I.

OBJECTIVE OF THE GENERAL OBJECTIVES After establishing a nurse-patient interaction and comprehensive assessment and providing care to the clients and vigilant study of the clients condition, student will be able to gain knowledge, developed skills, achieve comprehensive evaluation and enhance attitude through the utilization of the nursing process on the care and management of the patient with Myasthenia Gravis. II. SPECIFIC OBJECTIVES The student is expected to: 1. Define what Myasthenia Gravis is. 2. Identify its clinical manifestation. 3. Present the Anatomy and Physiology. 4. Trace the pathophysiology of the disease. 5. Establish a good and therapeutic nurse-patient interaction. 6. Determine the status of the patient through: a. General data b. Physical Assessment c. Present history of the illness d. Family Health History e. Personal and Social History 7. Analyze laboratory results and correlate it with patients present condition. 8. Familiarize self with diagnostic procedures done to patient. 9. Identify and understand the importance of medicine in relation to patients present condition. 10. Render nursing care through implementation of Nursing Care Plan. 11. Evaluate the effectiveness of nursing care plan and medical management.

III. INTRODUCTION OF THE DISEASE Much has been written about myasthenia gravis (MG) in recent years, because there now seems to be a plausible, scientific explanation for the cause of this disease. The word "gravis" seems no longer appropriate, as current forms of treatment virtually have allowed patients to live fully functional and independent lives. This review will summarize the therapeutic advances that have been made in the ocular form of MG, stressing the most effective and practical ways to manage double vision (diplopia) and droopiness of one or both lids (ptosis). Myasthenia is an autoimmune neuromuscular disease leading to fluctuating muscle weakness and fatiguability. It is an autoimmune disorder, in which weakness is caused by circulating antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction, inhibiting the stimulative effect of the neurotransmitter acetylcholine. Myasthenia is treated medically with cholinesterase inhibitors or immunosuppressants, and, in selected cases, thymectomy. At 200400 cases per million it is one of the less common autoimmune disorders. MG must be distinguished from congenital myasthenic syndromes that can present similar symptomatology but offer no response to immunosuppressive interventions. IV. ANTOMY AND PHYSIOLOGY MUSCULAR SYSTEM MG is the paradigm of an autoimmune disorder, i.e., it is caused by an antibody which antibodies viruses MG is in is and which referred a attacks normal bacteria, there to is as daily or an and diminishes the integrity of one of the body's own components. Making process from the moment we're born and exposed to such foreign proteins as even snake venom. When a patient makes an antibody against themselves, as in anomalous antibody produced against the receptor end plate of voluntary muscles, it autoimmune. This autoimmune attack on the muscles end plate accounts for the

symptoms

and

signs

of

ocular and generalized MG. All the muscles in our body are activated by nerve impulses which travel along nerve junction, released resulting contraction. Patients with MG enigmatically produce a blocking antibody which deposits on the neuromuscular transmission leads to muscular fatigue and sometimes frank paralysis. Characteristic of which moves treatment AcH neuromuscular junction. The muscular system is the anatomical system of a species that allows it to move. The muscular system in vertebrates is controlled through the nervous system, although some muscles (such as the cardiac muscle) can be completely autonomous. Muscles There are three distinct types of muscles: skeletal muscles, cardiac or heart muscles, and smooth (non-striated) muscles. Muscles provide strength, balance, posture, movement and heat for the body to keep warm. MG moves the is at face, to the is one arm either the eye or randomness of neuromuscular blockade. It may be confined only to a small muscle upward, outward, downward or laterally; or to one of the larger muscles which leg or breathing muscles. Regardless of the muscles involved, the goal of effective reduce the concentration of the blocking antibody or to increase the concentration of receptor muscle membrane and prevents the entry of AcH molecules. The resulting attenuation of in a trunks the called muscular emanating point from the brain and spinal cord. When these nerve impulses reach the neuromuscular at which a nerve fiber synapses with or terminates on a muscle fiber, a chemical is acetylcholine (AcH), which attaches to a receptor on the muscle membrane,

