Fluid and Electrolytes Part Two

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Fluid and Electrolytes Part Two
2013-04-02 21:20:58

Flashcards over second half of the Lecture (Electrolytes)
Show Answers:

  1. What is the major cation for the generation of the action potential?
  2. What electrolyte is important for regulating normal serum osmolarity?
  3. What organ excretes excess sodium taken in?
  4. What is normal sodium serum osmolarity?
    275-290 mOsm/L
  5. What is the normal sodium level? (mEq/L)
    135-145 mEq/L
  6. Below what value is considered hyponatremia?
    <130-135 mEq/L
  7. What is the most common cause of hyponatremia?
    Excess free water
  8. Above what value is considered hypernatremia?
    >150 mEq/L
  9. What are common causes of hypernatremia?
    • Excessive water excretion
    • Excessive sodium intake
    • Inadequate water intake
  10. How much sodium is required per day for infants? for adults?
    • Infants: approx. 3 mEq/kg/day
    • Adults: approx. 1.5 mEq/kg/day
  11. True or False:
    Hyper/hyponatremia is referring to the plasma concentration, not the total body sodium.
  12. What hormone regulates the plasma concentration of sodium?
  13. What hormones regulate total body sodium?
    Aldosterone and ANP
  14. Normally, the amount of sodium excreted by the kidneys is ____ to the sodium intake.
  15. What are some situations in which sodium loss is significant?
    • Sweating
    • Vomiting
    • Burns
    • Diarrhea
  16. Disorders of total body sodium go along with:
    A. increase or decreases in plasma volume
    B. concentration of the sodium in the plasma

    B= referring to hypo/hyper natremia
  17. What two systems regulate total body sodium and the concentration of sodium in the plasma?
    Endocrine and Renal
  18. We normally form: ___mL of urine for every ___ mOsm of solute excreted by the kidneys.
    10 ml of urine for every 1 mOsm of solute excreted by the kidneys
  19. In a free water challenge, kidneys respond through:
  20. In a sodium challenge (aka sodium load) kidneys respond through:
    Natiuresis (aka sodium excretion)
  21. If there is a reduction in body water, the body will: _______ to compensate.
  22. If there is a reduction in sodium, the body will ______ to compensate.
    Antinatiurese (retain sodium)
  23. Causes of natriuresis (sodium excretion) in volume expanded state:
    • Excessive intake of sodium
    • Inappropriate ADH
  24. Causes of natriuresis (sodium excretion) in volume depleted state:
    • Addisons Disease
    • High sodium excretion by the kidneys
    • Diuretic excess/abuse
  25. Causes of Antinatriuresis (sodium retention) in an edematous state.
    • Heart Failure
    • Chronic Liver Disease
    • Nephrotic Syndrome
    • Acute Glomerulonephritis
    • Idiopathic Edema
  26. Cause of Antinatriuresis (sodium retention) in non-edematous state.
    • Hemorrhage
    • Decreased sodium intake
    • Diuretic withdrawal
    • Acute mineralcorticoid administration
    • Sodium loss via sweat/vomiting
  27. Hyponatremia Decision Tree
  28. What are some things that cause an increase in ADH secretion?
    • *Pain
    • *Sympathetic Nervous System stimulation
    • *Nausea

    *Our patients typically have increased ADH secretion
  29. An increased in ADH causes what?
    Increased water re-absorption

