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ANATOMY AND PHYSIOLOGY OF THE EYES

The eye is essentially an opaque eyeball filled with a water-like fluid. In the front of the eyeball is a transparent opening known as the cornea. The cornea is a thin membrane that has an index of refraction of approximately 1.38. The cornea has the dual purpose of protecting the eye and refracting light as it enters the eye. After light passes through the cornea, a portion of it passes through an opening known as the pupil. Rather than being an actual part of the eye's anatomy, the pupil is merely an opening. The pupil is the black portion in the middle of the eyeball. Its black appearance is attributed to the fact that the light that the pupil allows to enter the eye is absorbed on the retina (and elsewhere) and does not exit the eye. Thus, as you sight at another person's pupil opening, no light is exiting their pupil and coming to your eye; subsequently, the pupil appears black. Like the aperture of a camera, the size of the pupil opening can be adjusted by the dilation of the iris. The iris is the colored part of the eye - being blue for some people and brown for others (and so forth); it is a diaphragm that is capable of stretching and reducing the size of the opening. In bright-light situations, the iris adjusts its size to reduce the pupil opening and limit the amount of light that enters the eye. And in dim-light situations, the iris adjusts so as to maximize the size of the pupil opening and increase the amount of light that enters the eye. Light that passes through the pupil opening, will enter the crystalline lens. The crystalline lens is made of layers of a fibrous material that has an index of refraction of roughly 1.40. Unlike the lens on a camera, the lens of the eye is able to change its shape and thus serves to fine-tune the vision process. The lens is attached to the ciliary muscles. These muscles relax and contract in order to change the shape of the lens. By carefully adjusting the lenses shape, the ciliary muscles assist the eye in the critical task of producing an image on the back of the eyeball. The inner surface of the eye is known as the retina. The retina contains the rods and cones that serve the task of detecting the intensity and the frequency of the

incoming light. An adult eye is typically equipped with up to 120 million rods that detect the intensity of light and about 6 million cones that detect the frequency of light. These rods and cones send nerve impulses to the brain. The nerve impulses travel through a network of nerve cells. There are as many as one million neural pathways from the rods and cones to the brain. This network of nerve cells is bundled together to form the optic nerve on the very back of the eyeball. Each part of the eye plays a distinct part in enabling humans to see. The ultimate goal of such an anatomy is to allow humans to focus images on the back of the retina How the Human Eye Works In a number of ways, the human eye works much like a digital camera: 1. Light is focused primarily by the cornea the clear front surface of the eye that acts like a camera lens. 2. The pupil of the eye functions like the diaphragm of a camera, controlling the amount of light reaching the back of the eye. 3. The eye's crystalline lens located directly behind the pupil further focuses light. Through a process called accommodation, this lens helps the eye automatically focus on near and approaching objects, like an internal autofocus camera lens. 4. Light focused by the cornea and crystalline lens (and limited in intensity by the pupil) then reaches the retina the light-sensitive inner lining of the back of the eye. The retina is similar to the electronic image sensor of a digital camera. Like an image sensor, it converts optical images into electronic signals. The optic nerve then transmits these signals from the eye to the visual cortex the part of the brain that controls our sense of sight. Process of vision

Light waves from an object (such as a tree) enter the eye first through the cornea, which is the clear dome at the front of the eye. It is like a window that allows light to enter the eye. The light then progresses through the pupil, the circular opening in the center of the colored iris. Fluctuations in the intensity of incoming light change the size of the eyes pupil. As the light entering the eye becomes brighter, the pupil will constrict (get smaller), due to the pupillary light response. As the entering light becomes dimmer, the pupil will dilate (get larger). Initially, the light waves are bent or converged first by the cornea, and then further by the crystalline lens (located immediately behind the iris and the pupil), to a nodal point (N) located immediately behind the back surface of the lens. At that point, the image becomes reversed (turned backwards) and inverted (turned upside-down). The light continues through the vitreous humor, the clear gel that makes up about 80% of the eyes volume, and then, ideally, back to a clear focus on the retina, behind the vitreous. The small central area of the retina is the macula, which provides the best vision of any location in the retina. If the eye is considered to be a type of camera (albeit, an extremely complex one), the retina is equivalent to the film inside of the camera, registering the tiny photons of light interacting with it. Within the layers of the retina, light impulses are changed into electrical signals. Then they are sent through the optic nerve, along the visual pathway, to the occipital cortex at the posterior (back) of the brain. Here, the electrical signals are interpreted or seen by the brain as a visual image. Actually, then, we do not see with our eyes but, rather, with our brains. Our eyes merely are the beginning of the visual process. Aqueous Humor