Skeletal muscle Skeletal muscle fibres are multinucleated, with the cell's nuclei located just beneath the plasma membrane. The cell comprises a series of striped or striated, thread-like myofibrils. Within each myofibril there are protein filaments that are anchored by tendons. The fiber is one long continuous string-like structure. The smallest cross section of skeletal muscle is called a sarcomere which is the functional unit within the cell. It extends from one Z line to the next attached Z line. The individual sarcomere has alternating thick myosin and thin actin protein filaments. Myosion forms the center or middle of each M line. Thinner actin filaments form a zig zag pattern along the anchor points or Z line. Upon stimulation by an action potential, skeletal muscles perform a coordinated contraction by shortening each sarcomere. The best proposed model for understanding contraction is the sliding filament model of muscle contraction. Actin and myosin fibers overlap in a contractile motion towards each other. Myosin filaments have club-shaped heads that project toward the actin filaments. Larger structures along the myosin filament called myosin heads are used to provide attachment points on binding sites for the actin filaments. The myosin heads move in a coordinated style, they swivel toward the center of the sarcomere, detach and then reattach to the nearest active site of the actin filament. This is called a rachet type drive system. This process consumes large amounts of adenosine triphosphate (ATP). Energy for this comes from ATP, the energy source of the cell. ATP binds to the cross bridges between myosin heads and actin filaments. The release of energy powers the swiveling of the myosin head. Muscles store little ATP and so must continuously recycle the discharged adenosine diphosphate molecule (AOP) into ATP rapidly. Muscle tissue also contains a stored supply of a fast acting recharge chemical, creatine phosphate which can assist initially producing the rapid regeneration of ADP into ATP. Calcium ions are required for each cycle of the sarcomere. Calcium is released from the sarcoplasmic reticulum into the sarcomere when a muscle is stimulated to contract. This calcium uncovers the actin binding sites. When the muscle no longer needs to contract, the calcium ions are pumped from the sarcomere and back into storage in the sarcoplasmic

At rest, the body produces the majority of its ATP aerobically in the mitochondria without producing lactic acid or other fatiguing byproducts. During exercise, the method of ATP production varies depending on the fitness of the individual as well as the duration, and intensity of exercise. At lower activity levels, when exercise continues for a long duration (several minutes or longer), energy is produced aerobically by combining oxygen with carbohydrates and fats stored in the body. Activity that is higher in intensity, with possible duration decreasing as intensity increases, ATP production can switch to anaerobic pathways, such as the use of the creatine phosphate and the phosphagen system or anaerobic glycolysis. Aerobic ATP production is biochemically much slower and can only be used for long-duration, low intensity exercise, but produces no fatiguing waste products that can not be removed immediately from sarcomere and body and results in a much greater number of ATP molecules per fat or carbohydrate molecule. Aerobic training allows the oxygen delivery system to be more efficient, allowing aerobic metabolism to begin quicker. Anaerobic ATP production produces ATP much faster and allows near-maximal intensity exercise, but also produces significant amounts of lactic acid which render high intensity exercise unsustainable for greater than several minutes. The phosphagen system is also anaerobic, allows for the highest levels of exercise intensity, but intramuscular stores of phosphocreatine are very limited and can only provide energy for exercises lasting up to ten seconds. Recovery is very quick, with full creatine stores regenerated within five minutes. Control of muscle contraction Neuromuscular junctions are the focal point where a motor neuron attaches to a muscle. Acetylcholine, (a neurotransmitter used in skeletal muscle contraction) is released from the axon terminal of the nerve cell when an action potential reaches the microscopic junction, called a synapse. A group of chemical messengers cross the synapse and stimulate the formation of electrical changes, which are produced in the muscle cell when the acetylcholine binds to receptors on its surface. Calcium is released from its storage area in the cell's sarcoplasmic reticulum. An impulse from a nerve cell causes calcium release and brings about a single, short muscle contraction called a muscle twitch. If there is a problem at the neuromuscular junction, a very prolonged contraction may occur, tetanus. Also, a loss of function at the junction can produce paralysis. Skeletal muscles are organized into hundreds of motor units, each of which involves a motor neuron, attached by a series of thin finger-like structures called axon terminals. These attach to and control discrete bundles of muscle fibers. A coordinated

and fine tuned response to a specific circumstance will involve controlling the precise number of motor units used. While individual muscle units contract as a unit, the entire muscle can contract on a predetermined basis due to the structure of the motor unit. Motor unit coordination, balance, and control frequently come under the direction of the cerebellum of the brain. This allows for complex muscular coordination with little conscious effort, such as when one drives a car without thinking about the process. EYE Eyes are organs that detect light, and convert it to electro-chemical impulses in neurons. In The connect higher simplest light to organisms photoreceptors movement.

complex neural pathways exist that connect the eye, via the optic nerve to the visual cortex and other areas of the brain. Complex optical systems with Schematic diagram of the vertebrate eye. resolving power have come in ten fundamentally different forms, and 96% of animal species possess a complex optical system. Image-resolving eyes are present in molluscs, chordates and arthropods. The simplest "eyes", such as those in unicellular organisms, do nothing but detect whether the surroundings are light or dark, which is sufficient for the entrainment of circadian rhythms. From more complex eyes, retinal photosensitive ganglion cells send signals along the retinohypothalamic tract to the suprachiasmatic nuclei to effect circadian adjustment.

