1
NUR2063 Pathophysiology – Examination Blueprint – Final exam
Modules 7-8-9-10
Use previous blueprints for Modules 1-6 for final preparation
Neurologic pathophysiology
1. Neuro system features – structure of neurons with myelin sheaths
a. Needs of neuro system to function: Oxygen and Glucose
b. Autonomic nervous system: Controls smooth muscle, unconscious response affecting the heart
rate, BP, intestinal motility
i. Parasympathetic: Rest and Digest vs. sympathetic systems: Fight or Flight
2. Disorders
a. Hydrocephalus: Common condition with excess CSF accumulation
i. Risk factors: premature, pregnancy complications, nervous system tumors, CNS
infections, cerebral hemorrhage, severe head injury
ii. Manifestations – children: Large head in infancy, bulging fontanel, Lethargy; irritability,
Seizures, Eyes that gaze downward, High-pitched cry, Feeding difficulties vs. adults:
Headache with N/V, Blurred vision or diplopia, Uncoordinated movements, Irritability;
personality changes, Sluggish pupil reactions
iii. Diagnosis: H & P, including measurement of head circumference, Neuro assessment,
Cranial CT/MRI/Xray, Prenatal US
iv. treatment: Surgical repair of blockage, Shunt placement, Antibiotic treatment if caused
by infection, Lifelong follow-up exams, Multidisciplinary team management
b. Meningitis: Inflammation of the meninges usually due to infection
i. What can cause it: Bacterial: Neisseria meningitidis, Streptococcus pneumoniae,
Haemophilus influenzae Viral: Enterovirus; measles, Influenza; herpes, Tumors, Allergens
ii. Risk factors: Less than 25 yrs old, living in community setting, Pregnancy,
Immunodeficiency, Working with animals
iii. Complications: Permanent neuro damage, Seizures, Hearing loss, Blindness, Speech
difficulties, Renal failure, Shock, Death
iv. Manifestations: Headaches, altered mental status, phonophobia, muscle fatigue, sever
muscle pain, dislike bright lights, NV,
v. Diagnosis: H & P, Throat cultures, Lumbar puncture with CSF analysis, PCR, Head CT
vi. Treatment: Antibiotics (if bacterial), Hydration, Fever management, Preventative vaccine
c. Encephalitis
i. What is it: Inflammation of brain and spinal cord, usually d/t infection
ii. what happens:
iii. Causes: Bacterial: Lyme disease, TB, Syphilis
1. Viral causes: Coxsackievirus, Poliovirus, Herpes virus, Cytomegalovirus, Measle,
Mumps, West Nile virus
iv. Manifestations: Flu-like symptoms, Headache/nuchal rigidity (neck pain), Confusion;
hallucinations, Personality changes, Diplopia, Seizures, Muscle weakness; tremors;
paresthesia or paralysis, Loss of consciousness, Abnormal deep tendon reflexes, Rash
v. Diagnosis: H & P, Head CT/MRI, EEG, LP with CSF analysis, PCR, Serum viral antibodies
vi. Treatment: Rest, Nutrition + sufficient hydration, Respiratory support, Reorientation &
emotional support, Analgesics & antipyretics to relieve headaches and fever, Antiviral
agents (if viral), Antibiotic therapy (if bacterial), Corticosteroids to reduce cerebral
edema, Sedatives to treat irritability and restlessness, PT, OT, Speech therapy,
, 2
NUR2063 Pathophysiology – Examination Blueprint – Final exam
Prevention, Vaccinations, Wear protective clothing (mosquito prevention), Eliminating
standing water sources
d. Traumatic brain injury (TBI)
i. What it is: A sudden violent blow or jolt to the head (closed), penetrating (open) head
wound
ii. What are causes: Falls, MVC, penetration of object, assaults
iii. Complications: Can be from one event or multiple mild events, Changes in thinking,
sensation, language or emotions, Seizures, Memory decline, Depression, Death,
Alzheimer’s disease, Parkinson’s disease
iv. Closed: the brain jolts forward hitting the frontal bone, then back to the occipital bone.
