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Phys exam 3 > Muscle Pathology > Flashcards

Muscle Pathology Flashcards

1
Q

atrophy caused by

A 
inactivity 
ischemia 
malnutrition 
aging 
chronic disease
denervation 
corticosteroid induced myopathy
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2
Q

necrosis

A

common response to muscle injury from primary muscle disease

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3
Q

types of injury

A

external - toxin

internal - structural disturbance

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4
Q

what 2 things happen during muscle necrosis?

A
  • myophagocytosis

- satellite cells become myoblasts & repair the injury

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5
Q

in chronic disorders what role does necrosis play with regeneration

A

muscle fiber necrosis wins out over regeneration = fibrosis

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6
Q

Rhabdomyolysis

A

dissolution of skeletal muscle fibers that release myoglobin into the circulation

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7
Q

Necrosis Rhabdomyolysis secondary to

A 
Hypertension 
Viruses
Mild Exercise
Anesthesia
EtOH
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8
Q

Myositis

A
  • inflammation of muscle
  • autoimmune
  • lymphocytes infiltrate the muscle and damage it
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9
Q

Clinical Presentation of Myositis

A 
malaise
fever
muscle swelling
pain
tenderness
lethargy
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10
Q

Fibrosis

A
  • muscle cell loss
  • limited capacity for regeneration
  • fibrotic tissue lacks strength and distensibility
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11
Q

Inflammatory Myopathies

A

non specific muscle weakness secondary to identifiable disease or condition

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12
Q

what type of disorder is Inflammatory Myopathies

A

autoimmune origin

associated with other autoimmune and connective tissue disorders

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13
Q

Morphology of Inflammatory Myopathies

A
  • inflammatory cells are present
  • necrosis and phagocytosis
  • regeneration and atrophy
  • fibrosis
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14
Q

Inflammatory Myopathies symptoms

A
  • symmetrical proximal muscle weakness
  • insidious onset & gets worse
  • includes neck muscles & larynx
  • can have cardiac involvement & pulmonary muscle weakness
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15
Q

Other causes of Inflammatory Myopathies

A

Bacterial infections (wound, trauma, spread from adjacent structures, sepsis)

Viral infection

Parasitic infection

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16
Q

3 types of muscle diseases

A
  1. Neurogenic muscle atrophy
  2. Myopathy or primary muscle disease
  3. Disease of neuromuscular junction
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17
Q

Neurogenic muscle atrophy

A

denervation

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18
Q

Myopathy or primary muscle disease

A

destruction & loss of muscle mass

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19
Q

Types of Myopathy or primary muscle disease

A
  • dystrophies
  • congenital myopathies
  • inflammatory myopathies
  • toxic or metabolic myopathies
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20
Q

diseases of neuromuscular junction

A

Myasthenia gravis (MG)

Lambert-Eaton Myasthenic Syndrome (LEMS)

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21
Q

Causes of Neurogenic Atrophy

A

Lower Motor Neuron Disease

PNS

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22
Q

Denervation Atrophy of Neurogenic Atrophy

A

Atrophy is secondary to loss of myofibrils and myofilaments

  • reinnervation attempts w/ every episode of denervation
  • adjacent motor units help to try and “plug in”

-if not re-innervated = complete loss of fibrils and filaments

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23
Q

Spinal Muscular Atrophy (SMA)

A

4 types - Type I - IV

  • Degeneration of anterior horn cells
  • 2nd most common lethal autosomal recessive disorder
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24
Q

Type I: Werdnig-Hoffman (infantile SMA)

A

Progressive & severe weakness in early infancy

Absent survival motor neuron gene

Degeneration can begin in utero after motor units have been established

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25
Q

Type II: Intermediate form (SMA)

A

Progressive but stabilizes

Moderate to severe hypotonia

Shortened life span

Attain the ability to sit at some point

Reliance on power mobility

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26
Q

Type III: Kugelberg-Welander (Juvenile SMA)

A

Later onset & not necessarily progressive

Attain the ability to ambulate at some point - wheelchair dependent

“Limb-girdle muscular dystrophy”

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27
Q

Non-inherited Muscular Dystrophy

A

spontaneous mutation (30% of cases)

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28
Q

Inherited Muscular Dystrophy

A

Severe & Progressive X-linked degeneration of skeletal muscle

Mother is carrier
Affects boyd

Progressive wasting of pelvic and shoulder girdle

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29
Q

Duchenne MD Pathogenesis

A

Mutation of the gene that codes for dystrophin

Without it = muscle cells cannot regulate the influx of Ca2+ == causes disintegration & weakness

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30
Q

where is dystrophin located?

A

sarcolema

31
Q

Duchenne MD Degeneration of muscle fibers

A
  • Degeneration outpaces regeneration
  • Progressive diseases in number of muscle fibers
  • Progressive increase in fibrofatty connective tissue
32
Q

Clinical Features of Duchenne MD

A

Elevated CK-MM

pelvic and shoulder girdle weakness

usually becomes evident at 2-4 years

Pseudohypertrophy of calf muscles (fibrofatty connective tissue)

33
Q

Clinical Presentation of Duchenne MD

A
  • Develop contracture
  • Gower’s sign
  • In wheelchair by age 9-10
34
Q

most common causes of death Duchenne MD

A
  • Respiratory insufficiency

- Cardiac Dysthymia

35
Q

Fibrofatty connective tissue

A

end stage of neuromuscular disease

muscle was stained & replaced by fibrofatty connective tissue

36
Q

Becker’s Muscular Dystrophy

A

dystrophin connects in the cytoskeleton of muscle fiber to the surrounding extracellular matrix through cell membrane

