PATHO WLO Answers

PAIN - What are nociceptors, where are they found, and what activates them?

Free nerve endings found in most tissues. Mechanical injury, extreme temperature, and irritating chemicals activate them; brain tissue itself lacks nociceptors.

PAIN - What are the four steps of nociception?

Transduction converts injury into an impulse; transmission carries it to the brain; perception recognizes pain; modulation increases or decreases the signal.

PAIN - How do A-delta and C fibers differ?

A-delta fibers carry fast, sharp, localized pain. C fibers carry slow, dull, burning, or poorly localized pain.

PAIN - What is the gate-control theory?

Touch input can activate inhibitory spinal neurons that reduce pain transmission. This explains why rubbing an injured area can decrease pain.

PAIN - What three systems shape pain perception?

Sensory-discriminative identifies location and intensity; affective-motivational creates the emotional response; cognitive-evaluative uses thoughts, culture, and past experience.

PAIN - How do endorphins decrease pain?

They bind opioid receptors and inhibit release or transmission of pain signals in the brain and spinal cord.

PAIN - How do acute and chronic pain differ?

Acute pain begins suddenly and often raises heart rate or blood pressure. Chronic pain lasts beyond expected healing and may occur with normal vital signs.

PAIN - How do somatic, visceral, and referred pain differ?

Somatic pain comes from skin, muscle, bone, or joints and is more localized. Visceral pain is diffuse and comes from organs. Referred pain is felt away from the source.

PAIN - How do neuropathic, peripheral, central, and radicular pain differ?

Neuropathic pain results from nerve dysfunction. Peripheral pain follows a damaged peripheral nerve; central pain follows brain or cord injury; radicular pain follows an irritated nerve root.

PAIN - What are allodynia, hyperalgesia, and analgesia?

Allodynia is pain from a normally painless stimulus. Hyperalgesia is an excessive response to pain. Analgesia is absence of pain from a normally painful stimulus.

PAIN - How is pain assessed and treated?

Use OLDCARTS plus a pain scale. Main treatments are nonpharmacologic measures, acetaminophen or NSAIDs, and condition-specific drugs such as opioids or neuropathic-pain agents.

TEMPERATURE - How does the body normally regulate temperature?

The hypothalamus compares core temperature with its set point and activates heat production, conservation, or heat loss.

TEMPERATURE - How does the body produce, conserve, and lose heat?

Metabolism and shivering produce heat; vasoconstriction conserves it. Radiation, conduction, convection, and evaporation remove heat.

TEMPERATURE - What causes fever?

Pyrogens increase hypothalamic prostaglandin E2, raising the temperature set point. The body shivers until it reaches the new set point.

TEMPERATURE - How are fever and hyperthermia different?

Fever is a regulated rise in the hypothalamic set point. Hyperthermia is an unregulated temperature rise without a set-point change.

TEMPERATURE - How do heat cramps, heat exhaustion, and heatstroke differ?

Cramps cause painful spasms after salt and water loss. Exhaustion causes heavy sweating and weakness. Heatstroke causes temperature above 40 C (104 F) with altered mental status.

TEMPERATURE - What is malignant hyperthermia and its priority treatment?

An inherited hypermetabolic reaction to certain anesthetics or succinylcholine causes rising CO2, rigidity, and rapid fever. Stop the trigger and give dantrolene.

TEMPERATURE - What is hypothermia and what findings matter most?

Core temperature below 35 C (95 F) slows metabolism. Important findings are confusion, bradycardia or dysrhythmias, and slowed breathing.

TEMPERATURE - What special temperature risks appear in CNS injury and older adults?

CNS trauma can cause central fever that responds poorly to antipyretics. Older adults have reduced sweating, shivering, vasoconstriction, and temperature perception.

SLEEP - How are sleep and rest different, and why is sleep needed?

Sleep is a repeating biologic cycle that supports memory, energy restoration, and tissue repair. Rest is a hypoactive state without the full sleep cycle.

SLEEP - How do NREM and REM sleep differ?

NREM has slower brain and body activity and includes deep restorative sleep. REM has vivid dreaming, rapid eye movements, muscle atonia, and variable vital signs.

