Eye and Ear Disorders PDF

Pathophysiology (2) (MBS 253M) Lecture 9 Disorders of the Eye and Ear Textbook ;Pathophysiology for the Health Professions, 4th edition, 2011 Chapter 24 (p.529-544)  Lecture 9 Disorders of the Eye a...

Pathophysiology (2) (MBS 253M) Lecture 9 Disorders of the Eye and Ear Textbook ;Pathophysiology for the Health Professions, 4th edition, 2011 Chapter 24 (p.529-544)  Lecture 9 Disorders of the Eye and Ear lecture outline:- The Eye Review of Normal Structure and Function Diagnostic Tests Structural Defects Infections and Trauma Glaucoma Cataracts Detached Retina Macular Degeneration The Ear Review of Normal Structure and Function Hearing Loss Ear Infections Otitis Media Otitis Externa Chronic Disorders of the Ear  Otosclerosis  Ménière’s Syndrome  Lecture 9 Disorders of the Eye and Ear Learning objectives: After studying this lecture ,the student is expected to: 1. Describe the common structural defects impairing vision: hyperopia, presbyopia, myopia, astigmatism, amblyopia, and nystagmus. 2. Describe common infections in the eye and their possible effects on vision. 3. Explain how intraocular pressure may become elevated and how it may affect vision. 4. Compare the signs of chronic glaucoma, acute glaucoma, cataract, macular degeneration, and detached retina, include the rationale for each. 5. Describe how the retina may become detached and the possible effects on vision. 6. Describe the types of hearing loss with an example of each. 7. Describe otitis media and its cause, pathophysiology, and signs. 8. Describe the pathophysiology and signs of otosclerosis and of Ménière’s syndrome. 9. Explain how permanent hearing loss is caused by acute otitis media, chronic otitis media, Ménière’s syndrome, and damage to the auditory area of the brain.  REVIEW OF NORMAL STRUCTURE AND FUNCTION Protection for the Eye The Eyeball Fluids in the Eye The Visual Pathway  The eye sits in a protective bony socket called the orbit. Six extraocular muscles move the eye up and down and side to side, and rotate the eye. The extraocular muscles are attached to the white part of the eye called the sclera. This is a strong layer of tissue that covers nearly the entire surface of the eyeball. The surface of the eye and the inner surface of the eyelids are covered with a clear membrane called the conjunctiva.  Tears lubricate the eye and are made by lacrimal gland which sits under the outside edge of the eyebrow (away from the nose) in the orbit. Tears drain from the eye through the tear duct. Light is focused into the eye through the clear, dome- shaped front portion of the eye called the cornea. Behind the cornea is a fluid-filled space called the anterior chamber. The fluid is called aqueous humor. Behind the anterior chamber is the eye’s iris and the dark hole in the middle called the pupil. Muscles in the iris dilate (widen) or constrict (narrow) the pupil to control the amount of light reaching the back of the eye.  Directly behind the pupil sits the lens, which focuses light toward the back of the eye. The lens is surrounded by the lens capsule. The vitreous cavity lies between the lens and the back of the eye. A jellylike substance called vitreous humor fills the cavity, nourishing the inside of the eye and helping the eye hold its shape. Light that is focused into the eye by the cornea and lens passes through the vitreous onto the retina — the light-sensitive tissue lining the back of the eye. A tiny but very specialized area of the retina called the macula is responsible for giving us our detailed, central vision. The other part of the retina, the peripheral retina, provides us with our peripheral (side) vision.  The retina has special cells called photoreceptors. These cells change light into energy that is transmitted to the brain. There are two types of photoreceptors: rods and cones. Rods perceive black and white, and enable night vision. Cones perceive color, and provide central (detail) vision. The retina sends light as electrical impulses through the optic nerve to the visual cortex in brain.  How the eye works Light is focused primarily by the cornea, which acts like a camera lens. The iris of the eye functions like the diaphragm of a camera, controlling the amount of light reaching the back of the eye by automatically adjusting the size of the pupil (aperture). The lens is located directly behind the pupil and further focuses light. By accommodation, this lens helps the eye automatically focus on near and approaching objects. Light focused by the cornea and lens (and limited by the iris and pupil) then reaches the retina. The retina acts like an electronic image sensor of a digital camera, converting optical images into electronic signals. The optic nerve then transmits these signals to the visual cortex — the part of the brain that controls our sense of sight.  