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ABIM NEP Na + H2O

ABIM NEP Salt & water

QuestionAnswer
Typical water content (TBW)? women & elderly & obese 50% TBW; men 60% TBW
What is physiologic serum osmolality? 285 – 290 mOsm/kg
ICF vs ECF TBW%s? ICF is 2/3 of TBW; ECF is 1/3 of TBW (plasma & intersitium)
Changes in plasma tonicity cause changes in ________? cell volume
AVP affects? urinary free water excretion
What structure has tonicity receptors? hypothalamus to changes in tonicity
What is AVP? arginine vasopressin, A.k.a. antidiuretic hormone (ADH). Made in hsupraoptic & paraventricular nuclei of hypothalamus, Carried via axonal transport dwon pituitary stalk to posterior hypophysis for storage
What makes renal interstium hypertonic? Na pumps cause absorption of salt in ascending limb, which is NOT permeable to water.
Effect of urea on cell volume? None. It freely crosses cell membranes and does not change volume
Effect of glucose on cell volume? None. It freely crosses cell membranes and does not change volume
Effect of saline on cell volume? hypertonic saline decreases cell volume by acting as effective osmoles facilitating water movement from cells that leads to cell shrinkage/less cell volume.
What are non-osmotic stimuli for vasopressin release? decreased effective circulating volume (CHF, cirrhosis, vomiting) need to release of vasopressin by causing discharge from parasympathetic afferent nerves in carotid sinus baroreceptors. Also: nausea, Post op pain, Pregnancy
Higher vasopressin levels are achieved with what physiologic changes? 7% decrease in volume vs. hyper osmolality
Vasopressin binds where? V1a (vascular and hepatic), V1b (ant pituitary), V2 (collecting duct).
V2 receptor function? needs to increase in water permeability via Aquaporin 2 (AQP2)
Aquaporin 1 versus 2 location/effects? AQP1 located in apical/basolateral prox tubular epith cells & desc limb of Henle is constitutively expressed (not regulated by AVP). AQP2 found in apical plasma membrane & intracellular vesicles of collecting duct principal cells —> controlled by AVP.
What are stimuli for thirst? hypertonicity (major one), hypovolemia, hypotension, angiotensinII.
_______ is the most potent stimulus for thirst? hypertonicity, only 2-3% change in plasma osmolality results in strong thirst (usu 290-295 mosm/kg).
What suppresses vasoppressin secretion? hypertonic interstitial fluid
Free water clearance? Cosm ~ Uosm x V/Posm; C of H2O ~ V[1-Uosm/Posm]. Normal < 3L/day… electrolyte free water clearance is better
Causes of polyuria aside from osmotic, 3 main causes: primary polydipsia, NDI, CDI
Osmotic diuresis? urine isosthenuric (SG near 1.010). UOsm (>1000/day) >>POsm. Osmotic diuretics are not easily reabsorbed by renal tubules. Ex: Uosm 450 mOsm/L w/ U flow rate 10 mL/min yields osm excr rate of 4.5 mOsm/min, a value 9X > usual in adult (0.5 mOsm/min)
Usually, specific gravity of more than _____ implies preserved concentrating ability. 1.018
Primary polydipsia Uosm << POsm + polyuria + hyponatremia. [Uosm should be > Posm]
Criteria to dx SIADH normal renal, thyroid, adrenal fcn. Posm<275; Uosm>100; clinical euvolemia; Hi UNa.
Pseudo hyponatremia is seen when? solid phase of plasma is increased by excess lipids or proteins. Happens because usual measurements of Na measure [Na] in whole plasma, not liquid phase. Assoc w/ normal serum osmolality.
Whole plasma osmolality?
True serum osmolality obtained by? measure only aqueous component using Direct ion-selective potentiometry
Formula to estimate water excess? 0.6W x {1-[Na]obs/140}
Formula to estimate water deficit? 0.6W x{[Na]obs/140 - 1}
Sodium reabsorption in thick ascending limb affected by? reduced by diuretics, osmotic diuretics, Interstitial disease
The ____ is impermeable to water in the absence of vasopressin. collecting duct. Permeability is increased by drugs and vasopressin
Thiazide diuretics work by? reducing NaCl absorption in distal convoluted tubule
Synonyms for antidiuretic hormone? ADH, arginine vasopressin, AVP, Vasopressin
Rs Acute hyponatremia 100-ml bolus of 3% hypertonic saline
Limits not to be exceeded to avoid osmotic demyelination syndrome? <10 mEq/L in the first 24 hours (ideally “6 in 6 then wait 24h), <18 mEq/L by 48 hours, and <20 mEq/L by 72 hours.
