Parkinsons, Seizures, MS, MG Flashcards

1
Q

Parkinson’s Disease

A

PROGRESSIVE DEGENERATIVE DISORDER of the dopamine secreting neurons that control muscle movement

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2
Q

Forms of Parkinson’s Disease

A
Idiopathic Parkinson's Disease (Primary)
Secondary Parkinsonism (caused by trauma, infection, tumor, atherosclerosis, toxins)
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3
Q

Primary Parkinson’s Causes

A

Idiopathic = etiology unknown

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4
Q

Secondary parkinson’s causes

A

trauma, infection, tumor, atherosclerosis, toxins

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5
Q

Dx of Parkinson’s

A

it’s CLINICAL = no lab tests for it
can do a CT or MRI to rule out other causes for the symptoms
15% dx <50; mainly dx in 60-70s

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6
Q

Parkinson’s Pathophysiology

A

Deficiency of dopamine and relative excess of acetylcholine at the synapse = rigidity, tremors, and bradykinesia (slow movement)

Dopamine deficiency prevent affected brain cells from performing their normal inhibitory functions in the CNS - dopamine (inhibitory) AcH (excitatory)

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7
Q

What does dopamine do

A

deep in basal ganglia and influences initiation, modulation, and completion of movement

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8
Q

What are the manifestations of Parkinson’s

A

Resting tremor
Bradykinesia
Rigidity
Postural dysfunction

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9
Q

Resting tremor

A

usually in hand and feet - can do “pill rolling” to help decrease the tremor
Disappears during sleep, and worse with stress/anxiety
Intermittent and progressively gets worse, but stops when they do things

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10
Q

Bradykinesia

A

generalized slowness of movement and failure of agnostic muscles to relax (loss of walking, swallowing, blinking etc)

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11
Q

Rigidity

A

involuntary contraction of striated muscles
Stiffness of limbs; resistance to ROM
ex. Lead pipe = jerky and whole thing is rigid
Cogwheel rigidity = gears of mvmt. and stiffness

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12
Q

Postural dysfunction

A

shuffling gait and balance problems
lose postural reflexes = falls or stooped posture = leaning to one side
festinating gain = short, accelerating steps until fall

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13
Q

Other manifestations of Parkinson’s

A

Fine motor deficits = micrographia (small, cramped handwriting)
Hypomimia = mask like faces
Freezing = stuck in place when trying to initiate a step
“En bloc” turn = turn entire body and hesitant doing so
Less blinking, drooling and dysphagia
ANS DYSFUNCTION - orthostatic hypotension, constipation, urinary retention

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14
Q

Parkinson’s Complications

A
Injury from falls
Aspiration/difficulty swallowing
UTI
Pressure ulcers (b/c they have difficulty moving)
Dementia
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15
Q

Parkinson’s Tx

A

NO CURE AT THIS TIME
only goal is to relieve symptoms and maintain function

PT = PROM, walking, baths (loosens muscles) massages
Surgery
Drugs = dopaminergic, anticholinergetics

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16
Q

Parkinson’s Nursing Care

A

Education, and referral to support groups
Exercise program
Assess - chewing, swallow depression
Speech Therapy, Home Safety, Clothing Choices

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17
Q

Seizure Disorder (Epilepsy)

A

neurons are firing off extra/abnormal signals to the brain

typically highest in childhood and old age

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18
Q

Types of Epilepsy

A

Primary - idiopathic (born with it and don’t know why)

Secondary - structural changes or metabolic alterations = increased automacticity

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19
Q

Febrile seizures

A

typically in infants/increased temp to 103-104 and child has seizure; doesn’t mean that kid will have a seizure disorder…just deals with the fact that the neurological system is NOT fully developed.