DIAGNOSTIC TESTS The Snellen chart is an eye chart – used to measure visual acuity Visual field tests – used to check central and peripheral vision. Tonometry – assesses intraocular pressure An ophthalmoscope – used to examine the interior structures. Gonioscopy measures the angle of the anterior chamber. Muscle function and coordination can also be tested.  STRUCTURAL DEFECTS Interfere with the focusing of a clear image on the retina: Myopia, – Nearsightedness – eyeball is too long – the image is focused in front of the retina,  STRUCTURAL DEFECTS Hyperopia, – farsightedness, – the eyeball is too short – the image focused behind the retina  STRUCTURAL DEFECTS Presbyopia – farsightedness associated with aging, – loss of elasticity reduces accommodation Astigmatism – an irregular curvature in the cornea or lens. Strabismus (squint or cross-eye) – results from a deviation of one eye, – resulting in double vision (diplopia). – may be caused by a weak or hypertonic muscle, a short muscle, or a neurologic defect. – In young children, must be treated immediately to prevent the development of amblyopia, the suppression by the brain of the visual image from the affected eye.  STRUCTURAL DEFECTS Nystagmus – an involuntary abnormal movement of one or both eyes. – This abnormality may result from neurologic causes, from inner ear or cerebellar disturbances, or from drug toxicity. Diplopia (double vision) Paralysis of the upper eyelid (ptosis) may be caused by trauma to the cranial nerves, resulting in paralysis of the extraocular muscles.  INFECTIONS AND TRAUMA A stye – an infection involving a hair follicle on the eyelid – usually by staphylococci. – A swollen, red mass forms on the eyelid Conjunctivitis; Trachoma Keratitis  Conjunctivitis – A superficial inflammation or infection – Involving the conjunctiva lining the eyelids and covering the sclera. – Allergens or irritating chemicals in the air are a frequent cause – Symptoms: redness, itching, and excessive tearing – Staphylococcus aureus cause the “pink eye” occurs frequently in children. The sclera of the eye and eyelid appears red, and there is a purulent discharge. spread by the fingers or contaminated towels. – Occurs with Contact lenses , contaminated medication or makeup. Antibiotic treatment is required to reduce contagion and prevent damage to the cornea  Conjunctivitis Other causes : Chlamydia trachomatis and N.gonorrhea Both cause infection in the reproductive tract May infect the eyes of newborns, May be transferred to the eyes by self- inoculation. Infection with N. gonorrhea is characterized by redness & heavy discharge.  Trachoma Caused by Chlamydia trachomatis Follicles develop on the inner surface of the eyelids. Can occur in any age group. “Scratchy” eye and no exudate is normally present. – Everting the upper eyelid shows the characteristic pearl- like follicles. Treated with antibiotic ointments, – if not treated, the eyelids become scarred and the lashes turn inward to abrade the cornea………lose of transparency. Globally, trachoma is the most common cause of vision loss – Where no adequate water and inadequate hygiene occurs  Keratitis Inflammation of the cornea. Severe pain and photophobia (sensitivity to light) Herpes simplex virus is a cause of corneal inflammation and ulceration. – transferred from a herpes lesion around the mouth by the fingers, or in a dental office, by spray of contaminated saliva. Keratitis --------increased risk of ulceration eroding the cornea Scar tissue interfering with vision. Trauma to the cornea also increases risk of visual loss. Damage from chemicals, splashes, or fumes.  GLAUCOMA Pathophysiology Results from increased intraocular pressure caused by an excessive accumulation of aqueous humor. May be acute or chronic Signs and symptoms Appearance of “halos” around lights at night – Due to corneal edema and altered light refraction Loss of peripheral vision As the pressure increased ,eye pain, nausea, and headache develop, – vision is blurred, – the cornea appears bulging and cloudy. – The pupil is dilated and unresponsive to light.  1- Acute (narrow or closed angle ) glaucoma A sudden marked increase in intraocular pressure. Occurs when angle between the cornea and the iris in the anterior chamber is decreased. Caused by a developmental abnormality, aging, or scar tissue in the eye from trauma or infection. Acute episodes of glaucoma may be triggered by pupil dilation resulting from adrenergic drugs, by stress, or by prolonged periods in darkened rooms.  1- Acute (narrow or closed angle ) glaucoma Signs&Symptoms: pressure rises rapidly, eye pain, nausea, and headache develop, vision is blurred, cornea appears bulging and cloudy. The pupil is dilated and unresponsive to light May require surgery, such as removal of part of the iris, to open a passageway for drainage into the canal of Schlemm (iridectomy) Laser iridotomy is a popular noninvasive procedure.  