Extraocular muscles The extraocular muscles are the six muscles that control the movements of the (human) eye. The actions of the extraocular muscles depend on the position of the eye at the time of muscle contraction. List of muscles

Inserted Muscle Innervation Origin Insertion Primary function Secondary Tertiary function function into the sclera distance Superior Superior branch rectus nerve Inferior Inferior branch rectus nerve of oculomotor of oculomotor Annulus of from tendinous ring Annulus of from tendinous ring Annulus of from tendinous ring Annulus of of from tendinous ring Annulus of via of oblique which forms 'pulley system'. Inferior Inferior branch nerve of Maxillary oblique oculomotor bone eye (posterior, inferior, lateral surface) Extorsion Elevation Abduction a Zinn the (posterior, Depression Abduction[3] lateral surface) Zinn Zinn Zinn Zinn eye (anterior, superior surface) eye (anterior, inferior surface) eye (anterior, lateral surface) eye (anterior, medial surface) Adduction 5.5mm Abduction 6.9mm Depression Extorsion Adduction 6.5mm Elevation Intorsion Adduction 7.7mm

Lateral rectus

Abducens nerve

Inferior Medial rectus branch nerve oculomotor

Trochlea eye Superior Trochlear oblique nerve superior superior, Intorsion

Importance Since only the fovea provides sharp distinct vision, the eye must move to follow a target. It must be precise and fast. This is seen in scenarios like reading, wherein the reader must shift gaze constantly, or following a small object like a golf ball, in which the extraocular muscles must lead the eye to follow the head movements. Although under voluntary control, most movement is done without thinking, such as those based on head or other body movement, or movement of objects in the area. Researchers still have some work in order to find the parallel nature of the environment-based (involuntary) and voluntary control. Innervation The nuclei or bodies of these nerves are found in the brain stem. The nuclei of the abducens and oculomotor nerves are connected. This is important in coordinating motion of the lateral rectus in one eye and the medial action on the other. In one eye, in two antagonistic muscles, like the lateral and medial recti, contraction of one leads to inhibition of the other. Muscles shows small degrees of activity even when resting, keeping the muscles taut. This "tonic" activity is brought on by discharges of the motor nerve to the muscle. Actions Note that intorsion and extorsion are not included in the following table; their actions are accounted for via summation of other actions. Medial (towards nose) Lateral (towards temple) Elevation, abduction: Elevation, adduction: Superior rectus Adduction: inferior oblique Abduction: adduction:

Medial rectus Lateral rectus Depression, abduction: Depression, Inferior rectus

Superior oblique

These motions are only for eye examinations. Note that they are different from the intrinsic motor functions of each muscle. This is done in an exam to separate out the muscle being tested specifically.

In an eye examination, the inability of the patient to move the eye in the specified direction can indicate a problem with the associated muscle, and the nerve associated with that muscle.

Coordination of Movement Between Both Eyes Intermediate directions are controlled by simultaneous actions of multiple muscles. When one shifts the gaze horizontally, one eye will move laterally (toward the side) and the other will move medially (toward the midline). This may be neurally coordinated by the central nervous system, to make the eyes move together and almost involuntarily. This is a key factor in the study of squint, namely, the inability of the eyes to be directed to one point. There are two main kinds of movement: conjugate movement (the eyes move in the same direction) and disjunctive (opposite directions). The former is typical when shifting gaze right or left, the latter is convergence of the two eyes on a near object. Disjunction can be performed voluntarily, but is usually triggered by the nearness of the target object. A "see-saw" movement, namely, one eye looking up and the other down, is possible, but not voluntarily; this effect is brought on by putting a prism in front of one eye, so the relevant image is apparently displaced. To avoid double vision from noncorresponding points, the eye with the prism must move up or down, following the image passing through the prism. Likewise conjugate torsion (rolling) on the anteroposterior axis (from the front to the back) can occur naturally, such as when one tips one's head to one shoulder; the torsion, in the opposite direction, keeps the image vertical. The muscles show little inertia - a shutdown of one muscle is not due to checking of the antagonist, so the motion is not ballistic. Paths

