be recycled
mvmt of Cl down conc gradient in 2nd 1/2 PT creates waht?
positive charge in lumen which promotes Na and Ca reabsorption
waht is the FLNa?
FLNa= GFR *plasmaNa
= 180 * 140 = 25,200 mEq/day
where is most of the filterd Ca reabsorb?
PCT: 70%
80% paracellularly as Cl is reabsobed creates postivie lumen that promotes Ca reabsorb
waht is cystinuria and where is the problem
problem in PT w/ Na independent aa tranpsorters
genetic defect in transporter for dibasic amino acids (COLA)
increased excretion of cystine
formation of cystine stones
why do only cystine kidney stones form? where do they form?
b/c cystine in insoluble
form crystals in CD that are excreted into calxy
"renal colic"
waht is the problem in Type II RTA and where does it occur?
PT disfxn
genetic defect in Na/H antiporter
decrease in Tm for HCO b/c decrese FL
poor HCO3 reabsorption in PT therefore metabolic acidosis
this lowers ECV which stimulates RAA
develop hypokalemia b/c of incresaed Na delivery to CD leading to K wasting
what happens in Type II RTA when you give the pt HCO to try to increase HCO reabsop?
they will spill the HCO b/c changed the Tm
get high urinary pH
why do we see hypokalemia in Type II RTA?
b/c HCO can't be reabsorbed it is sitting in lumen longer. this incresaes the delay which makes the lumen extra negative
the negative lumen draws more K out of cells
Nephritic sydrome think? nephrotic?
nephritic: I for inflammation; hematuria
nephrotic: O for prOteinuria; heavy protein and lipids
waht is Fanconi syndrome?
defect in PT transport of amino acids, glucose, phosphate, uric acid, protein, and electrolytes
*aminoaciduria, hypophosatemia
seen with multiple myeloma
waht would you expect to see in urine of pt with renal glucosuria that would make you Dx Fanconi?
amino acids
action of Probencid?
inhibits tubular secretion of organic acids like Penicillin therefore increase plasma levels
decreases reabsorb of uric acid at PT thereby promoting its excretion and decreasing serum uric acid levels
what can help penicilin stay in blood longer?
probencid by ihibiting the renal tubuar secretion
Cimetidine can inhibit secretion of ?
what channel will you find specifically in TAL?
Na-2Cl-K symporter
fxns primarly as Cl pump thus leaves post charge in lumen which promotes reab of Ca and Mg
where are Ca and Mg reaborption?
in TAL b/c Na-2Cl-K symporter leaves post charge in lumen that promotes reab of Mg and Ca
reabsorption in TAL is ___
load dependent
what is TAL necessary for?
both diluting (reab Na) and concentrationg (NaCl reasb exits BL into interstituum ) urine
why do you need Na/H antiporter in apical memb of TAL?
to promote HCO reasborb and H secretion
fxn of Furosemide (lasix) loop diuretic?
inhibits Na-2Cl-K
incresae urinary excretion of NaCL
inhibits reabsob of Ca
incresaes water excretion by reducing osmolality of interstitial fluid in medulla
what channel is present in DT?
Na-Cl symporter
Na pump
lumen becomes negative
fxn of DT?
continue the dilution of urine b/c apical membrane is imperm to Water
why doesn't hte DT contribute to medullary gradient?
bc DT in cortex
this is the reason that loops are more servere
action of Thiazide diuretics?
inhibit Na-Cl symporter in early DT
reducing the ability to dilute urine
stimulate Ca reasbsorption
affect on Ca of loop vs thiazides? why is this useful?
loops: decrease Ca reasb which is ueful in emergent Tx of hypercalcemia
thiazide: increase Ca reab which is useful in Tx renal stone disease
what are the 1st line Tx for hypertension?
where do all diuretics act?
they act on brush border of tubular cells (lumen) thus they must enter tubular lumen in order to have an effect
what 2 things stimulate aldosterone?
ang II and hyperkalemia
waht does aldosterone do to principal cells and interalated cell?
incresae #fxnl Na and K channels on apical and levels of Na/K on bL
directly stimualaes H secretion by intercalated by stimulating H-ATPase
what drives K into lumen in principal cells?
the reasp of Na creates a neg lumen
what will a pt with hyperaldosteronism look like?
metabolic alkalosis
less renin
what is Liddle's syndrome?
AD sydnrome affectin principal cells
activates Na selective channels
-hyperaldosteronism like
excessive Na reabsorb and K secretion
what is pseudohypoaldosteronism?
