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N361: Pathophysiology II > Module 11 - Parkinson's, Seizures, & MS > Flashcards

Module 11 - Parkinson's, Seizures, & MS Flashcards

1
Q

Nerve Cell Hillock

A

location where the axon leaves the cell body

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2
Q

What causes the signals generated in neurons?

A

The sum of the inputs that are excitatory or inhibitory at the axon hillock

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3
Q

Nerve signals are what kind of phenomenon

A

all or nothing

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4
Q

When the cell gets to threshold…

A

propagation occurs and the signal can go to another nerve cell or to a motor end plate

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5
Q

The more myelin…

A

the faster the conduction

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6
Q

__ is needed to make myelin

A

Fat

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7
Q

Nodes of Ranvier

A

areas of ion flow where the action potential jumps from node to node

Clustering or NaK channels allow for saltatory conduction in one direction as channels close behind them

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8
Q

Saltatory Conduction

A

pattern of myelinated axons allowing increased speed of conduction of action potentials

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9
Q

In Multiple sclerosis we are worried about what

A

demyelination of central nerves and loss of saltatory conduction in certain areas

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10
Q

Parkinson’s Disease

A

A progressive degenerative disorder of dopamine secreting neurons that control muscle movement

Incurable

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11
Q

What causes Parkinsons Disease

A

depletion of dopamine and excess of acetylcholine

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12
Q

Excitatory Inputs are made with what Neurotransmitter

A

Acetylcholine

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13
Q

Inhibitory Inputs are made with what Neurotransmitter

A

Dopamine

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14
Q

Is Parkinson’s Fatal?

A

no, but death may occur from complications

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15
Q

Forms of Parkinsons Disease

A

Primary Idiopathic PD

Secondary Parkinsonianism

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16
Q

Primary Idiopathic Parkinson Disease

A

PD without a known cause

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17
Q

Secondary Parkinsonianism

A

Parkinson’s disease caused by some other event like trauma, infection, tumor, atherosclerosis, toxins

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18
Q

What kind of genetically inherited forms of Parkinsons Disease are there

A
  1. A rare autosomal dominant form
  2. An early onset autosomal recessive form
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19
Q

Parkinson’s could be from an interaction of what things? Or a result of what?

A

Interaction between genetics and environment

Or it could be a side effect of anti psychotic medicines that block dopamine receptors

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20
Q

___ is not effected until later in Parkinson’s Disease

A

Cognition

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21
Q

What usually kills in Parkinsons Disease

A

the complications from immobility not the disease itself

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22
Q

The majority of Parkinson’s Disease patients are what age when diagnosed

A

60s to 70s

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23
Q

How is Parkinson’s Disease diagnosed?

A

Diagnosis is CLINICAL - there are no lab tests for it

However, diagnostic tests can be done to rule out other things such as CT or MRI to rule out stroke or tumor

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24
Q

Area Affected in Parkinson’s

A

Dopamine secreting neurons deep in the basal ganglia (Extrapyramidal brain nuclei)

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25
Q

What does the impact on dopamine secreting neurons in the basal ganglia have on a Parkinsons Patient

A

Influences initiation modulation and completion of movement

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26
Q

For fine motor movements what must be balanced?

A

Acetylcholine (Excitatory) and Dopamine (Inhibitory) release balance

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27
Q

Degeneration of dopaminergic neurons leads to…

A

Deficiency of dopamine and relative excess of acetylcholine at the synapse –> this causes rigidity tremors and bradykinesia

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28
Q

Dopamine deficiency prevents…

A

affected brain cells from performing their normal inhibitory function in the CNS

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29
Q

Extrapyramidal System

A

Neural network of motor systems that control involuntary reflexes and movement

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30
Q

Pyramidal System

A

the motor cortex and voluntary movements

The nerves leaves the motor cortex and axons cross at the medulla oblongata

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31
Q

__ __ cannot occur without dopamine

A

Smooth Coordination

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32
Q

Normally, what is the dopamine:acetylcholine ratio

A

1:1

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33
Q

Classic Manifestations of Parkinson’s

A

Resting Tremor

Bradykinesia

Rigidity

Postural Dysfunction

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34
Q

What is the Resting Tremor like in Parkinson’s Disease

A

Asymmetric, rhythmic, low amplitude (not spastic

Usually unilateral in hands and feet

Pill Rolling

Disappears during sleep but worsens with stress

Intermittent –> progressively worsens

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35
Q

What is the Bradykinesia in Parkinson’s Disease like

A

slowness of voluntary movement

generalized slowness of movement

failure of antagonistic muscles to relax

loss of ability to walk, blink, or swallow saliva

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36
Q

What is the Rigidity like in Parkinson’s Disease

A

involuntary contractions of striated muscle

Stiffness of limbs

resistance to ROM

Uniform –> lad pipe rigidity or jerky –> cogwheel rigidity NOT spasticity

You have to work against it to get moving and it will become bilateral with progression