View 1

of =

right Annulus

eye

from tendineus

the

right: communis

2 3 4 5 6 7 8 9 10 11 12 = Optic nerve = =

= = = = = = Levator

Superior Inferior Medial Lateral Superior Trochlea Inferior palpebrae = = of

rectus rectus rectus rectus oblique superior oblique superioris

muscle muscle muscle muscle muscle oblique muscle muscle Eyelid Eyeball

Five with paths from annulus of zinn Five of the extraocular muscles have their origin in the back of the orbit in a fibrous ring called the annulus of Zinn. Four of these then course forward through the orbit and insert onto the globe on its anterior half (i.e., in front of the eye's equator). These muscles are named after their straight paths, and are called the four rectus muscles, or four recti. superior rectus inserts on the globe at 2

inferior rectus - inserts on the globe at 3 medial rectus - inserts on the globe at 4 lateral rectus - inserts on the globe at 5

(Note that lateral and medial are relative to the subject, with lateral toward the side and medial toward the midline, thus the medial rectus is the muscle closest to the nose). Two with more complex paths The other two extraocular muscles follow more complicated paths.

The superior oblique muscle originates at the back of the orbit (a little closer to the medial rectus, though medial to it, getting rounder as it goes and courses forward to a rigid, cartilaginous pulley, called the trochlea, on the upper, nasal wall of the orbit. The muscle becomes tendinous about 10mm before it passes through the pulley, turning sharply across the orbit, and inserts on the lateral, posterior part of the globe. Thus, the superior oblique goes backward for the last part of its path, and because it goes over the top of the eye, it pulls it downward and laterally

The last muscle is the inferior oblique, which originates at the lower front of the nasal orbital wall, and passes under the LR to insert on the lateral, posterior part of the globe. Thus, the inferior oblique pulls the eye upward and laterally .

Rolling The superior and inferior recti are not strictly vertical. The oblique pull of the obliques causes a rolling opposite each other. Although bearing mutual strict antagonism, the superior and inferior rectus team up with the inferior and superior oblique to move the eye up or down, respectively. The extent of rolling in the recti is less than the oblique, and opposite from it. Mnemonics A good mnemonic to remember which muscles are innervated by what nerve is to paraphrase it as a molecular equation: LR6SO4R3. or (LR6SO4)3 i.e. "LR 6 SO 4 Whole 3."

Lateral Rectus - Cranial Nerve VI Superior Oblique - Cranial Nerve IV the Rest of the muscles - Cranial Nerve III.

Another way to remember which nerves innervate which muscles is to understand the meaning behind all of the Latin words.

The fourth cranial nerve, the trochlear, is so named because the muscle it innervates, the superior oblique, runs through a little fascial pulley that changes its direction of pull (the trochlea of superior oblique). This pulley exists in the superiomedial corner of each orbit, and "trochl-" is Latin for "pulley."

The sixth cranial nerve, the abducens, is so named because it controls the lateral rectus, which abducts the eye (rotates it laterally) upon contraction. The third cranial nerve, the oculomotor, is so named because it is in charge of the movement (motor) of the eye (oculo-). It controls all of the other muscles.

IV. OVERVIEW OF THE DISEASE

Myasthenia gravis is characterized by fluctuating weakness increased by exertion. Weakness increases during the day and improves with rest. Presentation and progression vary.

Extraocular muscle (EOM) weakness or ptosis is present initially in 50% of patients and occurs during the course of illness in 90%. Bulbar muscle weakness is also common, along with weakness of head extension and flexion.
o

Weakness may involve limb musculature with myopathiclike proximal weakness greater than distal muscle weakness. Isolated limb muscle weakness as the presenting symptom is rare and occurs in fewer than 10% of patients.

Patients progress from mild to more severe disease over weeks to months. Weakness tends to spread from the ocular to facial to bulbar muscles and then to truncal and limb muscles.5
o

On the other hand, symptoms may remain limited to the EOM and eyelid muscles for years. Rarely, patients with severe, generalized weakness may not have associated ocular muscle weakness. The disease remains ocular in only 16% of patients. About 87% of patients generalize within 13 months after onset. In patients with generalized disease, the interval from onset to maximal weakness is less than 36 months in 83% of patients.

Intercurrent illness or medication can exacerbate weakness, quickly precipitating a myasthenic crisis and rapid respiratory compromise. Spontaneous remissions are rare. Long and complete remissions are even less common. Most remissions with treatment occur during the first 3 years of disease.

