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48 Cards in this Set
- Front
- Back
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some stats
what % of BF does the kidney receive what % of plasma is filtered? what % of the BF to kidney goes to nephron, where does the remainder go? how much filtrate is made each day, what does this say about reabsorption |
25%
20% (GFR/RPF) 90%, rest to support the capsule and fatty tissue 180L, LOTS of reabs |
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wht is the filtration fraction
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FF= GFR/RPF
RPF = RBF x (1-HCT) **usually 20% of plasma is filtered |
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if you know RBF how do you determine PBF, what can PBF tell us
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RPF = RBF x (1-HCT)
FF= GFR/RPF **usually the filtration fraction os 20%, this ism 20% of our plasma is filtered |
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what does SNS do to RBF and GFR, how
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a1 constriction on afferent (primarily)
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name 5 things that will decrease GFR adn RBF
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1. SNS stim- a1 constriction
2. ANG II 3. ADH 4. ATP 5. endothelin |
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what will cause dilation and increase RBF
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1. ANP
2. glucocorticoids 3. NO 4. Prostaglandins (PGE2 PGI2) |
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what is "antialdosternone" what does it do to Na
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ANP
**promotes Na loss |
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what does it do to GFR
1. SNS 2. NO 3. Glucocorticoids 4. ANG II 5. ANP 6. ADH 7. Endothelin 8. prostaglandins |
what does it do to GFR
1. SNS: D 2. NO: I 3. Glucocorticoids: I 4. ANG II: D 5. ANP: I 6. ADH: d 7. Endothelin: d 8. prostaglandins: i |
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what is the afferent arteriole more sensitive to?
what is the effernt arteriole more sensitive to?> |
Afferent: a1 SNS constriction
Effernt: ANG II **both decrease GFR and RBF |
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what responds to ANG II
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effernt arteriole is more sensitive
**constrict and decrease GFR RBF |
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at arterial pressures of what is there constant BF nad GFR, what mech allows this
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80-180
**autoregulation **wide range of pressure without an effect on GFR/RBF |
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what can overide the autoreg that keeps GFR/RBF constant at arterial pressure of 80-180 (2)
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1. SNS tone, **decrease GFR/RBF
2. severe blood loss, decrease RBF/GFR |
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what happens to GFR/RBF with large hemmorage
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decerase
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autoregulation of the kidney refers to what? what are the mechanisms
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constant BF when pressure is 80-180
1. myogenic: intrinsic property of VSM to contract in reponse to stretch 2. Tubuloglomerular feedback (flow dependent): increased GFR increases NaCl transport past the macula densa, MD responds by increasing afferent arteriole Pressure to decrease GFR |
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the 2 mechanisms of autoregulation of GFR do what?
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alter resistance of afferent arteriole
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explain how the tubuloglomerular feedback works
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increased GFR increases NaCl that passes the MD, MD senses this increase and respinds by constricting the afferent arteriole and increasing pressue so GFR decreases
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what is the myogenic mechanism?
