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188 Cards in this Set
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Hyperopia
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Farsightedness
Objects at infinity are not seen clearly unless accommodation is used, and near objects may not be seen because accommodative capacity is finite. |
Corrected with convex lenses.
Experience presbyopia at an earlier age than emmetropia (normal state of vision) |
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Myopia
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Nearsightedness
The unaccommodated eye focuses on objects closer than infinity Able to focus on VERY near ojects without glasses; objects beyond this distance cannot be seen without the aid of corrective lenses. |
Corrected with minus, concave lenses
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Astigmatism
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Refractive errors in the horizontal and vertical axes differ.
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Corrected with cylindrical lenses
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Presbyopia
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Natural loss of accommodative capacity with age.
Persons with emmetropia usually notice inability to focus on objects at a normal reading distance at about age 45. Earlier occurrence in Farsighted individuals |
Corrected with Plus Lenses for near work.
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Entropion
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inward turning of usually the lower lid; occurs in older people as a result of degeneration of the lid fascia, or may follow extensive scarring of the conjunctiva and tarsus.
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Ectropion
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Outward turning of the lower lid.
Common with advanced age. Surgery is indicated if there is excessive tearing, exposure keratis, or a cosmetic problem. |
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Basal cell carcinoma
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Most common cancer.
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Dacryocystitis
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an infection of the lacrimal sac due to obstruction of the nasolacrimal system. Can be acute or chronic. Occurs often in infants and persons over 40 years old.
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Conjunctivitis
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The most common eye disease. Can be acute or chronic. Most are due to viral or bacterial infection.
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viral conjunctivitis
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Adenovirus is the most common cause of viral conjunctivitis. There is usually bilateral disease with copious watery discharge, often with marked foreign body sensation and a follicular conjunctivitis.
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Infection spreads easily. Eye clinics and contaminated swimming pools are sometimes the source of infection.
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Bacterial conjunctivitis
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The organisms isolated most commonly in bacterial conjunctivitis are staphylococci, streptococci, Haemophilus species, Pseudomonas, and Moraxella.
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Gonococcal Conjunctivitis
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Usually acquired through contact with infected genital secretions, typically causes copious purulent discharge.
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Trachoma
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Most common infectious cause of blindness in the world. Manifests as bilateral follicular conjunctivitis, epithelial keratitis, and corneal vascularization (pannus).
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• Blepharoptosis (Ptosis)
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• A clinical diagnosis of drooping of the upper eyelid. The function of the levator muscle is the key distinguisher of types and treatment.
• 5 subtypes |
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Involutional Blepharoptosis
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1 of 5 subtypes of blepharoptosis
AKA aponeurotic This is due to the disinsertion, vcentral dehiscence or attentuation of the levator aponeurosis. • most common type of ptosis • associated with aging, eye surgery or trauma, pregnancy and chronic eyelid swelling. • Levator function is good. |
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Mechanical Blepharoptosis
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1 of 5 subtypes of blepharoptosis
Due to the mass effect of tumors, dermatochalasis or blepharochalasis to tethering of the eyelid by scarring (“cicattrical ptosis”). o Levator function is good. |
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Myogenic Blepharoptosis
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due to muscle disorders such as chronic progressive external ophthaloplegia, myotonic dystrophy and myasthenia gravis.
• This is an uncommon form of ptosis with • extremely poor levator function. |
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Neurogenic Blepharoptosis
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due to faulty innervation to the levator (Cranial Nerve III palsy) or Müllers mucsle (Horner’s Syndrome) or to multiple sclerosis.
• Levator function is variable depending on the underlying defect. |
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Congenital Blepharoptosis
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usually myogenic and unilateral due to fibrosis and fat infiltration of the levator muscle.
• Levator function is poor from birth |
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Clinical Presentation of Blepharoptosis
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o Symptoms
o Eyelid droop, patients report seeing upper eyelashes or a defect in the superior vision o Signs o Eyelid droops and does not elevate fully on upgaze (levator function) o Eye often appears smaller and the lid crease is abnormal o Ptosis is usually accentuated in downgaze but often in congential ptosis the ptotoic lid is higher than the unaffected lid (lid lag) o Other deficits are common in myogenic and neurogenic types |
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Dacrocystitis - Physical Exam
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Cotton swab - apply gentle pressure to lacrimal sac in nasal corner of lower eyelid,
obtain a Gram stain of discharge Assess EOM’s, check for proptosis to assess for orbital cellullitis, Examine all systems for systemic infection, Do NOT attempt to probe or irrigate the lacrimal system during the ACUTE stage |
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Blepharitis Treatment
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Anterior - Scrub eyelid margins 2x/day w/mild shampoo, warm compresses for 10-15 mins 4x/day, antibacterial ointment to eye if moderately severe
Posterior - more difficult, perform and teach pt to express material, artificial tears, acute flares treated systemically w/oral antibiotics, anti-inflammatory drugs |
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Vitreous Floaters Signs/Symptoms
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Showers or sparks of lightning flashes (photopsia) that accompany a shower of floaters
-these require urgent evaluation of the retinal by a specialist |
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Vitreous Floaters Description
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Chronic: considered harmless.
Acute: Showers of floaters occur with vitrous hemorrhage or detachment or with retinal tears. |
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Retinal Detachment Description and Symptoms
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Separation of the sensory retinal from the underlying pigment epithelium. 3 major types: Rhegmatogenous (most common), exudative/serous and tractional
No pain or redness. “a curtain came down over my eye” floaters flashing lights |
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Viral Conjunctivitis TREATMENT
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Topical sulfonamides to prevent secondary bacerial infection and cold compress to reduce the discomfort. -lasts 2 weeks
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Gonococcal Conjunctivitis Treatment
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A single 1g dose of intramuscular Ceftriaxone is usually adequate. Topical abx such as erythromycin and bacitracin may be added
It is a ophthalmologic emergency because the corneal involvement may rapidly lead to perforation. |
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Cataracts - Clinical Findings and treatment
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On exam of a dilated pupil, the fundus is poorly visualized, eventually a red reflux is lost. Decreased VA, contrast sensitivity and color vision (blue) is lost
Early stages can be improved by glasses. Definitive tx is surgery |
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Granulomatous
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Chronic inflammation
The WBCs that have infiltrated this tissue are macrophges and eosinophils They make a thickened wall No erythema Not irritated Ex: Chronic Dacrocystitis |
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Chemosis
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swelling of the conjunctiva
Ex: conjunctivitis |
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4 things to assess in glaucoma
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– assessment of pressure (palpation and tonometry)
Intraocular pressure is evaluated grossly by palpation and more specifically by tonometry. – assessment of the anterior chamber angle – assessment of the optic disk – assessment of the visual fields The greatest loss is in the inferior region initially, later “tunnel” vision develops |
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Acute Closed Angle Glaucoma
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• Signs and symptoms include
– Rapid onset – Severe pain and profound visual loss. – Red eye, steamy cornea, dilated pupil. – Hard eye. – Minutes to hours – subacute – Sudden attack of symptoms, fluid can’t drain – Affects the cornea – Pressure buildup, then dilation, boom |
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Primary Open Angle Glaucoma
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• This is the most frequent type of glaucoma
• High risk populations include elderly, African Americans and those with positive family history • Onset is painless, insidious, with gradual loss of peripheral vision. • Evaluation parameters: – Elevated tonometry pressure with repeated measurements – Anterior chamber angle is normal (NO crescent shadows) – angle is big enough for light to get through – Optic disc cupping > 0.3 or asymmetry of the two disks – GRADUAL loss of peripheral visual fields - generally: abnormal drainage of the aqueous humor– angle of canal of schlemm is blocked infiltrated trebecula (endothelial linng Schlemm’s canal) – occurs with normal aging (starts at 30 y/o) |
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Cataracts P/E
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Red Reflex - present with a defect
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Clinical Presentation of Cortical Cataracts
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– Blurred vision, progressive over months or years. Patients often report the need for increased light to see clearly.
