Renal Physio

Front 1

percent total weight that is extracellular

Back 1

20% total weight (1/3 of total body water)

Front 2

percent total weight that is intracell

Back 2

40% total weight (2/3 of total body water)

Front 3

percent total body water that's intracell

Back 3

66% (2/3) or 40% total weight

Front 4

plasma volume is under what catergory

Back 4

extracellular fluid, along with "interstitial"

Front 5

interstital volume, % total weight

Back 5

3/4 of ECF (15% total weight, ECF 20% total weight)

Front 6

how much of ECF is plasma

Back 6

1/4 (3/4 is interstitial)

Front 7

how measure plasma volume

Back 7

radiolabelled albumin

Front 8

how measure ECV

Back 8

inulin

Front 9

how measure ICV

Back 9

total water-ECV
where ECV measured by inulin

Front 10

secretion/filter prop of inulin

Back 10

freely filtered and is neither reaborbed nor secreted

Front 11

how calculate GFR

Back 11

GFR=urine concentration inuline x volume / plasma inulin
or GFR=UixV/Pi

Front 12

name layers of glomerular filtration barrier

Back 12

fenestrated cap endothelium, fused BM, podocytes

Front 13

what creates charge barrier in kidney

Back 13

heparan sulfate BM (which is lost in nephrotic syndrome)

Front 14

how calculate clearance of "s"

Back 14

C=UsxV/Ps

Front 15

properties of PAH

Back 15

all filtered and secreted, (all PAH excreted) so used to estimate RPF

Front 16

does PAH under or over estimate RPF? why?

Back 16

under by 10%, bc not all regions filter/secrete PAH, so really it's calculating an effective RPF

Front 17

RBF=

Back 17

RBF=RPF/1-Hb

Front 18

compare contrast PAH, inulin

Back 18

inulin is all picked up out of plasma so can be used to measure GFR, PAH is all excreted and is used for RPF

Front 19

filtration fraction with NSAID? with ACEI?

Back 19

NSAID=constrict afferent, so decrease both GFR and RPF, no change FF
ACEI=prevents constrict of efferent, decreases RPF, increases GFR, increases FF

Front 20

effect ACEI on kidney (RPF,GFR,FF)

Back 20

prevents constrict of efferent, decreases RPF, increases GFR, increases FF

Front 21

effect NSAID on kidney

Back 21

constrict afferent, so decrease both GFR and RPF, no change FF

Front 22

Filtration fraction

Back 22

GFR/RPF

Front 23

calculate free water clearance

Back 23

C=V-(UxV)/P
where U is urine osmolarity, P is plasma osmolarity, V=urine flow rate

Front 24

transport occurring in PCT

Back 24

reabsorb all glu,aa, most bicarb, Na, H2O
secretes ammonia (to buffer H)
-PAH secreted by carrier mediated 2 active transport
-PTH decr P reabsorb here

Front 25

where PAH secreted

Back 25

PCT by carrier mediated 2 active transport

Front 26

transport of TAL

Back 26

-actively reabsorb Na, K, Cl
-indirectly reabsorbs Mg, Ca
-impermeable to H20

Front 27

transport in DCT (what absorbed, regul?)

Back 27

-actively reabsorbs Na, Cl with NaCl symport
-Ca/P under control of PTH, P in PCT, Ca in DCT

Front 28

very general transport in CD

Back 28

reabsorb Na/secrete K or H (aldos)
-reabsorb H2O (ADH)

Front 29

describe RAA axis
(include trigger, what secretes it, peptide lengths)

Back 29

decr BP in JG secrete renin, cleaves angiotensinogen to angioI (decapeptide).
in lung: angioI -> II (octapeptide) by ACE

Front 30

actions Ang II

Back 30

-vasoconstrict
-rel aldos from adrenal cortex
-rel ADH from p. pit
-stim thirst (hypothal)

Front 31

what composes JGA, what type of cells

Back 31

JG cells (modified sm m of afferent arteriole) and macular densa (Na sensor part of DCT)
--NOTE: JG cells also secrete EPO

Front 32

what JG cells respond to (3)
what 2nd thing do JG cells do?

