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Aphasia, difficulty with language comprehension or production, typically results from left cerebral hemisphere strokes affecting Broca’s or Wernicke’s areas, where language-processing neural networks reside. Right hemisphere strokes impair non-verbal functions, such as spatial awareness and perception, due to disruption of parietal and occipital lobe circuits, making aphasia an unlikely manifestation in this case.

Right-sided weakness is associated with left hemisphere strokes, as the brain’s motor cortex controls the contralateral body via the corticospinal tract. A right cerebral hemisphere stroke disrupts the right motor cortex, leading to left-sided motor deficits, not right-sided weakness, which is inconsistent with the client’s neurological presentation.

Left-sided weakness is common in right hemisphere strokes, as the right motor cortex governs the left body through crossed neural pathways. While this is a relevant motor deficit, the question focuses on a hallmark right hemisphere function, and visual spatial deficits are more specific to its role in spatial processing.

Some sedatives, like benzodiazepines, may cause minor blood pressure fluctuations, but this is not the primary concern in dementia patients. These medications primarily increase fall risk by inducing sedation and impairing coordination through GABA receptor modulation, making blood pressure elevation a less critical issue in this context.

Addiction is a potential risk with sedatives like benzodiazepines due to their effects on the brain’s reward system, but it is not the primary concern in dementia patients. The immediate risk of falls and confusion from sedation outweighs addiction, which is less relevant given the focus on safety in this vulnerable group.

Excessive sleepiness is a side effect of sedatives, resulting from enhanced GABA activity that depresses central nervous system function. However, in dementia patients, the primary concern is fall risk due to sedation and impaired coordination, as falls pose a greater threat of injury than excessive sleepiness in this context.

Aphasia, characterized by impaired language comprehension or expression, typically results from left hemisphere strokes affecting language centers like Broca’s or Wernicke’s areas. Right hemisphere strokes disrupt spatial and non-verbal processing, such as visuospatial skills, due to parietal lobe involvement, making aphasia an unlikely expectation in this client.

Right-sided weakness occurs with left hemisphere strokes, as the left motor cortex controls the right body via contralateral corticospinal tract pathways. A right hemisphere stroke affects the left side of the body, so expecting right-sided weakness is incorrect for a client with right-sided brain damage.

Left-sided weakness is a common outcome of right hemisphere strokes, as the right motor cortex controls left-sided motor function through crossed neural pathways. While relevant, the question emphasizes a hallmark right hemisphere deficit, with visual spatial deficits being more specific to its spatial processing functions.

Sitting at a 30° angle is insufficient for dysphagia management post-stroke, as it does not ensure safe swallowing. A 90° upright position minimizes aspiration risk by aligning the esophagus for gravity-assisted swallowing, making this statement incorrect and indicating ineffective teaching.

Placing food on the weaker side of the mouth is incorrect, as stroke-related dysphagia often involves weakened pharyngeal muscles on the affected side, increasing aspiration risk. Food should be placed on the stronger side to facilitate safer swallowing, showing the partner’s understanding is flawed.

Coughing while swallowing is dangerous, as it disrupts the coordinated swallowing process and increases aspiration risk in dysphagia. Stroke patients with impaired pharyngeal control need techniques to prevent choking, so this statement reflects a misunderstanding of safe swallowing practices.

Examining for skin breakdown is relevant for spinal cord injury care, as pressure ulcers are a risk. However, autonomic dysreflexia is triggered by noxious stimuli like bladder distention, causing sympathetic overactivity. Addressing the acute trigger is critical, making skin checks a lower priority in this emergency.

Checking for fecal impaction is relevant, as it can trigger autonomic dysreflexia by stimulating visceral reflexes. However, bladder distention is more common and urgent, as it rapidly activates sympathetic overdrive, leading to severe hypertension. Fecal impaction is a secondary consideration after addressing bladder issues.

No option is provided, so no specific action can be evaluated. In autonomic dysreflexia, the priority is identifying and removing the trigger, typically bladder distention, to halt the sympathetic surge. Without a viable option, this cannot be considered a correct or relevant response.

The Mantoux test detects TB exposure, not active infection status, and remains positive post-treatment due to immune memory. Treatment duration is based on bacterial eradication, not test results, so linking medication to a negative Mantoux test is incorrect and misleads the client.

Family members may need screening or prophylaxis if exposed, but routine preventive medication for all is not standard unless latent TB is confirmed. Active TB treatment focuses on the infected client, and blanket family treatment is unnecessary without evidence of infection.

Lifelong TB medication is incorrect, as 6 to 9 months of treatment typically cures active TB. Lifelong therapy is not required unless drug-resistant strains or relapse occur. This misinformation could discourage adherence due to perceived indefinite treatment duration.

DIC is characterized by decreased platelet counts due to widespread clotting consuming platelets and clotting factors. Elevated platelets are not associated with DIC, which involves a consumptive coagulopathy triggered by systemic inflammation, making this statement incorrect and misleading.

DIC is not controlled with lifelong heparin, as it is an acute condition treated with addressing the underlying cause (e.g., sepsis) and supportive measures. Heparin may be used cautiously in some cases, but lifelong use is inappropriate, making this statement incorrect.

DIC is not a genetic disorder or caused by vitamin K deficiency; it is an acquired condition secondary to triggers like sepsis or trauma. Vitamin K deficiency affects clotting factor synthesis, not DIC’s consumptive coagulopathy, making this statement inaccurate.