• Want brighter light in the room, can’t see, needs new glasses all the time • Read at a different angle by turning head – No pain or redness. • Signs – Lens opacities (may be grossly visible). – On examination of a dilated pupil, the fundus is poorly visualized, eventually the red reflex is lost entirely. Decreased visual acuity, contrast sensitivity and color vision (especially blue discrimination) – Color changes – especially blue – the blue spectrum is lost from vison → that’s why they need light |
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Cataract Management
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• In the early stages vision can be improved with glasses or contact lenses.
– Typically will leave it alone initially – Learning to live with gradual loss of vision until it is big enough to take out • Definitive treatment is surgery – ophthalmology – Put new lens in • Risk factors – determine progression length |
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Tx of ALL types of Glaucoma
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Reduction of aqueous humor production
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What determines intraocular pressure
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The rate of aqueous production;
The resistance to outflow of aqueous from the eye |
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Visual Fields of Patients with Glaucoma
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The greatest loss is in the inferior region initially, later “tunnel” vision develops
Lose periphery of visual fields Eventually can’t see anything but center AND macula |
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Primary Open Angle Glaucoma
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• This is the most frequent type of glaucoma
• High risk populations include elderly, African Americans and those with positive family history • Onset is painless, insidious, with gradual loss of peripheral vision. • Evaluation parameters: – Elevated tonometry pressure with repeated measurements – Anterior chamber angle is normal (NO crescent shadows) – angle is big enough for light to get through – Optic disc cupping > 0.3 or asymmetry of the two disks – GRADUAL loss of peripheral visual fields - Blockage of Canal of Schlemm by infiltrated trebecula (occurs with age) - aqueous humor can't drain |
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Primary Closed Angle Glaucoma
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• Closed angle glaucoma occurs in eyes with pre-existing anatomic narrowing of the anterior chamber and in elderly with enlargement of the lens. (flow problem, not a drainage problem)
Iris gets too close to lens (happens when eye is dilated). Blocks out flow. • High Risk populations include elderly, Asians and hyperopes. • Acute, Subacute and chronic forms exist. Accumulated damaged from acute and subacute episodes lead to chronic disease. |
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Acute Closed Angle Glaucoma
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• Signs and symptoms include
– Rapid onset – Severe pain and profound visual loss. – Red eye, steamy cornea, dilated pupil. – Hard eye. – Minutes to hours – subacute – Sudden attack of symptoms, fluid can’t drain – Affects the cornea – Pressure buildup, then dilation, then hemhorrage – Iris is injected with blood, fuzzy/blurry/steamy cornea – Go into movie theater, pupils dilate too much → causes spontaneous hemhorrage – This is why you always get a tonometry measurement/pressure before you dilate the eye!!! EMERGENCIA! |
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Vitreous Disorders (General)
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• Like the healthy lens, the vitreous is not normally visible.
• Visible elements therefore are the result of – Structural changes such as floaters (dark mobile spots that occur with age) Vitreous thickens, vision becomes less clear, will be there for the rest of your life – Invasive elements such as blood or fibrous tissues • Normal vitreous is best seen with a slitlamp, but large changes can be seen with the hand ophthalmoscope. |
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Vitreous Floaters
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• The most common symptom of an abnormal component of the vitreous, often associated with aging and more common in myopes.
– Typically start to occur around age 30 • A “floater” represents the patient’s awareness of the shadow that the opacity casts upon the retina. They may shift with eye movement and are most noticeable against a plain background like the sky. – Usually these are caused by condensation of vitreous proteins and collagens, and by small hemorrhages into the vitreous or fibrous coagulation. Recent hemorrhages are often seen as black streaks or cobwebs, which later break up into small spots. |
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Chronic Vitreous Floaters
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considered harmless, but a careful survey of the vitreous and retina is required.
– They are of “no clinical significance” and typically become less noticeable over time. – Document but typically don’t do anything |
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Acute Showers of Floaters
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occur with vitreous hemorrhage or detachment or with retinal tears or detachment. Showers of “sparks” or lightning flashes (photopsia) that accompany a shower of floaters are especially ominous.
– Pt sees black strings across eye – You will not even see the retina/fundus – the floaters of blood will block your view into the eye – Blood will mix with vitreous and sink to bottom – These require urgent evaluation of the retina by a specialist |
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Vitreous Hemorrhage
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• A vitreous hemorrhage can occur whenever the sensory retina is torn, there is occlusion of the retinal veins or longstanding hypertension.
• Symptoms include – Sudden increase, or onset of vitreous floaters – Sudden shower of small black dots or ring-like forms with clear centers. – Variable loss of visual acuity Usually one affected eye |
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Vitreous Hemorrhage and Retinopathy
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• Vitreous hemorrhage can be a result of hypertension.
• Hypertensive retinopathy is visible behind the vitreous hemorrhage. Damage shows as spots of yellow on fundus |
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Retinopathy
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• There are multiple local and systemic causes of retinopathy.
• Common signs of retinopathy include hemorrhages, ischemic cotton wool spots, drusen or hard exudates and a macular star, proliferation of blood vessels, nicking of the artiovenous crossing, Copper or Silver wiring, and optic disc edema. |
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Retinal Detachment
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• “Retinal Detachment” refers to the separation of the sensory retina (Photoreceptors and inner tissue layers) from the underlying pigment epithelium.
• There are three major types – Rhegmatogenous – characterized by a “tear” of the retina with infiltration of vitreous into the subretinal space. Most common type – Traction – characterized by a pull of the retina which “bulges” toward the examiner. The second most common type – Serous and Hemorrhagic – is due to fluid collections under the sensory retina and are uncommon. |
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Sxs of Retinal Detachment
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• Blurred vision in one eye becoming progressively worse. ("A curtain came down over my eye.")
• No pain or redness. • Central vision remains intact until the macula becomes detached. • On ophthalmoscopic examination, the retina is seen hanging in the vitreous like a gray cloud. |
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Retinal Detachment Treatment
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• Retinal Detachment requires urgent treatment by an Ophthalmologist!!