    Hyponatremia can result
  30. True or False
    Hyponatremia is usually dilutional, and doesn't represent total body Na increase.
  31. Hypovolemia and Hyponatremia together can be called a ________ sodium loss.
    Primary sodium loss
  32. Causes of Hyponatremia in Hypovolemic State
    • Hemorrhage
    • Burns (edema)
    • Peritonitis
    • Cerebral Salt Wasting Syndrome
    • Diarrhea
    • Vomiting
    • Diuretic Overuse
    • Addison's Disease
  33. Causes of Hyponatremia in Euvolemic State
    • SIADH
    • Psuedohyponatremia Syndrome
  34. Why does Addison's Disease cause hyponatremia?
    Decrease in Aldosterone secretion impairs the ability to reabsorb sodium and water
  35. True or False
    Usually we can excrete free water excess.
    • True!
    • (unless there's a problem with ADH)
  36. Causes of hyponatremia in hypervolemic State
    • CHF
    • Nephrotic Syndrome
    • Cirrhosis
    • TURP syndrome
  37. At least ___% of patients will develop hyponatremia when hospitalized.
  38. What is the most common electrolyte disturbance in hospitalized patients?
  39. In hyponatremic patients, their total body water sodium is usually:
    Normal or Increased
  40. What electrolyte imbalance is associated with an increase in mortality?
    • Hyponatremia
    • (could be electrolyte or underlying cause with hyponatremia as a symptom)
  41. Which imbalance is more serious: Acute or Chronic Hyponatremia? WHY?
    Acute Hyponatremia because it will produce more serious CNS symptoms
  42. Signs and symptoms of hyponatremia depend on: (2 things)
    • 1. Rate of Development
    • 2. Severity
  43. What level indicates severe hyponatremia?
    <120 mEq/L
  44. Symptoms of severe hyponatremia
    • Loss of Appetite
    • NV
    • Weakness
    • Cramps
    • Change in Level of Consciousness

    • can progress to:
    • Coma
    • Seizures
  45. CNS symptoms in hyponatremia are directly related to:
    Overhydration of the brain
  46. True or False
    The brain is relatively impermeable to water

    The brain is impermeable to sodium but permeable to water

    In hyponatremia, water moves into brain and brain rapidly compensates to changes in osmolarity (dangerous!)
  47. What does TURP syndrome cause? (or operative hysteroscopy)
    • intravascular absorption of irrigation fluid leads to: 
    • hypo-osmotic hyponatremia
  48. What are some general causes of hyponatremia?
    • Intraoperative State
    • Acute intracranial disease
    • Malignancy
    • Medications
    • Acute Pulmonary Disease (pulm. edema)
  49. If you correct hyponatremia too quickly, the brain:
  50. What is central pontine myelinolysis?
    Demylination of the neurons in the brain due to correcting sodium too quickly (especially with hypertonic solution)
  51. What is the correct method for correcting hyponatremia?
    Limit only <10-12 mEq/L per 24 hours or 18 mEq in 48 hours
  52. Treatment for hyponatremic, hypervolemic patient
    • Restrict water intake
    • Restrict Na
    • Give meds to improve cardiac output
    • Give meds to improve kidney function
  53. Treatment of euvolemic, hyponatremic patient
    • Reduce concentration of other solutes in the blood
    • (ex. urea) 

    By dialysis and free water retention
  54. Treatment for hypovolemic, hyponatremic patient
    • Restore volume with NS
    • Remove ADH stimulation if indicated
  55. Treatment for hyponatremia in SIADH patient
    • Free water restriction
    • Eliminate the cause (pain, postop state, intracranial disease)
  56. What are symptoms of central pontine myelinolysis?
    • Mild behavior disturbances
    • seizures
    • quadraparesis
  57. What two things are the main determinants of neurologic injury in hyponatremia?
    • 1. Magnitude/Chronicity of hyponatremia
    • 2. Rate of correction
  58. Hypernatremia is always associated with:
    a hyper osmolar state
  59. What are some common causes of hypernatremia?
    • Burns
    • GI loss
    • DI [central/nephrogenic]
    • Absolute or relative water deficit
  60. Mortality in hypernatremia is:
    A high
    B low
    A high!

