disorders of the CNS/PNS Flashcards

1
Q

what is meningitis (what, classified, observe for (2))

A

inflammation of the meninges, specifically the arachnoid and Pia mater
- classified by: septic (bacterial), aseptic (viral)
- observe for signs of direct communication to the CNS: otorrhea (ear drainage), rhinorrhea (nasal drainage)

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2
Q

viral meningitis (ASEPTIC) (common/uncommon?, no _____ found in CSF culture, causes (3), _____ _______ more likely to be temp…, treatment?)

A
  • most common type
  • no organisms found from the CSF culture
  • causes: viral, s/d cancer, weakened immune system (HSV-2, VZV, mumps, HIV)
  • neuro deficits more likely to be temporary and full recovery occurs as the inflammation resolves
  • treatment: administration of antiviral agents (via IV to cross blood brain barrier)
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3
Q

bacterial meningitis (SEPTIC) (common/uncommon, fairly high ________…, causes (2), highly _____________, occurs where?

A
  • MEDICAL EMERGENCY!!!
  • fairly high mortality rate, often within 24 HOURS
  • causes: streptococcus pneumoniae, Neisseria meningitidis
  • highly contagious
  • occurs in areas of high population density (first year college students, military, prisons)
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4
Q

what are the increased risk of bacterial meningitis (4)

A
  • tobacco use, upper respiratory viral infection (d/t increased amount droplet production
  • otitis media + mastoiditis (d/t increased risk bacterial meningitis can cross epithelial membrane and enter subarachnoid space)
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5
Q

s/sx meningitis (12)

A
  • headache (steady, throbbing, very severe)
  • fever
  • photophobia (sensitive to light)
  • nuchal rigidity (stiff neck d/t neck muscle spasms)
  • myalgia (muscle aches)
  • N/V
  • confusion/altered LOC
  • rash
  • positive kernig sign
  • positive brudzinski’s sign
  • seizures (d/t irritability of brain)
  • increased ICP (s/d diffuse brain swelling)
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6
Q

positive kernig sign

A

when patient lying with thigh flexed on abdomen, leg won’t completely extend
- B/L = meningeal irritation suspected

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7
Q

positive brudzinski’s sign

A

when patient neck flexed, flexion of knee and hip produced
- when LE passively flexed, similar movement seen on opposite extremity

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8
Q

what are signs of increased ICP (2)

A

decreased LOC
focal motor deficits

(if not attended to): pressure on brain stem -> brainstem herniation -> life threatening event (causes cranial nerve dysfunction + depresses center of vital functions + medulla)

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9
Q

meningitis nursing interventions (7)

A
  • prevention is KEY (vaccination: meningococcal conjugated vaccine, hand washing)
  • monitoring neurological status
  • give broad spectrum antibiotics ASAP and dexamethasone (inflammation), anticonvulsants for seizures, fluid volume expanders for dehydration/shock
  • monitor vascular status
  • maintain droplet precautions for bacterial meningitis (mode of transmission)
  • pain management PRN
  • maintain a quiet, cool, dark room for comfort
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10
Q

encephalitis (what, cause, can be _____ ________ or lead to _______ such as ____(4), ______ _______ causes _______ ____ ________ _______ -> further increase in _____ and potentially death)

A

inflammation of brain issue that affects cerebrum, brainstem, and cerebellum, and surrounding meninges
- cause: viral agent HSV (herpes simplex virus)
- can be LIFE THREATENING or lead to persistent neurological problems (d/t swelling of brain tissue) -> learning disabilities, epilepsy, memory deficits, fine motor deficits
- widespread edema causes compression of blood vessels -> further increase in ICP and possibly death

(local necrotizing hemorrhage that becomes more generalized, followed by edema. Progressive deterioration of nerve cell bodies)

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11
Q

encephalitis nursing interventions (3)

A
  • Prevention is KEY (wear protective clothing in mosquito infested areas)
  • pharmacological: acyclovir (Zovirax), ganciclovir (cytovene) for HSV encephalitis ASAP, pain management (analgesic agents)
  • supportive care: dimming lights, limit noise, ABC’s, educate families, control temp, neuro Q4H

TIP: monitor blood chemistry test results and urinary output (alerts nurse presence of renal complications r/t antiviral therapy)

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11
Q

what is demyelination (what, results in)

A

destruction of myelin - fatty and protein material that surrounds certain nerve fibers in brain and spinal cord
- results in impaired transmission of nerve impulses

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11
Q

multiple sclerosis (what, leading causes of?, characterized by, affects (6), causes ______ and ______ damage?)

