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Dysnatramias

The flashcards below were created by user yuiness on FreezingBlue Flashcards.

  1. What happens to total body water following Na+ infusion?
    It shifts (water moves from the ICF to the ECF)
  2. What happens to compartmental water balance following infusion of pure water?
    The water redistributes equally to both ICF and ECF (water is freely permeant across membranes)
  3. Why is it important to maintain a relatively constant serum osmolarity?
    The brain cannot tolerate small changes in osmolarity (it will swell or shrink)
  4. Consequences of brain shrinkage
    Pulls apart from meninges → hemorrhage, meningeal tears, neuronal/glial tears
  5. Consequences of brain swelling
    Herniation beyond the tentorium → compression of the brainstem
  6. Why can the brain tolerate minor changes in serum osmolarity?
    Blood-brain barrier
  7. Most dysnatremias are [mild, moderate, or severe] and SNa is in the range [#]-[#] mM
    Mild; 125-155 nM
  8. What kinds of patients most often have dysnatremias?
    Hospitalized, institutionalized, or “polypharmacied” patients
  9. T/F: Dysnatremias are often emergencies and require aggressive treatment
    False – most are non-emergent and require only a “tweak” in treatment
  10. Define osmoregulation
    Maintenance of constant Sosm (serum osmolarity)
  11. What areas of the brain sense changes in Sosm?
    • Supraoptic nucleus (SON)
    • Hypothalamic thirst nucleus
  12. Hypothalamic cells can sense Sosm changes of [%] once the level is about [#] mOsm
    1%; 285-290 mOsm
  13. How do these nuclei respond to increased Sosm?
    SON
    Hypothalamic thirst nucleus
    • ADH secretion
    • Increase thirst drive
  14. How do stimuli from the baroreceptor and brainstem nuclei affect ADH release?
    Lower the threshold for ADH release
  15. Stimuli that can lower the threshold for ADH release from the SON
    • Decreased PO2
    • Decreased BP
    • Decreased ECFV
    • Pain/stress
    • Nausea
    • Drugs
  16. ADH is released from the [anterior or posterior] pituitary
    posterior
  17. Operational definition of euvolemia
    Intravascular volume required to maintain the least preload for optimizing stroke volume
  18. How is preload measured?
    Swan-Ganz catheter
  19. Practical definition of euvolemia
    Intravascular volume that maintains stable BP and HR (lying or standing), without peripheral pitting edema or pulmonary vascular congestion
  20. Diuretics lead to which one?
    A. Too much water for the amount of salt
    B. Too little salt for the amount of water
    C. Too much salt and water, but more water than salt
    B. Too little salt for the amount of water
  21. Cirrhosis leads to which one?
    A. Too much water for the amount of salt
    B. Too little salt for the amount of water
    C. Too much salt and water, but more water than salt
    C. Too much salt and water, but more water than salt
  22. Molecular mechanism for SON response, leading to decreased ADH release
    Decreased Sosm → SON cell swelling → closure of stretch-inactivated cation channels → less depolarization → fewer APs → decreased Ca2+ entry at terminal → decreased ADH release
  23. Molecular mechanism for decreased ADH resulting in decreased urine osmolarity
    Decreased ADH binding at V2 receptors in collecting duct → less exocytosis of aquaporins into apical membrane → decreased water permeability → decreased urine osmolarity (urine is more dilute)
