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68 Cards in this Set

  • Front
  • Back
what fraction of total body water does the plasma comprise?

what are the fractions behind that?
1/12, because

1/3 of TBW is ECF
1/4 of extracellular fluid is plasma
most hyponatremia and hypernatremia are caused by
_____ ____ ____ ____
abnormal H2O intake or excretion
___ ions determine the tonicity of the ECF

____ ions determine the tonicity of the ICF
Na+ and its accompanying anions

K+ and its accompanying anions
definition of

tonicity vs. osmolality
tonicity: the effect that a fluid has on cell volume.

e.g. hypertonicity of the ECF makes the ICF shrink

osmolality: the number of solute particles dissolved in a kg of H2O
three different kinds of osmoles

and examples of them
cell-permeable, ineffective osmoles
--glucose in the presence of insulin

cell-impermeable, effective osmoles

--confined to plasma
if an osmole is "ineffective" what does that mean?
it does not affect plasma tonicity

i.e. it does affect H2O movement between the ECF and ICF
what's so special about Na+ as an osmole?

Na+ is the most important effective osmole in plasma

because of its

--high concentration
--exclusion from ICF
what's so special about albumin as an osmole?
even though it is only 1/290 mosm of plasma osmolality,

it's the only unique osmole in plasma

therefore it's the chief determinant of plasma oncotic pressure
Na+ and albumin are in what body compartment?
Na+ -- ECF

albumin -- plasma
osmolality equation
osmolality =

2 x Na+

+ glucose / 18

+ BUN / 2.8
milliequivalents =
millimoles x charge
_ is the big cause for H2O movement between the ECF and ICF
change in the plasma Na+ concentration
what are three big contributors to plasma osmolality?
Na+ 280

BUN 4-5
glucose 5-6
BUN can change

plasma _____ and _____
can change plasma osmolality

but NOT plasma tonicity
what's one bad effect that hyperglycemia immediately has on the body?
cellular dehydration
in the presence of insulin

tonicity =
2 x plasma Na+
5 osmoregulation mechanisms
CNS mechanisms
--release of vasopressin

renal mechanisms
--rate of fluid delivery to distal nephron
--NaCl reabsorption in water-impermeable portion of distal
--H2O permeability in medullary collecting ducts
what are a couple mechanisms that normally don't regulate intravascular volume, but in an emergency, it's okay to steal, and e.g. in hemorrhage, they'd pitch in and do their part?

formally state how they're regulated?
thirst and vasopressin

--normally regulated by changes in plasma osmolality

--can also be regulated by a substantial decrease in plasma volume
if osmolality is high, but blood volume is low (e.g. hemorrhage) is ADH released?

low blood volume has the trump card.
mechanisms to regulate plasma osmolality work to do one basic thing:
to increase or decrease H2O content in the ECF
vasopressin is released

from __ in the hypothalamus,
as a response to ____

but from __ in the hypothalamus
as a response to ____
supraoptic nucleus
increased plasma osmolality

paraventricular nucleus
decreased intravascular volume
plasma Na+ levels __ and __

and plasma osmolality ___ and ___

correspond to

urine osmolality __ and __
275, 295
135, 144
50, 1200
osmotic threshold to initiate the sensation of thirst
295 mosm/Kg H2O
where are thirst receptors located?
anterolateral hypothalamus
what's the most important mechanism that regulates intravascular volume?

3 other mechanisms?

natriuretic peptides


for a patient with volume depletion,

what's the anatomical pathway that regulates vasopressin release from the hypothalamus?
carotid sinus baroreceptors
atrial baroreceptors

paraventricular nuclei
__ and __ cause Na+ reabsorption

from what parts of the nephron?
aldosterone -- DCT and CCD
three things listed to increase thirst
increased osmolality

decreased intravascular volume

____ notices low intravascular volume

and causes ____ to release vasopressin
carotid sinus baroreceptors
atrial baroreceptors

paraventricular nuclei of hypothalamus
a low urine sodium is _____

and indicates what?
< 10 mEq/L

-- low dietary Na+
-- activation of the RAAS
there is no predictable relationship between plasma __ and urinary __

because ___ is regulated by...

and NOT by...
plasma Na+
urinary Na+

Na+ excretion is regulated by changes in

-- dietary Na+ intake
-- intravascular volume

not by changes in plasma [Na+]
if hypotonic fluid is added to the ECF, causing high volume and low sodium/low tonicity...

