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Pathophysiology II class notes > Ch. 36 Disorders of Neuromuscular Function > Flashcards

Ch. 36 Disorders of Neuromuscular Function Flashcards

1
Q

What is hypotonia?

A

Diminished resistance to passive movement.
Soft muscles on palpation.
Diminished deep tendon reflexes.

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2
Q

What is hypertonia?

A

Hyperexcitable stretch reflex causing rigidity and spasticity.

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3
Q

What is clonus?

A

Involuntary rhythmic muscular contractions and relaxations.

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4
Q

What does the suffix “plegia” mean?

A

Stroke or paralysis

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5
Q

What does “paralysis” mean?

A

Loss of movement.

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6
Q

What does the suffix “paresis” mean?

A

Weakness

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7
Q

What does the prefix “mono” mean?

A

One limb

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8
Q

What does the prefix “hemi” mean?

A

Both limbs on one side

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9
Q

What do the prefixes “di” and “para” mean?

A

Both upper limbs or both low limbs

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10
Q

What do the prefixes “quadri” and “tetra” mean?

A

all four limbs

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11
Q

What is paraparesis?

A

A defect causing weakness in both arms

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12
Q

What is hemiparesis?

A

A weakness in the right arm and leg

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13
Q

What is monoparalysis?

A

Inability to move one leg

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14
Q

What results from upper motor neuron damage?

A

Weakness and loss of voluntary control. The spinal reflexes remain intact but cannot be modulated by the brain.

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15
Q

What are the manifestations of upper motor neuron damage?

A

Increased muscle tone
Hypertonia/hyperreflexia
Spasticity

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16
Q

What neurons are affected by lower motor neuron damage?

A

Neurons directly innervating muscles are affected.

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17
Q

What occurs as a result of irritated neurons in lower motor neuron damage?

A

Involuntary muscle contractions: fasciculation (small/local)

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18
Q

What occurs as a result of death of neurons (lower motor neuron damage)

A

Spinal reflexes are lost.
Flaccid paralysis
Denervation atrophy of muscles.

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19
Q

What are the two causes of muscle atrophy?

A

Disuse and denervation

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20
Q

What is the pathophysiology of muscular dystrophy?

A

Contractile proteins not properly attached to cytoskeleton of muscle cell. Protein movement does not effectively contract muscle cell.

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21
Q

What is Duchenne Muscular Dystrophy?

A

Recessive X-linked
Affects 1 in 3500 male births
Females usually asymptomatic if carrier (or mild symptoms)

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22
Q

What is Becker Muscular Dystrophy?

A

Slower progression and less severe than DMD.

Occurs later in childhood than DMD

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23
Q

What is the clinical presentation of muscular dystrophy?

A 
Boys asymptomatic at birth.
Begins with hips/shoulder muscles.
Calf muscles pseudohypertrophy (fat/connective tissue).
by 2-3 years, abnormal posture, falls, contractures, joint immobility, scoliosis.
Wheelchair needed by teen years.
Incontinence.
Weak cough = resp infections.
CVS: cardiomyopathy.
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24
Q

How is muscular dystrophy diagnosed by the physician?

A 
Family history
Observation of voluntary movement
Elevated Creatine-kinase
Muscle biopsy
Echo, ECG
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25
Q

What is the treatment for muscular dystrophy?

A

Maintain ambulation (helps prevent deformities with bones)
Prevent deformity
Prevent respiratory infections
Death in young adulthood common

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26
Q

What is Gower’s sign?

A

Difficulty standing up and walking

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27
Q

Why are creatine-kinase levels elevated in muscular dystrophy?

A

Muscle damage causes elevated CK

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28
Q

What kinds of problems can arise with the neuromuscular junction?

A

Decreased acetylcholine release.
Decreased acetylcholine effects on muscle cell (receptors are lost).
Decreased acetylcholinesterase activity resulting in too much acetylcholine at neuromuscular junction, also interfering with nerve impulse.

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29
Q

What is myasthenia gravis?

A

An autoimmune disorder caused by antibody-mediated loss of acetylcholine receptors in the neuromuscular junction. It results in decreased motor response.

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30
Q

What are the risk factors for myastehnia gravis?

A

Early adulthood (women)
Older than 50 years of age (men)
Placental transfer from mother (10-15% only and often spontaneous resolution within months.)
Thymus tumor or hyperplasia in 75% of cases.

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31
Q

What is the autoimmune pathophysiology of myastenia gravis?

A

Gradual destruction of acetylcholine receptors in neuromuscular junction
Injury to postsynaptic muscle membrane
Receptor sites degraded and blocked d/t antibodies

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32
Q

What are the initial manifestations of myesthenia gravis?

