2204 Test 4 Aging Adult

Front 1

Asterognosis

Back 1

unable to identify by touching.

Identified with stage 2 of AD.

Front 2

Agraphia:

Back 2

inability to do and write.

Identified with stage 2 of AD

Front 3

Young Old:

Back 3

60-74

Front 4

Middle Old:

Back 4

75-84

Front 5

Old Old:

Back 5

84-100

Front 6

Centenarians:

Back 6

100 plus

Front 7

What was title 18 of social security act:

Back 7

Medicare

Front 8

What was title 19 of social security act:

Back 8

Medicaid

Front 9

Signifigance of 1900:

Back 9

Pension Laws enacted

Front 10

Significance of 1935:

Back 10

social security act

Front 11

What year was first congress on aging:

Back 11

1961

Front 12

Older Americans Act: nutrition, senior employment, and transportation programs was enacted in what year?

Back 12

1965

Medicare Title 18 of social security Act.
Medicaid Title 19 of social security Act.

Front 13

What was significance of 1972

Back 13

supplemental security income

Front 14

significance of 1987

Back 14

Omnibus Budget Reconciliation Act (Nursing Home Reform Bill)

Front 15

Robert Peck 1967.
Define

Back 15

x

Front 16

Echolalia

Back 16

repitition of words or phrases and scanning speech (searching for words.)

Front 17

Define Paraphasia

Back 17

using wrong word.

Front 18

Robert Peck 1968

Ego differentiation versus role preoccupation

Back 18

To develop satisfactions from oneself as a person rather than through parental or occupational roles

Front 19

Robert Peck 1968

Body transcendence versus body preoccupation

Back 19

To find psychological pleasures rather than become absorbed with health problems or physical limitations imposed by aging

Front 20

Ego transcendence versus ego preoccupation

Back 20

To achieve satisfaction through reflection on one’s past life and accomplishments rather than be preoccupied with the finite number of years left to live

Front 21

Define Geotranscendence

Back 21

Tornstam (2005) states that gerotranscendence suggests that “aging entails a transition from a rational, materialistic metaperspective to a cosmic and transcendent vision. As people age, they are less concerned with material possessions, meaningless relationships, and self-interests and instead desire a life of more significance and a greater connection to others.” (Elioppoulos, C., Gerontological Nursing, 7th ed. 2010, p. 19)

Front 22

Shortness of breath and confusion may be signs of:

Back 22

Myocardial Infarction

Front 23

Late stage heart disease may manifest as

Back 23

loss of appetite

Front 24

Define Delerium

Back 24

Acute confusion due to various causes
Poor oxygenation (respiratory or drug induced)
Decreased blood flow to the brain
Fever
Drug toxicity
Usually sudden onset
Treatment is to eliminate the cause and prevent injury

Front 25

What is apraxia?

Back 25

Difficulty with muscle coordination

Front 26

Describe Agnosia?

Back 26

Loss of ability to recognize and use familiar objects or to recognize people, sounds, and smells

Front 27

Describe Cognition

Back 27

perception, thought, and memory.

Front 28

What must be present with memory deficits on the DSM-IV-TR for a diagnoses of AD?

Back 28

Must have memory problems with one or more:
Aphasia, defined as difficulty articulating words or understanding written or spoken language. Residents demonstrating aphasia may substitute words linked by meaning (eg, time and clock) or words with similar sounds (eg, boat and coat).

Apraxia, defined as loss of the ability to perform tasks involving muscle coordination. For example, residents with apraxia may have difficulty buttoning a shirt or zipping a coat.

Front 29

Statistics for AD

Back 29

Age 65= 1:8, 75 = 1:5, 85 = 1:2 (44%)
Over 5 million Americans are diagnosed
Includes 4.9 million older than 65
And between 200,000 & 500,000 younger than 60
Over 11 million caregivers

Front 30

Describe the 10 warning signs of AD?

Back 30

Recall memory loss
Difficulty with familiar tasks
Language problems
Disorientation
Poor or decreased judgment

Problems with abstract thinking
Misplacing things
Mood / behavior changes
Personality changes
Loss of initiative

Front 31

Describe diagnostics for AD blood?

Back 31

Complete blood test and chemistry
B12 and folate
Thyroid profile
RPR-syphilis

Front 32

What diagnostic scans are used for AD?

Back 32

CT scan, MRI, Spectis a type of nuclear imaging test that shows how blood flows to tissues and organs., PET scan

Front 33

Describe Conditions That Mimic and/or Exacerbate Alzheimer’s Disease Symptoms

Back 33

Depression
Chronic alcoholism
Medication side effects
Drug-drug interactions

Dehydration
Thyroid disorders
Certain tumors, infections, or blood clots in the brain

Front 34

Describe Neuropsychological testing
for AD?

