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7313 Pathophysiology Shappy_Bringman > Exam 3 ppt 3 MS & ALS > Flashcards

Exam 3 ppt 3 MS & ALS Flashcards

1
Q

Multiple Sclerosis (everything below, but not detailed types and clinical manifestations):

What is it?

Epidemiology:

Etiology:

Pathophysiology:

Clinical Course (general):

Exacerbating Factors:

Non PT treatment:

PT Treatment:

A

What is it?

  • Chronic inflammatory demyelinating disease of CNS

Epidemiology:

  • Adult onset typically 20-40 years old
  • Race: white 2x more likely than African Americans
  • Sex: Females 2x more likely than males

Etiology:

  • Unknown
  • Best accepted theory is some sort of underlying viral disorder that causes autoimmune response
    • Some have suspected chalmydia, but this has not been proven and is debatable
  • Possible geneitc connection (15%)

Pathophysiology:

  • Autoimmune resonse sets of Immune system
  • •Something crosses BBB and causes demyelination (that can stop at any point)
    • attacks to myelin cause inflammation and then scar tissue develops,
    • oligodendrocytes are the glial cells that myelinate CNS axons and experience damage
      • shappy said they are the ones that are activated to respond (but microglial cells are like the phagocytes of the CNS, so I would think they have a large role in the innflammation and immue response - maybe oligodendrocytes try to regenerate?
    • You get inflammation first, then you will get the scar tissue after on the site (treat with inflammatory first)
  • •Slows conduction
  • •Decreasing transmission
  • •Results in weakness
  • Sort of like a CNS version of chronic Gillian Barre.

Clinical Course (general):

  • May be progressive or not, may have remissions and relapses. Very unpredictable.
  • optic nerve, motor and sensory cortex- not limited to these areas.
  • symptoms wax and wane which may or may not have an element of progression

Exacerbating Factors:

  • –Heat
  • –Stress

Non PT Treatment:

  • Anti-inflammatory at first to stop inflammatory response
  • may use IVIG to attack anitbodies that are created.
  • Oligodendrocytes can be repaired (remyelination can happen).
    • Remyelination can stop at any point.
  • For an Exacerbation:
    • Exacerbation (attack): symptoms get worse, treat immediately with anti-inflammatory (steroids), controls edema, after edema goes away the symptoms may also reduce. It is an argument to be as fit as possible before the attack

PT Treatment:

  1. –Help them avoid exacerbating factors
  2. –Exercise is okay, but not in hot environments (pools must be cool)
  3. –May need specialized outcome measures
    • Think of things that you can measure to show progress
      • Sensations (semmes weinstein, temperature, etc.)
    • •Need more research
      • •Including more short term and long term outcome measures
    • –Insurance companies don’t want to reimburse for maintenance
      • •Insurance companies like short term outcome measures
  4. Work on balanc and overall conditioning
  5. ”Strategic Weighting” Weighted belt can improve ability to move. There is certain spots for the weights on the belts. (sort of like jackets for scared dogs)
  6. Don’t forget wound care stuff
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2
Q

Multiple Sclerosis

What is it?

A

What is it?

Chronic inflammatory demyelinating disease of CNS

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3
Q

Multiple Sclerosis

Epidemiology:

A

Epidemiology:

  1. Adult onset typically 20-40 years old
  2. Race: white 2x more likely than African Americans
  3. Sex: Females 2x more likely than males
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4
Q

Multiple Sclerosis

Etiology:

A

Etiology:

  • Unknown
    • Best accepted theory is some sort of underlying viral disorder that causes autoimmune response
      • Some have suspected chalmydia, but this has not been proven and is debatable
    • Possible geneitc connection (15%)
How well did you know this?
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Not at all
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5
Q

Multiple Sclerosis

Pathophysiology:

A

Pathophysiology:

  • Autoimmune resonse sets of Immune system
  • •Something crosses BBB and causes demyelination (that can stop at any point)
    • attacks to myelin cause inflammation and then scar tissue develops,
      • oligodendrocytes are the glial cells that myelinate CNS axons and experience damage
        • shappy said they are the ones that are activated to respond (but microglial cells are like the phagocytes of the CNS, so I would think they have a large role in the innflammation and immue response - maybe oligodendrocytes try to regenerate?
    • You get inflammation first, then you will get the scar tissue after on the site (treat with inflammatory first)
      • •Can see Plaque build up
      • •Plaque is scar tissue
      • •Related to death of neuron
  • •Slows conduction
  • •Decreasing transmission
  • •Results in weakness
  • Sort of like a CNS version of chronic Gillian Barre.
How well did you know this?
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6
Q

Multiple Sclerosis

Clinical Course (general):

A

Clinical Course (general):

  1. May be progressive or not, may have remissions and relapses. Very unpredictable.
  2. optic nerve, motor and sensory cortex- not limited to these areas.
  3. symptoms wax and wane which may or may not have an element of progression
How well did you know this?
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7
Q

