Flashcards in SDL-5 Neuromuscular Disease Pathology Deck (22):
Type (I/II/III) muscle fibers are white, have 'fast' myosin, primarily used in strength and speed, and are rich in glycolytic enzymes and glycogen.
Type (I/II/III) muscle fibers are red, have 'slow' myosin, primarily used in endurance, and are rich in mitochondria and myoglobin.
(T/F) Normal muscle fibers have congregations of type I and type II fibers that largely remain segregated.
False. Normal muscle fibers have a diverse distribution of type I and II fibers, often resembling a "checkerboard" pattern.
What is the typical progression of chronic denervation in muscle?
I. Normal muscle is present
II. Motor unit loss to normal muscle causes small group atrophy
III. Collateral axonal sprouting follows motor unit loss. Re-innervation is attempted, and fiber type is "grouped" (reinnervated fibers switch to coincide with new axon) with giant motor units
IV. Further motor unit loss causes large group atrophy
Early denervation in neurogenic atrophy causes:
I. Formation of small angular fibers
II. Involvement of type I and II fibers
Chronic denervation in neurogenic atrophy results in:
I. Axonal sprouting and reinnervation
II. Formation of large motor units
III. Fiber type grouping
Late denervation of muscles in neurogenic atrophy causes:
I. Loss of large motor units
II. Large group atrophy of muscle fibers
_____________ is an autoimmune disease in which antibodies are produced against the body's acetylcholine receptors at synapses such as neuromuscular junctions.
What general myopathic changes may be observed in a patient with myasthenia gravis?
I. Myofiber degeneration and/or regeneration
II. Internalization of cell nuclei
III. Increased endomysial connective tissue (scar tissue formation)
Type II atrophy of muscle is typically seen accompanying:
II. Chronic disease
The two most common inflammatory myopathies are _____________ and ___________.
Intrafascicular inflammation is a pathology commonly seen in (polymyositis/dermatomyositis/inclusion body myositis).
The pathogenesis of polymyositis is caused by (humoral response/cytotoxic t-cells/degeneration of cellular structures).
Cytotoxic T cells
(T/F) Clinical presentation of polymyositis includes pain and a noticeable rash.
False. This is the clinical presentation of dermatomyositis. Polymyositis presents without rash. Only pain is present.
Extrafascicular inflammation and perifascicular atrophy are pathologies commonly seen in (polymyositis/dermatomyositis/inclusion body myositis).
The pathogenesis of dermatomyositis is caused by (humoral response/cytotoxic t-cells/degeneration of cellular structures).
Inclusions and rimmed vacuoles are pathologies commonly seen in (polymyositis/dermatomyositis/inclusion body myositis).
Inclusion body myositis
The pathogenesis of inclusion body myositis is caused by (humoral response/cytotoxic t-cells/degeneration of cellular structures).
Degeneration of cellular structures
(T/F) Inclusion body myositis presents clinically with resistance to steroids.
A general systemic deficiency of dystrophin results in (Duchenne MD/Becker MD/Myotonic MD).
A truncated dystrophin molecule caused by a multiple-of-three base deletion results in (Duchenne MD/Becker MD/Myotonic MD).