The aqueous is the thin, watery fluid that fills the space between the cornea and the iris (anterior chamber). It is continually produced by the ciliary body, the part of the eye that lies just behind the iris. This fluid nourishes the cornea and the lens and gives the eye it's shape. Tear Production The eye's tears are composed of three layers: oil, water and mucous. The outermost oily layer is produced by the meibomian glands which line the edge of the eyelids. The watery portion of the tear film is produced by the lacrimal gland. This gland lies underneath the outer orbital rim bone, just below the eyebrow. The mucous layer comes from microscopic goblet cells in the conjunctiva. With each blink, the eyelids sweep across the eye, spreading the tear film evenly across the surface. The blinking motion of the eyelids forces the tears into tiny drains found at the inner corners of the upper and lower eyelids. These drains are called puncta (plural for punctum). The tear film travels from the puncta into the upper and lower canaliculus, which empty into the lacrimal sac. The lacrimal sac drains into the nasolacrimal duct which connects to the nasal passage. This connection between the tear production system and the nose is the reason your nose runs when you cry. Some patients can actually taste eye drops as they drain from the nasal passage into the throat
ANATOMY AND PHYSIOLOGY OF THE NERVES

Nerve Tissue : Structure and Function Supporting Cells Supporting cells in the CNS are lumped together as neuroglia, literally, nerve glue. Neuroglia includes many types of cells that generally support, insulate, and protect the delicate neurons. In addition, each of the different types of neuroglia, also simply called glia has special functions. The CNS glia include: Astrocytes

Microglia Epindymal cells Oligodendrocytes

NEURONS Neurons, also called nerve cells, are highly specialized to transmit messages (nerve impulses) from one part of the body to another. Although neurons differ structurally, they have many common features. All have (A) have cell body, which contains the nucleus and is the metabolic center of the cell, and (B) one or more slender processes extending from the cell body. Cell body Rough ER, called Nissl substance, and neurofibrils, Dendrites Axons Axon hillock Myelin Schwann cells Nodes of Ranvier Synapse Axonal terminals - These terminals contain hundreds of tiny vesicles, or membranous sacs, that contain chemicals called neurotransmitters. The important neurohumoral neurotransmitters or chemical transmitters are: 1. Acetylcholine 2. Cholinesterase is the inactivator of acetylcholine. 3. Adrenaline 4. Noradrenaline CLASSIFICATION

Neurons may be classified either according to how they function or according to their strucuture. FUNCTIONAL CLASSIFICATION Sensory (afferent) neuron conduct impulses from sensory receptors (in the skin, viscera, muscles) to the central nervous system. o Cutaneous sense organs skin o Propioceptors muscles and tendons Types of sensory receptors: a. naked nerve endings (pain and temperature receptors) b.Meissners corpuscles (touch receptor) c. Pacinian corpuscles (deep pressure receptor) d. muscle spindle (proprioceptor) Motor (efferent) neuron transmit impulses from the CNS (brain of the spinal cord) to the viscera and/or muscles and glands. Association neurons (interneurons) complete the communication pathway between sensory and motor neurons; their cell bodies reside in the CNS. STRUCTURAL CLASSIFICATION Multipolar neurons Bipolar neurons Unipolar neurons

