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    Home > Active Ingredient News > Endocrine System > Can you answer these 5 questions about electrolytes correctly?

    Can you answer these 5 questions about electrolytes correctly?

    • Last Update: 2021-04-21
    • Source: Internet
    • Author: User
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    Although patients with mild electrolyte disturbances may have no symptoms, electrolyte imbalances can also lead to serious consequences, such as heart, nerve, and gastrointestinal problems.

    Electrolyte disorders are mainly caused by imbalances in sodium levels (hyponatremia, hypernatremia), potassium levels (hypokalemia, hyperkalemia), and calcium levels (hypocalcemia, hypercalcemia).

    Yimaitong compiles and organizes, please do not reprint without authorization.

    How much do you know about electrolyte disorders? Take a test now! 01 Regarding hyponatremia, which of the following descriptions is the most accurate? A.
    Loop diuretics are the most common cause of drug-related hyponatremia B.
    Hypervolemic hypotonic hyponatremia is the most common hyponatremia C.
    Most patients with hyponatremia are asymptomatic and It is often found accidentally during laboratory examinations.
    D.
    The correction rate of patients with chronic and severe symptomatic hyponatremia should be 2 mEq/L/h, and the total increase in serum sodium should be >10 mEq/L.
    Analysis: Most low Patients with natriemia have no symptoms, and most of them are found accidentally when checking the results of laboratory tests.

    Patients with hyponatremia may experience nausea and discomfort.
    The patient’s serum sodium level is slightly reduced, somnolence, decreased consciousness, and headache.
    In severe cases, it can also lead to epilepsy and coma.

    Usually, obvious neurological symptoms are mostly caused by low serum sodium levels (usually <115 mEq/L), which can cause translocation of intracerebral permeate and cerebral edema.

     The use of diuretics may cause hypovolemia and hyponatremia, but loop diuretics are not a common cause of hyponatremia.

     Normal blood volume hyponatremia is the most common hyponatremia, accounting for about 60%.

    The most common cause is syndrome of inappropriate antidiuretic hormone secretion (SIADH).

     Hypervolemic hyponatremia is characterized by clinically detectable edema or ascites, suggesting an increase in water and sodium in the body.

    However, paradoxically, the reduction of effective circulation and tissue perfusion can stimulate the pathophysiological mechanism of impaired renal excretion of water (the same as hypovolemic hypotonic hyponatremia).

    Common examples include liver cirrhosis, congestive heart failure, nephrotic syndrome, and severe hypoproteinemia.

     The guidelines recommend that the correction rate of patients with chronic and severe hyponatremia should be ≤0.
    5 mEq/L, and the total increase within 24 hours should be ≤8-10 mEq/L.

    The sodium ion concentration must be corrected within the normal range (usually ≤120 mEq/L) instead of the normal value.

     Answer: C02 Regarding hypernatremia, which of the following is the most accurate? A.
    The use of metformin is the biggest risk factor for hypernatremia.
    B.
    Polyuria and weight gain are the most common symptoms in patients with hypernatremia.
    C.
    Patients with hypernatremia have a higher urine sodium level, usually 20 mEq/ LD.
    For patients with asymptomatic or mild hypernatremia, the serum sodium correction should be ≤0.
    5 mmol/L/h, and should be limited to 10 mmol/L within 24 hours.
    Analysis: If the thirst response is intact and water is available, no May develop into hypernatremia.

    Under normal circumstances, an increase in osmotic pressure of 1%-2% will cause thirst, as well as hypovolemia and hypotension.

    There are multiple risk factors for hypernatremia, and the biggest risk factor is age> 65 years.

    Other risk factors include: ➤ mental or physical impairment; ➤ uncontrolled diabetes (solute diuresis); ➤ potential polyuria; ➤ diuretic treatment; ➤ living in a nursing home, lack of care; ➤ hospitalization.

     Drugs that may cause hypernatremia include: ➤ diuretics; ➤ sodium bicarbonate; ➤ sodium chloride; ➤ steroids (corticosteroids, corticotropin); ➤ hormones (androgens, estrogen).