Back 34

Mini-Mental Status Examination
Depression screen
Clock Drawing Task
Functional ability assessment

Front 35

Describe MMSE test

Back 35

Cognitive measurement
Brief, structured mental status examination
Sections
Orientation
Registration
Attention
Recall
Language/comprehension
Praxis
10 to 15 minutes to administer
Scores range from 0 (worst) to 30 (best

Front 36

Describe the Cognition test for AD

Back 36

Quick screening tool
Brief (1-5 minutes)
Minimal language requirement
Does not require specialized testing materials

Front 37

Care concerns for Stage 1 AD

Back 37

Having the opportunity to work through the person’s concerns
Health care directives
Financial and business concerns
Take the time to do some of the things the person always wanted

Front 38

Describe Care Concerns for Stage 2

Back 38

Safety, safety, safety!!
Falls
Behavioral problems
Wandering
Unsafe use of appliances, tools (apraxia)
Maintaining continence
Increasing need for cueing to remain relatively independent with ADLs

Front 39

Describe Important Concerns in Stage 3

Back 39

Aspiration
Skin breakdown
Malnutrition
Dehydration
Infections

“No” is not a four letter word

Front 40

Define Sequelae

Back 40

A pathological condition resulting from a disease. 2. A secondary consequence or result

Front 41

LIst the treatments for a client with AD?

Back 41

Good planning and medical management
Health care planning and directives
Pharmacological interventions
Treatment of concomitant mood disorders (depression, anxiety, psychosis)
Good nutrition
Activities and alternative therapies

Front 42

List the nonpharmacologic treatments for AD

Back 42

Keeping the environment consistent
Memory therapy
Activity therapy
Anti-stress measures
Music therapy

Front 43

Define Cognitive

Back 43

perception, thought, and memory

Front 44

Cognex

Back 44

(tacrine) anticholinesterase inhibitor. Introduced 1993

Front 45

Aricept

Back 45

(donepezil) anticholinesterase inhibitor Introduced 1996

MIld to moderate

Front 46

Exelon

Back 46

® (rivastigmine) anticholinesterase inhibitor. Introduced 2000

Gi UPset

Front 47

Razadyne

Back 47

(galantamine) anticholinesterase inhibitor. Introduced 2001

former called Reminyl

Front 48

Namenda

Back 48

(memantine HCl) which is the first and only NMDA-receptor (N-methyl-D-aspartate–receptor antagonist)
antagonist approved for the treatment of moderate to severe AD. Only drug besides donepezil currently approved for moderate to severe AD
Works differently than the cholinesterase inhibitors (different mechanism of action)

In AD, there is abnormal glutamate activity, resulting in damage to neurons (nerve cells)
Memantine blocks the activity caused by abnormal levels of glutamate

Front 49

Describe Acetylcholine's job

Back 49

Acetylcholine is a neurotransmitter (chemical messenger) that plays an important role in memory, thought, and judgment.
Acetylcholine is used by neurons (nerve cells) in areas of the brain involved in memory and learning, namely the hippocampus and the cerebral cortex.
Among others, 2 events known to occur in the brains of AD patients are the reduction in levels of acetylcholine and destruction of the hippocampal and cerebral cortex regions of the brain.
Cholinesterase inhibitors were designed to prevent or slow the breakdown of acetylcholine, thus allowing acetylcholine to remain in the synapse (very small gaps between neurons, across which neurotransmitters travel) longer.
By maintaining acetylcholine levels, ChEIs may compensate for the loss of cells in the hippocampus and cerebral cortex of AD patients.

Front 50

Describe the antidepressants used in AD treatment

Back 50

sertraline, escitalopram, paroxetine (paxil), amitriptyline (elavil trycyclic), fluoxetine, mirtazapine (NASSA), trazodone((SARI) )

Front 51

Describe a mood stabilizer used in the treatment of AD

Back 51

valproic acid

Front 52

Describe the antianxiety drugs used in the treatment of AD

Back 52

buspirone, lorazepam, alprazolam, clonazepam

Front 53

Name the anti psychotics used in the treatment of AD

Back 53

– aripiprazole, risperidone, quetiapine, olanzapine, haloperidol; (rarely) clozapine, thioridazine, thiothixene, chlopromazine and fluphenazine

Front 54

The 10 absolutes in AD care

Back 54

Never argue - agree
Never reason - divert
Never shame - distract
Never lecture - reassure
Never say “remember”
“I remember”
Never force - reinforce
Never say “I told you”
Repeat
Never say “you can’t”
“Do what you can”
Never command
Ask or model
Never condescend
praise or encourage

Front 55

Describe the affects of AD on the cerebral cortex of the brain

Back 55

loss of language skills and judgement.

Emotional outbursts and behavior (wandering & agitation) occur and become more frequent as the disease progresses.

Front 56

Name the enzyme that is necessary for synthesis of Acetylcholine

Back 56

choline acetyltransferase

Front 57

Describe the theory of mutation in AD?