The Medical Scientific Advisory Board (MSAB) of the Myasthenia Gravis Foundation of America (MGFA) formed a Task Force in May 1997 to address the need for universally accepted classifications, grading systems, and methods of analysis for patients undergoing therapy and for use in therapeutic research trials. Thus, MGFA Clinical Classification was created.6
o

Class I

Any ocular muscle weakness May have weakness of eye closure All other muscle strength is normal Mild weakness affecting other than ocular muscles

Class II

May also have ocular muscle weakness of any severity Predominantly affecting limb, axial muscles, or both May also have lesser involvement of oropharyngeal muscles Predominantly affecting oropharyngeal, respiratory muscles, or both May also have lesser or equal involvement of limb, axial muscles, or both

Class IIa

Class IIb

Class III

Moderate weakness affecting other than ocular muscles May also have ocular muscle weakness of any severity Predominantly affecting limb, axial muscles, or both May also have lesser involvement of oropharyngeal muscles Predominantly affecting oropharyngeal, respiratory muscles, or both May also have lesser or equal involvement of limb, axial muscles, or both

Class IIIa

Class IIIb

Class IV

Severe weakness affecting other than ocular muscles May also have ocular muscle weakness of any severity Predominantly affecting limb and/or axial muscles May also have lesser involvement of oropharyngeal muscles Predominantly affecting oropharyngeal, respiratory muscles, or both May also have lesser or equal involvement of limb, axial muscles, or both

Class IVa

Class IVb

Class V

Defined by intubation, with or without mechanical ventilation, except when used during routine postoperative management. The use of a feeding tube without intubation places the patient in class IVb.

A. REVIEW OF THE RELATED LITERATURE

 Description

Myasthenia gravis (mi-uhs-THE-ne-uh GRA-vis) is characterized by weakness and rapid fatigue of any of the muscles under your voluntary control. The cause of myasthenia gravis is a breakdown in the normal communication between nerves and muscles. There is no cure for myasthenia gravis, but treatment can help relieve signs and symptoms such as weakness of arm or leg muscles, double vision, drooping eyelids, and difficulties with speech, chewing, swallowing and breathing. While myasthenia gravis can affect people of any age, it's more common in women younger than 40 and in men older than 60. The disorder occurs in one or two people per 10,000. Symptoms Muscle weakness caused by myasthenia gravis worsens as the affected muscle is used repeatedly. Since symptoms typically improve with rest, your muscle weakness may come and go. While myasthenia gravis can affect any of the muscles that you control voluntarily, certain muscle groups are more commonly affected than others. Eye symptoms involve eye problems, such as:

muscles

In more than half the people who develop myasthenia gravis, their first signs and

Drooping of one or both eyelids (ptosis) Double vision (diplopia), which may be horizontal or vertical Blurred vision, which may come and go and throat muscles

Face

In about 15 percent of people with myasthenia gravis, the first symptoms involve face and throat muscles, which can cause difficulties with:

Speaking. Your speech may be very soft or sound nasal, depending upon which muscles have been affected. Swallowing. You may choke very easily, which makes it difficult to eat, drink or take pills. In some cases, liquids you're trying to swallow may come out your nose.

Chewing. The muscles used for chewing may wear out halfway through a meal, particularly if you've been eating something hard to chew, such as steak. Facial expressions. Family members may note that you've "lost your smile" if the muscles that control your facial expressions are affected.

Arm

and

leg

muscles

Myasthenia gravis can cause weakness in your arms and legs, but this usually happens in conjunction with muscle weakness in other parts of your body such as your eyes, face or throat. The disorder usually affects arms more often than legs. However, if it affects your legs, you may waddle when you walk. When to see a doctor

Talk to your doctor if you have trouble:

Breathing Seeing Swallowing Chewing Walking

Causes Your nerves communicate with your muscles by releasing chemicals, called neurotransmitters, which fit precisely into receptor sites on the muscle cells. In myasthenia gravis, your immune system produces antibodies that block or destroy many of your muscles' receptor sites for a neurotransmitter called acetylcholine. With fewer receptor sites available, your muscles receive fewer nerve signals, resulting in weakness. It's believed that the thymus gland, a part of your immune system located in the upper chest beneath the breastbone, may trigger or maintain the production of these antibodies. Large in infancy, the thymus is small in healthy adults. But, in some adults with myasthenia gravis, the thymus is abnormally large. Some people also have tumors of the thymus. Usually, thymus gland tumors are noncancerous. Some factors can make myasthenia gravis worse, including:

Fatigue Illness Stress Extreme heat

Some medications such as beta blockers, calcium channel blockers, quinine and some antibiotics

Complications Complications of myasthenia gravis are treatable, but some can be life-threatening. Myasthenic crisis

Myasthenic crisis is a life-threatening condition, which occurs when the muscles that control breathing become too weak to do their jobs. Emergency treatment is needed to provide mechanical assistance with breathing. Medications and blood-filtering therapies help people recover from myasthenic crisis, so they can again breathe on their own. Thymus tumors

About 15 percent of the people who have myasthenia gravis have a tumor in their thymus, a gland under the breastbone that is involved with the immune system. Most of these tumors are noncancerous. Other disorders

People who have myasthenia gravis are also more likely to have the following problems:

Underactive or overactive thyroid. The thyroid gland, located in the neck, secretes hormones that regulate your metabolism. If your thyroid is underactive, your body uses energy more slowly. An overactive thyroid makes your body use energy too quickly.