A

Muscle weakness (periorbital muscles, ptosis, diplopia)
Fatigue
These are progressive throughout the day.

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33
Q

What are the progressive manifestationos of myesthenia gravis?

A

Respiratory muscle weakness, difficulty speaking/chewing/swallowing, weak limbs.

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34
Q

What is a myasthenia crisis caused by?

A

Due to stress, infection, emotional upset, pregnancy, alcohol, cold, surgery, etc.

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35
Q

How is myesthenia gravis diagnosed?

A

History, physical exam
Rise in acetylcholine receptor antibodies (blood test)
Electrohysiologic studies to assess stage.

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36
Q

What is the treatment for myesthenia gravis?

A

Corticosteroid (immunosuppressant)
Thymectomy (if thymoma)
Plasmapheresis (remove specific antibodies from the blood and replace with immunoglobulin IgG)

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37
Q

What is carpal tunnel syndrome?

A

Mononeuropathy.

Compression of median nerve passing through carpal bones and ligaments.

38
Q

What causes carpal tunnel syndrome?

A

Inflammation of tendons, synovial swelling, tumor, RA, DM

Repetitive flexion-extension movements

39
Q

What are the manifestations of carpal tunnel syndrome?

A

Pain, paresthesis, numbness of thumb, 1st, 2nd, 3rd, and part of 4th digit
Wrist and hand pain, worse at night
Atrophy of abductor pollicus muscle.

40
Q

What is Tinel sign?

A

Light percussion over median nerve at wrist. Tingling sensation into palm = positive carpal tunnel

41
Q

What is Phalen maneuver?

A

Complete flexion x 1 minute

Parasthesia = positive carpal tunnel

42
Q

What is the treatment for carpal tunnel?

A

Anti-inflammatories, immobilization

43
Q

What is guillain-barre syndrome?

A

demyelinating polyneuropathy. It has an acute onset and is life threatening. It is immune mediated

44
Q

What bacteria is linked with guillain-barre syndrome?

A

Campylobacter jejuni most common. (also cytomegalovirus, epstein-barr virus, and mycoplasma pneumoniae

45
Q

What are the manifestations of Guillain-Barre Syndrome?

A 
Manifestations are progressive and variable.
Ascending muscle weakness/paralysis
Paresthesia, numbness
Loss of tendon reflexes
ANS involvement
Pain
46
Q

Where is pain located in Guillain-Barre syndrome?

A

Shoulder, back, posterior thighs.

47
Q

What are the signs of ANS involvement in Guillain-Barre syndrome

A

Postural hypotension, arrhythmias, flushing, sweating, urinary retention

48
Q

What are the risk factors for Guillain-Barre syndrome?

A

Possibly autoimmune
Association with immunizations
Frequently preceeded by mild respiratory or intestinal infection.

49
Q

What is the treatment for guillain barre syndrome?

A

Support ventilation
prevent complications
Plasmapheresis
IV immunoglobulin

50
Q

Define “choreiform” hyperkinesia

A

jerks

51
Q

Define “athetiod” hyperkinesia

A

twisting movements

52
Q

Define “ballismus” hyperkinesia

A

violent flinging movements

53
Q

Define dystonia

A

rigidity

54
Q

Which areas of the brain are affected by ALS?

A

Anterior horn of SC
Motor nuclei of brain stem
Cerebral cortex

55
Q

Which part of the brain is involved in Tourette’s Syndrome?

A

Cortical and subcortical regions (thalamus, basal ganglia, frontal cortex)

56
Q

What is Parkinson’s disease and what part of the brain does it involve?

A

Progressive disorder of basal ganglia and substantia nigral pathway resulting in depletion of dopamine.

57
Q

What are the risk factors for Parkinson’s?

A 
Post encephalitic syndrome
Antipsychotic drug s/e
Toxins
Carbon monoxide poisoning
Genetics
Brain tumours
CVA
Head trauma
Degenerative neurological diseases
58
Q

How do antipsychotic drugs cause Parkinson’s?

A

They block dopamine receptors and output, causing symptoms of Parkinson’s.

59
Q

What are the initial manifestations of Parkinson’s?

A

Rhythmic tremor of distal limbs that ceases with purposeful movement and sleep.

Rigidity (passive joint movement causes jerks).

Bradykinesis:

  • difficulty stopping voluntary movements
  • Shuffling when walking, freeze, lean forward to keep moving
60
Q

What are the late manifestations of Parkinson’s?

A 
Difficulty planning, starting, or carrying out tasks. 
Dementia/cognitive dysfunction (20-30%)
Motor function abnormalities.
Sleep disorders
Neuropsychiatric disorders
Autonomic Nervous System changes
61
Q

What are some examples of motor abnormalities that arise as a late manifestation of Parkinson’s?

