Neural Flashcards

1
Q

What occurs when the pressure in the brain presses on the blood vessels? What happens when that pressure continues to rise as blood flow is further impeded?

A

causes blood flow to the brain to slow causing cerebral hypoxa and ischemia

brain may herniate and blood flow ceases all together

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2
Q

What is a primary brain injury? Examples? What is a secondary injury/ Examples?

A

Primary injury: consequence of direct contact to head/brain during the instant of initial injury

Contusions, lacerations, external hematomas, skull fractures, subdural hematomas, concussion, diffuse axonal injury

Secondary injury: damage that evolves over ensuing days and hours after the initial injury

Cerebral edema, ischemia, or chemical changes associated with the trauma

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3
Q

What are signs of a fracture at the base of the skull? (basal fracture)

A

Bleeding from nose pharynx or ears

Battle sign: ecchymosis behind the ear
Halo sign: indicates a CSF leak. Ring of fluid around the blood stain from drainage

Raccoon eyes: bruising into the tissue around the eyes

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4
Q

What are manifestations of increased ICP?

A

Altered level of consciousness, restlessness, irritability
Pupillary abnormalities (a fixed dilated pupil is ominous)
Cranial nerve dysfunction
Sudden onset of neurological deficits and neurological changes; changes in senses, movement, and reflexes
Posturing such as decorticate or decerebrate
Cushing triad – late sign (hypertension, bradycardia, irregular slow RR)
Headache, NV
Seizures

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5
Q

What are the 3 signs of late ICP with Cushing’s triad?

A

hypertension
bradycardia,
irregular slow RR)

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6
Q

What are manifestations of a concussion or mild traumatic brain injury? What is post-concussion syndrome?

A

Change in neurologic function (H/A, dizzy, difficulty concentrating)
No identified brain damage if imaging done
Usually resolves within 72 hrs.

Persistent cognitive and physical manifestations

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7
Q

What are manifestations of a cerebral contusion?

A

Brain is bruised
Forceful injury resulting in bruising of a part of the brain
Can present with decreased LOC,vomiting, confusion
More severe than a concussion
Unconsciousness possible
May lie motionless, faint pulse, shallow breathing, pale skin
Bladder and bowel incontinence
Presents similar to shock (low BP)
Varying outcomes

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8
Q

What is a diffuse axonal brain injury?

A

Widespread shearing injury of axons
Usually from a severe forceful rotational force
Imaging will not reveal the injury
Results in coma

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9
Q

What is a intracranial hemorrhage?

A

Collection of blood in the epidural, subdural, or intracerebral space

Chronic subdural or subacute bleeding; the manifestations are delayed for weeks to mont

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10
Q

What is an epidural hematoma? Manifestations? Is it an emergency? Treatment?

A

Blood collection in the space between the skull and the dura, usually a result from an impact to thetemple area

Client may have a brief loss of consciousness with return of lucid state; then, as hematoma expands, increased ICP will often suddenly reduce LOC

An emergency since arterial bleeding will rapidly expand!

Treatment includes measures to reduce ICP, remove the clot, and stop bleeding
Burr holes or craniotomy, IV mannitol, or 3% N/S
Client will need monitoring and support of vital body functions and respiratory support

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11
Q

What is a subdural hematoma? Who are they commonly seen in? What are manifestations of an acute subdural hematoma? Subacute? Chronic?

A

Collection of blood between the dura and the brain

Common in elderly, especially with use of anticoagulants
Bleeding is from bridging veins that tear easily in elderly clients

Acute: symptoms develop over 24 to 48 hours
Changes in LOC, pupillary signs, hemiparesis, confusion, ataxia

Subacute: symptoms develop over 48 hours to 2 weeks
Requires immediate craniotomy for drainage and control of ICP

Develops over weeks to months
Causative injury may be minor and forgotten
Clinical signs and symptoms may fluctuate
Severe HA, intermittent; alternating focal neurologic signs; personality changes; mental deterioration; focal seizures
Treatment is evacuation of the clot

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12
Q

What is an intracerebral hemorrhage? Causes? Most common cause? Treatment?

A

Hemorrhage occurs into the substance of the brain

May be due to trauma or a nontraumatic cause
HTN, aneurysm, tumors, bleeding disorders, anticoagulant therapy

Most common cause is chronic hypertension

Treatment
Supportive care
Control of ICP
Administration of fluids, electrolytes, and antihypertensive medications
Craniotomy or craniectomy to remove clot and control hemorrhage unless area is inaccessible

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13
Q

What should always be assumed with any traumatic brain injury? Treatment for increased ICP includes what measures? What are the supportive measures?

A

cervical spine injury until ruled out

Adequate oxygenation
Elevating HOB
Maintaining normal blood volume
Drain CSF if needed
Mannitol IV or 3% N/S IV
Hyperventilation with ventilator

Ventilator
Seizure prevention
Fluids and electrolyte maintenance
Nutritional support
Management of pain and anxiety

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14
Q

What is the priority assessment with a brain injury? What other 2 primary assessment should be monitored regularly?

A

ABCDs (priority assessment)
Assess airway, breathing, circulation to ensure oxygenated blood is feeding the brain
Brain injury or death occurs within 3 to 5 minutes of hypoxia
Changes in LOC using the GCS provide the earliest indication of neurologic deterioration

Cranial nerve function
Eye blink response, tongue and shoulder movement
Assess pupils for size, equality, and reaction to light

Bilateral sensory and motor response

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15
Q

What are nursing interventios with head injuries?