NERVE IMPULSES Neurons have two major functional properties: Irritability and conductivity A neuron not carrying an impulse is in the state of Polarization, with Na+ ions more abundant outside the cell , and K+ ions and negative ions more abundant inside the cell. The neuron has positive charge on the outside of the cell membrane and a relative negative charge inside. A stimulus (such as neurotransmitter) makes the membrane very permeable to Na+ ions, will rush into the cell. This brings about

depolarization, a reversal of charges on the membrane. The outside now has negative charge, and the inside has positive charge. saltatory conduction- Transmission of electrical impulses is very rapid. The presence of an insulating myelin sheath increases the velocity of impulses, since only the nodes of Ranvier depolarize

MYASTHENIA GRAVIS

Comes from the Greek and Latin words meaning " grave muscular weakness." The most common form of MG is a chronic autoimmune neuromuscular disorder that is characterized by fluctuating weakness of the voluntary muscle groups. A disease characterized by progressive fatigue and generalized weakness of the skeletal muscles, especially those of the face, neck, arms, and legs, caused by impaired transmission of nerve impulses following an autoimmune attack on acetylcholine receptors. Risk Factors Gender: Female Age: 20-40 years old Thymic Tumor-

Is it hereditary? In general, Myasthenia Gravis is not an inherited disease; there are no tests for genetic screening. Infants of mothers with Myasthenia Gravis may be born with neonatal Myasthenia Gravis. The child is weak at birth, but within a few weeks attains normal strength. This is NOT a permanent condition. Signs and Symptoms Ptosis and Diplopia Dysarthria and DysphagiaSkeletal muscle weakness

Classifications A. Ocular FormB. Generalized Form Diagnostic Test

Tensilon Testing Electromyogram (EMG)


Serum Radioimmunoflurescence

Computed tomography (CT) or magnetic resonance imaging (MRI) A special examination called pulmonary function testing

Medical Management 1. Drug Therapy Anticholinesterase drugsCorticosteroids Immunosuppressive drugs

2. Plasmapheresis Complications of drug Therapy 1. Myasthenic Crisis 2. Cholinergic Crisis Surgical Management

Thymectomy

Nursing Management 1. Promote effective breathing pattern 2. Improved Airway Clearance 3. Ensure adequate nutrition 4. Increase activity tolerance 5. Provision of optimum vision Nursing Diagnosis 1. Ineffective Breathing Pattern related to respiratory muscle weakness. 2. Impaired Physical Mobility related to weakness of voluntary muscles. 3. Self-Care Deficit related to muscle weakness, general fatigue 4. Imbalanced Nutrition: Less than Body Requirements related to dysphagia, intubation, or muscle paralysis. New Trends in MG Recent advances in the diagnosis and treatment of acquired myasthenia gravis (MG) are reviewed. Increased awareness about the need for more uniform methods of reporting treatment trials for MG has prompted systematic review of the literature and inspired an effort to develop better classifications and disease-specific outcome measures. New antibodies have been discovered in patients with seronegative MG, possibly defining an immunologically distinct form of the disease. A new immunosuppressant, mycophenolate mofetil, may be an additional and safe option in the treatment of MG. Other work supports the possibility of developing a vaccine against MG suitable for trial in humans. Duke University Medical Center, 932 Morreene Road, Room 230, Durham, NC 27705, USA. ciafa001@mc.duke.edu