3 hormones are inhibited or increased in response? how exactly?

urinary Na+ excretion is decreased or increased?
low tonicity inhibits vasopressin

(as it should. this increases H2O excretion. we have more than enough total water.)

the irony is that the high volume
--inhibits renin release
--increases ANP release

and both of these last two cause
--increased Na+ excretion

IN SPITE OF the low plasma tonicity
what's the relationship between urine specific gravity

and urine osmolality?
usually parallel

(they increase or decrease by similar amounts)

exception: radiocontrast dyes disproportionately increase urine specifiic gravity
true hyponatremic disorders result from

(2) broad mechanisms
massive water intake
impaired renal water excretion
all true hyponatremic disorders feature

(2) lab findings
parallel reduction in

serum tonicity
serum Na+
two unusual types of hyponatremia

(that aren't "true hyponatremia")
(isotonic hyponatremia)

the gist of the problem is _ _ _ _ _
elevated serum lipids or proteins
isotonic hyponatremia is aka ____
(isotonic hyponatremia)


no treatment

the elevated serum lipids or proteins lower the [Na+] in a liter of plasma (solids plus water)

but the concentration of Na+ dissolved in the water phase of plasma doesn't change
(hypertonic hyponatremia)

the gist of what causes it
increase in plasma osmolality > 295

caused by e.g. mannitol or glucose in the absence of insulin

causes H2O to shift from the ICF into the ECF

thereby decreasing plasma Na+ concentration
plasma Na+ decreases by ___

for each _____ increase in glucose

plasma Na+ decreases ~ 2 mEq/L

for each 100 mg/dL increase in plasma glucose above 100 mg/dL
hypertonic hyponatremiai:

reduce the concentration of the elevated non-Na+ solute (e.g. mannitol or glucose) in the ECF

e.g. give insulin!

[? for mannitol or some others, I'm guessing you might do dialysis?]
the first step in the evaluation of hyponatremia is...

to measure plasma osmolality

in order to rule out isotonic and hypertonic conditions

is classified in 3 categories

and one of those categories has 3 subcategories. rank those in order of frequency

hypotonic hyponatremia
--hypervolemic (most common)
--hypovolemic (least common)
(hypotonic hyponatremia)

hypovolemic is caused by three things

they all share (broadly speaking) the same underlying thing going wrong / ~ mechanism
aldosterone deficiency

cerebral salt wasting

secretory diarrhea
excessive sweating

--Na+ lost in excess of H2O
--Na+ and H2O losses replaced with pure H2O
(hypotonic hyponatremia)

hypovolemic has 3 causes. list them and their

urine osmolality
urine Na+
aldosterone deficiency

≥ 20:1
> 400
> 20

cerebral salt wasting
≥ 20:1
> 100
> 40

secretory diarrhea
excessive sweating

≥ 20:1
> 400
< 10
hypovolemic hypotonic hyponatremia

aldosterone deficiency

urine osmolality
urine Na+

what mechanisms cause these lab values to be observed?
≥ 20:1
> 400
> 20

decreased Na+ reabsorption in the distal nephron
--> volume loss
--> stimulates RAAS, vasopressin

ATN II and vasopressin do what they can do
--this explains BUN/creatinine,Uosm

there remains the aldosterone problem / Na+ loss in distal tubule
--this explains the high urine Na+
hypovolemic hypotonic hyponatremia

orthostatic hypotension
resting tachycardia
low jugular venous pressure

[these he did not put in bold:
recent weight loss
poor skin turgor
dry axilla]
two possible initial, root cause mechanisms for cerebral salt wasting