A

Maintain c-spine precautions until cleared by x-ray or clinically

Report presence of CSF from the nose or ears to the provider

Monitor fluid, electrolytes, and osmolality to detect changes in sodium regulation (DI or SIADH)

Provide adequate fluids to maintain cerebral perfusion pressure

When giving large amounts of IVF, monitor for fluid overload and cerebral edema

Maintain safety and seizure precautions

Assess/monitor respiratory status, cranial nerve function, and bilateral sensory and motor responses

Support the client’s family- coping can be difficult
If brain death occurs, support the family when deciding whether to donate organs

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16
Q

What are the 3 cardinal signs of brain death?

A

coma
absence of brain stem reflexes
apnea

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17
Q

What is a spinal cord injury? What can be the result of a C-spine injury? T1 or below injury? C4 or above injury?

A

Involve the loss of motor function, sensory function, reflexes, and control of elimination
Level of injury dictates the consequence

C-spine injuries can result in quadriplegia

T1 or below injuries can result in paraplegia

C4 or above injuries can result in impaired ventilation d/t involvement of phrenic nerve

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18
Q

What is primary and secondary SCI?

A

Primary injury is the result of the initial trauma and usually permanent

Secondary injury resulting from SCI include edema and hemorrhage

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19
Q

What constitutes the autonomic nervous system? What can occur with injury to the SC from above T6?

A

Sympathetic chain of nerves is mainlyadjacent to the thoracic spinal cord

Spinal injuries above T-6 can result in neurogenic shock from sympathetic chain injury

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20
Q

What is spinal shock? What is the cause? Manifestations? How long can the loss last?

A

A sudden, but temporary loss of all reflexes and autonomic function below the level of spinal injury

The loss of reflexes, motor and sensation are all directly related to the spinal cord injury not the sympathetic nervous system

Muscular flaccidity and lack of sensation and absent deep tendon reflexes
Loss of sensation below the spinal cord injury level
Paralytic ileus from the loss of autonomic function

Loss of reflexes can last days to weeks, then become hyper-reflexic

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21
Q

What is neurogenic shock? Manifestations? Timeframe? Treatment?

A

Sudden loss of communication within the sympathetic nervous system with a SCI

Blood pressure & heart rate decrease, and cardiac output decreases
Venous pooling occurs due to peripheral vasodilation
Paralyzed portions of the body do not perspire because sympathetic activity is damaged- watch for early detection of fever

Can occur within 24 hours of injury and can last for several weeks

Keeping the mean arterial pressure at least 85 mm Hg can prevent further damage
Administer IV isotonic fluids (N/S or L/R)
Norepinephrine IV may be required

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22
Q

What are nursing actions when treating neurogenic or spinal shock?

A

Spinal shock and neurogenic shock often occur together following a SCI

Stabilize the spinal cord with proper positioning/ immobilizing

Monitor/assess: VS, temp, respiratory status, I&O, neuro status, muscle strength and tone, sensation, GI/GU function, and dependent edema

Treat with appropriate medications (vasopressors such as norepinephrine or atropine to increase HR) and IV fluids

Monitor for skin breakdown and ulcer formation

Client is at greater risk for venous thromboembolism (VTE)
Monitor for manifestations such as leg swelling, areas of warmth and/or tenderness
Administer anticoagulants as prescribed for DVT prophylaxis

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23
Q

What is a common complication of SCI? Cause?

A

orthostatic hypotension

Caused by an interruption in functioning of the autonomic nervous system and pooling of blood in lower extremities when in an upright position

*Change positioning slowly
*Use a reclining wheelchair
*Use thigh-high hose or elastic wraps to increase venous return that may extend all the way up the client’s leg and include the abdomen

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24
Q

What are nursing care actions relating to muscle strength and tone? What type occurs with acute injury? What about later stages? What is the risk in later stages? Treatment?

A

Determine baseline and monitor for increased loss of muscle strength

Encourage active ROM and assist if the client lacks all motor function

Flaccid type of paralysis following acute injury

Spastic muscle tone in later stages
If severe, they can develop pressure injuries

Administer muscle relaxants (baclofen and dantrolene) for severe spasticity
Monitor for drowsiness and muscle weakness

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25
Q

What type of injuries can result in a spastic neurogenic bladder? How is it managed for both males and females? What type of injueris can result in a flaccid neurogenic bladder? How is it managed?

A

upper neuron injuries in the brain

Males use a condom catheter and micturition reflex stimulation (tugging on the pubic hair)
Females use an indwelling urinary catheter d/t unpredictable urine release

lower neuron injuries in the spinal nerves

Males’ and females’ interventions include intermittent catheterization and Crede method (downward pressure placed on the bladder to manually express the urine)

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26
Q

What are nursing actions to maintain skin integrity when dealing with SCI?

A

Change position every 2 hours, every 1 hour if in wheelchair

Pressure ulcers can develop within 6 hours

Monitor Cervical collars- skin breakdown under chin, on the shoulders, and at the occiput

Use pressure relief devices continuously

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27
Q

What is autonomic dysreflexia? Triggers? Why is it an acute emergency? What types of SCI can result in this complication?

A

An abnormal, overreaction of the involuntary (autonomic) nervous system to astimulus
The stimulus causes an overreaction by the injured sympathetic systemand an attempt to compensate by the parasympathetic system

Sympathetic stimulation is usually caused by a triggering stimulus in the lower part of the body
Distended bladder
MOST COMMON CAUSE
CHECK PATENCY OF FOLEY CATHETER
Distention or contraction of visceral organs
Such as constipation
Stimulation of the skin by a compressive dressing or a skin infection

because of the resulting extreme hypertension

SC lesion above T6

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28
Q

What are symptoms of autonomic dysreflexia?

