Disorders of Volume Balance Flashcards
What are the following normal values in the blood plasma?
[Na+]
[K+]
[Cl-]
[protein]
osmolality
[Na+] = 142 mM
[K+] = 4.4 mM
[Cl-] = 102 mM
[protein] = 1 mM
osmolality = 290 mOsm
What are the following normal values in the interstitial fluid?
[Na+]
[K+]
[Cl-]
[protein]
osmolality
[Na+] = 145 mM
[K+] = 4.5 mM
[Cl-] = 116 mM
[protein] = 0 mM
osmolality = 290 mM
What are the following normal values in the intracellular fluid?
[Na+]
[K+]
[Cl-]
[protein]
osmolality
[Na+] = 15 mM
[K+] = 120 mM
[Cl-] = 20 mM
[protein] = 4 mM
osmolality = 290 mOsm
effective arterial blood volume (EABV)
the part of the extracellular fluid that is in the arterial system and is effectively perfusion the tissues (~700 cc in a 70 kg person)
in physiological terms, EABV is the pressure perfusion the arterial baroreceptors in the carotid sinus and glomerular afferent arterioles
What are the high pressure volume receptors?
carotid sinus
aortic arch
left ventricle
juxtaglomerular apparatus
What are the low pressure volume receptors?
cardiac atria
right ventricle
pulmonary vessels
What is normal serum sodium? What is a good measure of? And what does it mean when it is high? Low?
normal value - 140 mEq/L
best measure of relative proportion of solute to water ratio in the body
low values indicate relative water excess
high values indicate relative water deficit
volume regulation vs. osmoregulation
volume regulation is the renal handling of salt, and thereby volume
(volume is sensed (EABV) with multiple regulators and urine sodium excretion is primarily affected)
osmoregulation is the measurement of plasma osmolality and the subsequent response to high or low osmolality
(sensed by hypothalamic osmoreceptors, stimulating either thirst or water excretion, plasma osmolality is change dthrough water balance)
causes of low volume hyponatremia
GI losses
diuretics
salt losing nephropathy
causes of euvolemic hyponatremia
hyperthyroidism
glucocorticoid def.
ADH release
SIADH
polydipsia
causes of high volume hyponatremia
CHF
cirrhosis
nephrosis
renal failure
effectors of osmoregulation
ADH
thirst
effectors of volume regulation
RAA
sympathetic nerves
ANP
ADH
pressure natriuresis
What is the body’s response to a high osmolality?
stimulates release of ADH and stimulates thirst
water intake and ADH water retention by the kidneys causes plasma osmolality to decrease
What is the body’s response to a low osmolality?
little or no ADH would be released, and there would be no thirst stimulation
lack of ADH would allow for the excretion of dilute urine and therefore water loss from the body and an increase in the serum osmolality
What are the effector mechanisms integral for volume regulation?
RAAS
sympathetic nervous system
atrial natriuretic peptide (ANP)
ADH
pressure natriuresis
At the extremes is osmolality or volume more important to the body?
volume statis is more important
at the extremes, the body will retain or release ADH despite the osmolality stimulus
What are the criteria for successful urinary concentration?
intact medullary osmotic gradient
ADH is present and cells can respond
slow flow to allow osmotic equilibrium
What are the criteria for successful urinary dilution?
sufficient delivery of fluid through nephron
optimal solute transport out of urinary space in thick ascending limb
no ADH present
fast flow through tubules
How is GFR releated to sodium load?
in the steady state, sodium intake is equal to output (~100 mEq/day)
therefore the kidney filters > 20,000 mEq/day, but only 100 mEq are excreted in the urine in one day
Describe the distribution of sodium reabsorption in the nephron.
67% filtered in the proximal tubule
25% filtered in the TAL
5% filtered in the DCT
3% filtered in the CCD
urinary excretion is ~100 mmole/day
0.4% filtered load remaining
What is the equation for the fractional excretion of sodium?
fractional excretion = amount excreted x 100%/filtered load
(Ux/Px) / (Ucr/Pcr)
Describe the channels in the proximal tubule cell.
