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NSG 3280 Exam 3 Pathophysiology (2026/2027) | Galen College of Nursing | 150 Q&A with Rationales | Neuro, Stroke, SCI, Neurodegenerative

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Complete NSG 3280 Exam 3 Study Guide – Pathophysiology – Galen College of Nursing (2026/2027 Academic Year) This digital download is a comprehensive 150-question practice exam for NSG 3280 Pathophysiology – Exam 3 at Galen College of Nursing. Designed for undergraduate nursing students mastering the pathophysiological basis of neurological disorders, stroke, spinal cord injury, neurodegenerative diseases, and musculoskeletal/sensory conditions. What's included: 150 multiple-choice questions with detailed rationales 6 organized sections covering all exam topics Answers with evidence-based rationales – learn the "why," not just the "what" Section 1: Increased Intracranial Pressure (ICP) & Traumatic Brain Injury (Q1–35) Normal ICP: 0–15 mm Hg; sustained 20 mm Hg requires intervention Monro-Kellie doctrine: cranial vault fixed volume (brain tissue 80%, CSF 10%, blood 10%) Earliest sign of increasing ICP: change in level of consciousness (LOC) GCS classification: Mild TBI 13–15, Moderate 9–12, Severe ≤8 Primary injury: initial mechanical damage (irreversible) Secondary injury: delayed cascade (ischemia, hypoxia, inflammation, edema) Coup-contrecoup injury: impact site (coup) + opposite side (contrecoup) Epidural hematoma: arterial bleeding (middle meningeal artery) – lucid interval then rapid deterioration Subdural hematoma: venous bleeding from bridging veins Subarachnoid hemorrhage: bleeding into CSF – sudden "thunderclap" headache Basilar skull fracture: CSF rhinorrhea/otorrhea (halo sign) Herniation: most severe complication of elevated ICP Vasogenic edema: increased capillary permeability (tumors, inflammation) Cytotoxic edema: cellular energy failure (ischemia, hypoxia) Levels of consciousness: delirious (acute confusion) → obtunded (falls asleep unless stimulated) → stuporous (vigorous stimulation required) → comatose (unable to arouse) Decorticate posturing (flexor – cerebral hemispheres) vs. decerebrate posturing (extensor – brainstem, more ominous) Doll's eye reflex & cold calorics: test brainstem function Lumbar puncture contraindicated in increased ICP (risk of herniation) Section 2: Cerebrovascular Disorders & Stroke (Q36–60) Thrombotic stroke: in-situ clot on atherosclerosis plaque Embolic stroke: clot travels from heart (atrial fibrillation) Hemorrhagic stroke: vessel rupture (aneurysm, AVM, hypertension) Non-contrast CT: first-line imaging (differentiates ischemic vs. hemorrhagic) TIA: transient focal deficits resolving 24 hours – warning sign for future stroke Uncontrolled hypertension: single most important modifiable risk factor Left hemispheric stroke: aphasia + right-sided weakness Right hemispheric stroke: impulsivity, neglect, left-sided weakness Broca's aphasia: non-fluent, effortful speech (expressive) Wernicke's aphasia: fluent but meaningless speech ("word salad"), poor comprehension Cerebral aneurysm: focal arterial dilation; risk factors: hypertension, cocaine, connective tissue disorders, polycystic kidney disease AVM: congenital arteriovenous shunt (no capillary bed) – rupture risk Subarachnoid hemorrhage: most common cause = ruptured aneurysm Cushing's triad (late sign of increased ICP): hypertension, bradycardia, irregular respirations (sympathetic response to brainstem ischemia) Section 3: Seizure Disorders & CNS Infections (Q61–80) Seizure mechanism: paroxysmal abnormal electrical discharges from altered membrane potential Status epilepticus: continuous seizure 5 minutes or recurrent without return to baseline – medical emergency Absence seizure (petit mal): brief staring spell in children (5–30 seconds) Meningitis: inflammation of meninges (bacterial vs. viral) Encephalitis: inflammation of brain parenchyma (usually viral) Bacterial meningitis CSF: cloudy, ↓ glucose, ↑ protein, ↑ neutrophils Viral meningitis CSF: clear, normal glucose, lymphocytic predominance Classic meningitis triad: fever, nuchal rigidity, altered mental status Kernig's sign: resistance to knee extension with hip flexed Brudzinski's sign: neck flexion causes involuntary hip/knee flexion Bell palsy: acute idiopathic facial nerve (CN VII) palsy – unilateral facial droop, decreased blink, hyperacusis Trigeminal neuralgia: CN V – sudden excruciating facial pain Glutamate: primary excitatory CNS neurotransmitter Ischemia vs. hypoxia: ischemia = reduced blood flow; hypoxia = reduced oxygen "Time is tissue": rapid intervention