A

Extreme hypertension
Severe pounding headache- Why? What is the risk?
Pallor below the level of SC lesion’s dermatome
Flushing and profuse diaphoresis above the spinal level of lesion
Blurred vision
Restlessness
Nausea
Nasal congestion
Bradycardia

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29
Q

What are nursing action for autonomic dysreflexia?

A

Place client in sitting position immediately- this is priority!

Notify the healthcareprovider

Determine and treat the cause
Check patency of urinary catheter or insert catheter for distended bladder
Remove fecal impaction
Assess for injury (skin, fractures, infection)
Remove tight clothing
Adjust room temperature and block drafts

Monitor VS
Administer antihypertensives (nitrates or hydralazine)

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30
Q

What is a halo traction/cervical tong? Nursing actions?

A

Provides traction and or immobilizes the spinal column

Nursing actions
Maintain body alignment and ensure weights hang freely
Monitor skin integrity- assessing under the vest
Provide pin care
Do not use the device to turn or move the client
Good skin care- dry, no powder
Teach vest care- liner should not get wet, liner should be changed periodically

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31
Q

What is a decompressive laminectomy? Nursing actions?

A

Decompressive laminectomy removes a section of lamina, removes bone fragments, foreign bodies, or hematomas that can place pressure on the cord
Donor bone is often obtained from the iliac crest and is used to fuse the vertebrae together
Paravertebral rods are used to immobilize several vertebral levels

Assess for airway compromise from swelling or hemorrhage with cervical fusions
Assess neurological status and VS every hour the first 4 hrs. post op

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32
Q

What is menigitis? What are the 3 types and common conditions that cause them?

A

Inflammation/infection of the meninges which cover brain and spinal cord

Types
Bacterial- a contagious infection with ahigh mortality rate
Otitis media, sinusitis can spread to meninges

Viral- the most common form that usually resolves without treatment
Measles, mumps, herpes, West Nile virus

Fungal meningitis is common with AIDS or immunosuppression
Cryptococcus neoformans

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33
Q

What are the 3 vaccines that help to prevent meningitis?

A

Hemophilus influenzae type b (Hib)
Infants, 4 doses starting at 2 months of age

Pneumococcal polysaccharide vaccine (PPSV)
Also intended to prevent respiratory infections
For adults who are at risk (immunosuppressed or crowded living conditions)

Meningococcal vaccine (MCV4)
Adolescents prior to living in a college dorm or military base
Recommended at age 11 or 12 with a booster at age 16

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34
Q

What are the manifestations of meningitis?

A

Excruciating, constant headache

Nuchal rigidity (stiff neck)

Altered level of consciousness

Positive Kernig sign- thigh flexed on abdomen, can’t fully extend

Positive Brudzinski sign- with neck flexed, flexion of knees and hips is produced

Fever and chills

Nausea and vomiting

Behavioral changes

Photophobia

Hyperactive deep tendon reflexes

Tachycardia

Seizures

Red macular rash (petechiae)

Restlessness, irritability

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35
Q

How is meningitis accurately diagnosed? What does the appearance of spinal fluid indicate? What will labs indicate?

A

lumbar puncture

Cloudy: bacterial
Clear: viral

Elevated WBC
Elevated protein
Decreased glucose: bacterial
Elevated CSF pressure

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36
Q

What are isolation precaustions for meningits?

A

Isolate the client as soon as meningitis is suspected!

Droplet precautions

Continue precautions until antibiotics have been administered for 24 hrs. and secretions are no longer infectious.

Those with bacterial meningitis may need precautions continuously. Follow hospital policy.

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37
Q

What are nursing actions when treating meningitis?

A

Monitor VS and assess for septic shock

Implement fever-reduction measures

Bedrest with HOB at 30°

Monitor for increased ICP. Avoid increasing ICP

Seizure precautions

Provide a calm and quite environment with dim lights

Report meningococcal infections to the public health department

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38
Q

What are meds used with meningitis?

A

Ceftriaxone or cefotaxime in combination with vancomycin
Given until C&S results are available
Early administration of high doses of appropriate IV antibiotics for bacterial meningitis

Phenytoin
Anticonvulsant if ICP increases or the client has a seizure

Acetaminophen, ibuprofen
Analgesic for HA and/or fever
Prefer nonopioids to avoid masking changes of LOC

Prophylactic antibiotics (ciprofloxacin, rifampin) for those in close contact with the client

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39
Q

What are complications related to meningitis?

A

Increased ICP
Leads to brain herniation and death
Monitor signs of increased ICP and treat with mannitol

SIADH
Monitor blood and urine labs (serum Na, and urine specific gravity)
Provide interventions such as demeclocycline and restrict fluids
Daily weights

Septic emboli
Can occur in the hands and feet
Lead to gangrene and DIC

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40
Q

What is a brain abscess? Who is at riak? Prevention? Diagnostics?

A

Collection of infectious material within brain tissue

Risk is increased in immunocompromised clients

Prevent by treating otitis media, mastoiditis, sinusitis, dental infections, and systemic infections promptly

Diagnosis by MRI or CT
CT-guided aspiration is used to identify the causative organisms

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41
Q

What are S/S of a brain abscess? Managment? Nursing care?

A

Headache that is usually worse in the morning
Fever
Vomiting
Neurologic deficits- weakness, decreasing vision
Signs and symptoms of increased ICP- decreasing LOC and seizures

Control ICP
Drain abscess
Antibiotic therapy
Treat cerebral edema- corticosteroids

Conduct frequent and ongoing neurologic assessment and responses to treatment
Ensure client safety and protect from injury
Provide supportive care
Monitor for neurologic deficits

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42
Q

What is encephalitis? Causes? S/S? Medical management? Nursing care?

