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Flashcards in Diseases Group 3 Deck (104):

Opthalmia neonatorum

Conjunctivitis or keratoconjunctivitis occurring within first four weeks of birth.

Timing can help predict etiology.

Key organisms: N. gonorrhoeae, C. trachomatis, Staph, Strep. etc.

Treamtent: prophylactic erythromycin ointment.

Cultures and smears for diagnosis



Infection of the eyelid



Infection of the thin conjunctiva.

Symptoms: Discharge, red eye, irritation, and sensitivity to palpitation; caused by dilation and congestion of sub epithelial vessels.

DDX: Bacterial vs Viral vs Allergic (Other include Rhinoconjunctivitis, chemical reaction, meds, neoplasm, foreign body)

Bacterial: 50 to 74% bilateral, mucopurulent discharge, 32-39% acute otitis media.

Children: S. aureus, S. pneumoniae, H. influenza

Adults: S. aureus

Viral: 35% bilateral, mild watery discharge, redness, 10% acute otitis media

Neonates: HSV

Adults: Adenovirus (overall most common cause)

Allergic: Usually bilateral, discharge is rare, usually red, no otitis media, MAJOR PRURITIC

*AdenoPlus Test to test for viral vs. bacterial.



Infection of the conjunctiva and cornea



Infection of the choroid and retinal layers



Rare infection of the aqueous and vitreous humor.

Symptoms: Pain, redness, and decreased vision

Cause: Bacteria/Fungi

Exogenous - recent intraolcular eye surgery esp. cataract with agent coming from normal flora: Pseudomonas, Staph, and Candida

Endogenous - Hematogenous spread

Treatment - Fluoroquinolone



Localized inflammation often on lower lid due to bacterial growth in eyelash.

Treatment - Keep lid clean. Warm compress or massage to open gland. Erythromycin ointment.


Allergic rhinoconjunctivitis

IgE response (Hay fever)

Affects 20% of US pop.

Onset: Rarely before 2; always before 20

Dx: HISTORY! Recurrent episodes of sneezing, rhinorrhea, nasal congestion, and lacrimation. Pruritis is highly suggestive.

Testing: Skin testing (anitgen exposure) In vitro testing - radioallergosorbent testing (RAST) and enzyme linked immunosorbent testing (ELISA)

Management - Antihistamines, mast cell stabilizers, NSAIDS, avoid antigen, and glucocorticoid


Viral conjunctivitis

Neonatal - HSV

Post natal - Adenovirus (most common) Coxsackie, HSV, VZV (pain before redness), EBV, rubella, mumps, influenze


Acute bacterial conjunctivitis


Children - Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae

Adults - Staphylococcus aureus

Self-limited, but decreased morbidity and transmission with treatment. Empiric w/ gram pos and negative coverage. Trimethoprim and polymixin opthalmic drops (Polytrim) or more expensive moxifloxacin drops


Hyperacute bacterial conjunctivitis

Causative agent: Neisseria gonorrhea

Symptoms: Copious yellow-green discharge (purulent), preauricular adenopathy

Gram negative intracellular diplococci that grows on chocolate agar.

Treat promptly with systemic ceftriaxone.


Chylmydia trachomatis

Inclusion conjunctivitis (serogroups D-K)

Trachoma (serotypes A-C) leading cause of blindness worldwide due to multiple infections since no long lasting immunity

Treatment - Azithromycin and improve hygeine; treat sexual partner. (widespread prophylaxis is being used to try to eliminate Trachoma by 2020.


HSV - 1 keratoconjunctivitis

Similar presentation to adenovirus although lesions can be painful especially if scarring of the cornea occurs and often only one eye.

Avoid corticosteroids since can facilitate corneal penetration.

If corneal involvement treat with trifluridine and systemic acyclovir. Consider prophylactic treatment with erythromycin to prevent bacterial superinfection.



Symptoms: Vison defects, photophobia, pain, and foreign body sensation

Risk factors: trauma, drying of epithelia, and hypoxia increase susceptibilty

Causative agents: HSV-1, S. aureus and epidermidis, P. aeriginosa, and Bacillus cereus, Acanthamoeba

Treatment - Moxifloxacin eye drops for bacteria; Acyclovir and trifluridine for HSV-1



Inflammation of uveal tract can lead to blurred vision and permanent vision loss.