• Treatment in the clinic include positioning the patient so gravity pulls the tear toward its normal area, and keeping the patient calm • The Ophthalmologist will reposition the retina via pressure with gas, opening the eye or external pressure. • Sealing the retina is done by laser or cryotherapy. |
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Occlusive Disease of the Retina
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• The arteries and veins of the retina are subject to occlusion, with resultant characteristic changes in the retina.
• Painless, unilateral sudden visual loss is the presenting symptom of all occlusive disorders. • Increased age, increased serum lipids and atherosclerosis are risk factors. Glaucoma is also a risk factor. |
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Occlusive Disease of the Retina
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• The arteries and veins of the retina are subject to occlusion, with resultant characteristic changes in the retina.
• Painless, unilateral sudden visual loss is the presenting symptom of all occlusive disorders. • Increased age, increased serum lipids and atherosclerosis are risk factors. Glaucoma is also a risk factor. |
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Retinal Artery Occlusion
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• Retinal Artery Occlusions are analogous to a myocardial infarction.
• These can be in the central retinal artery or in a branch of it. • The patient complains of painless, sudden visual loss. The degree of loss varies by the portion of the artery affected. • For central artery occlusion, there will be an afferent pupillary defect within minutes. • Later the retina becomes opacified, with a pale optic disc if the occlusion is central. |
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Late Central Retinal Artery Occlusion
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• Pale optic disc
• Pale fundus • Cherry-red macula • Total loss of vision |
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Late Central Retinal Artery Occlusion - Treatment
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• This is a medical emergency
– There is irreversible damage after 90 minutes • Treatment includes – Immediate assistance by an ophthalmologist – laying the patient flat – ocular massage – high concentrations of inhaled oxygen – intravenous acetazolamide – anterior chamber paracentesis – Thrombolysis medications should be considered. |
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Branch Retinal Artery Occlusion
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• The same disease as retinal artery occlusion, but on a smaller scale.
• The pupils will react as some light will strike the retina. • Visual loss is limited to the visual field of the affected area. • The optic disc is not as affected. |
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Retinal Vein Occlusion
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• Retinal vein occlusion, either central or branch vein, leads to engorgement and hemorrhage of the vein.
• Ophthalmoscopic signs include disk swelling, venous dilation and tortuosity, retinal hemorrhages, and cotton-wool spots. • Branch occlusion may have a subacute onset of visual loss. It also has a better prognosis for visual return. • Edema of the macula and cotton-wool spots are commonly seen as the condition resolves. |
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Central Retinal Vein Occlusion
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• Increasing age (> 50 yrs) and cardiovascular disease are risk factors.
• Patients often report the vision loss as occurring during the night. It is painless, even with extensive hemorrhages. • Onset can be more gradual than arterial occlusion |
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Branch Retinal Vein Occlusion
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• Always occurs as the site of an artiovenous crossing.
• The hemorrhages are segmental, but macular edema and cotton-wool spots can develop in the surrounding areas. |
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Dx of Acute Otitis Media
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Requires:
1. hx of acute onset of signs and symptoms |
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Tympanometry
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Quantitative method of evaluating the pressure in your eye
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Keratoconjunctivitis (epidemic)
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SIGNS: usually bilateral, but may begin in one eye. Hyperemia at onset, moderate pain and tearing. Edema of eyelids, chemosis. Follicles and subconjunctival hemorrhages often occur within 48 hrs. Photophobia 5-14 days later and minute erosions of cornea upon staining, tender preauricular lymphnodes. Petechial hemorrhages and pseudomembranes possible but not common
SYMPTOMS: corneal sensation normal, sudden onset of red, irritated eyes, watery discharge. Photophobia. |
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Hazards of corticosteroid therapy
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i. Herpes Simplex (dendric) keratitis
ii. Fungal infection iii. Open-angle glaucoma iv. Cataract formation v. In EXTREME cases: perforation of cornea after the corticosteroid is used for herpes simplex keratitis |
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Hazards of systemic corticosteroid use
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i. Hypertension
ii. Diabetes mellitus iii. Gastritis iv. Osteoporosis v. Glaucoma |
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Systemic Effects of Ocular Drugs
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a. There is systemic absorption of topical drugs through the conjunctival vessels and lacrimal drainage system.
b. Some Medical Contraindications i. With timolol (ophthalmic solution of non-selective B-blockers): 1. May worsen bradycardia or cause CHT or asthma.-so these things are contraindicators. ii. phenylephrine eye drops: 1. May precipitate hypertensive crisis and angina. c. To BE SAFE i. Only use 1-2 drops at a time and… ii. Do a few minutes of nasolacrimal occlusion and eyelid closure. |
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Chemosis
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– conjunctival edema ranging from mild with a boggy appearance to extensive with tense ballooning (sometimes mistaken for a blister by the patient)
o swelling o puffs up and swells out, sclera balloons out o happens with gonorrhea o puffy sclera, breakup of light throughout |
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Papillae
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small to large fibrovascular mounds containing a central vascular tuft.
o Papillae result from long term edema and leakage of fluid from vessels and are a nonspecific finding seen on the palpebral (tarsal) conjunctiva (inside of upper/lower lid) - chronic allergies |
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Follicles
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small translucent avascular mounds of plasma cells and lymphocytes that are usually most prominent in the inferior fornix or bulbar conjunctiva. (inflammatory rxn)
o These are seen in viral, chlamydial and toxic conjunctivitis and are well-circumscribed foci of lymphoid hypertrophy due to reactive hyperplasia. |
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Pseudomembrane
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a loosely attached avascular fibrinous exudate seen in epidemic keratoconjunctivitis and mild allergic or bacterial conjunctivitis
o viral infection for example with a cold o forms when the fibrinous excretory or inflammatory exudate that is secreted by invading microorganisms or ocular tissues permeates the superficial layers of the conjunctival epithelium |
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True Membrane
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• True membrane is a fibrinous exudate (something pushed/exuded it out from the conjunctiva
• vascularized tissue • firmly adherent to the palpebral (Tarsal) conjunctiva that bleeds and scars when removed. • It occurs in bacterial conjunctivitis. o has fiber in it, thicker, stronger o if pull on it its so hard that it will tear and bleed o occurs in bacterial conjunctivitis!!! HINT o if firm, don’t try to pull on it with pickups |
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Orbital cellulitis
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• Orbital cellulitis is manifested by an abrupt onset of fever, proptosis, restriction of extraocular movements, and swelling and redness of the lids.
o upper and lower lids • Common causes include o Sinusitis – sinuses can drop infections material into soft tissues around eyes o Extension of local infections (Dacrocystitis, tooth abscess) o Post Traumatic – fist fight o Post Surgical • Immediate treatment with intravenous antibiotics is necessary o Refer to ophthalmologist |
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Bacterial Conjunctivitis
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• Acute
o Gonorrhea (very thick purulent discharge) and other invasive bacteria • Medical emergency! o The more common Haemophilus influenzae or Streptococcus pneumoniae with mucopurulent discharge. • Chronic o Chronic dacrocystitis and some rare bacteria • Spread by eye-hand contact, damp washcloths or towels, bedclothes • Usually self-limited • Untreated it lasts 10-14 days, if treated it lasts 1-3 days • Gram stain will demonstrate the organism |
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Pharyngoconjunctival Fever
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• Common cold (Viral)
• “Pharyngoconjunctival Fever” is the characteristic Upper Respiratory “Sore Throat” infection seen most commonly. • Conjunctivitis is a component of the disease and is associated with follicles in the conjunctiva, hyperemia and tearing. It can be unilateral or bilateral. • Other characteristic symptoms are fever (101-1030 F) sore throat and pharyngitis. • Nontender preauricular lymphadenopathy is characteristic. o Eye drains into lymph in front of ear. o Get swollen, but nontender • There is a usual course of about 10 days. |
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Epidemic Keratoconjunctivitis
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• “Epidemic Keratoconjunctivitis” is also common. It is spread by contaminated solutions and instruments. In children it becomes systemic, in adults it remains confined to the eye.
