Analyze the following clinical manifestations and determine whether they are characteristic of Anticholinergic or Cholinergic Toxicity.
Hypertension
Urinary Retention
Diaphoresis
Bronchoconstriction
Salivation
Hyperthermia
The Correct Answer is {"A":{"answers":"A"},"B":{"answers":"A"},"C":{"answers":"B"},"D":{"answers":"B"},"E":{"answers":"B"},"F":{"answers":"A"}}
- Hypertension: Seen in anticholinergic toxicity due to decreased parasympathetic tone and possible unopposed sympathetic stimulation. The body's inability to relax vascular tone may contribute to elevated blood pressure.
- Urinary Retention: A classic feature of anticholinergic toxicity. Inhibition of muscarinic receptors leads to impaired detrusor muscle contraction, making urination difficult or impossible.
- Hyperthermia: Results from inhibited sweating (anhidrosis), which is a hallmark of anticholinergic toxicity. Without the ability to cool through evaporation, body temperature rises dangerously.
- Diaphoresis: Excessive sweating is mediated by muscarinic receptor activation in cholinergic toxicity. It's often part of the SLUDGE symptoms seen in organophosphate poisoning or cholinesterase inhibitor overdose.
- Bronchoconstriction: Caused by overstimulation of muscarinic receptors in the airways, leading to narrowed bronchi and increased respiratory secretions — a dangerous feature of cholinergic excess.
- Salivation: Prominent in cholinergic toxicity due to unopposed parasympathetic activation. It may occur along with lacrimation, bradycardia, and other signs of excessive cholinergic stimulation.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is B
Explanation
A. Cardiotoxicity: While NSAIDs can contribute to cardiovascular risks such as hypertension and fluid retention, nephrotoxicity is the more direct explanation for the elevated kidney function tests and potassium level. Cardiotoxicity typically presents with symptoms like heart failure or arrhythmias rather than kidney-related lab abnormalities.
B. Nephrotoxicity: NSAIDs inhibit prostaglandin synthesis, which plays a key role in maintaining renal blood flow, especially in older adults or those with preexisting renal impairment. Chronic NSAID use can reduce glomerular filtration, leading to elevated creatinine, hyperkalemia, and worsening blood pressure control, all of which are evident in this patient.
C. Neurotoxicity: Neurotoxic effects are not commonly associated with NSAID use. Symptoms of neurotoxicity include confusion or seizures, which are not relevant to the clinical findings in this scenario.
D. Hepatotoxicity: NSAID-induced liver injury is rare and would typically present with elevated liver enzymes (AST, ALT), not elevated creatinine or potassium. The current lab findings and blood pressure changes are more consistent with kidney involvement.
Correct Answer is D
Explanation
A. Dry Cough: A dry cough is not typically associated with salicylate toxicity. It is more commonly seen in conditions like ACE inhibitor use, respiratory infections, or asthma, and does not help distinguish salicylate overdose.
B. Xanthopsia (Yellow Vision): This visual disturbance is more classically linked to digoxin toxicity, not salicylates. Patients experiencing digoxin toxicity may report seeing halos or yellow-tinted vision, but this is not seen with aspirin overdose.
C. Moon Facies: This refers to a rounded facial appearance typically caused by chronic corticosteroid use and is a hallmark of Cushingoid features, not salicylate toxicity.
D. Tinnitus: Ringing in the ears (tinnitus) is a classic early symptom of salicylate toxicity. It often precedes more serious effects like metabolic acidosis, hyperventilation, confusion, and even seizures. It serves as an important clinical clue when assessing patients with possible aspirin overdose.
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