Multiple Sclerosis

Exacerbating Factors:

A

Exacerbating Factors:

–Heat
–Stress

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8
Q

Multiple Sclerosis

PT Treatment:

A

PT Treatment:

  1. –Help them avoid exacerbating factors
  2. –Exercise is okay, but not in hot environments (pools must be cool)
  3. –May need specialized outcome measures
    • Think of things that you can measure to show progress
      • Sensations (semmes weinstein, temperature, etc.)
    • •Need more research
      • •Including more short term and long term outcome measures
    • –Insurance companies don’t want to reimburse for maintenance
      • •Insurance companies like short term outcome measures
  4. Work on balanc and overall conditioning
  5. ”Strategic Weighting” Weighted belt can improve ability to move. There is certain spots for the weights on the belts. (sort of like jackets for scared dogs)
  6. Don’t forget wound care stuff
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9
Q

Multipule Sclerosis: Clinical Manefestations/What does MS affect? (9 examples)

A

Anywhere CNS nerves are

  1. –Sensory Cortex
  2. –Pain
  3. –Visual Changes (optic nerve)
  4. –Motor dysfunction (motor cortex)
  5. –Speech/swallowing
  6. –Cognitive
  7. –Depression
  8. –Affective
  9. •Autonomic changes
  • –Cardiovascular
  • –Bladder
  • –Bowel
  • –Sexual dysfunction

•Basically everything in CNS

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10
Q

Multiple Sclerosis: Four autonomic functions affected

A

Autonomic changes

  1. –Cardiovascular
  2. –Bladder
  3. –Bowel
  4. –Sexual dysfunction
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11
Q

Multiple Sclerosis

Non-PT Treatment

What about for an exacerbation?

A

Non PT Treatment:

  1. Anti-inflammatory (steroid) at first to stop inflammatory response
  2. may use IVIG to attack anitbodies that are created.
  3. Oligodendrocytes can be repaired (remyelination can happen).
    1. Remyelination can stop at any point.

For an Exacerbation:

  1. Exacerbation (attack): symptoms get worse, treat immediately with anti-inflammatory (steroids), controls edema, after edema goes away the symptoms may also reduce. It is an argument to be as fit as possible before the attack
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12
Q

Can you see plaques on an MRI for someone with MS?

A

Scars plaque can be found anywhere in CNS

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13
Q

Is MS easy or hard to diagnose?

A

Manifestations can be hard to put a label on because the symptoms are vague. Easy to miss the diagnosis

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14
Q

How many categories of MS are there?

A

6 categories of Primary Progressive MS

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15
Q

What are the 6 Categories of Primary Progressive MS?

A
  1. .Benign MS (about 20%)
    • •Mild disease with full function greater than 15 years)
  2. 2Malignant MS (also called Marburg Disease ) – malignant does not mean cancer, just that it is fast and hard
    • •Rapid onset, continued progression. Significant disability or death
  3. Relaxing Remitting MS (70%) – she likes to test on this one
    • •Acute episodes followed by remission/improvement without disease progression
  4. Secondary Progressive MS
    • •Develops from relaxing remitting
    • •However is more progressive
    • •Occasional relapses to differentiate it with minor remissions
      • •A lot of these people will plateau during the remission period (you will not see them return to full function)
    • •pts are older at this age
  5. Progressive Relapsing
    • •Intervals between relapses actually show disease progression (so in between exacerbations you are still getting worse)
    • •Occurs with aging
  6. Primary Progressive (the little version of the big category of all of this)
    • •Disease progression without or with progression
    • •If you don’t fit into one of the other 5 categories, so you just say that it is Primary Progressive
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16
Q

Characteristics of Benign MS? (2)

A

.Benign MS

  • (about 20% of MS
  • •Mild disease with full function greater than 15 years)
17
Q

Characteristics of Malignant MS? (3)

A

Malignant MS

  1. also called Marburg Disease ) – malignant does not mean cancer, just that it is fast and hard
  2. •Rapid onset, continued progression.
  3. Significant disability or death
18
Q

characteristics of relaxing Remitting MS: (2)

A

Relaxing Remitting MS

  1. 70% of all MS – she likes to test on this one
  2. •Acute episodes followed by remission/improvement without disease progression
19
Q

characteristics of Secondary Progressive MS: (4)

A

Secondary Progressive MS:

  1. •Develops from relaxing remitting
  2. •However is more progressive
  3. •Occasional relapses to differentiate it with minor remissions
    • •A lot of these people will plateau during the remission period (you will not see them return to full function)
  4. •pts are older at this age
20
Q

Characteristics of Progressive Relapsing MS: (2)

A

Progressive Relapsing

  1. •Intervals between relapses actually show disease progression (so in between exacerbations you are still getting worse)
  2. •Occurs with aging
21
Q

characteristics of Primary Progressive MS (the little version of the big category of Primary Progressive MS): (2)

A

Primary Progressive (the little version of the big category of all of this)

  1. •Disease progression without or with progression
  2. •If you don’t fit into one of the other 5 categories, so you just say that it is Primary Progressive
22
Q

what does ALS stand for?

