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165 Cards in this Set

  • Front
  • Back
Chronic inflammation of eyelid margin
May or may not have symptoms
-Burning early morning
-red eye and scratchy
common in nursing home & debilitated
oils build up and colonized by Staph
exotoxin into eyes

Warm compression
Non-irritating shampoo
Gentomycin or erythromycin
-May have hereditary component
-Dig stuff out of eyes in morning
Anterior stye
Abscess of internal lamellum

Warm compression
Focal pressure
Lance if it does not go away

-May have defect in AA which causes secretions to be thicker
-NOT infectious
Anterior stye
Abscess of internal lamellum Warm compression
Focal pressure
Lance if it does not go away
Basal cell carcinoma
Basal cell carcinoma Central ulceration
Takes years to form

Punch biopsy

-may be confused with Hordeolum
Preceptal cellulitis
(infront of orbital septum)
-Caused by insect bit around eyelid
or abrasion
-swelling & redness of eyelids
-warm to touch

Oral antibiotics

-make sure it’s not an infection of orbital proper
Orbital Cellulitis
-infection of orbital proper
-unable to move eye
-lots of pain
-eye pushes out (proptosis)
-optic nerve dysfunction
reduced visual acuity
abnormal papillary response
optic disk swollen Hospitalization—life threatening
IV antibiotics (high)
Surgical debridement if fungal
Consults: ophth & ENT
Culture: conjunctiva, nasopharynx, blood
Xray: sinuses
CT scan

-due to penetrating trauma or ethmoid sinusitis
-common organism
Staph, Strep
H.flu (6 mon-5yrs)
Fungus (diabetic&immunocomp)
cavernous sinus thrombosis
Inflammation of lacrimal sac
Focal mass with surrounding
Very tender (pt will jump)*
Pressing may see purulent

Oral antibiotics
If recurrent, drain area
May have to re-route tear drainage
Into nose

-common organisms
staph, strep
H. flu
Gram negatives
-inspect nose to r/o tumor or polyps
Red eye
Clear cornea b/c able to see iris detail
Good eye reflex

Treatment depends on type

Causes by order
1-tear deficiency
Allergic conjunctivitis
Itching, red, nasal congestion, sneezing
String white discharge
Dark circle around eye
Kemosis (swelling of conjunctiva) Topical/oral antihistamine
Topical mast cell stabilizer
refractory: topical steroid

Associated with hay fever, asthma,
Type I-IgE mediated (mast cell)
Type IV-contact allergy (chemical
Or drugs)
Viral Conjunctivitis
Clear watery discharge
Preauricular lymph node
Blurry b/t blinks
Normal acuity
Past family history
Starts one eye than the other
Some pain
Assoc. with URI (sorethroat, fever)

Antibiotics to prevent bacterial

Most common: Adenovirus
Bacterial conjunctivitis
Pus like discharge
Matting of lids upon awakening

Broad spectrum antibiotics
Topical antibiotics if difficulty
Warm compression and cleansing

Causes: staph, strep, Haemophilius
Hyperacute bacterial conjunctivits
Due to N. meningitis or N. gonorrhea
Manifest w/in hours
Preauricular node
Corneal opaciffication*
Neck maybe stiff

IV antibiotics (high)
Treat systemic infection

Risk of meningitis
What is a major cause of blindness worldwide?
Chlamydia trachomatis
neonatal conjunctivitis

Chemical (silver nitrate)
Used for Neisseria prophylaxis
12-24 hours later

Clears w/in 48 hours
Supportive care

US—use erythromycin b/c Neisseria and Chlamydia prophylaxis
neonatal conjunctivitis

1-2 days after birth
acquired in birth canel
severe eyelid edema

Single—no cornea involvem.
5 day-if cornea involved
topical erythromycin &

If untreated, can develop corneal ulcer
neonatal conjunctivitis

Other bacteria
Staph (aureus and pneumonia)
Strep (group A & B)
GN (E.coli, Pseudom, Hemoph)
3-4 days after birth
bilateral purulent conjunctivitis
culture/gramstain are helpful

Staph & Strep—erythromycin
(gentamycin or tobramycin)
neonatal conjunctivitis

1 week
vesicles on skin around eyes
called Dendritic Keratitis
Giemsa: intranuclear inclusion
Viral culture

neonatal conjunctivitis

(Neonatal inclusion conjunctivitis)
1-6 weeks
*most common
acquired in birth canel
Giemsa: intracytoplamic inclusion
Monoclonal antibody test

Erythromycin or tetracycline
Erythromycin for systemic inf.
Subjunctival hemorrhage
Fragile break of conjunctival BV
Idiopathic (rubbing eyes)
Valsalva (coughing, vomiting, Having a baby)
Coagulopathy (rare)—may see Bruising and petechiae

Raised yellowish area of bulbar conjunctiva
subepithelial tissure degenerate and thickens
Degenerative disease
Associated w/ aging, UV exposure, dry eye
Cosmetic problem
May get pingueculitis (inflammation)

Topical antihistamine
Vasoconstrictive agents
Fibrovascular response where tissue grows into cornea
(Bowman’s layer)
damage of subepithelial collagen
degenerative disease
associated w/ UV exposure, dry eye
common closer to equator (desert environments

Artificial tear
Topical vasoconstriction
Surgically remove if
1. affect vision
2. distort cornea causing astigmatism
--deeper & more invasive when grows back
Inflammation of superficial vascular plexus
(on top of sclera)
autoimmune and deep to conjunctiva
see secondary conjunctiva congestion
common middle age & young adults
relatively innocuous may see recurrences
usually different locations & sectoral

Oral NSAIDS for several weeks

Cotton tip on eye will move
Conjunctival vessels
Episleral vesses don’t move
Funduscopic—more purple color
SOME patients have systemic dx
More severe & painful than episcleritis
Inflammation of collagen lamellae of sclera
Sclera thickens & bulges out like a tumor
See secondary episclera & conjunctival

