Flashcards in ECFV and Tonicity Deck (29):
What are the distributions of body water in different compartments?
body water 60% weight for men, 50% for women
2/3 of body water intracellular, 1/3 extra
1/4 of extra cellular is intravascular
What are the uses and limitations of the physical exam in the assessment of effective arterial volume?
increase in pulse or decrease in BP indicate large decreased volume
postural changes in pulse or BP more sensitive = tilt or orthostasis
also look for dry mucous membranes, JVD, sunken eyes, edema, pulm congestion, turgor
not applicable in autonomic neuropathies
What are the uses and limitations of the plasma analysis in the assessment of effective arterial volume?
low volume leads to increased BUN and urea and vice versa
must be sure another process not causing this
BUN/creatinine ratio >20 suggest low volume
What are the uses and limitations of the urine analysis in the assessment of effective arterial volume?
low fractional excretion of Na and Cl indicate decreased volume - more accurate than spot urine
must be sure low fractional excretion not due to primary Na retention
What is the difference in solute composition of the intracellular and extracellular fluid?
no osmotic gradients usually because most cells freely permeable
Na and its salts in EC fluid - when measured indicates total body osmolality so low Na means low K in IC also
What is the osmolar gap?
difference between calculated osmolality and measured plasma osmolality - measured >10 more indicates some uncalculated substance
What are four (five) substances that can increase the osmolar gap?
What compartment do sensing mechanisms determining Na handling sense?
intravascular only = effective arterial volume
What are the different sensors for osmoregulation vs. volume regulation?
low and high pressure baroreceptors
both affect ADH secretion
What are the different effectors in osmoregulation and volume regulation?
AVP and thirst
Aldo, AII, catechols
thirst mechanism kicks in later than AVP
What is the difference between osmolality and tonicity?
tonicity only includes particles that can't penetrate cell membranes and thus osmotically pull water
urea is ineffective
What do changes in plasma osmolality or EABV do to ADH secretion?
small increases in plasma osmolality lead to ADH secretion but larger decreases in EABV needed to do this
hypotonicity usually do to low EABV
What is the pathophysiology giving rise to impaired renal water excretion?
decreased EABV causes inappropriate ADH secretion - low in patients with volume depletion or edematous states
What is psuedohyponatremia?
increases in plasma triglycerides or protein can cause error in measurement of Na
increases in glucose lead to hyponatremia but no changed osmolality - as glucose rises, serum Na falls
What is primary/psychogenic polydipsia?
dilution normal - patient drinking more than kidney can excrete
evaluate by checking urine osmolality - should be normally dilute
What is SIADH?
EABV normal, body fluids hypoosmolar, concentrated urine and high ADH levels inappropriate
diseases of CNS - those affecting hypothalamus, pulm diseases, carcionmas
also glucocorticoid def, certain central acting drugs, and renal failure
What is the approach to a hyponatremic patient?
check plasma osmolality to see if matches Na
urine osmolality to rule out psuedo
urine osmolality high - assess EABV
What are the three different types of hypernatremia and examples of each?
hypovolemic - loss of more water than Na -GI (diarrhea, vomiting), skin (burns, fever) kidney (osmotic diuresis)
euvolemic - diabetes insipidus
hypervolemic - hypertonic Na admin or feedings
What conditions can lead to enhanced renal water loss (and thus hypernatremia)?
osmotic diuresis, central diabetes insipidus, nephrogenic DI
present as polyuria and polydipsia
What is central DI?
conditions where ADH secretion from posterior pituitary is inhibited - trauma, tumors, granulomas, infection, familial
What is nephrogenic DI?
ADH levels appropriate but still overly dilute urine - ADH resistance - urinary obstruction, hypokalemia, hypercalcemia, amyloidosis, sickle cell, polycystic KD, drugs, familial
How can central and nephrogenic DI and primary polydipsia be distinguished?
response of urine osmolalilty to water deprivation and ADH admin -
PP - urine concentrates with water dep
CDI - urine concentrates with ADH
NDI - no urine concentration
What are the clinical observations of a patient with hyponatremia?
acute - cerebral edema and sig. CNS symptoms - seizures or coma
chronic - neurologic symptoms unusual even with large losses
What is the pathophysiology behind the clinical observations of hyponatremia?
Water moves into cells in brain causing swelling - cells and brain that transport solutes out to return to normal
What can happen if chronic hyponatremia is returned to normal too quickly?
central pontine myelinolysis - cells shrink - quadriparesis, swallowing dysfunction, inability to speak, decreased mental status, psuedobulbar palsy
What time period differentiates acute and chronic development of hypo/hypernatremia?
Why can acute hyponatremia be treated rapidly?
brain cells haven't had time to transport solutes out yet
IV admin of hypertonic saline
can add furosemide if volume expansion is a problem
What can happen if chronic hypernatremia is returned to normal too quickly?