A

lifelong inflammatory disease causing demyelination and axonal injury of unknown etiology that affects the brain and spinal cord (affects myelin sheath of CNS -> interrupted transfer of messages
- leading causes of neurological disabilities in young adults
- characterized by periods of remission and exacerbation aka relapsing remitting course
- affects: optic nerves, chiasm, tracts, cerebrum, brainstem, spinal cord
- causes permanent and irreversible damage

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11
Q

encephalitis s/sx (14)

A
  • high fever
  • N/V
  • stiff neck (nuchal rigiditiy)
  • changes in mental status
  • motor dysfunction
  • hallucinations
  • photophobia
  • fatigue
  • increased ICP
  • behavioral changes
  • joint pain
  • headache
  • vertigo
  • focal seizures
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11
Q

s/sx multiple sclerosis (18)

A
  • muscle weakness and spasiticity
  • fatigue
  • intention tremors
  • dysmetria (inability to perform accurate, smooth movements)
  • numbness/tingling sensations
  • hypalgesia (decreased sensitivity to painful stumuli)
  • ataxia (impaired coordination)
  • dysarthria (slurred speech)
  • dysphagia (difficulty swallowing)
  • diplopia (double vision)
  • nystagmus (rapid involuntary eye movement)
  • scotomas (blind spots)
  • decreased visual and hearing acuity
  • tinnitus/vertigo
  • bowel/bladder dysfunction
  • cognitive changes
  • depression
  • alterations in sexual function
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12
Q

multiple sclerosis nursing interventions (goal, 7)

A

Goal: delay progression of disease, manage chronic sx., treat acute exacerbations
- preventing exacerbations
- managing symptoms (rest)
- improve function
- enhance bladder and bowel control (antispasmodics - baclofen, anticholinergics - seroquel, alpha adrenergic blockers - coreg, tamsulosin)
- complementary and alternative therapies
- pharmacological: immunomodulators, anti-inflammatory, steroid, daily analgesic

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13
Q

myasthenia gravis (what, may take many _____ -> ?, types)

A

progressive and acquired autoimmune disease characterized by muscle weakness caused by distorted acetylcholine receptors (AChRs) in the muscle motor end plate membranes
- may take many forms -> mild disturbances of the cranial and peripheral motor neurons to a rapidly developing, generalized weakness that may lead to death from respiratory failure
- 2 types: ocular (affects eyes), generalized (affects other systems)

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14
Q

MG classes (5)

A

1) class 1: any ocular weakness, may have weakness of eye closure; all other muscle strength is normal
2) class 2: mild weakness affecting other than ocular muscles; may also have ocular weakness
3) class 3: moderate weakness affecting other than ocular muscles; may also have ocular weakness
4) class 4: severe weakness affecting other than ocular muscles; may also have ocular weakness
5) class 5: defined by the need for intubation (except when used during routine postoperative management)

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15
Q

myasthenia gravis s/sx (7)

A
  • progressive muscle weakness that worsens with repetitive use and usually umproves with rest
  • fatigue
  • poor posture
  • ocular palsies (decrease muscle strength), ptosis (drooping eyelids), incomplete eyelid closure, diplopia (double vision)
  • dysphagia, voice weakness
  • loss of bowel/bladder control
  • respiratory complications
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16
Q

the tensilon test (what)

A

pharmacologic tests with the cholinesterase inhibitors edrophonium chloride (tensilon) and neostigmine bromide (prostigmin) may be performed
- drug INHIBITS breakdown of ACh at postsynaptic membrane, which increases availability of ACh for excitation of postsynaptic receptors
- 2mg IVP then 8mg IVP after 30 seconds
- within 30-60 seconds, most MG patients show a marked improvement in muscle tone that lasts up to 5 minutes

GOLD STANDARD FOR DIAGNOSIS OF MG

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17
Q

cholinergic crisis (MG)

A

when patient receives TOO MUCH cholinesterase inhibitor drugs (too much ach available)
- tensilon will actually increase weakness and fasciculations around the eyes and face may be seen (HOLD ALL ANTICHOLINERGIC MEDS)

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18
Q

cholinergic crisis s/sx (10)

A

(SLUDGE)
- salivation
- lacrimation
- urination
- diarrhea
- gastrointestinal distress (cramping)
- emesis

  • excessive bronchial mucus production and secretion, miosis (pupils constrict), skeletal muscle spasms/fasciculations
  • bradycardia
  • respiratory failure, flaccid paralysis
  • death CAN OCCUR
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19
Q

cholinergic crisis treatment (2)

A
  • anticholinergics (eg. atropine)
  • benzodiazepines (eg. diazepam)
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20
Q

myasthenia crisis (what)