     Symptoms of hypernatremia include: ➤ Cognitive ability: drowsiness, sleepiness, confusion, language abnormalities, restlessness, seizures, nystagmus, myoclonic convulsions; ➤Clinical symptoms of dehydration or volume reduction: orthostatic blood pressure Changes, tachycardia, oliguria, dry oral mucosa, swollen skin, dry armpits; ➤Other findings: weight loss, general weakness.

     Hypernatremia can be diagnosed based on the serum sodium level (>145meq/L).

    Laboratory tests can determine the cause of hypernatremia: ➤ Serum electrolytes (sodium, potassium, calcium); ➤ Glucose level; ➤ Urea; ➤ Creatinine; ➤ Urine electrolytes (sodium, potassium); ➤ Urine and plasma osmotic pressure; ➤ 24h urine output; ➤plasma arginine vasopressin level (if indicated).

     The first step in diagnosing hypernatremia is to assess the patient's volume status.

    Volume contraction may be reflected by low urine sodium levels (usually <20 mEq/L).

     The Endocrine Society recommends avoiding excessive correction of hypernatremia.

    For patients with acute hypernatremia, serum sodium should be corrected at a rate of 5 mmol/L within the first hour (or until symptoms improve), and should be limited to 10 mmol/L within 24 hours.

    For asymptomatic or mild hypernatremia patients, serum sodium correction should be ≤0.
    5 mmol/L/h, and it should be significantly less than 10 mmol/L within 24 hours.

     Answer: D 03.
    Which of the following is the most accurate description of hypokalemia? A.
    Eating disorders or excessive alcohol consumption are related factors for the high incidence of hyponatremia.
    B.
    Hypertension is usually associated with hypokalemia caused by the use of laxatives, and hypotension is indicative of potential diseases other than hypokalemia.
    C.
    Serum kidney is recommended The detection of aldosterone, aldosterone, and cortisol is the first-line test for all patients with hyponatremia.
    D.
    Angiotensin-converting enzyme inhibitor (ACEI) is recommended for hypokalemia with renal insufficiency or taking potassium supplements/diuretics Patient analysis: Prescription drugs that increase urination (such as diuretics) are the most common cause of hypokalemia.

    Severe vomiting or diarrhea can also cause excessive potassium loss.

    Other causes of hypokalemia include: Excessive drinking; Eating disorders; Chronic kidney disease; Diabetic ketoacidosis; Excessive use of laxatives; Excessive sweating; Folic acid deficiency; Primary aldosterone Hyperplasia; ➤ Application of antibiotics.

     Symptoms of hypokalemia are non-specific, mainly related to muscle or heart function.

    Patients usually experience symptoms of weakness or fatigue.

    The physical examination results are usually within the reference range.

     Hypokalemia patients develop hypertension or indicate primary aldosteronism, renal artery stenosis, use licorice, or have rare hereditary hypertension syndromes (such as congenital adrenal hyperplasia, Liddle syndrome).

    Relative hypotension in patients with hypokalemia may indicate laxative and diuretic use, binge eating disorder, or rare inherited renal tubular diseases, such as Bartter syndrome or Gitelman syndrome.

     In most cases, the cause of hypokalemia can be determined through medical history and physical examination.

    The measurement of potassium concentration in urine is very important because it establishes the pathophysiological mechanism behind hypokalemia, which helps in differential diagnosis.

    In addition, the determination of serum magnesium is conducive to differential diagnosis and treatment, and can be used as a first-line detection program.

     An electrocardiogram can determine whether hypokalemia affects heart function or whether the patient is poisoned by digoxin.

    The electrocardiogram of patients with hypokalemia shows that the amplitude of U wave increases, which can reach more than 0.
    2mV, which exceeds the amplitude of T wave.
    The increase of U wave is most obvious in leads V2 to V4 (it is relatively specific for the diagnosis of hypokalemia); T wave is low or flat or inverted; ST segment depression is ≥0.
    05mV; QTU interval is prolonged; P wave is increased; arrhythmia: ventricular premature beats, ventricular tachycardia, ventricular fibrillation in severe cases.

