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Cardiac muscle tissue is found only in the heart. It is striated and involuntary.
The fibers are quadrangular in shape and usually contain a single centrally placed nucleus.
Compared to skeletal muscle, cardiac muscle tissue has more sarcoplasm, more mitochondria, less well-developed sarcoplasmic reticulum, and larger transverse tubules located at Z discs rather than at the A-I band junctions.
Cardiac muscles branch freely and are connected via gap junctions.
Intercalated discs provide strength and aid in conduction of muscle action potentials by way of gap junctions that are located in the discs.
Intercalated discs are what make cardiac muscle appear like sheets of bamboo under the microscope.
Unlike skeletal muscle tissue, cardiac muscle tissue contracts and relaxes rapidly, continuously and rhythmically.
ATP is generated aerobically by large, numerous mitochondria that are found in cardiac muscle.
Cardiac muscle can contract without extrinsic stimulation and can remain contracted longer than skeletal muscle.
Cardiac muscle has a long refractory period. This allows the heart to relax in between beats and this prevents tetani in the muscle.
Smooth muscle is nonstriated and involuntary.
Smooth muscle fibers are considerably smaller than skeletal muscle fibers and are thickest at the center and taper at the ends.
Each fiber contains a single oval, centrally located nucleus and thick and thin myofilaments.
Smooth muscle fibers contain intermediate filaments and dense bodies which function as Z discs.
Visceral or single unit smooth muscle is found in the walls of hollow viscera and small blood vessels; The fibers are arranged in a network.
Multiunit smooth muscle is found in large blood vessels, large airways, the arrector pilli muscle and the iris of the eye. The fibers operate singly rather than as a unit.
The duration of contraction and relaxation of smooth muscle is longer than in skeletal muscle.
In smooth muscle, the regulator protein that binds calcium in the cytosol is calmodulin (which takes the place of troponin in striated muscle).
Calmodulin activates the enzyme myosin light chain kinase which facilitates myosin-actin binding and allows contraction to occur at a relatively slow rate.
Smooth muscle fibers contract in response to nerve impulses, hormones and local factors.
Smooth muscle fibers can stretch considerably without developing tension; this phenomenon is termed the “stress-relaxation response.”
Regeneration of Muscle Tissue
Skeletal muscle fibers cannot divide and have limited powers of regeneration; growth after the first year is due to enlargement of existing cells rather than an increase in the actual number of fibers.
Cardiac muscle fibers cannot divide or regenerate.
Smooth muscle fibers have limited capacity for division and regeneration.
Homeostatic Imbalances of Muscle Tissue
Fibromyalgia : Refers to a group of common non-articular rheumatic disorders that are statistically more common in women and are characterized by pain, tenderness and stiffness of muscles, tendons and ligaments. Frequent sites are the lower back (often referred to as “lumbago”), neck, chest and thighs (termed a “charleyhorse”).
Muscular Dystrophy refers to a group of inherited muscle-destroying diseases that are characterized by degeneration of individual muscle fibers, leading to progressive atrophy of skeletal muscle.
The most common form is Duchenne Muscular Dystrophy , for which there is hope that gene therapy may someday be employed to replace one affected gene for another to stop the progressive muscle loss.
Types of Muscular Dystrophy
Becker’s muscular dystrophy
Duchenne muscular dystrophy
Facioscapulohumeral muscular dystrophy
Limb-girdle muscular dystrophy
Emery-Dreifuss muscular dystrophy
Symptoms of Muscular Dystrophy
Symptoms vary with the different types of muscular dystrophy. Some types (Duchenne muscular dystrophy) are deadly while other types cause little disability and are associated with normal life span.
The muscles affected vary, but can be around the pelvis, shoulder, face or elsewhere. Muscular dystrophy can affect adults, but the more severe forms tend to occur in early childhood.
Symptoms of Muscular Dystrophy
Muscle weakness that slowly gets worse
Delayed development of muscle motor skills
Problems walking or a delay in walking
Difficulty using one or more muscle groups
Eyelid drooping (ptosis)
Mental retardation (only present in some types of the condition)
Hypotonia (low muscle tone)
Joint contractures (clubfoot, clawhand, or others)
Scoliosis (curved spine)
Some types of muscular dystrophy involve the heart muscle, causing cardiomyopathy or arrhythmias.
Note: Not all symptoms are seen in every patient
Diagnosis of Muscular Dystrophy
A complete physical examination and medical history will determine the type of muscular dystrophy. Specific muscle groups are affected by different types of muscular dystrophy.
Often, there is a loss of muscle mass or wasting, which may be hard to see because some types of muscular dystrophy cause a build up of fat and connective tissue that makes the muscle appear larger. This is called pseudohypertrophy.
Diagnosis of Muscular Dystrophy
A muscle biopsy may be used to confirm the diagnosis. In some cases, a DNA blood test may be all that is needed.
Myoglobin - urine/serum
LDH (lactate dehydrogenase) – Exercising muscles convert glucose to lactate which is then released into the blood and is later taken up by the liver. LDH is used to check for muscle health.
Serum Creatinine - levels vary according to a person's size and muscle mass; is also used to measure kidney function.
AST (Aspartate aminotransferase) – used to check for muscle & liver damage
Aldolase - involved in the breakdown of glucose, fructose, and galactose to generate energy in the form of ATP; found in high concentrations in muscle.
Treatment of Muscular Dystrophy
There are no known cures for the various muscular dystrophies. The goal of treatment is to control the symptoms.