SLEEP - What controls the normal sleep-wake cycle?

NREM and REM repeat about every 90 minutes. The hypothalamic suprachiasmatic nucleus aligns circadian rhythm with light, while nighttime melatonin promotes sleep.

SLEEP - What is insomnia and its main treatment?

Difficulty starting or maintaining restorative sleep with daytime effects. Sleep hygiene and cognitive behavioral therapy for insomnia are first-line treatments.

SLEEP - How do obstructive and central sleep apnea differ?

Obstructive apnea results from repeated upper-airway collapse. Central apnea results from loss of respiratory drive without airway obstruction.

SLEEP - What are the key findings, diagnosis, and treatment for obstructive sleep apnea?

Loud snoring, witnessed apnea, and daytime sleepiness are common. Polysomnography confirms it; weight management and nightly CPAP are major treatments.

SLEEP - What is narcolepsy?

A REM-regulation disorder causing sudden daytime sleep attacks, sometimes with cataplexy, sleep paralysis, or hallucinations. Treatment focuses on scheduled sleep and wake-promoting medication.

SLEEP - What are the major categories of sleep disorders?

Insomnia, hypersomnolence such as narcolepsy, breathing disorders such as apnea, circadian disorders such as shift work, parasomnias such as sleepwalking, and movement disorders such as restless legs.

CONSCIOUSNESS - How do consciousness, arousal, awareness, and orientation differ?

Consciousness is the overall state. Arousal is the stimulation needed to awaken. Awareness is understanding self and environment. Orientation identifies person, place, time, and situation.

CONSCIOUSNESS - How do alert, lethargic, obtunded, stuporous, and comatose levels differ?

Alert needs no stimulation; lethargic awakens easily; obtunded needs repeated stimulation; stuporous responds only to vigorous or painful stimulation; coma has no purposeful response.

CONSCIOUSNESS - What neurologic findings are most important when consciousness changes?

Level of consciousness is most sensitive. Also assess breathing pattern, pupils, eye movements, and motor response.

CONSCIOUSNESS - How can brain injury alter breathing, vomiting, pupils, eye movement, and motor responses?

Brainstem injury alters breathing, vomiting, pupillary, and eye-movement reflexes. Cortical, corticospinal, basal ganglia, or cerebellar injury changes movement and posture.

CONSCIOUSNESS - What is brain death?

Irreversible loss of all functions of the entire brain, including the brainstem. Formal clinical and apnea testing are required; a flat EEG alone is not enough.

CONSCIOUSNESS - What is cerebral death?

Irreversible loss of cerebral hemispheric function while the brainstem may still support breathing, circulation, and sleep-wake cycles.

CONSCIOUSNESS - What is a persistent vegetative state?

Wakefulness without awareness: eyes can open and sleep-wake cycles remain, but there is no purposeful communication or cognitive response.

CONSCIOUSNESS - What is a minimally conscious state?

Severely impaired consciousness with inconsistent but definite purposeful responses, such as following a simple command or giving a yes/no response.

CONSCIOUSNESS - What is locked-in syndrome?

The client is conscious and cognitively intact but nearly completely paralyzed from pontine injury. Vertical eye movement or blinking may permit communication.

COGNITION - How do retrograde, anterograde, and global amnesia differ?

Retrograde amnesia loses past memories. Anterograde amnesia cannot form new memories. Global amnesia combines both.

COGNITION - What is an executive attention deficit?

Difficulty sustaining attention, using working memory, planning, judging, correcting errors, or changing behavior when conditions change.

COGNITION - What is an image or data-processing deficit?

The person cannot correctly organize sensory information, form concepts, understand abstractions, or reason about relationships.

COGNITION - What are aphasia, agnosia, apraxia, and neglect?

Aphasia impairs language; agnosia impairs recognition; apraxia impairs learned purposeful movement; neglect causes inattention to one side.

COGNITION - Which brain regions strongly affect emotion and behavior?

Frontal and prefrontal injury alters judgment, inhibition, and personality. Limbic or temporal injury alters emotion and memory; parietal injury can cause neglect.