Refer to Rheumatologist
Systemic immunosupp. Ression

Always systemic disease
Polyartheritis nodosa
Weggener’s granulomatosis
Relapsing polychondritis
If not controlled, get avascular
Situation where BV disrupted &
Scleral thins
(scleromalacia perforans)
Keratoconjunctivitis sicca
(tear deficiency)
Burning, foreign body, dry eye
Tearing when reading
Common in postmenopausal female
Severe dry eye will cause corneal epit
To break down b/c there is an
Activation of collagenases in
Basement membrane which
Destroys the stroma and cornea
May perforate

Artificial tear
Lubricating ointment at night
Punctual occlusion to prevent
Tears from leaving
Environmental modification
Cyclosporin topical-help
Produce more tears

RA—damage to lacrimal gland
Steven Johnson syndrome—globlet cells
Which secretes mucin over cornea
So tears don’t spread evenly
Systemic medication—anticholinergic
Exagerbate dry eye
Sjogren’s syndrome--triad
Dry eye(keratoconjunctivitis sicca)
Dry mouth (xerostomia)
CT disorder (RA or LUPUS)
Exposure keratoconjunctivitis
Due to incomplete lid closure
See sclera on top of eyes
Thyroid disease
Facial nerve palsy
Lagothalmos—eyes open while asleep

Ointment at night
Tape eyelid shut
Herpes keratitis
Coneal opacification
Often recurrent each time more scars
Not much pain
Vesicular eruption (intranuclear

NO topical steroids
b/c suppresses T cell which is necessary to monitor herpes

oral acyclovir

Fluorocein staining: dendritic branch pattern
“cold sore in eye” HSV I>HSV II
trigeminal ganglion
Steroids side effects:
1. elevate IOP
2. cataract formation
3. enhance corneal penetration for fungi and herpes
Anterior uveitis
(iritis, iritocyclitis)
Circumcorneal redness-ciliary body inflamed
Sore/achy pain
May or may not have decreased vision
Miosis-sphincter muscle inflamed
Hypopyon—WBC layered in anterior chamber
Posterior synechiae—nonround pupil
Keratic precipitate—opacities when doing red
Reflex (lymph stuck to back of cornea)

Topical corticosteroid
Dilation of pupils help relieve
Discomfort and prevent
Posterior synechiae

Systemic associations:
JRA (younger)—chronic uveitis
Highest risk
Female, ANA+, JRA
HLA-B27 genotype
Ankylosing spondylitis
Psoriatic arthritis, IBS
Writer’s syndrome
Acute glaucoma
(closed angle)
Sudden rise of IOP
Severe deep pain and redness
Cornea not clear (steamy)
Mid-dilated pupils, unreactive to light (unilateral)
Seeing halos around light
Blurred vision
Headache (around eye)
Nausea and vomiting

Medical emergency
Topical beta blocker
Oral isosorbide
Prevention: peripheral irodotomy

Predisposed individuals (hypopia)
Increase IOP will cause ischemia to
Iris, retina, and damage corneal
“great masquerader”
Chronic glaucoma
(open angle)
More common
Painless, no redness
Pupils and cornea normal
*moderately elevated pressure (<22 mmHg)
*abnormal cup to disc ratio
*loss in visual field exam
blockage of aqueous outflow in region near
trabecular meschwork & canel of schlemm

Decrease secretion:
Beta blocker
Carbonic anhydrase inhibitor
Alpha 2 agonist
Increase outflow:
Pilocarpine (constrictor)
Epinephrine (dilator)
If fails, surgery (incising trabecular
Auricular hematoma
-Hematoma b/t cartilage & perichondrium
this depreves cartilage of O2  avascular necrosis occurs leading to cauliflower ear
-occurs in wrestlers
-ear swells & large and blue losing the outline of conchal folds
“redish puple with shapeless elevation”

-pressure and bolster dressing
-antibiotic ointment to prevent infection
Frostbite of the ear
-thermal injury
-blistering of pinna
-mild casesuperficial reversible (red & slight pain)
-severe casesblistering, edema, gangrene (painless) -rapid warming
-heparin to prevent venous clotting
-antibiotics to prevent superinfection
-avoid manipulation
-inflammation of cartilage
-infection of pinna after trauma
-lead to deformity and necrosis
-painful and swollen ear


Autoimmune perichondritis (relapsing)
deformity with repeated bouts
Acute otits Externa
“swimmer’s ear”
-infection of external auditory canal
-factors: heat, humidity, moisture, trauma
-common pathogens: Pseudomonas & Staph (Proteus, Strep pyrog)
-otalgia worsened by manipulation of outer ear
(does not happen to OM)
-sometimes: otorrhea from outer ear or middle ear
-swollen lymph nodes
-itching, ear pain

-debride and clean ear
-topical antibiotics drops (Quinolone, cipro)
-analgesic since it’s painful
-oral antibiotics if systemic signs (fever, cellulites, lymph nodes)
Chronic otitis externa
-painless, itching, scant cerumen (skin flaky and red)
-risk factors:
elderly patient
immunocompromised, AIDS

-steroid ointments
-fungal infection in external auditory canal
-common pathogens: Aspirgillis, candida
-main complaint: ITCHING
-hyphae in canal

-cleaning ear (for 1 month)
-antifungal drops
-gentian violet (old treatment)
-m-cresyl acetate
Necrotizing otits externa (malignant)
-bone destroying infection
granulation tissue at chondroosseous junction that’s able to spread thru fissure to temporal bone causing skull death
-occurs in diabetics, AIDS, immunosupressed
-caused by Pseudomonas
-progressive otalgia

-antibiotis (aminoglycoside, quinolones)
-surgical debridement
Preauricular cyst &
-absence of antihelical fold
-protruding ear
-familial tendency

-cosmetic problem
-can be surgically corrected (otoplasty)
Preauricular appendages
-skin tags infront of ear
-ear may be perfect or not