Lupus. Lupus is a disease in which your immune system attacks certain parts of your body. Common symptoms include painful or swollen joints, hair loss, extreme fatigue and a red rash on the face.

Rheumatoid arthritis. This type of arthritis is caused by problems with your immune system. It is most conspicuous in the wrists and fingers, and can result in joint deformities that make it difficult to use your hands.

Preparing for your appointment While you might first discuss your symptoms with your family doctor, he or she will probably refer you to a neurologist for further evaluation. What including: you can do

Because appointments can be brief, plan ahead and write lists of important information,

Detailed descriptions of all your symptoms, including whether anything seems to make them better or worse All your medications and dosages, including nonprescription drugs and supplements Questions for the doctor, such as what tests or treatments he or she may recommend

What

to

expect

from

your

doctor

Your doctor will want a detailed description of your symptoms and your past medical history. In addition to a physical exam, your doctor may also check your neurological health by testing your:

Reflexes Muscle strength Muscle tone Senses of touch and sight Coordination Balance Tests and diagnosis By Mayo Clinic staff The key sign that points to the possibility of myasthenia gravis is muscle weakness that improves with rest. Tests to help confirm the diagnosis may include:

Edrophonium

test

Injection of the chemical edrophonium (Tensilon) may result in a sudden, although temporary, improvement in your muscle strength an indication that you may have myasthenia gravis. Edrophonium acts to block an enzyme that breaks down acetylcholine, the chemical that transmits signals from your nerve endings to your muscle receptor sites.

Blood receptor sites where nerve impulses signal your muscles to move.

analysis

A blood test may reveal the presence of abnormal antibodies that disrupt the

Repetitive

nerve

stimulation

This is a type of nerve conduction study, in which electrodes are attached to your skin over the muscles to be tested. Small pulses of electricity are sent through the electrodes to measure the nerve's ability to send a signal to your muscle. To diagnose myasthenia gravis, the nerve will be tested many times to see if its ability to send signals worsens with fatigue.

Single-fiber

electromyography

(EMG)

Electromyography (EMG) measures the electrical activity traveling between your brain and your muscle. It involves inserting a very fine wire electrode through your skin and into a muscle. In single-fiber EMGs, a single muscle fiber is tested. Most people find this test to be somewhat uncomfortable.

Imaging abnormality in your thymus.

scans

Your doctor may order a CT scan or an MRI to see if there's a tumor or other

Treatments and drugs

Doctors use a variety of treatments, alone or in combination, to relieve symptoms of myasthenia gravis. Medications

Cholinesterase inhibitors. Drugs such as pyridostigmine (Mestinon) enhance communication between nerves and muscles. These drugs don't cure the underlying problem, but they do improve muscle contraction and muscle strength.

Corticosteroids. These types of drugs inhibit the immune system, limiting antibody production. Prolonged use of corticosteroids, however, can lead to serious side effects, such as bone thinning, weight gain, diabetes, increased risk of some infections, and an increase and redistribution of body fat.

Immunosuppressants. Your doctor may also prescribe other medications that alter your immune system, such as azathioprine (Imuran), cyclosporine (Sandimmune, Neoral) or mycophenolate (CellCept).

Therapy

Plasmapheresis (plaz-muh-fuh-RE-sis). This procedure uses a filtering process similar to dialysis. Your blood is routed through a machine that removes the antibodies that are blocking transmission of signals from your nerve endings to your muscles' receptor sites. However, the beneficial effects usually last only a few weeks.

Intravenous immune globulin. This therapy provides your body with normal antibodies, which alters your immune system response. It has a lower risk of side effects than do plasmapheresis and immune-suppressing therapy, but it can take

a week or two to start working and the benefits usually last less than a month or two. Surgery About 15 percent of the people who have myasthenia gravis have a tumor in their thymus, a gland under the breastbone that is involved with the immune system. If you have such a tumor, you'll need to have your thymus removed. For people with myasthenia gravis who don't have a tumor in the thymus, it's unclear whether the potential benefit of removing the thymus outweighs the risks of surgery. This is an individualized decision between you and your doctor, but most doctors don't recommend surgery if:

Your symptoms are mild Your symptoms involve only your eyes You're over 60 years old

Lifestyle and home remedies

Supplementing your medical care with these approaches may help you make the most of your energy and cope with the symptoms of myasthenia gravis:

Adjust your eating routine. Try to eat when you have good muscle strength. Take your time eating and rest between bites. More frequent, smaller meals may be easier to handle. Also, try soft foods and avoid sticky foods that require lots of chewing.