critical to prevent irreversible neuronal damage Section 4: Neurodegenerative Disorders (Q81–105) Multiple Sclerosis (MS): autoimmune demyelination of CNS white matter – optic neuritis (painful monocular vision loss) ALS: degeneration of upper and lower motor neurons – weakness, atrophy, fasciculations, hyperreflexia; respiratory failure is most common cause of death Parkinson's disease: dopamine neuron degeneration in substantia nigra – triad: resting tremor (pill-rolling), rigidity, bradykinesia Alzheimer's disease: beta-amyloid plaques + neurofibrillary tangles (hyperphosphorylated tau); earliest pathology in hippocampus (memory loss) Guillain-Barré syndrome: acute inflammatory demyelination of peripheral nerves – ascending paralysis; often post-infection (Campylobacter jejuni); priority: respiratory function Myasthenia gravis: autoimmune destruction of acetylcholine receptors at NMJ – fatigable weakness (worsens with use, improves with rest); Tensilon test improves strength in myasthenic crisis Huntington's disease: autosomal dominant – GABA neuron degeneration in striatum; triad: chorea, dementia, psychiatric symptoms Upper motor neuron signs: hyperreflexia, spasticity, Babinski sign Lower motor neuron signs: hyporeflexia, flaccid weakness, atrophy, fasciculations Section 5: Spinal Cord Injury & Autonomic Dysfunction (Q106–125) C5 injury: high risk for respiratory compromise (phrenic nerve C3–C5) Neurogenic shock: loss of sympathetic tone (T1–L2) → hypotension, bradycardia, warm dry skin (below injury level) Autonomic dysreflexia: life-threatening emergency in SCI at or above T6 – triggered by noxious stimulus below injury (bladder distention most common) → sudden severe headache, hypertension, bradycardia; first action: identify and remove stimulus Spinal shock: temporary flaccid paralysis, areflexia, loss of sensation (days to weeks) Complete SCI at T10: paraplegia (preserved upper extremity function) Brown-Séquard syndrome: hemisection – ipsilateral motor loss + contralateral pain/temperature loss Central cord syndrome: greater upper extremity weakness (hyperextension injury in elderly) Anterior cord syndrome: loss of motor and pain/temperature; preserved proprioception Cauda equina syndrome: compression of lumbar/sacral nerve roots – saddle anesthesia, bowel/bladder dysfunction (LMN signs) Conus medullaris syndrome: injury to sacral spinal cord segments (S2–S5) – early bowel/bladder dysfunction Poikilothermia: inability to regulate body temperature after SCI (environmental temperature) Section 6: Musculoskeletal & Sensory Disorders (Q126–150) Compartment syndrome: increased pressure within closed fascial compartment – surgical emergency; "5 Ps": Pain (out of proportion), Pallor, Pulselessness (late), Paresthesia, Paralysis (late); common in diabetics/smokers Osteoarthritis: degenerative loss of articular cartilage and subchondral bone Osteoporosis: decreased bone density – associated with estrogen deficiency, thyroid hormone suppression Paget's disease: viral etiology suspected – excessive bone resorption then chaotic formation Giant cell tumor: young adults (20–40), female predominance, around the knee Avulsion fracture: tendon/ligament pulls bone fragment Myositis ossificans: heterotopic bone formation in muscle after trauma Delayed healing: caused by poor circulation (diabetes, PVD, smoking) Conductive hearing loss: cerumen impaction, otitis media – sound conduction blocked Sensorineural hearing loss: cochlea or CN VIII damage – noise exposure, ototoxicity, presbycusis (age-related) Otosclerosis: middle-aged Caucasian women – conductive hearing loss Cranial nerves: CN III (oculomotor – eye movement), CN VII (facial – Bell palsy), CN VIII (vestibulocochlear – hearing/balance), CN V (trigeminal – facial sensation) Migraine: severe unilateral/throbbing pain, photophobia, nausea; aura in 25% Neuropathic pain: nerve injury (not tissue inflammation) Herpes zoster (shingles): painful unilateral vesicular rash along a single dermatome (VZV reactivation) Why this guide works: 150 unique questions – comprehensive coverage of Exam 3 content Detailed rationales – understand pathophysiological mechanisms, not just memorize facts Clinically relevant – prepare for NCLEX and clinical practice Exam-ready – mirrors the difficulty and style of Galen College of Nursing NSG 3280 Format: PDF (150 questions + answer key + rationales) Institution: Galen College of Nursing Course: NSG 3280 – Pathophysiology Term: 2026/2027 Exam: 3 of 3 (Neuro, Stroke, SCI, Neurodegenerative, Musculoskeletal, Sensory) Instant download – study on any device or print for offline use.