• The conjunctivitis is usually bilateral, but begins in one eye (which is more severely affected). o At onset there is hyperemia, moderate pain and tearing. Edema of the eyelids and chemosis is common. With follicles and subconjunctival hemorrhages often appearing within 48 hours. o 5-14 days later there is photophobia and minute erosions of the cornea seen on staining. • Corneal sensation is normal • Petechial hemorrhages and Pseudomembranes may occur, but are not common. |
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Vernal Keratoconjunctivitis
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• Extreme itching and a ropy, proteinaceous discharge with a pseudomembrane(not distinctive to viruses/allergies.
• Milky appearance of the conjunctiva, with fine papillae on the lower tarsal conjunctiva • The upper palpebral conjunctiva often has giant papillae with a cobblestone appearance. • Red eye, not as swollen, cobblestoning (rubbing eyes and nose), papillae, stringy |
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P/E finding of all cataracts
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Red Reflex - "present with a defect"
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Cataract
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Opacification of the LENS
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Risk Factors for Cataracts
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Risk factors include African-American ethnicity, smoking and exposure to ionizing radiation such as X-rays and sunlight.
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Symptoms of cortical cataracts
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• Primary symptoms are - painless, blurry, color change, opacity, don’t always lead to leukocoria!
– Blurred vision, progressive over months or years. Patients often report the need for increased light to see clearly. • Want brighter light in the room, can’t see, needs new glasses all the time • Read at a different angle by turning head – No pain or redness. |
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Cataract Management
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• In the early stages vision can be improved with glasses or contact lenses.
– Typically will leave it alone initially – Learning to live with gradual loss of vision until it is big enough to take out • Definitive treatment is surgery – ophthalmology – Put new lens in • Risk factors – determine progression length |
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Glaucoma
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• Glaucoma is a disease of increased intraocular pressure associated with optic disc changes and visual field loss.
Unnecessary for most patients End result – eye is hard as a rock Hard, sightless, painful and PREVENTABLE Blockage of intraocular fluid |
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GENERAL tx for all forms of glaucoma
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• Reduction of aqueous production is used to treat all forms of glaucoma. Other drugs and surgical options
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Types of Primary Glaucoma
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– Open angle glaucoma (Chronic)
– Closed angle glaucoma in Acute, Subacute and Chronic forms |
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The Sx that is a DIRECT indicator of the severity of glaucoma
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cup-disc ratio - Over time, the cup becomes increasingly enlarged, as the disc is smashed into it, due to increasing pressure from the aqueous humor.
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Primary Open Angle Glaucoma
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• This is the most frequent type of glaucoma
• High risk populations include elderly, African Americans and those with positive family history • Onset is painless, insidious, with gradual loss of peripheral vision. • Evaluation parameters: – Elevated tonometry pressure with repeated measurements – Anterior chamber angle is normal (NO crescent shadows) – angle is big enough for light to get through – Optic disc cupping > 0.3 or asymmetry of the two disks – GRADUAL loss of peripheral visual fields - generally: abnormal drainage of the aqueous humor– angle of canal of schlemm is blocked infiltrated trebecula (endothelial linng Schlemm’s canal) – occurs with normal aging (starts at 30 y/o) |
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Primary Closed Angle Glaucoma
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• Closed angle glaucoma occurs in eyes with pre-existing anatomic narrowing of the anterior chamber and in elderly with enlargement of the lens. (flow problem, not a drainage problem)
Iris gets too close to lens (happens when eye is dilated). Blocks out flow. • High Risk populations include elderly, Asians and hyperopes. • Acute, Subacute and chronic forms exist. Accumulated damaged from acute and subacute episodes lead to chronic disease. |
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Acute Closed Angle Glaucoma
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• Signs and symptoms include
– Rapid onset – Severe pain and profound visual loss. – Red eye, steamy cornea, dilated pupil. – Hard eye. – Minutes to hours – subacute – Sudden attack of symptoms, fluid can’t drain – Affects the cornea – Pressure buildup, then dilation, then hemorrhage – Iris is injected with blood, fuzzy/blurry/steamy cornea – Go into movie theater, pupils dilate too much → causes spontaneous hemorrhage – This is why you always get a tonometry measurement/pressure before you dilate the eye!!! – The aqueous never moved beyond the iris toward the drainage system – Medical emergency – Numb, ER, ophtalmologist – EXTREME pain |
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Causes of typical vitreous floaters
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– Usually these are caused by condensation of vitreous proteins and collagens, and by small hemorrhages into the vitreous or fibrous coagulation
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Photopsia
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General term for acute showers of sparks or lighting flashes in visual field
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Vitreous Hemorrhage Signs/Sxs
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• Acute showers of floaters occur with vitreous hemorrhage or detachment or with retinal tears or detachment. Showers of “sparks” or lightning flashes (photopsia) that accompany a shower of floaters are especially ominous.
– Pt sees black strings across eye – You will not even see the retina/fundus – the floaters of blood will block your view into the eye – Blood will mix with vitreous and sink to bottom – These require urgent evaluation of the retina by a specialist. |
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Vitreous Hemorrhage
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• A vitreous hemorrhage can occur whenever the sensory retina is torn, there is occlusion of the retinal veins or longstanding hypertension.
• Symptoms include – Sudden increase, or onset of vitreous floaters – Sudden shower of small black dots or ring-like forms with clear centers. – Variable loss of visual acuity Usually one affected eye |
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Exam of Vitreous Hemorrhage
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• On examination there is
– A variable amount of blood will be visible in the dependent portions – The amount of blood varies with the underlying cause of the bleed. – Fresh blood is red, then darkens and ultimately becomes absorbed as pale streaks. Pt upright vs pt supine – fundus will look different because the blood is mobile and will settle differently |
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Rhegmatogenous Retinal Detachment
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characterized by a “tear” of the retina with infiltration of vitreous into the subretinal space. Most common type
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Traction Retinal Detachment
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characterized by a pull of the retina which “bulges” toward the examiner. The second most common type
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Serous and Hemorrhagic Retinal Detachment
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is due to fluid collections under the sensory retina and are uncommon.