Causes of polyuria? Solutes (glu, Na, urea, mannitol) or aquaresis (primary polydipsia, Central DI, nephrogenic DI
Causes of acquired vasopressin deficiency? trauma, surgery, granulomatous diseases, autoimmune, vascular
Rapid increase in serum [Na] in setting of hyponatremia can cause? Central pontine and extrapontine myelinolysis, similar to what occurs after rapid correction of chronic hyponatremia
What occurs after rapid correction of chronic hyponatremia? CPM
Patients with ODS typically present when? two to six days after overly rapid correction of Na
Factors that increase risk of ODS serum sodium of ≤105 meq/L, alcoholism, liver disease, malnutrition, hypokalemia
Damage from overly rapid correction of hyponatremia treated? relowering [Na] with both dDAVP and D5W
What has been reported to abort early ODS following overcorrection of hypoNa? Relowering the serum sodium with D5W and desmopressin
Describe results of water deprivation in Central DI water deprivation raises uosm (usu ≥300 mosmol/kg) but submaximal. Then desmopressin resulting in a rise in Uosm: > 100 % - complete central DI and 15 to 50% - partial central DI
Describe results of water deprivation in Nephrogenic DI water restriction results in Uosm less than isotonic(<300 mosmol/kg). Then desmopressin causes little or no elevation in UOsm if have complete nephrogenic DI … BUT …<45%elevation UOsm in partial nephrogenic DI
Describe results of water deprivation in Complete central DI UOsm rises > 300 (submaximally). Then desmopressin results in a rise in Uosm: > 100 %
Describe results of water deprivation partial central DI UOsm rises > 300 (submaximally). Then desmopressin results in a rise in Uosm of 15-50%
Describe results of water deprivation complete Nephrogenic DI Water restriction results in Uosm less than isotonic (<300 mosmol/kg). Then desmopressin causes little or no elevation in UOsm if have complete nephrogenic DI …
Describe results of water deprivation partial Nephrogenic DI Water restriction results in Uosm less than isotonic(<300 mosmol/kg). Then desmopressin causes <45%elevation UOsm in partial nephrogenic DI and > 100% in complete DI
Urine that is not maximally concentrated DDX? think either partial DI or primary polydipsia, which “washes out” the concentration gradient in the renal medulla
Effect of injury/transection of the pituitary stalk (describe) DI->SIADH->DI!! First) DI occurs because interruption of nerve impulses means AVP cannot be released. 2cnd) SIADH from unregulated release of stored AVP from degenerating neurons. 3rd) Once AVP stores depleted, permanent DI seen.
Vasopressinase effects? Nlly in gestation vasopressinase causes subclinical cDI or nDI w polyuria responsive to DDAVP & AVP. In 3rd trimester, conditions can develop that respond to DDAVP (not AVP) causing decreased metabolism of vasopressinase (HELLP, acute fatty liver.)
What hormone is resistant to vasopressinase? DDAVP, not AVP
Significance of pituitary bright spot? loss of the posterior pituitary hypertensity is nonspecific finding with cDI. Bright spot maybe preserved early in AD cDI.
Nausea with free water intake can cause? hyponatremia d/t increased AVP release
Hyponatremia with Uosm <<100 (max dilute 50) mOsm/L? water intoxication, Beer potomania, tea & toast diet
Hyponatremia with Uosm >>100? low GFR, thiazides, excess AVP (hypovol inadequate circulation, SIADH),
SIADH and urine Na? reflects sodium intake, d/t no tendency to retain sodium. Usu high since increase Uosm causes less H20 excr + H20 cause overfilled art circulation (then causes low renin/ATII etc) and more Na excreted in urine. Usu >30 mEQ/L.
What is cerebral salt wasting? described before SIADH understood Colin lo plasma volume, lo CVP, hi natriuretic peptide. Hi U[Na] + vasopressin present despite hypoNa, low renin/aldo
What are organic osmolytes? aka “idiogenic osmoles” include glutamine, glutamate, taurine, myo-inositol, aspartate, creatine, CPK, glycerophosphocholine. Are intracellular osmotically active solutes that help Brain adapt to osmotic stress.
Within HOURS of sodium disturbance inside cells, there is shift of ______ in effort to adapt potassium. Lost in hypoNa, gained in hyperNa.
Within DAYS of sodium disturbance inside cells, there is shift of ______ in effort to adapt organic osmolytes. Lost in hypoNa, gained in hyperNa.
Complications of hyponatremia? cerebral edema, Seizures, pulm edema, herniation
Complications of hypernatremia? Brain hemorrhage, demyelination causing apoptosis of astrocytes (CPM)
Rapid correction of HYPOnatremia causes? demyelination, Central Pontine Myelonolysis
Rapid correction of HYPERnatremia causes? cerebral edema, especially in infants, with seizures
How do you treat over correction hyponatremia (unwelcome aquaresis!)? D5W plus DDAVP; DDAVP is effective to re-lower Na, is well tolerated, and prevents myelinolysis.
