Renal Flashcards
Where is the macula densa? JG cells?
Macula densa are cells w/in DCT
JG cells are modified SmM of aff art, make connection w/ DCT and macula densa
Body water is where?
60-40-20 (% of body wt)
60% TBW, 40% ICF, 20% ECF (1/4 pl vol, 3/4 interstitial vol)
Clearance =
vol of pl from which the substance is cleared per unit time:
C [ml/min] = [U] x V / [P]
GFR =
- Cr over or underest’s GFR?
use inulin:
GFR = CL(inulin) = UV/P, where U is the urine conc of inulin, P is the pl conc of inulin, and V is the urine flow rate
- slightly overest’s bc is secreted
ERPF =
RBF =
Is ERPF really RPF?
use PAH for est’d renal pl flow bc all PAH that enters kidneys is excreted:
ERPF = UV/P = CL of PAH
- RBF = RPF / (1-Hct)
- no, ERPF underest’s true RPF by about 10%
FF =
nl is?
Filtered load =
FF = GFR/RPF, nl is 20%
Filtered load = GFR x pl conc
What effect do PGEs and ATII have on FF?
PGEs don’t affect FF bc they incr RPF -> incr’d GFR
ATII incr’s FF bc decr RPF -> incr’d GFR
What effect do NSAIDs and ACEIs have on FF?
NSAIDs constric aff art (prevent dilation) -> decr’d RPF and GFR -> no change in FF
ACEIs dilate eff art (prevent constriction) -> incr’d RPF and decr’d GFR -> decr’d FF
Filtered load =
Excretion rate =
How to calc reab’n? secretion?
GFR x [P]x
V x [U]x
Reab’n = filtered - excreted
Secretion = excreted - filtered
Pl glc reab’n threshold?
Glc reab’n sat’n max at?
- What happens in nl preg?
~160 -> glucosuria
350 -> all transporters fully sat’d (Tm)
- Reduced reab’n of glc -> glucosuria and aminoaciduria (also not ab’d as well)
Hartnup’s dz =
defic in neutral AA (Tryptophan) transporter -> pellegra
ATII’s affect on kidneys?
PTHs 2 affects on kidneys?
- PT: stim’s Na/H exchange -> reab’n of Na, water, bicarb -> contrac alkalosis
- PT: inhib’s Na/phos cotrans -> phos excretion; and DCT: stim’s Ca/Na exchange -> incr’d Ca reab’n
What 3 things stim renin release from kidney?
Decr’d BP (sensed by JG cells)
Decr’d Na deliv (sensed by MD cells)
Incr’d symp tone (on b1 Rs)
Why don’t you get reflex brady w/ incr’d BP from ATII?
ATII also affects baroR func -> limits reflex brady
ADH reg’s?
Aldos reg’s?
ADH reg’s osmol’s (except w/ low bl vol then incr’s water reab’n to save vol)
Aldos reg’s bl vol
EPO is made by?
Act’d VitD is made where?
- Interstitial cells in the peritubular capillaries
- In the PT cells by 1a-hydroxylase
3 things that stim PTH release?
Decr’d pl Ca
Incr’d pl PO4(3-)
Decr’d pl 1,25-(OH)2 VitD
Insulin defic -> what effect on K?
Thus incr’d insulin does what?
Causes hyperK bc decr’d act’n of Na/K pump
- Incr’d INsulin shifts K INto cells (hyopK)
HyperK shows what on EKG?
HypoCa causes?
HypoMg causes?
- wide QRS and peaked T waves, arrhythmias
- tetany, seizures
- tetany, arrhythmias
Winter’s formula =
- use for?
PCO2 = 1.5(bicarb) + 8 +/-2
to determine what PCO2 should be w/ simple metab acidosis (determine if resp compensation is adequate of it there is a mixed acid-base d/o)
AG =
- check when?
AG = Na - Cl - HCO3-
check w/ metab acidosis to see if it’s gap or non-gap acidosis
Causes of gap metabolic acidosis?
MUDPILES Methanol (formic acid) Uremia DKA Propylene glycol Iron tab's or INH Lactic acidosis Ethylene glycol (oxalic acid) Salicylates (late)
Causes of non-gap metab acidosis?
HARD-ASS Hyperalimentation Addison's dz (decr'd aldos) RTA D Acetazolamide Spironolactone Saline infusion
Salicylate poisoning causes what change in bl pH first? then later?
Early: rep alkalosis bc stim’s resp center -> hypervent
Late: metab acidosis bc of acid