2- Chronic (wide or open-angle ) glaucoma  A common degenerative disorder in older persons, usually beginning after age 50 The trabecular network and canal of Schlemm become obstructed, The outflow of aqueous humor gradually diminishes. Signs & symptoms: Onset is insidious, pressure increases slowly and usually asymptomatically.  2- Chronic (open-angle )glaucoma Increased intraocular pressure is often the only sign. – compresses the blood flow to the retinal cells, causing ischemia and damage to the retinal cells. – The anterior portion of the retina is affected first, including the receptor cells for peripheral vision If pressure inside the eyeball continues to increase, more of the retina and the optic nerve will be damaged. – The optic disc appears eroded or “cupped” as the optic nerve fibers are compressed – Damage to the retina and optic nerve is irreversible, and eventually blindness results. Blurred vision and the appearance of “halos” around lights Corneal pain  2- Chronic (open-angle )glaucoma, Treated by regular administration of eye drops to reduce secretion of aqueous humor (e.g., timolol or betaxolol, beta-adrenergic blocking agents) or to constrict the pupil (e.g., pilocarpine, a miotic or cholinergic agent).  CATARACTS Progressive opacity or clouding of the lens The size, site, and density of the opacity vary among individuals and may differ in one individual’s two eyes Degeneration of proteins in the lens related to – Aging or metabolic abnormalities such as diabetes. – Excessive exposure to sunlight may be a factor. – Congenital cataracts are usually a result of maternal infection due to rubella or toxoplasmosis. – Traumatic cataracts are the result of blows to the eye Blurred vision that progresses over the visual field and becomes darker with time is the only indicator. Damaged lens can be removed and replaced by an artificial intraocular lens. Appearance of the eye with cataract  DETACHED RETINA An acute problem that occurs when the retina tears away from the underlying choroid because of ; – marked myopia, – degeneration with aging, or – scar tissue that creates tension on the retina Vitreous humor flow increase behind the loose retinal portion, – retina is lifted away from the choroid. – retinal cells cease to function – results in an area of blackness in the visual field. No pain related to the tear, Initially the patient may see light or dark floating spots in the visual field, resulting from blood or exudate leaking from the tear. A darkened or blind area develops, which increases in size with time. as a “dark curtain” drawn across the visual field. Surgical intervention such as scleral buckling or laser therapy is required as soon as possible  MACULAR DEGENERATION Age-related macular degeneration (AMD) is a common cause of visual loss in older persons. – Arise from a combination of genetic factors and environmental exposure (e.g., ultraviolet rays and drugs). – A similar condition found in younger persons has a stronger genetic basis. Degeneration occurs at the fovea centralis in the macula lutea, with its high density of cones, at the central point of the retina. Two types. : – Dry or atrophic AMD, more common type, deposits form in retinal cells gradually destroying them. – Wet or exudative form, neovascularization occurs, with the formation of abnormal, leaky blood vessels, rapidly destroying the retina. In both types, nutrients can no longer pass from the choroids to the retina. Central vision with high acuity first becomes blurred, and then is lost. There is no treatment to reverse the effects. Depth perception is also affected. There is no pain. Peripheral vision is not affected Normal vision Age-related macular degeneration  MACULAR DEGENERATION Visual field tests and angiography assist diagnosis. Photodynamic therapy (photosensitive drug plus laser) may help seal off neovasculature in some persons with the wet type. For the dry type of AMD, – Nutrition is assessed to ensure that vitamin, mineral, and antioxidant intake are sufficient. – A high-dose formulation of antioxidants and zinc has been shown to reduce the risk of advanced AMD and its associated vision loss.  THE EAR REVIEW OF NORMAL STRUCTURE AND FUNCTION Parts of the Ear Pathway for Sound The Semicircular Canals Structure of The Ear  Anatomy of the ear The ear is divided into three anatomic sections, the external ear, the middle ear, and the inner ear : The external ear consists of the pinna, and the external auditory meatus or canal. This canal passes through the temporal bone to the tympanic membrane or eardrum, which marks the separation between the external and middle ear. The middle ear consists of the tympanic cavity, a hollow area in the bone, which contains three tiny bones, the malleus, incus, and stapes, which compose the ossicles. The malleus is adjacent to the tympanic membrane, and the stapes fits against the oval window, a membrane connecting the middle ear and the inner ear. The middle ear cavity opens into the auditory or eustachian tube, which connects to the nasopharynx. This tube equalizes pressure in the middle ear with pressure in the external ear canal.  