HEENT Exam 1 Cards Flashcards
Part of the eye that controls the lens shape
Ciliary body
Substance in the back of the eye
Vitreous humor
Substance in the front of the eye
Aqueous humor
Pigmented part of the retina located in the very center of the eye
Macula
Area of greatest visual acuity in the eye
Fovea
The lens in our eye is a _____________ lens
Convex
What does the lens do when we want to see something that is near?
The ciliary muscles contract, suspensory ligaments slacken, making the lens thicker and the focal length shorter
What does the lens do when we want to see something far away?
Ciliary muscles relax, suspensory ligaments tighten, making the lens thinner and the focal length longer
2 things that can cause myopia
Too curved cornea, too long eyeball
Correction for myopia
Use a concave lens to diverge light rays and make objects look smaller
2 things that can cause hyperopia
Not enough curvature of the cornea, Eye too short
Correction for hyperopia
Use a convex lens to converge light rays and make objects look larger
An irregular shape of the cornea or lens leading to multiple focal points
Astigmatism
Presbyopia
Age related farsightedness
Cornea becomes cone shaped causing blurred vision
Keratoconus
Purpose of aqueous humor
Maintains intraocular pressure
Where does aqueous humor come from and where does it go
Produced in ciliary body and absorbed by trabecular meshwork
Purpose of vitreous humor
Maintain shape of eyeball and hold retina in place
Result of a lesion before the optic chiasm
Blindness in one eye
Result of a lesion at the optic chiasm
Bitemporal hemianopsia
Result of lesion in the optic tract (after optic chiasm)
Homonymous hemianopsia (left or right visual field loss in both eyes) on the opposite side as the lesion
Parasympathetic pupillary effect
Constriction
Sympathetic pupillary effect
Dilation
One pupil being naturally larger that the other
Anisocoria
Cotton wool spots
Yellow-white lesions that look like clouds on the retinal surface - Caused by micro ischemia and nerve infarction
Physiologic anisocoria
The pupillary difference is the same in the light and dark
MCC of cotton wool spots (2)
Diabetic retinopathy, hypertensive retinopathy
Anisocoria that is more pronounced in the dark
The small pupil is abnormal
Anisocoria that is more pronounced in the light
Large pupil is abnormal
Marcus Gunn Pupil
Pupil only reacts to consensual light, not direct - indicates an optic nerve lesion
Horner syndrome triad
Ptosis, Anhydrosis, Miosis,
PAM Horner
Horner syndrome triad
Ptosis, Anhydrosis, Miosis,
PAM Horner
Cause of horner syndrome
Loss of sympathetic innervation to the eye
Adie’s pupil
Sluggish direct and consensual reaction to light couples with diminished DTRs
Accommodation reflex
The pupils get smaller looking at closer objects and larger looking at far away objects
Agyll Robertson pupil
Pupils have an accommodation reflex but NO pupillary reflex (to light)
ARP - Accommodation Reflex Present
Pupillary reflex Absent
Patient complains of a “curtain coming down over 1 eye”
Retinal detachment
Swelling of the optic nerve
Papilledema
4 signs of papilledema
Disc elevation
Venous distension and tortuosity
Obscured disk margin
Absent venous pulsations
Blood and thunder fundus
Widespread retinal hemorrhages with venous dilation and tortuosity
Cause of a cherry red spot on the fovea
Central retinal artery occlusion
Cause of blood and thunder fundus
Retinal vein occlusion
Cause of retinal boxcar segmentation
Retinal artery occlusion
A-V Nicking
A small artery crosses and small vein and compresses it - seen in hypertensive retinopathy and atherosclerosis
Silver and Copper wiring
Seen in hypertensive retinopathy and atherosclerosis - Silver is more serious
Hard exudates
Yellow/white spots with distinct borders - caused by a breakdown of blood retina border and due to diabetes
Flame hemmorhages
Caused by necrotic blood vessels bleeding into the retina caused by diabetes or hypertension
Dot-Blot hemmorhages
Caused by micro aneurism rupture in the deeper retinal layers
Optic cupping
Blood flow to the optic nerve is diminished because of damage to the nerve, the optic cup grows larger
2 conditions in which we might see fundoscopic neovascularization
DM retinopathy and macular degeneration
Retinal Drusen
Yellow deposits under the retina - dead retinal epithelial cells caused by age-related macular degeneration
What does a slit lamp look at?
