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Topical analgesics relieve pain but do not address psoriasis’s underlying inflammation or scaling. Psoriasis involves immune-mediated epidermal hyperproliferation, causing scaly, burning plaques. Analgesics may reduce discomfort temporarily but fail to target the inflammatory process driven by T-cell activation, making this choice ineffective for managing psoriasis symptoms.

Colloidal oatmeal-based lotion soothes irritated skin but is insufficient for psoriasis, which requires anti-inflammatory treatment. Oatmeal reduces itching in conditions like eczema but does not address psoriasis’s silvery scales or immune-driven inflammation, making it an inadequate choice for controlling the client’s burning, bleeding plaques.

Topical antifungals treat fungal infections, not psoriasis, which is an autoimmune condition with no fungal etiology. The silvery, scaly plaques result from rapid keratinocyte turnover, not fungal growth, so antifungals are irrelevant, failing to reduce inflammation or scaling in this chronic inflammatory dermatologic condition.

Rinsing the mouth after ipratropium use is unnecessary, as this anticholinergic bronchodilator does not cause oral candidiasis like corticosteroids. However, it is not harmful and does not indicate misunderstanding of critical administration technique. This action is less concerning than incorrect priming, which affects drug delivery.

Attaching a spacer to the ipratropium inhaler is appropriate, as it improves drug delivery to the lungs by reducing oropharyngeal deposition. This enhances bronchodilation in COPD by ensuring more medication reaches the airways, indicating correct understanding and requiring no additional teaching.

Storing ipratropium at room temperature is correct, as extreme heat or cold can degrade the canister’s propellant, impairing drug delivery. This action shows understanding of proper storage to maintain the inhaler’s efficacy, requiring no further teaching for effective COPD treatment.

Assessing body temperature monitors for infection but is not specific to vancomycin administration. Clostridium difficile causes fever, but oral vancomycin’s safety depends on renal function, as it is minimally absorbed but can accumulate in renal impairment, making temperature less critical before the first dose.

Measuring oxygen saturation assesses respiratory status, irrelevant to oral vancomycin for Clostridium difficile, which primarily affects the gut. While severe infections may cause systemic symptoms, oxygenation is not a direct concern for vancomycin’s safety or efficacy, making this choice inappropriate.

Auscultating bowel sounds evaluates gastrointestinal motility, relevant to Clostridium difficile’s diarrheal effects but not vancomycin’s administration safety. Oral vancomycin targets gut bacteria, and bowel sounds do not indicate renal or systemic risks, making this less critical than renal function assessment.

C-reactive protein indicates systemic inflammation but is non-specific for wound infections. Purulent drainage requires pathogen identification via culture to guide therapy. While elevated CRP may support infection suspicion, it does not direct antibiotic choice, making it less critical than culture results.

Serum blood glucose is relevant for wound healing, as hyperglycemia impairs immune response, but it does not identify the infection’s cause. Purulent drainage requires microbiological data from culture to select antibiotics, making glucose levels secondary for immediate infection management.

Blood pH level assesses acid-base balance, irrelevant to localized wound infection. Purulent drainage indicates bacterial infection, requiring culture to identify pathogens. pH may be altered in systemic sepsis, but culture is the priority for guiding therapy in postoperative wound infections.

Orienting to a color-coding system is impractical, as Huntington’s cognitive impairments, like executive dysfunction, hinder processing complex visual cues. This approach overwhelms the client, increasing confusion, and is less effective than physical escorting to ensure safe and direct cafeteria navigation.

Using a hospital map relies on spatial reasoning, which is impaired in Huntington’s due to basal ganglia degeneration. The client’s cognitive and motor deficits make map-based navigation challenging, increasing disorientation risk, making this less effective than escorting for cafeteria access.

Step-by-step verbal directions require intact memory and processing, compromised in Huntington’s due to cortical and striatal atrophy. Verbal instructions may confuse the client, leading to navigation errors, making physical escorting a more reliable method to ensure safe cafeteria arrival.