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20
Q

Causes of Seizure Disorders

A
Idiopathic
Anoxia (no O2)
PKU or TB
Hypoglycemia (metabolic disorders) or even low calcium or low sodium
CVA = stroke
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21
Q

Diagnostics of Seizure Disorders

A

Have to have 1 or more seizures
EEG - records electrical activity in brain to see if there is anything abnormal going on
CT or MRI to reveal STRUCTURAL brain abnormalities
Serum chemistries to evaluate metabolic units

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22
Q

In an EEG what indicates whether or not they had a seizure

A

high fast voltage spikes in all leads

No seizure = rounded spike waves

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23
Q

Pathology of Seizure disorders

A

Epileptogenic (means seizure forming) neurons in the brain depolarize or become hyper excitable = fires more readily when stimulated
Resting membrane potential is less negative or inhibitory connections are missing = lower threshold
Epilpetogenic fires and spreads the current to surrounding tissues = 1 side of brain (partial) or full brain (generalized)
INCREASE IN METABOLIC DEMAND FOR O2

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24
Q

If the metabolic demand for O2 is not met in a seizure what could happen

A

brain damage

If they inhibitory neurons cannot fire enough to cause the excitatory neurons to stop it could result in status epilepticus (w/o tx anoxia is FATAL)

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25
Manifestations of seizure disorders
``` RECURRENT SEIZURES Aura (prodrome) - type of sign that the pt feels indicating a seizure is coming (see/smell something) Postictal State (after seizure) = slow return to consciousness, combative/lethargic, confusion, headache, fatigue) ```
26
Partial Seizures
arise from a local areal and cause focal symptoms
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Simple Partial (jacksonian) Seizure
beings in a specific area and DOES NOT ALTER CONSCIOUSNESS Sx = flashing lights, smells, auditory hallucinations ANS Sx = sweating pupil dilation Psychic Sx = dream states, anger, fear
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Complex Partial Seizure
ALTERS CONSCIOUSNESS generally lasts 1-3 minutes and pt may follow simple commands Amnesia for events that occur during and immediately after the seizure
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Generalized Seizures
affect the entire brain and can be convulsive or non-convulsive
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Absence (petit mal) seizure
brief change in LOC and lasts 1-10 sec
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Myoclonic seizure
bilateral; brief involuntary muscular jerks of the body and extremities Consciousness usually NOT affected
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Generalized tonic-clonic (grand-mal)
MOST COMMON; about 2-5 min | typically begins with a loud cry= loss of consciousness = body falls = body spasms (TONIC) and then relaxes (CLONIC)
33
Atonic
loss of postural tone, and temporary loss of consciousness (drop attacks)
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Status epilepticus
THIS IS A MEDICAL EMERGENCY It's a continuous seizure state and can happen in all types Most life threatening is the generalized tonic clonic status epilepticus Will see respiratory distress= hypoxia/anoxia
35
What are some reasons Status epilepticus might occur
Abrupt withdrawal of anticonvulsant medications Acute head trauma Hypoxic/Metabolic encephalopathy
36
Ungeneralized seizure
seizures that do not fit characteristics of partial or generalized seizure or status epilepticus
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Complications of Seizure Disorders
Hypoxic brain damage/Mental Retardation Depression and Anxiety Social Isolation
38
Tx of Seizure Disorders
#1 identify type of seizure/ NOTE TIME AND ACTIVITY Reverse the cause of disorder Drugs/pharmacologic Surgery Vagal nerve stimulators = reduce frequency of seizures in some patients Counseling
39
Seizure disorder Nursing Care
``` Cushion head and loosen any ties or buttons near neck to (protect from injury) Turn on size Maintain airway (nothing in mouth) Lood for ID (and DON'T HOLD PERSON DOWN) Apply O2 and monitor response ```
40
What do Nurses want to to for their pts after a seizure
Administer aniconvulsants per oder Monitor the therapeutic effects of meds Education about precipitating factors
41
Multiple Sclerosis (MS)
DEMYELINATION of the white matter of the brain and spinal cord damage to nerve fibers and their targets Characterized by exacerbations and remissions
42
MS facts