The anterior portion of the eye
Use of fluorescence staining
Helps us highlight corneal abrasions and foreign bodies
Presentation of bacterial conjunctivitis (3 things)
Purulent discharge, conjunctival injection, mild discomfort
3 MCCs of Bactierial conjunctivitis
S. aureus - Adults
Strep Pneumo - Children (followed by other OM causes)
Pseudomonas - Contact wearers
Treatment for mild bacterial conjunctivitis
Polymixin B/Trimethoprim (Polytrim)
3 treatments for severe bacterial conjunctivitis or pseudomonal conjunctivitis
Moxifloxacin (vigamox), Ofloxacin opthalmic (Ocuflox) Ciprofloxacin
Treatment for gonococcal conjunctivitis
Rocephin (ceftriaxone) with Erythromycin or bacitracin
Treatment for chlamydial conjunctivitis
1 dose azithromycin PO
Presentation of gonococcal conjunctivitis
Perfuse purulent exudate
Presentation of trachoma
Chlamydial conjunctivitis - Yellow follicle spots on inner eyelid
Clinical presentation of viral conjunctivitis
Usually bilateral, watery discharge, foreign body sensation, preauricular lymphadenopathy
MCC of viral conjunctivitis
Adenovirus from eye clinics or swimming pools
Treatment for viral conjunctivitis
Supportive care
Presentation of allergic conjunctivitis
May be seasonal. stringy discharge with cobblestone papillae on inner eyelid (big bumps), pruritis
Chemosis
Swelling of the conjunctiva - seen in allergic conjunctivitis
Treatment for allergic conjunctivitis
2 drugs
Topical antihistamines such as Ketotifen or Olopatadine
Uvea
Structures of the eye beneath the sclera
The iris
The ciliary body
The choroid
MC type of uveitis
Acute, nongranulomatous, anterior uveitis
Posterior Uvea
Choroid
Anterior Uvea
Iris and Ciliary body
1 thing NOT to do with opthalmic herpes
DONT give steroids
Non-granulomatous uveitis
Inflammation with predominantly polymorphonuclear cells rather than giant cells - usually presents acutely
Granulomatous uveitis
Inflammation where macrophages are the predominant cell - usually indolent with blurred vision
Causes of non-granulomatous anterior uveitis
Often linked to autoimmune condition such as UC or arthritis
Causes of anterior granulomatous uveitis
Syphillis, TB, Toxoplasmosis, Herpes
Fundus of ocular syphillis
Salt and pepper fundus
Diagnosis and clinical presentation of anterior uveitis
Use a slit lamp - Hypopyon or collection of pus in the cornea, Keratitic deposits seen - larger with granulomatous inflammation
General presentation of uveitic eyes
Red and painful with redness around the cornea
Old v New Posterior Uveitic lesions
New have less defined borders and are yellow, old have more definite margins
Clinical presentation of posterior uveitis
Gradual vision loss with floaters and often bilateral
Cause of posterior uveitis
Idiopathic, autoimmune, pars plantis, or agents that cause anterior granulomatous uveitis
Treatment for anterior uveitis
Topical corticosteroid with pupil dilation - treat agent if identified
Treatment for posterior uveitis
Corticosteroid therapy given more invasively - treat agent if identified
Keratitis
Inflammation of the cornea
Causes of bacterial keratitis
Most common in contact lenses worn overnight - most commonly pseudomonas, moraxella, staph or strep
Presentation of bacterial keratitis
Hazy cornea with ulcer, hypopyon, difficulty keeping eye open
Treatment for bacterial keratitis
Emergent referral and fluoroquinolone drops
Cause of viral keratitis
HSV
Key sign of herpes simplex keratitis
Dendritic (branching) lesion of the cornea
Treatment for viral keratitis
Urgent referral with topical or oral acyclovir or valacyclovir
Hutchinsons sign
Involvement of the tip of the nose or lid margins in HSV predicts eye involvement
Fungal kerititis
Candida, aspergillis, fusarium
Often from injury in an agricultural setting or with contacts and the immune compromised
Presentation of fungal keratitis
Feathery corneal infiltrate with satellite lesions and multiple stromal abscesses
Treatment for fungal keratitis
Natamycin, Amphotericin, Voriconazole
Acanthamoeba keratitis
Severe pain with ring shaped corneal infiltrate
Treatment for acanthamoeba keratitis
Needs long term treatment with topical biguamide (Polyhexamethylene or chlorahexadine)
Why does acanthamoeba keratitis need long term treatment
It can encyst with the corneal stroma
Subconjunctival hemmorhage
Well defined area of hemorrhage under the conjunctiva - usually self limiting and caused by HTN or trauma
How long does a subconjunctival hemorrhage usually last?