Or side to side vs. open head injuries: fractures or something penetrating the head
v. Manifestations: unable to recall details, pupil unequal in side, asymmetrical facial
features, impaired senses, lack of coordination, bradypnea, hypotension
vi. Diagnosis: H & P with Glasgow Coma Scale, Head CT/MRI, ICP monitoring
vii. Treatment: Rest, Analgesics (specifically acetaminophen), Cold compresses, Osmotic
diuretics (ex: mannitol), Antiseizure meds, Sedatives, Surgery, Rehabilitation, PT, OT,
Speech
viii. Prevention: seatbelts, car seats, helmets,
e. Increased intracranial pressure
i. Causes: TBI, Tumors, Hydrocephalus, Cerebral edema, Hemorrhage
ii. Manifestations: pupillary changes, impaired eye movement, changes in mobile ability,
seizures, high systolic BP, Low pulse, vomiting, change in speech,
iii. Compensatory mechanisms
1. Monro-Kellie hypothesis: Increase in volume of one component must be
compensated for by a decrease in volume of another. Accomplished mostly by
shifts in CSF and blood volume
2. Autoregulation: Blood vessels dilate to increase blood flow and constrict if ICP
increases
3. Cushing’s reflex: The hypothalamus increases sympathetic stimulation when the
mean arterial pressure (MAP) pressure drops below the ICP
Causes vasoconstriction, increased cardiac contractility and increased cardiac
output
a. Cushing’s triad: Increased blood pressure, Bradycardia, Cheyne-Stokes
respirations
iv. Diagnosis: same as TBI
v. Treatment: Based on underlying cause, Respiratory support, Semi-Fowler’s position,
Drain excess CSF, Medications, seizure precaution
vi. Complications: Brain herniation, feared complication of increased ICP, Not reversible,
Death is the result
f. Hematomas
i. What they are: A collection of blood in tissue developed from ruptured blood vessels
ii. Types
1. Epidural – Bleeding between dura and skull –usually an arterial tear
2. Subdural – Between dura and arachnoid layers – usually due to a small venous
tear
, 3
NUR2063 Pathophysiology – Examination Blueprint – Final exam
3. Subarachnoid – Results from bleeding in the space between arachnoid and pia
mater. presentation is severe headache with a sudden onset
4. Intracerebral: Result from bleeding in the brain tissue
iii. What happens with hematoma: Bleeding leads to localized pressure on nearby tissue
and increases ICP. Blood may coagulate and form a solid mass. The hematoma becomes
encapsulated by fibroblasts and blood cells lyse within the capsule. Fluid from hemolysis
exerts osmotic pressure, drawing more fluid into the capsule. Edema increases the mass
size, applying pressure on the nearby tissue and increasing ICP.
iv. Diagnosis: H & P, including Glasgow Coma Scale, Head CT, MRI, Cerebral angiogram, ICP
monitor
v. Treatment: May/may not be required or removing blood may not be possible
Surgical removal of blood through burr hole or craniotomy, PT/OT/Speech therapy
g. Spinal cord injury
i. What it is: Results from direct injury to the spinal cord or indirect damage to surrounding
tissues
ii. Causes: Motor vehicle crashes, Falls, Violence, Sports injuries, Weakened vertebral
structures: Ex: osteoporosis or rheumatoid arthritis, Compression of spinal cord d/t,
Hemorrhage, Fluid accumulation, Edema, Spinal shock
iii. What is spinal shock: Temporary suppression of neurologic function d/t spinal cord
compression; neuro function gradually returns
iv. Complications: Loss of neurologic functioning, Varying degrees of paralysis, Autonomic
hyperreflexia, Massive sympathetic response, Usually injuries above T6, Neurogenic
shock, Respiratory failure, Effects of immobility, Changes in bowel/bladder function, Chronic
pain, Death
v. What is neurogenic shock: Abnormal vasomotor response secondary to disruption of
sympathetic impulses
vi. Manifestations: Cervical spine injuries most devastating: Affects upper and lower
extremities, Paralysis, Impacts respiratory system, Unstable BP (initially)/temp
fluctuations, Diaphoresis, Loss of bowel/bladder control, Paresthesia/sensory changes,
Spasticity, Pain. Thoracic injuries: Affect lower extremities, Manifestations same as for
cervical. Lumbar/sacral injuries: Varying degrees of presentation, Manifestations can be
same as cervical spinal except for respiratory problems
vii. Diagnosis:
viii. Treatment
1. Immediate: Immobilize the spine, administer corticosteroids to reduce swelling,
Spinal traction to reduce fracture & immobilize, Surgical repair, Respiratory
