Podcast
Questions and Answers
What is the classification for severe hyponatremia?
In chronic hypervolemic hyponatremia, what is a recommended way to reduce the neurohumoral influence on water retention?
What should be avoided in hypervolemic hyponatremia as it impairs urinary dilution?
For chronic, asymptomatic hyponatremia, what is recommended to use once the underlying cause is treated?
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Why should Chronic hyponatremia be treated cautiously with gradual correction?
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Which medication can be used as an ADH antagonist in the treatment of hyponatremia?
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Why should loop diuretics be preferred over thiazides in hypervolemic hyponatremia?
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What is the appropriate approach to chronic, asymptomatic hyponatremia?
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Why should severe hyponatremia be cautiously treated with gradual correction?
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In hypovolemic hyponatremia, what is the purpose of restoring ECF volume with isotonic saline?
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What is the recommended approach for chronic, asymptomatic hyponatremia after treating the underlying cause?
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What should be used to excrete free water in hypervolemic hyponatremia once a negative Na+ balance has been achieved?
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In chronic hypervolemic hyponatremia, what is the first treatment that should be focused on?
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What is a possible consequence of severe hyponatremia during the perioperative period?
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which type of hyponatremia associated with significant perioperative morbidity.
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for accurate diagnosis of hyponatremia we should use?
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hyponatremia is usually observed in conjunction with ?
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in which situations, osmolality is normal or raised in hyponatremia?
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pseudohyponatremia is accompanied with ?
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Which treatment option is recommended for hypovolemic hyponatremia?
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mild preoperative hyponatremia is associated with?
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What is the main physiological mechanism that can lead to postoperative hyponatremia?
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Which group is particularly at high risk for neurologic symptoms due to postoperative hyponatremia?
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What is the typical Na+ level at which elderly women become symptomatic from hyponatremia?
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What percentage of hyponatremic patients may develop encephalopathy postoperatively?
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What is a potential consequence of failure to recognize hyponatremia as a cause of postoperative symptoms?
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Why might inadequate treatment of hyponatremia based on fears of causing osmotic demyelination contribute to poor outcomes?
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Prevention of postoperative hyponatremia should be a key goal of postoperative fluid therapy, based on ?
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What is the primary reason for terminating surgery if 1000 to 1500 mL of fluid has been absorbed in females?
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What is the recommended intravesical pressure limit for endometrial procedures to prevent TURP complications?
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In severe hypoosmolar hyponatremia with neurologic symptoms, what is the treatment of choice?
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What is the purpose of monitoring the patient's neurologic status using regional anesthetic techniques during surgery?
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What treatment should be considered if intravascular volume overload is present in a patient?
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What is the preferred treatment when osmolality is normal or slightly decreased in a patient with hyponatremia?
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What is the primary cause of TURP syndrome?
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Which factor is NOT listed as a risk factor for developing TURP syndrome?
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What is the recommended replacement for distilled water as an irrigant to prevent TURP syndrome?
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How can TURP syndrome be prevented during surgery?
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What should be assessed if a significant amount of irrigation fluid has been absorbed during a TURP procedure?
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Why is the use of conducting irrigant with bipolar diathermy recommended to prevent TURP syndrome?
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during TURP . Early hypervolemia-related hypertension may be followed by profound hypotension as a result of?
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by which mechanism Glycine lead to seizures ?
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side effect due to glycine during TURP?
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what is the treatment for the excitatory effects of glycine?
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What is the recommended initial rate of hypertonic 3% saline infusion for patients with symptomatic hyponatremia?
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What is the recommended goal of increasing [Na+] when using hypertonic 3% saline for symptomatic hyponatremia treatment?
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What should be primarily focused on in treating chronic, asymptomatic hyponatremia once the underlying cause is addressed?
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For patients with moderate symptoms of symptomatic hyponatremia, what treatment may be used to increase [Na+] by 1 mEq/L/h for 3 to 4 hours?
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What is the primary approach for optimally treating chronic hypervolemic hyponatremia?