Once they start moving, hard to initiate and modulate stopping and turning - take fast short steps

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37
Q

What is the Postural Dysfunction like in Parkinson’s Disease

A

Shuffling gait and balance problems

Loss of postural reflexes causing high fall risk

Stooped posture - leans to one site when seated

Festinating Gait

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38
Q

Festinating (Parkinsonian) Gait

A

short, accelerating steps

hard to initiate and hard to modulate in order to stop and turn

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39
Q

What is not affected in Parkinson’s Disease

A

Intellect - so they are aware of symptoms and deficits and cannot control what the body does – therefore it is disturbing to them

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40
Q

What are some other Parkinson’s Disease Manifestation

A

Fine Motor deficits (fingers and hand) are slow and difficult

Micrographia

Hypomimia

Dysarthria and Monotone, high pitch low voice volume

Freezing

Slight foot drag

Turns are hesitant and En Block

Dandruff, oily skin, and seborrhea

Less blinking

Drooling and dysphagia leading to swallowing issues

Autonomic dysfunction - urine retention, diaphoresis, orthostatic hypotension, constipation

Depression and Anxiety

Dementia in late stages

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41
Q

Micrographia

A

Small Cramped Handwriting

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42
Q

Hypomimia

A

Decrease in facial expression

masklike faces

less blinking

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43
Q

What is the voice like in Parkinson’s disease

A

low volume hoarse and breathy

high pitch and monotone

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44
Q

Parkinson’s Disease patients have a very high __ risk

A

fall

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45
Q

Why are UTI rates high in Parkinson’s disease?

A

They cannot control autonomic functions like relaxing and contracting the bladder easily

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46
Q

Complications from Parkinson’s Disease

A

Disability to varying degrees

Difficulty performing ADLs

SE from medications

Late - Dementia

Injury from Falls

Aspiration

UTI

Pressure Ulcers

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47
Q

What is usually less affected in Parkinson’s Disease

A

Intelligence and Lifespan

*Can have a full life and not die early but you know what is happening to you - you are aware

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48
Q

What is the goal of Parkinson’s treatment

A

There is NO CURE at this time –> so the goal is to relieve symptoms and maintain function through pharmacologic, surgical, and PT means

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49
Q

What sort of drugs may be given to Parkinson’s pts?

A

Dopaminergic (Levodopa-Carbidopa)

Anticholinergic (Artane, Cogentin)

Other (Eldpryl, Tasmar, Symmetrel)

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50
Q

Levodopa-Carbidopa

A

A dopaminergic drug given to PD patients

Levidopa is an inactive dopamine form that can cross the blood brain barrier and convert to dopamine in the brain - but there are enzymes in the periphery that do this do so we use Carbidopa to inhibit periphery conversion before crossing since active dopamine cannot cross

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51
Q

What are anticholinergics good for in Parkinson’s Disease patients but can cause what?

A

Good for stopping drooling, but they cause dry mouth and cause more drinking with risk for aspiration of fluids

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52
Q

What sort of surgeries may be done on Parkinson’s patients

A

Pallidotomy by Stereotactic Neurosurgery

Fetal tissue Transplants

Deep Brain Stimulation

these are not used as much

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53
Q

What is the mainstay treatment for Parkinson’s

A

Levodopa-Carbidopa Drugs

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54
Q

Pallidotomy by Stereotactic Neurosurgery

A

obliteration of ventrolateral nucleus of the thalamus and Globus pallidus which prevents involuntary movement

For PD

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55
Q

Fetal Tissue Transplants

A

For PD

transplanting cells from the basal ganglia or adrenal medulla of fetuses into the caudate

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56
Q

Deep Brain Stimulation

A

Pacemaker like brain implants that decrease tremors and is controlled by the patient via a magnet

for PD

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57
Q

When are surgical measures sued for Parkinson’s?

A

When they are not responding to medication management.

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58
Q

Why is PT so important in Parkinson’s?

