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Pathology > Myopathy > Flashcards

Myopathy Flashcards

1
Q

What are the primary muscle disease classifications?

A 
Atrophy
Dystrophy
Inflammatory-autoimmune disorders
congenital myopathy
metabolic myopathy
neoplasm
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2
Q

Basic Pathological Changes include

A

Atrophy
Hypertrophy–in the presence of disease–pseudohypertrophy
Pathological degeneration–nerve injury
Limited regeneration

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3
Q

Clinical Features

A

Fatigue
Weakness
Wasting
Pain

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4
Q

Clinical Exam Assessment

A

Muscle testing

weakness and wasting

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5
Q

assessment–Electromyography (EMG)

A

Motor unit potentials are of shorter duration and smaller in amplitude in myopathic disease (eg…dystrophies)

Longer and Larger in Neuropathic Disease

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6
Q

assessment–Serum ENZYME Assays

A

“creatine kinASE” (CK) increase in DMD(duchane muscular dystrophy) look for–muscle damage to the heart!!!
Other enzymes
Lactic dehydrogenase (LDH)
Glutamine oxaloacetic transaminASE (GOT)
Pyruvic KinASE (PK)

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7
Q

assessment–Muscle Biopsies (LM, EM, Immunoflorescence)

A

Necrosis and regeneration

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8
Q

Muscle Atrophy

A

Generalized muscle cell wasting

muscle fiber death secondary to predisposing causes

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9
Q

Generalized muscle cell wasting causes .. a.Generalized Primary Disorders

A

Chronic malnutrition
anterior pituitary atrophy–horomonal—growth horomone
prolonged immobilixation (disuse)
systemic lupus
erythematosis (SLE)
diffuse ischemia (aging (normal), diabetes(pathological))

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10
Q

Normal Skeletal Muscle what Dr TATE said

A

Cross Section and longitudinal
muscle polygonal in shape–if you cut through–multinucleated, equal in size
Fibers all mixed up–stains show the differences in the muscle types

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11
Q

Muscle atrophy

A

Cellular shrinking and misshaping

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12
Q

Generalized muscle cell wasting causes b. Localized

A

Primary denervation
neuropathies–polio
Results–smaller with the loss of myofilaments and organelles
—Denervation atrophy

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13
Q

Extra information on UMN and LMN during muscle atrophy

A
  1. UMN disease wasting and disuse tends to affect type II FT myofibers involved in rapid contractions initially
  2. LMN disease (poliomyelitis) affect both Type I and Type II myofibers
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14
Q

Pathology of Muscle atrophy

A
  1. Descreased mypfiber size
  2. increased sarcolemma
  3. Later stages
    - -loss of striation
    - -lipofuscin pigment accumulation
    - ——metabolic waste product
    - -increased CT in muscle
    - -Fat Cell accumulation
  4. Results of immobilization
    - -decreased number of sarcomeres
    - -sarcomeres in shortened position
    - -% changes in FAST TWITCH and Slow Twitch fibers
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15
Q

Muscle Hypertrophy

A

Increase in size of myofibers

  • Exercise Increases # of sarcomeres and organelles–not the # of fibers
  • –“Pseudohypertrophy is increase in size of gross muscle without true hypertrophy of all myofibers”
  • —–Increase in DCT
  • —-Increase in adipose tissue
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16
Q

What are the causes of skeletal muscle hupertrophy

A

Compensatory
Neurogenic
Myopathic

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17
Q

Compensatory muscle hypertrophy

A

normal conditions, due to increased unaccustomed workload, the opposite of disuse atrophy

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18
Q

Neurogenic muscle atrophy

A

chronic denervation-reinnervation neuropathies, Charcot-Marie-Tooth disease
poliomyelitis
spinal muscular atrophy
ALS

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19
Q

Myopathic

A

Secondary to muscular dystrophies

20
Q

Muscular Dystrophy

A

A group of similar inherited or acquired neuromuscular diseases marked by ‘primary wasting and progressive weakness’ of skeletal muscles

21
Q

Muscular Dystrophy (MD) population

A

Thousands of Americans affected /2/3rds of children.
Different types strike any age
No known cure