A

Acute, inflammatory process of the brain tissue

Causes
Viral infections
HSV
West Nile
St. Louis
Fungal infections

Headache
Fever
Confusion
Changes in LOC
Vector-borne rash
Flaccid paralysis
Parkinson-like movements

Acyclovir for HSV infection
Amphotericin B and/or other antifungal agent for fungal infection
Control seizures
Control ICP

Frequent and ongoing assessment
Dim lights
Limit noise
PRN pain meds
Use cautiously- may mask neuro symptoms
Monitor intake and output- be alert for presence of renal complications from antiviral therapy
Monitor for seizures

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43
Q

What is MS? Where are the most common locations of damage?

A

A chronic progressive immune-related demyelination disease of the CNS
Demyelination interrupts the flow of nerve impulses
Plaques can occur on axons
Unable to regenerate and causing irreversible damage

Most common areas include optic nerve, cerebrum, brainstem, cerebellum, and spinal cord

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44
Q

What are S/S of MS?

A

Fatigue
Weakness
Numbness
Difficulty in coordination
Loss of balance
Pain or paresthesia
Visual disturbances
Difficulty with speech
Muscle spasticity
Bowel and bladder dysfunction
Cognitive dysfunction
Sexual dysfunction

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45
Q

What is nursing care with MS?

A

Monitor the following
Visual acuity
Speech patterns
Swallowing
Activity intolerance
Skin integrity
Urinary incontinence

Discuss coping mechanisms and resources

Encourage fluid intake and other measures to decrease the risk of UTI
Assist with bladder elimination
Establish a voiding time schedule
Every 1.5 to 2 hours

Monitor cognitive changes

Plan interventions to promote cognitive function

Reorient as needed, place objects used in routine places

Use a communication board as needed

Apply eye patches to treat diplopia
Alternate eyes every few hours
Teach scanning technique

Exercise and stretch affected muscles

Balance activity and rest

Maintain a safe environment- fall risk!
Walk with feet apart- widen base of support
Watch the feet while walking

46
Q

What are meds used with MS, MOA and AEs?

A

Interferons beta-1a and beta-1b (injections)
Start early in the course of disease
Used to prevent and treat relapses
Adverse effects: flu-like symptoms

Corticosteroids (prednisone, dexamethasone, methylprednisolone)
Reduce inflammation in acute exacerbations (very high doses used)
Adverse effects: infection, hypervolemia, hypernatremia, hypokalemia, hyperglycemia, GI bleeding, and personality changes, insomnia, weight gain

Antispasmodics (dantrolene, baclofen, diazepam) for muscle spasticity

Anticonvulsants (carbamazepine, gabapentin, pregabalin) is used to treat paresthesia

Anticholinergics (oxybutynin, tolterodine) is used for bladder dysfunction

47
Q

What is myasthenia gravis?

A

Impaired transmission of impulses across the neuromuscular junction

Loss of acetylcholine receptors on muscles due to autoimmune destruction

Considered a motor disorder- varying degrees of weakness of the voluntary muscles

48
Q

What are S/S of myasthenia gravis? Most concerning symptom?

A

Symptoms frequently occur in the face
Diplopia
Ptosis
Weakness of facial muscles
Dysphonia- caused my laryngeal involvement
Dysphagia- increased choking and aspiration
Generalized weakness- affects extremities, intercostal muscles whichleads to respiratory failure

Most concerning symptom with a new diagnosis is shortness of breath, or increasing work of breathing from respiratory muscle weakness

49
Q

What is medical management of myasthenia gravis?

A

Pharmacologic Therapy: (2 parts to medication treatment)
Anticholinesterase meds- inhibits breakdown of acetylcholine (pyridostigmine)
Immunosuppressant meds: an autoimmune disease (azathioprine, cyclosporine)

Therapeutic Plasma Exchange (Plasmapheresis)
Exchange of plasma
Reduces the number of antibodies circulating in the bloodstream
Temporary relief from symptoms- few weeks

Surgery
Thymectomy- removal produces antigen-specific immunosuppression and clinical improvement
Frequently done to control myasthenia gravis long-term

50
Q

What is nursing care with myesthenia gravis?

A

Medication management- understanding actions of meds and schedule of taking them
Conservation of energy- identify times of rest throughout the day
Risk of aspiration- meals should coincide with peak effects of anticholinesterase meds
Impaired vision- tape eyes closed for short periods, artificial tears, eye patches
Avoid factors that exacerbate symptoms- emotional stress, infections, rigorous activity, heat
Support groups

51
Q

What is a myasthenic crisis relating to MG?

A

Result of disease exacerbation or a precipitating event, most commonly a respiratory infection
THE COMMON COLD!!!

Severe generalized muscle weakness with respiratory distress or failure

Monitor for any shortness of breath, tachypnea, or increased work of breathing

Client is admitted to ICU and closely monitored

52
Q

Whatis guillain barre syndrome? S/S

A

Autoimmune disorder with acute attack of peripheral nerve myelin sheath
Rapid demyelination of peripheral nerves starting in legs and arms
Ascending weakness
May produce respiratory failure and autonomic nervous system dysfunction with CV instability (changes in BP,HR)
Most often follows a viral infection

Muscle weakness
Muscle paralysis
Paresthesias
Pain
Diminished or absent reflexes that start in the lower extremities and progress upward
Cranial nerve syndromes (peripheral nerves)
Changes in vital signs- vagus nerve affected- tachycardia, bradycardia, hypertension, orthostatic hypotension

53
Q

What causes bells palsy? manifestation? What is the diffence in manifestations of bells palsy and a stroke?

