72 terms

SGU Physiology - Renal

EPO (erythropoietin)
hormone: glycoprot, dec PO2 -> fibroblasts secrete in renal interstitium -> inc RBCs => people w/ renal failure dev anemia
principal cells
2/3 of distal tubule/collecting duct, cells for Na/H2O balance (Ald action)
intercalated cells
1/3 of the cells in the distal tuble/collecting duct, for acid/base bal
cortical nephrons
85% of nephrons, have a short LOH + PCT
juxtamedullary nephron
15% of nephrons, have a long LOH + vasa recta, have greater filtration, reabs, "salt-conserving"
180 liters
norm daily GFR
RBF (renal blood flow)
Upah*V/Apah, est w/ PAH, 20% CO = 1L/minute = 350mL/minute/100g, which is 7x that of brain
RPF (renal plasma flow)
(1-Hct)RBF = UpahV/Ppah = Cpah, 687 mL/min
bridges gap betw GBM podocyte foot procs, defect in Congenital Nephrotic Syndrome
GFR (glomerular filtration rate)
Puf Kuf = ultrafiltration P ultrafiltration coeff, Kuf = permability * SA, est w/ Insulin or Creatinine
myogenic mechanism
GFR autoreg: distend afferent arteriole -> open non-spec cation chans -> depol -> VGCa2+ open -> contract smooth mm -> inc R -> restore Q to norm
TGF (tubuloglomerular feedback)
GFR autoreg: inc NaCl to macula densa (how it senses inc flow) -> inc ATP -> adenosine -> A1 on afferent arteriole -> vasoconstrict
adenosine R: aff. arteriole vasoconstrict
adenosine R: metabolic vasodilation
UxV/Px = volume of plasma rendered free of a subst in 1 min = amt subst per min / []subst in pl
Gault-Cockcroft Forumula
GFR = (140-age)weight/([Cr]pl72)
ERPF (effective renal plasma flow)
use PAH Cl to calc RPF through functional nephrons
FF (filtration fraction)
FL (filtered load)
Excretion Rate (ER)
FE (fractional excretion)
ER/FL = UzV/(GFR*Pz)
Tm (transport maximum)
where reabs curve asymptotes
renal threshold
[] where excr (vs reabs) is first recorded
weird filter/reabs lines due to nephron heterogeneity
familial renal glycosuria
clinical: SGLT2 muts
clinical: AR -> dibasic AA carrier mut => kidney stones
Hartnup's disease
neutral AR -> AA carrier mut => pellagra s/s
drug: dec CA => dc Na/HCO3- transport -> metab acidosis -> inc resp
exchanger: Na/H+ in proximal tubules
Fanconi Syndrome
clinical: excr everything w/out reabs => acidosis + polyuria
Bartter's Syndrome
clinical: mut NKCC2, ROMK, or CLC-Kb of TALH -> waste NaCl, lose lots of Ca2+ + Mg
Gittelman's syndrome
clinical NCCT muts -> hyperkalemia, hyperchloremia, alkalosis
liddle's syndrome
clinical: ENaC GoF mut -> Na+ hypertension
PHA (pseudohypoaldosteronism)
clinical: ENaC LoF mut -> hypovolemic, dec ability to excrete K+
thiazide diuretics
drug: diuretics that act on Na/Cl cotransporter of DCT, inc Ca2+ reabs -> hypercalcemia, kyperkalemia
loop diuretics
drug: diuretics that act on NKCC in LoH, Tx for CHF, edema, renal failure
potassium sparing diuretics
drug: diuretics that act on CD
glomerulotubular balance
reg NaCl reabs by bal betw GFR + tubular reabs
action of AII, NE, Ald, ADH on Na+ reabs
action of Dopa, PGE2, ANP, and NO on Na+ reabs
inc Na+ reabs in PCT by inc NHE3, inc NaKATPase -> inc transcellular reabs
inc Na+ reabs in TALH by inc NKCC2, ROMK, cation transport, imp for countercurrent mult sys
inc Na+ reabs in principal cell of CD by inc ENaC, ROMK, NA/K ATPase => also inc K+ secr
ANP (atrial natriuretic peptide)
dec Na+ reabs in prinicpal cell of CD by dec ENaC
ADH receptor for vasoconstriction on vasc smooth mm
ADH receptor for water retention on TALH, CD -> inc cAMP, ins AQP2 vesicles into apical memb, inc transporters (NKCC2, ROMK)
"diluting seg" since undergoes NaCl reabs
water reabs under control of ADH
water reabs in prox nephron NOT ADH controlled
diabetes insipidus
clinical: bad ADH reg -> polydipsia, polyuria, Central = PosPit ADH rel prob, Nephrogenic = kidney V2 prob, Psychogenic = mental prob
effective circulating volume (ECV)
the "fullness" of circ
11-HSD (11-hydroxysteroid dH)
enzyme: converts glucocorticoids to inactive metabolites
second most abund intracellular cation (after K+), 65% reabs in LoH, 25% in PT (reverse of Na+ + Ca2+ handling)
paracellular Mg2+ channel in TALH, affected by loop diuretics
CaR (extracellular Ca2+ sensing Receptor)
senses fall in [Ca2+]free, ionized -> G protein -> PTh -> PTH
alkaline phosphate
HPO42-, 80% of phosphate
ion: 80% reabs in PCT (Na/P cotransport), PTH dec reabs
3.5-5.5 mEq/L
normal [K+]
alpha-intercalated cells
respond to low [K+]pl -> inc H/K-ATPase -> inc [H+] => acidemia
limits of ECF pH compatible w/ life
normal reg pH range
volatile acid (~15kmMols produced per day)
aka fixed or metabolic acids, includes organic acids, P + S acids
any subst that can rev bind H+ ions
buffering power
# mols of strong acid in 1 L of sltn to reduce pH by 1 OR mols of strong B added to 1 L of sltn to inc pH by 1
NBC (Na Bicarbonate Cotransporter)
Na+ + 3 HCO3- cotransporter on basolateral PCT memb, uses HCO30 from action of cyto CA
beta-intercalated cells
cells in CD that have apical Cl-/HCO3- exchangers active in response to inc pH, minor fx in rel to amt of HCO3- that is reabs, filtered, or created
volume contraction alkalosis
dec ECV -> metabolic alkalosis
base excess
amt of strong HA or B (mEq/L) to titrate pH of 100% ox bl to 7.4 @ 37 dec C @ 40mm Hg, norm range = -2 to + +2, (<-2 = metab acidosis, > +2 = metab alkalosis)
anion gap
[Na+] - ([Cl-] + [HCO3-]), norm = 8-16mmol/L (> 18 = unmeas anions, oft in metabolic acidosis), metab acidosis w/ norm anion gap found in hyperchloremia (due to HCO3-/Cl- exch)
35-45 mmHg
norm PaCO2 range (< = resp alkalosis, > = resp acidosis)
norm HCO3- range (< = metab acidosis, > = metab alkalosis)