Resorbs within 2 weeks
Dacryoadenitis
Inflammation or infection of the lacrimal gland
Dacryocystitis
Infection of the lacrimal sac/duct
Clinical Presentation of dacryoadenitis
Unilateral rapid onset swelling in the supratemporal region
Dacryocystitis clinical presentation
epiphora(overflow of tears), rapid unilateral onset, and inframedial swelling
2 potential causes of dacryoadenitis
Mumps, and autoimmune inflammatory
MC organisms for acute and chronic dacryocystitis
Acute - Staph aureus
Chronic - Staph epidermidis
Treatment for dacryoadenitis
Treat underlying cause and use systemic antibiotics if bacterial
Treatment for acute dacryocystitis
Lacrimal sac massage
Topical Tobramycin and Moxifloxacin if discharge only
Augmentin systemic if other s/s of infection are present
Treatment for chronic dacryocystitis
Can be kept latent with antibiotics - Surgery to relieve obstruction is definitive treatment
Anterior blepharitis
Involves the eyelids skin and eyelashes, may be associated with ulcers or seborrhea of the scalp, brows, and ears
Posterior blepharitis
Inflammation of meibomian glands at inner portion of the eyelid can be cause by infection, dysfunction, or skin conditions
Meibomian glands
Located in eyelids - secrete oily substance used to lubricate eyeball and prevent tear evaporation
Clinical presentation of anterior blepharitis
Red rimmed eyes with scales seen on eyelashes
Clinical presentation of posterior blepharitis
Greasy or frothy tears with rolled in lid margin with telangiectasia and hyperemesis - Waxy, congealed meibomian glands
Treatment for anterior blepharitis
Remove scales with a hot washcloth use bacitracin or erythromycin for an antistaph ointment
Treatment for mild poterior blepharitis
Meibomian gland expresseion and lid massage
Treatment for conjunctival and corneal inflammation
Tetracycline long term, Prednisolone short term
Hordeolum
Localized red, tender area of the eyelid caused by a staphylococcal abcess
External Hordeolum
Usually smaller and on the margin of the eyelid
Internal hordeolum
Often a Meibomian gland abscess pointing into the conjunctival surface of the lid, can cause lid cellulitis
Treatment for Hordeolum
May need to change any cosmetics, warm compress, and I&D if no progress
Antibiotics NOT indicated
I&D
Incision and Drainage
Chalazion
Hard, Non-tender swelling with redness of adjacent conjunctiva
Chalazion treatment
Often resolves on own with warm compress etc, may need to refer refractory for incision or steroids
Cause of Orbital cellulitis
Caused my OM pathogens and S. Aureus - often connected with a sinus infection (cause the sinuses are nearby)
Orbital cellulitis or Preseptal cellulitis - which one is an emergency
Orbital - think - it’s closer to the brain!!
Orbital cellulitis pathology
Infection of the fat and soft tissue that holds the eye in its socket
Clinical presentation of orbital cellulitis
Fever, Painful swelling, Proptosis, Ptosis, Limited movement
One thing you should do to assess for severity of preorbital cellulitis
Check pupillary reaction to light to assess ocular nerve involvement
Treatment for orbital cellulitis
Immediate IV Vanc and a later gen cephalosporin
May add metronidazole or Clinda for anaerobes
Orbital cellulitis treatment after symptoms are under control
Switch to oral Bactrim, Augmentin, or FQone for 2-3 weeks
Preseptal/Periorbital cellulitis
Bacterial infection superficial to the orbital septum - Usually secondary to another eyelid infection such as conjunctivitis
2 common agents of preseptal cellulitis
S. Aureus and S. Pneumo
Clinical presentation of preseptal/periorbital cellulitis
NO fever, NO proptosis, Eyelid swelling, Erythema, No vision impairment
Treatment for Preseptal/Periorbital cellulitis
PO - Augmentin or Omnicef with Bactrim or Clinda
Ciliary flush
Definitive for corneal pathology - red/violet streaks spreading out from the edges of the cornea
4 clinical presentations of a corneal ulcer
Ciliary flush, Irregular pupil, dendritic ulcer, mucopurulent discharge
Characteristics of Psudomonas Corneal ulcer
Gray/Yellow infiltrate at a break in the cornea, Contact lens wearing hx,
Treatment for corneal ulcer with pseudomonas
FQone or Tobra/Gentamycin
Characteristics of group A strep corneal ulcer
May include a hypopyon, Edematous corneal stroma, not as specific
Characteristic of a staph infected corneal ulcer
Ulcer bed feels firm when scraped
3 drugs to treat staph infected corneal ulcers
Cefazolin, Moxifloxacin, Gatifloxacin
Characteristics of Fungal corneal ulcers
Gray, irregular edged infiltrate with satellite lesions -slow growing
Treatment for fungal corneal ulcer
Amphotericin B, Voriconazole, Posaconazole
Characteristics of viral corneal ulcers
Hx of fever or blisters, Dendritic ulcer, photophobia
Treatment for viral corneal ulcer
Acyclovir PO or Idoxuridine/Gancyclovire Topical
Corneal ulcer placement and size
Can be a small dot at the EDGE of the cornea
Entropion
Inward turning of the eyelid - often in elderly patients
Treatment for entropion
Surgery if eyelashes rub against the cornea
Botulinum toxin injections may be used
Ectropion
Outward turning of the lower eyelid - associated with tear leakage
Blepharospasm and treatment
Abnormal eyelid muscle contraction (eye twitching) - treated by alleviating stress and possibly botox
3 Neurological diseases that can cause Ptosis
Horner’s syndrome
3rd nerve palsy
Myasthenia gravis
Mild, Moderate, and Severe Ptosis
2, 3, and 4 mm drop
Treatment for Ptosis
Oxymetazoline eye drops (alpha adrenergic stimulators)
Surgery usually reserved for those with an obscured visual field
Pterygium
Encroachment of the conjunctiva onto the nasal side of the cornea - often due to prolonged exposure to wind, sand, dust, etc.