This tube equalizes pressure in the middle ear with pressure in the external ear canal. This equalization is important if atmospheric pressure changes suddenly, as when an airplane takes off. Chewing or swallowing helps to equalize the pressure on either side of the tympanic membrane. The middle ear cavity is also continuous with the mastoid air cells in the mastoid process of the temporal bone around the ear. A continuous mucous membrane lines the middle ear cavity, the mastoid cells, the auditory tube, and the respiratory tract. This is significant because it provides a path for direct spread of infection through these structures.  The inner ear is called the labyrinth. It is composed of two parts, the cochlea and the semicircular canals, joined by a vestibule. These structures consist of a bony labyrinth filled with a fluid, perilymph, inside of which is a membranous labyrinth filled with endolymph. The cochlea contains a complex arrangement of membranes surrounding the organ of Corti, where specialized hair cells (nerve receptors) provide stimuli to the sensory neurons for hearing. These neurons form the cochlear branch of the auditory nerve (cranial nerve VIII), which conducts impulses to the temporal lobe for reception and interpretation of sound.  Pathway for Sound 1. Sound waves enter the external ear canal and strike the tympanic membrane, causing it to vibrate. 2. Vibration of the tympanic membrane causes the malleus to vibrate, and then the incus and the stapes. 3. The motion of the stapes against the oval window initiates movement of the perilymph and endolymph in the cochlea. 4. These “water waves” stimulate movement of the membranes and hair cells in the organ of Corti, which converts the stimulus into a nerve impulse. 5. The nerve impulses are conducted to the auditory area in the temporal lobe of the brain, where the sound is received and interpreted.  The semicircular canals in the inner ear include three structures, each at right angles to the other two; the sense of balance and equilibrium is focused in the crista ampullaris, located in the ampulla of each semicircular canal and in the macula in the vestibule. These contain the receptor hair cells, which can be stimulated by motion of the endolymph fluid in response to head movements or position changes. Because of the arrangement of the canals, movement in any direction can be detected. Any stimulus is conducted by the vestibular branch of the auditory nerve to the medulla oblongata and other parts of the brain. Vestibular damage causes vertigo, a sense of rotation of self or the environment.  Ear disorders HEARING LOSS EAR INFECTIONS – Otitis Media – Otitis Externa CHRONIC DISORDERS OF THE EAR – Otosclerosis – Ménière’s Syndrome  HEARING LOSS Two basic types, – Conduction deafness – Sensorineural deafness (sometimes sensorineural is broken down into sensory and neural deafness). Tests comparing conduction by air through the external canal and conduction through the mastoid bone can assist in differentiating the type of deafness.  HEARING LOSS Conduction deafness ; Sensorineural impairment develops with damage to the organ of Corti or occurs when sound is the auditory nerve. blocked in the external For example: ear or middle ear. – Viral infection (rubella, infleunza, HSV) For example: – Head trauma – Ototoxic drugs such as the antibiotics – An accumulation of wax (streptomycin, neomycin), analgesics or a foreign object in the (asprin, ibuprofen), diuretic (furosemide) external ear canal can The early sign of toxicity is often tinnitus, a ringing or buzzing in the ears block sound waves. – Sudden, very loud sounds or prolonged – Scar tissue or adhesions exposure to loud noise (damage hair cells) may impair the function – Presbycusis is the sensorineural loss that occurs in elderly people of the tympanic – Congenital deafness (infection or trauma) membrane or ossicles. Hearing impairment in young children often interferes with speech and social development, as well as other interactions with persons and with learning ability.  HEARING LOSS Newborns are screened for hearing deficits Audiologists, otolaryngologists, and speech-language pathologist are helpful. Lip reading and sign language (American Sign Language, ASL) may be learned. Many assistive devices are now available to improve communication skills. Hearing aids have been used to compensate hearing deficit. Cochlear implants are used in cases of sensorineural loss in very young congenitally deaf children or adults.  