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Retinal Detachment: Signs/Sxs
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• Blurred vision in one eye becoming progressively worse. ("A curtain came down over my eye.")
• No pain or redness. • Central vision remains intact until the macula becomes detached. • On ophthalmoscopic examination, the retina is seen hanging in the vitreous like a gray cloud. |
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CERUMEN
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• Cerumen is a mixture of oily secretions, shed hair and dead skin cells from the external auditory canal.
– Cerumen is good! – Protects the canal and removes debris • Cerumen normally exits the canal as a viscous fluid – thickens and dries with aging or chronic inflammation – packs with “Q-tip trauma” |
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Cerumen Impaction
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– Common symptoms include
– Hearing loss, discomfort, tinnitus, dizziness and chronic cough |
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Tx of Impacted Cerumen
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– Two phase process
– Phase 1 – removal – There are multiple methods for removal – Manual Removal – Irrigation – Cerumenolytics • water based • oil based • Mixed – Home remedies – Phase 2 – Patient Education – Q-tips aka Cotton buds – Normalization of cerumen |
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Cerumen Related Referral Indications
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– Persistent pain
– Vertigo with irrigation when water is at body temperature – Patients with a history of perforation, radiation or surgery – Very swollen canals |
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Otitis Media
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inflammation, infection or fluid changes in the structures between the tympanic membrane and the round window.
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Autophony
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an exaggerated ability to hear oneself breathe and speak, occurs with bilateral external ear or unilateral middle ear disorders.
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Tinnitus and Vertigo
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are common inner ear symptoms.
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Otitis Externa Causes
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• Otitis externa can occur from a variety of conditions which predispose the canal to inflammation.
– Skin conditions such as eczema, Seborrheic dermatitis or atopy. – Furuncles – Moist humid environments – Mechanical trauma • Typically unilateral disease occurs from acute processes, bilateral disease occurs from chronic disease . |
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Sxs of Otitis Externa
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– Otalgia which is exacerbated by movement of the pinna or tragus. Discomfort limited to the external auditory canal is the most characteristic symptom
– Pruritus – Discharge • Purulent if infection is present, watery discharge if eczema or atopic disease, mucoid if tympanic membrane is opened or combinations of purulent and mucoid. – Erythema and edema of the ear canal skin, extending to the lateral surface of the tympanic membrane – Hearing loss with Autophony Severe pain or granulation of the external auditory canal in patients with diabetes or those who are immunocompromised. |
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Otitis Externa Tx
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Avoid moisture and trauma in the external auditory canal to prevent recurrence.
Acidification with 2 percent acetic acid combined with hydrocortisone (VoSoL HC Otic) for inflammation is effective treatment in most cases and, when used after exposure to moisture, is an excellent prophylactic. |
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AOM
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infection of the middle ear.
Acute otitis media (acute ear infection) occurs when there is bacterial or viral infection of the normally present fluid of the middle ear, which causes production of fluid or pus. This may be accompanied by bleeding in the middle ear. Acute Otitis Media is defined by the presence of acute illness and a red, bulging tympanic membrane under positive pressure. |
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OME
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fluid in the middle ear.
Otitis Media with Effusion is defined by the absence of signs and symptoms of acute infection (other than reduced hearing) and the presence of a retracted or neutral tympanic membrane under negative pressure, or under no pressure but with fluid in the middle ear space. Inflammation of the ear (sterile otitis or serous otitis) may occur when there is a collection of sterile fluid in the ear. This may be caused by overproduction of fluid by the structures in the middle ear. It may also be caused by blockage of the eustachian. The presence of excess fluid causes the ear to become irritated and inflamed. |
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OM causes
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Pressure from fluids associated with ear infection may cause the eardrum to rupture. Conversely, a ruptured eardrum can result in ear infection by allowing bacteria or viruses direct entry to the middle ear. Ear infections are most common following respiratory infections, or if the sinuses or eustachian tube are blocked from allergies or enlarged adenoids.
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P/E of OM
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The typical physical findings are erythema and decreased mobility of the tympanic membrane. Rarely, when middle ear empyema is severe, the tympanic membrane can be seen to bulge outward. Mastoid tenderness is common.
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P/E of OME
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Tympanic membrane is dull and hypomobile, occasionally accompanied by air bubbles in the middle ear and conductive hearing loss.
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Complications of Otitis Media
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Extracranial
• Rupture of Tympanic Membrane with Otitis Externa • Mastoiditis • Facial Paralysis • Rupture into Inner Ear with Labrynthitis • Osteomyelitis • Sinus Thrombosis Intracranial • Central Nervous System infections Mengitis, Intracranial abscesses • Osteomyelitis • Sinus Thrombosis |
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Otitis Externa
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– Infection or inflammation of the inner ear is much less common as it is usually well protected by the local anatomy.
– Middle ear infections which rupture through and viral infections are the most frequent infectious causes. – Symptoms include o Vertigo (associated with labrynthitis, often vomiting and nausea) o Tinnitus (cochlear inflammation or injury) |
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Peripheral Vertigo
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– Occurs due to lesions in the ear and vestibular nerve
– Tends to occur episodically, no neurologic symptoms or loss of consciousness – Common types are Benign Paroxysmal Postitional Vertigo, Viral Labrynthitis and Meniere’s Disease – The type of vertigo seen with ototoxic drugs |
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Central Vertigo
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– Due to lesions in the central nervous system
– Symptoms are constant and neurologic signs or loss of consciousness is common – Common causes are migraine, stroke , epilepsy cardiovascular insufficiency |
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Benign Paroxysmal Positioning Vertigo
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The most common cause of peripheral vestibular vertigo is BPPV
– It is characterized by sudden, brief and sometimes violent vertigo after a change in head position and is often noticed when a patient lies down, arises or turns over in bed. It may even awaken a person from sleep. – The actual sensation of vertigo usually lasts for only a few seconds – As a rule, BPPV does not cause hearing loss, ear fullness or tinnitus. If these symptoms are present, it is likely that an additional inner-ear problem exists. |
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Viral Labyrinthitis
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Viral labrynthitis is also termed Vestibular Neuronitis and is presumed to have a viral etiology because it is often associated with a recent history of a flu-like illness. The virus produces acute loss of unilateral vestibular function.
• It is characterized by acute onset of intense vertigo associated with nausea and vomiting that is unaccompanied by any neurologic or audiologic symptoms. • These usually reach a peak within 24 hours and gradually subside. • During the first 24 to 48 hours of a vertiginous episode, severe truncal unsteadiness and imbalance are present. • The patient has difficulty focusing visually because of spontaneous nystagmus. |
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Meniere's Disease
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A disorder which is due to abnormal endolymph in the inner ear.
• It is characterized by episodic attacks of vertigo, which is often severe and associated with nausea and vomiting. • Hearing loss, of fluctuating level, either unilateral or bilateral. • Tinnitus, which usually worsens prior to an attack and is described as of a low tone and “blowing”. • Aural fullness, described as a pressure, fullness or warm feeling in the ear. |
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Tinnitus
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• Tinnitus is the symptom of noise in the ear.