Treatment for pterygium
Artificial tears, NSAIDS and steroid can be used, surgery in extreme cases
Pinguecula
Yellow/orange raised conjunctival lesion that DOES NOT cross into the cornea - exposure or dust caused
Clinical findings of dry eye
Itching, Absence of tear meniscus on lower lid, Excess mucous production, blurred vision
Tests to detect dry eye
Fluorescence staining to find dry spots
Rose Bengal and Lissamine Green for epithelial defects
Schirmer’s tear production test
Tear breakup time
3 complications of dry eye
Corneal scarring and vascularization, Corneal ulceration, Impaired vision
First line treatment for dry eye
Artificial tears 3-4 times a day and ointment, Plugs, Cyclosporine for immune inhibition
Cataract
Lens opacity usually resulting from age, can also be related to smoking and alcohol use
Clinical presentation of cataracts
Progressive blurring of vision, monocular double vision, cloudy lens, Glare with bright lights
Cataract treatment
Refer to ophthalmology for surgery
Part of the eye effected by cataracts
Lens not the cornea
Clinical presentation of macular degenerations
Loss of central vision first that is usually bilateral
Atrophic macular degeneration (dry)
Atrophy and degeneration of the retina and retinal pigment with retinal drusen
Retinal drusen
Hard, discrete, yellow retinal deposits
Neovascular (wet) macular degeneration
Excess growth of vasculature under the retina leads to fluid accumulateion, hemorrhage, and fibrosis - more rapid vision loss
Narrow angle glaucoma
Acute glaucoma - a medical emergency
Open angle glaucoma
Chronic glaucoma - less emergent
Glaucoma
Neuropathy of the optic nerve with or without intraocular pressure, also with cupping of the optic disk
Creation and drainage of aqueous humor
Made by ciliary body, drained by trabecular meshwork
Etiology of acute angle closure glaucoma
Lens is pushed forward leading to closure of the angle between the cornea and the iris and impaired drainage of aqueous humor
3 risk factors for narrow angle glaucoma
Asian descent
Female, 40-50 years old
Farsightedness
Primary angle closure glaucoma
Lens located too far forward anatomically, leading to closed angle
Secondary angle closure glaucoma
Conditions that push the ciliary body forward or pull on the iris creating a closed angle
Clinical presentation of acute angle closure glaucoma
Halo’s around lights, with onset more common when it is dark, Red steamy cornea with sluggish dilated pupils and IOP over 50mmg
Gold standard diagnostic for narrow angle glaucoma
Gonioscopy is the gold standard for diagnosis - views the irideocorneal angle
Initial treatment for angle closure glaucoma
Place the patient supine and refer to opthalmology urgently
Pharmacology for Narrow angle glaucoma
First line: Acetazolamide (CAI) PO or IV
Pilocarpine drops administered later
Recheck IOP every 30-60 minutes
3 Non-first line topicals for acute angle closure glaucoma
Latanoprost, Timolol, Apraclonidine
Definitive treatment for angle closure glaucoma
Laser peripheral iridotomy, creates a hole in the peripheral iris to releive the pupillary block
5 things to give someone with Angle closure glaucoma while waiting for the ambulance
Lie on back
Acetazolamide
Pilocarpine
Anagesia
Antiemetic
Clinical presentation of open angle glaucoma
Gradual peripheral vision loss with high IOP (over 40mmHg)
Screening recommendations for glaucoma
every 5-10 years for under 40
to ever 1-2 years over 65
Refer any pt with cupping!
IOP at which to refer
30-40 is Urgent, anything higher is emergent
3 types of therapy for open angle glaucoma
Pharm - acetazolamide
Laser therapy
Surgery
4 drugs for open angle glaucoma
Topical prostaglandins - Lataprost
Topical beta blockers - Timolol
Topical Alpha 2 agonists - Apraclonidine
(reduces aqueous humor production by dilating eyes)
Cholinergic agonists - Pilocarpine
Surgical therapy for any glaucoma
Laser periperal iridotomy - put a hole in the peripheral iris for drainage
Cause of a corneal abrasion
Often from trauma - fingernail, contact lens, paper, etc.