    • 40-50%
    • *question over whether its a marker or a cause
  61. What is the serum sodium level above in hypernatremia?
    >145-150 mEq/L
  62. In a healthy adult, typically, what two things compensate for elevated sodium levels?
    • 1. thirst mechanism
    • 2. ADH secretion
  63. Which state is more stable with better outcomes?
    A. acute hypernatremia
    B. chronic hypernatremia
    B chronic hypernatremia
  64. Which patient populations have an altered thirst mechanism?
    • 1. elderly*
    • 2. infants
    • 3. patients under anesthesia

    *elderly patients also have a decreased ability to concentrate urine
  65. What are some common symptoms of hypernatremia?
    • Renal Insufficiency (renal failure)
    • Decreased ability of the kidneys to concentrate urine
    • Kidneys could be excreting large amounts of unconcentrated urine

    *can be causes or symptoms
  66. A polyuric, hypernatremic patient most likely has a diagnosis of:
    Diabetes Insipidus

    • -decreased ADH secretion
    • -increased volume of dilute urine

    -urine Osm <150 in setting of hypertonicity (increasedOsm) and polyuria= diagnostic of DI
  67. Two categories and associated values for hypovolemic hypernatremia
    • Non Renal Losses 
    • Urine Na <10-15 mEq/L
    • Urine Osm >400 mOsm/L
    • Renal Losses
    • Urine Na >20 mEq/L
    • Urine Osm <300 mOsm/L
  68. Two categories and associated values for Euvolemic hypernatremia
    • Non Renal Losses 
    • Urine Na variable
    • Urine Osm >400 mOsm/L
    • Renal Losses
    • Urine Na variable
    • Urine Osm <290 mOsm/L
  69. Two categories and associated values for hypervolemic hypernatremia
    • Iatrogic
    • Mineralcorticoid Excess
    • Urine Na >20 mEq/L
    • Urine Osm >300 mOsm/L
  70. True or False:
    There is no set pace for treating hypernatremia, you can treat it as fast or as slow as you want.

    Needs to be corrected slowly because there's a risk of neurologic sequelae (ex. cerebral edema)
  71. In general, a hypovolemic hypernatremic patients volume is replace over:
    24-48 hours
  72. What is the standard rule for lowering sodium in hypernatremia?
    Don't lower sodium by more than 1-2 mEq/L/hour
  73. Treat hypovolemia in hypernatremia with what fluid?
    Normal Saline!

    -will treat volume deficit but will also decrease plasma sodium concentration
  74. Treatment of hypernatremia in hypervolemic patient
    • Enhance sodium removal
    • -loop diuretics, dialysis
    • Replace water deficiency
    • -hypotonic fluids
  75. Treatment of hypernatremia in Euvolemic patient
    • Replace water deficit
    • -hypotonic fluid
    • Control DI
    • -central
    • -nephrogenic
  76. Treatment for Hypernatremia in Central (neuro) DI
    DDAVP (vasopressin)
  77. Treatment of hypernatremia in patient with nephrogenic DI
    • Restrict sodium
    • restrict water
    • thiazide diuretics
  78. What is the relationship between ADH and:
    Central DI vs. Nephrogenic DI
    In central DI insufficient ADH levels

    In nephrogenic DI, the kidneys don't respond to ADH (so giving more ADH won't help!)
  79. Treatment of Hypernatremia in Hypovolemic Patient
    • Hypovolemia Correction
    • -.9% NaCl
    • Hypernatremia Correction
    • -hypotonic fluids
  80. What is a major intracellular cation?
  81. What is the normal intracellular concentration of potassium?
    150 mEq/L
  82. What is the normal extracellular concentration of potassium?
    3.5-5 mEq/L
  83. What is the usual daily potassium intake?
    50-150 mEq/day
  84. True or False
    We usually excrete the same amount of potassium we take in.
  85. How is potassium excreted in the body?
    Mostly through the kidneys, but some in feces
  86. What three things typically cause potassium to move INTO the cell?
    • 1. Insulin
    • 2. Beta agonists
    • 3. Alkalosis (decreased pH)
  87. What two electrolytes together are responsible for the resting membrane potential?
    Sodium and Potassium
  88. What two things regulate potassium excretion?
    • 1. Aldosterone
    • 2. Plasma protein level
  89. For Potassium:
    As long as the GFR is >_____mL/minute and dietary intake is normal, we excrete the same amount of potassium we take in.
  90. What is the difference between plasma and serum?
    • Plasma: liquid blood that is NOT clotted
    • Serum: liquid blood that IS clotted

