A. Initiate isolation precautions — This is the first action the nurse should take. Bacterial meningitis is highly contagious (often spread via droplet transmission), and immediate isolation (droplet precautions) helps prevent spread to others.
B. Administer antibiotics after collecting cultures — This is a critical next step, but only after the client is placed in isolation to protect others.
C. Prepare for a lumbar puncture after ruling out increased ICP — While a lumbar puncture is important for diagnosis, increased ICP must be ruled out first, and this is not the immediate first action.
D. Start IV fluids — Supportive care is important, but it is not the priority over infection control measures.

A. Ischemia and neuronal death – Cerebral perfusion pressure (CPP) is the pressure needed to ensure adequate blood flow to the brain. If CPP drops too low, the brain doesn't receive enough oxygen and glucose, leading to ischemia and eventually neuronal death.
B. Improved cognitive function – Low CPP results in decreased oxygen and nutrient delivery, which impairs cognitive and neurological function.
C. Increased blood flow to the brain – Low CPP means reduced blood flow, not increased.
D. Undetectable intracranial glucose levels – While glucose delivery may decrease, levels are not necessarily undetectable and this is not the primary concern with low CPP.

A. Administer antibiotics only if the client has a high fever on two separate occasions – Waiting for multiple fevers delays critical treatment and is not evidence-based.
B. Start antibiotics immediately, even before confirmation of diagnosis – In suspected bacterial meningitis, early administration of broad-spectrum antibiotics is life-saving. Delaying treatment until confirmation can lead to rapid deterioration due to the severity and speed of disease progression.
C. Wait for confirmation of diagnosis before starting antibiotics – Delaying antibiotic treatment while waiting for lab confirmation (e.g., lumbar puncture) puts the patient at risk of worsening illness and complications.
D. Avoid antibiotics altogether as they are not effective against bacterial meningitis – Antibiotics are the mainstay of treatment for bacterial meningitis and significantly reduce mortality and morbidity.

A. Rejuvenation –. This is not a physiological term used in the context of ICP or brain compensation.
B. Autoregulation –This is the brain’s ability to maintain consistent cerebral blood flow (CBF) despite changes in systemic blood pressure. In early stages of increased ICP, autoregulation helps maintain oxygen and nutrient delivery to brain tissue by adjusting cerebral vessel diameter.
C. Percolation –This term is not relevant in neurophysiology or ICP management.
D. Demarcation –This refers more to distinguishing boundaries between tissues (e.g., in gangrene), not compensatory mechanisms for ICP.

A. Move the person immediately to a more comfortable location – Moving a person with a suspected brain or spinal injury can worsen the injury, especially if there’s a cervical spine injury.
B. Administer pain medication to alleviate discomfort –Pain meds should only be given under medical supervision after evaluation, as they can mask symptoms or interfere with assessment.
C. Keep the person still and call for medical assistance –. Immobilization is critical to prevent worsening of a possible spinal or brain injury. Emergency medical services should evaluate and transport the person safely.
D. Perform head rotations to test range of motion –This can cause serious or irreversible damage if a cervical spine injury is present.

A. According to the Monroe-Kellie doctrine, the skull is a closed compartment, and the total volume of brain tissue, blood, and cerebrospinal fluid (CSF) must remain constant. If one component increases, the others must decrease to maintain normal intracranial pressure (ICP).
B. Even small changes in volume can affect ICP and brain function if compensation mechanisms are exceeded.
C. The skull is rigid and does not expand, so any volume increase without compensation leads to increased ICP.
D. The components are interrelated and changes in one directly affect the others due to the closed nature of the intracranial space.

A. Hydrocephalus is not a normal variation — it is a neurological disorder that requires medical attention.
B. Hydrocephalus is caused by an increase, not a decrease, in cerebrospinal fluid (CSF) in the brain's ventricles.
C. While inflammation (like meningitis) can lead to hydrocephalus, the condition itself is not defined by brain tissue inflammation.
D. Hydrocephalus is characterized by an abnormal buildup of CSF in the brain’s ventricles, leading to ventricular enlargement and increased intracranial pressure. This can be due to obstruction, poor absorption, or overproduction of CSF.

A. It enlarges the heart chambers – This is typically seen with volume overload, not pressure overload. Volume overload leads to chamber dilation, not wall thickening.
B. It strengthens heart valves – Afterload does not improve valve function; in fact, high afterload can worsen conditions like aortic stenosis over time.
C. It thickens heart walls – The heart compensates for increased afterload (e.g., from chronic hypertension or aortic stenosis) by hypertrophying (thickening) the ventricular walls. This is called concentric hypertrophy, a structural adaptation to increased pressure.
D. It thins the heart walls – Thinning occurs in conditions like dilated cardiomyopathy where the problem is decreased contractility and volume overload, not increased afterload.

A. Increased systemic blood pressure – While systemic vasoconstriction may occur to maintain perfusion, it is a result of compensatory mechanisms like RAAS, not a primary mechanism leading to fluid retention and edema.

B. Renin-angiotensin-aldosterone activation – RAAS leads to:

Sodium and water retention via aldosterone

Vasoconstriction via angiotensin II

These changes increase intravascular volume, contributing to fluid overload and edema.

C. Ventricular hypertrophy – This is a structural adaptation to increased workload (pressure overload), not directly responsible for fluid retention.

D. Ventricular dilation – Dilation occurs as a result of chronic volume overload, not as a compensatory mechanism causing fluid retention.

A. Hyperthermia, increased thirst, and polyuria are not related to Cushing's Triad; these symptoms suggest other conditions such as diabetes insipidus.
B. Confusion, blurred vision, and dizziness are nonspecific symptoms and do not define Cushing’s Triad.
C. Cushing's Triad is a classic neurologic emergency that indicates increased intracranial pressure. It is characterized by the triad of bradycardia (slow heart rate), decreased or irregular respirations, and hypertension (high blood pressure). This response is the body’s attempt to maintain cerebral perfusion in the face of rising intracranial pressure.
D. Tachycardia, shallow respirations, and hypotension are not consistent with Cushing’s Triad.