Explain osmotic demyelination syndrome? develops 2-6 days after excessive correction of HYPOnatremia —> causes quadriparesis, locked in syndrome, swallow dysfcn (pontine sx) and non-pontine sx of seizures,AMS, movement d/o.
Risk factors of osmotic demyelination syndrome? chronic hypoNa, ETOH, malnutrition, liver dz, burns, hypoK, [Na} < 105
Acute hyponatremia Time frame? < 48 hrs requires emergency treatment with 3% NaCL of 513 mEq at 1 ml/kg results in 1 mEq/L increase in Na with goal to raise Na 4-6 mEq/L. {raise Na 6 in 6hrs then STOP}
3% NaCl effects? 513 mEq/L has the effect that 1 ML equals 0.5 mEq. 1 ml/kg results in 1 mEq/L increase in Na for max increase of 6 mEq/6 hrs then stop.
Correction of hypoNa with KCL? 400 mMol KCl ~ 3% NaCl
Therapy for DDAVP induced hyponatremia (usu isotonic NaCl)? cont DDAVP and 3% NaCl + fluid restrict. stopping DDAVP leads to marked and rapid rise in Na. can start w 100 cc bolus of 3% NaCl then gtt 0.3 ml/kg/hr.
Speed of correcting hypernatremia? acutely should correct as fast as it developed. Chronically, correct < 12 mEq/L to avoid cerebral edema.
Why is there no edema with SIADH? excess ADH causes water retention despite low Posm. Volume receptors become activated leading to appropriate increased UNa and H20 excretion. Thus it’s combo of H20 retention + solute loss so UNa usu > 40
Rx SIADH water restrict (difficult), vaptans do not require H20 restriction
Effect of vaptans? block AVP effects causing fewer AQP2 channels in apical membrane—> more H20 excreted sodium
Rx lithium induced nephrogenic DI amiloride blocks entry of Li via ENaC.. lithium enters cell via ENaC and little extruded, inhibits cAMP formation in coll duct,
What is w/u lithium induced polyuria? if Posm high with low Uosm and hyponatremia, picture clearly not psychogenic
Name causes of drug induced hypoNa analogs (DDAVP, oxytocin); potentiate AVP (tylenol, NSAIDS, cyclophosphamide, chlorpropamide); Xtra AVP release (SSRI, ifosfamide, chlorpropamide, narcs, vincristine, clofibrate, tegretol); unk (haldol, amytriptiline, thioridazine, fluoxetine, ecstacy)
Explain water deprivation test. goal is to raise serum Na > 144 to stimulate concentration of urine. If the serumNa is already high, water deprivation not needed!
T/F continuous furosemide infusion this better than bolus therapy FALSE. Intermittent bolus therapy is similarly effective to get.
Ototoxicity from furosemide is worse w what route of administration? bolus rx. Continuous infusion carries a lower risk
Benefits of bumetanide vs furosemide? Bumetanide has more hepatic clearance and is sometimes more effective PO.
Furosemide is dependent on ____ for its biological action. adequate plasma albumin. It is 95% albumin bound, which is component that reaches proximal tubule to then gain entry into tubular lumen. Low alb causes less furosemide to enter tubular lumen + has higher vol distribution.
Bumetanide binds to ______? albumin and globulins, where is furosemide only binds to albumin.
Psychogenic polydipsia resembles true DI since causes polyuria + low Uosm BUT plasma osm is normal/low in PP whereas high in DI.
How do thiazide diuretics work to Treat NDI? thiazides + low sodium diet inhibit salt re absorption in DCT causing mild vol depletion. Hypovolemia then stimulates fluid resorption in proximal tubule thereby lowering H20 delivery to AVP sensitive sites in DCT.
Therapy of NDI? thiazides + low Na diet, PG inhibitors like NSAIDS, amiloride
Therapeutic hypernatremia for cerebral edema and prevention of herniation? 30 ml of 23.4% NaCl (~234 ml of 3% NaCl) usu raises Na by 5 mEq/L
Emergency Rx of hypoNa with neurologic deficits? 1-3 “100 mL" boluses 3% NaCl. The preferred Rx bring Na up by 4-6 mEq/L (and less than 10 mEq/L over 24 hours) to reduce the risk of cerebral edema.
Describe Exercise Assoc HypoN. Lg hypotonic fluid intake (even sports drinks) during and after exercise assoc w/ weight gain compared with the pre-race weight. Other independent risk factors: longer race time, female, low bBMI, & NSAIDs use.
Created by: ka1usg