Multiple sclerosis

Multiple sclerosis (MS) is a disease in which the nerves of the central nervous system (brain and spinal cord) to degenerate. Myelin, which provides a covering or insulation for nerves, improves the conduction of impulses along the nerves and also is important for maintaining the health of the nerves. In multiple sclerosis , inflammation causes the myelin to disappear. Consequently, the electrical impulses that travel along the nerves decelerate, that is, become slower. In addition, the nerves themselves are damaged. As more and more nerves are affected, a person experiences a progressive interference with functions that are controlled by the nervous system such as vision, speech, walking, writing, and memory. (medicinenet.com) Most researchers believe MS is an autoimmune disease -- one in which white blood cells, meant to fight infection or disease, are misguided to target and attack the bodys own cells. This attack causes inflammation in the CNS, which may damage the myelin and ultimately injure the nerves. Areas of inflammation are known as active lesions. Areas of thick scar tissue, known as plaques, form along the damaged myelin. The changes in size, number, and location of the lesions and plaques may determine the type and severity of symptoms. The term multiple sclerosis originates from the discovery of the plaques. Multiple refers to many; sclerosis refers to scars. (Multiple sclerosis association of America, 2007). Prevalence About 350,000 people in the U.S. have multiple sclerosis. Usually, a person is diagnosed with multiple sclerosis between 20 and 50 years of age Multiple sclerosis is twice as likely to occur in Caucasians as in any other group. Women are twice as likely as men to be affected by multiple sclerosis earlier in life. (Medicinenet.com) the occurrence of this disorder is positively correlated with latitude.

People living beyond the 40-degree mark north or south of the equator are far more likely to develop MS than those living in the warmer climates near the equator. This is especially true for people in North America, Europe, and southern Australia, while Asia continues to have a low incidence of MS.

More prevalent among those of northern European or Scandinavian ancestry, Caucasians are far more likely than those of African heritage to develop this disease.

Causes/Etiology The cause of multiple sclerosis is still unknown. However, researchers have focused on the following: a. Disorders of the immune system b. Slowacting viruses c. Deficiency in Vitamin D d. Genetics e. Cigarette Smoking SIGNS AND SYMPTOMS Symptoms of multiple sclerosis may be single or multiple and may range from mild to severe in intensity and short to long in duration. Complete or partial remission from symptoms occurs early in about 70% of individuals with multiple sclerosis. FATIGUE It is also not contagious.

VISUAL DISORDERS NUMBNESS Numbness of the face, body or extremities (arms and legs) is one of the most common symptoms of MS. Often its the first symptom experienced by those eventually diagnosed with MS. The numbness may be mild or so severe that it interferes with the ability to use the affected body part. For example, a

person with very numb feet may have difficulty walking. Numb hands may prevent writing, dressing, or holding objects safely. DIZZINESS/VERTIGO BLADDER DYSFUNCTION BOWEL DYSFUNCTION WEAKNESS AND IMPAIRED MOBILITY TREMORS SEXUAL DYSFUNCTION SLURRED SPEECH SPASTICITY (LEG STIFFNESS) SWALLOWING DISORDERS CHRONIC ACHING PAIN DEPRESSION, MANIC DEPRESSION, PARANOIA OR AN UNCONTROLLABLE URGE TO LAUGH OR WEEP MILD COGNITIVE AND MEMORY DIFFICULTIES TYPES OF MULTIPLE SCLEROSIS There are types of multiple sclerosis. These are: RELAPSING REMITTING FORM OF MS SECONDARY-PROGRESSIVE (SP) MS PRIMARY-PROGRESSIVE (PP) MS BENIGN

PROGRESSIVE RELAPSING MS MALIGNANT OR FULMINANT MS DIAGNOSIS OF MULTIPLE SCLEROSIS MS diagnosis is based upon an individuals history of clinical symptoms and neurological examinations. Other conditions with similar symptoms must be ruled out, often requiring various lab tests.

Magnetic resonance imaging (MRI) of the brain has been Cerebrospinal fluid (CSF) analysis CSF eval: presence of oligoclonal banding presence of IgG antibody in CSF An electro-physiological test (evoked potential tests) VEP (visual evoked potentials) BAEP (brain stem auditory evoked potentials) SSEP (somatosensory evoked potentials) MEDICAL MANAGEMENT Many experts now recommend treatment as early as possible with one of the five approved agents. Studies show that treating after the first attack can significantly delay time to the second attack. Early treatment is also thought to possibly limit axonal (nerve) injury, which may be irreversible, and later lead to progressive disease. The treatment of MS generally falls into two categories: 1. treatments that address symptom management 2. treatments that change the course of the disease by modifying the number and severity of attacks and the progression of disability. Interferon-Beta products Betaseron (interferon beta-1b) Avonex (interferon beta-1a) Rebif (interferon beta-1a) Glatiramer Acetate Copaxone (glatiramer acetate) A Monoclonal Antibody
Tysabri (natalizumab)

