A client is admitted to the emergency department (ED) with symptoms of arm numbness, chest pain, and nausea/vomiting. The examining healthcare provider (HCP) believes that the client has experienced an acute myocardial infarction (AMI) within the past three hours, and would like to initiate tissue plasminogen activator (tPA) therapy. Which client history findings contraindicate the use of tPA?

Choice A reason: Sodium bicarbonate levels affect acid-base balance, not cystic fibrosis (CF) secretions. CF results from defective sodium and chloride transport, causing thick mucus that impairs gas exchange. This choice is incorrect, as bicarbonate does not drive the respiratory issues or secretion buildup in CF pathophysiology.

Choice B reason: Excess potassium chloride is unrelated to cystic fibrosis. CF involves a CFTR gene mutation, disrupting sodium and chloride transport, leading to thick secretions. Potassium chloride does not cause mucus buildup or respiratory issues, making this an incorrect explanation for the child’s symptoms in CF.

Choice C reason: Increased sodium chloride content in sweat is a CF diagnostic marker, but it does not directly cause insufficient oxygen supply. Thick secretions from faulty ion transport obstruct airways, impairing gas exchange. This choice misrepresents the link between sodium chloride and CF’s respiratory pathophysiology.

Choice D reason: Cystic fibrosis results from a CFTR gene mutation, impairing sodium and chloride transport across cell membranes. This causes dehydrated, thick, sticky secretions that obstruct airways, leading to respiratory issues. This explanation accurately describes CF’s pathophysiological process, addressing the parents’ concerns about secretions and breathing difficulties.

Choice A reason: Tissue ischemia from vasospasm is associated with conditions like stroke, not multiple sclerosis (MS). MS involves immune-mediated demyelination of the central nervous system, causing exacerbations. Ischemia does not drive MS exacerbations, making this incorrect, as scarring of the myelin sheath is the hallmark pathological change.

Choice B reason: Destruction of norepinephrine receptors is unrelated to multiple sclerosis. MS exacerbations result from immune attacks on myelin, leading to scarred plaques that disrupt nerve conduction. Norepinephrine receptor issues may affect autonomic functions, but they are not part of MS’s pathophysiology, making this an incorrect choice.

Choice C reason: Multiple sclerosis exacerbations result from immune-mediated destruction and scarring (sclerosis) of the myelin sheath, forming plaques that impair nerve signal transmission. This causes neurological symptoms like weakness or sensory loss. Progressive demyelination and scarring are the core pathologic changes, aligning with MS’s clinical and histopathological features.

Choice D reason: Over-secretion of excitatory neurotransmitters may occur in epilepsy or neurotoxicity, not multiple sclerosis. MS exacerbations stem from myelin sheath scarring, disrupting nerve conduction, not neurotransmitter imbalances. This choice is incorrect, as it does not reflect the immune-driven demyelination central to MS’s pathological process.