Clinical presentation of a corneal abraision
Tearing, Foreign body sensation, may have ciliary flush or change in visual acuity, photophobia
Complications for a corneal abrasion
Bacterial keratitis leading to ulcers and hypopyon
Diagnostics for a corneal abraision
Evert eyelid to rule out foreign body, check visual acuity, stain to find abrasion
3 treatments for corneal abrasions
Antibiotics - bactrim-polymixin
NSAID eye drop
Cycloplegic to stop ciliary spasms and pain
Are alkali or acidic burns worse?
Alkali
4 factors effecting the severity of a chemical eye injury
Toxicity
Length of exposure
Depth of penetration
Area of involvement
Treatment for chemical eye injury
Irrigate with pH monitoring
May use a cycloplegic
Presentation of welder’s flash photophobia
6-12 hours after exposure to UV radiation, Staining reveals corneal speckles
Treatment for welder’s flash potophobia
Binocular patching with Cyclopentolate (cycloplegic drug)
What MUST you do when you suspect a foreign body?
Always evert the eyelid
Rust ring
formed by an iron containing foreign body - remove if not resolved in 2-3 days
Hyphema
Injury causing a hemorrhage into the anterior chamber of the eye causing pain, photophobia and blurred vision
Non-pharm management for a hyphema
Prevent further bleeding, keep patient supine with head elevated 45 degrees and a hard eye shield
Pharm management of hyphema
NO NSAIDs or Aspirin
Pain meds and antiemetics
Bone at the top of the orbit
Frontal bone
2 Bones on the outside edge of the orbit
Zygomatic bone and sphenoid bone
2 Bones on the bottom of the orbit
Maxilla and zygomatic bone
2 Bones on the inside edge of the orbit
Maxilla and ethmoid bone
Bones in back of the orbit (4)
Sphenoid, Palatine, Ethmoid, Maxilla
Action of the inferior oblique
Moves the eye upwards and inwards
Action of superior oblique
Moves the eye downwards and inwards
Most common bone injured in an orbital blowout fracture
Maxilla
Clinical presetation of an orbital blowout fracture
Pain and ecchymosis around the eye
Decreased movement - especially looking upwards due to trapped inferior rectus
Localized facial anesthesia (trigeminal nerve)
Enopthalmos (sunken in eyes - indicates inferior displacement of orbital contents through the orbital floor)
3 Evaluation steps for an orbital blowout
Obtain mechanism of injury
Examine eye contents and check visual acuity
CT of the orbit
4 things to look for on an orbital CT from an orbital blowout fracture
Emphysema (air in the orbit) with crepitus
Fracture of floor or medial wall of orbit
Soft tissue extending into maxillary sinus (could become ischemic)
Opacification of maxillary sinus from blood or edema
3 things we do not want someone with an orbital blowout fracture doing
Throwing up
Sneezing
Blowing nose
(or anything like unto it)
2 pharm treatments for orbital blowout
Systemic antibiotics and steroids for swelling
3 symptoms that are indicative of a ruptured globe in penetrating trauma
Teardrop shaped pupil, eyeball appears deflated, afferent pupillary defect
Afferent pupillary defect
Response to light is more sluggish in one eye
3 treatment points for penetrating trauma or ruptured globe
Protective eye shield
Elevate head 45 degrees
Vancomycin and Ceftazidime or FQone
Amaurosis fujax
Transient monocular blindness, symptom not a diagnosis
3 things that might cause amaurosis fujax
Migraine, Retinal emboli, giant cell arteritis
Clinical presentation of amaurosis fujax
Described as a curtain coming down over the visual field with a few minutes of complete vision loss
Monocular ischemia pattern and mechanism
Monocular rapid onset due to a retinal embolism
Giant cell arteritis vision loss pattern and mechanism
Usually monocular w/ headache, due to optic nerve ischemia
Papilledema vision loss pattern and mechanism
Monocular graying or blurring with diplopia from elevated intercranial pressure
Idiopathic retinal vasospasm
Accompanied by a headache and monocular vision loss
Migraine vision loss
Binocular due to cortical depression and possible retinal vasospasm
Vision loss of vertebrobasilar ischemia
Homonymous hemianopia caused by an embolism
Vision loss of an ictal seizure
Binocular and lateralized due to epileptic discharge
Postictal vision loss
lasts 20+ minutes, binocular visual field loss due to cortical inhibition
Clinical presentation of central retinal artery occlusion
Sudden profound painless monocular loss of vision with a cherry red spot and afferent pupillary defect and boxcar segmentation
Management for central retinal artery occlusion
Lay patient flat, give acetazolamide and vasodilators and ocular massage with O2. Thrombolysis given CAREFULLY
Treatment for giant cell arteritis
High dose corticosteroids
~Pexy
Root for fixation of something
Clinical presentation of Central retinal vein occlusion
Painless monocular vision loss often first noticed upon awakening with a blood and thunder fundus - starts out blurry
Treatment for retinal vein occlusion
Anti VEGF first line
Intravitreal corticosteroids second line
Laser photocoagulation
Laser photocoagulation
Uses lasers to seal leaky vessels and prevent VEGF formation
2 common risk factors for retinal detachment
Nearsighted (longer eyeball)
Cataract extraction
Clinical findings of a retinal detachment
Monocular decreased vision, Eye pain, Central vision is last to go
Flashing lights and floaters
Treatment of retinal detachment
Can often be cured surgically, prognosis depends upon length of time and extent of detachment
Optic neuritis
Strongly associated with MS - inflammation of the optic nerve can also be HSV or autoimmune
Clinical presentation of optic neuritis
Pain behind the eye with loss of color vision/perception andcentral field loss
Unilateral w/ pupillary defect
Fundoscopic findings for optic neuritis
Swollen disc with diffuse borders and a few homrrhages
Treatment for Optic neuritis
IV methylprednisone for 3 days and then oral prednisone
May need more prolonged therapy for chronic/non-acute cases
Optic disk swelling due to intercranial pressure
Papilledema
Clinical presentation of papilledema
Bilateral with blurred margins and flame hemorrhages - may have NO visual symptoms
Treatment for Papilledema
DONT perform a lumbar puncture!!