    *serum potassium is .5 mEq higher than plasma because of lysis of cells that occurs during clotting (potassium is released during clotting)
  91. Na/K Pump:
    __ Sodium Ions move out of the cell as __ potassium ions move into the cell.
    3 sodium ions move out of the cell as 2 potassium ions move into the cell.
  92. What effect does acidosis have on the movement of potassium?
    Acidosis causes potassium to move OUT of the cell
  93. What effect does alkalosis have on the movement of potassium?
    Alkalosis causes potassium to move INTO the cell
  94. What effect do ACE inhibitors have on potassium?
    ACE inhibitors block aldosterone, which helps to control secretion of potassium: hyperkalemia
  95. True or False: 
    Plasma concentration is a good reflection of total body electrolyte concentration.

    Plasma concentration is a poor reflection of total body concentration.

    Hypo/hyper imbalances are only plasma concentration! NOT representative of total body concentration
  96. True or False:
    Hypokalemia is uncommon in healthy patients.
  97. Hypokalemia is a frequent side effect of:
    • Diuretics
    • Antibiotics
    • Hormones (aldosterone, glucocorticoids)
    • Chemotherapy
  98. What lab level is definitive for hypokalemia?
    <3.5 mEq/L
  99. Typically, symptoms for hypokalemia are manifested in what two systems?
    • Cardiovascular
    • Neuromuscular
  100. What are typical symptoms for hypokalemia?
    • Skeletal muscle weakness- lead to paralysis
    • Arrythmias- prominent U waves, ST depression, flat/inverted T waves
  101. What is the treatment for hypokalemia?
    • Replace the Potassium! (slowly!)
    • Correct precipitating factors (alkalosis, Mg, Meds)
  102. If severe hypokalemia, bolus __-__ mEq KCl.
    5-6 mEq KCl
  103. During severe hypokalemia, it is important to have continuous:
    EKG monitoring
  104. What is the recommended KCl replacement for mild hypokalemia? (>2.0 mEq/L)
    Replace with IV KCl at ≤ 10 mEq/hr
  105. What is the recommended KCl replacement for severe hypokalemia? (≤ 2 mEq/L)
    Replace with IV KCl at ≤ 40 mEq/hour
  106. Acute hypokalemia causes _____ of the cardiac cells.
    • Hyperpolarization
  107. By what mechanism do our sedative hypnotics work?

    Benzo's, propofol, barbs all cause Chloride to move into cell and make the intracellular space MORE NEGATIVE: causing sedation
  108. In severe hypokalemia, (≤2 mEq/L) what symptoms are you likely to see?
    • Paralysis
    • EKG changes
  109. What effect does hypokalemia have on digoxin? "nursing 101"
    Hypokalemia increases digoxin binding, pharmacologic effect is more profound

    There is an increased risk of digoxin toxicity in a state of hypokalemia
  110. What electrolyte imbalance contributes to hypertension? (especially on a low sodium diet)
  111. How does hypokalemia effect diabetic patients?
    • Impairs insulin secretion
    • Decreases end organ sensitivity to insulin
  112. True or False
    There is no set potassium level that we'd cancel surgery.
  113. A potassium level of ≤____ mEq/L is associated with perioperative rhythm disturbances. (especially prior to heart surgery)
    3.5 mEq/L
  114. What are some predisposing factors for hyperkalemia?
    • Renal Insufficiency
    • Diabetes
    • Hypoaldosteronism
  115. What are examples of medications that increased potassium levels?
    • ACE inhibitors
    • NSAIDs
    • K sparing diuretics
  116. Hyperkalemia is defined as a potassium level ≥ ___ mEq/L.
    ≥5 mEq/L
  117. Lethal symptoms of hyperkalemia are focused on:
    The heart! (cardiac)

    ex. arrythmias, cardiac arrest
  118. What are some causes of hyperkalemia under anesthesia?
    • Succinylcholine*
    • *Denervation Injuries
    • *Burns
    • Medications
  119. How does succinylcholine effect electrolytes?
    Causes hyperkalemia