management, Bed rest
2. Long term management: PT/OT/speech therapy, Mobility assistive devices, Long
term respiratory management, Antispasmodic agents & Botox injections to treat
muscle spasms, Prompt treatment of infections, Meticulous skin care,
Bowel/bladder training or management, Pain management, Nutritional support,
Electronic devices (brain/computer interfaces), Psychosocial support
h. Brain disorders
i. TIA ( Transient ischemic attack) –what are these: “mini stroke”
1. Risk factors: Migraines, Smoking, Diabetes mellitus, Age, Inadequate nutrition,
Hypercholesterolemia, OCPs, Excess alcohol consumption, Illicit drug use
NUR2063 Pathophysiology – Examination Blueprint – Final exam
Modules 7-8-9-10
Use previous blueprints for Modules 1-6 for final preparation
Neurologic pathophysiology
1. Neuro system features – structure of neurons with myelin sheaths
a. Needs of neuro system to function: Oxygen and Glucose
b. Autonomic nervous system: Controls smooth muscle, unconscious response affecting the heart
rate, BP, intestinal motility
i. Parasympathetic: Rest and Digest vs. sympathetic systems: Fight or Flight
2. Disorders
a. Hydrocephalus: Common condition with excess CSF accumulation
i. Risk factors: premature, pregnancy complications, nervous system tumors, CNS
infections, cerebral hemorrhage, severe head injury
ii. Manifestations – children: Large head in infancy, bulging fontanel, Lethargy; irritability,
Seizures, Eyes that gaze downward, High-pitched cry, Feeding difficulties vs. adults:
Headache with N/V, Blurred vision or diplopia, Uncoordinated movements, Irritability;
personality changes, Sluggish pupil reactions
iii. Diagnosis: H & P, including measurement of head circumference, Neuro assessment,
Cranial CT/MRI/Xray, Prenatal US
iv. treatment: Surgical repair of blockage, Shunt placement, Antibiotic treatment if caused
by infection, Lifelong follow-up exams, Multidisciplinary team management
b. Meningitis: Inflammation of the meninges usually due to infection
i. What can cause it: Bacterial: Neisseria meningitidis, Streptococcus pneumoniae,
Haemophilus influenzae Viral: Enterovirus; measles, Influenza; herpes, Tumors, Allergens
ii. Risk factors: Less than 25 yrs old, living in community setting, Pregnancy,
Immunodeficiency, Working with animals
iii. Complications: Permanent neuro damage, Seizures, Hearing loss, Blindness, Speech
difficulties, Renal failure, Shock, Death
iv. Manifestations: Headaches, altered mental status, phonophobia, muscle fatigue, sever
muscle pain, dislike bright lights, NV,
v. Diagnosis: H & P, Throat cultures, Lumbar puncture with CSF analysis, PCR, Head CT
vi. Treatment: Antibiotics (if bacterial), Hydration, Fever management, Preventative vaccine
c. Encephalitis
i. What is it: Inflammation of brain and spinal cord, usually d/t infection
ii. what happens:
iii. Causes: Bacterial: Lyme disease, TB, Syphilis
1. Viral causes: Coxsackievirus, Poliovirus, Herpes virus, Cytomegalovirus, Measle,
Mumps, West Nile virus
iv. Manifestations: Flu-like symptoms, Headache/nuchal rigidity (neck pain), Confusion;
hallucinations, Personality changes, Diplopia, Seizures, Muscle weakness; tremors;
paresthesia or paralysis, Loss of consciousness, Abnormal deep tendon reflexes, Rash
v. Diagnosis: H & P, Head CT/MRI, EEG, LP with CSF analysis, PCR, Serum viral antibodies
vi. Treatment: Rest, Nutrition + sufficient hydration, Respiratory support, Reorientation &
emotional support, Analgesics & antipyretics to relieve headaches and fever, Antiviral
agents (if viral), Antibiotic therapy (if bacterial), Corticosteroids to reduce cerebral
edema, Sedatives to treat irritability and restlessness, PT, OT, Speech therapy,
, 2
NUR2063 Pathophysiology – Examination Blueprint – Final exam
Prevention, Vaccinations, Wear protective clothing (mosquito prevention), Eliminating
standing water sources
d. Traumatic brain injury (TBI)
i. What it is: A sudden violent blow or jolt to the head (closed), penetrating (open) head
wound
ii. What are causes: Falls, MVC, penetration of object, assaults
iii. Complications: Can be from one event or multiple mild events, Changes in thinking,
sensation, language or emotions, Seizures, Memory decline, Depression, Death,
Alzheimer’s disease, Parkinson’s disease
iv. Closed: the brain jolts forward hitting the frontal bone, then back to the occipital bone.