Physical therapy may help patients maintain muscle strength and function. Orthopedic appliances such as braces and wheelchairs can improve mobility and self-care abilities. In some cases, surgery on the spine or legs may help improve function.
Corticosteroids taken by mouth are sometimes prescribed to patients to keep them walking for as along as possible.
The person should be as active as possible. Complete inactivity (such as bed rest) can make the disease worse.
Myasthenia Gravis: An autoimmune disorder characterized by great muscular weakness and caused by antibodies directed against Ach receptors at the neuromuscular junction; more Ach receptors are affected as the disease progresses, making the muscle increasingly weaker.
What is Myasthenia Gravis?
Myasthenia gravis is a chronic autoimmune neuromuscular disease characterized by varying degrees of weakness of the skeletal (voluntary) muscles of the body. The name myasthenia gravis, which is Latin and Greek in origin, literally means "grave muscle weakness." However for the majority of individuals with myasthenia gravis, life expectancy is not lessened by the disorder.
The hallmark of myasthenia gravis is muscle weakness that increases during periods of activity and improves after periods of rest. Certain muscles such as those that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are often, but not always, involved in the disorder. The muscles that control breathing and neck and limb movements may also be affected.
What causes Myasthenia Gravis?
Myasthenia gravis is caused by a defect in the transmission of nerve impulses to muscles. It occurs when normal communication between the nerve and muscle is interrupted at the neuromuscular junction. Normally when impulses travel down the nerve, the nerve endings release a neurotransmitter substance called acetylcholine. Acetylcholine travels through the neuromuscular junction and binds to acetylcholine receptors which are activated and generate a muscle contraction.
In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction which prevents the muscle contraction from occurring. Thus, myasthenia gravis is an autoimmune disease because the immune system mistakenly attacks itself.
Symptoms of Myasthenia Gravis
Although myasthenia gravis may affect any voluntary muscle, muscles that control eye and eyelid movement, facial expression, and swallowing are most frequently affected. The onset of the disorder may be sudden. Symptoms often are not immediately recognized as Myasthenia Gravis.
In most cases, the first noticeable symptom is weakness of the eye muscles. In others, difficulty in swallowing and slurred speech may be the first signs. The degree of muscle weakness involved in myasthenia gravis varies greatly among patients, ranging from a localized form, limited to eye muscles (ocular myasthenia), to a severe or generalized form in which many muscles are affected.
Symptoms, which vary in type and severity, may include a drooping of one or both eyelids (ptosis), blurred or double vision (diplopia) due to weakness of the muscles that control eye movements, unstable or waddling gait, weakness in arms, hands, fingers, legs, and neck, a change in facial expression, difficulty in swallowing and shortness of breath, and impaired speech (dysarthria).
Myasthenia gravis occurs in all ethnic groups and both genders. It most commonly affects women under 40 and men over 60 but it can occur at any age.
In neonatal myasthenia, the fetus may acquire immune proteins (antibodies) from a mother affected with myasthenia gravis. Generally, cases of neonatal myasthenia gravis are transient (temporary) and the child's symptoms usually disappear within 2-3 months after birth. Other children develop myasthenia gravis indistinguishable from adults. Myasthenia gravis in juveniles is common.
Myasthenia gravis is not directly inherited nor is it contagious . However, the disease may occur in more than one member of the same family.
Rarely, children may show signs of congenital myasthenia or congenital myasthenic syndrome. These are not autoimmune disorders, but are caused by defective genes that produce proteins in the acetylcholine receptor or in acetylcholinesterase.
Diagnosis of Myasthenia Gravis
Unfortunately, a delay in diagnosis of one or two years is not unusual in cases of myasthenia gravis. Because weakness is a common symptom of many other disorders, the diagnosis is often missed in many individuals.
The first steps of diagnosing myasthenia gravis include a review of the individual's medical history, and physical and neurological examinations. The signs a physician must look for are impairment of eye movements or muscle weakness without any changes in the individual's ability to feel things.
Diagnosis of Myasthenia Gravis
If the doctor suspects myasthenia gravis, several tests are done to confirm the diagnosis:
A blood test is done to detect the presence of immune molecules or acetylcholine receptor antibodies. Levels are elevated in Myasthenia Gravis patients.
The edrophonium test. This approach requires the intravenous administration of edrophonium chloride or Tensilon(r), a drug that blocks the degradation (breakdown) of acetylcholine and temporarily increases the levels of acetylcholine at the neuromuscular junction. In people with myasthenia gravis involving the eye muscles, edrophonium chloride will briefly relieve weakness.
A single fiber electromyography (EMG) test. Here, single muscle fibers are stimulated by electrical impulses. EMG measures the electrical potential of muscle cells. Muscle fibers in myasthenia gravis do not respond as well to repeated electrical stimulation compared to muscles from normal individuals.
A pulmonary function test. This test measures breathing strength and helps to predict whether respiration may fail which would lead to a myasthenic crisis.
Treatment of Myasthenia Gravis
Myasthenia gravis is controlled but not cured.
Medications used to treat the disorder include anticholinesterase agents such as neostigmine and pyridostigmine , which help improve neuromuscular transmission and increase muscle strength.
Immunosuppressive drugs such as prednisone , cyclosporine and azathioprine may also be used. These medications improve muscle strength by suppressing the production of abnormal antibodies.
These drugs must be used with careful medical follow-up because they can cause serious side effects.