Flashcards in Renal: Body Fluids Deck (74):
Molarity = what
# moles per liter SOLUTION (includes solute)
Molality = what
number moles per kg solvent (does not include solute)
when is there a big diff between molarity and molality?
when there is a considerable concentration of solute
in PLASMA, is there a difference between molarity and molality?
YES, there are enough solutes to make a difference between molarity and molality
colligative property of solution. total numbre of particles in solution regardless of the nature of those particles.
what is osmolality of NS?
290 mOsm/kg H20
how will lab report osmotic concentration?
as osmolality. Lab - osmoLality
define an effective osmole
solute with permeability less than water. will suck water to its own side in order to equilibrate osmolality
how do cells behave in terms of NaCl?
behave as if they are impermeable to NaCl.
Is NaCl an effective osmole across the capillary membrane?
NO, because endothelial cells are permeable to it.
what is the reflection coefficient? what does a reflection coefficient of 0 indicate? 100?
the probability that a solute will NOT be able to cross the membrane. 0 means that a solute will always cross membrane, 100 means that it will cross as freely as water.
what is the Donnan effect?
the effect of charged particles to osmotic pressure. If there is a + charged particle on one side of a membrane that cannot cross, it will pull - charged particles to its side and therefore change the osmotic pressure.
Describe the fluid compartments of the body.
BW = body weight
TBW = total body water
ICFV = 2/3 of TBW, CELLS
ECFV = 1/3 of TBW, extracellular
PV = 25% ECFV
ISFV = 75% ECFV
what people tend to have high % body water? low?
Fat has a LOW % body water comparted to muscle. So lean athletes have a higher % water than overweight people.
what drives the pressure for osmotic water entry?
macromolecules within the cell (proteins)
ICFV is determined by the presence of what ion? ECFV?
ICFV: K content
ECFV: Na content
is K higher in the cell or outside the cell?
Much higher INSIDE the cell
what might the osmolar gap indicate
difference between lab osmolarity (measured) and calculated osmolarity. can indicate presence of toxin (anything that is not glucose, BUN, NaCl)
where can pure water move?
what happens if you eat salty food?
salt is restricted to the ECFV compartment (since Na is an effective osmole to cells). will draw water out of cells and portion it in ISFV and PV proportionately.
what are effective osmoles in capillaries?
describe Starling forces
relationship of movement between ISFV and PV. dependent on filtration coefficient, hydrostatic pressures, reflection coefficient, and osmotic pressures. hydrostatic pressures OPPOSE osmotic pressures. along the capillary, osmotic pressures are roughly equal, but hydrostatic pressures decline. at beginning of capillary, net force is OUT. at end of capillary, net force is IN.
what could happen if there is a huge drop in blood volume?
hydrostatic pressure will decline, osmotic pressure will cause fluid to be drawn out of interstitium. autotransfusion.
what 2 qualities of the Starling eqn can lead to edema?
too much hydrostatic pressure (high BP) or too low osmotic pressure (absence of proteins)
best way to lower ICFV?
IV hypertonic solution, will draw free water out of cells.
why can't we infuse pure water?
too hypotonic: will cause hemolysis. infuse with D5W or D2.5W instead
what compartment will NS expand?
will expand mainly ECFV, but also ICFV.
best way to expand PV?
colliods, which contain proteins which cannot cross endothelial membrane
is NS a good way to expand PV?
Not really. It won't expand cells, but 75% will go into ISFV and only 25% will go to PV.
will pure water change the hematocrit?
NO because water distributes freely across all compartments.
the size of a fluid compartment in the body is determined by..
the number of osmotically active particles residing in the compartment
to expand ICFV with minimal effect on ECFV, use what?
pure water. actually, since pure water will lyse cells, use D5W.
blood flow through kidneys is how much of total cardiac output?
what is the main user of energy in the kidney?
what drives O2 consumption in kidney?
blood flow. kidney PO2 is independent of flow. Therefore kidney is a good site to monitor changes in arterial O2 content.
where is the site for countercurrent multiplication?
what are the 3 pressure forces within the glomerulus?
PGC: pressure of glomerular capillary. towards nephron.
PBS: pressure of Bowman's space. towards capillary.
pi-GC: oncotic pressure of glomerular cap. Pull towards capillary.
what is the biggest difference between glomeruli and other body capillaries?
bigger GFR through body capillaries.
what is the eqn for Filtration Fraction?
FF = GFR/RPF
Constrict Afferent: what happens to GFR, RBF, FF?
GFR decr, RBF decr, FF decr
Dilate Afferent: what happens to GFR, RBF, FF?
GFR incr, RBF incr, FF incr
Constrict Efferent: what happens to GFR, RBF, FF?
GFR incr, RBF decr, FF incr
Dilate efferent: what happens to GFR, RBF, FF?