A

Amyotrophic Lateral Sclerosis

23
Q

what is an alternate name for ALS?

A

Lou Gheric’s Disease

24
Q

What is ALS ?

A

•Motor neuron disease

  1. –Degenerative spinal cord, brain, brainstem motor neuron loss.
  2. –Typically develops in UE first, then progresses to lower
    • •One of few conditions where Diplegia is present in UE
25
Q

ALS Epidemiology

A

Epidemiology

  1. –Men more common than women (2:1)
  2. –10-15% seem to have familial link
  3. –30K cases in USA (15 diagnosed per day)
26
Q

ALS Etiology

A
  • Unkown
  • –A number of theories
    1. •Free radical build up
      • –Enzymes whose job it is to elimiate free radicals are dysfunctional (superoxide)
    2. •Neurotransmitter issues
      • –Glutamate is typically elevated
    3. •Motor neuron degeneration
    4. •Autoimmune
    5. •Unscheduled apoptosis
27
Q

ALS: prognosis

A

From onset of symptoms to death: 5-10 years (usually from respiratory problems)

28
Q

What are the 5 theories of ALS Etiology?

A
  1. •Free radical build up
    • –Enzymes whose job it is to elimiate free radicals are dysfunctional (superoxide)
  2. •Neurotransmitter issues
    • –Glutamate is typically elevated
  3. •Motor neuron degeneration
  4. •Autoimmune
  5. •Unscheduled apoptosis++
29
Q

ALS Pathophysiology

A

•Pathophysiology

  1. –Motor neuron progressive degeneration
  2. progression
    1. – from cranial nerves
    2. –Can progress to sensory
    3. –Bowel and bladder
  3. –Typically develops in UE first, then progresses to LE
    • •One of few conditions where Diplegia is present in UE
  4. –Distal to proximal
  5. –Ultimately can affect breathing
30
Q

What are three types of motor neurons that ALS affects?

A
  1. LMN
  2. UMN
  3. Bulbar neurons
31
Q

Clinical Manifestations of ALS affecting LMN (3)

A
  1. •UE tend to be first LE second
  2. •Distal to proximal
  3. •Can affect reflexes (typically flaccid)
32
Q

Clinical Manifestations of ALS affecting UMN (1)

A

•Spasticity if affects reflexes

33
Q

Clinical Manifestations of ALS affecting Bulbar tract neurons (4)

A
  1. •Face
  2. voice
  3. swallowing
  4. speaking
34
Q

Does ALS affect cognition?

A

Cognitive function is generally spared for most people, although some (about 5%) also develop frontotemporal dementia.

per wikipedia: http://en.wikipedia.org/wiki/Amyotrophic_lateral_sclerosis#Diagnosis

35
Q

Managment of ALS

A
  1. •We usually go straight to power chair with multiple different concepts on how to get it to move, partly because UE goes first
    • •Sip and puff and eye devices
  2. •Computerized technology for speech
    • –Lots of very expensive technology for very short period of time

Wikepedia says:

Management of ALS attempts to relieve symptoms and extend life expectancy. This supportive care is best provided by multidisciplinary teams of health care professionals working with the person and their caregivers to keep them as mobile and comfortable as possible

Then lists the following:

  1. medications
  2. breathing support
  3. Therapy
    1. physical
    2. occupational
    3. speech
  4. nutrition
  5. pallitiave care (care meant to keep pt comfortable but not improve condition as they approach death)
36
Q

ALS DIagnosis

A

ALS is a very difficult disease to diagnose. To date, there is no one test or procedure to ultimately establish the diagnosis of ALS. It is through a clinical examination and series of diagnostic tests, often ruling out other diseases that mimic ALS, that a diagnosis can be established. A comprehensive diagnostic workup includes most, if not all, of the following procedures:

  1. electrodiagnostic tests including electomyography (EMG) and nerve conduction velocity (NCV)
  2. blood and urine studies including high resolution serum protein electrophoresis, thyroid and parathyroid hormone levels and 24-hour urine collection for heavy metals
  3. spinal tap
  4. x-rays, including magnetic resonance imaging (MRI)
  5. myelogram of cervical spine
  6. muscle and/or nerve biopsy
  7. thorough neurological examination

http://www.alsa.org/about-als/diagnosing-als.html

37
Q

Physical therapy for ALS

A

from wikipedia

Physical therapy plays a large role in rehabilitation for individuals with ALS. Specifically, physical and occupational therapists can set goals and promote benefits for individuals with ALS by delaying loss of strength, maintaining endurance, limiting pain, preventing complications, and promoting functional independence.

7313 Pathophysiology Shappy_Bringman (13 decks)

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