37
Q

who is carrier in Becker’s Muscular Dystrophy

A

5 in 100,000 live male births

mother is carrier

38
Q

Clinical Presentation Becker’s Muscular Dystrophy

A

Long life expectancy

Stay ambulatory for a long period of time (toe walkers = calf hypertrophy)

Involvement of proximal musculature first then distals

39
Q

Contractures of Becker’s Muscular Dystrophy

A
  • Elbow flexors
  • Forearm pronators
  • Wrist Flexors
  • Plantar and Knee Flexors
  • Hip Adduction
40
Q

implications for PT during MD

A

maintain function in unaffected muscle groups for as long as possible

avoid eccentric exercises

contracture management

Glucocorticoid therapy

41
Q

Facioscapulohumeral Dystrophy

A

Genetic defect

Autosomal dominant

42
Q

Clinical Presentation of Facioscapulohumeral Dystrophy

A

mild form of MD

Starts with weakness and atrophy of facial muscles and shoulder girdle

Lower extremity weakness is delayed

43
Q

do individuals develop contractures, skeletal deformities, or muscle hypertrophy in Facioscapulohumeral Dystrophy

A

NO

44
Q

Myotonic Dystrophy

A

most common form of adult dystrophy

prolonged muscle spasm that cannot relax after contraction

45
Q

what type of disorder is Myotonic Dystrophy

A

inherited autosomal dominant disorder

46
Q

Type 1 Myotonic Dystrophy

A

slow twitch

fiber type atrophy

47
Q

Type II Myotonic Dystrophy

A

fast twitch

Hypertrophy

48
Q

Myotonic Dystrophy compared to Duchenne MD

A

far less necrosis and regeneration

49
Q

Adult Clinical Presentation of Myotonic Dystrophy

A

20-30 y.o

progressive muscle weakness & stiffness of distal limbs

facial & jaw muscles are always effects

Personality deterioration

testicular atrophy

smooth muscle involvement

50
Q

Congenital Clinical Presentation of Myotonic Dystrophy

A

seen only in offspring of women who have symptoms

infants born with severe muscular weakness

high incidence of mental defects

51
Q

most common cause of toxic and metabolic myopathies

A

alcoholism

directly affects muscle cells = Rhabdomyolysis

Liver damage affects metabolism of lipids & carbohydrates

52
Q

Toxic and Metabolic Myopathies drugs

A

Vitamin E overdose
Lead
Methotrexate
Penicillin

53
Q

Metabolic Myopathies

DM
Cushing's 
Addison's
Hyper/Hypo Thyroidism 
Hormonal Imbalances
A

DM = secondary to vasculopathy

Cushing = too much cortisol = break down of tissue

Addison’s = decreased glucocorticoid = decreased gluconeogenesis = decreased glycogen stores = weakness

Hyper/Hypo thyroidism = proximal weakness = pelvis>shoulders

54
Q

Myasthenia Gravis

A

Disease of the Neuromuscular Junction

abnormal muscular fatigability

circulating antibodies to Ach receptors at the neuromuscular junction

55
Q

What type of disorder is Myasthenia Gravis

A

acquired autoimmune disease

56
Q

Incidence of Myasthenia Gravis

A

all races

twice as common in women

young adulthood

histologically - no muscular pathologic changes

57
Q

Myasthenia Gravis effect on antibodies & Ach at the motor end plate

A

antibodies attach to Ach receptors = blocks the binding sites for Ach

  • blocked receptor sites
  • atrophic motor end plants
  • decreased number of receptors
  • widened synaptic space
58
Q

Role of Thymus in Myasthenia Gravis

A

40% of patients have thymoma

75% have thymic hyperplasia

59
Q

Clinical Features of Myasthenia Gravis

A
  • fatigue and muscle weakness
  • weakness of extraocular muscles
  • dysphagia
  • trunk weakness (respiratory insufficiency)
  • arm weakness
60
Q

Treatment of Myasthenia Gravis

A

Thymectomy, plasmapheresis & cholinesterase inhibitors

61
Q

Lambert-Eaton Myasthenic Syndrome (LEMS)

A

muscle weakness

wasting

fatigability of proximal limbs and trunk

usually associated with small cell lung CA

62
Q

How does Lambert-Eaton Myasthenic Syndrome (LEMS) defect Ach release ?

A
  • Ca2+ channels are necessary for Ach release

- Ca2+ channels are reduced on the presynaptic side

63
Q

Two forms of Lambert-Eaton Myasthenic Syndrome (LEMS)

A

1 associated w/ SC lung CA

auto-immune

64
Q

Torticollis

A

“Wry neck” - muscular fibrosis

65
Q

Torticollis is contracture of what muscle

A

SCM

66
Q

How does Torticollis occur

A

breach & forcep delivery - vacuum extraction & cesarean section

67
Q

Spasmotic Torticollis

A

Cervical dystonia

3 in 10,000 adults

central disorder vs. muscle disorder

68
Q

Arthrogryposis Multiplex Congenita

A

multiple congenital contractures present at birth

69
Q

3 types of Arthrogryposis Multiplex Congenita

A

Amyoplasia
Distal
“everything else”

70
Q

Arthrogryposis Multiplex Congenita other abnormalities

A

cleft palate, cardiac, urinary tract malformations

71
Q

Clinical Manifestation of Arthrogryposis Multiplex Congenita

A

joint contracture

articular rigidity

muscle weakness

fibro-fatty tissue

72
Q

Frog Posture Arthrogryposis Multiplex Congenita

A

slower to roll but quicker to sit and scoot

can hold standing once placed

73
Q

In adulthood Arthrogryposis Multiplex Congenita

A

DJD secondary to overuse

May need powered mobility to project joints

Phys exam 3 (5 decks)

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