-small ear
-absence of ear
Cerumen impaction
->90% occlusion will affect hearing
-different types of wax

-removal by irrigation or cerumolytic
-complication: hematoma, laceration, perforation
-tiny bones in ear canal
-may be asymptomatic
-history of surfing and swimming in cold water

-drilling if completely blocking ear canal
Epidermal inclusion cyst
-benign neoplasm of outer ear

-excised under local
-benign neoplasm of outer ear
-predisposed individual, happens after trauma

-excision but keloid may come back worse
-local steroid injection
Winkler’s disease
(Chondrodermatitis nodularis chronica helices)
-common, benign neoplasm of outer ear
-Very painful nodules (ulcerated) at superior helical rim
-idiopathic inflammatory condition
-males > 40 yrs old

-topical steroid
-inject sterior
-surgical excision
Basal cell carcinoma
Malignant Neoplasm of outer ear
Squamous cell carcinoma
Malignant Neoplasm of outer ear
-able to metastasis
Malignant melanoma
-able to metastasis more than squamous cell -wide excision
-excision of lymph nodes
Glomus Tumor
-benign vascular tumor from jugular bulb in middle ear
-pulsatile tinnitus & conductive hearing loss
-can lead to problem if it gets bigger (CN VII, IX, X, XI)
-reddish mass behind TM
-fluid behind ears
Squamous cell carcinoma of temporal bone
-severe otalgia and bloody otorrhea
-facial paralysis
-poor prognosis (eating away temporal bone)

Bell’s palsy
-unilateral facial paralysis
-lesion may have immune causes or viral disease or ischemia
-compression of CNVII in narrow confines or temporal bone
-distortions of face (sagging corners of mouth, inability to smile, drooping eyebrows, inability to close eye, eversion of lower eyelid)
-also cause:
decreased lacrimation, loss of taste in anterior 3/2 out tongue (chorda tympani)
painful sensitivity to sounds (n to stapedius)
deviation of lower jaw and tongue (n. to digastric)

-patch eye when sleeping
-surgical decompression is rare
Herpes zoster oticus
(Ramsy Hunt syndrome)
-invastion of CN VIII and geniculate ganglion of CN VII by Herpes virus
-severe otalgia, facial paralysis, hearing loss, vertigo
-decrease lacrimation, salvation, taste
-vesicles seen on pinna and in ear canal

-patch eye when sleeping
Bullous myringitis
-inflammation of tympanic membrane
-see blebs or hemorrhagic vesicles on TM
-severe otalgia
-deafness is conductive hearing loss
-organisms: Strep pneumo, H. influenza, Moraxella

-analgesics for pain
Barotrauma (Aerotitis)
-result of sudden pressure changes between Middle ear and Atmosphere
increased pressure causes eustation tube to shut
-predisposing: Upper respiratory infection or allergies
-otalgia, fullness in ear, tinnitus, vertigo
-conductive hearing loss with effusion of middle ear
-ear drum appears to be blue b/c bleeding behind it
-TM retracts inward

-auto inflation of ear
-myringotomy (aspirate effusion)
topical/oral decongestant
chewing gum
freq swallowing
ear planes (slowly equalize pres)
Otitis media
-inflammation of middle ear
-common illness in children
-3 categories
1. acute suppurative otitis media (AOM)
2. otitis media with effusion (OME)
3. chronic suppurative otitis media (CSOM)

1. infection
2. eustation tube dysfunction
3. allergy
4. ciliary dismotility
5. eustation tube obstruction
• adenoid hypertrophy
• nasopharyngeal tumor
Acute otitis media
-otalgia, fever, irritability, tugging ear, hearing loss, otorrhea
-extension of infection (vertigo, tinnitus, facial paralysis, mastoid swelling) EMERGENCY
-common organisms:
strep pneumo, H. influenza, moraxella catarrhalis
-red inflamed TM, cloudy, bulging or perforated
-risk factors
1. <24 months b/c eustation tube is more horizontal,cartilage undeveloped
2. males
3. down syndrome
4. family history
5. maternal smoker
6. native American, native Alaskan, caucasion American
7. recent URI
8. fall thru spring
9. bottle feeding
10. daycare
11. lower social economic status

-antibiotics (amoxicillin, augmentin, erythromycin, sulfonamide)
-tympanostomy tubes
-decongestants, antihistamine, OMM
Otitis media with effusion
-hearing loss, aural fullness, but often no symptoms
-air fluid level, TM is immobile
-commonly OME is seen after previous acute OM has started to heal

-**antibiotic does NOT help b/c it’s not suppurative process
Chronic supperative otitis media
-persistent purulent discharge of middle ear
-perforation of TM
-no pain
-hearing loss
-organisms: Pseudomonas, Staph
-problem ingrowth of squamous epith into middle ear
causing cholesteatoma (white cyst)
-can be infection & spread to adjacent tissues & ossicles

-tympanoplasty with mastoidectomy
-antibiotics (3rd, 4th gen cepalosporins)
-extension of middle ear infection into air cell of mastoid
-see mass behind ear

-drainage of abscess
Vestibular migraine
-history of migraine headache
-motion intolerance (car sick)
-episodic, variable duration
-association: headache, photophobia, phonophobia, visual aura
Vestibrobasilar insufficiency

(Central causes of vertigo)
-dizziness (lightheadedness)
-diplopia, dysphasia
-drop attack with normal neurologic exam b/t attacks

-antiplatelet/anticoagulant therapy
Multiple sclerosis

Central causes of vertigo
-vertigo with nystagmus (bizarre up beating)
-impaired position and vibrating sensation
-optic neuritis on MRI

Central causes of vertigo
-diagnosis of exclusion
-occurs in elderly
-decrease hearing loss exp upper frequencies
1. impaired vestibular function
2. loss muscle strength
3. diff. gait
4. impaired vision