Back 57

a mutation for encoding amyloid precursor protein and alteration of apolipoprotein E.

Front 58

Describe Parkinson's Disease

Back 58

A progressive degenerative disease of the basal ganglia
Balance is lost between the excitatory and the inhibitory neurotransmitters. dopaminergic nigrostriatal (pigmented pathway) degenerates which in turn causes a decrease in the # of dopamine receptors.
Leads to loss of voluntary motor function
Atrophy within the substantia nigra results in deficiency of dopamine
Failure to inhibit acetylcholine is the underlying basis for the manifestations of PD

Front 59

Define secondary Parkinsonism

Back 59

Parkinson’s like symptoms, called secondary parkinsonism, may result from other disorders such as trauma, encephalitis, tumors, toxins and drugs

Front 60

Name the drugs that can cause drug-induced Parkinson

Back 60

neuroleptics, antiemetics, antihypertensives, and illegal designer drug MPTP.
carbon monoxide and cyanide also.

Front 61

Name the difference between Acetylcholine and Dopamine neurotransmitters.

Back 61

Acetylcholine is a excitatory neurotransmitter.
Dopamine is an inhibitatory neurotransmitter.

Front 62

Describe first stage of PD

Back 62

Unilateral involvement only, usually with minimal or no functional impairment on one side.

Front 63

Describe 2nd stage of PD

Back 63

Bilateral or midline involvement, without impairmet of balance.

Front 64

Describe 3rd stage of PD

Back 64

III – 1st indications of balance problems though the person remains independent. Starts having falls.

Front 65

Describe stage 4 of pd.

Back 65

– fully disabling disease

Front 66

Describe stage 5 of PD

Back 66

person confined to bed or wheelchair

Front 67

Define Pill rolling

Back 67

Pill rolling is usually the 1st symptom of PD. NOnintention tremors.

Front 68

List the characteristics of PD

NO antipsychotics for these patients.
No neuroleptics

Back 68

Bradykinesia(abnormal slowness of movement)
(Akinesia)-absence, poverty, or loss of control of voluntary muscle movements.
Postural loss
Festinating gait (an involuntary tendency to take short accelerating steps in walking.)
Retropulsion-an abnormal gait in which the body is bent backward.
Cogwheel rigidity is common
Muscle rigidity with mask-like face and soft voice results from delayed movements in the eyes, mouth and voice

Front 69

LIst symptoms of Loss of Autonomic Nervous System

Back 69

Constipation
Urinary hesitation
Urinary frequency
Orthostatic hypotension
Eczematous skin changes
Sebborhea-crusting head?

Front 70

Describe PD manifestations in the Brain

Back 70

Both depression and dementia are pathologies associated with PD.

Bradyphrenia (slow thinking) may also occur and result in slow thinking and a decreased ability to form thoughts, plan and decide

Approximately 50% of persons with PD will eventually develop some form of dementia.
Lewy body dementia
Dementia of the Alzheimer’s type
Or both

Front 71

List the manifestations required for a PD diagnoses

Back 71

Based on having two of the following manifestations
Tremor at rest
Bradykinesia (abnormal slowness of movement.)
Rigidity
Postural instability

Front 72

List the Diagnostic Tests to rule out PD

Back 72

CBC - anemia
Chemistry – hypoproteinemia
Drug screen – potential secondary parkinsonism causing agents
EEG – slowing and disorganization
GI series – delayed emptying and / or delayed swallow

Front 73

What will a PET scan show when diagnosing PD?

Back 73

PET scan will show decreased uptake of 6-[18F]-fluro-dopa

Front 74

bromocriptine

Back 74

(Parlodel)
Dopamine Agonist
Activate dopamine receptors in the brain
Increase the effect of levodopa
Adverse reactions similar to levodopa

Front 75

pergolide

Back 75

Permax
Dopamine Agonist
Activate dopamine receptors in the brain
Increase the effect of levodopa
Adverse reactions similar to levodopa

Front 76

pramipexole

Back 76

(Mirapex, Mirapexin, Sifrol)
Dopamine Agonist
Activate dopamine receptors in the brain
Increase the effect of levodopa
Adverse reactions similar to levodopa

Front 77

ropinirole

Back 77

Requip, Ropark, Adartrel
Activate dopamine receptors in the brain
Increase the effect of levodopa
Adverse reactions similar to levodopa

Front 78

trihexyphenidyl

Back 78

Artane (anticholinergic)
Used early in disease or when levodopa no longer effective; may be adjunctive
Side effects may be severe in the elderly
Wean slowly to prevent exacerbation of S&S
eases drooling, tremors, rigidity

Front 79

benztropine

Back 79

Cogentin (anticholinergic)
eases drooling, tremors, rigidity.
Used early in disease or when levodopa no longer effective; may be adjunctive
Side effects may be severe in the elderly
Wean slowly to prevent exacerbation of S&S

Front 80

Levodopa

Back 80

Dopar, Laredopa
Dopamenergics
for stage 3 & up
Levodopa crosses the blood/brain barrier
Giving with pyridoxine (B6) decreases effectiveness
“On/off” phenomenon may be problematic
Patient will eventually “burnout”
Nausea – take with food
Orthostatic hypotension – teach to change position slowly
Multiple drug interactions – anticholinergics, pyridoxine, antipsychotics
Severe constipation and/or urine retention
Protein bound – may need to alter diet; decreases availability. Divide protein intake for meals.