MRI for diagnostics and treat underlying cause
Why no lumbar puncture for papilledema
Risk of herniation
Ischemic optic neuropathy
Inadequate perfusion of ciliary arteries leading to infarction of the optic disk
Clinical presentation of Ischemic optic neuropathy
PAINLESS monocular vision loss usually affecting the superior and inferior visual field
Treated with HIGH dose corticosteroids and referral
Fundoscopic exam for ischemic optic neuropathy
Optic disk swelling, central cotton with flame shaped hemorrhage (nonarteric) Large central palor/cotton wool spot (Arteric)
6 eye complaints that can be treated in primary care w/o urgent follow up
Hordeolum
Chalazion
Blepharitis
Subconjuntival Hemorrhage
Conjunctivitis
Dry eye syndrome
3 eye complaints that can be treated in primary care BUT need urgent follow up
Corneal Abrasion
Corneal foreign body
Contact lens over wear
3 ophthalmic signs of hypertension
Cotton wool spots, Open angle glaucoma, Copper and silver wiring
3 signs of diabetic retinopathy
Hard exudates, Neovascularization, Ischemic optic neuropathy
3 ophthalmic signs of thyroid disease
Protruding eyes, Color dullness, difficulty moving eyes
2 ophthalmic signs of hyperlipidemia
Macular degeneration, Blood and thunder fundus from venous occlusion
2 ophthalmic signs of sarcoidosis
Granulomatous anterior uveitis
Optic neuritis
Ophthalmic signs of myasthenia gravis
Diplopia and ptosis due to muscle weakness
Ocular signs of HIV/AIDS (4)
Patchy salmon appearance from conjunctival lymphoma
Opportunistic fungal infections
Cytomegalovirus with yellow around vascular distribution
Something w/ blue sclera in newborns
4 things that need to be determined in a hearing loss evaluation
Nature of impairment
Severity of impairment
Anatomy of impairment
Etiology of impairment
3 times that we screen hearing
Within 1 month of birth
Kindergarten
Pre-employment/Military service
2 screening tests for infants
Otoacoustic emissions (bounces sound waves off of the tympanic membrane)
Auditory brainstem responses
Otoacoustic emissions
Tests the ears response to sound - can tell if sound is responded to or not - should be an echo if hearing is intact
Auditory brainstem response
Uses electrodes to detect whether or not the brain is receiving sound information in a clear manner
What do you do is a baby does not pass initial hearing screenings?