CNS injury leads to two separate problems...
*BNP* release from hypothalamus

- - - - - - - - - - - - - - - -

+ SV, CO
how does cerebral salt wasting cause hyponatremia?
all of these are falling dominoes:

increased GFR and BNP

decreased Na+ reabsorption throughout much of the nephron

polyuria > 3 L /day

decreased intravascular volume

vasopressin release
H2O reabsorption
what two sodium problems are seen respectively in

aldosterone deficiency

primary hyperaldosteronism
hypotonic hyponatremia

hypervolemic hypernatremia
what two sodium problems are seen respectively in


hypotonic hyponatremia

hypovolemic hypernatremia
CNS problems including tumors, trauma, infections, etc.

can cause these two sodium issues
cerebral salt wasting
(hypovolemic hypotonic hyponatremia)

(isovolemic hypotonic hyponatremia)
secretory diarrhea
excessive sweating
... and _____

can cause what two sodium problems?

how does it cause one, or the other?
hypovolemic hypotonic hyponatremia
--loss of more Na+ than H2O
--(vomiting is also listed for this one)

hypovolemic hypernatremia
--when H2O losses are not replaced
cerebral salt wasting causes what category of sodium problem?

hypovolemic hypotonic hyponatremia
elevated serum lipids or proteins can cause what category of sodium problem?

isotonic hyponatremia
mannitol or glucose in the absence of insulin can cause what category of sodium problem?

hypertonic hyponatremia
cerebral salt wasting's lab values:

urine osmolality
urine Na+

explain the findings
1. ≥ 20:1
2. > 100
3. > 40

1. this reflects
--volume depletion (is RAAS activated or not?!)
--vasopressin's effect on BUN reabsorption

2. polyuria causes volume loss,
which stimulates vasopressin

but the urine is not strongly concentrated because

--Na+ losses and polyuria prevent formation of hypertonic medullary interstitum
--natriuretic peptides antagonize the concentrating effect of vasopressin in the medullary collecting ducts

3. increased GFR and BNP decrease Na+ reabsorption throughout much of the nephron
secretory diarrhea
excessive sweating

can cause hypovolemic hypotonic hyponatremia

what lab values are observed for

urine osmolality
urine Na+

explain the findings
≥ 20:1
> 400
< 10

volume depletion stimulates RAAS and vasopressin
the three categories of hypotonic hyponatremia

listed in order from most common to least common
hypervolemic hypotonic hyponatremia

peripheral edema
elevated jugular venous pressure

[not in bold:
history of recent weight gain]
hypervolemic hypotonic hyponatremia:

there are two different groups of problems that cause it.

in each, what is the gist mechanism in terms of Na+ and H2O?
heart failure
nephrotic syndrome

retaining Na+ and H2O
but more H2O than Na+

acute tubular necrosis
chronic kidney failure

H2O retention in excess of Na+
particularly when H2O intake exceeds capacity for its excretion
what are the disease states that cause

hypervolemic hypotonic hyponatremia?
the most common causes:
--heart failure
--nephrotic syndrome

--acute tubular necrosis
--chronic kidney failure
chronic kidney failure is listed as causing what sodium problems?

hypervolemic hypotonic hyponatremia

hypovolemic hypernatremia
heart failure
nephrotic syndrome

can cause hypervolemic hypotonic hyponatremia. list and explain the lab findings.

urine osmolality
urine Na+
≥ 20:1
> 400
< 10

reduced effective intravascular volume stimulates RAAS and vasopressin
acute tubular necrosis
chronic kidney failure

can cause hypervolemic hypotonic hyponatremia

list and explain the lab findings:

urine osmolality
urine Na+
≤ 15:1
isotonic to plasma ~ 300
> 20

Na+ and H2O reabsorption are impaired

therefore urea reabsorption is also impaired

the failing kidneys are unable to dilute or concentrate the urine
the two sodium problems


that are caused by ADH disturbances
--isovolemic hypotonic hyponatremia

diabetes insipidus
--isovolemic hypernatremia
isovolemic hypotonic hyponatremia

what causes it?
SIADH is the most common cause

other causes:

i. glucocorticoid deficiency

ii. hypothyroidism

iii. carbamazepine

iv. exercise-associated hyponatremia

v. primary psychogenic polydypsia