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What is a key factor in determining the symptoms of hyponatremia?
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At what Na+ concentration do symptoms of seizures and coma typically occur?
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In hypovolemic hyponatremia, why is isotonic saline used for treatment?
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What should be considered when treating chronic hyponatremia (>48 hours) due to cerebral compensation?
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Why are sudden increases in osmolality discouraged in the treatment of chronic hyponatremia?
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What should be tailored when deciding on the treatment for hyponatremia?
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what is the initial treatment of Severely symptomatic hyponatremia (coma, seizures, ) of acute onset?
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What percentage of critically ill patients may develop hypernatremia?
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What is the rapid guide to urine osmolality in cases where urgent treatment is being considered?
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What is the treatment approach for hypovolemic hypernatremia after correcting the intravascular volume deficit?
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What is the major mechanism leading to hypernatremia due to excessive water loss?
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Which condition is characterized by the excretion of large quantities of inappropriately dilute urine?
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What is the recommended treatment for hypervolemic hypernatremia after stopping exogenous Na+ administration?
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In which circumstances does central DI typically occur?
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In central diabetes insipidus with a urine output greater than 250 mL/h, what medication is indicated to reduce urine output?
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What is the risk associated with administering higher acute doses of desmopressin acetate in central diabetes insipidus?
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What clinical feature is associated with hypernatremia?
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How is the diagnosis of hypernatremia typically established?
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What is the appropriate treatment for euvolemic hypernatremia after replacing deficit and ongoing losses?
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In which circumstances does nephrogenic DI typically occur?
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what is the complication hypernatremia due DI If the patient is unable to accept compensatory fluid orally ?
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how hypernatremia is defined ?
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severe hypernatremia defined as Na more than
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Appropriate hypernatremia Treatment should be
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mortality rate due to severe hypernatremia?
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what is the diagnosis for : Hypovolemia, TBW ↓↓ TBNa+ ↓. U[Na+] >20 ?
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what is the diagnosis for : Hypovolemia, TBW ↓↓ TBNa+ ↓. U[Na+] <20 ?
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what is the diagnosis for : Euvolemia, TBW ↓, TBNa+ normal,U[Na+]Variable.
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what is the diagnosis for : Hypervolemia, TBW ↑, TBNa+ ↑↑,U[Na+]>20?
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What is a possible cause of hypokalemia according to the text?
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What is a potential consequence of using anticoagulated samples for K+ tests?
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What is the primary mechanism of failure of renal secretion leading to hyperkalemia?
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What is a common cause of elevated plasma K+ levels due to sampling artifacts?
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what is the key role of potassium on excitable tissue ?
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What is a potential consequence of dyskalemia during the perioperative period?
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What ECG changes are seen with hyperkalemia at K+ levels greater than 7.5 mEq/L?
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In the context of anuric renal failure, what level of hyperkalemia is an indication for acute dialysis?
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What is the primary goal of the acute treatment of hyperkalemia?
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What is a characteristic feature of chronically induced hyperkalemia, such as in chronic renal failure?
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What is the mechanism of action for eliminating potassium in more chronic cases of hyperkalemia?
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What are the initial ECG changes seen with hyperkalemia when K+ levels are between 5.5 and 6.5 mEq/L?
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What are the initial ECG changes seen with hyperkalemia when K+ levels are between 6.5 and 7.5 mEq/L?
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What are the initial ECG changes seen with hyperkalemia when K+ levels Greater than 9.0 mEq/L
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Ratios between intracellular and extracellular K+ concentrations in acute hyperkalemia
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What is the primary cause of TURP syndrome?
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HYPOKALEMIA defined as k level less than ?
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Moderate-to-severe hypokalemia defined as k Level between ?
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Moderate-to-severe hypokalemia (2-2.5 mEq/L) leads to
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why Hypokalemia should be pragmatically corrected in the perioperative period to
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treatment is of prime importance when acute arrhythmias exist, and K+ should be maintained at greater than ?