Home safety
Benign paroxysmal positional vertigo

Peripheral causes of vertigo
-vertigo with certain head position
-otoliths dislodged from utricles and saccules and enter the posterior semicircular canal
-can be intense and short
-history of trauma and vibration or none
-abnormal Hallpike-Dix test

-canal repositioning therapy
Meniere’s disease

Peripheral causes of vertigo
-vertigo lasting hours
-aural pressure in the involved ear
-tinnitus in involved ear
-sensorineural hearing loss (fluctuating & low frequency)
-progressive permanent hearing loss
• Overproduction or under absorption of endolymp in stela media resulting in bulging membrane symptoms when rupture of membraneous labyrinth occurs
• Inner ear hair cells are exposed to high K+ killing them and leading to vertigo and hearing loss

-salt restriction (3 grams Na)
-vestibular suppressant medicin
-diuretics if more frequent
-allergy (if involved)
-surgery (severe cases) by removing endolymph
Vestibular neuronitis

Peripheral causes of vertigo
-vertigo lasting for days
-very ill (vomiting)
-absence of other ear symptoms (no hearing loss)
-causes: viral inflammation of vestibular nerve

-supportive care (hosp, IV)
benzodiazepam, anticholinergic
if chronic,
vestibular rehab
Acoustic schwannoma

Peripheral causes of vertigo
-unilateral asymmetric sensorineural hearing loss
-benign tumor arising from (cochlear) auditory nerve
-if vestibular nerve is involved, see dizziness
-sudden hearing loss, but usually more progressive
-diagnosis made by MRI

hearing loss
possible facial paralysis
Chemical injury
Irrigation—several liters
Antibiotic ointment
Remove particular matter

Prognosis depends on
-what got into eye
-how soon flush out
Base—damage to collagen lamella
Transplantation unsuccessful b/c
Eye is unvascularized
Corneal abrasion
Very painful
Red eye
Tearing photophobic
Secondary Uveitis (small pupils)
Flourescein test

Cyclophlegic agent (anticholin)
Paralyze iris and ciliary body
Cool compress
Topical antibiotics (erythromycin)
Patch eye
Tylenol or advil for pain

**do NOT patch contact lens abrasions**
Corneal foreign body
Feels like something there
Red eye

If embedded, numbing drop with sterile TB syringe and needle
Then treat as an abrasion
Foreign body in tarsus
Red eye
Sensation of foreign body but no
Foreign body in cornea
Flourescein shows scratches up
& down

Evert eyelid
Use swab and take it out
Apply antibiotic
Artificial tear
Blood layer in anterior chamber
Due to blunt trauma
A tear of peripheral artery at the
Root of the iris

Goal: prevent rebleeding
Bed rest 5 days with no mov’t of eye
*no aspirin
topical anti-inflammatory agent
steroid to reduce bleeding
cytoplegic agent to paralyze muscle
wear shield

Due to blunt trauma:
Soccer ball
Paint ball
Diabetic retinopathy

Clinical Presentation
• Most common retinal vascular disease
• 2nd leading cause of blindness in US (20-64 year old)
Nonproliferative DR
o Microaneurysm (sm round lesion) “blot&dot” if leaky, lipids make hard exudates
o Intraretinal hemorrhage
o Retinal ischemia (occlusion of end arterioles; leading to microinfarction) see cotton wooly spots
o 2 complications:
1. ischemic maculopathy
-ischemia at macula   visual acuity
-irreversible but can improve if improve underlying condition (HTN, anemia, heart failure)
2. macula edema
-see hemorrhage & exudates
-treatable with laser
Proliferative DR
• signs of NDR + neovascularization
• signs of gobla ischemia  causing new vasculature
• complications:
1. vitreous hemorrhage
-blood infront of retina due to new vessel bleeding
-pt complains of floaters and cobwebs
2. Gliosis (scar tissue)
-contact into a mass causing Traction Retinal detachment
Diabetic Retinopathy

Yearly ophthalmic scope exam with dilated pupils

Control glucose, HTN, hyperlipid

-laser to eliminate microaneruysm &
leaky blood vessels

PDR: kill ischemic retinadec sign of neovascularization
-laser (panretinal photocoagulation)
most common
-freezing (panretinal cryrethinopexy)
older; used if unable to see retina
Side effects:
Constriction of periph visual field
Decrease night vision
Reduced near vision
Possible reduction in visual acuity
Diabetic retinopathy notes
Risk factors
1. inc. duration of DM
2. other syst vascular cond.
3. poorly controlled blood sugar
-goal HgA1C <6.0
-loss or renal fxn
-loss of extremities

DMI (insulin dep)
-free of retinopathy 1st 5 years
-95% if 15 or more yrs

-retinopathy at time of diagnosis (maybe 1stsign)
-80% if 15 yr or more

leading cause of blindness in world is Trachomoa
HTN Retinopathy
Arteriolar sclerosis (more light reflex > 1/3)
Arteriolar constriction (arterioles <1/2 of venules)
AV nicking
Retinal hemorrhage (flamed) & exudates (usually soft)
Optic disc swelling (in severe, acute HTN)

-arteriolar narrowingnarrowing with focal constrictioncotton wooly exudates and flamed hemorrhagepapilliedema

-broden light reflexAV nickingcopperwiring (arteriolar) silver wiring

Control hypertension
Branch Retinal Vein occulusion (BRVO)
-Caused by HTN when AV nicking compelety compresses venule causing blood to back up in wedge shape pattern
-symptoms of vision loss if it’s in temporal arcade b/c near fovea
-retinal hemorrhage
-can result in neovascularization
Central Reinal vein occlusion (CRVO)
-All quadrants involved b/c occlusion is w/in disk proper
-leading cause of neovascular glaucoma
-visual impairment is 1st noticed upon waking in morning
-opthalmoscopic signs:
disk swelling
venous dilation & tortuosity
retinal hemorrhage
cotton wooly spots
unilateral: assoc HTN, DM, smoking
bilateral: blood dyscrasia, hight viscosity, myeloma, Waldensrom’s macroglobinemia
Central retinal artery occlusion (CRAO)
-Central reinal artery w/in disk is occluded due to embolus sudden vision loss
-retina turns white b/c ischemia and infracted
-cherry red spots usually at fovea