Iritis (anterior uveitis) - often not infectious, photophobia, pain, and decreased visual acuity. Caused by Treponema pallidum, HSV, and VZA

Chorioretinitis (posterior uveitis) - most common, floaters, no pain.



Symptoms - blurred vision and visual field defects

Pathophysiology: Blood borne route via retinal arteries, frequently manifestation of systemic disease

Congenital - Toxoplasma and CMV are most common (HIV +)

Two parasitic worm infections (Toxocara canis and Onchocerca volvulus) cause eye infx



Most common parasitic disease, late term congenital infections are more likely to produce progressive blindness, diagnose with IgM serology

Treatment: Pyrimethamine (blocks DHFR) and sulfadiazine (blocks pteridine synthetase)


Cauliflower Ear

shearing forces applied to anterior auricle which separates from underlying cartilage. Tears auricular blood vessels creating a hematoma and then stimulates new cartilage growth


Conductive Hearing Loss

increase in hearing thresholds due to decrease in sound transmission through external and/or middle ears. Air conduction is reduced but bone transmission is unaffected.

Positive Rinne and Weber lateralizes to affected ear.

Main causes: Otitis media, otosclerosis, ruptured TM



Pathophys: abnormal growth of bone in middle ear causing immobilization of stapes

Initially causes increase in stiffness (low freq) rapidly results in increased mass (high freq)

 Bone growth can occur into cochlea  sensorineural hearing loss

 Common cause of bilateral, gradual hearing loss in adults (60-70% hereditary, females>males, Caucasians)

 Low freq sounds affected first  high freq almost always affected by time pt seeks tx

Treatment: Stapedectomy or hearing aids. Fluoride prevents.


Otitis media

Acute middle ear space infection. Tubes often blocked. fluid, inflammation under TM

Most or Second most common reason that children visit MD

Risk factors: Day care attendence, smoke exposure, bottle feeding (lack of maternal Anitibodies)

Common etiologic agents: Strep pneumo 25-50%, Haem infl. 15-30%, Moraxella catarrhalis 3-20%, Viral (RSV, rhinovirus) 5-22%, No pathogen identified

May cause tympanic membrane rupture

Sx: Otalgia, Aural fullness, hearing loss, tinnitus. Hearing loss temporary which can cause significant impact on speech development for kids.

Tubes are shorter and less slanted in children

Low freq sounds (speech) affected first – threshold elevations

High freq sounds not affected until mass of middle ear bones is increased --> both low and high frequency sounds are reduced = conductive hearing loss

Complications: Perforated TM, Acute mastoiditis, Abcess, labyrinthe fistula, facial nerve paralysis, meningitis, and more


Choanal atresia

Improper opening of choanae due to failure of apoptosis of oronasal membrane.

"My newborn is having difficulty breathing and can't breastfeed."

"My daughter's nose is always running; she cannot breathe through it."


Anterior lip and palate defects

Due to the failure of fusion of maxillary prominences with the fused medial nasal prominences.

Involve upper lip, alveolar part of maxilla, and primary palate.

1 in 1000 births and 60-80% males increasing with increasing maternal age.


Posterior palate defects

Due to failure of fusion of the palatine shelves with one another with the nasal septum and with the posterior margin of the primary palate.

Involves hard and soft palate (secondary palate)

1 in 2500 births and 2x as common in girls. No link with maternal age

Wide variation: all of hard and soft palate, only soft palate, only uvula (bifid uvula); unilateral or bilateral


Fetal Alcohol Syndrome (FAS)

Characteristic facial features. (Many FAS don't show facial features) Classic signs are flat face, small palpebral fissures, small jaws

Majority of features are neurological.

Only 4-6% show physical signs.


Congenital coloboma

Defective closure of the choroid or optic fissure.

It is positioned in the infero-nasal quadrant, relective of the location of the optic fissure during fetal development


Detached retina

Failure of retinal layers to fuse and obliterate intraretinal space between neural retinal layer and retinal pigmented epithelium.

Presents as sudden partial vision loss in one eye. Painless, progressive, and often floaters.

Can occur congenitally (linked with Marfans and Down Syndrome), or later in life secondary to trauma or type II DM. Linked with myopia.

Surgical emergency = lasar demarcation of retinal tear, or scleral buckling procedure.


Congenital cataracts

Lens becomes opaque during intrauterine life.