A

when the patient DOES NOT GET ENOUGH cholinesterase inhibitor drug (too little ACh)
- worsening of muscle weakness, resulting in respiratory failure that requires intubation and mechanical ventilation
- tensilon will result in improved muscle strength

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21
Q

myasthenia crisis s/sx (6)

A
  • generalized weakness
  • severe bulbar (oropharyngeal) weakness
  • mydriasis (dilated pupils)
  • tachycardia
  • respiratory failure
  • death CAN OCCUR
22
Q

myasthenia crisis treatment

A
  • neuromuscular agent (neostigmine) to increase muscle tone and treat MG
23
Q

myasthenic (6) vs. cholinergic crisis (7) vs. both (6)

A

myasthenic:
- increased pulse and respiration
- rise in BP
- bowel/bladder incontinence
- decreased urine output
- absence of cough and swallow reflex
- IMPROVEMENT of symptoms with TENSILON TEST

cholinergic: SLUDGE
- flaccid paralysis
- hypersecretion
- n/v/d
- abdominal cramps
- miosis, blurred vision
- pallor
- WORSENING of symptoms with TENSILON TEST

both:
- apprehension
- restlessness
- dyspnea
- dysphagia
- generalized weakness
- respiratory failure

24
Q

myasthenia gravis nursing interventions (6 including pharmacological (5)

A
  • respiratory support: manually assisted coughing, pulmonary hygiene, suctioning, oral care
  • plasmapheresis (plasma exchange) or IVIG (IV immunoglobulins)
  • improving function: energy conservation s/sx
  • surgery: life long circulatory t cells
  • supportive care: mobility aids, prevent dysphagia, energy conservation

pharmacological:
- anticholesterases/cholinesterase inhibitors (pyridostigmine)
- cholinergic drugs
- immunosuppressive drugs
- corticosteroids
- plasmapheresis

25
Q

plasmapheresis (what, side effects (8))

A

removes circulatory antibodies thought to be responsible for the disease
- plasma is selectively separated and removed from white blood
- 3-4 treatments but may require a second round
- nurses must weigh the patients before and after the procedures and care for the shunt/line

side effects of plasmapheresis:
- citrate-induced hypocalcemia
- urticarial reactions (skin reaction that causes itchy welts/hives)
- depletion coagulopathy (blood can’t coaguate)
- immunoglobulin depletion (
- risk for infection (sepsis through single line)
- fluid shift or depletion
- sensitivity reactions
- site specific complications

26
Q

IV immunoglobulins (IVIG) (what, side effects (2))

A

contains pooled immunoglobulin G (IgG) immunoglobulins from the plasma of approximately a thousand or more blood donors

side effects of IVIG:
- minor discomforts (chills, mild fever, myalgia, headache)
- major complications (anaphylaxis, aseptic meningitis, retinal necrosis, acute renal failure)

27
Q

guillan barre syndrome (what, result of, antibodies attack?, leads to, healing occurs in _____)

A
  • acute inflammatory polyradiculoneuropathy that affects the axons and/or myelin of the peripheral nervous system, causing motor weakness and abnormalities in sensory perception
  • result of IMMUNE MEDIATED PATHOLOGY
  • antibodies attack the myeline sheath that surrounds the axon of the peripheral nerves
  • leads to acsending paralysis: progressive motor weakness starting in legs and spread upwards (respiratory failure)
  • healing occurs in the REVERSE
28
Q

acute guillain barre syndrome stages (3)

A

1) stage 1: acute or initial phase (1-4 weeks)
- begins with onset of first symptoms, ends when no further deterioration occurs
2) stage 2: the plateau period (several days - 2 weeks)
- healing through interventions
3) stage 3: the recovery phase (4-6 months to 2 years)
- thought to coincide with remyelination and axonal regeneration

29
Q

chronic guillian barre syndrome stages

A

some patient do NOT completely recover and have permanent neurologic deficits

30
Q

guillian barre syndrome s/sx motor (5)

A

motor manifestations
- ascending symmetric muscle weakness -> flaccid paralysis without muscle atrophy
- decreased or absent DTRs
- respiratory compromise (dyspnea, diminished breath sounds, decreased tidal volume, reduced SpO2, respiratory failure)
- loss of bowel/bladder control
- ataxia

31
Q

guillian barre syndrome s/sx sensory (2)

A
  • parasthesia
  • pain (cramping)
32
Q

Guillian barre syndrome s/sx cranial nerve manifestation (4)

A
  • facial weakness
  • dysphagia
  • diplopia
  • difficulty speaking
33
Q

guillian barre syndrome s/sx autonomic manifestations (3)

A
  • labile BP
  • cardiac dysthymias
  • tachycardia
34
Q

guillian barre syndrome nursing interventions (7)

A
  • airway management
  • plasmapheresis or IVIG
  • develop similar communication techniques
  • referrals: physical and occupational therapy, speech language pathologist, dietician
  • perform passive ROM exercises Q2-Q4
  • VTE prophylaxis
  • pharmacological: pain med, opioids, gabapentin, TCA (tricyclics)
35
Q

trigeminal neuralgia (what, _____ nature of pain, associated with?)