    As a result of fasciculations: causes release of K from ICF to ECF

    Exaggerated in patients with burns and denervation injuries due to up regulation of Ach receptors
  120. What patient populations is succinylcholine contraindicated?
    • Denervation Injuries
    • Burns
  121. Effects of hyperkalemia on the cardiac muscle are exaggerated by:
    • Hypocalcemia
    • Hyponatremia
    • Acidosis
  122. What are common symptoms of hyperkalemia?
    • Muscle weakness
    • EKG changes
  123. With a potassium level <6, what cardiac effects will you see?
    Miminal cardiac effects, may see a peaked T wave
  124. What a potassium of >7, what cardiac and respiratory symptoms are you likely to see?
    Cardiac: ↑ PR interval, QRS complex widens...can progress to cardiac standstill

    Respiratory: ascending muscle weakness, inability to phonate, flaccid paralysis, respiratory arrest
  125. Treatment of hyperkalemia is aimed at:
    • Treating the Cause
    • Reversing membrane hyperexcitability
    • Getting of excess Potassium! (either excrete it or move ECF→ICF)
  126. What can be given to help stabilize the heart rhythm and depress membrane potential in hyperkalemia?
    Calcium Gluconate
  127. How do Beta2 agents affect potassium?
    • Increase uptake of potassium by skeletal muscles
    • (ex. albuterol)
  128. How can we assist the kidneys in removing excess potassium?
    • Diuretics
    • Dialysis
  129. How can we assist the GI tract in removing potassium?
  130. Where is calcium homeostasis housed for us?
    Thyroid and Parathyroid
  131. What % of the calcium is protein bound?
  132. What % of the calcium is complexed to anions?
  133. What % of the calcium is ionized?

    Only part of calcium that is physiologically active
  134. Which calcium in the body is the physiologically active one?
    Ionized calcium!
  135. How will acute alkalemia affect ionized calcium?
    Acute alkalemia will decrease ionized calcium
  136. How will acute acidemia affect ionized calcium?
    Acute acidemia will increase ionized calcium
  137. The plateau of cardiac action potential is dependent on which electrolyte?
  138. What electrolyte is responsible for the pumping action of the heart? (excitation/contraction coupling in the heart and skeletal muscle)
  139. What electrolyte is responsible for neurotransmitter release and secretion of enzymes and hormones?
  140. Is calcium most prevalent in the intracellular fluid or the extracellular fluid?
    extracellular fluid
  141. A decreased ionized calcium is seen in ___% of critically ill elderly patients.
  142. __% of hospitalized, non-ICU patients will have hypocalcemia.
  143. What are the early, first signs of hypocalcemia?
    Circumoral tingling and numbness
  144. What lab level indicates hypocalcemia?
    Ionized calcium <4 mg/dl; <1 mmol/L; <2 mEq/L
  145. Hypocalcemia is typically caused by a problem in the:
    parathyroid hormone [usually not just a calcium deficiency alone]
  146. What are the cardiovascular symptoms of hypocalcemia?
    dysrhythmias, digoxin insensitivity, EKG changes, heart failure, hypotension
  147. What are the neuromuscular symptoms of hypocalcemia?
    • *TETANY-hallmark symptom(due to irritability of neuronal membranes)
    • muscle spasm, papilledema, seizures, weakness, fatigue
  148. What are the respiratory symptoms of hypocalcemia?
    apnea, laryngospasm, bronchospasm, respiratory arrest
  149. How does hypocalcemia affect smooth muscle?
    • Irritates it! Causing spasms...
    • abdominal cramping, bronchospasms, urinary frequency
  150. What are some psychiatric symptoms of hypocalcemia?
    anxiety, dementia, depression, psychosis, irritability
  151. What are some causes of hypocalcemia?
    • surgical removal of the parathyroid glands
    • increased phosphate levels
    • increased/decreased magnesium levels
    • lysis of cells due to chemo
    • cell destruction from rhabdo
    • hypothermia
    • blood products (due to citrate)
    • Packed RBC's [5U+] (due to citrate)
    • hyperventilated patients (increased pH)
    • large administration of bicarbonate
  152. What is chvostek's sign? What does a positive sign indicate?
    • -Tap on facial nerve and it twitches
    • -indicates hypocalcemia
  153. What is trousseau's sign? What does a positive sign indicate?
    • -Inflate a blood pressure cuff to 20mmHg above systolic blood pressure, will cause ischemia to the radial and ulnar nerve, will cause carpal spasm
    • -Hypocalcemia
  154. What is important to consider when diagnosing hypocalcemia?
    • Pt age/history
    • Renal Function
    • Serum Phosphate (normal or low indicates Vit D or mag deficiency)
    • General status
    • Duration of hypocalcemia
  155. What are treatments for hypocalcemia?
    • Calcium Gluconate/Calcium Chloride- Rule of 10's!
    • -10 mL's of 10% CaCl/CaGluconate over 10 minutes followed by continuous infusion