Mitoxantrone Novantrone (mitoxantrone)

Steroid Treatment For acute relapses a. IV or oral corticosteroids b. Methylprednisolone, followed by oral Prednisone taper c. Azathioprine (Imuran) d. Cyclophosphamide (Cytoxan) Treating exacerbations Interferon B (Betaseron) used for ambulatory pts. [genetically engineered complex protein w both antiviral and immunoregulatory properties which reduce the number of exacerbations Symptomatic treatment: pharmacologic treatment of the symptoms a. Bladder dysfunction: oxybutynin (ditropan), propantheline, urecholine, b. Constipation: psyllium hydromucilloid, bisacodyl c. Fatigue: amantadine, modafinil d. Muscle spascity: baclofen diazepam, dantrolene e. Tremors: propranolol, thenobarbial, clonazepam f. Trigeminal neuralgia: carbamazepine, phenytoin, amitriptyline g. Dysesthesia: TENS transcutaneous electrical nerve stimulation

NURSING MANAGEMENT 1. Promotes physical mobility activity and rest no vigorous physical exercise frequent rest periods walking and gait exercises minimize spasticity and contractures warm packs, daily muscle stretching

activities: swimming, stationary bike, progressive wt bearing Minimize effects of immobility; skin integrity; cough and deep breathing exercises. 2. Prevent injury walk with feet wide apart, environment awareness and modification, gait training. Use of assistive devices walker, cane etc. 3. Promote bladder & bowel control - Urinal/bedpan readily available, po fluids intake schedule/voiding schedule, increase fiber in diet, intermittent self-catheterization 4. Improve sensory and cognitive function: Vision eye patch for diplopia; prism glasses for reading; talking books Speech slurred, low volume, problems with phonation speech therapist cognitive & emotional responses forgetfulness, easily distracted, emotionally labile, social activities; hobbies. 5. Development of coping strengths education about diseases process; stress relief; network of services social, speech, PT, psychological, homemaker/meal on wheels 6. Improve self care assistive devices, raised toilet seat, shower bench, reached tongs, decrease physical and emotional stress, decrease exposure of extreme temperatures 7. If patient needs instruction on assistive devices, or learn muscle tone to remain active; conduct ROM exercise 8. Adapting to sexual dysfunction counseling, plan sexual activity, willingness to experiment. 9. Administer medications as needed. 10. Watch for adverse reactions to administered medications. 11. Educate the patient and his/her family about this chronic disease. 12. Increase patient comfort with massages and relaxing baths. 13. Promote emotional stability. Help the patient establish a daily routine to maintain optimal functioning. NURSING DIAGNOSES

Impaired physical mobility related to fatigue & weakness Activity intolerance r/t weakness, dizziness, and unsteady gait Self-esteem disturbance r/t loss of health & lifestyle changes

Guillain barre Syndrome

- defined as an inflammatory disorder of the peripheral nerves (those outside the brain and spinal cord). Its characterized by the rapid onset of weakness and, often, paralysis of the legs, arms, breathing muscles, and face (Springhouse,1997) - It affects the peripheral nervous system and results in loss of myelin (a segmental demyelination) and edema and inflammation of the affected nerves, causing a loss of neurotransmission to the periphery.

Subtypes of Guillain-Barr syndrome Several variants of GBS are recognized. These disorders share similar patterns of evolution, symptom overlap, and probable immune-mediated pathogenesis. Recovery varies. a. Acute inflammatory demyelinating polyneuropathy b. Acute motor axonal neuropathy c. Acute motor-sensory axonal neuropathy d. Miller-Fisher syndrome e. Acute panautonomic neuropathy

f. Pure sensory Guillain-Barr syndrome. g. Other variants Statistics The syndrome affects males 1.5 times more frequently than females and is typically seen in adults, although it is observed in all age groups. Worldwide the incidence has varied from 0.4 to 1.7 cases per 100,000 persons disorder. (Simmons, 2010) Etiology: The etiology of this disorder is unknown, but it is believed to be a cell-mediated immunologic reaction directed at the peripheral nerves. Viral infection history of upper respiratory and GI infection Campylobacter jejuni is the most recognize organism associated with Guillain Barre Syndrome. C. jejuni gastroenteritis is thought to precede Guillain Barre syndrome in 30% of cases. Other potential pathogens include: per year. With adequate supportive care, 85% to 95% of patients recover completely from this

