extracellular

intracellular

plasma volume (1/4 ECF, 1/12 TBW)

interstitial fluid (3/4 ECF, 1/4 TBW)

TBW = 60%

ICF = 40% weight

ECF = 20% body weight

can use dilution methods in which a known amount of a substance is given and the subs is allowed to equilibrate and then the [] in plasma is measured, allowing the vol of distribution to be calculated as follows:

V = (amount given - amount excreted)/[plasma]

TBW : D2O

ECF : mannitol, inulin, sulfate

Plasma : radioiodinated albumin

ICF : ECF - Plasma

Intracellular : TBW - ECF

the volume of the body fluid compartment

get an increase in ECV

no fluid shift occurs because shifts are only going to occur with changes in osmolarity.

[plasma protein and hemtocrit] decrease

(RBCs do not shrink or swell bc isotonic)

arterial BP increases

ECF volume decreases.

because there's no change in osmolarity, no fluid shift occurs. RBCs do not shrink or swell

Hct and plasma protein [] increase.

the osmolarity of the ECF increases, so do get a fluid shift from the ICF -> ECF.

ICF vol decreases, ECF vol increases

is known as hyperosmotic vol expansion

[plasma and Hct] decrease as ECF increases

decsribe the process of hyperosmotic volume contraction

(eg sweating in a desert)

lose H20, so osmolarity of ECF increases, inducing a fluid shift from the ICF -> ECF

ICF volume decreases

ECF volume also decreases

 ICF osmolarity increases as fluid shifts out, so get net increase of osmolarity of both ECF and ICF

plasma prot [] increases bc of decreased ECF vol, but since the osmolarity it increased, fluid is drawn out of RBCs -> Hct stays the same

decsribe what happens in hypo-osmotic volume expansion.

eg SIADH

osmolarity of ECF decreases bc of retained H2O-> fluid shift from ECF to ICF

ICF osmolaity decreases until = ECF, and ICF vol increases

since water is moving into the RBCs, the hematocrit stays the same, but [protein] in the plasma decreases

explain what occurs with hypo-osmotic volume contraction

eg adrenocortical insufficiency

since you're losing Na+ from the ECF, get a fluid shift from ecf -> ICF causing ICF osmolarity to decrease until = ECF osmolarity

ICF volume increases

[plasma prot] increases bc of decrease in ECF vol, and Hct increases bc of decreased vol and swell due to entry of water

arterial BP drops

the volume of plasma cleared of a substancer per unit time

units = mL/min or mL/24hr

C = (UV)/P

C = clearance

U = urine [] mg/mL

V = urine flow rate(mL/min)

P = plasma [] (mg/mL)

by changing the renal vascular resistance. if arterial BP changes, a proportional change occurs in renal vasc R to maintain a constant RBF

RBF remains constant over a range of arterial pressures, from 80-200mmHg

myogenic mech: afferent arterioles contract when stretched

tubuloglomerular feedback: increased fluid delivery to macula densa causes constriction of nearby afferent arterioles to maintain constant pressure

the clearance of PAH is used to estimate RPF

Clearance PAH = (U[PAH]xV)/P[PAH]

by looking at the clearance of inulin.

also look at the serum levels of BUN and creatinine, both of which are waste products normally cleared by the kidney. increased levels indicate depressed renal function.

can also be expressed as the starling eqn

GFR= K[(HPgc-HPbs)-(OPgc-OPbs)]

the fraction of RPF filtered across the glomerular capillaries

FF = GFR/RPF

reabsorbance and secretion rates:

if the filtered load is > excretion rate, then net reabsorption has occured

if  FL < excretion rate, then net secretion of the substance has occured

filtered load = GFR x [plasma]

excretion rate = [urine] x V

reabsorption = FL - ER

secretion = ER - FL

at glucose []'s > 350 mg/dL = Tm of carriers

threshold, or [] at which glucose first appears in urine, = 250mg/dL

the term splay refers to the excretion of glucose in urine before the saturation of reabsorption (Tm) is fully achieved

be able to C&C Tm curves for glucose and PAH

weak acids have an HA and an A- form

the HA form is readily reabsorbed

HA form predominates at acidic pH, so don't get excretion of weak acids with acidic urine

alkaline urine, HA predominates, get increased excretion

(so alkalinize urine to get rid of ASA)

weak bases have a BH+ and B form

B form readily reabsorbed

at acidic pH, BH+ form predominant, increased excretion

at basic pH, B form predominant, decreased excretion

67% reabsorbed at proximal tubule

is isosmotic (Na+ H2O reabsoprtion proportional)

early PCT: transported along with aa, glucose, phosphate and lactate

also reabsorbed by counter-transport with H+ (directly linked to HCO3- reabsorption) CA inhibitors = diuretics that work here.

late PCT: Na+ is reabsorbed w Cl- (bc glucose, aa etc have all been reabsored at this point)

glomerulotubular balance in PCT means will always reabsorp 67% regardless of GFR. so if GFR increases, filtered load of Na+ also increases and Na+ reabsorption also increases to maintain reabsoprtion of 67%

causes increased reabsorption.

volume contraction increases peritubular capillary protein [] and decreases capillary pressure both of which act to draw H2O, and thus Na+ (bc is isosmotic reabsorption here) back into the capillaries, increasing proximal tubular reabsoprtion

ECF vol expansion does the opposite

reabsorbes 25% of filtered Na+

Na+/K+/2Cl- cotransporter

(Loops!!!)

this portion is impermeable to water, so get dilution of urine here = diluting segment

has lumen-positive potential difference (from back-diffusion of K+ through luminal channels) This + lumen potential drives paracellular diffusion of Ca2+ and Mg2+

8% Na+ reabsorbed

early DCT: Na+/Cl- contransporter

(Thiazides!!!)

also impermeable to H2O, = cortical diluting segment

late DCT and CD: 2 cell types

principle cells- reabsorb Na+ and H2O, secrete K+, affected by aldosterone (increased Na+ reabsorbed, increased K+ secreted), and ADH (increases H2O permeability at this segment)

intercalated cells- secrete H+ (H+-adenosine triphosphatase) which is stimulated by aldosterone, reabsorbs K+ using H+,K+ATPase

50% normally passively reabsorbed in PCT

all other segments are usually impermeable. under influence of ADH, inner medullary CD's become permeable to urea, which helps establish a strong osmotic gradient to further drive reabsorption of water!!

85% normally reabsorbed in PCT using Na+/phosphate cotransport

distal segments are impermeable

PTH inhibits phosphate reabsorption in PCT by decreasing activity of cotransporter (so decreases interaction bt increased Ca2+ and phosphate)

most filtered K+ is reabsorbed in the PCT(70%) and loop of henle (25%), and most K+ excreted in the urine is carried out by cortical CD principle cells (ranges from 1-15%)

when dietary K+ changes, renal excretion changes in the same direction, mostly thru effects on the CD principle cells

I. elevated K+ -> increased activity of basolateral K+/H+ATPase of PC -> increased intracellular K+ and increased secretion and excretion

II. K+ acts in adrenal cortex to increase aldosterone which acts on principle cells ->

1. increased luminal Na+ permeability

2. increased # and activity of basolateral NaKATPase

3. increase luminal permability to K+

all promoting K+ secretion