Front 81

Carbidopa-Levodopa

Back 81

Sinemet
Levodopa crosses the blood/brain barrier
Giving with pyridoxine (B6) decreases effectiveness
“On/off” phenomenon may be problematic
Nausea – take with food
Orthostatic hypotension – teach to change position slowly
Multiple drug interactions – anticholinergics, pyridoxine, antipsychotics
Severe constipation and/or urine retention

Protein bound – may need to alter diet; decreases availability. Divide protein intake for meals.

Patient will eventually “burnout”

Carbidopa, an inhibitor of aromatic amino acid decarboxylation, is a white, crystalline compound,

Front 82

Amantidine

Back 82

Symmetrel (discontinued)

Front 83

selegiline

Back 83

(Eldepryl) MAO- B inhibitors – delays destruction of dopamine
stages 1& 2
Used alone or as adjunct to levodopa therapy
Does not cause as much depression
Monitor for hypertension and/ or orthostatic hypotension
Monitor for sleep pattern disturbances

Front 84

What is a Pallidotomy?

Back 84

destroy the affected areas in the globus pallidus
May restore gait, balance and language
Long-term results not known

Front 85

Describe Deep brain stimulation.Activa TM tremor control therapy

Back 85

Uses implanted pacemaker-like device to block tremors
Wire is placed in the thalamus and pulse generator placed under the clavicle
Patient can increase or decrease stimulus

Front 86

Describe Stereotaxic thalamotomy

Back 86

used for medication failure in younger patients – electrode used to destroy tissue in the ventrolateral nucleus of the thalamus

Front 87

Describe Autologous adrenal medullary?

Back 87

medullary transplant very controversial

another procedure Fetal tissue transplant of substantia nigra tissue into the caudate nucleus under study

Front 88

What is multiple sclerosis?

Back 88

chronic demyelinating neurologic disease of the CNS (brain, optic nerves, spinal cord). associated with an abnormal immune response to an environmental factor.

Front 89

When in a patients life is onset of MS?

Back 89

20 to 50 years, with a peak at 30. Leading cause of neurologic disability in young adults.

Front 90

MS primarily affects which race?

Back 90

norther europeon, however does occur in people of northern Europeon ancestry; however, ms does occur in people of african, Asian, and Hispanic descent. Genetic factors do set people up for susceptability. MS usually occurs in more temperate climate such as northern US.

Front 91

Describe Pathophysiology of MS

Back 91

believed to occur as a result of an autoimmune response to a prior viral infection in a genetically susceptible person. the infection, which is thought to occur early in life, activates T cells. T cells usually move in and out of the CNS across the blood-brain barrier, but for an unkown reason, they remain in the CNS in people with MS.The T cells facilitate infiltration by other leukocytes, and an inflammatory process follows. Inflammation destroys myelin and oligodendrocytes (myelin producing cells), leading to axon dysfunction.

Front 92

Name the 4 classifications of MS

Back 92

Relapsing remitting-most common clinical course, exacerbations (accute attacks) with either full recovery or partial recovery with disability.

Primary progressive:steady worsening from onset with occastional minor recovery.

Secondary progressive: relapsing-remitting but steadily becomes worse between exacerbations.

Progressive relapsing-rare continues to progress from onset but also has exacerbations.

Front 93

Describe brief manifestations attacks of MS

Back 93

short lived or paroxysmal. Conditions that cause short lived attacks include 1) minor increases in body temperature or calcium concentrations. 2) functional demands that exceed conduction capacity. Paroxysmal attacks are sensory or motor manifestations that occur abruptly and last for only seconds or minutes; parathesias, dysarthria, and ataxia, and tonic head turning. Paroxysmal attacks, occur many times a day because of transmission of nerve impulses between adjacent demyelinated axons.

Front 94

What is required for a diagnoses of MS?

Back 94

one of the following: 1) two or more exacerbations seperated by one month or more and lasting 24 hours. 2) a history of repeated exacerbations and remissions with or without complete recovery, followed by progressively more severe manifestations lasting 6 months or more 3) slowly increasing manifestations for at least 6 months.

Front 95

Diagnostics to detect MS

Back 95

MRI-brain lesions

Cerebrospinal fluid analysis (not just for MS) reveals increased # of T cells. 80% of patients have elevated levels of immunoglobulin G (IGG) in csf.

CT of brain shows atrophy and white matter lesions in 25% of clients with MS, enlarged ventricles are visible.