AR syndrome affecting principal cells
INactivating mutation of Na channels
hypotenisve due to Na wasting
action of Amiloride?
blocks the entry of Na in principal cells so Na can't be reabsorbed
less K leaves b/c lumen is postive
decrese Na extrusion across BL via Na/K
stimulates RAA to reasbsrb Na in PT
besides blocking Na reabsorb what else do K spares block?
blcok Li entry: Li normally comopetes with Na to enter principal cells
increasing the oncotic pressure in cell of PT does what to reabsorb?
improve reasbsorption
increasing the oncotic presssure ouside will decresae reabsorb
if you lower the Pc what will happen to reabsopriton
increase b/c Pc is inversely proprortional to the resistance of both aff and eff arterole
oncotic pressure in capillaries is qual to what?
FF=GFR/RPF = oncotic pressure in cap
what portion of the nephron do starling forces not affect?
do not affect transport by Henle's loop, DT, and CD bc of decreased water permeability
Pc is inversely proportional to what?
R of afferent and efferent
if you constict aff/eff the Pc wil decrease which promotes reeabsorption
oncotic pressure of Capillaireis is proporitonal to what?
GFR at constant RBF (proportional to FF_
what happens to oncotic pressure of capilllaries as GFR decreases at constant RBF?
then FF decreases
less ultrafiltrate produced
plasma proteins less concentrated
decrease oncotic pressure, less reabsorb
what happens to oncotic pressure of capillaries as GFR increases at constant RBF
then FF incresaes
then more ultrafiltrate produced
plasma proteins more concentrated
increses reasborption of NaCl and water from PT
waht happens to osmotic prssure as capillaries go through glomerulus?
form ultrafiltrate
efferent oncotic > afferent oncotic
when will you see a decrease in FF?
dilate efferent arteriole b/c decrased GFR more than RBF
when wil you see an increase in FF?
constrict eff b/c increase GFR
action of prostaglandins
come into play ony when pt and kidney severely stressed
inhibit the vasoconstrictor effects of sympathetics to prevent renal ischemia
what is the response of the kidney to high BP in the PT?
less Ang II produced therefore less Na/H transporters in apical membrane
what increases in response to low ECV? what are the action?
ang II: most potent stimulus for reabosrption in PT of NaCl and water
Ang II stimulates release of aldostereone which stimulates the reabsorption of NaCl in TAL, DCT, CD
what is secreted in response to incresaed BP and ECV?
ANP from atria
BNP from ventricles
urodilatin from DT, CD
all inhibit NaCl and water reabsorption
alteration of plasma Na (hypernatremia or hyponatremia) are problems of waht?
water balance
ex: Na=130 means excess water not a deficiency of water
alterations in ECF vol (edema, hypertension) are problems of waht?
water balance
waht happens to osmolality levels when you decrease ADH?
decrease ADH, increase diuresis
decrease urine osmolality
increase plasma osmoality
where is ADH made and how sensitive is it?
made in neuroendocrine cells w/n supraoptic and paraventricular nuclei of hypothalamus
*very sensitive: stimulated by 1% increaese in osmolality via osmoR's, and 5-10% decrease in ECV
what will nausea and stress stimulate?
Ang II
why don't you want to give a postsurgical pt large volumes for free water or D5W?
b/c after surgery for several days ADH levels are still high (stimulated by stress) tehrefore if given water tehy will become hyponatremic
what is the ADH set point? what happens below the set point?
genetically dtermined
decreaeses by a decreased ECV and pregnancy
below set point no ADH released
waht will decrease the ADH set point?
decreased ECV and pregnancy
if you are hyperosmolar, what do you want secreted?
ADH to dilute the plasma
what would/could it mean if you are hyponatremic?
could mean your ADH set point is set too low or your are postsurgery
will small acute reductions in vascular volume stimulate ADH?
no! only stimulate renin and norEpi release, but will not cause release of ADH therefore increase in PT reabsorb of Na is stimulated by Ang II will restore volume
what are the 3 factors taht will inhibit release of ADH?
decreased plasma osmolalality
increased blood presesure
increasd blood volume
waht are the 3 factors that will stimuate the release of ADH?
increased plasma olsmolality
low BV
low BP
what will the kidney sacrifice to increase blood volume? ex?
sacrifice osmoles to incresaed volume
ADH stimulated b/c low volume, drink water which expands vascular volume but Na concentration decreses--become hypnatremic in order to restore volume
what is the problem in central DI?
inadequate release of ADH therfore get a large volume of dilure urine
the polyuria sitmulates polydipsia to compensate for water loss to maintain osmolality
when does a central DI occur?
after head trauma or brain tumors
see inadequate release of ADH
how do you correct central DI?
exogenous ADH
how will you know if pt has central DI or nephrogenic DI?
if you give pt exogenous ADH, if they have central DI they will respond to it and the urine osmolality will increase
if they have nephrogenic DI, there will be no change in urine osmolality b/c they don't respond at all to ADH
what is the Triphasic response seen in central DI?
initially polyruia
antidiruetic phase: release of stored ADH
permanent CDI
how is the CD made permeable to water?