ALZHEIMER DISEASE - What is the definition?

A chronic, progressive, irreversible neurodegenerative disease causing worsening memory, cognition, and ability to function.

ALZHEIMER DISEASE - What are the main risk factors?

Increasing age, family history or APOE-e4, and Down syndrome. Vascular risks, low activity, and poor sleep can also increase risk.

ALZHEIMER DISEASE - What is the pathophysiology?

Beta-amyloid plaques collect outside neurons and tau tangles form inside neurons. Synapses and acetylcholine are lost, causing neuronal death and cerebral atrophy.

ALZHEIMER DISEASE - What are the top manifestations by stage?

Early: recent-memory and word-finding problems. Middle: worsening judgment and ADL dependence. Late: loss of communication or mobility with dysphagia.

ALZHEIMER DISEASE - What are the main complications?

Falls, malnutrition or dehydration, and aspiration pneumonia from late swallowing impairment.

ALZHEIMER DISEASE - How is it evaluated?

Cognitive and functional testing, laboratory tests for reversible causes, and CT or MRI. Biomarkers can support diagnosis; tissue examination confirms classic pathology.

ALZHEIMER DISEASE - What are the main treatments?

Provide structure, safety, activity, and caregiver support. Donepezil or another cholinesterase inhibitor may slow symptoms; memantine is used in moderate-to-severe disease.

SEIZURES - How are a seizure and epilepsy different?

A seizure is one sudden burst of abnormal cerebral electrical activity. Epilepsy is an enduring tendency to have recurrent unprovoked seizures.

SEIZURES - What is the basic pathophysiology?

Excess excitation or inadequate inhibition makes neurons fire synchronously. The affected brain area determines motor, sensory, behavioral, or awareness changes.

SEIZURES - What commonly provokes or causes seizures?

Brain injury or tumor, stroke or infection, and metabolic problems such as hypoglycemia or electrolyte imbalance. Sleep loss and alcohol withdrawal can lower the threshold.

SEIZURES - How do generalized, focal, and unknown-onset seizures differ?

Generalized begins in both hemispheres. Focal begins in one hemisphere and may spread. Unknown onset means the starting site is not yet known.

SEIZURES - What are the aura, ictal, and postictal phases?

Aura is a possible focal warning; ictal is active seizure activity; postictal is recovery with confusion, fatigue, or amnesia.

SEIZURES - How do the common seizure manifestations differ?

Tonic stiffens; clonic jerks; tonic-clonic combines both with loss of consciousness; absence causes brief staring; myoclonic causes brief jerks; atonic causes sudden loss of tone.

SEIZURES - What is status epilepticus?

A seizure lasting at least 5 minutes or repeated seizures without recovery between them. It can cause hypoxemia, brain injury, and death.

SEIZURES - How are seizure disorders evaluated?

History or witness description, EEG, glucose and electrolyte tests, and brain CT or MRI when a structural cause is possible.

SEIZURES - What are the main treatments?

Correct the cause and use an antiseizure drug matched to seizure type. Status epilepticus requires airway support and a rapid benzodiazepine such as IV lorazepam.

SEIZURES - What nursing actions protect a client during a seizure?

Protect the head, turn to the side, clear hazards, and time the seizure. Do not restrain the client or place anything in the mouth.

INCREASED ICP - What is ICP and what does the Monro-Kellie doctrine explain?

ICP is pressure inside the rigid skull. Brain tissue, blood, and CSF share fixed space, so an increase in one must be offset by a decrease in another or ICP rises.

INCREASED ICP - What are the main causes?

Cerebral edema or tumor, intracranial hemorrhage, and excess or obstructed CSF such as hydrocephalus.

INCREASED ICP - How are CPP and autoregulation affected?

CPP equals MAP minus ICP. Autoregulation normally adjusts vessel diameter to maintain cerebral flow, but severe ICP disrupts it, lowering perfusion and causing ischemia.

INCREASED ICP - What happens in stages 1 and 2?

Stage 1 uses CSF and blood-volume compensation with few findings. Stage 2 causes subtle confusion, restlessness, drowsiness, or slight pupil and breathing changes.