PET (positron, emission tomorgraphy) measures brain activity. MS patients show changes in glucose metabolism.

Evoked response testing visual, auditory, somatosensory impulses --delayed conduction.

Front 96

Name the Immunomodulators for MS

Back 96

Interferon beta-1a (Avenox)

Interferon beta-1b (betaseron)(decrease lesions)

Glatiramer Acetate (copaxone, Copolymer-1)

Relapsing remmiting patients.
No pregnancy
monitor cbc and wbc every 3 months
pain and redness are common
administor within 3 hours of reconstitution
avoid prolonged sunlight

Front 97

Name the Adrenalcorticosteroid therapy for MS

Back 97

Adrenocortocotropic hormone (ACTH) (ACTHAR)-given to induce remission. given IV for 1 week. Prednisone therapy is followed. another protocol ACTH iv 3 days then IM every 12 hours for 1 week.

Prednison (Deltasone, Meticorten, Orasone)

Methylprednisolone (Medrol, SoLU-Medrol)

Front 98

Name the Muscle relaxants used in MS

Back 98

Baclofen (Lioresal) suppresses CNS reflexes. Stop treatment after 2 weeks. Do not stop abruptly.

Dantrolene (Dantrium) acts directly on skeletal muscles. may cause liver toxicity. Monitor liver enzymes and bilirubin.

Diazepam (valium) suppresses CNS reflexes.

Front 99

Name the Immunosuppresants for MS

Back 99

Azathioprine (Imuran) may cause hepatitis

Cyclophospamide (Cytoxan) hemorrhagic cystitis, sterility, stomatitis.

Front 100

MS patients with foot drop can do what?

Back 100

surgery Achilles tenotomy, a surgical procedure in which the Achilles tendon is transected.

Front 101

Health Promotion for MS patients should include?

Back 101

fatigue, avoid stress, extremes hot and cold, high humidity, physical overexertion, and infections.

Front 102

Heat & MS

Back 102

avoid heat it delays the impulse transmission across demyelinated nerves, which contributes to to fatigue.

Front 103

PD patients experience vivid dreams when what 3 drugs are combined?

Back 103

bromocriptine, levodopa, espicially, if used with an anticholinergic,

Front 104

Define Huntington's disease

Back 104

progressive, degenerative, inherited neurologic disease characterized by increasing dementia and chorea (jerky, rapid, involuntary movements). Single gene autosomal-dominant inherited disease that causes localized death of neurons of the basal ganglia.

there is a decrease in gamma-aminobutyric acid (GABA) which is a inhibitory neurotransmitter in the basal ganglia.
Frontal lobe

Front 105

What is the patho for huntingtons?

Back 105

destruction of cells in the caudate nucleus and putamen areas of the basal ganglia. Frontal lobes may atrophy. GABA and acetylcholine are decreased.

DOPAMINE is not affected! but decrease in acetylcholine results in a relative excess of dopamine in basal ganglia.

Excess dopamine causes opposite effect in Huntington's excessive, uncontrolled movement.

Psychologic manifestations are more debilaitating than choreiform (rapid and jerky) movements.

Front 106

Name some early manifestations of Huntington's

Back 106

depression memory loss decreased ability to concentrate, emotional liability and impulsiveness.

Petruding tongue
slurred speech poor articulation

Front 107

Dysarthria

Back 107

condition in which problems occur with the muscles that help one talk

Front 108

Describe diagnoses for huntingtons


(genetic)

Back 108

genetic testing. both blood and amniotic fluid may be tested for presence of a gene mutation on chromosome 4 using DNA analysis.

Front 109

Which antipsychotics are used with Huntington's disease?

Back 109

Phenothiazines and butyrophenones, are effective.

They block dopamine receptors in the brain.

Antidepressants are prescribed early in the disease.

Front 110

Define Amyotrophhic lateral Sclerosis

Back 110

Lou Gehrig's disease. rapidly progressive and fatal neurologic disease characterized by weakness and wasting of muscles under voluntary control without loss of cognitive or sensory. Muscle atrophy

Front 111

Pathophysiology of Amyotrophic Lateral sclerosis (Lou Gehrigs)

Back 111

results from degeneration and demyenation of the both upper and lower motor neurons in the anterior horn of the spinal cord, brain stem, cerebral cortex.
Death of motor neurons results in axonal degeneration, demyelination, glial proliferation, and scarring along the corticospinal tract.

Abnormal glutamate metabolism and hydrogen peroxide production being studied.

Front 112

Describe in Amyotrophhic lateral Sclerosis the symptoms of upper motor motor neurons

Back 112

spastic, weak muscles, increased deep tendon reflexes,

Front 113

Describe in Amyotrophhic lateral Sclerosis the symptoms of Lower motor

Back 113

muscle flaccidity, paresis (weakness), paralysis, and atrophy. Weakness and paresis are common early manifestations.
Depends on which muscle group is being affected fasciculations (twitching) is common in early stage.