A

Facial paralysis caused by unilateral inflammation of the seventh cranial nerve

unilateral facial muscle weakness or paralysis with facial distortion,decreased lacrimation, and painful sensations in the face; may have difficulty with speech and eating due to weak muscles,increased sound sensitivity, loss of taste to affected side, increasedtearing (loss from eye leading to dry eye), and decreased saliva production

bells palsy includes forehead, stroke does not

54
Q

What are diagnostic measures for brain tumors? What are risks and benefits of a biopsy?

A

CT, MRI, PET scan, cerebral angiogram
Determines size, location and extent of the tumor

Cerebral biopsy
Usually guided by CT or MRI scan
Abnormal cerebral tissue is sent to pathology

Benefits-minimally disruptive to the rest of the brain, decreased recovery time, and not associated with risk of an open craniotomy
Negative- does not remove or debulk the tumor, results can be inconclusive, and possible misdiagnosis

55
Q

What are brain tumor meds and managment?

A

Non-opioid analgesics
Avoid opioids as they can decrease LOC

Corticosteroids (dexamethasone)
Reduce cerebral edema
Relieves headaches, improves LOC

Osmotic diuretics (mannitol)
Decrease fluid content of the brain
Decreases ICP

Anticonvulsant medication (phenytoin)
Control and prevent seizures

H2-antagonist (famotidine)
Decreases the risk of stress ulcers

Antiemetics (ondansetron)

Radiation/chemotherapy
Craniotomy (if surgery is possible)

56
Q

What is parkinsin’s disease?

A

Slowly progressing and debilitating disorder of movement
Decreased levels of dopamine which allows acetylcholine to dominate in substantia nigra

57
Q

What are assessment findings of parkinson’s?

A

Four primary findings
Tremor/pill-rolling tremor of fingers
Muscle rigidity
Bradykinesia
Postural instability/stooped posture

Fatigue
Slow, monotonous speech
Masklike facial expression
Difficulty chewing and swallowing
Drooling
Dysarthria
Mood swings
Cognitive impairment/dementia (late)
Autonomic findings
Orthostatic hypotension
Flushing
Diaphoresis

58
Q

What are the 2 main meds and MOAs for parkinson’s? Signs of toxicity?

A

Levodopa (dopaminergic) is converted to dopamine in the brain
Carbidopa protects levodopa from being metabolized before it reaches the brain
Allows for smaller doses and less adverse effects

Muscle twitching
Facial grimacing
Spasmodic eye winking

59
Q

What are other med treatmens for parkinson’s? AEs?

A

Dopamine agonists (pramipexole)
Combine with dopaminergic for better results
Adverse effects: orthostatic hypotension, dyskinesias, and hallucinations

Anticholinergics (benztropine)
Decrease tremors and rigidity
Adverse effects: anticholinergic effects

COMT inhibitors (entacapone)
Decrease the breakdown of levodopa
Adverse effects: dark urine, diarrhea

MAO-B inhibitors (selegiline)
Reduce the wearing off phenomenon
Avoid foods high in tyramine- can cause hypertensive crisis

60
Q

What are therapeutic procedures for parkinson’s?

A

Stereotactic pallidotomy or thalamotomy
When clients are unresponsive to other therapies
Causes destruction of a small portion of the brain

Deep brain stimulation
Electrode is implanted in the thalamus
Current is delivered through a small pulse generator implanted under the skin of the upper chest
Decreases tremors and involuntary movements

61
Q

What is Huntington’s disease? Pathology? S/S?

A

A chronic progressive hereditary (autosomal dominant) disease that results in choreiform movement and dementia

Pathology involves premature death of cells in the striatum of the basal ganglia (control of movement) and the cortex (thinking, memory, perception, judgment)
Occurs at midlife (30-50)

Chorea
Intellectual decline
Emotional disturbance
Uncontrollable movement
Tics and grimaces
Speech problems- slurred, hesitant, explosive
Dysphagia- risk for aspiration
Disturbed gait with eventual bedrest
Impaired judgment and memory
Anger, dementia, and psychosis eventually ensue

62
Q

What are the 3 stages of alzheimer’s?

A

Three general stages
Mild Alzheimer
Stages 1-3
ModerateAlzheimer
Stages 4 and 5
Severe Alzheimer
Stages 6 and 7

63
Q

What are pharmaceutical management of AD?

A

Antipsychotics
Antidepressants
Anxiolytics
AD Medications may temporarily improve activities of daily living
Donepezil prevents the breakdown of acetylcholine
Memantine blocks nerve cell damage caused by excess glutamate
Adverse effects: frequent stools,upset stomach, and dizziness/headache, unsteady gait

64
Q

What is ALS?

A

amyotropic lateral sclerosis (Lou Gehrig)

Unknown cause
Progressive illness
Loss of motor neurons in the anterior horn of the spinal cord and loss of motor nuclei of the lower brainstem
Occurs most between 40 and 60 years of age

65
Q

What are S/S of ALS?

A

Fatigue
Progressive muscle weakness
Cramps
Fasciculations (twitching)
Incoordination
Difficulty in talking
Difficulty in swallowing
Difficulty in breathing

66
Q

What is the patho of muscular dystrophies?

A

Incurable disorders characterized by progressive weakening and wasting of skeletal and voluntary muscles
Most are inherited disorders
Muscle tissue is replaced with connective tissue

67
Q

How do disc herniations manifest? Medical managment? Nursing care?