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during treatment of hypokalemia, speed of the infusion should be
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during treatment of hypokalemia, speed of the infusion should be
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at which concentration the K solution should be given via central venous catheter
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Treatments for Hyperkalemia: what is the indication for using CaCl2 10% (10 mL) or Calcium gluconate
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Treatments for Hyperkalemia: duration of action of CaCl2 10% (10 mL) or Calcium gluconate (Antagonize cardiac toxicity)
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Treatments for Hyperkalemia: what is the indication for using “Intracellular potassium shift” insulin
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Treatments for Hyperkalemia: what is the indication for using “Intracellular potassium shift” NaHCO3 1 mEq/kg
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Treatments for Hyperkalemia: what is the indication for using “K+ elimination” Kayexalate
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Treatments for Hyperkalemia: what is the indication for using "Increase renal excretion” Furosemide
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Which of the following is a symptom characteristic of hypocalcemia?
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What is a sign of hypocalcemia that involves facial twitching induced by tapping on the facial nerve?
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In which patient population may ionized hypocalcemia from citrate chelation be particularly severe and prolonged?
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What ionized calcium concentration is considered the threshold for specific coagulopathy due to hypocalcemia?
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What is the recommended ionized calcium level that should be aimed for in situations requiring supplemental calcium due to hypocalcemia?
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Which symptom is NOT characteristic of hypocalcemia?
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In critical illness, what circumstance warrants Ca2+ supplementation?
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Which symptom is associated with hypercalcemia?
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What treatment is recommended for symptomatic hypercalcemia to increase renal Ca2+ excretion?
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Which medication could contribute to a mild reduction in Ca2+ levels during the rehydration phase?
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What is the purpose of Bisphosphonates in the treatment of severe hypercalcemia?
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Which condition may lead to low Mg2+ levels during hypocalcemia?
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What is the recommended IV dose of pamidronate for moderate hypercalcemia?
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What should be considered before administering Bisphosphonates for hypercalcemia treatment?
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When is Calcitonin given in the treatment of hypercalcemia?
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Why might calcium gluconate be preferred for peripheral administration over CaCl2 for hypocalcemia treatment?
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IV calcium gluconate vs CaCl2 for hypocalcemia treatment?
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The causes of hypocalcemia are related to
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when Glucocorticoids indicated as treatment in hypercalcemia?
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combination of volume expansion with isotonic saline and loop diuretics. how much It can reduce Calcium level?
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in how long time the IV dose of pamidronate 60 mg cam bring claim level to normal?
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what is the most common cause typically manifests with mild hypercalcemia ?
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What is one of the reasons why serum Mg2+ concentration may be a poor indicator of total body content?
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Which group of patients are particularly prevalent to hypomagnesemia?
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What are some common symptoms associated with hypomagnesemia?
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What can lead to relative depletion of magnesium in the body?
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How are intraerythrocyte or intralymphocyte Mg2+ levels related to total body and tissue stores?
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What is one of the cardiovascular manifestations associated with acute hypomagnesemia?
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What is the recommended initial dose of IV Mg2+ in the presence of seizures or acute arrhythmias?
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What are the symptoms associated with Mg2+ concentration between 24 to 48 mg/dL?
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What is a key consideration when administering Mg2+ to patients with kidney disease?
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Which complication may arise if Mg2+ is used without caution in patients with a background impairment of neuromuscular transmission?
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What is the primary purpose of administering IV Ca2+ during treatment of acute hypermagnesemia?
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What is the definitive treatment for hypermagnesemia, especially in the presence of renal disease?
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what is the magnesium Therapeutic levels in the treatment of preeclampsia
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hypomagnesemia are associated with cardiovascular morbidity and are particularly prevalent in diverse hospitalized patients, which patients has the highest risk for hypomagnesemia?
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treatment of Asymptomatic patients with moderate-severe hypomagnesemia ?
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what is the indication to start treatment for hypomagnesemia?
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symptoms of hypomagnesemia often relate to common coexisting ?