    Vit D to increase enteric uptake
  156. What other electrolyte imbalances potentiate the neuromuscular and cardiovascular effects associated with hypocalcemia?
    • Hyperkalemia
    • Hypomagnesium
  157. True or False
    It is important to remember to NOT overtreat a mild case of hypocalcemia.
  158. Hypercalcemia is caused by:
    • Malignancy
    • Hyperparathyroidism
  159. Ionized calcium in hypercalcemia is a level of:
    • ≥1.5 mmol/L
    • OR
    • ≥3 mEq/L
  160. Hypercalcemia is characterized by a total serum calcium of ≥ ____ mg/dl
    10.5 mg/dl
  161. What effect does hypercalcemia have on the kidneys?
    Impairs the kidneys ability to concentrate urine
  162. What hormone has the greatest effect on calcium homeostasis?
    Parathyroid Hormone
  163. What are some treatment options for hypercalcemia?
    • Hydration 
    • with .89 NaCl to dilute out Ca
    • Calcitonin
    • not a first line treatment
    • hormone made my thyroid to regulate calcium
    • will lower calcium in 24-48 hours
    • more effective when given with glucocorticoids (cortisol)
  164. Symptoms in association with total serum calcium levels
    • <11.5: usually asymptomatic
    • 11.5-13: lethargy, anorexia, nausea, polyuria
    • >13: muscle weakness, stupor, coma, hypertension, arrythmias, cardiac arrest, lysis of bone 
    • >14: MEDICAL EMERGENCY! Hydrate! Lasix UO goal of 200-300 hour
  165. Phosphate is freely filtered at the:
  166. Reabsorption of phosphate is controlled mainly by the:
    parathyroid hormone
  167. What % of phosphate is found in the bone?
  168. What  % of phosphate is found in the intracellular fluid?
  169. What % is phosphate is found in the extracellular fluid?
  170. What % of phosphate is a free ion?
  171. What % of phosphate is complexed to an anion?
  172. What % of phosphate is protein bound?
  173. What is the normal total level of phosphate? (mg/dl)
    2.7-4.5 mg/dl
  174. Why is phosphate important? What are the 'roles' of phosphate?
    • ATP- phosphate is the energy bond
    • Second messager system [cAMP]
    • Nucleic acids
    • Cell membranes (phospholipids)
    • Part of 2,3 DPG (release O2 from Hgb)
    • Urinary Buffer
  175. Phosphate of < ___ mg/dl will result in severe organ dysfunction.
    <1 mg/dl
  176. How is ATP affected in hypophosphatemia?
    Phosphate is the energy bond in ATP

    With a decrease in phosphate, could leave to cellular energy depletion
  177. What are symptoms of hypophosphatemia?
    N: parasthesias, myopathy, encephalopathy, delirium, seizures, coma