A

Cervical disc herniation (cervical radiculopathy)
Lumbar disc herniation (sciatica)
Spondylosis- degenerative changes in disc and adjacent vertebral bodies
Paresthesia- numbness, tingling, pins & needles
Pain and stiffness in the neck and shoulders
Low back pain, especially with activity
Postural deformity

Medications- analgesics, NSAIDs, muscle relaxers, corticosteroids
Surgery- discectomy with or without fusion

Nursing Management
Relief of pain
Improve mobility
Monitor for bleeding / hematoma (following surgery)
Frequent neuro checks- spinal cord compression may produce rapid or delayed onset of paralysis
Monitor for dysphagia- anterior approach cervical surgery

68
Q

What is client positioning with disc herniation?

A

side-lying with pillow between legs
supine with pillow under lower legs

69
Q

What is the CNS? PNS? ANS?

A

Central nervous system
Brain and spinal cord
Peripheral nervous system

Includes cranial and spinal somatic nerves (motor and sensory) and the Autonomic nervous system

70
Q

What is the ANS? Sympathetic? parasympathetic? what regulates these systems?

A

Functions to regulate activities of internal organs and to maintain and restore internal homeostasis

Sympathetic nervous system
“Fight or flight” responses
Main neurotransmitter is norepinephrine
Sympathetic divisionis mainly from the thoracic sympathetic ganglion

Parasympathetic nervous system
“Rest and digest” responses
Controls mostly visceral functions
Parasympathetic division is mainly from cranial nerves and sacral nerves

Regulated by centers in the spinal cord, brainstem, and hypothalamus

71
Q

A neurologic assessment is assessing the health history of what manifestations? It includes assessment of what systems?

A

Pain
Seizures
Ataxia (abnormal balance or movement) and vertigo (illusion of movement, usually rotation)
Visual disturbances
Weakness
Abnormal sensations
Past health, family, social history

Consciousness and cognition
Cranial nerves
Motor system
Sensory system
Reflexes

72
Q

What are the cranial nerves? Mneumonic?

A

1 olfactory
2 optic
3 oculomotor
4 trochlear
5 trigeminal
6 abducens
7 facial
8 vestibulocochlear
9 glossopharyngeal
10 vagus
11 accessory
12 hypoglossal

Some Say Marry Money, But My Brother Says Big Boobs Matter Most

73
Q

Where does the spinal cord end?

A

T12-L1

74
Q

What are concerns for CT contrast administration?

A

Allergies to shellfish/iodine
Assess BUN and Cr
NPO 4 hours prior for contrast
Monitor for allergic reaction
Flushing out contrast by increasing PO fluids
Stop metformin prior to IV contrast

75
Q

What is a PET scan and a SPECT? What do they do? How is this accomplished?

A

positron emission tomography
single photon emission computed tomography

Both are nuclear imaging exams
Produce 3D images of static (depicting vessels) or functional (brain activity)
Determines tumor activity and/or response to treatment
Determines dementia (the brain does not respond to the tracer)
Both use radiation

PET
Glucose-based tracer is injected into the blood stream prior  initiates regional metabolic activity  documented by PET scanner
SPECT
Uses a radioisotope to initiate metabolic activity

76
Q

What is MRI? What does it do and by what means? What can it identify?

A

magnetic resonance imaging

Cross sectional images
Images are obtained using magnets (not radiation)
Safe for pregnancy
Not compatible with some artificial devices (pacemakers,surgical clips,any metallic objects)
Use MRI-approved equipment to obtain VS and provide ventilation/oxygen

Done with or without contrast
Capable of discriminating soft tissue from tumor or bone
Determine tumor size and blood vessel location

77
Q

What is cerebral angiography? What does is assess? What can is be used for? Nursing actions?

A

Looks at circulation to the brain with a contrast agent

Assesses narrowing of vessels, aneurysms, strokes, vascularity of tumors

Used to inject medications to treat blood clots or administer chemo
Contrast agent is injected into the femoral or carotid artery

Nursing Actions
NPO 4 to 6 hours prior
Assess BUN and Cr
Determine history or bleeding or anticoagulant use
Hydrate before procedure
Void immediately before procedure
Mild sedation for relaxation can be used
Warmth in face, behind eyes or in mouth, and metallic taste with dye injection
Frequent neuro checks after the exam (embolism/arterial dissection)
Assess puncture site (bleeding/hematoma) and circulation
Activity restriction
Ice pack to insertion site

78
Q

What is an EEG? What does it do?

A

electroencephalography

A non-invasivetest
Assesses the electrical activity of the brain
Most done to assess for seizure disorders
Also used to evaluate sleeping disorders and behavioral changes
Used to determine brain death

79
Q

What is pre, intra, post nursing procedures with an EEG?

A

Preprocedural
Review medications
Client education: wash hair, stay awake the night before the test (to achieve sleep-deprivation which can induce a seizure), during the exam you might be exposed to flashing lights or asked to hyperventilate for 3-4 minutes, and avoid sedating or stimulant medications 24 hrs. prior

Intraprocedural
Procedure takes 45 to 120 minutes
Small electrodes are placed on the scalp
Notations are made when stimuli is present

Postprocedural
Resume normal activities

80
Q

What is the location of a lumbar puncture? What are its therapeutic uses? What are some results from CSF analysis and what could they potentially indicate?

A

Spinal tap- L3/L4, L4/L5 as spinal cord ends L1, small amount of CSF is removed

Can determine disease processes (MS, meningitis,syphilis)
Also used to reduce ICP by removing fluid, instill contrast media for imaging,or administer chemotherapy directly to central nervous system for malignancies

Obtain CSF samples for analysis
Clear vs. pink-tinged (bleeding in brain)
Cell count (WBC elevated with inflammation/infection)
Culture (viral cultures for encephalitis, bacterial cultures for meningitis)
Glucose (reduced with bacterial infection)
Protein (elevated with MS, Guillain-Barre syndrome, and infections)

81
Q

How long should client be flat after a limbar puncture? what are possible complications?