A

PROM, walking, bathing, speech therapy, massages are all important to maintain independent function which we want to promote as long as possible safely

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59
Q

Nursing Care measures for Parkinson’s

A

Education

Referral to support groups

Exercise program – maintain mobility and safety

Assess: Chewing, swallowing, depression, nutrition (as it may be hard to chew and swallow or get food)

Speech therapy for dysarthria

Home safety (bars, etc anything to make the home safer)

Clothing choices: Non-skid Velcro shoes, shirts without buttons, slacks with elastic waistbands,

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60
Q

Epilepsy

A

Seizure Disorder

Condition of the brain characterized by susceptibility to recurrent seizures

These are not just a febrile seizure when they were kids, its seizures every once in a while

It is from Paroxysmal events associated with abnormal electrical discharges of neurons in the brain

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61
Q

Epileptogenic Focus

A

area of the cerebral cortex causing the seizures - where the brain is making the electric storm

Neurons in the brain depolarize or become hypoexcitable –> fires more readily than normal when stimulated as a result

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62
Q

Types of Epilepsy

A

Primary

Secondary

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63
Q

Primary Epilepsy/Seizure Disorder

A

Idiopathic - no apparent structural brain changes occur

We do not know what is causing it

The brain cells fire and reset and electrical discharges keep going throughout the brain causing varying symptoms depending on location

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64
Q

Secondary Epilepsy/Seizure Disorder

A

Structural changes or metabolic alterations in the brain leading to increased automaticity

Could be something like a brain tumor, atherosclerosis, or a metabolic disorder

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65
Q

What is the prevalence of epilepsy

A

1-2% –> 2 million people

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66
Q

When is the occurrence/diagnosis of Epilepsy most commonly seen?

A

Highest in childhood and with old age

even babies can get it though, anyone can

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67
Q

What is Epilepsy’s prognosis with treatment?

A

Very good

68
Q

Anytime pH is ___ a baby will have a seizure

A

<7

69
Q

Anoxia

A

Brain starved of oxygen

70
Q

The majority of epilepsy is ___

A

idiopathic (50%)

71
Q

Potential causes for a Seizure Disorder

A

Idiopathic ( ~ 50%)

Birth trauma

Perinatal infection

Anoxia

Infection

Toxins

Brain Tumors

PKU or TB

Head injury/trauma

Metabolic disorders

CVA

72
Q

What is diagnosis of Seizure Disorders primarily based on?

A

Based on occurrence of one or more seizures - not just one

73
Q

What is the diagnostic test for choice for seizures? What is the catch?

A

EEG - the catch is it may have normal findings if they are not actively having a seizure

74
Q

What may a CT or MRI or Skull X Ray show for seizure disorders?

A

structural brain abnormalities or assessments for bony structures

75
Q

What can serum chemistries do for seizure disorder diagnosis?

A

It can allow evaluation of metabolic conditions (BUN, CBC, Ketones, Uric Acid etc)

76
Q

What does an EEG show with a tonic clonic seizure

A

high fast voltage spikes in all leads

77
Q

What does an EEG show if there is no seizures?

A

Rounded spike wave complexes

78
Q

What is the pathophysiology of a Seizure Disorder

A

Neurons in the brain depolarize and become hyperexcitable by lowering the threshold –> this causes firing more readily than normal in this epileptogenic focus area

The resting membrane potential is less negative or inhibitory connections are missing d/t GABA activity or electrolyte shifts (lower threshold to fire)

Once the epileptogenic focus fires electric currents spread out to surrounding cells firing with greater amplitude and cause impulse cascades around the brain

This increased firing increases metabolic demand and can lead to brain damage

Eventually inhibitory neurons should stop this firing

79
Q

Where can impulse cascades of epileptogenic fire occur?

A

Partial Seizure - One side of the brain

Generalized Seizure - both sides of the brain

Cortical, subcortical, and brain stem areas

80
Q

What happens to metabolic demand in seizuires?

A

demand for O2 and nutrients increase by 200% and if they are not met then brain damage will occur

81
Q

What happens if inhibitory neurons cannot stop a seizure?

A

Status Epilepticus occurs and without treatment fatal anoxia will occur

82
Q

Why is the resting membrane potential lower/ less negative for seizures?