  24. Increased renal free water clearance → [increase or decrease] in Sosm
    increase
  25. 4 major causes of hyponatremia
    • Stimulus for inappropriate thirst
    • Stimulus for massive ADH release
    • Salt wasting with water replacement
    • Overactivation of CVMP
  26. Osmolarity of the most dilute urine possible
    50 mOsm/L
  27. ADH release is inappropriate if Sosm falls below [#]
    280 mOsm
  28. CVMP is a [non-osmolar or osmolar] drive for ADH secretion
    non-osmolar
  29. Methods for determining a patient’s volume status
    • Weight
    • Recent photograph
    • Orthostatic BP changes
    • Central venous pressure
  30. How can cancer cause hyponatremia?
    Paraneoplastic secretion of an ADH-like substance
  31. How can CNS inflammation or injury cause hyponatremia?
    Cytokine stimulation of SON neurons → ADH release
  32. How can affective disorders cause hyponatremia?
    • Psychotic thirst
    • Antidepressants → non-osmotic induction of ADH release
  33. The urine of a hyponatremic patient should be below [#] mOsm
    100 mOsm
  34. How can you measure renal function?
    Serum creatinine
  35. The urine of a hyponatremic patient should have UNa below [#] mEq/L
    20 mEq/L
  36. A hyponatremic patient should be hyper-osmolar, with Sosm < [#] mOsm
    285-290 mOsm
  37. What could produce a falsely reduced serum sodium?
    Hyperlipidemia (lipids take up too much of the non-protein component of blood; if you subtract the lipid component, SNa is normal)
  38. What hormone might have residual activity if the urine of a hyponatremic patient is not maximally dilute?
    ADH
  39. SIADH
    What does it stand for?
    It is also called “[?] hyponatremia”
    • Syndrome of inappropriate ADH secretion
    • Euvolemic
  40. SIADH occurs in the [presence or absence] of ineffective intravascular volume
    Absence
  41. In SIADH, SNa and Sosm are low enough that [hormone] should be shut off, but it isn’t
    ADH
  42. In SIAD, the urine [is or is not] maximally dilute
    is not
  43. 2 possible causes of SIADH
    • Osmostat has been reset
    • Autonomous ADH secretion (paraneoplastic syndrome)
  44. SIADH results in primarily [ECF or ICF] overload
    ICF
  45. Is pitting edema often seen in SIADH?
    No – SIADH causes an increase in ICF, not ECF
  46. Describe the following in SIADH:
    Volume status
    Renal function
    Hypothyroid or Addison’s?
    Urine osmolarity
    Urine sodium
    • Euvolemic
    • Intact
    • No
    • Less than maximal (Uosm > 75-100 mOsm)
    • UNa > 20 (off diuretics) – not low
  47. Patients with SIADH [are or are not] in sodium balance, and they put out [too much or too little] water
    are; too little
  48. What is psychogenic polydypsia?
    Inappropriate thirst → massively increased water intake
  49. Excretable sodium load on a normal diet
    800-900 mOsm/day
  50. On a normal diet, what is the maximal volume or urine possible (if it is maximally dilute)?
    16-18 L/day
  51. Excretable sodium load on a poor diet
    300 mOsm/day
  52. Patients with hypovolemic hyponatremia have decreased [?] volume
    intravascular
  53. How can patients develop hypovolemic hyponatremia?
    • Loss of fluid from body
    • Sequestration of fluid in a third space (e.g., intestinal lumen, lymph, muscle, pancreas, pleural cavity, peritoneal cavity)
  54. What conditions can result in hypervolemic hyponatremia?
    • CHF
    • Hepatic cirrhosis
    • Nephrotic syndrome
  55. Chronic use of thiazide diuretics can result in [?] hyponatremia, due to ongoing loss of [?]
    euvolemic or hypovolemic; Na+
  56. Use of thiazide diuretics results in a decrease in intracellular [K+ or Na+] and an increase in intracellular [K+ or Na+]
    K+; Na+
  57. Treat hyponatremia if SNa is less than [?] mEq/L
    120-125 mEq/L
  58. T/F: Hyponatremia might be correctable with simple fluid restriction
    True
  59. When treating hyponatremia, what is the maximum safe rate of SNa increase?
    8-10 mEq/day
  60. 2 methods for treating hyponatremia
    • Solute loading + loop diuretic (to get rid of hypotonic fluid)
    • Aquaresis with ADH V2 receptor blocker
  61. What are vaptans?
    Non-peptide ADH V2 receptor blockers
  62. Do vaptans produce…
    Natriuresis?
    Kaliuresis?