A

4-8 hrs

Brain herniation due to removal of fluid with high ICP
Spinal hematoma compression of cauda equina and paralysis
Infection introduction of the spinal canal
Post- LP headaches

82
Q

How is the Glasgow coma scale measured?

A

Eye opening
4 spontaneous
3 to sound
2 to pain
1 none

verbal
5 coherent and oriented
4 incoherent and disoriented
3 makes no sense
2 sounds, not words
1 none

motor
6 follows commands
5 local reaction to pain
4 withdraws from pain
3 decorticate posture
2 decerebrate posture
1 none

83
Q

What is decorticate posturing? Think core

A

elbows flexed on chest, arms adducted to sides, legs internally rotated, feet flexed

84
Q

What is decerebrate posturing?

A

arms adducted and extended, hand flexed, feet flexed

85
Q

What is the normal intracranial pressure range?

A

10-15 mmHg

86
Q

What does the HTN component of cushing triad look like?

A

systolic increased
diastolic decreased

87
Q

What is cerebral perfusion pressure? Equation? Normal range? Range of brain damage?

A

CPP is closely linked to ICP
CPP is determined by mean arterial pressure minus intracranial pressure
Provides an estimation of the blood pressure that allows blood to flow to brain

CPP = MAP – ICP

Normal CPP is 70 to 100 mm Hg
A CPP of less than 50 results in permanent damage

88
Q

What are nursong acctions with a craniotomy?

A

Administer mannitol and dexamethasone every 6 hrs. for 24 to 72 hrs. post-op to reduce ICP and cerebral edema

Administer phenytoin or diazepam to prevent seizure activity

Monitor ICP

Supratentorial surgery
Maintain HOB of at least 30° with proper body positioning to prevent increased ICP

Infratentorial
Keep client flat and on either side for 24 to 48 hrs. to prevent pressure on the neck incision site

Maintain a calm environment
Provide emotional support (brain surgery is an extremely fearful procedure)

89
Q

What are 5 types of seizures?

A

Tonic-clonic seizure
Breathing can stop, cyanosis, biting, incontinence
Period of confusion and sleepiness follows the seizure

Tonic seizure
Sudden increased muscle tone, loss of consciousness, and autonomic manifestations (vomiting, incontinence, salivation)

Clonic seizure
Muscles contract and relax, can last several minutes

Myoclonic seizure
Brief jerking or stiffening of the extremities for few seconds

Atonic or akinetic seizure
Muscle tone is lost, clients frequently fall
Confusion follows the seizure

90
Q

What is a partial or focal seizure? What are the 2 types and how do they manifest?

A

Involves only one side of the hemisphere

Two types
Simple partial
Consciousness is maintained
Can cause unusual auras as well (sense of déjà vu, offensive smell)
Results in focal symptoms such as movement of an arm or leg

Complex partial
Associated with automatisms (unaware of lip smacking or picking at clothes)
Can cause a loss of consciousness or black out for several minutes
Amnesia can occur immediately before and after

91
Q

What are risk factors for seizures?

A

Genetic predisposition
Cerebrovascular disease
Hypoxemia
Fever (childhood)
Head injury
Cerebral edema
Hypertension
Central nervous system infections like encephalitis or meningitis
Metabolic (hypoglycemia or hyponatremia)
Brain tumor
Drug and alcohol withdrawal
Allergies
Abrupt cessation of antiepileptic drugs
Toxins
Stroke
Heart disease
Fluid and electrolyte imbalances

92
Q

What is status epilepticus? Causes? Complications? Treatment?

A

Repeated seizure activity within a 30-min time frame without full recovery or a single,prolongedseizure lasting more than 5 minutes (ATI, 2023)
Medical emergency to stop the seizure (prevent hypoxemia/ischemia to brain)

Usual causes
ETOH withdrawal, sudden withdrawal from antiepileptic drugs, head injury, cerebral edema, infection, metabolic disturbances

Complications
Decreased oxygen levels, inability to return to normal functioning, and continued assault on neuronal tissue

Treatment
ABC, oxygen, IV access, ECG, and O2 sat monitoring
IV/IM diazepam or lorazepam followed by IV phenytoin infusion

93
Q

What are the stages of a migraine with aura (classic migraine)

A

Prodromal phase- awareness of symptoms before onset of headache (irritability, depression, food cravings, diarrhea, constipation, frequent urination); often hours to days prior to headache

Aura stage- numbness/tingling, confusion, visual disturbances; minutes to hours prior to headache. Can be confused with a stroke due to initial neurological symptoms

Second stage- severe throbbing headache that intensifies over several hours, NVD, vertigo, photophobic, and phonophobia

Third stage- dull headache that lasts 4 to 72 hrs.

Recovery- with pain and aura subsiding, muscles ache, physical activity worsens pain

94
Q

What is pharm treatment for mild migraines? Severe?

A

NSAIDs (ibuprofen, naproxen) or acetaminophen products
Antiemetics such as metoclopramide or ondansetron

Triptans (sumatriptan)
Cause vasoconstriction to treat the migraine HA
Educate the client to notify the provider for continuous or severe chest pain
Contraindicated for those who have a history or are at risk for MI

Ergot alkaloids (ergotamine)
Cause powerful vasoconstriction to control migraine HA
Can cause hypertension,chest pain, and ischemia to fingers and toes
Adverse effects: GI discomfort with nausea and vomiting
Toxicity: paresthesia in fingers and toes, peripheral ischemia
Not for long-term use to avoid physical dependence
Pregnancy category X

95
Q

What is a TIA? How long does it last? What is it indicated could happen

A

transient ischemic attack
Temporary neurologic deficit resulting from a temporary impairment of blood flow

All neurological function returns to normal, usually within minutes to hours

“Warning of an impending stroke” in the future

96
Q

What are the FAST signs of a stroke?

