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SKIN (INTEGUMENT) LECTURE 6
• Histology Textbooks ‘Basic Histology’,
Junqueira,13 th Edition.
• ‘Colour Atlas of Histology’ Gartner and Hiatt
SELECTED REFERENCES
LECTURE OBJECTIVES
describe the process of skeletal muscle remodeling and its relevance to atrophy
and hypertrophy.
outline the physiology of the neuromuscular junction and describe the
pathogenesis and clinical features of myasthenia gravis.
state how neuromuscular transmission is disrupted in botulism and
organophosphate poisoning.
describe the pathophysiology of Duchenne muscular dystrophy.
outline the pathophysiology of malignant hyperthermia.
Alteration of Neuromuscular Transmission.
Muscular Dystrophies
Other Myopathies
Continual
Replacement of contractile proteins in 2 weeks
Destruction-replacement =atrophy
Replacement-destruction=hypertrophy
Remodeling of Muscles
Although skeletal muscle has a remarkable capacity to repair and adapt to
exercise-induced muscle damage, there is a limit to this capacity for
remodelling. The precise impact of repeated bouts of muscle damage and
repair, over a number of years, on the remodelling capacity of skeletal
muscle is not known. However, there is evidence to suggest that athletes
who expose their muscles to rigorous training and racing regimes may
exceed the muscles finite capacity for repair and adaptation
Remodeling of Muscles
Muscle paresis/paralysis, hypotonia/atonia, and hyporeflexia/areflexia are
usually seen immediately following an insult. The extensor Babinski reflex is
usually absent. Muscle wasting, fasciculations and fibrillations are typically
signs of end-stage muscle denervation. Another feature is the segmentation
of symptoms - only muscles innervated by the damaged nerves will be
symptomatic.
Lower motor neuron lesion
http://en.wikipedia.org/wiki/Paresishttp://en.wikipedia.org/wiki/Paralysishttp://en.wikipedia.org/wiki/Hypotoniahttp://en.wikipedia.org/wiki/Hyporeflexiahttp://en.wikipedia.org/wiki/Plantar_reflexhttp://en.wikipedia.org/wiki/Plantar_reflexhttp://en.wikipedia.org/wiki/Plantar_reflexhttp://en.wikipedia.org/wiki/Muscle_wastinghttp://en.wikipedia.org/wiki/Muscle_wastinghttp://en.wikipedia.org/wiki/Muscle_wastinghttp://en.wikipedia.org/wiki/Fasciculationhttp://en.wikipedia.org/wiki/Fibrillationhttp://en.wikipedia.org/wiki/Denervationhttp://en.wikipedia.org/wiki/Innervation
Neuromuscular Disorders
Myasthenia Gravis
Autoimmune destruction of the end-plate Ach receptors
Loss of junctional fold at end-plate
Widening of synaptic cleft
Symptoms of Myasthenia Gravis
Fatigability and sudden falling-due to reduced to Ach release
Drooping eyelides-double vision
Effected by general state of health and emotion.
Myasthenia gravis
The hallmark of myasthenia gravis is fatigability. Muscles become
progressively weaker during periods of activity and improve after periods of
rest. Muscles that control eye and eyelid movement, facial expressions,
chewing, talking, and swallowing are especially susceptible. The muscles that
control breathing and neck and limb movements can also be affected., the
first noticeable symptom is weakness of the eye muscles. In others, difficulty
in swallowing and slurred speech may be the first signs.
http://en.wikipedia.org/wiki/Fatigabilityhttp://en.wikipedia.org/wiki/Chewinghttp://en.wikipedia.org/wiki/Manner_of_articulationhttp://en.wikipedia.org/wiki/Swallowinghttp://en.wikipedia.org/wiki/Breathhttp://en.wikipedia.org/wiki/Eye_muscleshttp://en.wikipedia.org/wiki/Eye_muscleshttp://en.wikipedia.org/wiki/Eye_muscles
Myasthenia gravis
Treatment
Acetylcholinesterase inhibitors ,e.g.neostigmine , physostigmine.
Other conditions affecting Neuromuscular transmission
Botulism (toxins block Ach release)
Organophosphate poisoning (inhibit acetylcholinesterase irreversibly)
Botulism is a rare and potentially fatal paralytic illness caused by a toxin produced by
the bacteria Clostridium botulinum. The disease begins with weakness, trouble
seeing, feeling tired, and trouble speaking.This may then be followed by weakness of
the arms, chest muscles and legs. The disease does not usually affect consciousness or
cause a fever.
Botulism
http://en.wikipedia.org/wiki/Paralytichttp://en.wikipedia.org/wiki/Clostridium_botulinumhttp://en.wikipedia.org/wiki/Clostridium_botulinumhttp://en.wikipedia.org/wiki/Clostridium_botulinumhttp://en.wikipedia.org/wiki/Consciousness
Botulism is a rare and potentially fatal paralytic illness
caused by a toxin produced by the bacteria Clostridium
botulinum. The disease begins with weakness, trouble
seeing, feeling tired, and trouble speaking.This may then be
followed by weakness of the arms, chest muscles and legs.
The disease does not usually affect consciousness or cause a
fever.
http://en.wikipedia.org/wiki/Paralytichttp://en.wikipedia.org/wiki/Clostridium_botulinumhttp://en.wikipedia.org/wiki/Clostridium_botulinumhttp://en.wikipedia.org/wiki/Clostridium_botulinumhttp://en.wikipedia.org/wiki/Consciousness
Genetic disorders. Progressive muscle weakness and wasting .
characterized by progressive skeletal muscle weakness, defects in muscle proteins,
and the death of muscle cells and tissue. These conditions are generally inherited,
and the different muscular dystrophies follow various inheritance patterns. However,
mutations of the dystrophin gene and nutritional defects (with no genetics history) at
the prenatal stage are also possible in about 33% of people affected by DMD. The
main cause of the Duchenne and Becker types of muscular dystrophy is the muscle
tissue's cytoskeletal impairment to properly create the functional protein dystrophin
and dystrophin-associated protein complex
Duchenne muscular dystrophy (DMD)
http://en.wikipedia.org/wiki/Skeletal_musclehttp://en.wikipedia.org/wiki/Proteinhttp://en.wikipedia.org/wiki/Cell_(biology)http://en.wikipedia.org/wiki/Biological_tissuehttp://en.wikipedia.org/wiki/Cytoskeletalhttp://en.wikipedia.org/wiki/Dystrophinhttp://en.wikipedia.org/wiki/Dystrophin-associated_protein_complexhttp://en.wikipedia.org/wiki/Dystrophin-associated_protein_complexhttp://en.wikipedia.org/wiki/Dystrophin-associated_protein_complex
is the most common childhood form of muscular dystrophy; it generally
affects only boys (with extremely rare exceptions), becoming clinically
evident when a child begins walking. By age 10, the child may need braces
for walking and by age 12, most patients are unable to walk. Life span ranges
from 15 to 51. In the early 1990s, researchers identified the gene for the
protein dystrophin which, when absent, causes DMD. The amount of
dystrophin correlates with the severity of the disease (i.e., the less
dystrophin present, the more severe the phenotype). Since the gene is on the
X chromosome, this disorder affects primarily males, and females who are
carriers have milder symptoms.
muscular dystrophy
http://en.wikipedia.org/wiki/Dystrophin
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