Unexplained weight loss is not directly relevant to pyridostigmine administration. Myasthenia gravis affects neuromuscular junctions, and pyridostigmine enhances acetylcholine, improving muscle strength. Weight loss may indicate systemic issues, but it does not affect the drug’s immediate safety or efficacy, making this choice secondary.

Trouble sleeping is unrelated to pyridostigmine’s administration. The drug targets acetylcholinesterase, increasing muscle strength in myasthenia gravis, but does not typically affect sleep. Insomnia may reflect other conditions, but it is not a critical pre-administration concern compared to cholinergic side effects.

Recent oral intake is relevant for gastrointestinal side effects, as pyridostigmine may cause nausea, but it is less critical than urinary issues. Taking the drug with food can mitigate nausea, but urinary retention poses a greater immediate risk, making this choice secondary.

Administering an antiemetic addresses vomiting but is not the first priority. Confusion and projectile vomiting in MS suggest increased intracranial pressure or brain injury post-fall, requiring neurological assessment to identify life-threatening conditions like hematoma, which takes precedence over symptom management.

Determining the last corticosteroid dose is relevant for MS management but not urgent. Confusion and vomiting suggest acute neurological injury, requiring immediate assessment. Steroid history may guide long-term care but is secondary to evaluating current neurological status post-fall.

Determining the neurological baseline is useful but not the first action. Acute confusion and vomiting require immediate assessment to detect changes like brain injury. Baseline data provide context but delay critical evaluation of current neurological status, making this choice less urgent.
 

Temporary use until pressure stabilizes is incorrect, as open-angle glaucoma is a chronic condition requiring ongoing intraocular pressure control. Eye drops, like beta-blockers, reduce aqueous humor production, but stopping them risks pressure spikes, leading to optic nerve damage and vision loss.

Using drops only during symptomatic episodes is incorrect, as glaucoma is often asymptomatic until advanced. Consistent eye drop use prevents pressure buildup, protecting the optic nerve. Symptomatic treatment fails to address chronic pressure elevation, risking progressive vision loss.

Discontinuing drops once vision improves is incorrect, as vision improvement is not expected in glaucoma. Eye drops maintain intraocular pressure to slow disease progression, not reverse damage. Stopping treatment allows pressure to rise, accelerating optic nerve damage and vision loss.

Hyperventilation rapidly eliminates carbon dioxide, causing respiratory alkalosis, not acidosis. In respiratory acidosis, hypoventilation retains CO2, increasing blood carbonic acid, lowering pH. This contradicts the client’s condition, as rapid CO2 loss would raise, not lower, blood pH.

Blood oxygen levels stimulating respiration may occur in hypoxia but do not directly cause respiratory acidosis. Low oxygen can coexist with CO2 retention, but acidosis results from high CO2, not oxygen-driven respiratory changes, making this choice irrelevant to the pathophysiology.

Carbon dioxide conversion in kidneys occurs during bicarbonate buffering, a compensatory mechanism, not the primary cause of respiratory acidosis. Acidosis results from pulmonary CO2 retention, not renal processes, which are secondary and slower, making this choice incorrect for the acute condition.

Using tiotropium for sudden shortness of breath is incorrect, as it is not a rescue inhaler. Tiotropium provides sustained bronchodilation over 24 hours, not rapid relief. Short-acting beta-agonists like albuterol are used for acute symptoms, indicating a need for further teaching.

Using another inhaler between tiotropium doses suggests misunderstanding, as tiotropium is a once-daily maintenance therapy. Additional inhalers may be prescribed, but this statement implies incorrect timing or overuse, which could lead to improper COPD management, requiring clarification.

Expecting thinner sputum is incorrect, as tiotropium does not affect mucus viscosity. It dilates airways, not liquefying secretions, which is the role of mucolytics. This misunderstanding indicates a need for teaching about tiotropium’s bronchodilatory, not mucolytic, effects in COPD.