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21 Cards in this Set

  • Front
  • Back
Total body water distribution
50-60% body weight
2/3 intracellular
1/3 extracellular (1/4 of which is in vasculature)
Volume regulation:
Sensors
Effectors
EABV sensed by baroreceptors
AII, catechols, aldosterone retain/excrete NaCl from kidneys
Osmolality regulation:
Sensors
Effectors
Osmolality sensed by hypothalamic osmoreceptors
ADH/AVP/vasopressin released to retain water from kidneys
Thirst
Physical exam findings of EABV
Orthostatic changes in pulse/BP: dec EAV
JVD, edema, ascites, pulmonary congestion: inc EAV
Skin turgor, dry mucosa, sunken eyes: dec EAV
Lab findings of EABV
FE Na/Cl: low = dec EAV; high = inc EAV
BUN, uric acid: inc = dec EAV (high ratio = dec EAV)
Effective vs. Ineffective osmols
Effective (tonicity): Na, glucose, mannitol
Ineffective: Urea, alcohols, acetone
Calculating osmolality
Plasma osm = 2 x Na + glucose/18 + BUN/2.8
Plasma tonicity = 2x Na + glucose/18
ADH response to osm or EAV
Inc osm: sensitive, linear inc ADH
Dec EAV: less sensitive inc ADH
ADH pathways
Inc vascular tone (V1)
Inc H2O resorption and release vWF (V2)
H2O resorption via Gs, inc cAMP, PKA, aquaporin insertion into the collecting duct
Pseudohyponatremia
High triglycerides/protein levels leading to "diluted" measurement
Primary polydipsia
Excess H2O consumption
Urine osmolality is appropriately dilute
Corrects with fluid restriction
HYPOnatremia
SIADH
Inc urine osmolality but normal EAV
Inappropriate ADH secretion by the CNS
HYPOnatremia
Volume depletion
Diarrhea, diuretics
Inc urine osm, low EAV and low extracellular fluid volume
HYPOnatremia
Edematous disorders
CHF, cirrhosis, nephrosis
Inc urine osm, low EAV, normal extracellular fluid volume
HYPOnatremia
Hypertonicity with dec volume
Renal loss (osmotic diuresis, diuretics)
Extrarenal loss (resp, skin, GI)
Central DI
CNS ADH secretion is inhibited (trauma, tumors, infection, genetic)
Corrects with ADH administration but not with fluid restriction
Nephrotic DI
ADH resistance
Urinary obstruction, kypokalemia, hypercalcemia, amyloidosis, sickle cell disease, PCKD, drugs, genetic
Does not respond to ADH or fluid restriction
Hypertonicity with inc volume
Iatrogenic administration of hypertonic solutions
Effects and treatment of HYPOnatremia
Acute: cerebral edema
Chronic: cells dec osm to accommodate for dec osm of plasma
Correct slowly (0.5 mEq/L/hr) to avoid central pontine myelinolysis
Effects of HYPERnatremia
Acute: cells shrink
Chronic: cells import/synthesize solutes to inc osm
Correct slowly to avoid cerebral edema (correct volume depletion first if present)
Approach to polyuria/polydipsia
U osm: inc = osmotic diuresis; dilute - fluid deprivation
Fluid dep: inc U osm = primary polydipsia; dilute - ADH admin
ADH: inc U osm = central DI; dilute = nephrogenic DI