     In patients with hypokalemia, the following tests can also be performed, but they should not be used as a first-line test, unless the disease is highly suspected: ➤ Screen urine and/or serum for diuretics, amphetamines or other drugs Sympathetic stimulants; ➤ Serum renin, aldosterone and cortisol levels; ➤24h urinary aldosterone, cortisol, sodium and potassium levels; ➤ pituitary imaging to evaluate Cushing syndrome; ➤ adrenal imaging to evaluate adenomas; ➤Assessment of renal artery stenosis; ➤Enzyme testing for 17-beta hydroxylase deficiency; ➤Tyroid function testing in patients with tachycardia (especially Asian patients); ➤Sera anion gap (such as testing toluene toxicity).

     Under normal circumstances, in patients who need potassium supplementation or sustained potassium loss (such as patients taking thiazide diuretics), oral potassium chloride treatment should be given.

    In these patients, maintenance therapy with potassium chloride is necessary.

    Under normal circumstances, potassium-sparing diuretics are only used for patients with normal renal function and prone to hypokalemia.

     ACEI can inhibit the excretion of potassium by the kidneys, thereby partially improving hypokalemia caused by thiazide diuretics or loop diuretics.

    However, it can also cause severe hyperkalemia in patients with renal insufficiency taking potassium supplements or potassium-sparing diuretics.

    Answer: A 04 For hyperkalemia, which of the following is the most accurate description? A.
    Compared with reduced renal potassium excretion, excessive intake of potassium is more likely to cause hyperkalemia.
    B.
    Drugs that cause hyperkalemia include angiotensin receptor blockers (ARB) and non-steroidal anti-inflammatory drugs (NSAID) C.
    All patients with suspected hyperkalemia should undergo renal tubular potassium concentration gradient (TTKG) measurement.
    D.
    Hemodialysis should be performed even in patients with hyperkalemia without abnormal electrocardiogram.
    Analysis: The decrease in potassium excretion is high The most common cause of potassiumemia.

    Excessive potassium intake and the transfer of potassium ions from intracellular to extracellular are also potential pathophysiological mechanisms of hyperkalemia.

     Many patients with hyperkalemia are asymptomatic.

    The symptoms of hyperkalemia are non-specific, mainly related to muscle or heart function.

    Weakness and fatigue are the most common symptoms of hyperkalemia patients, and sometimes patients may also experience obvious muscle paralysis or shortness of breath.

    Patients may also experience symptoms such as palpitations, chest pain, nausea, and vomiting.

    Asking the medical history helps to clarify the cause of hyperkalemia.

     The following drugs may damage the potassium excretion function of the kidneys: ➤potassium-sparing diuretics, especially for the treatment of liver cirrhosis and chronic heart failure; ➤NSAID; ➤ACEI; ➤combined application of spironolactone and ACEI; ➤ARB; ➤direct renin inhibition Drugs, such as Aliskiren; ➤ Calcineurin inhibitors, such as tacrolimus, cyclosporine; ➤ antibiotics; ➤ aminocaproic acid; ➤ oral contraceptives, such as drospirenone.

     In addition, the authenticity of elevated potassium levels should also be clarified.

    For patients who do not have a tendency to hyperkalemia, blood tests should be repeated before potassium-lowering treatment, except for related ECG changes.

    The electrocardiogram manifestations of hyperkalemia are mainly: ①High tip of T wave and disappearance of P wave; ②Prolonged PR interval; ③Enlarged QRS wave; ④Sine wave-like ECG changes; ⑤Bundle branch or branch block, sinus arrest, escape rhythm , Ventricular fibrillation.

     Kidney function testing is also very important.

    If the patient has renal failure, blood calcium levels should also be tested (hypocalcemia can aggravate arrhythmia).

    Patients can also be checked for electrocardiogram, urine potassium, sodium, osmotic pressure, complete blood count and metabolism.

     Although the TTKG measurement is still used to assess whether the reduction in renal potassium excretion can lead to hyperkalemia, some studies question its accuracy, and some experts also recommend abandoning the TTKG measurement.

     The treatment of hyperkalemia is related to the development speed of the disease.

    The faster the potassium level rises, the greater the cardiotoxicity, and the more aggressive treatment should be carried out.

    If the patient's potassium level is moderately elevated and there is no abnormality in the electrocardiogram, cation exchange resins or diuretics can be used to increase potassium excretion, and the excessive potassium source needs to be corrected.