* Cytomegalovirus * Epstein-Bar Virus * Human Immunodeficiency virus * Rubella & Rubeola * Varicella Clinical Manifestations Pain Bilateral weakness in the legs Paresthesia (numbness and tingling) Hypotonia (reduced muscle tone)

Areflexia (lack of reflexes) Respiratory dysfunction Low blood pressure or poor blood pressure control Dysphagia CN VII (facial) Horners syndrome paralysis of the symphathetic nerves o Ipsilateral ptosis o Enophthalmos

Complications: Respiratory Failure Immobility from the paralysis can cause problems such as: Paralytic ileus Muscle atrophy Deep vein thrombosis Pulmonary emboli Skin breakdown Orthostatic hypotension Nutritional deficiencies

Diagnostic Tests CSF analysis Electromyography

Medical Management 1. Plasmapheresis 2. Immunoglobulin infusion 3. Steroids 4. Ace inhibitors

5. Medications: 4AS (Antibiotics, Analgesic, Anticoagulants, Azathripine & Cyclophosphamide) 6. Maintaining Respiratory Function Nursing Diagnoses: Impaired spontaneous ventilation related to progression of disease process resulting in respiratory muscle paralysis Risk for aspiration related to dysphagia Acute pain related to paresthesias, muscle aches and cramps, and hyperesthesias Impaired verbal communication related to intubation or paralysis of the muscles of speech Fear related to uncertain outcome and seriousness of the disease Self-care deficits related to inability to use muscles to accomplish activities of daily living Nursing Management: 1. Maintaining Respiratory Function 2. Enhancing physical mobility 3. Providing adequate nutrition 4. Improving communication 5. Decreasing fear and anxiety 6. Monitor respiratory status through vital capacity measurements, rate and depth of respirations, and breath sounds. 7. Monitor level of muscle weakness as it ascends toward respiratory muscles. Watch for breathlessness while talking which is a sign of respiratory fatigue. 8. Monitor the patient for signs of impending respiratory failure. 9. Monitor gag reflex and swallowing ability. 10. Position patient with the head of bed elevated to provide for maximum chest excursion. 11. Avoid giving opioids and sedatives that may depress respirations.

12. Position patient correctly and provide range-of-motion exercises.


13. Provide good body alignment, range-of-motion exercises, and change of position

to prevent complications such as contractures, and dependent edema. 14. Ensure adequate nutrition without the risk of aspiration. 15. Encourage physical and occupational therapy exercises to help the patient regain strength during rehabilitation phase. 16. Provide assistive devices independence and activity. 17. If verbal communication is possible, discuss the patients fears and concerns. 18. Provide choices in care to give the patient a sense of control. 19. Teach patient about breathing exercises or use of an incentive spirometer to reestablish normal breathing patterns. 20. Instruct patient to wear good supportive and protective shoes while out of bed to prevent injuries due to weakness and paresthesia. 21. Instruct patient to check feet routinely for injuries because trauma may go unnoticed due to sensory changes. 22. Urge the patient to maintain normal weight because additional weight will further stress monitor function. 23. Encourage scheduled rest periods to avoid fatigue. Prognosis Recovery can take weeks, months, or years. Most people survive and recover completely. According to the National Institute of Neurological Disorders and Stroke, about 30% of patients still have some weakness after 3 years. Mild weakness may persist for some people. A patient's outcome is most likely to be very good when the symptoms go away within 3 weeks after they first started. as needed (cane or wheelchair) to maximize

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