Muscle atrophy then paralysis.
Usually first affects hands, shoulders, upper arms, and finally legs.
Increasing brain stem involvement causes progressive atrophy of the tongue and facial muscles dysphagia, dysarthria. No dementia involved.
eventually need gastrostomy tube

Diagnoses is usually testing to rule out other diseases and the manifestations.

Front 114

Fasciculations

Back 114

"muscle twitch", is a small, local, involuntary muscle contraction and relaxation which may be visible under the skin. Or detected by EMG testing.

Front 115

What medications is used to treat Amyotrophhic lateral Sclerosis?

Back 115

Riluzole (Rilutek) antiglutamate. First medication developed to treat ALS. Inhibits presynaptic release of glutamic acid in the CNS and protects neurons against excitotoxicity (nerve cells are killed by excessive neurotransmitter) of glutamic acid.

Front 116

Interventions Amyotrophhic lateral Sclerosis?

Back 116

baseline breathing, turn X 2.
elevate head of bed 30

Front 117

Describe Myasthenia gravis

Back 117

chronic autoimmune neuromuscular disorder characterized by fatigue and severe weakness of skeletal muscles. Clients experience periods of remission and exacerbation, and mild forms of the disorder exist.
Especially hits ocular muscles.
mostly women

Front 118

What medications are used for treatment of Myasthenia Gravis

Back 118

anticholinesterase.

Front 119

Patho for Myasthenia Gravis

Back 119

Axons of motor neurons divide as they enter skeletal muscles, and each axonal ending forms a neuromuscular junction.
Antibodies destroy or block neuromuscular junction receptor sites resulting in a decreased number of acetylcholine receptors.
Sometimes associated with a tumor of thymus.

Front 120

IN myasthenia gravis define Cholinergic crisis

Back 120

overdose of anticholinersterase (cholinergic).

Differentiation is based on clients response to edrophonium chloride (Tensilon).

In myasthenic crisis test is positive, and in cholinergic crisis the test is negative

Front 121

Describe the medications used to treat Myasthenia gravis.

Back 121

is the anticholinesterases. These drugs act at the neuromuscular junction and allow acetylcholine to concentrate at the receptor sites, promoting muscle contraction.

Eye muscles usually the first muscle group affected
Ptosis, diplopia
Dysarthria and dysphagia lead to eating difficulties
Fatigue is severe
DTRs normal!
Myasthenic crisis and / or Cholinergic crisis are life-threatening (Tensilon differentiates)

Careful history
Tensilon test (edrophonium Cl)= improvement for short time is positive test for myasthenia
EMG = < amplitude
CT to check the thymus
Serum assay to check ACTH antibodies

Pyridostigmine (mestinon) is used the most.
immunosuppresive agents, such as cyclosporine or azathioprine (imuran).

Neostigmine (prostigmin)
Ambenonium (mytelase caplets)
Pyridostigmine (mestinon, regonol administer 30 minutes before meals.v)
edrophonium chloride (Tensilin) test.

Plasmapheresis is to remove the antiacetylcholine receptor antibodies, thus improving sever muscle weakness, fatigue, and other manifestations.

Front 122

Describe Guillain-Barre syndrome

Back 122

acute inflammatory demyelinating disorder of the peripheral nervous system characterized by an acute onset of motor paralysis (usually ascending).
20% have respiratory. May have to be ventilated.
Miller fisher variant. Opthalmegalia, areflexia

Front 123

What bug is identifiable in the cause of Gulliane Bar syndrome?

Back 123

Campylobacter jejuni

gbs is thought to be humoral and cell mediated.

loss of autonomic nervous system

Front 124

Define Creutzfeldt-Jakob disease (also called spongiform encephalapothy)

Good hand washing

Back 124

rapidly progressive, degenerative, neurologic disease that causes brain degeneration without inflammation.
Abnormal form of a cellular glycoprotein known as prion protein.

New variant CJD "mad cow disease". from bovine spongiform encephalopathy.

Front 125

Define Stochastic theorie

Back 125

aging is random cellular damage.

Front 126

NONSTACHASTIC

Back 126

we are genetically programmed to age

Front 127

list 3 psychosocial theories of aging.

Back 127

disengagement theory-withdraw from customary roles and become more introspective

activity theory-successful aging comes from continued activity

continuity-personality stays the same and behavior becomes more predictable.

Front 128

Another name for Lewy body Dementia

Back 128

picks disease.

Front 129

Describe Multi-infarct dementia

Back 129

vascular

Front 130

Another name for Huntingtons'

Back 130

Huntingtons chorea

Front 131

Tertiary Syphulus

Back 131

hides in brain

3rd phase

Front 132

Vernicke's encephalopathy

Back 132

mimic alheimers

Front 133

GAD

Back 133

Geriatric assessment depression

Front 134

Functional Ability Test

Back 134

takes 4 hours close family member or caregiver needs to be there.

