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A Glasgow Coma Scale motor score of 5 indicates localized movement to pain, not an inability to move extremities. The client can move purposefully, ruling out complete paralysis. The total GCS score of 13 suggests mild impairment, not severe motor deficits, making this conclusion incorrect.

A verbal score of 5 on the Glasgow Coma Scale indicates oriented speech, meaning the client can vocalize and respond appropriately. This contradicts the conclusion of being unable to make vocal sounds, as the score reflects intact verbal ability, not mutism or severe impairment.

An eye-opening score of 3 indicates the client opens eyes to speech, not specifically when spoken to, as this could include spontaneous opening to sound. The conclusion is imprecise, and the total GCS score of 13 suggests mild impairment, not specific to this action.

Brudzinski’s sign involves involuntary flexion of the hips and knees when the neck is flexed, indicating meningeal irritation in meningitis. It differs from Kernig’s sign, as it is elicited by neck movement rather than leg extension. While both signs suggest meningitis, Brudzinski’s sign is not observed in the described leg extension scenario.

Nuchal rigidity refers to neck stiffness, a common meningitis symptom, where the client resists neck flexion due to meningeal inflammation. Unlike Kernig’s sign, it is not associated with leg movement. It reflects irritation of the meninges but is not the specific condition observed during the leg extension test described in the scenario.

Bradykinesia, characterized by slow movement, is typically associated with neurological disorders like Parkinson’s disease, not meningitis. It involves impaired motor control due to basal ganglia dysfunction, unrelated to meningeal inflammation or leg extension pain. Therefore, it does not correspond to the clinical presentation described in the meningitis assessment scenario.

Providing fluid hydration is not the primary purpose of an osmotic diuretic in this context. Osmotic diuretics, like mannitol, draw fluid from tissues into the bloodstream, reducing intracranial pressure by decreasing brain edema. Hydration may occur as a secondary effect, but it is not the goal in treating increased intracranial pressure.

Increasing cell size in the brain is not the purpose of osmotic diuretics. These medications reduce brain cell swelling by drawing water out of cells into the vascular compartment. Enlarging brain cells would exacerbate intracranial pressure, counteracting the therapeutic goal of managing cerebral edema in this condition.

Expanding extracellular fluid volume is not the primary goal of osmotic diuretics in this context. While they increase blood volume temporarily by drawing fluid from tissues, the aim is to reduce brain edema and intracranial pressure, not to expand extracellular fluid, which could worsen pressure dynamics in the brain.

Discontinuing intravenous access is inappropriate for a STEMI client, as IV access is critical for administering medications like anticoagulants, antiplatelets, and thrombolytics, or for emergency interventions. Maintaining IV access supports rapid treatment to restore coronary blood flow, which is essential in managing acute myocardial infarction effectively.

A non-contrast CT scan is not typically indicated for STEMI management. STEMI is diagnosed via EKG and requires urgent revascularization, often through cardiac catheterization. CT scans may be used for other conditions, like stroke, but they do not address the urgent need to restore coronary artery perfusion in STEMI.

Holding anticoagulant therapies is contraindicated in STEMI, as these medications (e.g., heparin) prevent further clot formation and stabilize the existing thrombus. Anticoagulants are critical in conjunction with revascularization procedures like cardiac catheterization to improve blood flow and reduce myocardial damage in acute infarction.

Placing the client with the head reclined back is unsafe for dysphagia, as it increases aspiration risk by allowing food or liquid to enter the airway. Proper positioning involves an upright posture (90 degrees) to facilitate safe swallowing by aligning the esophagus and reducing the chance of aspiration.

Encouraging brief exercise before meals may promote appetite but is not directly related to feeding safety in dysphagia. The priority is preventing aspiration and ensuring safe swallowing, which involves techniques like upright positioning and small bites, rather than focusing on appetite stimulation in this context.

Placing food on the affected side of the mouth is incorrect for dysphagia management. Food should be placed on the unaffected side to leverage stronger muscle control for swallowing. The affected side may have impaired sensation or motor function, increasing aspiration risk if food is placed there.

Administering a nitrate antihypertensive is not the first action for autonomic dysreflexia. While it may help manage hypertension, the priority is identifying and removing the triggering stimulus, such as bladder distention, which causes the autonomic response. Addressing the cause prevents further escalation of the life-threatening hypertensive crisis.

Obtaining the client’s heart rate provides additional data but is not the priority. Autonomic dysreflexia is characterized by severe hypertension due to a noxious stimulus below the spinal injury level. Checking for triggers like bladder distention is critical first to eliminate the cause and stabilize blood pressure.

Placing the client in a high-Fowler’s position may help manage hypertension by reducing preload, but it is not the first action. Autonomic dysreflexia requires identifying and removing the trigger, such as bladder distention, to prevent ongoing sympathetic overactivity, which drives the hypertensive crisis in spinal cord injury clients.

Cardiac enzymes, such as troponin, do not diagnose pulmonary congestion, which is assessed via imaging or clinical signs like crackles. These enzymes (troponin, CK-MB) are released from damaged myocardial cells during an MI, indicating heart tissue injury rather than lung-related conditions like congestion.

Cardiac enzymes do not assess heart structure or valve mobility, which are evaluated using imaging techniques like echocardiography. Enzymes like troponin and CK-MB are specific to myocardial damage, rising in the blood post-MI to indicate the extent of heart tissue injury, not structural details.

Cardiac enzymes do not pinpoint the exact location of an MI. Localization is achieved through EKG changes or imaging like cardiac catheterization. Enzymes indicate the presence and extent of myocardial damage but lack specificity for identifying which coronary artery or heart region is affected.

Wearing sunglasses is not an appropriate intervention for homonymous hemianopia, a visual field defect from stroke affecting the same side of both eyes. Sunglasses may reduce glare but do not address the loss of left visual field or help compensate for the neurological deficit.

Scanning from left to right is incorrect for left homonymous hemianopia. This would prioritize the intact right visual field, neglecting the affected left side. Clients need to scan toward the affected side (right to left) to compensate for the visual loss and ensure awareness of their environment.

Applying eye ointment is irrelevant for homonymous hemianopia, which results from brain damage (e.g., occipital lobe stroke) rather than ocular issues. Ointment may treat dry eyes or infections but does not address the neurological visual field defect caused by disrupted visual pathways.