A

Either:

a. Inhibitory connections are missing because of GABA

or

b. Electrolyte shifts like hyponatremia, hyperkalemia, and hypocalcemia occur

83
Q

GABA

A

gamma aminobutyric acid

chief inhibitory NT in the CNS

without it seizure can occur from a lowered threshold

84
Q

What are the 3 major manifestations of a Seizure Disorder

A
  1. Characterization by recurrent seizures
  2. Aura in the Prodrome phase
  3. Postictal State after generalized seizure
85
Q

Aura

A

a sensory sign indicating an imminent seizure in the prodromal phase of epilepsy

could be anything depending on area of brain impacted like visual, auditory, kinesthetic, olfactory, etc

86
Q

Prodrome

A

something that comes right before another event

87
Q

Postictal State

A

In generalized seizure, consciousness is loss and once returned they must reorient slowly

May cause loss of bowel and bladder

Can be embarrassing

HA, Confusion, Fatigue, Combativeness, Lethargy, and a Slow Return to consciousness occurs

88
Q

Partial Seizure

A

come from a local area and cause focal problems

89
Q

2 Kinds of Partial seizures

A

Simple Partial (Jacksonian)

Complex Partial

90
Q

Simple Partial (Jacksonian) Seizure

A

Begins locally and does NOT cause alteration in consciousness

Sensory sx (flashing lights, smells, hallucinations), Autonomic Sx (sweating, flushing), and Psychic sx (dream states, anger, fear) occur

S.A.P.

Since they are conscious, they know they’re having a seizure

91
Q

Complex Partial Seizure

A

Partial seizure that DOES alter consciousness

Amnesia for events that occur during and immediately after the seizure occurs

During, the patient may still follow simple commands

Lasts 1-3 minutes

92
Q

Generalized Seizure

A

Most commonly thought of seizure

A generalized electrical abnormality within the brain

can be convulsive (tonic clonic) or non convulsive ( no movement)

93
Q

Tonic Clonic

A

a convulsive seizure with movement

94
Q

4 Types of Generalized Seizures

A

Absence (Petit Mal)

Myoclonic

Grand Mal

Atonic

95
Q

Absence Seizure (Petit Mal)

A

Brief generalized seizure with change in LOC lasting 1-10 seconds

Look like they are daydreaming and not paying attention

Blank out and teachers may notice

96
Q

Myoclonic Seizures

A

Bilateral massive epileptic myoclonus generalized seizures

May be rhythmic

Brief involuntary muscular jerks of body or extremities occurs - not normal to happen in an entire side of the body though

Consciousness usually NOT affected

97
Q

Generalized Tonic Clonic (Grand Mal) Seizure

A

Generalized seizure

Classic seizure

Rhythmic movements: quiet period, movement, quiet period etc

Begins with a loud cry –> Loss of Consciousness –> Body falls –> body spasms (tonic phase) and relaxes (clonic phase)

Usually 2-5 minutes long

98
Q

Atonic Seizure

A

Generalized seizure

Loss of postural tone and temporary loss of consciousness

“Drop Attacks”

99
Q

Status Epilepticus

A

A medical emergency

Continuous seizure state that can occur in ALL seizure types

It is accompanied by resp distress followed by hypoxia or anoxia

100
Q

What may Status Epilepticus be due to

A

Abrupt withdrawal of anticonvulsant medications

hypoxic encephalopathy

acute head trauma

metabolic encephalopathy

septicemia d/t encephalitis or meningitis

101
Q

What is the most life threatening form of status epilepticus?

A

Grand Mal / Generalized Tonic Clonic Status Epilepticus (huge metabolic demand)

102
Q

Status epilepticus can occur in what seizure types?

A

ALL of them

More common in grand mal, simple partial, and complex partial though

103
Q

Unclassified Seizures

A

seizures that do not fit characteristics of partial or generalized seizures or status epilepticus

104
Q

Complications from Seizure Disorders

A

Hypoxic brain damage and mental deficiencies as a result

Depression and Anxiety

Social Isolation (do not want embarrassment, danger from driving, triggers)

105
Q

Treatment for Seizure Disorders

A

Identify type of seizure – note time & activity (can help allow for better treatment)

Reverse cause of disorder if possible

Pharmacologic - Based on seizure type

Surgery (last line treatment)

Vagal nerve stimulators – reduce frequency of seizures in some patients

Counseling

106
Q

What sort of surgeries may be done for seizure disorders?

A
  1. Resective surgery to excise the epileptogenic focus
  2. Corpus collostomy –> remove connections between hemispheres to limit activity - but this can affect all aspects of life
107
Q

Note what things about a seizure?