    • No
    • No
  63. How do vaptans interact with the ADH V2 receptor?
    • Bind deep in the GPCR and prevent ADH binding superficially
    • Prevent interaction of the GPCR with the G-protein
  64. Hypernatremia + fluid [intake or restriction] → “eunatremic”
    intake
  65. Hyponatremia + fluid [intake or restriction] → “eunatremic”
    restriction
  66. 2 general causes of hypernatremia
    • Diabetes insipidus (hypodipsea + urinary concentrating deficit)
    • Abnormal loss of hypotonic fluid without access to free water
  67. Cause of central diabetes insipidus
    Reduced ADH secretion secondary to surgery, intrapituitary bleed, head trauma, intracranial malignancy (i.e., damage to the pituitary)
  68. Causes of nephrogenic diabetes insipidus
    • Reduced ADH response due to receptor or aquaporin deficit
    • Reduced transport of Na+ or urea into medullary interstitium
    • Loss of vasa recta (sickle cell disease)
  69. Causes of hypernatremia secondary to abnormal hypotonic fluid loss
    • Impaired skin integrity
    • Intense sweat + fever/heat exposure
    • Heat exhaustion or stroke
    • Osmotic diarrhea
    • Hyperventilatory water loss
  70. In osmotic diarrhea, the lost fluid is [hypertonic or hypotonic]
    hypotonic
  71. 3 drugs that result in nephrogenic diabetes insipidus
    • Lithium
    • Amphotericin B
    • Calcium
  72. Drug-induced diabetes insipidus results in disruption of the [hormone] pathway, causing decreased insertion of [?] in the apical [nephron segment] membrane
    ADH; aquaporins; collecting duct
  73. How does lithium cause ADH blockade?
    Enter cell through ENaC → inhibit adenylate cyclase → interrupt ADH signaling cascade
  74. How does amphotericin B cause ADH blockade?
    Amphotericin B monomers form a non-selective cation channel in the apical membrane of the collecting duct → Na+ enters cell and K+ leaves → loss of K+ causes malfunction of adenylate cyclase → interrupt ADH signaling cascade
  75. How does calcium cause ADH blockade?
    Ca2+ binds its own GPCR in the basolateral membrane → release of an inhibitory G-protein subunit → inhibition of adenylate cyclase → interrupt ADH signaling cascade
  76. Urinary concentration deficits secondary to lithium/amphotericin B/calcium have a [rapid or slow] onset
    rapid
  77. Treat hypernatremia if serum sodium is > [#] mEq/L
    155 mEq/L
  78. Why must hypernatremia always be treated?
    Patients could develop significant CNS pathology
  79. Maximum rate of SNa decrease when treating hypernatremia
    Consequences if SNa decreases too quickly
    • 0.5 mEq/L/hr (12 mEq/day) until SNa = 150
    • Brain swelling
  80. Treatment for acute hypernatremia
    Infusion of D5W (5% dextrose; essentially “free water”)
  81. Treatment options for chronic hypernatremia
    • ADH agonist (DDAVP)
    • SON stimulant
    • Mild reduction in GFR (tricky)
  82. Treatment for a hypovolemic hypernatremic patient
    • First, correct hypovolemia with normal saline
    • If patient is still hypernatremic, infuse D5W
  83. During treatment of hypernatremia, rebound will occur if you don’t…
    replace urinary and insensible free water loss
  84. Formula for estimated water deficit in hypernatremic patients
    0.45*(lean body weight)*(measured SNa/140 – 1)
  85. In the formula for estimated water deficit, what does “0.45” represent?
    Fraction of body weight that is total body water (in a lean person)
  86. T/F: The calculated water deficit might not be accurate depending on the BMI of the patient
    True
  87. T/F: Vaptans (ADH receptor antagonists) can be used to treat hypernatremia
    True – they are effective in both hypo- and hypernatremia
  88. Mechanism of vaptans in the treatment of hypernatremia
    Vaptans enter cell → bind defective ADH receptor → chaperone the receptors through the ER/Golgi → insertion in the basolateral membrane of the collecting duct
  89. Mechanism of cGMP phosphodiesterase inhibitors in the treatment of hypernatremia
    Raise intracellular [cGMP] → cGMP acts like cAMP → target aquaporins to the apical membrane of the collecting duct
  90. Example of a cGMP phosphodiesterase inhibitor
    Viagra
  91. Hypernatremic patients have [oliguria or polyuria]
    polyuria
  92. Major cause of hypernatremia in the elderly
    Defect in thirst (or lack of accessibility to water)
Author
yuiness
ID
39192
Card Set
Dysnatramias
Description
Dysnatremias
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