ECFV and Tonicity Flashcards

1
Q

What are the distributions of body water in different compartments?

A

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

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2
Q

What are the uses and limitations of the physical exam in the assessment of effective arterial volume?

A

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

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3
Q

What are the uses and limitations of the plasma analysis in the assessment of effective arterial volume?

A

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

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4
Q

What are the uses and limitations of the urine analysis in the assessment of effective arterial volume?

A

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

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5
Q

What is the difference in solute composition of the intracellular and extracellular fluid?

A

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

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6
Q

What is the osmolar gap?

A

difference between calculated osmolality and measured plasma osmolality - measured >10 more indicates some uncalculated substance

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7
Q

What are four (five) substances that can increase the osmolar gap?

A
ethanol
methanol
ethylene glycol
isopropyl alcohol
(acetone)
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8
Q

What compartment do sensing mechanisms determining Na handling sense?

A

intravascular only = effective arterial volume

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9
Q

What are the different sensors for osmoregulation vs. volume regulation?

A

hypothalamic osmoreceptors
low and high pressure baroreceptors
both affect ADH secretion

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10
Q

What are the different effectors in osmoregulation and volume regulation?

A

AVP and thirst
Aldo, AII, catechols
thirst mechanism kicks in later than AVP

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11
Q

What is the difference between osmolality and tonicity?

A

tonicity only includes particles that can’t penetrate cell membranes and thus osmotically pull water
urea is ineffective

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12
Q

What do changes in plasma osmolality or EABV do to ADH secretion?

A

small increases in plasma osmolality lead to ADH secretion but larger decreases in EABV needed to do this
hypotonicity usually do to low EABV

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13
Q

What is the pathophysiology giving rise to impaired renal water excretion?

A

decreased EABV causes inappropriate ADH secretion - low in patients with volume depletion or edematous states
causes hyponatremia

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14
Q

What is psuedohyponatremia?

A

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

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15
Q

What is primary/psychogenic polydipsia?

A

dilution normal - patient drinking more than kidney can excrete
evaluate by checking urine osmolality - should be normally dilute

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16
Q

What is SIADH?

A

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

17
Q

What is the approach to a hyponatremic patient?

A

check plasma osmolality to see if matches Na
urine osmolality to rule out psuedo
urine osmolality high - assess EABV

18
Q

What are the three different types of hypernatremia and examples of each?

A

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

19
Q

What conditions can lead to enhanced renal water loss (and thus hypernatremia)?

A

osmotic diuresis, central diabetes insipidus, nephrogenic DI

present as polyuria and polydipsia

20
Q

What is central DI?

A

conditions where ADH secretion from posterior pituitary is inhibited - trauma, tumors, granulomas, infection, familial

21
Q

What is nephrogenic DI?

A

ADH levels appropriate but still overly dilute urine - ADH resistance - urinary obstruction, hypokalemia, hypercalcemia, amyloidosis, sickle cell, polycystic KD, drugs, familial

22
Q

How can central and nephrogenic DI and primary polydipsia be distinguished?

A

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

23
Q

What are the clinical observations of a patient with hyponatremia?

A

acute - cerebral edema and sig. CNS symptoms - seizures or coma
chronic - neurologic symptoms unusual even with large losses

24
Q

What is the pathophysiology behind the clinical observations of hyponatremia?

A

Water moves into cells in brain causing swelling - cells and brain that transport solutes out to return to normal

25
Q

What can happen if chronic hyponatremia is returned to normal too quickly?

A

central pontine myelinolysis - cells shrink - quadriparesis, swallowing dysfunction, inability to speak, decreased mental status, psuedobulbar palsy

26
Q

What time period differentiates acute and chronic development of hypo/hypernatremia?

A

48 hours

27
Q

Why can acute hyponatremia be treated rapidly?

A

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

28
Q

What can happen if chronic hypernatremia is returned to normal too quickly?

A

cerebral edema

29
Q

How should hypernatremia be corrected?

A

water admin at rate leading to half correction in 24 hours