ADH stimulates the secreteion of Aqua2 channels
ADH binds to BL side, Aqua channels inserted on apical
waht is the problem in neprhogenic DI?
ADH doesn't work on principal cells to increase prodxn of Aqu2 channels
therfore have decresad ability to maximllay concentate the urine
waht stimulates teh thrist center and how high does the plasma osmolarity be to see a change?
incresaed plasma osmolarlty of only 2-3%
Ang II stimulates thirst center
what will hapen to a cave dweller that is attacked by a tiger and loses 500cc blood? waht wif he has access only to water?
stimulate SNS
release renin, produce Ang II
increse reabsob Na from PT
stimulate thirst
decrease FeNa
if no food=no salt
thirst will be stimulated and Ang II will stimulate reab Na but with no Na in diet the kidney will stil reabsorb water via ADH even though serum osmolarity decreases=sacrifice osmoles
waht is uniqe about the tubular fluid leaving PT?
isotonic w/ plasma
what must you do to dilute urine?
reabsorb Na > water
what must be done to concentrate urine? what is the stimuls?
reabsorb water > NaCl
via ADH and hyperosmotic medulla
what is unique about the medullary CD?
permeable to water and urea w/o ADH
cortical CD is only permeable to water w/ ADH
how does the TAL concentrate the medulla
active transport of Na via Na-Cl-K
then fluid in desc limb could be 2ndarily concentrated via reasb of water thus providing delivery of highly concentrated urine to the thin AL
in the presence of ADH, what is the conc of Na vs urea at the turn of loop of henle?
Na is greater in the tubule
urea is greater in teh interstium
thus as go into ascending limbs, Na is actively reabsorbed and urea enters tubles b/c of gradient
waht happens as urea goes through TAL and DCT? what is the pupose of urea?
becomes more concentrated which allows it to leave CD and diffuse back into thin AL continuaosly increasing conc gradient
in the prescence of ADH, what happens to urea?
leaves the CD and floods the interstitum to increase the concentration gradient
1/2 of the 1200 mOsm/L concentration gradient is due to urea!
what happens to the insterstium in medullary asending limb?
it is made hyperosmotic by reabsorption of NaCl w/o water
when is urea able to leave the CD?
when ADH is preseent, water is reaborbed from cortical and med CD, but cortical CD are imperm to urea so the conc of urea increases in tubular fluid
the urea is then able to be reab in medullary CD
what does the urea that accumulates dependent on?
indirectly dependent upon active NaCl transport in thin AL
how will you tell the difference b/n a physogenic water drinker and person with DI?
if you withhold water, DI pt will dehydrate and serum Na wil increase, the same will initially happen in physo b/c ADH has been off for so long
BUT 2-3 days later the medullary gradient will be restored via ADH
why isn't the vasa recta straight?
to minimize the removal of excess intersital solute
what would happen if the vasa recta were straight?
solute would continue to be taken in to the blood and water would be lost from teh blood. now the water that is being reabsorbed from the tubules would not have any way of entering the bloodstream to reduce the plasma osmolality
waht are the reqts for max free water clearance?
ADH must be absent
tubules that dilute the urine (Thin AL, TAL,DT, and CD) must fxn normally
must be adequate delivery of tubular fluid to diluting sites
waht are the tubules that dilute the urine?
thin AL, TAL, DT, CD
waht will impair the ability to maximllay dilute the urine?
decreased GFR or increased prox reabsorption
diuretics and/or volume depletion will impair dilution
why do you give a pt with nephrogenic DI thiazide?
you want to decrease the polyuria that is associated with nephrogenic DI
thiazide inhibits the Na-K-2Cl so there is no Na reab
they already don't have ADH so the 2 being blocked will stimulate RAA b/c the body assumes volume depletion which will decrease the polyuria
increase Na reab in PT and water reab which means less Na and water are delivered to ADH sensitive sites in CD
how does amilioride work to help pts with reveresible Li nephrotoxicity?
amilioride will block the Na selective channels so less Na will be reabsorbed
less Na reabsorbed will stimuluate the RAA system
the Li also competes with the Na selective channels so toxicity will decrease
which diuretic will lower the urine output in nephrogenic DI?
thiazide will decrease urine output by stimulating vol depletion
loop will not lower the urine ouput b/c it blocks the accumulation of NaCl in the mullary interstitium that is essential for the prodxn of concentrated urine and inducing relative ADH resistance: no NaCl in medulla to pull water from CD
no more water in CD=more pee
why don't you want to give a person on Li a diruetic?
b/c anything that promotes Na reab wil increase the amt Li reabsorbed wich can lead to Li toxicity
what do prostaglandins antagonize?
the action of ADH
prostaglandins inhibit the action of sym nervous system which acts to stimualte ADH
we give NSAIDs to block prostaglandins
what are the 4 things you would use to Tx Nephrogenic DI?