Describe the channels in the thick ascending limb cell.
Describe the channels in the distal convoluted tubule cell.
Describe the channels in the principal cell.
What is considered low urine Na? What are the exceptions?
low urine Na is less than 15-20 mEq/L
this suggests decreased EABV in the appropriate clinical setting
exceptions include low sodium diet in a steady state, renal ischemia
What does low FeNa (<1%) suggest?
a prerenal state (decreased EABV) or normal physiology
What are the effects of angiotensin II?
sympathetic activation
smooth muscle vasoconstriction
decreased bradykinin
Na/H2O retention (via aldosterone)
What is the effect of increased sympathetic signals on the kidneys?
increased renin, angiotensin II, and aldosterone
increased Na+ reabsorption both directly and thorugh AGII and Aldo
increased EABV/ECV and cardiac output as a result
natriuretic peptide
peptide released from the cardiac atria, activates guanylyl cyclase through attachment to membrane receptor
stimulus for release is atrial stretch
acts as vasodilator and promotes urinary Na+ and water excretion through increased GFR and inhibition of Na+ reabsorption in the medullary collecting tubule
What is pressure natriuresis?
a backup physiological phenomenon that does not rely on humoral or neural control
unclear mechanism
probably does not play a large role in day to day volume balance, when the other effector systems are in place
How does hypertension affect pressure natriuresis? Hypotension?
in the absence of neurohumoral factors, hypertension promotes Na+ excretion and hypotension promotes Na+ retention
underfilling theory
as plasma leaks out of the capillaries, the kidney senses an “underfilled” vascular tree (a decreased EABV) and holds onto salt and water
can result in edema over time
treating with diuretics may decrease perfusion
overfilling theory
the kidney inappropriately holds onto salt and water, creating an “overfilled” vascular system and edema
treatment with diuretics is usually safe
What are the clinical features of nephrotic syndrome?
proteinuria
edema - periorbital, peripheral
mechanism of edema in nephrotic syndrome
overfilling secondary to abnormal kidney retaining Na+
underfillying if capillary hemodynamics are altered by hypoalbuminemia
protein in urine creates a low plasma oncotic pressure and fluid movement into the interstitium
the result is a response to retain additional volume
treatment of edema in nephrosis
cure the underlying disease
restrict NaCl intake
ACE-inhibitors may decrease proteinuria, improve cardiac function
diuretics to improve symptoms of edema
mechanisms of edema in heart failure
increase in venous (hydrostatic pressure) behind the heart
lack of forward force to appropriately stimulate the high pressure receptors
low EABV results, the kidney retains Na+
treatment options for heart failure
ACE inhibitors - reduce afterload (DM)
beta-blockers (DM)
spironolactone - antagonizes aldo (DM)
digoxin - improves cardiac function
diuretics - remove fluid
salt and water restriction for edema
bradykinin
a vasodilator that results from angiotensin II release
clinical features of cirrhosis
ascites
lower extremity edema (below the diseased liver)
mechanism of edema in liver cirrhosis
splanchnic vasodilation and decreased systemic vascular resistance make the kidney perceive a decreased EABV due to the increased diversion of blood to the other abdominal organs, and retain salt and water
primary sodium retention (overfiling) - observed early in cirrhosis
decreased EABV, and resultant underfilling found later
treatment of liver cirrhosis
fix the liver
restrict NaCl intake
water restriction if hyponatremic
diuresis if needed
What is hepatorenal syndrome? How is it treated?
primary liver failure, renal failure, and low urine Na+ in the settin gof eu- or hypervolemia
treatmet - combination of midodrine (an oral alpha1 adrenergic stimulator) and octreotide (a splanchnic vassoconstrictor)
