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47 Cards in this Set

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intracellular and extracellular fluid - what percentages of TBW do they represent and how are they divided, what are the major cations/anions?
TBW = 60% of body weight.

2/3 is intracellular, where the major cations are Mg+ and K+. Major anions are proteins and phosphates (ATP, etc)

1/3 is extracellular, where the major cation is Na+. Anions are Cl- and HCO3-.

note that the extracellualr is further divided: 3/4 are interstitial fluid, 1/4 is plasma.

therefore, plasma is about 1/12 of TBW.
what's the 60 40 20 rule?
TBW is 60% of body weight.

ICF is 40% of body weight

ECF is 20% of body weight.
what markers can be used to measure water and compartments?
for ECF, use mannitol or inulin (both are large proteins that can't get into cells, so stay in the extracellular space). also use sulfate.

for plasma, use RISA or evans blue, as labels albumen.

TBW can be used with D20.

calculate ICF by determining both TBW and ECF and subtracting.

interstitial = extracellular fluid - plasma
how are dilution problems solved?
volume = Amount Injected (minus lost, if given) / concentration.

VAC. V = A/C
what happens if you give isotonic sodium?
extracellular fluid expands but doesn't move into the intracellular fluid compartment. proteins get diluted out which can affect capillary filtration, but generally water doesn't move in. BLOOD PRESSURE GOES UP. So no osmolarities change in the body.
what about diarrhea?
loss of isotonic solution - again, only ECF is affected but no osmolarity change happens. No movement between ECF and ICF. Protein concentration goes up. BP down.
What about excessive NaCl intake?
Hyperosmotic volume expansion:

osmolarity of ECF goes up and ICF has to match - so water shifts out of ICF into ECF. ICF volume goes down, ECF up. Plasma proteins go down.
what happens when you sweat?
this is the loss of hypoosmotic water, so the ECF osmolarity increases.

water shifts out of ICF into the ECF and ICF osmolarity goes up, too.

plasma protein concentration goes up.
what if you have too much ADH around?
you're going to retain too much fluid in your ECF, and this isn't good.

ECF becomes hypoosmotic and fluid begins to accumluate there AND shift into the ICF, decreasing its osmolarity too.

Plasma protein concentration goes down.
what's our urine clearance equation?
C = UV/P

were U is urine concentration, V is urine volume, and P is plasma concentration.

So urine concentration times volume divided by plasma concentration is the clearance - which is how much plasma was cleared per minute. also how much is lost per minute.
Renal blood flow - what percentage of cardiac out put is it?
dilation and contraction of efferent and afferent arterioles - what can cause it and how does this change RBF?
contraction of the efferents happens with light Ang II influence and serves to INCREASE GFR.

ACE inhibitors dilate the efferents and cause a drop in GFR. seems weird 'cause ace inhibitors help bring down blood pressure.

prostiglandins help dilate the arterioles, increasing RBF. Happens from bradykinin, NO, and dopamine.
what's RBF autoregulation and what is it trying to do?
trying to keep RBF constant. works between 80 and 200mmHg.

happens with myogenic mechanism: renal arterioles clamp when pressure is high, release when it's low.

TGF: macula densa detects increased fluid delivery and constricts nearby afferent arterioles.
how do we measure renal plasma flow?
use PAH - it's secreted and filtered, and represents renal plasma flow well (underestimates by 10%).

use same equation: urine concentration times urine volume divided by plasma concentration. add 10%.
if we have renal plasma flow, how can we calculate renal blood flow?
RBF = RPF / 1- HCT
how about measuring GFR?
use INULIN (same thing used to measure ECF).

it's filtered but not reabsorbed or secreted.

can also use serum creatinine.
what's filtration fraction?
amount of renal plasma flow that ends up getting filtered, usually 20%.

it's GFR/RPF. 80% then leaves via the efferent arterioles.
what's our starling equation for kidneys?
GFR = Kf [(P gc - P bs) - (Pi c - Pi bs)]
how are proteins kept from getting into the urine?
negatively charged glycoproteins should line the glomerular capillaries. in renal disease, these can be lost and you get protenuria.
so if plasma protein concentration goes up, how is GFR affected?
more plasma proteins decrease GFR by increasing Pi C and pulling more fluid back out of bowman's space.

note that Pi bs should be zero as there should be no protein in bowman's space.
talk about glucose and reabsorption:
filtered glucose goes up if glucose concentration goes up. (filtered = GFR * [Glucose]

there's Na+/Glucose cotransport in the proximal tubule, but this is limited.

above 350 mg/dl, they're saturated and can't reabsorb.
what does the TF/P ratio tell you?
tubular fluid concentration / plasma plasma concentration.

if they're the same, then no net reabsorption of secretion has happened.

if TF > P (high ratio), then there's been secretion OR water's been pulled out faster than the substance.

if TF < P, then there's been reabsorption of our substance.

if TF = P, then there's been nothing OR it's been reabsorbed in the exact proportion with water. This is what happens to salt in the proximal tubule.
talk about the early proximal tubule: then talk about the middle/late
here, Na+ reabosorbed with glucose.

Na+ also counter transported in with H+ out to get bicarb into the cell.

once all the glucose and bicarb are back in, have to transport Na+ with Cl-.
what's glomerular/tubular balance in the proximal tubule?
always resorb 2/3 of Na+ and H20 in the proximal tubule, regardless of GFR.

if GFR went up, you'd probably filter less unless there was a way to increase resorption, and there is. with higher GFR, there's more colloid pressure in the capillaries to reabsorb more. So, it stays constant.
what's the lumen charge in the thick ascending and what interesting transporter is there?
the Na/K/2Cl- transporter is there, and that's where loop diuretics work.

note that this is the diluting segment, so TF < P.

what about the early distal tubule? interesting transporters?
has the Na/Cl COTRANSPORTER. This is where thiazide diuretics work.
late distal tubule? what substances work here to regulate it?
two cells: principle and intercalated.

principle: secrete K+, absorb Na and H20 (first time it's water permeable since descending loop).

this is where aldosterone works (increases Na+ absorption and K+ secretion) and ADH comes in to add H20 transporters. Note that without ADH, the principle cells are impermeable to water.