A

tic douloureux
- chronic pain syndrome characterized by paroxysms of sudden pain in the area innervated by any of the three branches of the fifth cranial nerve
- unilateral nature of pain
- associated involuntary contraction of the facial muscles can cause sudden closing of the eye or twitching of the mouth, hence the former name tic douloureux (painful twitch)

can affect any/all nerves *mainly 3, not BL

36
Q

trigeminal neuralgia assessment (3)

A

1) sudden intense facial pain (spasm like)
- excruciating, sharp, shooting, piercing, burning, jabbing pain (jaw, mandibular division, occular)

2) usually provoked by minimal stimulation of a trigger zone

3) unilateral and confined to the area innervated by the trigeminal nerve

37
Q

trigeminal neuralgia nursing interventions (3, pharmacological (4))

A

pharmacological: anticonvulsant
- AED: carbamazepine (tegretol)
- gabapentin (neurontin)
- pregabalin (lyrica)
- baclofen (lioresal)

  • acupunture
  • surgery (help with neurovascular decompression, radial frequency, thermoregulation)

RISK: infection!

38
Q

bell’s palsy (what, cause, remission?)

A

(facial paralysis)

unilateral inflammation of the 7th cranial nerve, which results in weakness or paralysis of the facial muscles on the affected side
- cause: inflammation triggered by a formerly dormant HSV-1 (cyclivir)
- most patients go into remission within 3 months

39
Q

bells palsy s/sx (6)

A
  • paralysis over 2-5 days on one side
  • pain
  • cannot close the eye, wrinkle forehead, smile, whistle, grimace
  • tearing may stop or become excessive
  • impaired taste
  • tinnitus
40
Q

bells palsy nursing interventions (3, pharmacological 4)

A

pharmacological:
- corticosteroids
- antivirals
- mild analgesics
- artificial tears

  • warm/moist heat
  • massage/exercise
41
Q

brain tumor (what, effects, type of changes resulting in _______(4))

A

occupies space within the skull, growing as a spherical mass or diffusely infiltrating tissue
- effects of brain tumors are caused by inflammation, compression, and infiltration of tissue
- a variety of physiologic changes result, causing any or all of the following:
increased intracranial pressure (ICP) or cerebral edema, seizure activity and focal neurological signs, hydrocephalus, altered pituitary function

42
Q

cerebral tumors s/sx (9)

A
  • headache
  • vomiting unrelated to food intake
  • changes in vision, diplopia
  • hemiparesis or hemiplegia
  • hypokinesia: diminished motor activity
  • hyperesthesia (hyper sensitive to stimuli), paresthesia (pins and needles), decreased tactile discrimination
  • seizures
  • aphasia
  • changes in personality or behavior
43
Q

brainstem tumors s/sx (9)

A

(lower functioning)
- hearing loss (acoustic neuroma)
- facial pain and weakness (CN 5 or trigeminal neurlgia)
- dysphagia, decreased gag reflex (CN 9)
- nystagmus: rapid involuntary eye movement
- hoarseness
- ataxia or dysarthria (cerebellar tumors): difficulty speaking d/t weak muscles
- apnea: stop breathing
- bradycardia
- hypotension

44
Q

brain tumor nursing interventions (5, pharmacological (4))

A
  • surgery
  • radiation
  • assist the patient in compensating for self care deficits (ROM, feeding)
  • improve nutrition (potential nutrition supplementation - protein, lipids, carbs, etc.)

pharmacological:
- chemotherapy: to control tumor growth or decrease tumor burden (doesn’t last)
- analgesics: given for headache (NSAIDs, steroids, antiepileptic)
- steroids: given to control cerebral edema (Dexamethasone - decadron)
- AEDs: to prevent or treat seizures

45
Q

parkinson disease (what, 4 cardinal signs)

A

progressive neurodegenerative disease as a result of DOPAMINE LOSS in the brain
- debilitating disease affecting motor ability and is characterized by four cardinal symptoms:
1) tremors
2) muscle rigidity
3) bradykinesia/akinesia
4) postural instability
- reduces sympathetic nervous system: influences heart and blood vessels