    H: dysfunction of RBCs, WBCs, platelets

    muscle weakness, respiratory muscle dysfunction, rhabdo
  178. Why can low phosphate increase susceptibility to sepsis?
    Hypophosphatemia affects the white blood cells, which act as phagocytes; if there is dysfunction in the phagocytes, patients are more susceptible to sepsis
  179. What is used to treat moderate hypophosphatemia?
    15 mmmol (456 mg) boluses mixed with 100 mL of NS over 2 hours
  180. What is used to treat chronic hypophosphatemia?
    .2-.68 mmol/kg (5-16 mg/kg)
  181. What causes severe hypophosphatemia in post operative and trauma patients?
    • 1.Phosphate shifts intracellularly
    • 2. Increased loss of phosphate by kidneys
    • 3. Decreased absorption in the GI tract
    • 4. Hyperventilation
  182. What effect does hyperventilation have on phosphate levels?
    Hyperventilation decreases phosphate levels significantly, effect will last long after hyperventilation ends
  183. Why should one be careful when correcting hypophosphatemia in patient who are also hypocalcemic?
    Increased phosphate=Decreased calcium

    Don't want to cause more severe hypocalcemia!
  184. Hyperphosphatemia is primarily related to decreased levels of what other electrolyte?
  185. Hyperphosphatemia is a level > ____ mg/dl
    5 mg/dl
  186. What are two common causes of hyperphosphatemia?
    • Rapid lysis of cells (from rhabdo, chemo)
    • Renal Failure**

  187. Renal excretion of phosphate is adequate as long as the GFR is > ___ ml/min.
    20-25 ml/min
  188. What are treatments for hyperphosphatemia?
    • Correct underlying cause
    • Correct associated hypocalcemia
    • Restrict Intake & Increase Excretion 

    [increase excretion by: NS, acetazolamide, aluminum hydroxide, dialysis]
  189. Normal plasma level of Magnesium
    • 1.5-1.9 mEq/L
    • 1.8-2.8 mg/dl
  190. What % of Magnesium is found in the bone?
  191. What % of Magnesium is found intracellularly?
    50% (half of this is in the muscle)
  192. What % of Mag is found in the plasma?
  193. What electrolyte is an important divalent cation in the intracellular space?
  194. What examples doe Mag act as a co-factor in enzyme reactions?
    • DNA&protein synthesis
    • Energy metabolism
    • Glucose utilization
    • Fatty Acid Synthesis and Breakdown
  195. Magnesium is a calcium ______.
  196. Which electrolyte partially regulates PTH secretion?
  197. Which electrolyte regulates/stabilizes membranes?
  198. What % of Magnesium is ionized?
    • 55% 
    • *only ionized is active
  199. What % of Mag is protein bound?
  200. What % of Mag is bound to an anion?
  201. What 3 enzyme systems does Magnesium act as a primary regulator/cofactor for?
    • 1. NaK Pump
    • 2. CaATPase Pump
    • 3. Slow Ca Channels
  202. What conditions is therapeutic hypermagnesemia indicated?
    • premature labor
    • pre-eclampsia
    • eclampsia
    • arrythmias
  203. What is Magnesium indicated for treatment of arrythmias?
    • directly effects myocardial membrane
    • prolongs the effective refractory period
    • depresses conduction
  204. How does Magnesium function in potassium metabolisM?
    primarily through regulating Na+K ATPase and controls potassium absorption by renal tubules (esp in K depleted states)
  205. What electrolyte prevents vasospasms and release of catechols from adrenergic nerve endings?
  206. What effects does decreased Magnesium have on the muscle?
    Decreased Magnesium causes muscle to contract more to a stimulus; muscle is more prone to tetany
  207. True or False:
    Magnesium is used to treat Torsades
  208. In relation to the axonal membrane, HypoeMagnesemia:
    • Decreases the threshold of axonal stimulation
    • Increases the nerve conduction velocity