Or side to side vs. open head injuries: fractures or something penetrating the head
v. Manifestations: unable to recall details, pupil unequal in side, asymmetrical facial
features, impaired senses, lack of coordination, bradypnea, hypotension
vi. Diagnosis: H & P with Glasgow Coma Scale, Head CT/MRI, ICP monitoring
vii. Treatment: Rest, Analgesics (specifically acetaminophen), Cold compresses, Osmotic
diuretics (ex: mannitol), Antiseizure meds, Sedatives, Surgery, Rehabilitation, PT, OT,
Speech
viii. Prevention: seatbelts, car seats, helmets,
e. Increased intracranial pressure
i. Causes: TBI, Tumors, Hydrocephalus, Cerebral edema, Hemorrhage
ii. Manifestations: pupillary changes, impaired eye movement, changes in mobile ability,
seizures, high systolic BP, Low pulse, vomiting, change in speech,
iii. Compensatory mechanisms
1. Monro-Kellie hypothesis: Increase in volume of one component must be
compensated for by a decrease in volume of another. Accomplished mostly by
shifts in CSF and blood volume
2. Autoregulation: Blood vessels dilate to increase blood flow and constrict if ICP
increases
3. Cushing’s reflex: The hypothalamus increases sympathetic stimulation when the
mean arterial pressure (MAP) pressure drops below the ICP
Causes vasoconstriction, increased cardiac contractility and increased cardiac
output
a. Cushing’s triad: Increased blood pressure, Bradycardia, Cheyne-Stokes
respirations
iv. Diagnosis: same as TBI
v. Treatment: Based on underlying cause, Respiratory support, Semi-Fowler’s position,
Drain excess CSF, Medications, seizure precaution
vi. Complications: Brain herniation, feared complication of increased ICP, Not reversible,
Death is the result
f. Hematomas
i. What they are: A collection of blood in tissue developed from ruptured blood vessels
ii. Types
1. Epidural – Bleeding between dura and skull –usually an arterial tear
2. Subdural – Between dura and arachnoid layers – usually due to a small venous
tear
, 3
NUR2063 Pathophysiology – Examination Blueprint – Final exam
3. Subarachnoid – Results from bleeding in the space between arachnoid and pia
mater. presentation is severe headache with a sudden onset
4. Intracerebral: Result from bleeding in the brain tissue
iii. What happens with hematoma: Bleeding leads to localized pressure on nearby tissue
and increases ICP. Blood may coagulate and form a solid mass. The hematoma becomes
encapsulated by fibroblasts and blood cells lyse within the capsule. Fluid from hemolysis
exerts osmotic pressure, drawing more fluid into the capsule. Edema increases the mass
size, applying pressure on the nearby tissue and increasing ICP.
iv. Diagnosis: H & P, including Glasgow Coma Scale, Head CT, MRI, Cerebral angiogram, ICP
monitor
v. Treatment: May/may not be required or removing blood may not be possible
Surgical removal of blood through burr hole or craniotomy, PT/OT/Speech therapy
g. Spinal cord injury
i. What it is: Results from direct injury to the spinal cord or indirect damage to surrounding
tissues
ii. Causes: Motor vehicle crashes, Falls, Violence, Sports injuries, Weakened vertebral
structures: Ex: osteoporosis or rheumatoid arthritis, Compression of spinal cord d/t,
Hemorrhage, Fluid accumulation, Edema, Spinal shock
iii. What is spinal shock: Temporary suppression of neurologic function d/t spinal cord
compression; neuro function gradually returns
iv. Complications: Loss of neurologic functioning, Varying degrees of paralysis, Autonomic
hyperreflexia, Massive sympathetic response, Usually injuries above T6, Neurogenic
shock, Respiratory failure, Effects of immobility, Changes in bowel/bladder function, Chronic
pain, Death
v. What is neurogenic shock: Abnormal vasomotor response secondary to disruption of
sympathetic impulses
vi. Manifestations: Cervical spine injuries most devastating: Affects upper and lower
extremities, Paralysis, Impacts respiratory system, Unstable BP (initially)/temp
fluctuations, Diaphoresis, Loss of bowel/bladder control, Paresthesia/sensory changes,
Spasticity, Pain. Thoracic injuries: Affect lower extremities, Manifestations same as for
cervical. Lumbar/sacral injuries: Varying degrees of presentation, Manifestations can be
same as cervical spinal except for respiratory problems
vii. Diagnosis:
viii. Treatment
1. Immediate: Immobilize the spine, administer corticosteroids to reduce swelling,
Spinal traction to reduce fracture & immobilize, Surgical repair, Respiratory
management, Bed rest
2. Long term management: PT/OT/speech therapy, Mobility assistive devices, Long
term respiratory management, Antispasmodic agents & Botox injections to treat
muscle spasms, Prompt treatment of infections, Meticulous skin care,
Bowel/bladder training or management, Pain management, Nutritional support,
Electronic devices (brain/computer interfaces), Psychosocial support
h. Brain disorders
i. TIA ( Transient ischemic attack) –what are these: “mini stroke”
1. Risk factors: Migraines, Smoking, Diabetes mellitus, Age, Inadequate nutrition,
Hypercholesterolemia, OCPs, Excess alcohol consumption, Illicit drug use