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hypomagnesemia usually present with hypocalcemia, hypokalemia, or both which also should also be treated? which one should be treated first ?
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What are the symptoms associated with Mg2+ concentration between 5 to 10 mg/dL?
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what is the main cause of HYPERMAGNESEMIA
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What may precipitate symptoms of hypophosphatemia in patients with chronic depletion?
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What metabolic change leads to intracellular electrolyte depletion particularly phosphate despite normal plasma levels during starvation?
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What phenomenon leads to profound hypophosphatemia as a result of refeeding after a period of prolonged starvation?
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Which disorder may be observed on commencement of nutrition after prolonged starvation and could manifest postoperatively?
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symptoms of severe hypophosphatemia (<1.5 mg/dL), may include
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during hypophosphatemia , IV PO43− replacement carries a risk for precipitating
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indications of IV PO43− replacement therapy during hypophosphatemia
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IV PO43− replacement for hypophosphatemia. protocols should be based on ?
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what is the most common cause in clinical practice for HYPERPHOSPHATEMIA?
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HYPERPHOSPHATEMIA due to renal failure
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The features of hyperphosphatemia may be related to
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what is the effect on phosphate and calcium due to increased PTH secretion
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Hypocalcemia due to hyperphosphatemia is mediated via
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hypophosphatemia cause by?
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hyperphosphatemia caused by?
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How does exogenous Cl− administration from isotonic saline affect the plasma SID and therefore pH?
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In disease states with hyperchloremia and hypernatremia, what impact do they have on the plasma SID and pH?
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What should initial investigation and treatment of 'matched' electrolyte imbalances target?
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Which electrolyte imbalances can affect acid-base balance according to the text?
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Causes and Mechanisms of Chloride Abnormalities- HYPOCHLOREMIA
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Causes and Mechanisms of Chloride Abnormalities- HYPERCHLOREMIA
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Study Notes
Chloride Disorders
- Hypernatremia: [Na+] >145 mEq/L, less common than hyponatremia, affecting up to 10% of critically ill patients
- Causes: excessive water loss, inadequate compensatory intake, lack of ADH, administration of exogenous sodium
- Symptoms: altered mental status, lethargy, irritability, seizures, hyperreflexia, spasticity
- Diagnosis: assessment of intravascular volume status, urinary osmolality, and Na+ concentration
- Treatment: tailored to intravascular volume status, correction of Na+ concentration no more rapid than 10 mEq/L/day
- Hypochloremia and hyponatremia do not affect SID or pH
- Causes of Cl– abnormalities: matched electrolyte imbalances, targeting dysnatremia first
Magnesium Disorders
- Hypomagnesemia: associated with cardiovascular morbidity, prevalent in hospitalized patients (12% of general inpatients, 19% of preoperative cardiac surgery patients, 65% of critical care patients)
- Causes: reduced Mg intake, increased renal losses, relative depletion in times of increased cell turnover and protein production
- Symptoms: nonspecific; relate to coexisting hypocalcemia or hypokalemia
- Treatment: tailored to severity of symptoms and degree of hypomagnesemia, asymptomatic patients receive oral supplementation, IV Mg2+ for symptoms or Mg2+ <1 mg/dL
- Hypermagnesemia: typically iatrogenic, caused by excessive Mg2+ administration
- Symptoms: reflect effect on neurologic and cardiac function, relate to serum Mg2+ levels
