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SKIN (INTEGUMENT) LECTURE 6

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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