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61 Cards in this Set

  • Front
  • Back
percent total weight that is extracellular
20% total weight (1/3 of total body water)
percent total weight that is intracell
40% total weight (2/3 of total body water)
percent total body water that's intracell
66% (2/3) or 40% total weight
plasma volume is under what catergory
extracellular fluid, along with "interstitial"
interstital volume, % total weight
3/4 of ECF (15% total weight, ECF 20% total weight)
how much of ECF is plasma
1/4 (3/4 is interstitial)
how measure plasma volume
radiolabelled albumin
how measure ECV
how measure ICV
total water-ECV
where ECV measured by inulin
secretion/filter prop of inulin
freely filtered and is neither reaborbed nor secreted
how calculate GFR
GFR=urine concentration inuline x volume / plasma inulin
or GFR=UixV/Pi
name layers of glomerular filtration barrier
fenestrated cap endothelium, fused BM, podocytes
what creates charge barrier in kidney
heparan sulfate BM (which is lost in nephrotic syndrome)
how calculate clearance of "s"
properties of PAH
all filtered and secreted, (all PAH excreted) so used to estimate RPF
does PAH under or over estimate RPF? why?
under by 10%, bc not all regions filter/secrete PAH, so really it's calculating an effective RPF
compare contrast PAH, inulin
inulin is all picked up out of plasma so can be used to measure GFR, PAH is all excreted and is used for RPF
filtration fraction with NSAID? with ACEI?
NSAID=constrict afferent, so decrease both GFR and RPF, no change FF
ACEI=prevents constrict of efferent, decreases RPF, increases GFR, increases FF
effect ACEI on kidney (RPF,GFR,FF)
prevents constrict of efferent, decreases RPF, increases GFR, increases FF
effect NSAID on kidney
constrict afferent, so decrease both GFR and RPF, no change FF
Filtration fraction
calculate free water clearance
where U is urine osmolarity, P is plasma osmolarity, V=urine flow rate
transport occurring in PCT
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
where PAH secreted
PCT by carrier mediated 2 active transport
transport of TAL
-actively reabsorb Na, K, Cl
-indirectly reabsorbs Mg, Ca
-impermeable to H20
transport in DCT (what absorbed, regul?)
-actively reabsorbs Na, Cl with NaCl symport
-Ca/P under control of PTH, P in PCT, Ca in DCT
very general transport in CD
reabsorb Na/secrete K or H (aldos)
-reabsorb H2O (ADH)
describe RAA axis
(include trigger, what secretes it, peptide lengths)
decr BP in JG secrete renin, cleaves angiotensinogen to angioI (decapeptide).
in lung: angioI -> II (octapeptide) by ACE
actions Ang II
-rel aldos from adrenal cortex
-rel ADH from p. pit
-stim thirst (hypothal)
what composes JGA, what type of cells
JG cells (modified sm m of afferent arteriole) and macular densa (Na sensor part of DCT)
--NOTE: JG cells also secrete EPO
what JG cells respond to (3)
what 2nd thing do JG cells do?
-decr renal BP
-decr Na delivered to DCT
-incr sympathetic tone
--NOTE: JG cells also secrete EPO
stimulants of renin
-decr renal BP
-decr Na delivered to DCT
-incr sympathetic tone (beta one)
name endocrine functions of kidney
EPO, activate vitD, renin, PG (to incr GFR)
where, when EPO made
in response to hypoxia, endothelial cells of peritubular capillaries
how vit D activated
by 1 alpha-hydroxylase which is activated by PTH
ANF: trigger, action
trigger=incr atrial P
action=incr GFR, incr Na sxn
aldosterone: trigger, action
trigger=incr K, ATII
effect=incr Na reabsorp (inde of ATII), incr K and H sxn in collecting tubules
PTH: trigger, action on kidney
trigger=decr Ca, P
effect=incr reabsorb Ca in DCT and inhibits reabsorb P in PCT, stim activated vit D (by alpha hydroxylase)
PTH: effect on bone
stim Ca and P release
directly stim osteoblast, indirectly osteoclast causing net bone resorption
PT reabsorption: hypo, iso, or hyperosmotic
secondary causes HTN
-renal a stenosis
-primary hyperaldosteronism
-genetic (Liddle, gluco remedial aldost, SAME)
others: acromegaly, hypo/hyperthyroid, Cushing (glucocort have some mineral fxn), coaract aorta, scleroderma (excess collagen deposition->renal crisis)
AD, Na duct in CD is always open.
low K, HTN, incr volume, (low renin, aldos)
tx: amiloride to block Na channel
overall Na/H2O transport at each segment
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
describe renal artery anatomy
renal a, arcuate, interlobular
1) afferent, GC, efferent, peritub
2)stellate, interlobular, arcuate, interlobar, renal v
places reabsorb Na
67% PCT, 25% TAL, 5% DCT, 3%CD
where in kidney regulate acid/base
Na channel used in PT?
Na/H antiport (linked to reabsorb HCO3), cotransport with glu, aa, P, lactate
what section of kidney performs hyposmotic net
the loop!
urea is reabsorbed where
in the intermedullary CD, ADH increases the permeability--used to increase concentration gradient.
otherwise 50% urea reabsorbed passively in PT,
how does ECF volume effect PT fxn
decrease in ECF volume increases reabsorption
TAL transporters
triport: Na/K/2Cl
channels and ion movement of CD
principal cells reabsorb Na and H2O, secrete K
a intercalated cells secrete H by H/ATPase and reabsorb K by H/K/ATPase
channel of DCT
NaCl symport
how is K secreted in TAL
due to positive lumen potential
are Mg, Ca transported in TAL
yes, indirectly, interstitially
which regions of the nephron are impermeable to H2O
early distal tube, thick ascending limb
hypokalemia can be caused by alkalosis or acidosis
alkalosis (pull H+ out to fix alkalosis, K+ goes in)
how does ECF volume effect PT reabsorption
volume contraction increases reabsorption just bc of the forces
how does systemic acidosis affect K sxn in kidney
(bc less positivity in lumen)
how do loop and thiazide diuretics affect K reabsorb DCT, CD
increase flow rate thru DCT causing dilution of K, this increases the drive to secrete K