Front 135

Mini Mental test takes how long?

Back 135

10-15 minutes

Front 136

How long does clock Test take?

Back 136

1-5 minutes

Front 137

Primary Progressive is more common in who?

Back 137

men

Primary Progressive is 2nd stage of the 4 of ms

Front 138

Define Spinal Cord Syndrome MS. Weakness in leg, Foot drop,

Back 138

exacerbation of MS with hot water.
Uhtoffs Syndrome
Weakness in leg, Foot drop
bowel and bladder dysfunction
Parethesia's
Lerhmitte's sign shocklike (tips head to touch chin to chest)

Front 139

Define Cerebral Syndrome

Back 139

affect cerebral cortex
amouratic
optic neuritis
muscle weakness
hemiphareses
could be new seizure disorder

Front 140

Define Brain Stem Syndrome

Back 140

cranial nerves 3-12
dysarthria (slurred speech)
explosive speech late sign
eye pain nystagmus
Ataxia
Weakness with hypotonia
Intention tremors

Front 141

Define Cerabellar Syndrome

Back 141

ataxia
impaired gate
flacid arm
intention tremors (hand shake)

Front 142

Describe Stage 1, 2, 3 of Guillian Barre

Back 142

acute severe rapid weakness progressing quadriplegia, respiratory failure, nocturnal pain(stocking glove effect, loss of autonomic nervous system usually lasts 2 weeks.

stabilizing plateua, occurs 2-3 weeks, after onset. Leveling off stage.

recovery MAY take months up to 2 years. Strength returns in reverse order from where onset began. Recovery is usually complete. OT/PT is a must.

Front 143

Trigeminal Neuralgia

carbamazepine (tegretol)

Back 143

(ticdouloureux) maxillary divisions or cranial nerve 5. Severe pain. not sure cause.
infections such as flu may be cause.
trauma
infection of teeth or jaw
pressure on the nerve aneuyrism

Chronic disease of the maxillary and/ or mandibular divisions of cranial nerve V which result in episodic severe pain
Cause unknown though contributing factors may include flu like illnesses, trauma or infection of the teeth or jaw, and pressure on the nerve from an aneurysm, tumor or pressure on an artery close to the nerve
Follows pattern of remission-exacerbation with less time and more severity between episodes

Chronic disease of the maxillary and/ or mandibular divisions of cranial nerve V which result in episodic severe pain
Cause unknown though contributing factors may include flu like illnesses, trauma or infection of the teeth or jaw, and pressure on the nerve from an aneurysm, tumor or pressure on an artery close to the nerve
Follows pattern of remission-exacerbation with less time and more severity between episodes


flare ups
middle older females

treatment:
anticonvulsants-carbmazepine and occ
phenytoin to decrease pain
muscle relaxants-baclofen to decrease spasms.

rhizotomy last resort surgically removing nerve root.

Front 144

ergoloid mesylates

Treatment for AD

Back 144

(hydergine)
improves cognitive function

Front 145

Describe the Diagnostics for this Lecture

Back 145

CSF analysis = ↑ T lymphocytes with ↑ antigens. Elevation of IgG is common during serial exacerbations
MRI revealing multifocal lesions in the white matter is diagnostic of MS
EEG during exacerbations reveals generalized slowing

Front 146

Which drugs are used in Relapsing Remitting MS

Back 146

Interferon beta-1a (Avonex) and beta-1b (Betaserone)

Front 147

Which drugs are used in during Exacerbations and to suppress immune system in MS

Back 147

ACTH (glucocorticoids) used to treat inflammation and suppress the immune response during exacerbations

Front 148

Which drugs may used monthly in MS

Back 148

Cytoxan and Imuran (immunosuppressives) may be used monthly

Front 149

Which antispasmodics are used with MS

Back 149

Antispasmodics / muscle relaxants (Baclofen, Flexeril

*Plasmapheresis to remove antibodies

Front 150

Define Amyotrophic Lateral Sclerosis
(lou gar)

Back 150

EMG shows fibrillations of the muscles at rest
Muscle biopsy reveals atrophy
Progressive degeneration and demyelination of the motor neurons in the anterior horn of the spinal cord the and brain stem leading to eventual paralysis of the diaphragm
Usual onset between 40 and 60, male dominant
Weakness and paresis, fasciculation's of the involved muscles may be earliest signs
Death is usually within 2 to 5 yrs of diagnosis


Serum creatine kinase may be elevated
Pulmonary function studies are ordered for those with respiratory involvement

Front 151

***************The only drug prescribed for Amyotrophic Lateral Sclerosis

Back 151

Riluzole (Rilutek) is the only disease specific drug available
Decreases the release of glutamate
Most effective for those with swallow problems

Front 152

Describe the clinical manifestations of Guillian Barre

Back 152

Ascending (most common) – begins in the legs and moves caudally. Respiratory loss in 50 %.

