A client presents with magnesium toxicity, what antidote should the nurse prepare?
Calcium gluconate
Sodium bicarbonate
Naloxone
Potassium chloride
The Correct Answer is A
Magnesium toxicity occurs when serum levels exceed the therapeutic range (4-7 mEq/L), leading to neuromuscular blockade and respiratory depression. The excess magnesium antagonizes calcium at the presynaptic nerve terminals, inhibiting acetylcholine release. Immediate reversal is required to restore deep tendon reflexes and prevent cardiac arrest.
A. Calcium gluconate: Calcium serves as a direct physiological antagonist to magnesium at the neuromuscular junction. Intravenous administration of 10% calcium gluconate rapidly displaces magnesium, reversing respiratory depression and cardiac dysrhythmias. It is the mandatory first-line antidote for magnesium-induced toxicity.
B. Sodium bicarbonate: This alkalizing agent is primarily used to treat metabolic acidosis or specific tricyclic antidepressant overdoses. It does not possess antagonistic properties against magnesium ions. Using it for magnesium toxicity would not address the underlying respiratory failure or muscular paralysis.
C. Naloxone: Naloxone is a competitive opioid antagonist used to reverse central nervous system depression caused by narcotics like morphine or fentanyl. It has no effect on magnesium-induced CNS depression. It targets mu-opioid receptors, which are not involved in the pathophysiology of hypermagnesemia.
D. Potassium chloride: Administering potassium is used to treat hypokalemia but is not indicated for magnesium overdose. In fact, magnesium and potassium levels are often linked, and hyperkalemia could potentially worsen cardiac instability. It provides no antidotal benefit for reversing magnesium's toxic effects.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
Phenylketonuria (PKU) is an autosomal recessive disorder caused by a deficiency of the hepatic enzyme phenylalanine hydroxylase. This leads to the toxic accumulation of the amino acid phenylalanine, which causes irreversible neurological damage and intellectual disability. Screening occurs via a neonatal heel stick shortly after birth.
A. Fluid restriction: There is no physiological basis for limiting fluid intake in infants with PKU. Adequate hydration is necessary for metabolic stability and renal function. Treatment focuses on the chemical composition of the intake rather than the total volume of fluid consumed.
B. Iron supplementation: While maintaining general nutrition is important, iron does not affect the metabolic pathway of phenylalanine. PKU management is specifically concerned with amino acid metabolism rather than hematological parameters. Iron status is managed independently of a PKU diagnosis.
C. High-protein diet: Standard high-protein foods like meat, dairy, and eggs are extremely high in phenylalanine and are strictly forbidden. Consumption of these foods would lead to a rapid rise in neurotoxic levels of the amino acid. A high-protein diet is contraindicated for these patients.
D. Phenylalanine-restricted diet: The mainstay of therapy is a life-long diet that limits phenylalanine while providing enough tyrosine and other essential nutrients. This involves special medical formulas and low-protein foods to maintain blood levels within the therapeutic range. This prevents cognitive impairment.
Correct Answer is B
Explanation
Alcohol is a known teratogenic agent that readily crosses the placental barrier, leading to a spectrum of developmental disorders. It disrupts cellular proliferation and migration within the developing fetal brain and organs. No amount of consumption has been proven safe during any stage of human gestation.
A. Only first trimester matters: While organogenesis is a high-risk period, alcohol exposure in the second and third trimesters causes significant neurodevelopmental impairment. Brain growth and synaptogenesis continue throughout the entire pregnancy. Risk is present from conception to delivery, making this statement medically inaccurate.
B. No alcohol is recommended: Complete abstinence is the only certain way to prevent fetal alcohol syndrome and associated cognitive deficits. There is no established threshold below which alcohol is guaranteed to be harmless to the fetus. This is the standard medical advice provided by all major health organizations.
C. Only small amounts are safe: Research has failed to define a safe minimum dose, as metabolic rates vary significantly between individuals. Even low levels of exposure are associated with behavioral problems and growth restriction. Recommending any amount poses an unacceptable risk to fetal health and development.
D. Limit to weekends: Binge drinking, often associated with weekend consumption, causes high peak blood alcohol levels that are particularly damaging to the fetal central nervous system. Frequency of use is less relevant than the fact that any exposure is potentially toxic. Total avoidance is the necessary clinical recommendation.
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