Decrease IOP
w/in 8 hours, thrombolytic to restore vision
Amaurosis Fugax
-retinal transient ischemic attack
-sudden, transient, painless monocular vision loss
-curtain passing vertically across visual field
-causes (occluding ipsilateral carotid)
Hollenhors plaque
-embolus containing cholersterol crystal wedge in retinal arterioles
-they are reflectal
Platelet-firin embolus

Ischemic optic neuropathy
-stroke of optic disk head
-unilateral optic disk swelling
-2 causes:
1. nonarthritic (age related)—occusion small end arteioles
2..arthritic—inflam. Of end arterioles & ciliary arteries due to giant cell arthritis

Aspirin to decrease occurrence

Glucocorticords to prevent blindness in other eye
Giant cell arthritis
-Elderly >60 y/o
-vasculitis of small medium sized arteries
-temporal pain and jaw claudication
-headache, malaise, night sweat, fever,anemia
-overlap with polymyalgia rheumaatica
-temporal arteiries are prominent, pulselss, indurated
-ESR elevated
-temporal artery biopsy

High dose of prednisone until remission

Biopsy soon b/c 10-14 days after treatment will see false neg.
Optic neuritis
-inflammation of optic nerve
-due to demylinating lesion associated with Multiple sclerosis or vinus or autoimmune disease (Lupus)
-unilateral swollen nerve
-decrease vision
-relative afferent papillary defect
-if recurrent, may get optic atrophy (white nerve)

Age-related macular degeneration
-leading form of IRREVERSIBLE blindness in US
-degeneration of outer retina & choroids
-common age 70 & up
-very gradual dec. in central vision
-blind spots
-hereditary correlation, but no gene ID
-usable vision in one eye

-vit E, C, A, zinc (lutein)

-laser photocoagulation
-subretinal surgery
excise new vessels
not good b.c removes too much RPE & cause hemor.

Atrophic form (dry)
-drusen (yellow deposits)
-pigmentary disturbance in macula

Exudative form (wet)
-subretinal scar (outer retina)
-complication of atrophic form
Vitreous separation
-will happen to everyone
-vitreous overtime liquefies causing gel to peel off retina
-if vitreous adheres to retina, see flashes of light
Rhegmatogenous retinal detachment
-vitreous goes thru retinal tear (b/t neurosensory retina and RPE)
-convex configuration
-due to trauma or idiopathic
-elevated, dark grayish corregated area that shifts with eye mov’t
-out of focus so dial + #’s for elevated portions
-pt complains of flashes & floaters
-abnormal vision
-pupillary defect

-freezing of laser to seal tear
-sclera buckle around eye to bring eye wall into retina

-remove vitreous and add gas bubble (vitrectomy)

Risk factors
-thinning of retina
-most common reversible vision loss in world & US
-any clouding of lens
-glare (night & dark)
-blurred vision at a distance then later reading and near vision
-see color changes

1. Nuclear cataract
-affect vision sooner
-most coomon aged related
2. cortical cataract
-white cataract
3. posterior subcapsular cataract
-inside posterior capsule
-thin placque on back of eye
-common: DM, steroid, trauma

-usually none
-surgery if significant visual impairment or affect daily activities

-complications (<1%)
retinal swelling or detachment
-pats are unable to accommodate
-capsule can opacify but cleaned with laser

1. aging
2. DM ( sugar level distort shape of lens)
3. hereditary (congenital or young)
4. injury (blunt trauma, vitetomy surgery)
5. meds (steroids)
6. UV exposure
Herpes simplex oralis
“cold sore”
-caused by HSV 1 that stays dormant in trigeminal ganglion
-painful fluid filled vesicles which occurs on any oral mucosal surface

-self limiting ;heals in about 1-2 wks
-if severe, acyclovir for few wks
-if pain, give analgesics
Recurrent aphthous stomatitis
“canker sore”
-unknown etiology
-white ulcer with surrounding erythema
-any oral mucosa except gingival & hard palate
-very painful

Nothing effective
If severe, topical or intraoral steroid
If multiple, systemic steroid and analgesic
(oral candidiasis)
-caused by Candida albicans
-results of broad spectrum antibiotic use
-if found in healthy individ. w/o antibiotic use, patient may have HIV
-common in neonates b/c no established NF
-burning sesation; soft white plaques on oral mucosa

Topical or systemic antifungal
-caused by Corynebacterium diphtheria
exotoxin produce local tissure inflame& necrosis
-2-4 day incubation
-gray adherent membrane in pharynx (pseudomembrane)

Antitoxins and antibiotics
Prevention: immunization

Looks like mono and acute bact tonsillitis
Infectious mononucleosis
Caused by EBV
-2-5 day of prodrome of fatigue, malaise, fever then pharyngitis (inflame of throat)
-severe and exudative pharyngitis
-worse caseu tonsillitis causing obstruction
-POSTERIOR and anterior cervical adenopathy
splenomegaly and hepatomegaly
-dx: CBC with smear (>10% atympical lymph)
+ monospot

Severe, give steroids
Really severe, (very painful, airway comp) give IV steroids
If IV not helpful, acute tonsillectomy
Ludwig Angina
Cellulites like
-infection of dental origin from rotten tooth or poor dental care
-extension of infection into submandibular, sublingual, submental space (strep, anaerobic strep)
-infection & edema will cause displacement of tongue posteriorly causing airway obstruction