Descending – begins in the cranial nerves and moves downward. Respiratory involvement rapid.

Miller-fisher variant – Ophthalmoplegia, areflexia and ataxia triad. No sensory and rare respiratory loss.

Pure motor – as in ascending without muscle pain or sensory loss.

Front 153

Describe Bell's Palsy

Back 153

Unilateral paralysis of cranial nerve VII
Cause unknown; possibly viral or traumatic
Occurs in all age groups though seen most often in those 20 to 60
Recovery is usually complete in a few weeks to several months
Treatment is symptomatic with special focus on preventing permanent injury to the eye on the affected side
Prednisone, NSAIDS and antivirals may help

Front 154

Creutzfeldt-Jakob disease

Back 154

Rare disease with spongiform degeneration of the gray matter of the brain; onset between 55 and 74; men and women equally effected
Is transmissible, though the causative agent is not known; Belief is a long-acting virus or a glycoprotein pathogen called a prion: England, Chile and Italy most common occurrences
Has been transmitted through corneal transplants and human growth hormone from cadavers
Is often fatal within 3 to 12 months: 1 to 30 per million

Front 155

Describe the differences in Creutzfeldt-Jakob disease and Variant Creutzfeldt-Jakob disease

Back 155

see slide 43 of Degenerative Neurological pp

Characteristic stages include:
Onset of memory changes, exaggerated startle reflex, sleep disturbances and nervousness
Progresses with a rapid decline in motor, sensory and language function
Tremors, hyper-reflexia, rigidity and + Babinski follow
Severe dementia follows in almost all cases
Final stage is coma with decorticate and decerebrate posturing

Front 156

New Variant CJD

Back 156

Also rare form believed to be due to ingestion of bovine sponigiform encephalopathy infected cattle products
Affects younger persons; so far, none in USA
Occurrences in England, France, Ireland, Italy and Canada

Diagnosis by neuro exam, EEG and CT
Postmortem exam is diagnostic
Often mistaken for AD in early stage
Support is symptomatic
Nursing care aimed at prevention of complications, family support
Standards precautions used to prevent infection of caregivers

Front 157

Postpolio Syndrome

Back 157

Complication of a previous infection from poliomyelitis infection (25 to 35 yrs post)
Occurs in approximately ½ of the 1.6 million persons previously infected by polio
Leads to motor neuron degeneration leading to fatigue, muscle and joint weakness that may lead to respiratory collapse
Death is usually by respiratory failure

May begin in previously affected muscle groups and spread to other groups
Neuromuscular symptoms include: cold intolerance, dizziness, headaches, urinary incontinence and sleep disturbances
Usually affects those with the worst previous cases of polio
Care is aimed at physical and emotional support

Front 158

Describe Rabies

Back 158

Rhabdoviral infection of the CNS by infected saliva entering the body through a bite or open wound
Nearly always fatal if symptomatic
Incubation period varies from 10 days to 1 year
Treatment is by rabies immune globulin and inactivated human diploid cell rabies vaccine

Intensive care in a quiet, darkened room
Maintain airway and oxygenation
Control seizures
Standard precautions to prevent transference to healthcare providers from contact with saliva
Never give both RIG and HDCV at the same time.
If globulin not available test patient for sensitivity to horse serum.

Front 159

Tetanus

Back 159

Neurologic disorder from effects of neurotoxin tetanospasmin from Clostridium tetani received from puncture or other wounds containing spores of the bacillus
Incubation is from 8 days to 15 weeks

Quiet, dark room to prevent muscle spasms and seizures; disturb as little as possible. Even minor stimulation can onset uncontrolled muscle spasms
Maintain oxygenation
IVFs and nutritional support
Meds for cardio support, antibiotics, electrolytes
Prevent of complications from immobility
(trismus) spasms of the jaw

Greater than 40% fatality with most cases occurring in those over 50
Infection leads to hyper-reflexia, severe muscle spasms, and seizures. There is no cognitive loss
Treat all punctures wounds with oxygen producing antiseptics (H2O2)

Front 160

Define Botulism

Back 160

Poisoning from ingestion of food contaminated with Clostridium botulium: dx by serum and fecal findings
Blocks the release of acetylcholine from nerve endings causing paralysis of skeletal muscles
Onset 12 to 36 hrs after ingestion
Visual disturbances noted first
Progression throughout skeletal muscles leads to respiratory failure requiring ventilator support.

Administer botulism antitoxin
Ventilator support
Parenteral nutritional support
Removal of toxins by cathartics, enemas and gastric lavage
Prevention of complications of immobility
Health promotion teaching especially related to food preparation

Front 161

Elders take how many days to develop a fever?

Back 161

3 a fever of 101 could be deadly.

Front 162

Spect test

Back 162

actually tells you which neurotransmitters is missing at that moment.