Obtain a full hearing evaluation before 3 months of age
Full infant hearing eval
Repeat ABR
See how baby reacts to sounds
See how ears respond to sound
5 signs of hearing loss in a baby
Not being startled by loud sounds
Not turning towards a sound after 6 months of age
Not saying single words at 1 year
Turns head it they see you but not if you call out their name
Seems to hear some sounds but not others
When should children at risk for hearing loss be retested
By 2.5 years
Visual reinforcement audiometry
6 months to 2 years - Child is trained to look towards the source of a sound
Conditioned play audiometry
2-5 years old - child is trained to perform and activity when a sound is heard
3 hearing tests for children and adults
Tuning fork, Whisper testing, Audiometric screening (with headphones)
Pure tone audiogram
Determines the faintest a tones a person can hear at pitches from low to high
X axis of audiogram
Frequency in Hertz
Y axis of audiogram
Hearing threshold level in decibels
6 hearing loss categories with dB number
Slight, Mild, Moderate, Moderately severe, Severe, Profound - start at 10 dB for slight and add 15 each time
Symbol for left ear
X
Symbol for right ear
O
2 symbols used for bone conduction on the right
[ or <
2 symbols used for bone conduction on the left
] or >
Tympanogram
Measures the motility of the tympanic membrane
Types A B and C
5 things that can be diagnosed with a tympanogram
Otitis Media, Fluid in middle ear space, Eustachian tube dysfunction, Indirectly diagnose hearing loss, Tympanic membrane perforation
How does a tympanogram work
It introduces pressure into the ear canal while emitting sound waves to see how the TM is responding - measures pressure and flexibility
Type A tympanogram
Normal finding - central peak
Type B tympanogram
Gentle decline - No compliance
Type C tympanogram
Early peak with rapid decline - Eustachian tube dysfunction (negative pressure in the ear space)
3 Rinne test results and what they mean
Air>Bone - No loss or sensoneurial
Bone>Air - Conductive hearing loss
3 Weber test results and what they mean
Hearing in both ears -Normal
Hearing in good ear - Sensorineural
Hearing in Affected ear - Conductive
Conductive hearing loss
Sound is not conducted efficiently through the outer or middle ear leading to better bone conductivity than air conductivity
Sensorineural hearing loss
Occurs because of damage to the inner ear or auditory nerve - may hear unclear or only low pitched sound
Correction of sensorineural hearing loss
Permanent loss usually
Infectious causes of hearing loss
TORCH
Toxoplasmosis
Other agents (Syphillis, Parvovirus, Listeria)
Rubella
Cytomegalovirus
Herpes Simplex Virus
Ototoxic drugs - what do they cause?
Cause BILATERAL tinnitus or hearing loss
List of ototoxic drugs (7)
Medications neglected can loss auditory vestibular system
M - Malaria and Macrolide
N - Nsaid
C - Cisplatin
L - Loop diuretic
A - Aminoglycoside
V - Vancomycin and Vincristine
S - Salcilic acid (ASA)
Otosclerosis
Stapes affixes to the oval window causing conductive hearing loss - autosomal dominant
Clinical presentation of otosclerosis
Slow uni or bilateral hearing loss with possible improved hearing of background noise
Treatment for otosclerosis
surgical with stapedectomy
Otoscopy findings of otosclerosis
Flamingo flush over the tympanic membrane or normal tympanic membrane
Otoscopy finding for tympanosclerosis
White chalky patches on tympanic membrane
Presbyacusis
Sensorineural - Bilateral age related hearing loss that is most remarkable at high frequencies - most severe in males
Age-related change to the cochlea
Degeneration of outer and inner hair cells
Ossicular change related to age
Joint between bones calcify and become thinner
Treatment for presbyacusis
Hearing aids, cochlear implants if severe, OTC CoQ may help
2 clinical signs of presebyacusis
Increased wax production with decreased TM compliance
Acoustic neuroma
Benign tumor of schwann cells on nerve VIII causing UNILATERAL sensorineural hearing loss (rarely affects CN VII)
Clinical presentation of acoustic neuroma
Progressive unilateral hearing loss with tinnitus, dizziness, and balance problems
Diagnostic and treatment for acoustic neuroma
MRI to diagnose
Depending on severity, monitoring, radiation, or surgery
Noise induced hearing loss
Permanent hearing impairment cause by hair cell death that results from prolonged exposure to high levels of noise
Decibel level that causes noise induced hearing loss and frequencies usually lost
85+ decibels
2000-4000 hertz
Decibels of a vacuum cleaner
70
2 causes of hearing loss that may not need a referral
Cerumen impaction and OM
What patient needs an urgent referral for hearing problems
Idiopathic, sudden sensorineural hearing loss - can use corticosteroids
People who should have routine audiologic screenings
Prior exposure to injurious noise and over 65
Gold standard for auditory rehabilitation
Cochlear implant
Dizziness
Imprecise symptom that can describe many conditions
Vertigo
Sensation of movement when there is none - can be caused by spinning or by vestibular dysfunction
Lightheadedness
Feeling like one is about to loose consciousness
Disequlilibrium
Feeling off balance may be CNS lesion or vestibular
Peripheral vertigo
Vertigo that originates OUTSIDE of the CNS
Central Vertigo
Vertigo that originates INSIDE the CNS - can be mixed (ie. migraines)
General presentation of peripheral vertigo
Often sudden with hearing symptoms
General presentation of central vertigo
Often gradual with no hearing symptoms or bilateral ones
Nystagmus
Involuntary back and forth movement of the eyes - can be suppressed by
Eye movement indication of cerebellar pathology
Abnormal pursuit/saccades
Head impulse test
Patient looks forward and their head is turned to the side
Positive head impulse test
Patient’s eyes move WITH the head - they can’t keep their gaze on the examiner or take time returning their gaze to the examiner after returning of head to its position - PATHOLOGICAL
Dix-Hallpike test
Patient sits upright with head turned 45 degrees, patient is layed down so that their head is 30 degrees below horizontal
Positive Dix-Hallpike test
Nystagmus upon performance
What does the Dix-Hallpike test test for
Benign Paroxysmal Positional Vertigo
What does the head impulse test test for?