A

Type and Activity like what they did did they yell first, etc

note time brain potentially went without oxygen

108
Q

Nursing Care During a Seizure

A

Protect from injury

Place on ground in side lying position

Maintain airway

Apply O2 and Monitor responses

Do NOT put anything in their mouth as they can chew through things and hurt themselves or others

Note auras and triggers

109
Q

Nursing Care After a Seizure

A

Administer anticonvulsants per order

Monitor therapeutic levels of meds

Education about factors that precipitate

110
Q

Tips for Things to do During a Seizure

A

Cushion Head

Loosen Neckware

Turn on Side

Nothing in Mouth

Look for ID

DO NOT HOLD DOWN

As seizure ends, offer help

111
Q

Pediatric Febrile Seizures

A

Typically occur between 3mo and 6 y/o age

lasts a few seconds to a few minutes - rarely goes beyond 15 minutes

Hypothesized as arising from fever affecting the developing brain

Can be grand mal to causing baby needing to reorient when waking up, becoming diaphoretic, or wetting themselves

112
Q

What fevers usually cause pediatric febrile seizures

A

greater than 100.4 F

113
Q

When is the peak for pediatric febrile seizures?

A

between 12-18 months - 1 to 1.5 years

114
Q

Most pediatric febrile seizures are outgrown…

A

most often by age 3 but almost all by age 5

115
Q

What should a caregiver do if a pediatric do if a child has a febrile seizure lasting more than 15 minutes?

A

Call 911 if longer than 15 minutes or sooner if they show signs of breathing issues

If its the first febrile seizure, the pediatrician will need to be seen soon after

116
Q

Multiple Sclerosis

A

Demyelination of the white matter of the brain and spinal cord (CENTRAL NERVOUS SYSTEM) - damage to nerve fibers and their targets occur

Characterized by exacerbations and remissions

117
Q

How does Gullain Barre syndrome differ from MS

A

GB is demyelination of peripheral nerves while MS is demyelination of CNS

118
Q

The major cause of chronic disability in young adults is…

A

multiple sclerosis

119
Q

When do s/s of MS begin to occur

A

between ages 20-40 with an average age of 27

120
Q

When do most MS diagnoses occur

A

between 55-64 years of age

121
Q

What is the ratio for Parkinson’s between Sexes?

A

Female:Male is 1:1

122
Q

What is the ratio for MS between Sexes?

A

Female:Male is 3.1:1

123
Q

What areas tend to have more MS incidence

A

Northern Areas rather than southern ones

124
Q

Where is gray and white matter in the brain? in the spinal cord?

A

Brain: Gray matter is cell bodies outside the brain with white matter inside

Spinal Cord: The white matter is outside with gray matter insides

125
Q

MS is thought to be caused by what?

A

An autoimmune disease allowing you to destroy your white matter

A virus may initiative this with a protein similar to proteins in the myelin sheath and this confuses the immune system which then attacks the white matter

126
Q

MS Syndromes

A

Corticospinal

brain Stem

cerebellar

cerebral

127
Q

Corticospinal MS

A

Symmetric muscular weakness and stiffness

spastic paralysis

bowel and bladder incontinence

128
Q

Brain Stem MS

A

Dysfunction of CN 3 through 12

leads to::

Ophthalmoplegia

Nystagmus

Dysarthria

facial and muscle weakness

Paresthesia

Ptosis

129
Q

Cerebellar MS

A

spastic gait

ataxia

intention tremors (a symptom not always means MS)

hypotonia

130
Q

Cerebral MS

A

optic neuritis

impaired vision

intellectual and emotional deterioration

131
Q

Ophthalmoplegia

A

double vision

132
Q

Ptosis

A

Droopy eyelid

133
Q

Nystagmus

A

involuntary eye movement horizontally or vertically

more of a central problem if vertical

134
Q

Optic Neuritis

A

visual clouding, loss of vision, and visual field pain when eye is moving

135
Q

Types of MS

A

relapsing

Primary progressive

secondary progressive

progressive relapsing

136
Q

Relapsing MS

A

remitting MS (25% of pop)

clear relapses (acute attacks or exacerbations) with full/partial recovery and lasting disability

disease does not worsen between attacks

There is initial events with remission back at baseline functioning with some more minor flares between events

137
Q

Primary progressive MS

A

uncommon - 15% of pop

steady progression from the onset with minor recovery or plateaus

Line steadily increases with some plateauing - never returns to baseline

138
Q

Secondary Progressive MS

A

40% of pop

Begins with clear relapses and recovery and lasting disability steadily progressive and worsens between attacks

Line will act much like relapsing with flares and remissions at baseline until eventually the flares do not return to baseline and continuously get worse and increase