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intrinsic property of VSM to contract in response to stretch,
one way kidneys autoregulate to have a constant GFR with pressures from 80-180 |
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again, the 4 parts of renal function
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1. Glomerular Filtration: protein free filtrate
2. Reabsorption: from tubule to blood 3. Secretion: from blood to lumen 4. Excretion: pee |
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what is the conc of small molecules in the filtrate in comparison to plasma
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isoosmotic
**the molecules that enter filtrate are isoosmotic to plasma initially |
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the fluid in bowmans capsule can be referred to as what
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protein free filtrate of blood plasma
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what are the main barriers to filtration
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BL: excludes negative things, lots of proteins in blood are negative
Filtration Slits: exclude big things (have diaphragms) **the fenestrae exclude RBC |
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what structures easily pass into bowmans space base on size, wht doesnt
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water
NaCl glucose inulin **proteins are excluded: albumin, hg **recall large things are excluded by filtration slits formed by pedicles of podocytes |
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what is the eq for GFR
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starling
GFR= K ((Pgc-Pbc) - (ngc-cbc)) **NFP= (Pgc-Pbc) - (ngc-gbc) **nbc is usually 0 bc no protein in bowmans capsule |
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what part of the equation for GFR is usually zero
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nbc
**No protein in capsule **oncotic pressure |
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Kf is what
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filtration coeffecient, the net filtration rate produced by each mmHg of NFP
**GFR= kf (Pgc-Pbc)- (ngc-nbc) |
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how does the filtration coeffecient for the kidney capillaries differ from those of other organs
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Kf is WAY higher for kidney, reflects the filter nature of kidney
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how do mesangial cells affect Kf
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they contract and decrease Kf to decrease GFR
**recall ANG II causes mesangial cells to contract |
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what is the driving force for NFP (net filtration pressure)
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pressure in glomerular capillary
Pgc |
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what are these components that tend to drive GFR
1. Pgc 2. Pbc 3. ngc 4. nbc |
Pgc: pressure of capillary to force fluid into bowmans space, driving force for filtration
Pbc: small back force ngc: oncotic pressure of glomerular capillary, force drive fluid into the capillary to dilute the capillary proteins nbc: oncotic pressure in bowmans space, 0. no protein here |
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what is the main part of NFP that decreases NFP
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ncg
**the oncotic pressure of the capillary, lots of proteins in capillary that want to drive water into the capillary **opposed by the high hydrostatic pressure of the capillary that drived fluidOUT of capillary |
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as plasma leaves capillary and enters bowmans space what happens to ngc
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increases, proteins have concentrated as filtrate enters the bowmans capsule
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because the glomerular capillary bed is made of 2 arterioles what pressure stays prtty constant
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hydrostatic pressure of capillary
Pgc |
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what is the ngc at afferent arteriole, what about at effernt
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Afferent: low, oncotic pressure of glomerular capillary
Afferent: much higher, solute is lost and protens are super concentrated by the time we get to efferent arteriole, increased force to drive water into the capillary |
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NFP is differnt at affernt and efferent end. why? how do they differ
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afferent: 45, low oncotic pressure of capillary
efferent: 0, NO filtration, but not - so no reabs here. The proteins in blood are super concentrated and so there is a large force that wants to drive water into the capillary. capillary oncotic pressure |
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what pressure is constant througout capillary system in glomerularus
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hydrostatic pressure of glom capillary
**affernet/efferent arteriole, same pressure |
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calc NFP
calc GFR Pgc= 45 Pbc= 10 ngc= 26 (nbc, not given. assume 0) Kf= 14 |
NFP= 45 - (10+26)
= 45 - 36 = 9 GFR= Kf + NFP = 14 x 9 |
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what is the formula for NFP
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driving force OUT - driving force IN
Pcg - (ngc+Pbc) |
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we say that GFR = kf + NFP
how do we calc NFP |
(Pcg-Pbc) - (ngc-nbc)
Rearrange: driving force OUT - driving force IN Pcg - (Pbc+ncg) |
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what does constriction to affernt art do to GFR
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decrease RBF and GFR, due to decrease Pcg
**SNS stim to constrict afferent will decrease glom P |
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what does constriction to effernt art do to GFR? what causes effernt constriction
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decrease RBF, increase P in glom, increase filtration
*8at low/mod ANG II effernt constricts |
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what if we constrict both afferent and efferent arterioles, what does GFR do RBF
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constant!
DRASTIC decrease in RBF |
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how can we decrease RBF and keep GFR constant
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constrict both efferent and affernet art
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when aff art constricts what happens to Pgc and RBF
what about effernet |
both decrease
RBF decrease, Pgc increase |
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what would make kf increase, how does this afect GFR
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increase glom SA, relax mesangial cells (no ANG II)
increase GFR |
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what wuld make Pgc increase, what does this do to GFR
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1. increase Renal Art p
2.decrease aff art resistance, dilate afferent 3. efferent constriction increase GFR |
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what would make Pbc to increaes, what does this go to GFR
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1. blockage of nephron (increase intratubular pressure)
decrease GFR |
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what would make oncotic pressure of capillary increase, what does this do to GFR
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1. increased plasma oncotic rpessure
2. decreased renal plasma flow GFR decrease |
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if we have icnreased RBF what happens to GFR? is there a chance we wont reach equilibrium
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increae GFR
sure thing! |
