Flashcards in Hormonal Control of Sodium and Water Balance Deck (26):
Contrast the actions of ADH and Aldosterone in water and sodium regulation.
ADH- enhances water reabsorption in response to osmolarity (hypothalamus) and then ECV (baroreceptors of carotid sinus and aortic arch)
Aldosterone: increases sodium reabsorption in response to ECV or when sodium levels in filtrate are low
What is characteristic of an "effective osmol."? What does that mean effective. ineffective osmolality?
particles that are trapped in one compartment (cannot diffuse across the membrane) will pull water from another to dilute themselves— these are called effective osmosis
compartments with effective osmols is hypertonic, one with fewer effective osmols is hypotonic
Give examples of ineffective and effective osmols. in cell dynamics.
ineffective: BUN, glucose (normally)
normally Na is the main determinant of ECF tonicity
What is the range of "normal" osmolarity of the ECF?
280-300 mosmols/kg of water
Where and how does ADH work?
acts at the distal nephron, ADH allows water reabsorption
binds to membrane receptor of principal cell in collecting duct, stimulates cAMP and insertion of water channels into the luminal membrane
What is required for normal water excretion and dilution of urine?
adequate renal blood flow
reabsorption of Na and Cl in thick distal limb
dilute urine must be maintained by lack closed water channels
water excreted cannot exceed the amount that can be excreted given the osmolality of max. dilute urine
Abnormalities in the serum sodium are almost always due to alterations in ______ ______ ____.
body water content: addition of water causing hyponatremia, loss of water causing hypernatremia
Symptoms of high and low Na are primarily ______ and are due to?
symptoms are primarily neurologic and are due to shrinking or swelling of brain cells, related to the severity and rapidity of Na change
What are the 3 kinds of hypnatremia?
isoosmolar (mostly a lab artifact due to elevated plasma proteins or lipids)
Describe the condition of hyperosmolar hyponatremia.
caused by accumulation of an effective osmol (other than Na)
most commonly in uncontrolled diabetes; excess sugar causes shift of fluid to ECF and dilutes the ECF sodium
** an individual with marked hyperglycemia and serum sodium concentration that is NOT LOW is in a state of severe water depletion (osmotic diuresis)
What is the most important next step in a patient that has low sodium and low osmolality?
determine their volume status (3 types of hypoosmolar hyponatremia)
What are causes of hypovolemic hypoosmolar hyponatremia?
usually not endocrine: due to loss of both water and salt, but more sodium than water (look for dry membranes, tacky and orthostatic hypotension)
renal losses in kidney disease, diuretic use, aldosterone deficiency (elevated urinary Na) or non renal GI losses, burns (urinary Na appropriately low)
What are causes of hypervolemic hypoosmolar hyponatremia?
usually not endocrine: due to gain of both water and sodium but more water than sodium- usually total body volume overload but low effective intravascular volume (CHF, cirrhosis)
look for peripheral edema, increased JVP
What are causes of euvolemic hypoosmolar hyponatremia?
caused by gain of water (constant input/output) without sodium- commonly due to SIADH, urine cannot be fully diluted; SIADH can be from pituitary secretion, ectopic ADH production or due to drugs (possibly hypothyroidisma, cortisol deficiency or psychogenic polydipsia)
leads to low [Na] and low serum osmolality, urine osmolality that is inappropriate (not maximally dilute)— tx with restriction of free water
What is the cause of Beer drinker's potomania?
poor diet leads to less than normal daily solute excretion which limits the amount of water that can be excreted with maximally dilute urine
Hypernatremia is almost always due to what?
deficit of free water, rarely due to addition of salt w/o water
hyperosmolality triggers ADH secretion and thirst so hypernatremia is rarely seen in those who have free access to water (excludes those with altered mental status, ICU, infants)
Describe the cause of diabetes insipidus (DI).
lack of ADH action either through deficiencies in production (central) or in resistance to ADH action (nephrogenic)
patients will produce large volumes of dilute urine leading to hyperosmolality— patients will often drink until osmolality normalizes if they have access
How do you differentiate between central and nephrogenic causes of diabetes insipidus?
create a stimulus for ADH secretion by the "water deprivation test"
hyperosmolality should serve as a strong ADH secretion stimulus (occurs only successfully in nephrogenic), after administer ADH and look for evidence of urinary concentration (occurs successfully only in central)
How do you treat nephrogenic and central DI?
central DI- give synthetic ADH
nephrogenic- partial (give high dose ADH), complete (give diuretics to induce volume depletion and induce aldosterone)
What determines ECF volume?
sodium content- mechanisms to regulate ECF are actually regulating ECF volume
How is Aldosterone release stimulated by RAAS?
renin is produced in JG apparatus and is produced when renal perfusion pressure is low or when sodium levels are low in the filtrate
renin convert angiotensiogen to AT1
ACE convert AT1 to AT2
AT2 stimulates aldosterone production
How does aldosterone work to increase sodium reabsorption?
bound to renal cortical collecting duct causes reabsorption of Na in exchange for potassium and acid (H+) out
What are the causes and presentation of someone with primary hyperaldosteronism?
state of aldosterone excess: either due to adrenal adenoma or hyperplasia (renin will be appropriately low)
presents with volume expansion, hypertension and +/-hypokalemia
What are diagnostic tests used in primary hyperaldosteronism and possible treatments?
confirmed by salt-loading or admin. of normal saline to expand volume; abnormal sources will not suppress
treated surgically or medically with drugs that block mineralocorticoid receptor (spironolactone or eplerenone)
What is the presentation of someone with hypoaldosteronism?
typically seen in primary adrenal insufficiency, aldosterone deficiency leads to an impairment in renal sodium reabsorption causing volume depletion and hyperkalemia