139
Q

Progressive Relapsing MS

A

rare

steadily progressive from the onset, but has clear acute attacks

140
Q

Causes for MS

A
  • Unknown cause but autoimmune - antibodies will attack self and destroy CNS neurons
141
Q

What are some current theory on the cause of MS

A
  1. Slow acting or latent viral infection stimulating autoimmune response
  2. Environmental and genetic factors
  3. Trauma toxins and nutritional deficiencies

perhaps also familial

142
Q

What is needed to make an MS diagnosis

A

evidence of 2 or more neurologic attacks

143
Q

How is diagnosis undergone for MS

A

Get evidence of 2 or more attacks with periodic testing and close observation

MRI will show multifocal white matter lesions that look dark when they should be white

EEG will show abnormalities in a third of patients

Lumbar punctures will have normal CSF proteins but increased CSF IgG

CSF Electrophoresis will show evidence of kappa light chains

Evoked Potentials will show slowed nerve impulse conduction

144
Q

What kind of nerves are affected in MS?

A

Central nervous system nerve, peripheral nerves are unaffected

145
Q

Pathophysiology of MS

A

sporadic patches of axon demyelination and nerve fiber loss throughout CNS –> widely disseminated and varied neuro dysfunction

Slowed neural impulses leads to alterations in movement, reflexes, and mental status

Swelling and edema occur causing further injury to neurons and development of scar tissue plaques on myelin

146
Q

What is causing the presence or absence of function in MS?

A

It is the presence or absence of axons determining function NOT loss of myelin.

This can either be autoimmune destruction of axon with subsequent myelin attacks OR autoimmune attacks against myelin that slow conduction

147
Q

Plaques

A

lesions of MS

Phase 1 Plaques - small inflammatory lesions develop

Phase 2 Plaques - lesions extend and consolidate to form scar tissue

These inhibit and slow nerve conduction

148
Q

What do manifestations of MS depend on

A

extent and location of myelin destruction, extent of remyelination, and adequacy of restored synaptic transmissions

149
Q

What are some manifestations of MS

A

Ocular disturbances

sensory impairment

muscle dysfunction

urinary disturbances

bowel disturbances

fatigue

speech problems

150
Q

Ocular Disturbances in MS

A

Optic Neuritis (from demyelination of optic nerve)

Diplopia

Ophthalmoplegia (large pupil)

Ptosis

Blurred Vision

Nystagmus

Scotoma

151
Q

Sensory Impairment in MS

A

burning (like electric signals burning body)

Pins and Needles

Electrical sensations (sometimes these symptoms occur with electrical storms like lightening)

152
Q

Muscle Dysfunction in MS

A

weakness

paralysis (monoplegia to quadriplegia)

spasticity

hyperreflexia

intention tremor

gait ataxia

153
Q

Urinary Disturbances in MS

A

incontinence

frequency

urgency

frequent infections

154
Q

Bowel Disturbances in MS

A

involuntary evacuation OR constipation

155
Q

Speech Problems in MS

A

poor articulation and dysphagia occur

156
Q

What is often the most debilitating s/s of MS

A

Fatigue

157
Q

Scotoma

A

blind spot in otherwise normal visual field

158
Q

S/S of MS are precipitated by what?

A

Stress and sometimes heat

159
Q

The key to MS Manifestations is knowing…

A

demyelination causes slowed nerve impulses, BUT axon destruction from plaques and scar tissues removes the function of the nerve

160
Q

Secondary complications of MS

A

injuries from falls

UTI

Constipation

joint contractures

pressure ulcers

rectal distention

pneumonia (have trouble coughing)

insomnia

161
Q

Tertiary complications of MS

A

depression from role changes and loss of independence

Loss of social support - social isolation

family/spousal stress - divorce

financial problems from unemployment

162
Q

Goals of MS Treatment

A

Treat acute exacerbations

treat disease process

treat related s/s

163
Q

Treatment of M mostly revolves around…

A

good treatments for s/s and complications that are controllable as there are not many treatments for the MS itself

164
Q

Pharmacologic treatments in MS are doing what…

A

treating what is happening, and are not a cure

165
Q

What is pharmacologic treatment like in MS

A

Immunosuppressant therapy - at disease onset and with any exacerbation

Antiviral drugs - to try and slow disease

SQ immune substance interferon beta - to decrease number and severity of exacerbations

Innovative therapies - to foster antigenic self tolerance

166
Q

Education to give MS Patients

A

bladder training

sexual functioning

avoidance of complications

avoidance of fatigue and stress

N361: Pathophysiology II (20 decks)

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