Use safety precautions at home. Install grab bars or railings in places where you may need support, such as next to the bathtub. Keep the floors and halls in your house clear of clutter, cords and loose rugs. Outside your home, keep the steps, sidewalk and path to your car clear.

Use electric appliances and power tools. Save your energy in the bathroom, in the kitchen or at the workbench by using electric appliances, such as toothbrushes, can openers and screwdrivers.

Wear an eye patch. If you have double vision, using an eye patch can help relieve this problem. Wear the patch while you read or watch television. To avoid eyestrain, periodically switch the patch from one eye to the other.

Plan. If you have a chore to do around the house, shopping to do or an errand to run, plan the activity to coincide with the time at which your medication provides

your peak energy level. If you're working on a project at home, gather everything you need for the job at one time, to eliminate extra trips that may drain your energy.

Ask for help. Depending on your energy level, you may not be able to do everything you have planned around the house or run every errand that you need to. Ask family members and friends to lend a hand.

Current Trends Protein From Tick Saliva Studied For Potential Myasthenia Gravis Treatment ScienceDaily (Apr. 4, 2009) Looking for a better treatment for the autoimmune disease myasthenia gravis, researchers have found that a protein in tick saliva shows promise in limiting the severity of the disease in an animal model in a study published in the Annals of Neurology. "This disease can leave patients weak and on breathing machines, and conventional treatments can be toxic," said Henry Kaminski, M.D., chair of the department of neurology and psychiatry at Saint Louis University and one of the nation's leading experts on myasthenia gravis. "There is a real need for better treatments. This study is a step in that direction." Myasthenia gravis is a highly debilitating, chronic neuromuscular disorder that affects about 400 to 600 per 1 million people, and roughly 1,100 to 1,700 people in the St. Louis area. Symptoms include weakness in the arms and legs, chronic muscle fatigue, difficulty breathing, difficulty chewing and swallowing, slurred speech, droopy eyelids and blurred or double vision. While drugs like prednisone, a corticosteroid, can be effective in treating the disorder, they also can carry a host of severe side effects, including pronounced weight gain, osteoporosis, glaucoma and diabetes. Other treatments, intravenous immunoglobulin and plasmapheresis, which involve blood plasma, are expensive and can have rare but serious side-effects such as infections, heart attacks and stroke. Doctors believe that myasthenia gravis is caused by an overreaction of the complement system, a component of the immune system that specifically defends against parasites, bacteria and other pathogens. Antibodies block nerve receptors at the neuromuscular

junction, the place where nerves connect with muscles, and then activate complement which prevents muscle contraction from occurring, causing weakness. To impede the complement system's misplaced response, researchers hope a new class of drugs, called complement inhibitors, may stop the body's defense system from attacking itself. Other researchers discovered that rEV576, a protein found in tick saliva, works as a complement inhibitor, allowing ticks to avoiding setting off an immune response in their human host. SLU researchers in collaboration with Varleigh Limited tested the protein on two groups of rats with mild and severe models of myasthenia gravis. The health of rats that were given the complement inhibitor rEV576 improved, with reduced weakness and weight loss. Researchers hope rEV576 could have therapeutic value in human myasthenia gravis. And, because ticks apply themselves to people without causing a reaction, researchers are optimistic that rEV576 will not cause allergic reactions or other negative side effects. "Complement inhibitors are a completely new class of drugs," said Kaminski. "This one will probably prove to be superior to what we've seen. Since complement is activated in many diseases such as Alzheimer's, stroke and rheumatoid arthritis, our studies may be important for other diseases."

V.CASE STUDY PROPER A.GENERAL DATA Personal Data Case no: 09111405 Hospital No: 200942112

Name: Villaruel Eric M. Address: Sto Domingo Quezon,City Age: 58y/o Sex: male Civil Status: Married Name of Father: DECEASED Name of Mother: DECEASED Nationality: Filipino Religion: Roman Catholic Place of birth: Mindoro Date of birth: October 27, 1968 Department: Neuro Ward Room no.: 202L C/c: Gen. Body Weakness Initial diagnosis: Myasthenia Gravis Admission Date: 3:59pm Feb.26, 2010 Final Diagnosis: Myasthenia Gravis Out of Crisis Class III Doctor: Da. Sunga/King

B. HISTORY OF PRESENT ILLNESS Patient is known of Myasthenia Gravis diagnosed last May 2009 in our institution. He was maintained on Pyridostigmine (Mestinon) 60mg/tab q4, Prednisone 20mg/tab BID and Azathioprine 50mg/tab OD. Patient is compliant with his medication. He was also to have Thymoma (May 2009) offered Thymectomy however due to financial constrained, procedure was not done. 12 Days Prior to admission Feb. 10,2010, patient experienced difficulty of initiation of swallowing on both solid and liquid, no associated odynophagia, hypophonia, DOB, cough, vomiting, abdominal pain or chest pain. Patient did not consult nor take any medication for the symptom.