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Voorbeeld van de inhoud

NSG 3280 EXAM 3 PATHOPHYSIOLOGY —
COMPLETE 150-QUESTION PRACTICE EXAM
Galen College of Nursing | 2026/2027 | Questions with
Answers & Rationales




SECTION 1: INCREASED INTRACRANIAL PRESSURE (ICP) & TRAUMATIC
BRAIN INJURY (Questions 1-35)

1. What assessment finding is the earliest indicator of increasing intracranial
pressure (ICP) in a client with acute brain injury?
A. Fixed dilated pupils
B. Change in level of consciousness
C. Cushing triad
D. Decerebrate posturing

Correct Answer: B
Rationale: A change in LOC is typically the first sign of rising ICP because
cerebral perfusion and reticular activating system function are affected early.
Late findings such as fixed pupils and posturing suggest worsening brain
compression.

2. The normal range of ICP is:
A. 0-5 mm Hg
B. 0-15 mm Hg

,C. 15-30 mm Hg
D. 30-45 mm Hg

Correct Answer: B
*Rationale: Normal ICP ranges from 0-15 mm Hg. Sustained pressures above
20 mm Hg are considered elevated and require intervention.*

3. If all three compartments of the cranium remain fixed and one
compartment increases, what can happen?
A. Increased cerebral perfusion
B. Possible brain herniation
C. Decreased blood pressure
D. Spontaneous resolution

Correct Answer: B
Rationale: The Monro-Kellie doctrine states the cranial vault is a fixed
volume. If one component (brain tissue, CSF, or blood) increases, others
must decrease to compensate. When compensation fails, ICP rises and brain
herniation can occur.

4. A client with suspected increased ICP develops headache, vomiting, and
blurred vision. How should the nurse interpret these findings?
A. They are late signs of brain herniation
B. They are initial manifestations of increased ICP
C. They indicate spinal cord injury
D. They suggest seizure activity only

Correct Answer: B
Rationale: Headache, vomiting (often projectile), and blurred vision

,(papilledema) are early signs of increased ICP. Late signs include Cushing
triad and posturing.

5. A client's Glasgow Coma Scale (GCS) score is 8. How should the nurse
interpret this finding?
A. Mild TBI
B. Moderate TBI
C. Severe TBI
D. Normal neurologic function

Correct Answer: C
*Rationale: GCS classification: Mild TBI = 13-15, Moderate = 9-12, Severe = 8
or less. A score of 8 or less indicates severe TBI and often correlates with
coma.*

6. The three components of the cranium include:
A. Brain tissue, CSF, and blood
B. Brain tissue, water, and electrolytes
C. Neurons, glial cells, and meninges
D. Gray matter, white matter, and ventricles

Correct Answer: A
Rationale: The cranial vault contains three volume components: brain tissue
(80%), cerebrospinal fluid (10%), and blood (10%).

7. GCS is taken first ______ hours after a TBI.
A. 24
B. 48

, C. 72
D. 96

Correct Answer: B
Rationale: The Glasgow Coma Scale is typically assessed within the first 48
hours after traumatic brain injury to establish baseline and monitor for
deterioration.

8. If a patient has increased ICP, should you perform a lumbar puncture?
A. Yes, it is diagnostic and therapeutic
B. Yes, but only with ultrasound guidance
C. No, it could cause brain herniation
D. No, it is only contraindicated in meningitis

Correct Answer: C
Rationale: Lumbar puncture is contraindicated in the presence of increased
ICP because the sudden release of CSF pressure below the level of the
brainstem can cause downward herniation.

9. Primary injury in TBI refers to:
A. Progressive delayed cell death
B. Initial damage from the traumatic event that is not reversible
C. Cerebral edema occurring 24-48 hours after injury
D. Ischemic damage from hypotension

Correct Answer: B
Rationale: Primary injury is the initial mechanical damage occurring at the
moment of impact. It is immediate and not reversible.

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