GFR decr, RBF incr, FF decr
how is the filtration barrier able to be selective?
Charge and size of particles
damage to the filtration mechanism may lead to what?
qualities of post-glomerular capillaries in terms of osmotic and hydrostatic pressure?
osmotic pressure is HIGHER (higher amt of protein/unit liquid); hydrostatic pressure is lower (lower fluid pressure after glomerulus). NET effect = more pressure in towards capillaries.
the volume of PLASMA completely cleared from a substance per unit time.
RPF can be measured using what metabolite?
PAH, because PAH is cleared fully from the blood after one pass through the kidney.
GFR can be measured by using what metabolite?
inulin, because once inulin is filtered, it is not secreted or reabsorbed. really use creatinine, made by muscles in consistent amount. creatinine is a slight over-estimation of GFR because a small amount is secreted.
Autoregulation. over what pressures are the kidneys autoregulated
2 mechanisms for auto-regulation of the kidney?
-tubuloglomerular feedback (MD senses high Na load and feeds back to afferent arteriole)
describe the RAAS pathway. what are the effects of AT II?
angiotensinogen to At I via renin. At I to At II via ACE. At II leads to aldosterone, thirst, salt appetite, constriction of efferent arteriole (slight constriction of afferent arteriole)
4 regulators of renin release?
afferent arteriolar pressure (more pressure, less renin)
sympathetic tone (renin incr)
NaCl load at MD (less renin)
pressor hormones (less renin)
what types of items are actively secreted back into the tubular fluid in the PT?
what is the main consumer of energy in the kidney?
reabsorption of Na
where is Na most reabsorbed?
what is reabsorbed in the PT?
2/3 of water, 2/3 of Na+, 80% bicarb, 80% phosphate, all nutrients. xenobiotics are secreted.
describe the reabs of bicarb. where?
in the PT. indirect: PT secretes H+ (via exchanger with Na+), combines with HCO3- that has been filtered -> H2CO3. Carbonic Anhydrase breaks it to H20 and CO2. both of those are reabsorbed into cell. once in cell, recombine to H2CO3, then break back down to H+ and HCO3-. H+ is recycled via exchanger, HC03- is reabsorbed with Na+ cotransporter.
does the osmolality of the fluid in the PT change?
NO becasue as Na+ is reabsorbed, so is water.
what happens with the concentration of Cl- along the PT?
the concentration increases. it then goes paracellularly to interstitum, leaving the lumen with a + charge. causes Na+ to follow paracellularly.
how are Na and Cl absorbed in the second half of the PT?
transcellular mechanisms: driven by Na/K ATPase -- drives Na/H exchanger, which drives Cl- in, whcih drives Cl- out on the basal side.
define glomerotubular balance. 2 ways it is controlled?
the PT always reabsorbs a constant fraction of the filtered load. roughly 2/3. controls: (1) increase in filtration yields more co-transported substances to fuel Na+ coupled reabsorption. (2) constriction at efferent cap increases GFR and decreases hydrostatic pressure at peritubular cap, while increasing oncotic pressure at peritubular cap. Yields increased reabsorption, reduced back-leak.
AtII does what to the Na/H enchanger?
2 inhibitors to Na absorption in the PT?
dopamine and ANP. both are stimulated by ECFV expansion.
where is water reabsorbed in the LOH?
in the descending limb. NOT in the ascending limb because it is largely imperbeable to water.
result of water/Na transport in the LOH?
water reabsorbed in the descending limb, Na reabsorbed in teh ascending limb. result: tubular fluid becomes hypo-osmotic (dilute) and medulla becomes hyper-osmotic. this drives water reabs in the CD.
through what kind of transported is salt reabsorbed in teh ascending loop?
mainly via the Na/Cl/K co-transported. driven by the Na/K ATPase. K is wated into the lumen, Cl- moves transcellularly through a channel.
how does the TAL protect itself against calcification?
the TAL does reabsorb significant Ca2+ and Mg2+ and bring them into the interstitium. There is a receptor in the interstitial side that senses Ca2+ concentration. When activated, this receptor inhibits apical K channels in the TAL, thus NOT generating the voltage + lumen that drives Ca2+ into the interstitium paracellularly. result: less reabsorption of Ca2+.
MD: what is primary form of co-transporter?
the triple cotransporter: Na/Cl/K.
distal tubule: primary transporter?
Na/Cl co transporter, Na/K ATPase, Cl channels to interstitium.
primary transporter in collecting duct?
Principal cells: Na channel, K channel, Na/K ATPase.
what type of diuretics work in teh collecting duct?
K sparing diuretics. block Na channel on apical side, or block aldosterone. result: reduce K excretion while still decreasing Na reabsorption. (since those two are disconnected in CD)
aldosterone has what effect in the CD?
stimualtes Na reabsorption by principal cells by opening Na channels and upregulating Na/K ATPase.