Thiazide diuretics
low salt diet
Li retention will occur with any cause of what?
effective vol depletion
where is mostof the Li reabsobed?
in PT: follows that of Na
waht would cause an eleveated BUN?
if >20:1, consider enhanced urea prodxn or vol depletion (ECV)
renal failure, high protein diet, blood in gut
what is the eqn to determine solute amt from plamsa osmolality and flow rate of urine?
S = U * V
waht is the problem with hyponatremia? what causes it?
water problem
decreased ECF
primary polydipsia (psychogenic drinker)
what is a combo of water retention and secondary solute loss?
what can caouse SIADH?
postoperative pt
neuropsychiatric pt
ectopic prodxn
waht is the net effect of SIADH?
low Na, normal volume
you have normal volume b/c the kidney compensated for that
how can you treat someone iwht SIADH?
water restriction
Na administration via hypertonic saline
Na + loop
ADH R antagonist
what type of saline do you give someone iwth SIADH?
hypertonic saline
if give isotonic, it will expand their water volum by 350cc that they don't need
*saline needs to be more concentrated than the urine to raise the plasma Na
why is water intox fatal?
water rushes into brain b/c higher osmolality therefore decrease blood flow to the brain
waht is the difference b/c hyponatremia in SAH vs SIADh?
SIADH: normal volume, low Na
SAH: vol depleted, high urine Na, low plasma Na
waht is impt about correcting hypnatremia?
must go slowly
<0.5mEq/L/hr or <12mEq/L/day
or cause irreverisble neurological damage b/c cause central pontine myelinolysis
waht is ECV?
portion of ECF taht is contained in arterial system
the pressure that is perfusing the arterial BaroR's
nl when ECF increases, ECV increases
what is happending to ECV and ECF in heart failure?
you hava a decrease in CO which causes decrease in ECV. kidney senses low ECV adn stimulates the RAA to increse volume in ECF which leads to edema
*same thing in cirrhosis
what are the 4 actions of Ang II?
stimulate the adrenal to releease aldosterone from zona glomerulosa
vasoconstric eff
stimulate ADH secretion from pos p and stimulate thirst
increse NaCl reab in PT
action of ANP
oppose RAA
dilate aff, constict eff to increase GFR
what is the mEq Na, g Na, and gNCl in normal diet?
137mEq Na
3 g Na
8 g NaCl
how would you determine someon'es dietery Na?
24hr urine specimen b/c dietary Na = urine Na
if you are on a low salt diet what happens to your K?
you reabsorb less Na therefore lose less K
what is the FLNa?
GFR * plasma [Na]
when is it ok to have a low FeNa?
when the pt is normal
only problematic if pt is oliguric
if oliguiric <1= vol depletion
impt b/c if you give ATN pt fluid they will be volume overloaded
why is it impt to find out FeNa?
b/c if pt is oliguruic, if over 2% they have ATN
don't want to give this persone fluid bc they wil become vol overloaded
how is FeNa tightly controlled? what happens if you intake larg amt of Na?
small change in FeNa can lead to a large change in fluid loss (dont' want to increse FeNa too fast)
if intake large amt of Na, FeNa increases gradually but can only remove 1/2 of what you took in in the first day. the rest wll be reab and you will gain wt
the wt gain will stimulate vol expansion and you will reab less Na, excrete mre Na
need wt gain to act as stimulus for increaed excretion
when is steady state reached?
steady state: uine Na=intake Na
what can act like aldosterone? when?
stimulate Na reab K secretion
if deficient in 17alpha or 11beta
what is the aldo escape?
normally aldo causes Na reab and K secretion but after 3g wt gain, spontan diuresis occurs returning plasma vol to normal
hypertension stimuates pressure natiruresis so you continue to lose K but no edema occurs b/c Na gain stops
low Na, low MAP
in a pt with chronic high BP why don't we see edema?
b/c of aldo escape: they will have aldo present but low Na reab b/c of the increased BP that creaeted a pressure natiruresis to decrease Na reab
what is the pressure natiruesis?
small increase in BP causes large urinary Na and water excretion
what happens to Na reab when ECV increeses (diff parts of nephron)?
decrese in PT
increase in TAL and DT b/c they are load dependent
decreaes in CD b/c aldo is decreased
what is the state of GFR, RBF, and FF in ECV expansion?
decrese sympathetics
aff > eff dilation
incrase GFR but greater increase in RBF therefore decrese FF
make less ultrafiltrate
decrease oncotic in capillaries
less reabsorbed
what is the state of GFR, RBF and FF in ECV contraction?
b/c sym increase aff>eff constriction
RBF decrease more than GFR decresae therefore FF icrease
increes Na reab in PT: decreas Pc and incresae oncotic in cap
less delivery to TAL