#1 - Disorders of Extracellular Fluid Volume and Tonicity Flashcards
ADH release stimulated by
increase in tonicity
Total body water = ___% body weight
60 for men; 50 for women
Total body water distribution
2/3 intracellular, 1/3 extracellular
Of extracellular fluid, ___ is intravascular
1/4
Intravascular volume sensed via
effective arterial volume - sensed by kidney
Volume regulation senses
EABV via baroreceptors, causes change in aldosterone and catecholamine release which affect urine Na+
Osmoregulation senses
Posm via hypothalamic osmoreceptors; stimulates AVP/ADH and thirst
Physical exam indications of decreased EABV:
increases in pulse, decreases in BP, “orthostatic hypotension” (a “tilt”), especially decreased diastolic pressure when standing
Most sensitive finding is BPM increase of 8/min or more
Renal retention of NaCl indicates
low EABV; calculate with FE (fractional excretion) which uses creatinine for comparison as it’s neither secreted nor reabsorbed
FE =
(Ux X Pcreat)/(Ucreat X Px)
Low is <0.5-1%, indicating low EABV
BUN and uric acid
blood urea nitrogen - increased in low EABV, as is uric acid (>20 and >5 respectively); protein metabolism or purine metab. can affect them
BUN/creatinine ratio >20 suggests low EABV
Hydration/dehydration related to ______
Salt status related to ____
osmoregulation; volume regulation
Tonicity
Effective osmolality - only counts particles that do not penetrate cell membranes such as Na, glucose.
Ineffective osmoles include urea, ethanol, ethylene glycol, acetone. These don’t affect fluid distribution
Osmolality =
2 x [Na+] + (glucose/18) + (BUN/2.8)
Normal = 280-300 mOsm/L
Usually only Na and glucose really needed to calculate it.
3 ways of detecting low effective arterial volume:
1) Postural changes - incr. pulse and decrease BP
2) Na/Cl retention - FE 20) & uric acid levels (>5)
3) Increased BUN/creatinine
Osmolar gap
difference between calculated and measured osmolality. Gap > 10 indicates accumulation of unmeasured substance such as ethanol, methanol, etc.
Ascending loop of Henle
water impermeable, dilutes urine
Collecting duct
ADH-dependent H2O permeability
ADH causes it to become more water permeable and reabsorb water
ADH
=AVP=vasopressin. Synthesized in hypothalamus and stored in post. pituitary in response to increased osmolality or decreased effective arterial volume
ADH levels at very low osmolality
undetectable because not at threshold
At higher osmolality, ADH
increases linearly. Thirst threshold is higher than ADH’s.
ADH also increases when ____
effective arterial volume decreased. This is inefficient because only 1/3 of retained water will be in ECF so only used in emergency states such as hemorrhage with >10% volume loss so it’s a backup system. ADH also causes release of vWF and pro-coagulation.
ADH secretion more sensitive to
increases in osmolality than decreases in BP as it takes a large decrease in blood volume to cause ADH secretion
Aquaporin 2
Phosphorylated and inserted into lumen membrane of cells of collecting duct in response to ADH
Marker for hypotonicity is
hyponatremia
Pseudohyponatremia
Lab artifact due to increases in TGs or protein which makes Na appear low when it’s actually normal
Polydipsia as cause of hypotonicity
Drinking more water (20+ L/day) than kidney can excrete, usually due to CNS problem or psychosis
- urinary osmolality appropriately dilute, less than 100 mOsm/L
Hyponatremia caused by renal defect shows
urinary osmolality greater than 100 mOsm/L
ADH secretion may be appropriate due to decreased EABV in pts. with low volume or edematous disorders
SIADH
Syndrome of inappropriate ADH - EABV normal, serum hyponatremia, concentrated urine and high ADH
- usually associated with CNS problems such as hypothalamus or carcinomas secreting ADH, certain drugs, glucocort. deficiency
Primary defense against hypernatremia is
thirst
Hypertonic challenges leading to hypernatremia
- decreased volume from renal loss or extra renal loss (skin burns, vomiting, diarrhea)
- isovolemic DI - renal water loss
- Increased volume from iatrogenic administration of hypertonic solution
Enhanced renal water loss presents with
polyuria and polydipsia. Can be DI, osmotic diuresis
Diabetes insipidus (DI)
inappropriate water loss by kidney in absence of osmotic diuresis
Central DI
ADH secretion impaired; urine concentration improves with ADH administration. Fluid restriction may help if not complete central DI.
Nephrogenic DI
ADH resistance due to urinary obstruction, hypokalemia, hypercalcemia, amyloidosis, sickle cell, X-linked disorder.
- urine concentration does not improve with fluid restriction nor ADH admin.
Hyperglycemia can cause increased
serum osmolality despite low Na. Glucose draws water into ECF in presence of somatostatin especially, diluting Na. Increased tonicity stim. thirst and AVP secretion.
IV gamma globulin can cause
hyponatremia and hyperkalemia as it often contains much sucrose which draws water and K+ from cells in to ECF
Principal danger of correcting hypo- or hypernatremia is
effects on CNS function due to brain size changes
If acute change, can change fast, if chronic need to change more gradually
Hyponatremia leads to ___ in CNS
swelling, cerebral edema if faster onset.
Must be treated accordingly as sudden return to increased ECF osmolality can cause cell shrinkage and Central pontine myelinolysis
- Don’t want to correct too quickly. May use furosemide to excrete some Na in urine and excrete water, with hypertonic saline.
- Fluid restriction will correct it
Hypernatremia causes brain
shrinkage initially. Correcting too quickly can cause cerebral edema with cell swelling as the cells have compensated by increasing their osmolality
- Should do half correction in 24 hours to avoid this