INCREASED ICP - What happens in stages 3 and 4?

Stage 3 causes falling consciousness, sluggish pupils, bradycardia, and widened pulse pressure. Stage 4 causes herniation, fixed pupils, abnormal breathing, and brainstem failure.

INCREASED ICP - What are the most important early and late findings?

Earliest: altered level of consciousness. Late: Cushing triad of widened pulse pressure, bradycardia, and irregular respirations.

INCREASED ICP - How is it evaluated?

Frequent neurologic examinations plus CT or MRI identify the cause. In selected clients, an invasive monitor directly measures ICP.

INCREASED ICP - What are the main treatments?

Elevate the head about 30 degrees, maintain oxygenation and perfusion, and treat the cause. Mannitol or hypertonic saline, CSF drainage, or surgery may be needed.

CEREBRAL EDEMA - What is it and what causes it?

Excess intracellular or extracellular brain fluid after trauma, ischemia, infection, hemorrhage, hypoxia, or tumor. It raises ICP and can cause herniation.

CEREBRAL EDEMA - How do vasogenic, cytotoxic, and interstitial edema differ?

Vasogenic leaks through a disrupted blood-brain barrier; cytotoxic swells injured cells after pump failure; interstitial moves CSF into tissue around obstructed ventricles.

CEREBRAL HERNIATION - What is it, and how do supratentorial and infratentorial types differ?

Brain tissue shifts from high to lower pressure. Supratentorial tissue shifts across the tentorium or falx; infratentorial tissue shifts near or through the foramen magnum.

CEREBRAL HERNIATION - What findings distinguish uncal, central, and tonsillar herniation?

Uncal causes an ipsilateral fixed dilated pupil and falling LOC. Central causes rapid coma and abnormal posturing. Tonsillar compresses the medulla, causing respiratory and cardiac failure.

HYDROCEPHALUS - What is the definition and pathophysiology?

Excess CSF enlarges the ventricles because of obstruction, impaired absorption, or rarely overproduction. Pressure damages white matter and can raise ICP.

HYDROCEPHALUS - How do communicating, noncommunicating, and normal-pressure types differ?

Communicating has impaired CSF absorption; noncommunicating has obstruction inside the ventricular system; normal-pressure hydrocephalus has enlarged ventricles with intermittently elevated pressure.

HYDROCEPHALUS - What are the key findings, diagnostics, and treatments?

Normal-pressure hydrocephalus causes gait change, urinary incontinence, and cognitive decline. CT or MRI evaluates ventricles; a ventricular shunt or endoscopic procedure restores flow.

MOTOR SYSTEMS - What are the CNS motor system and motor unit?

The CNS motor system plans and coordinates movement through brain and spinal pathways. A motor unit is one lower motor neuron plus all muscle fibers it controls.

MOTOR SYSTEMS - How do pyramidal and extrapyramidal systems differ?

Pyramidal tracts control precise voluntary movement. Extrapyramidal and basal-ganglia pathways support posture, tone, and automatic movement.

MOTOR SYSTEMS - What does the cerebellum do, and what indicates dysfunction?

It coordinates balance, timing, and accuracy. Dysfunction causes ataxia, intention tremor, and dysarthria.

MOTOR SYSTEMS - How do upper and lower motor neuron lesions differ?

UMN lesions cause spastic weakness and hyperreflexia. LMN lesions cause flaccid weakness, muscle atrophy or fasciculations, and reduced reflexes.

PERIPHERAL NERVES - How do segmental demyelination and axonal degeneration differ?

Demyelination slows or blocks conduction while the axon remains intact. Axonal degeneration destroys the axon distal to injury and recovers more slowly.

HEAD INJURY - How do primary and secondary traumatic brain injury differ?

Primary injury is immediate tissue damage from impact. Secondary injury evolves from edema, bleeding, inflammation, ischemia, and hypoxia.

HEAD INJURY - What are acceleration-deceleration, coup-contrecoup, and rotational forces?

Acceleration-deceleration moves the brain within the skull; coup injures the impact side and contrecoup the opposite side; rotation creates shearing.

HEAD INJURY - What is a concussion?