A

Falls
Voluntary facial movements become limited and slow = stiff, masklike expression
Tongue, palate, throat muscles become rigid
Slow speech, poor articulation

62
Q

What are some examples of autonomic nervous system changes that arise as a late manifestation of Parkinson’s?

A 
Lacrimation (flow of tears)
Sweating
Dysphagia
Orthostatic hypotension
Thermal regulation problems
Constipation
Impotence
Incontinence
63
Q

What are the nonpharmacologic treatments for Parkinson’s?

A

Group support, education, exercise, nutrition guidance.

64
Q

What are the pharmacologic treatments for Parkinson’s?

A

Levodopa (increases dopamine)
Bromocriptine, pramipexole, amantadine (stimulate dopamine receptors)
Selegiline, rasagiline (slows the breakdown of dopamine)

65
Q

What is the lifespan/prognosis of someone diagnosed with ALS?

A

80% die within 2-5 years of diagnosis

66
Q

Define “amyotrophy” as it pertains to ALS

A

Denervation/shrinkage of muscle fibres

67
Q

Define “lateral sclerosis” as it pertains to ALS

A

gliosis (scarring) of lateral columns of white matter

68
Q

What is the pathophysiology of ALS?

A

Genetic mutation that causes glutamate (neurotransmitter) accumulation. This causes calcium channels to open more than normal. This damages both upper and lower neurons controlling voluntary movement. Distal neurons are affected first in lower spinal cord, then the disease moves toward parent nerve.

69
Q

Which motor neurons are affected by ALS? (what part of the brain)

A

Anterior horn of SC
Motor nuclei of brain stem
Cerebral cortex

70
Q

In ALS, damage to which part of the brain causes weakness, lack of motor control, and spasticity?

A

Cerebral cortex

71
Q

What does ALS not affect in most cases?

A

Entire sensory system
Ocular motility
Intellect

72
Q

What are the early manifestations of ALS?

A 
Muscle cramps
One extremity progressively weakens and atrophies
Generalized weakness
Hyporeflexia
Fasciculations
Impaired fine motor control
73
Q

What does ALS stand for?

A

Amyotrophic Lateral Sclerosis

74
Q

What are the late manifestations of ALS?

A

Weakness of limbs and head.
Weakness of palate, pharynx, tongue (speech disorders, dysphagia)
Weakness of neck, shoulders, respiratory muscles
Aspiration
Death due to cerebral and respiratory complications
These manifestations are progressive.

75
Q

What are the treatments for ALS?

A

Riluzole (antiglutamate) decreases glutamate accumulation and slows progression.
Support of ADLs
Nutrition
Psychological assistance

76
Q

What is multiple sclerosis?

A

Inflammation and destruction of CNS myelin. It is immune mediated.

77
Q

Which demographic is the highest risk for multiple sclerosis?

A

Women ages 20-40

If immediate relative affected, 15 times more likely to develop.

78
Q

What occurs during the first stage of multiple sclerosis?

A

Sequential development of small inflammatory lesions.

79
Q

What occurs during the second stage of multiple sclerosis?

A

Lesions extend and consolidate, demyelination and gliosis occurs

80
Q

What parts of the nervous system are affected by multiple sclerosis?

A

Nerve fibres of white matter in brain, spinal cord, and optic nerve

81
Q

What are the characteristics of plaques in multiple sclerosis?

A

Hard, sharp-edged, sclerotic, patchy

82
Q

What are the manifestations of multiple sclerosis?

A 
Paresthesia
Sexual and bladder dysfunction
Fatigue, speech disturbances, mood swings
Optic nerve and muscle abnormalities
Lhermitte Sign
Muscle spasticity
83
Q

What are some examples of the optic nerve and muscle abnormalities that can occur as a manifestation of multiple sclerosis?

A

Neuritis, diplopia, gaze paralysis, nystagmus, vertigo

84
Q

What is the Lhermitte sign?

A

A shock-like response down the back and legs when the neck is flexed.

85
Q

What physical functions are affected when the corticobulbar tracts are affected by multiple sclerosis?

A

Speech/swallowing

86
Q

What physical functions are affected when the corticospinal tracts are affected by multiple sclerosis?

A

Muscle strength

87
Q

What physical functions are affected when the cerebellar tracts are affected by multiple sclerosis?

A

Gait, coordination

88
Q

What physical functions are affected when the spinocerebrellar tracts are affected by multiple sclerosis?

A

Balance

89
Q

What physical functions are affected when posterior cell columns of the spinal cord are affected by multiple sclerosis?

A

Position, vibratory sensation

90
Q

What are the four different types of multiple sclerosis?

A

Relapsing-remitting
Secondary progressive
Primary progressive
Progressive relapsing

Pathophysiology II class notes (15 decks)

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