Degen 4

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    Parkinson >unknown>viral infections

    >a progressive, degenerativedisease

    causing destruction of nerve cells

    in the basal ganglia of the brain

    depigmentation of the substantianigra of the BASAL GANGLIA

    loss of neurons

    dec. Dopamine

    >Pillrolling tremors ofthe fingers

    >Rigidity with muscle

    weakness-bradykinesia/akinesia

    -cogwheel rigidityabsence of arm swing

    in normal rhythmic gait>Parkinsons mask

    >Drooling of saliva

    >Dysphagia>Shuffling,festinating

    gait>Defects in judgment

    >Emotional instability

    -deppression, paranoiaand eventually confusion

    >Excessive sweating>No intellectual

    impairment

    Diagnostic Tests:

    >EEG, CT Scan>No test is diagnostic of

    Parkinsons dse.

    1.Encourage pt to maintainindependence as much

    as possible in hygiene

    and dressing.2.Position to prevent

    contractures; firm bed,no pillows, prone

    position when lying inbed, hold hands folded

    at the back when

    walking.3.Diet: residue, calorie, soft

    diet4.Aspiration precaution

    5. fluid intake to prevent

    constipation6.Anticholinergics. To reduce

    tremors.Anti_Parkinsonian

    (Dopaminergics)-improves muscle

    flexibility

    AntiviralAntispasmodics

    Antihistamines

    7.Gradual change ofposition,wear elastic

    stockings to prevent postural hypotension.

    8.Reddish brown urine harmless.

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    DISORDER ETIOLOGY PATHOPHYSIOLOGY CLINICAL

    MANIFESTATION

    MANAGEMENT

    Huntington

    chorea

    >transmitted as anautosomal dominant

    trait

    >hereditary, familyhx

    >affects men andwomen of all races

    >a chronic, progressive,hereditary disease of the

    nervous system that

    result in progressiveinvoluntary choreiform

    (dancelike) movementand dementia.

    Genetic dse inherited as

    an autosomal dominant

    trait

    gene is present onchromosome 4

    the gene encodes aprotein known as

    huntingtin

    gradually, accumulateswithin brain cells

    brain cells are damaged

    when levels ofhuntingtin rise

    Early S/Sx:>personality changes

    > cognitive abilities

    >irritability, anger orparanoia

    >difficulty in decision-making

    >mild balance problem>clumsiness

    >involuntary facial

    movementsS/Sx as the dse

    progress:>sudden jerky,

    involuntary movements

    (chorea) throughout thebody

    >a wide, prancing gait>severe problems with

    balance andcoordination

    >difficulty shifting

    your gaze without

    moving your head>hesitant, halting orslurred speech

    >inability to swallow

    >dementia

    Diagnostic Test:>positive family hx

    >CT Scan and MRI

    N/I:

    1.prevent injury2.maintain proper nutrition

    3.maintain fluid intake4.reduce stress

    5.employ relaxation techniques

    6.proper hygiene7.skin care

    8.encourage exercise9.moral support

    Treatment:>management is aimed to control

    signs and symptoms>long-term home care

    Medications:

    >tranquilizers

    >anti-psychotic

    >anti-depressant

    DISORDER ETIOLOGY PATHOPHYSIOLOGY CLINICAL

    MANIFESTATION

    MANAGEMENT

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    Myasthenia

    Gravis

    >caused by anacquired

    immunologic

    abnormality or by agenetic abnormality

    >between ages 20-50,

    > in women, youngadults

    >is an auto immunedisease which is

    characterized by

    fluctuating, sometimesfatal, muscle weakness.

    > neuromusculardisorder that results in

    the failure to transmitnerve impulses at the

    myoneural junction

    > acethylcholinesecretion by the motor

    end plate> cholinesterase at the

    nerve ending

    >specific muscleweakness, particularly

    in the eyes, face and

    neck>dysphagia

    >dyspnea> physical activity

    >double vision,strabismus

    >fatigue

    >ptosis>diplopia

    >impaired speech>snarl smile(smile

    slowly)

    >masklike facialexpression

    >drooling

    Diagnostic Test:>EMG

    >Tensilon Test

    (EndrophoniumChloride Test)

    1.Assess swallowing/gag reflexbefore feeding the client

    2.Administer medications 20-30

    mins a.c. to prevent aspiration3.Protect from falls.

    4.Aspiration precaution5.Star meal with cold beverage.

    6.Adequate ventilation7.Plasmapheresis

    Medications:>cholinergics(Anticholinesterase)

    Antacids

    Surgery:>Thymectomy

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    DISORDER ETIOLOGY PATHOPHYSIOLOGY CLINICALMANIFESTATION

    MANAGEMENT

    Amyotrophic

    Lateral Sclerosis

    Lou Grehrigs

    Disease

    Unknown

    Viral Infection

    Myelin Sheath

    Destruction

    Scar Tissue Formation

    Distortion / Blocking of

    nerve Impulse

    Fatigue

    Awkwardness of fine

    fingers

    Muscle weakness

    Atrophy

    Fasciculations

    Dysarthia

    Jaw clonus

    Respiratory

    difficulty

    Spasticity of flexor

    muscle

    Unilateral disability

    of upper extremities

    Death: 5 to 10 Years

    Diagnostic test EMG

    ( no definite test )

    Gastrostomy feeding

    Assist with ADL

    Prosthesis to support

    weakened muscle

    Promote effective

    airway clearance

    Avoid Aspiration

    Tucked chin position

    when eating drinkingto facilitateswallowing

    Emotional support

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    DISORDER ETIOLOGY PATHOPHYSIOLOGY CLINICAL

    MANIFESTATION

    MANAGEMENT

    Guillian Bare

    Syndrome

    Infectious

    Polyneuritis

    Relatively rare

    disease affecting the

    peripheral andcranial nerves

    Usually follows a viral

    infection

    Infectious Polyneuritis

    Ascending or

    descending paralysis

    which may progressto respiratory muscle

    paralysis

    Paralysis ascends

    and stay at

    maximum level 2 3weeks then slowly

    descendsAbnormal sensation of

    tingling or nubness

    No specific therapy,

    symptomatic,

    supportive care ofthe paralyze

    immobilized patient

    ROM

    Skin care

    Full recovery oftenoccurs if good

    supportive care duringillness is adequate

    implemented