Vestibulo-occular reflex
Normal caloric testing result
Warm beats ipsilateral
Cold beats contralateral
Abnormal caloric testing result
Lack of any nystagmus
Medications that can interfere with the caloric reflex
Antihistamines, anxiolytics, antidepressants
ENG or VNG testing
Uses electrodes to trace eye movements and record the presence of nystagmus
VEMP testing
Vestibular evoked myogenic potential
looks at the reaction time between a sound and muscle response
Cervical VEMP
Assesses Saccule
Ocular VEMP
Assess Utricle
Etiology of BPPV
Canalithiasis - calcium deposits in SCC can also be from a free floating otoconia
Presentation of BPPV
Vertigo appears upon changes in head position and presents with no other neurological deficits
BBPV of posterior canal
Upward rotary nystagmus
BBPV of anterior canal
Downward rotary nystagmus
Horizonal canal BBPV
Beating towards the floor
Otolith repositioning for BPPV
Epley maneuver
2 deconditioning exercises for BPPV
Brandt-Daroff and Sermont
Vestibular neuronitis
Viral or post viral inflammatory response only affecting that vestibular division of CN VIII
Vestibular labyrinthitis
Viral or post viral inflammatory response that effects the vestibular AND cochlear division of CN VIII
Clinical presentation of Vestibular neuronitis or labrynthitis
Sudden onset vertigo
Nystagmus AWAY from the affected side
Normal head impulse test for central lesion
Treatment for vestibular neuronitis/labrynthitis
Corticosteroids - prednisone or methyl prednisone for 10 days to 3 weeks
May try antivirals or antimicrobials if suspected
2 drugs for vertigo suppression and 2 for nasuea
Antihistamines and Benzodiazepines
Promethazine and Ondansetron
Meniere’s disease (endolymphatic hydrops)
Thought to be related to excessive fluid in the inner ear may be due to syphillis and blocked endolymphatic ducts
Classic meniere’s disease triad
Episodic vertigo, Unilateral hearing impairment, Tinnitus w/ low tone blowing
Aural fullness is also a symptom
Testing for meniere’s disease
2 spontaneous episodes lasting at least 20 minutes
Abnormal caloric testing
Hearing normal between attacks
Treatment for meniere’s disease
Restrict salt, alcohol, and caffeine
Medication for acute Meniere’s disease
Meclizine, diazepam, promethazine
Medication for chronic meniere’s disease
Acetazolamide - Diuretic to remove salt water
Perilymphatic fistula
Leakage of fluid from the inner to the middle ear
Perilymphatic dehiscence
Abnormal thinning or asence of bone above the superior semicircular canal
Clinical presentation of peri lymphatic fistula or semicircular canal dehiscence
Sensorineural hearing loss
Brief recurrent episodes of vertigo with specific triggers
Physical exam usually unremarkable
Treatment for peri lymphatic fistula or semicircular canal dehiscence
Referral, Bed rest with head elevation, meds for symptoms, may need a surgical patch if refractory
Barotrauma
Buildup of pressure between the middle and inner ear due to eustachian tube dysfunction, flight, SCUBA, etc.
Type of pressure usually present in barotrauma
Negative pressure in the middle ear
Presentation of Barotrauma
Pain, Pressure, Tinnitus, Hearing loss
Hemorrhage behind TM or perforation may be seen
Treatment for barotrauma
Most heal over time, refractory may need myringoplasty or tympanoplasty
Prevention of barotrauma
Decongestants, slow depth/altitude changes, Chewing gum or pacifier, frequent swallowing
Tinnitus
Sounds in the absence of an exogenous source - pulsatile or non-pulsatile. Continuous or intermittent
Pulsatile tinnitus
Can result from carotid bruits, Muscle spasms or open Eustachian tube (loud breath sounds)
Non-pulsatile tinnitus
Due to sensorineural hearing loss, otosclerosis, meniere’s disease, etc.
TL/DR - More directly ear related
Paragnaglioma
Tumor of the middle ear - causes pulsatile tinnitus and can be removed surgically
Look for high vascularity
Treat sugically
Patulous eustachian tube
Tube stays open leading to roaring from breath sounds and unusually loud hearing of one’s own voice
Treatment for patulous eustachian tube
Premarin (mucosal irritant)
Surgery
Exacerbating factors of tinnitus
Depression and insomnia
21% suicide rate
Therapy for tinnitus
Noise reducing generators with retraining therapy, Stress reducing CBT
Other interventions for tinnitus
BZD, Intra TM steroids, Misoprostol, Transcranial magnetic stimulation