– Objective Tinnitus may be heard by the examiner and are rare. Most causes are treatable however. – Subjective tinnitus is frequent and usually untreatable • Intermittent periods of mild, high-pitched tinnitus lasting for several minutes are common in normal-hearing persons. |
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Diseases Known to Cause Tinnitus
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– External ear: cerumen
– Middle ear: otosclerosis, middle ear effusion – Inner ear: Ototoxic drugs, trauma, noise-induced hearing loss, labrynthitis, Meniere’s Disease |
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4 mechanisms that cause conduction deafness
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Obstruction (cerumen)
Mass loading (MEE) Stiffness Effect (otosclerosis) Discontinuity (ossicular disruption) |
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Sensory Hearing Loss
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deterioration of the cochlea, usu. due to loss of hair cells from Organ of Corti
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Neural Hearing Loss
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Lesions of 8th nerve, auditory nuclei, ascending tracts or auditory cortex
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Otitis Externa
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Painful erythema and edema of ear canal skin
Purulent exudate May evolve into osteomyelitis of the skull base |
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Malignant external otitis
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osteomyelitis of the skull base, often in diabetic/immunocompromised pts
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Peripheral Vertigo
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– Occurs due to lesions in the ear and vestibular nerve
– Tends to occur episodically, no neurologic symptoms or loss of consciousness – Common types are Benign Paroxysmal Positional Vertigo, Viral Labrynthitis and Meniere’s Disease – The type of vertigo seen with ototoxic drugs, |
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Central Vertigo
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– Due to lesions in the central nervous system
– Symptoms are constant and neurologic signs or loss of consciousness is common – Common causes are migraine, stroke , epilepsy cardiovascular insufficiency |
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Benign Paroxysmal Positional Vertigo
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The most common cause of peripheral vestibular vertigo is BPPV
– It is characterized by sudden, brief and sometimes violent vertigo after a change in head position and is often noticed when a patient lies down, arises or turns over in bed. It may even awaken a person from sleep. – The actual sensation of vertigo usually lasts for only a few seconds – As a rule, BPPV does not cause hearing loss, ear fullness or tinnitus. If these symptoms are present, it is likely that an additional inner-ear problem exists. |
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Meniere's Disease
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A disorder which is due to abnormal endolymph in the inner ear.
• It is characterized by episodic attacks of vertigo, which is often severe and associated with nausea and vomiting. • Hearing loss, of fluctuating level, either unilateral or bilateral. • Tinnitus, which usually worsens prior to an attack and is described as of a low tone and “blowing”. • Aural fullness, described as a pressure, fullness or warm feeling in the ear. |
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Viral Labyrinthitis
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Viral labrynthitis is also termed Vestibular Neuronitis and is presumed to have a viral etiology because it is often associated with a recent history of a flu-like illness. The virus produces acute loss of unilateral vestibular function.
• It is characterized by acute onset of intense vertigo associated with nausea and vomiting that is unaccompanied by any neurologic or audiologic symptoms. • These usually reach a peak within 24 hours and gradually subside. • During the first 24 to 48 hours of a vertiginous episode, severe truncal unsteadiness and imbalance are present. • The patient has difficulty focusing visually because of spontaneous nystagmus. |
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Ear Diseases that cause tinnitus
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– External ear: cerumen
– Middle ear: otosclerosis, middle ear effusion – Inner ear: Ototoxic drugs, trauma, noise-induced hearing loss, labrynthitis, Meniere’s Disease • The quality of the tinnitus is useful in locating the site of origin: – The most common noise is a high-pitched, hissing or rushing noise. This is produced largely by the inner ear, as well as brain stem or auditory cortex. – Banging, popping or crackling noise originates in the middle ear, especially with effusions. – Pulsatile noise is heard from a normal carotid artery. |
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Alveolar Mucosa - Characteristics
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nonkeratinized, highly vascular, red, movable, and continuous with the buccal mucosa.
"the gingiva further from the crowns" |
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Dental Plaque - Clinical Findings
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– discolored, usually tan to brown, adherent crust located over the lower teeth.
– acute inflammation of the gingiva (“gingivitis”) with swelling and ulceration of the gums, often with bleeding and ulceration. – Chronic - calcification with extension into the periodontal ligament, loosening of the tooth and recession of the gingiva and caries. |
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Dental Plaque - Characteristics
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bacterial growth and the solidification of acid products next to the tooth.
Acid generated by oral bacteria is usually neutralized by the alkaline saliva. However if the bacteria is allowed to flourish, the materials thicken and adhere to the teeth at the gumline. The gumline is where bacterial growth is thickest. |
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Periodontitis
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a group of microorganism-induced inflammatory diseases that lead to destruction of the supporting structures of the teeth, including the alveolar bone, periodontal ligament, and adjacent soft tissues.
Gingivitis - mildest form |
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Periodontitis - Clinical Findings
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• Examination of the mouth and teeth by the dentist shows soft, swollen, red-purple gingiva. Deposits of plaque and calculus may be visible at the base of the teeth, with enlarged pockets in the gums. The gums are usually painless or mildly tender, unless a tooth abscess is also present. Teeth may be loose and gums may be receded
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Dental Caries - Clinical Findings
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– Focal destruction of the tooth appearing initially as a thinned chalky white area, later as a dark space or brownish-yellow to brownish-black spot.
– Insertion of an instrument reveals the depth of the cavity – If bacteria have invaded the tooth there is local pain and sensitivity to heat or cold |
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Primary Care Management of Dental Caries
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changing the microflora, using agents such as topical chlorhexidine and topical fluoride as a “swish and spit”
– reducing the amount of dietary sugars – decreasing the frequency of eating – adding fluoride, particularly through daily tooth brushing – increasing salivary flow, using mechanical stimulation during vigorous chewing or by using drugs |
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Dental Abscess
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• Spread of oral bacteria into the dental pulp space, tooth apex or periodontal spaces.
• Inflammatory response contains the infection. • Clinically – If apical - tooth tenderness and local pain on motion – If periodontal - Swelling and soreness and enlarged, tender mass below the gumline – Erythema of the local area. – Both processes may radiate pain into the ear - “referred otalgia”. |
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Gingival Abscess
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A localized acute infection of the marginal or interdental gingiva is usually caused by the impaction of a foreign object (ie, popcorn hull, peanut husk, toothbrush bristle, or toothpick splinter) that initiates the infection. Local débridement of dental plaque and removal of the foreign body are sufficient to abort the infection and permit healing
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Periodontal Abscess
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localized purulent inflammatory process, which is initiated by the pathogenic organisms associated with periodontitis and involves the subgingival periodontal structures. Comprehensive evaluation of the patient usually shows generalized periodontal disease in conjunction with the periodontal abscess. Often, the abscess is associated with root surface accretions and deep tortuous periodontal pockets. Clinically, patients present with pain and percussion sensitivity, mobility, and slight elevation of the involved tooth, or with a feeling of "pressure in the gums." Debridement of the affected root surface aborts the acute symptoms and leads to healing if the area is maintained plaque-free. The use of systemic antibiotics is rarely indicated.