A

Facial drooping (ask client to smile—look for unilateral facial drooping.)

Arm weakness (ask client to raise both arms—look for downward drift.)

Speech impairment or difficulty speaking (ask client to repeat a simple phrase—listen for unexpected findings such as slurred speech.)

Time to call 911 (if any of above findings present, call 911 immediately.)

97
Q

What are the 2 types of stroke?

A

Ischemic
Decreased oxygenation to the brain r/t vascular occlusion from thrombotic or embolic event
Thrombotic stroke:
Occurs secondary to a blood clot on an atherosclerotic plaque
Embolic stroke:
Caused by embolus traveling from another part of the body to a cerebral artery such as atrial fibrillation

Hemorrhagic
Bleeding into the brain from a ruptured artery or aneurysm
Main risk factor is chronic hypertension
Poorer prognosis
Significant ischemia and increased ICP

98
Q

What is the left cerebral hemisphere responsible for? What are manifestations of a LH stroke?

A

responsible for language, mathematics skills, and analytical thinking

Expressive or receptive aphasia (inability to speak or understand language)
Agnosia (unable to recognize familiar objects)
Alexia (reading difficulty)
Agraphia (writing difficulty)
Right hemiplegia (paralysis) and hemiparesis (weakness)
Hemianopsia (loss of visual field)
Slow, cautious behavior
Depression, anger, and quick to become frustrated

99
Q

What is the right cerebral hemisphere responsible for? What are manifestations of a RH stroke?

A

Responsible for visual and spatial awareness and proprioception

Altered perception of deficits
Unilateral neglect syndrome (more common in R)
Loss of depth perception
Poor impulse control and judgment
Left hemiplegia or hemiparesis
Hemianopsia

100
Q

What are diagnostic procedure in the event of a stroke?

A

Coagulation panel: PT/INR/aPTT prior to initiating fibrinolytic or anticoagulation medications
12 lead ECG
Doppler ultrasound: (carotid) to determine perfusion to the brain, check for occlusions or blockage
Non-contrast CT scan:
Used emergentlytoassess forstrokes
Perform within 25 minutes of arrival to theED!
Used to determine the type of stroke (ischemic or hemorrhagic) and whether the client is a candidate forthrombotic therapy (t-PA)
Cerebral Angiography:
Outlines the entire vascular tree to the brain
A cerebral CTA is often used (combination of a CT with angiography)
MRI:
Can identify edema, ischemia, and necrosis
Not used emergently since a much longer test to perform
GCS: to assess and follow the level of consciousness (LOC) with acute stroke
Dysphagia screening: Speech-language pathologist can perform a swallowing study

101
Q

What is treatment for an ischemic sroke?

A

Early treatment is important (time is brain tissue)
Thrombolytic therapy (also known as fibrinolytic therapy) if appropriate
Tissue plasminogen activator (t-PA)
Administer within 3 to 4.5 hours of initial manifestations
Only given for ischemic strokes

102
Q

What are therapeutic procedures for ischemic strokes?

A

Thrombectomy (Intra-arterial t-PA administration):
Directly infuses t-PA into occluded artery to dissolve the clot

Endovascular therapy:
With a guidewire system, the clot is removed from occluded artery

Carotid artery angioplasty with stenting (CAS)
Stent is placed to open a blockage
Performed within 6 hours of onset of manifestations

Carotid endarterectomy (if occluded carotid artery)
Removes atherosclerotic plaque in the carotid artery

103
Q

What are nursing actions with strokes?

A

Monitor VS every 1 to 2 hours

Monitor LOC and treat fever which can increase ICP (increase metabolic demands of brain)

Maintain SpO2 >92% if the client has a decreased LOC

Monitor ECG for cardiac dysrhythmias

Conduct a cardiac assessment to detect murmurs and irregularity

Monitor for hyperglycemia which is associated with poor neurologic outcomes

Elevate HOB to at least 30°, prevent extreme flexion/extension of head

Institute seizure precautions

104
Q

What is homonymous hemianopsia? Client instructions?

A

decreased visual field

Instruct the client to use a scanning technique when eating and ambulating
Put items in the room within the client’s view

105
Q

What is the normal CPP? What is the formula to calculate CPP? What would decrease the CPP?

A

cerebral perfusion pressure
70-100 mmHg

MAP - ICP = CPP

a low MAP or high ICP

106
Q

What are early manifestations of elevated ICP?

A

changes in LOC
restlessness, agitation, confusion
weakness in one side
drowsiness
HA increasing in intensity

107
Q

What are the late manifestations of elevated ICP?

A

respiratory and vasomotor changes
projectile vomiting
dixed dilated pupils
seizure coma posturing
changes in VS, Cushing’s triad

108
Q

What incidental circumstances that can elevate the ICP? Nursing actions?

A

increased CO2
suctioning
coughing/straining
neck/hip flexion or extenaion
laying flat, bed less than 30 degrees
constrictive clothing
Valsalva maneuver

HOB 30-45 degrees
keep head and neck still
ventilation
prevent constipation

109
Q

How are seizures aggravated when being monitored with an EEG?

A

sleep deprivation
flashing lights
hyperventilation

110
Q

What med is given IV to stop a seizure? If client is on seizure precautions what should be done ahead of time?

A

benzodiazepine followed by phenytoin

IV access in the event of a seizure

111
Q
A