Intercalated cells: pump out H+ with an ATPase, also stimulated by aldosterone. Also reabosrb K+ (last stop to reabsorb potassium).
talk about potassium specifically - where is most of it reabsorbed, and how is its concentration controlled?
2/3 resorbed in the proximal tubule (same with Na+ and H20).

thick ascending does another 20%. the remaining is played with later.

Reabsorbed in the intercalated cells with an EXCHANGE FOR H+ on the basolateral membrane.
So, if you're acidic, H+ is pumped from the blood into the intercalated cells and K+ goes into the blood, lowering the concentration of K+ in the cell and secreting less.

Secreted in the principle cells in response to aldosterone OR more salt in the tubule (anything that brings in more salt from the tubule will kick out more potassium). So, if you have hypoaldosteroneism, you'll end up HYPERKALEMIC 'cause you cant kick out potassium.

so - acidosis causes HYPERKALEMIA and alkalosis causes HYPOKALEMIA.
so what are our diuretics and what do they do?
loop and thiazide diuretics (loop block the Na/K/2Cl- while thiazides block the joint Na/Cl- resorption in the late distal tubule both increase potassium secretion by the principle cells by making more Na+ available for exchange.

amiloride acts directly on the principle cells and are potassium-sparing (cause hyperKALEMIA if not careulf). try to use both diuretics together.
talk about urea reabsorption:
50% in the proximal tubule.

that's usually it, unless ADH is around, where innermedularry collecting ducts become permeable and urea leaves the ducts for the interstitium.

this helps create the countercurrent
85% reabsorbed in the proximal tubule with a co-transport with Na+. The rest gets excreted.

NOTE: PTH causes phosphate excretion by messing with this transporter. PTH causes phosphoturia and urinary cAMP
90% reabsorbed in proximal/distal tubule. Note that PTH increases this resorption through cAMP.

Coupled to Na+ resorption, so loop diuretics cause pissing out of Ca++. Thiazide diuretics do the opposite.

NOTE: Mg and Ca++ compete for the same channels - so having hypercalcemia causes Mg to get peed out.
concentrating urine: what substance has to be secreted and what are the processes that have to be turned on?
ADH has to make counter current multiplication, urea recycling and countercurrent exchange (in the vasa recta) happen
what does ADH do to set up countercurrent exchange?
depends on NaCl resorption in the thick ascending - goes up with ADH to leave more salt in the interstitium.

help urea recycling happen too.
what's free water clearance calculation?
CH20 = V - Cosm

as in, urine flow - clearance of your substance

and we know clearance is urine concentration times urine flow divided by blood concentration.
what kinds of acids are made by the body?

what are our big buffers and where do the work?
volatile and non-volatile.

volatile is C02.

non-volatile is everything else.

extracellular buffer is HC03- and phosphate.

intracellular buffers are organic phosphates (ATP, etc) and proteins. remember that deoxyhemoglobin is a good buffer.
what's contraction alkalosis?
you tend to resorb more H2CO3- when volume contracted (it's an osmolite that can be used to force water resorption)

note that this is mediated by angiotensin II
go through the symptoms of hypoaldosteroneism (addison's disease)? what responds inappropriately?
decreased serum Na+, hyperKalemia, volume contraction (from inability to pull in Na+ and water), hyerpigmentation, weight loss, weakness.

hypotension from the volume depletion.

get inappropriate ADH release which resorbs water and makes the hyponatremia worse.
what does vomiting do? what responds inappropriately?
loss of H+ from stomach acids causes a metabolic alkalosis. respond with respiratory acidosis (decreased breathing).

also get decreased volume. this upps the renin system, leading to more aldosterone.

remember that one way Ang II works is to resorb HCO3- from the proximal tubule - so you're already alkalotic, now you're resorbing more HCO3-, it gets worse.
what must urine H+ excretion equal?
the daily production of H+ from cagtabolism and ingested H+ must equal excreted titratable acid and amonium
free water clearance and urine - to have a positive or negative free water clearance, must urine be hyper or hypo osmotic?
hyperosmotic urine = negative free water clearance.
what does dilation of the afferent arteriole do to GFR and RPF?
makes both go up.
diuretics and calcium - which affect calcium resorption/excretion?
they all do, but act differently.

usually, Na+ and Ca+ resorption are linked - so diuretics that stop Na+ resorption will stop Ca++ resorption.

thiazides are an exception - these increase Ca++ resorption.
how does SIADH differ from water deprivation?
SIADH means too much ADH around for no good reason, which will up water retention and make the plasma HYPOOSMOTIC.

water depravation will make the blood slightly hyperosmotic and then cause ADH release.
how does aldosterone affect pH balance?
ALdosterone causes ALkalosis

extra aldosterone makes the intercalated cells kick out more H+ and "make" more HCo3-
acidosis and alkalosis - what's associated with hyper and hypo kalemia?
acidosis is associated with hyperkalemia. remember that H+ ions can be exchanged for potassium through cellular membranes. so, too much H+ floating around will go into cells in exchange for potassium.

opposite for alkalosis.
Which cells does aldosterone work on in the collecting duct?
both intercalated cells and principle cells.

makes K+ enter the lumen. makes H+ enter the lumen. Pulls Na+ in.