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Simple Gingivitis
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first causes a deepening of the sulcus (gingival crevice) between the tooth and the gingiva, followed by a band of red, inflamed gingiva along one or more teeth, with swelling of the interdental papillae and easy bleeding. Pain is usually absent.
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Gingivitis
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- The inflammation can be localized or generalized
- Typically it is diffuse or confined to the free gingival margins or the interdental papillae - Early signs are loss of stippling and bleeding on gentle probing - The gingiva are light red in color with increasing red color as it progresses - The margins on the gingiva may be blunted, receded or hyperplastic - A localized tumorlike proliferation can occur on gingiva |
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Acute Necrotizing Ulcerative Gingivitis
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• A form of gingivitis not due to dental hygiene. It is also called “Trench Mouth” or Vincent’s Infection”
• Caused by local infection with spirochetes and fusiform bacilli and appears during periods of emotional or physical stress. A common problem in immunocompromised patients. • Characteristic gram stain findings are seen here. |
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Acute Necrotizing Ulcerative Gingivitis: P/E and Tx
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• Clinical Findings are
– Generalized painful gingival inflammation and bleeding – Gingival necrosis with resultant halitosis – Systemic signs such as fever, lymphadenopathy • Treatment is with local anti-infective measures (PeriDex or Hydrogen Peroxide swish and spit) and oral antibiotics. • Severe cases should be referred for gingival curettage. |
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Leukoplakia
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• Leukoplakia is an adherent white patch of plaque in the mucosa. It may be benign, such as lichen planus or secondary syphilis. It can be premalignant, especially if it occurs on the floor of the mouth or ventrolateral tongue.
• Clinical presentation – white patch varies from flat, smooth and slightly translucent macular areas to thick, firm, rough-surfaced and fissured, raised plaques – Occurs on the buccal mucosa, floor of the mouth, labial commissures, lateral borders of the tongue and mandibular and maxillary alveolar ridges • More common in males • Leukoplakia and Erythroplakia are considered pre-malignant lesions in the mouth. • If the lesion is red, speckled red-white or enlarging – biopsy is mandated. |
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Erythroplakia
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• A chronic red oral mucosal patch usually not attributed to traumatic, vascular or inflammatory causes
• Predominantly a disease of older men • Clinical Appearance – ASYMPTOMATIC*** red macule or patch on a mucosal surface, floor of mouth, tongue and palate – multiple lesions may be present – typical oral lesion is less than 1.5 cm. well-demarcated from the surrounding pink mucosa – The surface is typically a smooth, soft, velvety texture and regular in coloration • Leukoplakia and Erythroplakia are considered pre-malignant lesions in the mouth. • If the lesion is red, speckled red-white or enlarging – biopsy is mandated. |
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Candidiasis
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• Oral candidiasis is also know as “Thrush”.
• It is called “Curdy, thick, cheesy” and is often painful. • The key difference is that these lesions can be rubbed off, leaving a red base. |
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Aphthous Minor
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• Located on the labial or buccal mucosa, soft palate and the floor of the mouth. Usually single, may be multiple.
• Clinical Features: – small (0.5 mm- 10mm), shallow, crateriform edges, whitish-yellow bases painful – 1-2 days of tenderness and healing in 5-6 days in non-aphthous patients 7-10 days of pain and tenderness and healing in 10-14 days in patients with a predisposition for aphthous ulcers |
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Aphthous Major
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• Clinical Features:
– lesions are large (5-20mm) usually only 1 or 2 at a time – Crateriform and deeper – often last up to 6 weeks severe pain occur after puberty • Prognosis: scaring often occurs and recurrent episodes may continue to develop for up to 20+ years |
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Aphthous Ulcer Tx
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• Recurrence is common, especially when stressed.
• Treatment is symptomatic relief of pain, reduction of inflammation and hygiene. Intralesional injection with triamcinolone is done for severe lesions. For extensive ulceration monitor food and fluid intake – eating may be painful. |
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Primary Herpetic Gingivostomatitis
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One single virus can not produce disease and in order to achieve a substantial number of viruses intracellular replication take place in a prodromal period which is estimated to last one week, during which the patient does not present any symptomatology.
• Like Herpes Labalis, these present with initial burning, (may be tingling, or lack of sensation) • The gingiva is characterized by marked erythema, especially of the interdental papillae • This is followed by typical small vesicles that rupture leaving superficial ulcers and form white, moist scabs. • Highly contagious • The absence of a red base distinguishes them from aphthous ulcers. There is increased body temperature, regional lymphadenopathy and incapacity to eat properly due to the painful lesions. The primary infection lasts up to two weeks and resolves itself without leaving scars or sequelae. These primary lesions are highly contagious. The saliva of infected patients contains large number of shed virons. |
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Recurrent Herpetic Gingivostomatitis
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• Also called Herpes Labalis – usually less severe than the primary infection
• Excitants such as: GI upsets, stress, menses, solar radiation, extreme cold or other infections, will reactivate the virus in around 40% of carriers. This reactivation induces migration from the ganglion to the peripheral epithelial cells where the virus replicate. This new viral load will produce recurrent lesions which are generally less severe than the primary ones. As well as the primary lesions, the recurrent ones are also highly contagious. • The recurrent lesions on the lips go through several clinical stages which are: burning sensation, erythema of the affected area, vesiculation, ulceration and crust formation • Eventually the ulcer becomes covered by a dark red-brown crust. Episodes last 10 to 14 days. Secondary lesions also heal without scar formation. • The oral recurrent lesions generally occur in the lip's vermilion, but lesions may also develop in the attached gingiva and/or hard palate. |
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Tonsillitis
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• Inflammation of the tonsils is termed tonsillitis – this does not automatically mean bacterial infection. Many cases of tonsillitis are viral. AIDs may present as recurrent acute tonsillitis. Abscesses in the tonsils occur, usually unilaterally
• Exudates are usually indicative of infection, but not as to type. • Clinical findings include – Dysphagia – Halitosis – Fever – Cervical lymphadenopathy |
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β Hemolytic Strep Tonsillitis
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• β Hemolytic Streptococcus tonsillitis has some distinguishing characteristics:
– fever over 38 °C – tender anterior cervical adenopathy – lack of a cough – a pharyngotonsillar exudate. – odynophagia • The sore throat may be severe. |
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Pharyngitis
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• Inflammation of the posterior pharynx is termed Pharyngitis.
• This can be the result of infection (i.e. “Strep Throat”). • It can be the result of irritants, such as “post-nasal drip” or cigarette smoke. |
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Laryngeal Disease
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• Common signs of disease of the larynx include
– Hoarseness - localizes to the vocal cords and is due to abnormal flow of air past the vocal cord - “rough, raspy” or “breathy” – Stridor - noisy breathing resulting from an obstruction. Inspiratory stridor occurs from obstruction of the trachea or larynx. Expiratory stridor results from bronchial obstruction. – Dysphonia –are changes in the vocal quality, such as lowered pitch, loss of volume or lack of sound |
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Causes of Laryngitis
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• Laryngitis can be caused by any process which causes inflammation to the vocal cords. Common causes of acute laryngitis are:
– upper respiratory infections – vocal abuse (screaming, periods of high-pitched singing or speaking) – Tobacco smoke, perfumes – gastroesophageal reflux • The key symptom is hoarseness. |
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P/E of Laryngitis
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• The key symptom is hoarseness.