Secure airway
Drainage to relieve pressure
Xray: swelling in submental space
Retropharyngeal abscess
-puss in potential space b/t constrictors and prevertebral fascia
-occurs in children <4 yrs old
-occurs in adults if penetrating trauma to posterior pharyngeal wall
-difficulty swallowin (polled salivary secretion)
-respiratory distress (fullness posterior pharyngeal wall)
-neck rigidity w/ cervical adenopathy
-xray: widened retrophayngeal space on lateral xray

(inflame of adenoids)
-may be confused w/ sinusitis b/c both present w/ purulent rhinorrhea
-nasal obstruction, fever, otitis media
-difficulty to distinguish from URI or bacterial sinusitis
Obstructive Adenoid hyperplasia
-chronic nasal obstruction
-snoring at night
-mouth breathing
-hyponasal speech
dx: nasal endoscopy, lateral neck xray

Acrte tonsillitis
-sore throat, fever, dysphasia
-tender cervical adenopathy
-erythematous tonsils
-tonsillar exudates
Recurrent tonsillitis
>6 episodes in 1 year
>5 per year in 2 consecutive years
>3 per year in 3 consecutive years

fever, cervical adenopathy, tonsil exudates with no symptoms the rest of the year
Chronic tonsillitis
Chronic sore throat
Bad breath
Persistent, tender cervical adenopathy
Only temporally relief with antibiotics

Obstructive tonsillary hypertrophy
Sleep apnea
NO sore throat only dry, scratchy throat
abscess “Quins Peritonsillary”
-worsening sorethroat
-dysphagia, drooling, hot potato voice (hurts to use pharyngeal and palatal muscle)
-trismus (diff opening jaw due to inflame of muscles of mastication)
-swelling of superior tonsillar pole leading to deviation of uvula to unaffected side

Drainage (immediate relief)
Possible tonsillectomy
-wartlike growth on oral mucosa
-Squamous cell carcinoma

Surgical excision
Torus pallatinus
-hard bony protuberance in midline of hard palat

Nothing if severe, remove
Torus mandibularis
-hard bony protuberance on alveolar ridge of mandible
-blocked sublingual gland
-fluid filled
-not painful Excision by marsupial technique
-blocked minor salivary gland (inner lip)
-see lump in lip

Surgically excised
-unilateral tonsillar enlargement w/o infection or sore throat or URI type symptoms
Minor salivary gland malignancy
Bulging soft palate
Looks like torus palatinus but soft
Squamous cell carcinoma
-most common cancer or oral cavity 95% involve lower lip
-risk factors:
UV sun exposure
Oral tobacco
Unproper dentures
Betel nut chewing

Good prognosis b/c diagnosed early
Surgical excision
-most common newborn laryngeal abnormality
-since newborn having abnormal flaccidity of epiglottis b/c cartilage not well developed
-inspiratory stridor worsen when supine
“omega epiglottis” curling upon inspiration

Self limiting
Chalasia chair
Laryngeal web, atresia, stenosis
-congenital or post traumatic
-symptoms depend on degree of blockage of glottic closure due to scarring of laryngeal inlet or not fully developed
-atresia (complete blockage) present as sever distress at birth and requires ER airway

Laser laryngoscopy
Tracheotomy until problem is fixed
Acute epiglottis
“supraglottis”—inflam of larynx above vocal cord
-caused by type B Haemephilis influenza
-rapid onset & progression
-fever, odynophagia, drooling
-if airway compromised can lead to airway obstruction and death
-AVOID manipulation of larynx until operating room b/c can cause complete airway obstruction
*critical in children b/c smaller airway

-antibiotics does not help
index of suspecision
lateral xray—epiglottis see thumb print sign (widened epiglottis)

secure airway
steroid to dec inflammation
-viral infection of young children
-inflammation of subglottic larynx (below vocal cord)
-“barky” cough and stridor
-mimial laryngeal erythema

High humidiy O2 tent
Racemic epinephrine
Acute infectious laryngitis
-usually viral
-hoarseness, cough, low grade fever
-laryngeal erthema and edema

Voice rest
Humidification and hydration
Cough suppressant and mucolytics
Chronic infectious laryngitis
Risk factor
-smoking, alcohol
-vocal overuse and/or abuse
-gastric acid reflux
husky voice; must to layngeoscope since persistant
less red, swollen hypertrophy and edematous

Underlying condition
Tubercuous laryngitis
-associated with active pulmonary TB
-edema and erythema post 1/3 of vocal cord
-*can mimic laryngeal cancer (appearance, persistant hoarsness, if smoker)

Antituberculous chemotherapy
Vocal cord nodules
(screamers nodules)
-excessive vocal use (mucosal trauma)
-see in children and adults
-usually bilateral nodes on vocal cord
-begin as edema then progresses to fibrosis
-benign white lesion at jxn of anterior and middle 1/3 of vocal cord
-raspy voice

Voice rest
Voice therapy for 6 month
Surgery but not usually done
Vocal cord polyp
-result of vocal abuse or smoking
-pedunculated mass on vocal cord
-smooth surface
-usually unilateral

Surgical removal
Vocal cord granuloma
-arise on posterior vocal cord
causes: gastroesophageal reflex, traumatic incubation, prolonged intubation

Surgical removal but can recur
Laryngeal papillomatosis
-result of HPV
-more children
-stridor and airway obstruction
-multiple soft mucosal projection of vocal cord

Multiple surgical removal (CO2 laser) b/t recur quite often
Can regress after puberty
Laryngeal cancer
May be on vocal cord, epiglottis, aryepiglottic fold (meckmass with no hoarseness)
-almost always squamous cell carcinoma
-risk factors
males: females (8:1)
alcohol w/ smoking
-hoarseness best if on vocal cord 1st b/c present earliest
-other: sore throat, dysnea, dysphagia, wt loss, referred pain, neckmass

Depends on staging
Total layngectomy
Conservative surgery
Voice restoration
Esophageal speech
Electric larynx
Voic prosthsis
Vocal cord paralysis
-one side vocal cord paralyzed, thin, atrophies so will not move during phonation give hoarseness
-body tries to compensate