A mild TBI causing temporary functional disturbance, commonly confusion, headache, amnesia, or brief loss of consciousness without a major structural lesion.

HEAD INJURY - How do cerebral contusion and diffuse axonal injury differ?

Contusion is focal brain bruising, often frontal or temporal. Diffuse axonal injury is widespread shearing that commonly causes prolonged unconsciousness or coma.

HEAD INJURY - How do epidural and subdural hematomas differ?

Epidural bleeding lies between skull and dura, often arterial with a lucid interval. Subdural bleeding lies below the dura, usually venous and may develop slowly.

HEAD INJURY - What skull-fracture findings require urgent follow-up?

Depressed fracture can compress brain tissue. Basilar fracture may cause CSF drainage, Battle sign, or raccoon eyes. CT and rapid neurologic evaluation are priorities.

SPINAL CORD INJURY - What is the definition, and how do primary and secondary injury differ?

SCI disrupts motor, sensory, or autonomic pathways. Primary injury is immediate compression or tearing; secondary injury adds ischemia, edema, inflammation, and cell death.

SPINAL CORD INJURY - How do complete and incomplete injuries differ?

Complete injury has no sensory or motor function in the sacral segments. Incomplete injury preserves some function below the lesion and has greater recovery potential.

SPINAL CORD INJURY - How do paraplegia and tetraplegia differ?

Paraplegia affects both legs and lower trunk from thoracic or lower injury. Tetraplegia affects all four limbs from cervical injury.

VERTEBRAL INJURY - What are the four classifications?

Simple fracture, anterior compression or wedge fracture, comminuted or burst fracture, and fracture-dislocation.

VERTEBRAL INJURY - How do hyperflexion, hyperextension, axial compression, and rotation cause injury?

Flexion injures anterior structures; extension injures posterior cervical structures; axial force causes burst fractures; rotation adds shearing and instability.

SPINAL SHOCK - What is it and what are the key findings?

Temporary loss of reflex, motor, sensory, and autonomic function below an acute cord lesion. Flaccid paralysis, areflexia, and bowel or bladder dysfunction occur.

SPINAL SHOCK - What indicates it is ending?

Return of reflexes, often beginning with the bulbocavernosus reflex, followed by possible hyperreflexia and spasticity.

NEUROGENIC SHOCK - What is it and what are the key findings?

Loss of sympathetic tone, usually after injury above T6, causes hypotension, bradycardia, and warm dry skin.

SPINAL VS NEUROGENIC SHOCK - What is the difference?

Spinal shock is temporary loss of neurologic function below the lesion. Neurogenic shock is circulatory failure from loss of sympathetic tone.

AUTONOMIC DYSREFLEXIA - What is the pathophysiology?

After SCI at T6 or above, a stimulus below the lesion triggers massive sympathetic vasoconstriction that descending brain signals cannot stop.

AUTONOMIC DYSREFLEXIA - What commonly triggers it?

A distended bladder is most common. Bowel impaction and skin pressure or irritation are other major triggers.

AUTONOMIC DYSREFLEXIA - What are the key manifestations?

Sudden severe hypertension, pounding headache, and flushing or sweating above the lesion. Bradycardia can occur.

AUTONOMIC DYSREFLEXIA - What is the first treatment?

Sit the client upright, loosen restrictive items, check the urinary catheter or bladder, and remove the trigger. Give a rapid antihypertensive if hypertension persists.

INCOMPLETE SCI SYNDROMES - How do central, anterior, and Brown-Sequard syndromes differ?

Central cord weakens arms more than legs; anterior cord loses motor and pain-temperature function; Brown-Sequard causes same-side motor loss with opposite-side pain-temperature loss.

CAUDA EQUINA SYNDROME - What findings make it an emergency?

Saddle anesthesia, new urinary retention or incontinence, and progressive leg weakness suggest compressed lumbosacral roots requiring urgent MRI and decompression.

SPINAL CORD INJURY - What are the main acute treatments and complications?

Maintain immobilization, oxygenation, and blood pressure; decompress or stabilize when indicated. Monitor for respiratory failure, DVT, pressure injury, and bladder or bowel problems.