22
Q

Muscle Dystrophy is primarily a disease of

A

‘Muscle Tissue with similar pathology’
but the Distribution is
Very different
distinctive distribution

23
Q

Muscle Dystrophy timeline

A

demonstrates a progressive clinical course

24
Q

Muscle Dystrophy aquirement

A

genetically determined; inherited (familial) or acquired (sporadic)
—Sex-linked recessive, autosomal dominant or autosomal recessive

25
Q

MD Background Information

A

Dystrophy

  • -faulty nutrition (latin/greek)
  • -early visual observation of muscle tissue wasting away
    • –not properly nourished
26
Q

How do muscular dystrophies differ?

A 
By severity
age of onset
muscles first and most often affected
rate of progression
mode of inheritance
27
Q

MD Diagnosis–How do we diagnose

A
  1. Tests family history
    - –s/s may not appear until 50% muscle tissue is affected
  2. Clinical examination
  3. Muscle Biopsy–absence of dystrophin (protien in muscle architecture that helps provide support)
  4. Electromyogram
  5. Nerve Conduction Velocity
  6. Blood Enzyme Test–CK creatine kinase
  7. Urine Tests
28
Q

MD Physical THerapy Treatment

A

Exercise Programs–minimize contractures
–delay scoliosis
Orthopedic Devices
Respiratory Care

29
Q

MD Medical Treatment

A

Surgery for contracted tendons

Cardiac Pacemaker

30
Q

MD Drug THerapy (corticosteroids)

A

relieve muscle stiffness

does not affect muscle weakness–treat symptoms

31
Q

General Pathology for MD includes

A
  1. loss of normal polygonal cross section contour
  2. necrosis and phagocytosis of fibers(invasion by macrophages)
  3. Infiltration of fatty, fibrous conncetive tissue
  4. Loss of myofilaments(actin, myosin)–loss of cross striations
  5. Abnormal EMG Activity:increased membrane sensitivity to ACh; at rest fibrillation, spontaneous discharges
32
Q

Classified by presentation of muscle weakness and mode of inheritance can be

A

(X) sex linked
(AD) autosomal dominant
(AR) autosomal recessive

33
Q

Know Duchenne (X) and Becker(X)

A

Sex linked

34
Q

Autosomal Recessive Inheritance

A

Both Parents are Carriers
1 unaffected child
2 Carrier children
1 affected child

35
Q

Autosomal Dominant Inheritance

A

One affected Parent and on unaffected parent
2 affected children
2 unaffected children

36
Q

X linked Inheritance

A 
Carrier mother and unaffected father
1 unaffected daughter XX
1 unaffected son XY
1 carrier daughter XX
1 affected son XY
37
Q

When a man with X-linked MD has children

A

Non-carrier mother–Carrier Father

2 Carrier daughters and 2 unaffected sons

38
Q

Dystrophin Protein

A

protects the stability in the muscle
Provides stability in the cell
w/o it vigorous type of contraction–eccentric contractions–cause severe muscle pathology and distruction

39
Q

Duchenne’s MD

A

much more severe pathology also known as pseudohypertrophic MD

40
Q

Duchenne’s MD represents

A

50% of all cases and is the most severe

41
Q

Duchenne’s MD is a genetic disease

A

characterized by an X-linked recessive gene

42
Q

Duchenne’s age

A

Thought for years to only affect boys

diagnosed between age of 1-5 (inherited)

43
Q

Duchenne’s in females are carriers

A

some females ave been documented who manifest symptoms as heterozygous carriers..ie sporadic mutation

44
Q

Duchenne’s and Dystrophin

A

Dystrophin is found close to the cell membrane and sarcolemmal membrane

  • -It serves to couple the electrical activity with muscular contraction
  • -The lack of dystrophin accounts for muscular wasting
  • -Rise in internal calcium ions causes activation of proteolytic enzyme calpain–leads to muscle pathology
45
Q

Dushennes’s MD

A

Early on the limbs are loose and hypotonic; DTR’s normal or hyporeflexic; joints have full ROM

Pathology (5 decks)

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