Injection material under mucus memb of paralyzed vocal cord to bulk it up

Many causes: see list
(hereditary hemorrhagic telangiectasia)
Autosomal dominant
Fe anemia b/c of telangiectasia
Red-violet telangiectasias on face, lips, mucosal surface, tip of fingers and toes
Pulmonary RL shunt with TIA, CVA, brain abscess
Sjogren’s syndrome
Autoimmune to exocrine glands no longer make saliva/tears
mostly females middle aged
present with:
1. xerostomia (dry mouth)
2. keratoconjunctivitis sicca (dry eye)
3. systemic symptoms (1/3 of patients)
easily fatiqued low grade fevers
renal involvement
pulmonary involvement
enlarged parotid gland

Dx: autoantibody SSA,SSB, ANA, RF
Parotid biopsy(massive lymphs)
Vit B12 deficiency
Classic smooth atrophic tongue
Buring sensation—b/c rapid turn over of cells and DNA replication
Associated with pernicious anemia
Vit C deficiency
Hemorrhagic manifestation and abnormal dental formation
Due to improper diet
Latent for 3-6 mondths after reduction of Vit C to <10 mg
Impaired collagen formation
Gums swollen, frile, purple, bleeding
Vincent’s angina
(trench mouth)
(acute necrotizing ulcerative gingivitis)
Oral lesion of HIV & AIDS patient
Due to oral anaerobe (prevotella)
Necrosis, tissue toss, pain, bleeding
Buccal candidiasis
**esophageal candidiasis is diagnostic for HIV**
Oral hariy leukoplakia
Large white patch on side of tongue
Cause EBV
Sign of advancing immunodef (HIV) than clinical problem

Self Limiting
Kaposi;s sarcoma
Blue/red/purple bump on hard or soft palate
AIDS related (may occur with normal CD4 count (HIV))
Associated w/ herpes simplex virus 8
Behcet’s syndrome
Collagen vascular disease recurrent painful oral ulcers
Similar lesions on penis (pain) and vagina (painless)
Idiopathic etioloty
30’s more males than females 2x
see relapsing anterior uvelitis
High risk thyroid nodule
Firm nontender nodule, fixed when palpated
Lateral mass
Assoc cervical adenopathy
“cold” radionucleide scan
solid nodule on ultrasound or xray
vocal cord paralysis

Dx: fine needle aspiration is the best test!!

4 types:
1. papillary—malignant, not aggressive
2. follicular—malignant, not aggressive
3. anaplastic—LETHAL
4. medullary—familial
Thyroglossal duct cyst
Congenital, mid line
Freely movable w/ swallowing
May also see thyroductal duct fistula Surgically removed
Brachial cleft cyst
Congenital (remnant of 1,2,3rd branchial cleft)
Appears suddenly, lateral neck mass
1. along the SCM and ext. auditory canal
2. tonsillar fossae; bifurcation of carotid artery
3. periform recess of larynx

Surgically removed
CT to determine that it’s cystic
Cystic hygroma
Benign neoplasm of lymphatic orgin
Seen in infants
Soft, illdefined, transilluminate
May cause: disfiguration and respiratory compromise if it gets big

Surgical removal but since ill defined will recur
Air filled diverticulum arising from laryngeal ventricle
Can be internal (w/t structures of larynx) or external (w/in structures of the neck)
Caused by increase intralaryngeal pressure
Lateral selling in neck
Enlarge with valsalva maneuver
Hoarsness or dyspnea if large

Risk factors: glass blowers, trumpet players
Seen on CT scan

Surgical removal
Dermoid cyst
Midline neck mass
Will not move with swallowin
Common neck mass in newborns
See swelling in parotid gland
Will get smaller as the child ages
Cervical adenitis
Due to Strep, Staph, anaerobes
Other causes also viral, fungal (see list)
Enlarged tender lymph nodes

Appropriate antibiotics
Incision and drainage if abscessed
Cervical adenitis scrofula
Caused by Mycobacterium tuberculosis
Swollen, red, nontender lymph nodes

+PPD, acid fast bacillus

antituberculous chemotherapy
Deep space neck infections
Origin: dental, pharynx, tonsil, salivary glands
Typically mixed flora (strep, staph, bacteroides,)
Fever, pain, neck swelling, trismus, dysphagia

Secure airway
CT or MRI of neck
Surgical drainage if not responding to antibiotics
(salivary stones)
CaPO4 stones forms around nidus of mucous or foreign material
SMG>parotid>sublingual (depends on length of duct)
Recurrent sweeling of gland with meals
Severe pain

Sialogram, xray, or CT pick up small stone

Tx: hydration, surgical removal or stone
Acute sialadenitis
Bacterial infection of major salivary gland
Most likely parotid gland
Staph aureus
Seen in debilitated, dehydrated patients (salivary stasis)
Pain and tender gland, homogenously enlarged
Pus in ductal orifice

Drainage of abcess
(epidemic parotitis)
Caused by mumps virus
Parotid pain and swelling
Mostly bilateral
Sensorineural hearing loss

Symptomatic treatment
Salivary gland hypertrophy
• Obesity causes fatty infiltrate into parotid gland
• Herpertyroidism
• Diabetes
• Alcoholism
• Endocrinopathies
Salivary gland atrophy
• Aging
• Malnutrition
• Gout
• Radiation therapy
Salivary gland neoplasms
• Painless mass
• Parotid>minor>SMG

• Painless mass with facial paresis
• Minor>SMG>parotid

Removal of gland
Choanal atresia
Partition b/t nasal passageway and nasopharynx (lack of opening)
90% bony (other membranous)
bilateral or unilateral
8 french catheter—pass thru nasal passage to see if it gets in throat
nasopharyngogram—dye and see if it pools in saliva
CT scan—to confirm

Bilateral—as an infant
Unilateral—wait until older
Cleft palate
Causes septum to deviate as well
Problem with regurgitation and swallowing
Note: bifid uvula due to in complete joining of tensor vali palatini

Multiple reconstructive surgeries
Nasal vestibulitis
Infection of hair follicle in nasal vestibule
Pain and swelling of nasal tip, tender
Causes: Staph (most) , Strep
*complications: cavernous sinus thrombosis b/c drainage into facial and ophthalmic veins—high mortality.