    Hemodialysis is the ultimate treatment for kidney failure or insufficient medication.

    Patients with significantly elevated potassium levels should be treated with dialysis, and medication alone cannot reduce potassium levels in a timely and sufficient manner.

     Answer: B05 Regarding hypocalcemia and hypercalcemia, which of the following descriptions is the most accurate? A.
    The most common cause of hypocalcemia is hypoproteinemia.
    B.
    Most hypercalcemia is related to vitamin D.
    C.
    It is recommended that patients with mild hypocalcemia should be treated with intravenous calcium injection D.
    Loop diuretics are Analysis of contraindications in patients with hypercalcemia: Hypocalcemia means that when the serum protein concentration is normal, total serum calcium <8.
    8 mg/dl (<2.
    20 mmol/L) or serum ionized calcium concentration <4.
    7 mg/dl (<1.
    17) mmol/L).

    The range of serum calcium varies with age and gender.

    Hypocalcemia may be hereditary or acquired.

    Acquired factors include a variety of diseases, diet, drugs, and surgery.

     Hypoalbuminemia is the most common cause of hypocalcemia and can be caused by liver cirrhosis, kidney disease, malnutrition, burns, chronic diseases, and sepsis.

    In patients with hypoalbuminemia, the serum calcium concentration should be measured after correction for hypoalbuminemia.

     The manifestations of hypocalcemia are diverse and can be asymptomatic or life-threatening.

    Patients with hypocalcemia are often encountered in hospitalized patients.

    Depending on the cause, severe hypocalcemia that is unclear or improperly treated can lead to death.

    Most hypocalcemia is found through clinical suspicion and appropriate laboratory tests.

     The treatment of hypocalcemia depends on the cause, severity, symptoms, and speed of the development of hypocalcemia.

    Clinically, most cases of hypocalcemia are mild, requiring only supportive treatment and further laboratory evaluation.

    Mild patients can be treated with oral calcium.

    Severe hypocalcemia can lead to seizures, refractory hypotension or arrhythmia, etc.
    , which requires active treatment, including intravenous calcium infusion.

     The effect of hypocalcemia on myocardial action potential is to prolong phase 2 and phase 3 has no obvious effect.

    The ECG manifestations are: ST segment is flat and prolonged; QT interval is prolonged, T wave time is not prolonged; T wave is low or inverted in patients with severe hypocalcemia; U wave increases when combined with hypokalemia; low Calcemia can cause various premature beats, conduction block and other arrhythmias; hypocalcemia can increase the excitability of the vagus nerve and cause cardiac arrest.

    After the hypocalcemia is corrected, the electrocardiogram can return to normal.

     When too much calcium enters the extracellular fluid or the kidney's calcium excretion is insufficient, hypercalcemia may result.

    About 90% of hypercalcemia is caused by hyperparathyroidism or cancer, and the remaining 10% are caused by other conditions, including vitamin D-related problems, thiazide use, renal failure, and family diseases.

     The main manifestations of the electrocardiogram of hypercalcemia are: ① shortened QT interval; ②Osborn wave; ③increased ventricular excitability, ventricular fibrillation occurs; ④When severe hypercalcemia, QRS complex time and PR interval can be prolonged, and sometimes two Degree or complete atrioventricular block.

    The treatment of hypercalcemia includes: ➤ volume supplementation of isotonic sodium chloride solution; ➤ loop diuretic application; ➤ bisphosphonates application; ➤ denosumab; ➤ hemodialysis or peritoneal dialysis; ➤ parathyroid glands Surgical treatment of hyperfunction.

     Answer: A References: [1] Vecihi Batuman.
    Fast Five Quiz: Electrolyte Disorders.
    Medscape.
    March 23, 2021.
    [2] Lu Xilie, Ding Fang.
    Cardiovascular emergency treatment (11) Common electrocardiographic manifestations and treatment of electrolyte disorders ( Continued 10).
    Chinese Journal of Circulation, 2014, 29:664.
    [3] Five Electrolyte Disturbance ECGs: A Warning of Danger.
    Yimai Tongxin Internal Channel.
    2018-04-23.

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