46
Q

parkinson disease stages (5)

A

1) stage 1 (initial stage)
- unilateral limb movement, minimal weakness, hand and arm trembling

2) stage 2 (mild stage)
- bilateral limb involvement, masklike face, slow and shuffling gait

3) stage 3 (moderate stage)
- postural instability, increased gait disturbances

4) stage 4 (severe stage)
- akinesia, rigidity

5) stage 5 (complete ADL dependence_

47
Q

parkinson disease s/sx (posture (2), gait (5), motor (12))

A

1) posture: stooped posture, flexed trunk

2) gait: slow, shuffling, short hesitant steps, propulsive gait, difficulty stopping quick

3) motor:
- bradykinesia
- muscular rigidity
- akinesia
- resting tremors
- “pill rolling” movement
- mask- like face
- difficulty chewing and swallowing
- uncontrolled drooling
- fatigue
- difficulty changing positions
- reduced arm swing on one side of the body when walking
- micrographia (small handwriting effects)

48
Q

parkinson disease s/sx (speech (5), autonomic dysfunction (7), psychosocial (8))

A

4) speech: soft, low pitched voice, dysarthria, echolalia, hypophonia

5) autonomic dysfunction: orthostatic hTN, excessive perspiration, oily skin, seborrhea, flushing, changes in skin texture, blepharospasm (twitching eye)

6) psychosocial: emotionally labile, depressed, paranoid, easily upset, rapid mood swings, impaired cognition (dementia/delirium), delayed reaction time, sleep disturbances

49
Q

parkinson disease nursing interventions (5, pharmacological (2))

A

pharmacological:
1) dopamine agnosits: mimics dopamine by stimulating dopamine receptors in brain (apormorphine - apokyn, pramipezole (mirapex), ropinirole (requip), rotiigotine (neupro)
2) levodopa: better at improving motor function but LT use leads to dyskinesia (decreased motor movement)

  • improve mobility and enhance self care activities (safety, assisted devices ambulation, change position slowly, dysphagia precautions)
  • improve nutrition and elimination
  • maintain safety precautions
  • supportive care
50
Q

huntington disease (what, 3 stages)

A

hereditary autosomal dominant disorder (gene mutation on one of the chromosome associated with that pair, 50% inheritance) that causes both neurological and behavioral symptoms that usually begin between ages 30-50 and progressively worsens

3 stages -
1) stage 1: onset of neurological or psychological symptoms
2) stage 2: characterized by an increasing or dependence on others for care
3) stage 3: loss of independent function

51
Q

huntington’s disease s/sx (8)

A
  • dominant inheritance
  • choreiform movements (rapid jerky movements) in limbs trunk and facial muscles
  • progressive mental status changes leading to dementia
  • poor balance
  • hesitant or explosive speech
  • dysphagia
  • impaired respirations
  • bowel/bladder incontinence
52
Q

huntington disease nursing interventions (5, pharmacological (2))

A
  • no known treatment or cure for HD
  • genetic counseling
  • supportive care
  • end of life care

pharmacological:
- tetrabenazine (xenazine) to help with chorea movements
- benzodiazepines and neuroleptic drugs may also help with chorea

53
Q

amyotrophic lateral sclerosis (what, begins ____, ______ typically occurs within ___ years of diagnoses d/t _______ ________)

A

(Lou Gehrig’s disease)
- upper and lower motor neuron disease that is characterized by progressive weakness, muscle wasting, and spasticity that eventually leads to paralysis
- begins in one area of the body -> motor weakness and deterioration spread until the entire body is involved includes ability to talk, swallow, and breathe
- death typically occurs within 3 years of diagnoses d/t respiratory failure

54
Q

amyotrophic lateral sclerosis assessment (early clinical manifestations) (11)

A
  • tongue atrophy
  • weakness of hands and arms
  • beginning of muscle atrophy of arms
  • fasciculations of face or tongue
  • difficulty controlling crying or laughing
  • nasal quality of speech
  • dysarthria
  • dysphagia
  • fatigue while talking
  • stiff or clumsy gait
  • abnormal reflexes
55
Q

amyotrophic lateral sclerosis assessment (late clinical manifestations) (4)

A
  • muscle atrophy (typically in trapezius, sternocleridomastoid muscles)
  • respiratory depression
  • pneumonia: can’t clear seizures appropriately
  • death
56
Q

amyotrophic lateral sclerosis nursing interventions (5, pharmacological (2)

A
  • no prevention, no treatment, no cure
  • symptomatic treatment
  • supportive care
  • end of life care (pallative, hospice)

pharmacological:
- riluzole and edarav one can possibly extend survival time 3-6 months