• Physical findings – hoarseness, stridor is rare – Erythema and swelling of the cords – “sore throat” which is located at the larynx – Signs of viral illness |
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Chronic Laryngitis
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• Continued vocal use or exposure to irritants such as smoke lead to ulceration and permanent damage.
• This appears as generalized swelling of the vocal cords. |
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Vocal Cord Nodules
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• Vocal cord nodules occur as a result of excessive laryngeal use. They are common in “personalities who vocalize aggressively.”
• The repetitive striking of the cords under strain produces paired masses at the area of greatest stress. For higher pitches (such as singing and screaming) this is at the junction of the anterior and middle thirds of the vocal cords. • Physical findings – hoarseness, often described as “breathy, husky, with a low pitch quality” – No sore throat or signs of viral infections – Visible paired nodules at the junction of the anterior and middle thirds of the vocal cords. |
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Tx/Prognosis of Vocal Cord Nodules
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• Treatment is vocal retraining, rest. Surgical removal of the nodules is indicated if poor response to conservative measures, but it will not restore the voice completely.
• Hemorrhagic nodules are a sign of severe injury and may not be paired lesions. Much of this is due to the mechanism of the vocal trauma. |
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Laryngeal Cancer
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• The most common form of laryngeal cancer is squamous cell carcinoma. Benign tumors are rare, and it should be considered malignant until biopsied as benign.
• Smokers are at the greatest risk. • Clinical Findings are dependent on the stage of the disease. – Early cancer presents with prolonged hoarseness, often with odynophagia. – Later disease presents with dysphonia, dysphagia and weight loss, referred otalgia, hemoptysis, and metastatic lymphadenopathy. |
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Romberg Testing
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Stand w/feet together and close both eyes - pt may lose their balance.
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Dix-Hallpike Testing
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(quickly lowering the pt to the supine position w/the head extending over the edge and placed 0 degrees lower than the body, turned either to the L or R)
Will elicit a delayed onset (10 sec) fatiguable nystagmus in cases of benign positional vertigo. Nonfatiguable nystagmus in central etiology. |
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Lab tests for Vertigo
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w/persistent vertigo, or CNS is suspected:
ENG Audiologic eval caloric stimulation ENG VNG MRI |
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ENG
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objective recording of the nystagmus induced by the head nad body movements, gaze and caloric stimulation
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Meniere Syndrome
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2 causes: syphilis and head trauma
distension of endolymphatic compartment of inner ear lasts 20 mins- several hours fluctuating low frequency sensorineural hearing loss, tinnitus, and unilateral aural pressure Thermally induced nystagmus Tx: low salt diet, diuretics, intratympanic corticosteroid injections, endolymphatic sac decompression, gentamicin, labyrinthectomy |
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Labyrinthitis
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acute onset
continuous, severe vertigo lasting several days to a week hearing loss and tinnitus Cause unknown Tx: abx if febrile or sxs of bacterial infection Vestibular suppressants during acute phase Discontinue ASAP to avoid long-term dysequilibrium |
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BPPV
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recurrent spells of vertigo
several minutes per spell changes in head position occur in clusters that persists for days acute vertigo subsides after 10-60 seconds but remain imbalanced for several hours habituation - constant repetition of the positional change MRI - recurrent cases Physical Therapy Tx |
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Vestibular Neuronitis
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paroxysmal, single attack of vertigo without accompanying impairment of auditory fx
will persist for several days-week Nystagmus Absent responses to caloric stimulation Cause unclear, may be viral Tx: Diazepam, vestibular therapy |
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Traumatic Vertigo
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Labyrinthine Concussion
Sxs may diminish within several days, but may linger for a month or more basilar skull faractures severe vertigo several days to a week, and deafness in involved ear Chronic posttraumatic - cupulolithiasis - detached statoconia settle o nthe ampulla - excessive degree of cupular defection --> presents as episodic positioning vertigo tx: diazepam, vestibular therapy |
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perilymphatic fistula
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leakage of perilympathic fluid from the inner ear into the tympanic cavity via the round/oval window
--> cause of vertgio and sensory hearing loss physical injury, extreme barotrauma, valsalva tx: tissue graft |
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cervical vertigo
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triggered by neck movements after neck injury, particularly hyperextension
degenerative cervical spine disease is associated. triggered by assuming a SPECIFIC head position |
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Migrainous Vertgio
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temporally located
up to seeral hours occurs in the absence of headache at times NO associated hearing loss or tinnitus (distinguishes it from Meniere's) head pressure, visual and motion sensitivity, audio/photosensitivity |
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Nonproliferative Retinopathy
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manifests as dilation of veins, microaneurysms, retinal hemorrhages retinal edema and hard exudates.
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Backgound Retinopathy
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abnormalities are mild no vision changes.
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Maculopathy
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manifests as edema, exudates, or ischemia involving the macula.
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Proliferative Retinopathy
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manifests as edema, exudates, or ischemia involving the macula.
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Prophylaxis of Swimmer's Ear
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2% acetic acid
Can be slightly irritating |
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Common Anti-Infective Topical Agents
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Acetic Acid Soln - drying agent: sensitizer/ possibly ototoxic
Neomycin - Sensitizer, contact derm, ototoxic Polymixin B - No activity against Staphylococcus and Gram + Aminoglycosides - potential ototoxicity, expensive Quinolone - highly effective, expensive, NOT ototoxic. |
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Necrotizing Otitis Externa
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mortality rate is high
otalgia and headache are disproportionately more sever than the clincial signs Granulation tissue may be apparent at the bony cartilaginous junction. Confirm Dx w/CT or MRI ESR - monitor therapeutic response Tx of choice - flouroquinolones - antipseudomonal Surgical debridement - otolaryngologist |
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Pericoronitis
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Acute, localized infection caused by food particles and microbes trapped beneath the gingival flaps of a partially erupted tooth or impacted wisdom tooth.
Localized pain and limitation of movement on opening the jaw, facial swelling. Halitosis Localized Lymphadenopathy Tx: removal of food particles, good oral hygiene, hot salt water/chlorhexidine rinses, Severe --> Abx then refer |
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Major Sxs of Rhinosinusitis
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– Facial pain/pressure/fullness*
– Nasal obstruction/blockage – Nasal or postnasal discharge/purulence (by history or physical examination) – Hyposmia/anosmia – Fever (in acute rhinosinusitis only)§ |
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Minor Sxs of Rhinosinusitis
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– Headaches
– Fever (other than acute rhinosinusitis) – Halitosis – Fatigue – Dental pain – Cough – Ear pain/pressure/fullness |
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Pathogens in Bacterial Conjunctivitis
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Haemophilus Influenzae, Streptococcus pneumoniae, Gonorrhea
Do a gram |
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