Integrative Physiology I Regulation of Extracellular Fluid Osmolarity and Na Concentration Flashcards
in what ways can water be lost
-insensible loss by skin and lungs
- sweat
-feces
-urine
which does ADH effect: ECF osmolarity or plasma volume
both
how does ADH effect changes in ECF osmolarity? for excess water ingested
- excess water ingested -> decreased body fluid osmolarity -> decreased firing by hypothalamic osmoreceptors ->decreased ADH secretion ->decreased plasma ADH -> decreased tubular permeability to water in CD -> decreased water reabsorption in CD -> increased water excretion
how does ADH work with changes in plasma volume? for ex low plasma volume
- low plasma volume -> low venous, atrial, and arterial pressures -> increased ADH secretion -> increased plasma ADH -> increased tubular permeability to water in CD -> increased water reabsorption in CD -> decreased water excretion
is ADH more sensitive to changes in osmolarity or volume
osmolarity
what are the factors that increase ADH secretion
-increased ECF osmolarity
- decreased blood volume via low ANP
- decreased blood pressure via baroreceptor activity
- nausea
- hypoxia
- nicotine and morphine
- ANG II
what are factors that decrease ADH secretion
- low ECF osmolarity
- high blood volume via high ANP
- high BP via high baroreceptor activity and indirectly via decrease in ANG II
-ethanol
-cold
what is syndrome of inappropriate ADH (SIADH)
-excrete a concentrated urine
- too much ADH function
when is SIADH most often seen
neurologic disease, head injury, lung tumors or after major surgery
what does excessive ADH secretion cause
-hyponatremia
-decreased plasma osmolarity
-urine hyperosmolarity
what does excessive ADH secretion not cause
-sodium handling
- only defect is in water excretion
is there feedback inhibition of ADH
no
how is SIADH treated
ADH inhibitor drugs like demeclocycline
what happens in DI
-excrete a dilute urine
- too little ADH fcuntion
what are the types of DI
-hypothalamic or central DI
- nephrogenic DI
- polydipsic DI
what happens in hypothalamic DI
-defect in ADH synthesis or release
-decreased [ADH]plasma
what happens in nephrogenic DI
-defect in ADH action
-failure to maintain hyperosmotic medullary gradient
-elevated [ADH]plasma
what happens in polydipsic DI
-compulsive water drinking
what are the symptoms of DI
-polyuria
- nocturia
- polydipsia
what is polyuria defined as
greater than 3 liters urine/day
what are the 2 factors that determine urine volume
-amount of solute to be excreted (OUV)
- [ADH]plasma
what are the 3 major mechanisms of polyuria
- decrease in Na+ reabsorption (kidney disease, diuretics)
- reduced ADH secretion
- ADH resistance
what can cause ADH resistance
-lithium and tetracyclines
-hypercalcemic nephrogenic DI
what are the mechanisms of regulation of [Na+] ECF
-osmoreceptor -ADH system
- the thirst mechanism
- aldosterone and ANG II
- salt appetite
what are the primary mechanisms that regulate [Na+] ECF
-osmoreceptor-ADH system
- the thirst mechanism
how do aldosterone and ANG II regulate [Na+]ECF
-alter Na+ mass but NOT concentration
- changes in Na+ mass accompanied by volume changes (thirst, ADH)
what are the stimuli for thirst
-low plasma volume (MAP and ECF volume)
- increased plasma osmolarity
-dry mouth
what part of the brain responds to signals that initiate drinking
hypothalamic thirst center
where does ANG II act to increase thirst
centrally
what receptors detect low plasma volume for thirst response and what do they do
baroreceptors and cause increase in ANG II and directly stimulate thirst
what receptors detect high plasma osmolarity for thirst response and what do they do
osmoreceptors and directly cause thirst
what reduces thirst
metering of water intake by GI tract
what are stimuli that increase salt appetite
-sodium deficits
- decreased blood volume
-decreased blood pressure associated with circulatory insufficiency
what Na+ concentration do humans function normally at and what is the average consumption in the US every day
-function normally at 20 meq/day
- average: 200 meq/day
what is the response to increase in osmolarity but no change in volume
- ADH secreted -> increased renal water reabsorption
-thirst -> increased water intake -> increased ECF volume and increased BP -> kidneys excrete salt and water and osmolarity and volume returns to normal AND cardiovascular reflexes lower BP to return BP and volume to normal
what is the response to decrease in MAP without change in volume or osmolarity
- decreased BP -> decreased GFR -> decreased NaCl transport across macula densa of DT -> paracrines -> granular cells of afferent arteriole -> increase renin secretion
- decreased BP -> cardiovascular control center -> increase sympathetic activity -> granular cells of afferent arteriole -> increase renin secretion
- renin makes ANG I -> ANG II ->arterioles to vasocontrict, CV center in medulla increases CV response, hypothalamus increases ADH and thirst, adrenal cortex increases aldosterone which increases Na+ reabsorption -> all of which increase BP and volume to maintain osmolarity
what is the response to increased blood volume and no change in osmolarity
- increased BV causes atrial stretch ->atrial myocardial cells stretch and release ANP -> acts on hypothalamus to decrease ADH, kidney to increase GFR and decrease renin, adrenal cortex to decrease aldosterone, and medulla to decrease BP -> all of which increase NaCl and water excretion