11 prior to admission persistence of symptoms were noted, with generalized body weakness, inability to finish full meal and DOB. Patient was partially relieved by one dose of salbutamol nebulisation. Patient was noted to have decreased ability to do activity daily living. Patient preferred bed rest at most time of day. No cough and fever was noted. No consult was done. Few hours prior to admission, persistence of symptoms was noted, with generalized body weakness, inability to finish full meal and DOB. No fever and abdominal pain and cough noted. Patient was brought to our institution and hence no consult done. C. FAMILY HEALTH HISTORY For management of Myasthenia Gravis, the patient is usually brought in the hospital. Regarding the present illness, Eric brought to USTH for further examination and management.

D. PAST MEDICAL HISTORY According to him they do not have the history of DM and Hypertension. The common illness of their family is cough and colds. E. COURSE IN THE WARD Since I handled the patient, he was ordered MGH and importance of continuous intake of home medication must be emphasized. F. LABORATORY REPORTS Since I handled Mr. Villaruel and he was MGH the laboratory I found was in normal range. PHYSICAL EXAMINATION

General Conditon Eric Villaruel conscious and coherent Vital signs upon admission T= 36.9C P= 79 bpm

R= 20bpm BP= 100/70 mmHg Integument Skin The skin is slightly pale and He has a fair skin turgor. Hair The patient has evenly distributed black hair. Nails The nails are pinkish with capillary refill time of 2-3 seconds. It has convex curvature and with hard texture. HEENT Head The head is symmetrical with rounded skull contour. Eyes Eyebrows are evenly distributed. Eyelashes equally distributed and curled slightly outward. The patient has dyplopia and ptosis at the right eye The patient has slightly pale conjunctiva. No edema and redness over the lachrymal glands. The pupils are equally reactive to light accommodation. Ears Symmetrical in size and shape. It is in lined to the outer canthus of the eyes and recoils after it is folded. Cerumen noted on both ears. Nose Symmetrical Nasal septum intact and in midline. No redness and swelling noted in the nasal mucosa No discharges noted. Mouth Slightly pale and pinkish dry lips With pale oral mucosa With poor dentition

Neck The muscles are equal in size and strength. No scars or palpable mass noted. Not distended vein Thorax and lungs The chest is symmetric with skin intact and has uniform temperature. No crackle sounds heard on both lung fields upon auscultation. Spine vertically aligned. The patient is in not respiratory distress. Abdomen Soft abdomen upon palpation with no scars noted. Muscle tone is normal. There is abnormal bowel sounds, 9-20 per minute. Lower Extremities Upper and lower extremities are well flexed and warm to touch.

SOUTHERN LUZON STATE UNIVERSITY Lucban, Quezon

MYASTHENIA GRAVIS
A Case Study

Presented to the Faculty Of College of Allied Medicine

In partial fulfillment of the requirements for the Degree Bachelor of Science in Nursing

Submitted by: Arriola, Ericson L. BSN IIISLSU, Group 4

Submitted to: Mr. Gerald Villasenor

Summer Affiliation, 2010

Modifiable factors: fatigue misuse of antibiotics (penicillamine)

Non-modifiable factors: Familial predisposition Other underlying diseases (hypothyroidism)

Autoimmune disorder

Alteration in the development of Tcells and the selection of the T-cell receptors during antibody production

Circulating antibodies blocks the nicotinic acetylcholine receptor (nAChR) at the post-synaptic neuromuscular junction

Decrease cumulative activation of the nAChR leads to decrease influx of sodium ions therefore decreases release of calcium

Decreases muscle contraction

Muscle weakness

Subjective: Weakness in arms, hands, fingers, legs, and neck Dysphagia Shortness of breath

Objective: ptosis (a drooping of one or both eyelids) diplopia (double vision) due to weakness of the muscles that control eye movements unstable or waddling gait change in facial expression dysarthria (impaired speech, often nasal due to weakness of the velar muscles)

Complication: myasthenic crisis (a paralysis of the respiratory muscles)

Myasthenia Gravis