EAR INFECTIONS Otitis Media Otitis media is an inflammation or infection of the middle ear cavity. Pathophysiology Exudate builds up in the cavity, causing pressure on the tympanic membrane--------rupture of the tympanic membrane – interfering with the movement of the membrane and the ossicles. The auditory tube is obstructed by – inflammation, preventing drainage of the fluid into the nasopharynx. – Enlarged adenoids may compress the tube. Prolonged infection is likely to produce – scar tissue and adhesions, – permanent conductive hearing loss. – mastoiditis  Otitis Media (Etiology) The mucosa of the middle ear cavity may become inflamed due to: – allergies or infection that spreads along the continuous mucosa from the nasopharynx and respiratory structures More in infants and young children because; – the auditory canal is shorter and wider and forms more of a right angle to the nasopharynx, thereby facilitating drainage of respiratory secretions into the auditory tube – Infants tend to spend more time in a recumbent position, feeding in a supine position encourages reflux of fluid into the ear. More frequently in the winter months Common bacterial causes – Haemophilus influenza, particularly in young children, and pneumococci, beta-hemolytic streptococci, and staphylococci. – result in a purulent discharge.  Otitis Media Signs and symptoms Occasionally otitis media is asymptomatic. severe pain or earache (otalgia) related to the pressure on the tympanic membrane and the nerve receptors in the cavity. The tympanic membrane appears red and bulging. An infant or young child tends to rub or pull at the ear to express distress. Mild hearing loss or a feeling of fullness is common. Fever and nausea, may be present. Rupture of the tympanic membrane results in a purulent discharge from the external ear canal, accompanied by relief of pain.  Otitis Media Treatment Antibacterials Some physicians treat initial infections for at least 48 hours with ibuprofen or acetaminophen to reduce discomfort. Decongestants to reduce edema and obstruction of auditory canal. A person with an ear infection should use caution if he is planning to use air transportation because the pressures inside and outside the ear must be equalized to prevent additional damage (barotrauma). – Chewing gum or swallowing during rapid ascent or descent may help. – Tympanoplasty or mastoidectomy may be required.  Otitis Externa Otitis externa, sometimes called swimmer’s ear, An infection of the external auditory canal and pinna. Usually of bacterial origin but occasionally is fungal. May be associated with – swimming, – irritation or the introduction of organisms when cleaning the ear, – frequent use of earphones or earplugs. Pain, purulent discharge, and a hearing deficit are common signs of otitis externa. Otitis externa can be differentiated from otitis media because pain is usually increased with movement of the pinna. CHRONIC DISORDERS OF THE EAR 1- Otosclerosis Imbalance in bone formation and resorption. – With development of excess bone in the middle ear cavity, – the stapes becomes fixed to the oval window, blocking conduction of sound into the cochlea. A genetic factor, primarily in young adult females. Surgical removal of the stapes (stapedectomy) and replacement by a prosthesis restores hearing. If laser surgery is used in an early stage, the stapes may be freed and no prosthesis is required. CHRONIC DISORDERS OF THE EAR 2- Ménière’s Syndrome: An inner ear or labyrinth disorder beginning in adults 30 to 50 years of age. Affects one ear. Excessive endolymph develops intermittently, stretching the membranes and interfering with the function of the hair cells in the cochlea and vestibule. Rupture of the labyrinth membrane may allow perilymph to mix with endolymph, increasing volume and causing an attack. The increased fluid may also be of vascular origin.  Ménière’s Syndrome Each attack may last minutes or hours and causes severe vertigo, tinnitus (excess noise like a roaring motor or ringing), and unilateral hearing loss. – Vertigo, a sensation of whirling and weakness, is often – accompanied by loss of balance and falls, – nausea and sweating, – inability to focus, and nystagmus. – Repeated occurrences lead to permanent damage to the hair cells, with permanent loss of hearing and vertigo.  Ménière’s Syndrome The acute episodes occur over several months, followed by a brief period of relief, and then the cycle repeats. – Stress is a predisposing factor, – Other conditions that affect blood flow. – Changes in barometric pressure may precipitate an attack. Improvement occurs with – stress reduction; – avoidance of smoking, alcohol, and caffeine; – observance of a low-sodium diet; and use of a mild diuretic  Ménière’s Syndrome Diagnostic tests include ; – the balance test, electronystagmography (ENG), – the fluid test, electrocholeography (ECOG), – MRI to rule out a tumor or other abnormal structure. Treatment of attacks consists of Drugs such as ; dimenhydrinate, diazepam, or antihistamines. Home exercise programs have assisted in reducing the individual’s sensitivity to motion. In severe cases surgery may be helpful to provide a shunt, remove excess endolymph, or resect the vestibular nerve.