major cause of chronic disability in young adults usually sx by btwn 20-40 yrs Female > Male White> non white NORTH urbane areas (especially if you live there for the 1st 15 years of your life Higher Socioeconomic status more prone
43
MS syndromes
Corticospinal Brain Stem Cerebellar Cerebral **SOME FOLKES WILL HAVE ELEMENTS OF ALL OF THESE
44
Corticospinal MS Syndrome
symmetric muscular weakness and stiffness, spastic paralysis, bowel/bladder incontinence
45
Brain Stem MS Syndrome
dysfunction of CN III - XII = opthalmoplegia, nystagmus, dysarthria, facial and muscle weakness and paresthesias
46
Cerebellar MS Syndrom
affects your ability to move = spastic gait, ataxia, inanition tremors, hypotonia
47
Cerebral MS Syndromes
optic neuritis, impaired vision, intellectual and emotional deterioration
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Types of MS
Relapsing - remitting Primary progressive Secondary progressive Progressive relapsing
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Relapsing - Remitting MS
90% clear relapses with full/partial recovery and lasting disability Disease does NOT worse between attacks
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Primary progressive
10% | Steady progression from the onset with minor recovery
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Secondary Progressive
Begins with clear relapses and recovery and lasting disability steadily progressive and worsens between attacks
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Progressive Relapsing
Steadily progressive from the onset, but has clear acute attacks
53
Causes of MS
Unknown but auto immune = antibodies destroy neurons in the CNS Slow acting/late viral infection stimulates autoimmune response Environmental and genetic factors Trauma, toxins, nutritional deficiencies
54
MS Pathology
sporadic patches of axon demeylination and nerve fiber loss occurs throughout the CNS = neurologic dysfunction ****Presence or absence of axons is what determines how sick they are not just the loss of patches Peripheral nerves are unaffected SLOW NEURAL IMPULSES Swelling and edema causes further injury to neurons and development of scar tissue plaques on myelin
55
Dx of MS
``` Evidence of 2 or more neurologic attacks MRI (multifocal white lesions) EEG abnormalities LP (normal CSF protein but and increased CSF IgG CSF electrophoresis EPs = slowed nerve impulses ```
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Manifestations of MS
DEPENDS ON EXTENT AND LOCATION OF MYELIN DESTRUCTION ``` FATIGUE = most debilitating symptom Ocular disturbances = diplopia (double vision), nystagmus, scotoma (lack of center vision) Pins and needles/electrical sensations weakness, wobbly gain, paralysis incontince, frequent/urgent peeing ``` Stress and Heat can precipitate exacerbations
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MS complications
``` Secondary injuries from falls UTI Pressurer ulcers Pneumonia Insomnia ``` Tertiary Depression, Loss of support, Financial probe (unemployment)
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MS Tx
treat exacerbations and treat s/s aggressive immunosupressant drugs at start of disease antivirals may slow progression SQ immune substance to decrease exacerbations Innovative Therapies
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MS Nursing Care
``` Drugs Symptom management PT Educations Nutrition Safety ```
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Myasthenia Gravis
"grave muscular weakness" autoimmune disorder of transmission at the neuromuscular junction (Acetylcholine receptors destroyed, altered/not enough receptors d/t abnormal T- cell function)
61
Manifestations of MG
``` Drooping eyelid (ptosis) Weakness in arms and legs difficulty breathing, chewing,swallowing Blurred/double vision Slurred speech Chronic muscle fatigue ```
62
More MG manifestations
can progress from ocular to generalized weakness Extremity weakness usually greater in proximal parts rather than distal Symptoms usually at their quietest in the morning, and grow worse with effort throughout the day.
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Myasthenia Crisis
Affects respiratory system and may require ventilatory support and close airway management
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DX of MG
Hx of and Physical Exam Anticholinesterase test Nerve and muscle stimulation studies Testing for acetylcholine receptor antibodies
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Anticholinesterase test
administer an short acting acetylcholinesterase inhibitor IV to decrease the breakdown of Ach If MG there will be a dramatic improvement in muscle function
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Tx of MG
``` Anti-cholinesterase drugs Immunosuppressants Corticosteroids Plasmapheresis - to removed antibodies from circulation Thymectomy (removal of the thymus) ```