- Treatment: promote renal excretion, IV Ca2+ to antagonize Mg2+, definitive treatment may require dialysis
Potassium Disorders
- Hyperkalemia: may result from excess intake, failed excretion, or shift from ICF to ECF
- Symptoms: muscle weakness, paralysis, altered cardiac conduction, ECG changes
- Treatment: shifting K+ from ECF to ICF, antagonizing cardiac toxicity with Ca2+, increasing renal excretion, GI resin exchange
- Hypokalemia: may result from excess intake, failed secretion, or shift from ECF to ICF
- Causes: impaired principal cell function in the cortical collecting duct, hypomagnesemia, refeeding syndrome
- Symptoms: muscle weakness, paralysis, altered cardiac conduction
- Treatment: correction of underlying cause, potassium supplementation
Calcium Disorders
- Hypocalcemia: related to reduced PTH and/or vitamin D activity, increased bone deposition, Ca2+ chelation, or changes in binding protein concentration or ionized fraction
- Symptoms: neuromuscular irritability, circumoral and peripheral paresthesia, Chvostek sign, Trousseau sign, muscle cramps, laryngospasm, tetany, seizures
- Treatment: addressing underlying cause, correcting ionized Ca2+, supporting cardiac inotropy and neuromuscular function
- Hypercalcemia: occurs when ECF Ca2+ influx from GI tract and/or bone outweighs efflux to bone or excretion via kidneys
- Symptoms: neurologic symptoms, GI symptoms, renal manifestations, ECG abnormalities, potentiation of digoxin toxicity
- Treatment: addressing underlying cause, increasing renal Ca2+ excretion with isotonic saline and loop diuretics, bisphosphonates, glucocorticoids, calcitonin
Phosphate Disorders
- Hypophosphatemia: related to impaired enteral uptake, increased renal excretion, or shifts to the cellular compartment or bone
- Symptoms: precipitated by hyperventilation in patients with chronic depletion
- Treatment: addressing underlying cause, correcting phosphate levels
- Hypermagnesemia: not mentioned
Sodium Disorders
-
Hyponatremia: may be present preoperatively, develop as a consequence of perioperative events, or both
- Classification: mild (130-134 mEq/L), moderate (120-130 mEq/L), severe (<120 mEq/L)
- Symptoms: unusual due to cerebral compensation for hypoosmolar state
- Treatment: depends on underlying cause, hypovolemic hyponatremia requires ECF volume restoration, hypervolemic hyponatremia requires fluid restriction and optimization of underlying disease state### Hyponatremia
-
Classified as mild (130-134 mEq/L), moderate (120-130 mEq/L), or severe (<120 mEq/L or 48 hours or of unknown duration)
-
Treatment of chronic hyponatremia (>48 hours or of unknown duration) should be cautious to avoid cerebral compensation for the hypoosmolar state, leading to cerebral water loss and osmotic demyelination
Hypovolemic Hyponatremia
- Symptoms are unusual due to osmotic shifts in the brain being limited by the loss of both Na+ and water
- ECF volume should be restored with isotonic saline, which will also reduce ongoing ADH release
Hypervolemic Hyponatremia
- In chronic cases, focus on restricting water intake and optimizing the underlying disease state, such as improving cardiac output with ACE inhibitors to reduce neurohumoral influence on water retention in cardiac failure
- Loop diuretics can be used to excrete free water once a negative Na+ balance has been achieved
Chronic, Asymptomatic Hyponatremia
- No immediate correction of hyponatremia is required, and the underlying cause should be treated
- Fluid restriction, ADH antagonists (lithium, demeclocycline), and loop diuretics may be used
Postoperative Hyponatremia
- The surgical stress response, aggravated by hypotension and pain-related or physiologic stress-related sympathetic activity, can lead to a state of Na+ and water retention similar to SIADH
- Incidence of postoperative hyponatremia is 1% to 5%, with children and premenopausal females at high risk for neurologic symptoms
- Symptoms and neurologic sequelae may occur at Na+ levels as high as 128 mEq/L in these groups
Symptomatic Hyponatremia
- Typically euvolemic or hypervolemic
- In patients with moderate symptoms (confusion, lethargy, nausea, and vomiting), hypertonic 3% saline may be used at an initial rate of 1 mL/kg/h to increase [Na+] by 1 mEq/L/h for 3 to 4 hours
- Infusion rate should be modified to ensure that [Na+] is increased by no more than 10 mEq/L in the first 24 hours of treatment
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Description
Explore the diagnosis, classification, and treatment of hyponatremia disorders in the perioperative setting. Learn about the risks of sudden increases in osmolality and potential complications such as osmotic demyelination.