Antibiotics (oral or topical)
Drainage if abscess
Actue Rhinitis
Viral—adenovirus, rhinovirus
Irritants—smoke, dust
Bacterial—strep, staph, H. influenza, Moraxella
Exanthems—rubella, rubeola, pertussis, chicken pox

Red, swollen turbinates, clear nasal discharge, congestion

Nasopharyngitis, sinusitis, OM, pharyngitis, laryngitis, bronchitis

Viral symptomatic
Oral—sudaphedrine (sympathomimetic)—cautious with pt with heart conditions or HBP
Topical—oxymetazoline—warn pt about overuse
Antibiotics if bact. Infection
Topical nasal steroid spray for inflammation
Vasomotor rhinitis
Diagnosis of exclusion
Presents same way as acute rhinitis and allergic rhinitis
Runny stuffy nose; watery discharge, nasal congestion
Pathophysiology—inc parasymp stimulation to nasal mucosa resulting in vasodilation, edema, stuffiness
Exacerbated on by humidity, temperature, stress, irritants

Some cases, ipratropium bromide has worked
Allergic Rhinitis
Type I hyper sensitivity (IgE mediated)
Causes: inhalants, ingestants, contactants, injectants
Spikes in teenage years and still present in geriatrics
Sneezing, itching, watery discharge, nasal/ocular purities, congestion, nasal obstruction
Eyes: conjunctivits, dennie’s line, allergic shiners
Ears: otitis media with effusion, chronic otitis externa
Nose: pale blue turbinates, swollen mucosa, watery rhinnorrhea, nasal polys
Allergic salute, allergic crease
Throat—lymphatic cobble stoning, high arch palate, dumb look
Inherited problem

• nasal cytogram
PMN=acute infectious rhinitis
Eso=allergic infectious rhinitis
• allergy testing (in vivo or in vitro)

avoidance of antigen/environmental control
anti IgE antibodies (1000/month)
antihistamines (fexofenadine)
decongestants—if stuffy
mast cell stabilizer (cromolyn sodium)
nasal steroids
systemic steroids (really severe)
leukotrine inhibitors
Nasal polyps
*polys do not constrict with afrin nasal spray—helps differentiate it from turbin
pedunculated gray mass
bilateral but can be unilateral
blockage of the nose

Surgical removal if severe
After surgery, put on steroid spray to prevent
Inflammation of the mucosal lining of the sinuses
Most common health care complaint in US
Pathophysiology: sinus ostium obstruction causing  O2 so decrease ciliary function. Caused by allergic rhinitis or acute rhinitis
Other problems: infectious (staph, strep, H influ, moraxella)
Septal deviation, enlarged turbinates, neoplasm, etc)
Dx: facial pain/pressure, nasal obstruction/blockage, nasal discharge, hyposmia
Minor: headache, dental pain, ear pain
• acute up to 4 wks
• subacute 4-12 wks
• chronic >12 wks
• recurrent, acute >4 episodes/year but no symptoms in betwee

CT scan is good for diagnosis but xray too
Antibiotics—acute (4 1wk after resolution)
Decongestants (drainage)
Topical steroid (dec mucosal edema)
Mucolytics (liquefy)
Saline irrigation, moist heat
Endoscpic sinus Surgery (chronic sinusitis)
Goal: enlarge sinus opening
Complications: orbital celluitis periorbital or brain absess, meningitis, cavernous sinus thrombosis, osteomylitis
Intranasal foreign body
-unilateral nasal discharge (until proven otherwise)
-common in children
foul odor and no one wants to play with child

Deviated nasal septum
Born with or due to trauma
Usually no symptoms , but if so see nasal obstruction, headaches, recurrent sinusitis

Septoplasty—straightens up inside of nose
Septal perforation
Nasal crusting, epistaxis nose bleed , whistleing when breathing
Septoplasty, septohematoma, cauterization, granulomatous disease, cocaine, nasal steroid spray No symptoms—no treatment
Septal button
Rhinitis medicamentosa
Result from prolonged use of topical decongestants (OTC spray)
b/c or rebound, pts gets in a viscous cycle
pale congested nasal mucosa on exam

Discontinue the topical decongestant
Atrophic rhinitis
Body compensates for too little nasal resistance
Atrophy and crusting of nasal mucosa
Nasal discharge with odor may become infected (ozena)

Saline irrigations
Topical estrogen to thicken the nasal mucosa
Acne rosacea
Hyperemia of nasal tip
May lead to rhinophyma (hypertrophy of sebaceous glands) cosmetically disfiguring

Surgery for cosmetic
Inverted papilloma
Benign tumber but locally aggressive
Looks like a polyp
Bleeds easily will erode bone

Wide surgical resection
Juvenile angiofibroma
Benign tumor in the nasopharynx
Always males in 20’s
Recurrent epistaxis (severe—blood out of mouth) & nasal obstruction

Surgical resection
Worry about blood loss so preop embolization
Sinus malignancy
Most Squamous cell carcinoma
Slow growing unilateral nasal obstruction
Broadening of nose—changes in skeletal formation**
Epistaxis, pain, epiphoria (tearing), loosening of upper teeth
Xray or CT scan –see bone destruction

Surgery (remove cheek bone and eye)
Radiation follows
Poor prognosis
Nasopharyngeal malignancy
Nasal obstruction, post nasal discharge, epistaxis, pain
**unilateral OM with effusion w/o recent URI & CN involvement
posterior cervical adenopathy**
Squamous cell carcinoma

Radiation therapy
Risk factors: southern Chinese
Associated with EBV