Back 32

-decr renal BP
-decr Na delivered to DCT
-incr sympathetic tone
--NOTE: JG cells also secrete EPO

Front 33

stimulants of renin

Back 33

-decr renal BP
-decr Na delivered to DCT
-incr sympathetic tone (beta one)

Front 34

name endocrine functions of kidney

Back 34

EPO, activate vitD, renin, PG (to incr GFR)

Front 35

where, when EPO made

Back 35

in response to hypoxia, endothelial cells of peritubular capillaries

Front 36

how vit D activated

Back 36

by 1 alpha-hydroxylase which is activated by PTH

Front 37

ANF: trigger, action

Back 37

trigger=incr atrial P
action=incr GFR, incr Na sxn

Front 38

aldosterone: trigger, action

Back 38

trigger=incr K, ATII
effect=incr Na reabsorp (inde of ATII), incr K and H sxn in collecting tubules

Front 39

PTH: trigger, action on kidney

Back 39

trigger=decr Ca, P
effect=incr reabsorb Ca in DCT and inhibits reabsorb P in PCT, stim activated vit D (by alpha hydroxylase)

Front 40

PTH: effect on bone

Back 40

stim Ca and P release
directly stim osteoblast, indirectly osteoclast causing net bone resorption

Front 41

PT reabsorption: hypo, iso, or hyperosmotic

Back 41

isoosmotic

Front 42

secondary causes HTN

Back 42

-renal a stenosis
-primary hyperaldosteronism
-pheo
-genetic (Liddle, gluco remedial aldost, SAME)
others: acromegaly, hypo/hyperthyroid, Cushing (glucocort have some mineral fxn), coaract aorta, scleroderma (excess collagen deposition->renal crisis)

Front 43

Liddles

Back 43

AD, Na duct in CD is always open.
low K, HTN, incr volume, (low renin, aldos)
tx: amiloride to block Na channel

Front 44

overall Na/H2O transport at each segment

Back 44

PT: active Na, glu, aa reabsorbed, H2O, Cl and urea reabsorbed passively. secretion of H+ and ammonia
tDLH: no permeability for Na, passive reabsorb of water
tALH: active Na reabsorb, no H2O
TAL: active reabosrb Na, K
CT: reabsorb Na in exch for K or H
CD: active Na, K, Cl reabsorb, passive H2O

Front 45

describe renal artery anatomy

Back 45

renal a, arcuate, interlobular
1) afferent, GC, efferent, peritub
2)stellate, interlobular, arcuate, interlobar, renal v

Front 46

places reabsorb Na

Back 46

67% PCT, 25% TAL, 5% DCT, 3%CD

Front 47

where in kidney regulate acid/base

Back 47

PCT

Front 48

Na channel used in PT?

Back 48

Na/H antiport (linked to reabsorb HCO3), cotransport with glu, aa, P, lactate

Front 49

what section of kidney performs hyposmotic net

Back 49

the loop!

Front 50

urea is reabsorbed where

Back 50

in the intermedullary CD, ADH increases the permeability--used to increase concentration gradient.
otherwise 50% urea reabsorbed passively in PT,

Front 51

how does ECF volume effect PT fxn

Back 51

decrease in ECF volume increases reabsorption

Front 52

TAL transporters

Back 52

triport: Na/K/2Cl

Front 53

channels and ion movement of CD

Back 53

principal cells reabsorb Na and H2O, secrete K
a intercalated cells secrete H by H/ATPase and reabsorb K by H/K/ATPase

Front 54

channel of DCT

Back 54

NaCl symport

Front 55

how is K secreted in TAL

Back 55

due to positive lumen potential

Front 56

are Mg, Ca transported in TAL

Back 56

yes, indirectly, interstitially

Front 57

which regions of the nephron are impermeable to H2O

Back 57

early distal tube, thick ascending limb

Front 58

hypokalemia can be caused by alkalosis or acidosis

Back 58

alkalosis (pull H+ out to fix alkalosis, K+ goes in)

Front 59

how does ECF volume effect PT reabsorption

Back 59

volume contraction increases reabsorption just bc of the forces

Front 60

how does systemic acidosis affect K sxn in kidney

Back 60

decreases
(bc less positivity in lumen)

Front 61

how do loop and thiazide diuretics affect K reabsorb DCT, CD

Back 61

increase flow rate thru DCT causing dilution of K, this increases the drive to secrete K