MS I Alterations in Neuroregulation STUDENT COPY

8/2/2019 MS I Alterations in Neuroregulation STUDENT COPY

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Chronic Neurological Problems

Susan Greathouse RN BN MSN


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Headache

Tension-type Bilateral location and press/tightening

qualityMigraine Recurring, unilateral or bilateral throbbing

pain, trigger, history

Cluster Repeated headaches for weeks or months


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Seizure Disorders and

EpilepsySeizure is a paroxysmal, uncontrolledelectrical discharge of neurons in the

brain that interrupts normal functionEpilepsy is a condition in which aperson has spontaneously recurring

seizures caused by a chronic underlyingcause


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Generalized Seizures

Prodromal phase

Aural phase

Ictal phase

Postictal phase


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Metabolic Disturbances

Acidosis

Electrolyte imbalances

Hypoglycemia

Hypoxia

Alcohol and barbiturate withdrawalDehydration

Water intoxication


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Generalized Seizures

Tonic-Clonic Cyanosis, excessive salivation, tongue or

cheek biting, incontinenceAbsence Brief staring spell

Atypical absence seizures Staring accompanied by other s&s

Other Types excessive jerk, falling


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Partial Seizures

Partial focal seizures

Complex partial seizures

Temporal lobe absence

Automatism repetitive movements


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Status Epilepticus

Ventilatory insufficiency

Hypoxemia

Cardiac dysrhythmias

Hyperthermia

Systemic acidosisTreated with Lorazepam or Diazepam


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Drug Therapy

Antiseizure drugs (pg. 1538)

70% of the patients seizures are

controlled

Therapeutic ranges are guides fortherapy, not toxic ranges


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Acute Intervention

Carefully observe and record details

Exact onset

Course and nature, duration

Autonomic signs

Maintain a patent airwayDo not restrain

Suction and oxygen if needed


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Degenerative Diseases:

Multiple Sclerosis (MS)Results from damage/scarring of myelinsheath


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MS Epidemiology

Incidence

58/100,000

More common in cooler climates

Women > men

Peak age of onset = 20-40

Race = Caucasian most likely to beaffected (90%)


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MS Pathophysiology

Unknown trigger stimulates immuneresponse -> inflammatory response

->myelin sheath damage -> scar/plaqueformation -> nerve impulse interruption


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Types of MS

Relapsing-remitting

Primary-progressive

Secondary-progressive

Progressive-relapsing


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MS Assessment

History

Physical assessment

Motor changes Sensory changes

Cognitive changes

Psychosocial changesLabs

Radiology


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MS Interventions

Exercise/physical therapy

Medications

Steroids Immunosuppressants

Immunomodulators

Cholinergics anticholinergics

Complementary therapies


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Neurotransmitter Dysfunction:

Parkinsons DiseaseNeurotransmitter affected = Dopamine

Destruction of substantia nigra = loss of

dopamine

Pathophysiology

Movement = balance of ACh and DA

Loss of DA = loss of control of voluntarymuscles


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Parkinsons Disease

Demographics50,000 new cases per year

Age = usually > 50

More common in men 3:2 ratio


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Stages of Parkinsons Disease

Stage 1 = initial stage

Stage 2 = mild symptoms

Stage 3 = moderate symptoms

Stage 4 = severe disability

Stage 5 = complete dependence


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Assessment of Parkinsons

Posture

Gait

Motor function

Speech

Autonomic dysfunction

Psychosocial issues


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Parkinsons: Medical

InterventionsMedications Dopaminergics

Dopamine receptor agonists Anticholinergics

MAO inhibitors

COMT inhibitors

Physical and occupational therapy

Surgical management


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Parkinsons: Nursing

InterventionsSafety

Medications

Ambulation

Communication

Nutrition

Support


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Neurotransmitter Dysfunction:

Myasthenia Gravis (MG)Neurotransmitter affected = ACh

Pathophysiology

Auto-immune process: antibodies developed toACh receptor sites

Thymus gland abnormalities in 85% cases

Epidemiology

0.4/100,000

Women:men = 2-3:1

Peak age of onset = 20-30


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Myasthenia Gravis

AssessmentPhysical Exam

Progressive muscleweakness

Poor posture Ocular palsies

Ptosis

Diplopia

Fatigue Loss of bowel/bladder

control

Labs

Ach receptorantibodies

Radiology

CXR, Chest CT

EMG

Tensilon test


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Myasthenia Gravis

ManagementActivity Planning

Medications

Anticholinesterases Steroids

Immunosuppressantdrugs

Plasmapheresis

Respiratory support

Nutritional support

Communication

Eye protectionThymectomy

Education


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Restless Legs Syndrome

Unpleasant sensory and motorabnormalities of one or both legs

Cause unknownPrimary family history

Secondary iron deficiency, renal

failure, polyneuropathy, DM, RA,pregnancy

Remove aggrevating factors drug tx.


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Amyotrophic Lateral Sclerosis

(ALS) Lou Gehrigs

Pathophysiology

Progressive degeneration/death of motorneurons

Cause = unknown; ? abnormal

metabolism of glutamate


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ALS Epidemiology

1.5/100,000

Men more than women 2:1

Age of onset = 40-70


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ALS Assessment

Physicalassessment Fatigue while talking

Tongue atrophy

Dysphagia

Weakness ofhands/arms

Nasal quality ofspeech

Dysarthria

Labs = 0

Radiology = 0

Tests = 0Treatment

Experimental meds

Fluorouracil

Thalidomide


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Huntingtons Disease

Genetic, autosomal dominant disorder

30-50 years

Deficiency of neurotransmitters Ach andgama-aminobutyric acid

Abnormal and excessive involuntary

movements (chorea)Gait deterioration, intellectual decline,psychotic behavior


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Alzheimers Disease

Most common form of dementia, chronicprogressive, degenerative

5% of people 65-74

Diagnosed by presence ofneurofibrillary tangles, -amyloid

plaques, loss of connections betweencells and cell death at autopsy


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AD Early Warning Signs

Memory loss

Deterioration in personal hygiene

Loss of ability to concentrate andmaintain attention

Altered or unpredictable actions

Dysphasia, apraxia, visual agnosia,dysgraphia

Aggression and tendency to wander


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AD Drug Therapy

Cholinesterase inhibitors

Namenda

Management of behavior problems

Antipsychotic drugs

SSRI, TCA

Antiseizure

Hormones and herbs


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Guillain-Barre Syndrome

(GBS)Pathophysiology

Segmental demyelination of motor neurons

Inflammatory response, typically followinga viral infection, acute illness, trauma,surgery, or vaccination

Auto-immune process: T-cells becomesensitized to myelin


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GBS Epidemiology

1.9/100,000

Men = women

Age of onset = 30-50, higher rates inthose >50

More common in those with Hodgkins

disease, SLE, HIV

More common in Caucasians


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GBS Physical Assessment

Motor

Ascendingsymmetric weakness

Decreased/absentdeep tendon reflexes

Respiratorycompromise

Loss ofbowel/bladdercontrol

Sensory

Paresthesias

PainCranial Nerve

Facial weakness

Dysphagia

Diplopia

Difficulty speaking


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GBS Assessment

Autonomicdysfunction

Labile BP Cardiac

dysrhythmias

tachycardia

Labs

CSF

EMGRespiratory functionstudies


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GBS Interventions

Medications

ACTH

ImmunoglobinsPlasmapheresis

Supportive

Pulmonary

Immobility Pain

Communication

ADLs


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MS I Alterations in Neuroregulation STUDENT COPY

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