    -Mag functions as a regulator of membrane excitability
  209. What electrolyte competitively inhibits entry of calcium into the presynaptic nerve terminals?
  210. Which electrolyte serves as a structural component in both cell membrane and skeleton?
  211. How does Magnesium function as an endogenous calcium antagonist?
    • Magnesium regulation of slow calcium channels contributes to the
    • 1. maintenance of normal vascular tone
    • 2. prevention of vasospasms
    • 3. prevention of calcium overload in the tissue
  212. True or False
    Magnesium regulates PTH secretion
  213. Which electrolyte is important for maintenance of end organ sensitivity to both PTH and Vitamin D?
  214. True or False
    Abnormalities in ionized magnesium concentration can result in abnormal calcium metabolism.
  215. True or False:
    Decreased levels of Magnesium aggravate Congestive Heart Failure
  216. Causes of Hypo-Magnesium
    • Inadequare GI absorption
    • Excessive Mag losses (NG, drains)
    • Failure of Renal Magnesium conservation

    *Rarely caused by inadequate Mag intake
  217. __% of alcoholic hospitalized patients have hypo-Magnesium
  218. Treatment of MILD Hypo-Magnesium
  219. Medication related causes of Hypo-Magnesium
    • Aminoglycosides
    • Chemotherapy (cysplatin)
    • Cardiac glycosides
    • Diuretics
  220. True or False
    Decreased Magnesium can be caused by intracellular shifts of Magnesium due to insulin administration or thyroid hormone.
  221. Symptomatic Hypo-Magnesium Treatment
    8-16 mEq/L in bolus over 1 hour then 2-4 mEq/hr THEN 1 mEq/hr

    *always use cardiac monitor
  222. How can Hypo-Magnesium cause Hypokalemia?
    Renal Potassium Wasting- replacing potassium alone won't fix the issue (need to replace Magnesium as well)
  223. Symptoms of hypo-Magnesium
    Membrane irritability and tetany

    • 1.5-1.7 mg/dl: symptoms are rare
    • <1.2 mg/dl: weakness, fatigue, lethargy, muscle spasms, parasthesias, depression, coronary spasms, heart failure, dysrhythmias, hypotension

    Severe: seizures, coma, confusion
  224. What effect does hypo-Magnesium have on Digoxin?
    Aggravates Digoxin Toxicity

    -also increases myocardial sensitivity to Digoxin
  225. True or False
    NaK Pump depends on Magnesium
  226. Hyper-Magnesium lab levels: > ___ mg/dl
    2.5 mg/dl
  227. Hyper-Magnesium is caused by:
    Usually iatrogenic

    • antacids
    • enemas
    • parenteral feedings (esp if renal failure)

    • Rare causes:
    • hypothryoid, Addison's, lithium intoxication
  228. What effect does hyper-Magnesium have on nondepolarizing muscle relaxants?
    Hyper-Magnesium potentiates action of nondepolarizing muscle relaxants

    *Increased Magnesium= Decreased Potassium in response to succinylocholine
  229. True or False
    Increased levels of Magnesium antagonize the effect and release of achetylcholine at the neuromuscular junction
    • True
    • -depresses skeletal muscle function
    • -acts as a neuromuscular blockade
  230. Interrelationship between ___ & ___ in cardiac tissue has greatest clinical relevance in terms of dysrhythmias, Digoxin toxicity, and myocardial infarction.
    Magnesium and Potassium
  231. What effect does severe hypo-Magnesium or severe hyper-Magnesium have on PTH secretion?
    SUPPRESSES PTH secretion (can cause hypocalcemia)

    -severe hypo-Magnesium can impair end organ response to PTH
  232. Hyper-Magnesium Symptoms Associated with Lab Levels
    2.5-5: usually asymptomatic

    >5: Flushing, NV, decreased deep tendon reflexes, somnolence, hypotension, EKG changes

    Symptoms progress in severity as levels increase: to cardiac arrest, paralysis, and coma
  233. Hyper-Magnesium Treatment
    • Acute Treatment: Manage Neuro and Cardiac Toxicity!
    • 5-10 mEq Ca IV: buys time to institute a more definitive treatment (Ca is transient antagonist to Magnesium)

    • Then: 
    • Expand ECF volume, Lasix, Dialysis (if renal failure)