disorders of the CNS/PNS Flashcards
what is meningitis (what, classified, observe for (2))
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)
viral meningitis (ASEPTIC) (common/uncommon?, no _____ found in CSF culture, causes (3), _____ _______ more likely to be temp…, treatment?)
- 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)
bacterial meningitis (SEPTIC) (common/uncommon, fairly high ________…, causes (2), highly _____________, occurs where?
- 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)
what are the increased risk of bacterial meningitis (4)
- 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)
s/sx meningitis (12)
- 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)
positive kernig sign
when patient lying with thigh flexed on abdomen, leg won’t completely extend
- B/L = meningeal irritation suspected
positive brudzinski’s sign
when patient neck flexed, flexion of knee and hip produced
- when LE passively flexed, similar movement seen on opposite extremity
what are signs of increased ICP (2)
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)
meningitis nursing interventions (7)
- 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
encephalitis (what, cause, can be _____ ________ or lead to _______ such as ____(4), ______ _______ causes _______ ____ ________ _______ -> further increase in _____ and potentially death)
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)
encephalitis nursing interventions (3)
- 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)
what is demyelination (what, results in)
destruction of myelin - fatty and protein material that surrounds certain nerve fibers in brain and spinal cord
- results in impaired transmission of nerve impulses
multiple sclerosis (what, leading causes of?, characterized by, affects (6), causes ______ and ______ damage?)
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
encephalitis s/sx (14)
- 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
s/sx multiple sclerosis (18)
- 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
multiple sclerosis nursing interventions (goal, 7)
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
myasthenia gravis (what, may take many _____ -> ?, types)
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)
MG classes (5)
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)
myasthenia gravis s/sx (7)
- 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
the tensilon test (what)
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
cholinergic crisis (MG)
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)
cholinergic crisis s/sx (10)
(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
cholinergic crisis treatment (2)
- anticholinergics (eg. atropine)
- benzodiazepines (eg. diazepam)
myasthenia crisis (what)
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
myasthenia crisis s/sx (6)
- generalized weakness
- severe bulbar (oropharyngeal) weakness
- mydriasis (dilated pupils)
- tachycardia
- respiratory failure
- death CAN OCCUR
myasthenia crisis treatment
- neuromuscular agent (neostigmine) to increase muscle tone and treat MG
myasthenic (6) vs. cholinergic crisis (7) vs. both (6)
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
myasthenia gravis nursing interventions (6 including pharmacological (5)
- 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
plasmapheresis (what, side effects (8))
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
IV immunoglobulins (IVIG) (what, side effects (2))
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)
guillan barre syndrome (what, result of, antibodies attack?, leads to, healing occurs in _____)
- 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
acute guillain barre syndrome stages (3)
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
chronic guillian barre syndrome stages
some patient do NOT completely recover and have permanent neurologic deficits
guillian barre syndrome s/sx motor (5)
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
guillian barre syndrome s/sx sensory (2)
- parasthesia
- pain (cramping)
Guillian barre syndrome s/sx cranial nerve manifestation (4)
- facial weakness
- dysphagia
- diplopia
- difficulty speaking
guillian barre syndrome s/sx autonomic manifestations (3)
- labile BP
- cardiac dysthymias
- tachycardia
guillian barre syndrome nursing interventions (7)
- 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)
trigeminal neuralgia (what, _____ nature of pain, associated with?)
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
trigeminal neuralgia assessment (3)
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
trigeminal neuralgia nursing interventions (3, pharmacological (4))
pharmacological: anticonvulsant
- AED: carbamazepine (tegretol)
- gabapentin (neurontin)
- pregabalin (lyrica)
- baclofen (lioresal)
- acupunture
- surgery (help with neurovascular decompression, radial frequency, thermoregulation)
RISK: infection!
bell’s palsy (what, cause, remission?)
(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
bells palsy s/sx (6)
- 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
bells palsy nursing interventions (3, pharmacological 4)
pharmacological:
- corticosteroids
- antivirals
- mild analgesics
- artificial tears
- warm/moist heat
- massage/exercise
brain tumor (what, effects, type of changes resulting in _______(4))
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
cerebral tumors s/sx (9)
- 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
brainstem tumors s/sx (9)
(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
brain tumor nursing interventions (5, pharmacological (4))
- 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
parkinson disease (what, 4 cardinal signs)
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
parkinson disease stages (5)
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_
parkinson disease s/sx (posture (2), gait (5), motor (12))
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)
parkinson disease s/sx (speech (5), autonomic dysfunction (7), psychosocial (8))
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
parkinson disease nursing interventions (5, pharmacological (2))
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
huntington disease (what, 3 stages)
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
huntington’s disease s/sx (8)
- 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
huntington disease nursing interventions (5, pharmacological (2))
- 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
amyotrophic lateral sclerosis (what, begins ____, ______ typically occurs within ___ years of diagnoses d/t _______ ________)
(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
amyotrophic lateral sclerosis assessment (early clinical manifestations) (11)
- 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
amyotrophic lateral sclerosis assessment (late clinical manifestations) (4)
- muscle atrophy (typically in trapezius, sternocleridomastoid muscles)
- respiratory depression
- pneumonia: can’t clear seizures appropriately
- death
amyotrophic lateral sclerosis nursing interventions (5, pharmacological (2)
- 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
