Quiz 1 Flashcards
ineffective osmoles
reflection coefficient at equilibrium is t generate an osmotic effect.
osmolality calculation; osmolar gap
osmolality = 2[Na] + [glucose]/18 + [BUN]/2.8
osmolar gap = measured - calculated; alters you to the presence of a toxin in the blood at high enough concentration to affect measured osmolality
Fluid compartment rules
TBW=60% of BW, ICF=40% of BW, ECF=20%. ECFV is 75% ISFV and 25% PV.
forces driving fluid movement between plasma and ISF
hydrostatic pressure: plasma–>ISF
oncotic pressure due to plasma proteins: ISF–>plasma
filtration rate
Kf= [(Pc-Pi) - σ(πc - πi)]
ultrafiltration rate/day
180L/day, necessitating 20% of CO. Filtration is passive but reabsorption isnt.
O2 consumption by kidneys
determined by GFR, which varies based on RPF. A-V O2 difference is constant while O2 consumption, GFR and RBF increase
starling equation for GFR
GFR=Kf[(Pgc-Pbs)]-πgc]
different from other caps because of Kf
driven by Pgc
filtration fraction
GFR/RPF, ~20%, limited by πgc (increases as protein free filtrate leaves the glomerulus)
constriction of afferent arteriole
Pgc↓ so GFR ↓, RPF↓
constriction of efferent arteriole
Pgc↑ so GFR↑, RPF↓
renal clearance
virtual volume of plasma that would be completely cleared of a substance per unit time = Us x V’ /Pas (concentration in arterial plasma)
clearance of PAH
measures RPF, since PAH is both filtered and secreted and doesnt appear in the vein
RPF = Upah x V / Pa pah
clearance of inulin and creatinine
measures GFR, since its freely filtered but neither secreted nor reabsorbed from tubules. Creatinine is alternative, advantage is its endogenously produced but disadvantage is that its secreted in the PT, so that at low GFR, tend to overestimate
autoregulation of RBF and GFR
1) myogenic mechanism: ↑BP→intrinsic smooth muscle contraction
2) tubuloglomerular feedback: when RBF and GFR are high, MD senses higher NaCl load AND flow and alters afferent arteriole resistance, which bring RBF and GFR down
vasoactive effects on Na reabsorption in tubules
vasodilators are naturietic (increase Na discharge)
vasoconstrictors are antinaturietic (decrease Na discharge)
major regulators of renin release
afferent arteriolar pressure: ↑pressure - ↓renin
sympathetic tone: ↑activity - ↑renin
NaCl load @MD: ↑load - ↓renin
pressor hormone: ↑levels - ↓renin
effects of AII on renal hemodynamics
↑↑↑efferent tone
↓renin secretion
preserves GFR while counteracting reduced perfusion pressure
NSAIDS effect
when have congestive heart failure, can decrease GFR dramatically because prostaglandins counter vasoconstriction. When their synthesis is inhibited, high vasoconstriction will make GFR drop
characteristics of solute transport along nephron
transport capacity: decreases as →
driving force: increases as →
leakiness: decreases as →
energy efficiency: decreases as →
PT main functions
reabsorption of 2/3rds of Na and H2O, all nutrients, 80% of bicarb and phosphate, and secretion of xenobiotics.
Transporters: Na/nutrient coupled reabsorption, Na/H+ exchanger to aid in bicarb reabsorpt.
solvent drag from leaky TJs
late PT transport
[Cl-] increases, diffuses through TJ, lumen + voltage drives Na+ out of lumen paracellularly
regulation of Na/H2O trasnport in the PT
GT balance: PT always reabsorbs 2/3rds of filtered load despite changes in GFR. Main reason: high GFR creates high π and low hydrostatic P in peritubular capillaries, increasing reabsorption
functions of loop of henle
reabsorb 25% of filtered Na (only in ascending limb) but only 15% of filtered H2O (only in descending limb)
direct dilution of urine
indirect, permissive concentration of urine
TAL transport
Na+/2CL-/2K+ cotransporter; recycling of K+ creates a lumen + voltage that drives paracellular Na, Ca++, Mg++, K+ and NH4+ transport.
rate of paracellular = transcellular
regulation of LH transport
loop diuretics: inhibit Na/K/Cl transporter, used to treat edema assoc. w/ heart failure and hepatic cirrhosis
rate of Na reabsorption increases w/ Na delivery
Ca++ receptors on basolateral TAL cells sense high [Ca] and inhibit K+ channels letting K+ back into lumen.
also regulated by NO and prostaglandins
MD
transport via Na/K/Cl, contributes to renin secretion
main functions of DT
reabsorbs 5% of filtered NaCl via Na/Cl cotransporter, NO H2O, contributes to dilution of urine. Na transport is strictly transcellular
main functions of the CD
major role in regulation of Na balance (ECFV); 4% of Na reabsorption (strictly transcellular) and ~15% (0-20%) of H2O reabsorption. Regulation of H2O balance (exclusive site of regulated H2O transport)
ion transport in the CD
ENaC: apical Na channel driven by low intracellular [Na] and negative potential inside cell - can render tubular fluid nearly Na-free. K secretion is coupled to Na reabsorption; K sparing diuretics block ENaC and therefore conserve K.
aldosterone regulates Na
ADH regulates H2O
main stimulus for ADH secretion and thirst
increase in effective plasma osmolality
Osmotic control via ADH and thirst
ADH onset at approx plasma osmolality of 282 mOsm/kg H2O and plasma [Na] of approx 138 meq/L
Thirst onset at approx plasma osmolality of 290 mOsm/kgH2O and plasma [Na] of 145
volumetric control of ADH secretion
decrease in blood volume or pressure of >15%
volumetric control of H2O balance
high [Na]→ADH and thirst osmoreceptors→neurohypophysis secretion of ADH and thirst center stimulated, ADH acts on kidneys
renin secreted from kidneys→AII→increases thirst
ANP from heart inhibits ADH osmoreceptors
protection against overhydration
cold receptors and GI metering
countercurrent exchange
medullary vasa recta get teeny flow and sluggish movement to preserve Na gradient
countercurrent multiplier
hairpin structure of LH exploited to increase the osmolality of the interstitium and create a large axial Na gradient
effects of ADH
increased H2O permeability of all CD
increased urea permeability of medullary CD
renal handling of urea
50% is reabsorbed in PT via paracellular diffusion and solvent drag. High urea permeability in LH where up to 70% (but as little as 10%) moves back into lumen, then medullary CD has high urea permeability during antidiuresis→reabsorbs 90%, which creates large urea gradient and effectively uncouples urea excretion from needing H2O also.
diabetes insipidus
central: inadequate release of ADH
nephrogenic: kidney is resistant to ADH
SIADH
ectopic ADH secretion that is not suppressed by low plasma osmolality
free water clearance
rate at which water needs to be added to or subtracted from urine to render it isoosmotic with plasma. Excess h2o secretion=positive, excess solute=negative