Rubella infx of mom at 4-9 months
Chromosomal abnormalities


Perilymphatic fistula

Rupture of bony labyrinth causing CSF to flow through the cochlear aqueduct.


Benign Paroxysmal Positional Vertigo

Most common cause of vertigo. Caused by otoconia displacement from utricle into semicircular canal post trauma/ viral infx.

Symptoms are recurrent brief vertigo and ipsilateral nystagmus.

Normal Hearing

Diagnosed via Dix-Hallpike maneuver and treated with epley maneuver to move otoconia back into semicircular canal.



Inflammation of inner ear, usually viral cause (1-2 weeks after flu or otitis media) that spreads through round or oval window.

Symptoms: Sudden vertigo and sometimes temporary hearing loss/ tinnitus.

Rx: IV antibiotics, symptomatic control --> antiemetics for nausea and vomitting.


Sensorineuronal hearing loss

Increase in thresholds and/or loss of ability to transduce specific freq. due to damage to cochlea, auditory nerve, or cochlear nucleus.

More commonly due to hair cell damage due to noise (brief high sounds most potential to damage, but all are important)

Exposure/toxic drugs (aminoglycosides cause sterocilia damage and furosemide blocks NKCC in stria vascularis)

Genetic problems w/ endolymph changes possible too (commonly due to connexin genes regualting gap junctions)

Weber lateralizes to normal ear. Normal or absent rinne.


Central Auditory Processing Disorder

Defeciency in central processing of auditory stimuli resulting in "cocktail party effect" in which a patient can't filter out extra noise.

Generally old patients and will have normal audiograms when in isolated examination room.

Hearing aids often compound problem.



PERCEPTION of sound when no external stimulus is present. "ringing in the ears"

Very common and can be debilitating.

Cause may be central or peripheal (likely multiple types)

Worsened by loud noises, alcohol, nicotine, caffeine, and many medications (NSAIDS, Antibiotics, and more)

Many treatments



Loss of hearing that occurs gradually as people age. Affects 1/3 of people over 65.

Can be sensorineuronal, CAPD, or tinnitus

Both peripheral and central causes.



Calcium plaques from old old ear infx, perforation of drum, or tubes/surgery


Serous otitis media

negative pressure, clear fluid due to eustachian tube obstruction.

Symptoms: bubbles behind TM, do tympanogram if you can't see fluid (expect flat line result)

Tx: Time/Tubes


Eustachian tube dysfunction

Leads to negatve pressure and eventual erosion of ossicles. More concave TM w/ obvious bony landmarks.

Tx: decongestants, plug nose and blow out to open tube. . Tubes if chronic.



Skin cyst caused by long standing retraction pocket of eardrum into the middle ear. Cyst slowly erodes bone and can eventually cause facial paralysis, hearing loss, dizziness, and eventually erode into brain cavity

Tx: Mastoid operation.


Ear drum perforation

Not uncommon. Caused by Q-tip, loud noise, severe otitis media, or post tubes)

Tx: generally heal, sometimes tympanoplasty needed.



Blood in middle ear, generally post trauma. Order CT.



"The Goal is Control"

Most common causes: Disruption of nasal mucosa, facial trauma, scars, intranasal medications/ recreational drugs, hypertension and/or arteriosclerosis, and anticoagulant meds (High INR)

Most common areas are Kiesselbach's plexus on anterior septum (ethmoidal arteries) or Woodruff's plexus in posterior septum (sphenopalatine artery)

Treatment: 1.) local pressure 2.) Silver nitrate cautery 3.)Absorbable hemostat 4.) Pack or Rhinorocket (antibiotics for TSS) for

*Posterior epistaxis may need foley placement


External Ear Malformation

Failure of first cleft to invaginate.

Part of several syndromes: first arch syndromes, chromosomal abnormalities.

Present as:
-Auricular appendages/tags from excess hillock mesenchyme
-Auricular cysts (fistulas) from incomplete fusion of hillocks
-Microtia: abnormal shape or size of the ear which varies in severity. Can be unilateral or bilateral.
-Anotia: agenesis, inner ear may be normal and individual may have normal hearing.


Congenital Neurosensory deafness:

Neurosensory deafness:
- abnormal development of cochlea, cranial nerve VIII, or brain stem
-Rubella in first trimester can have defects in organ of Corti in 30% of cases
-Neural Crest defect: migratory melanocytes from NC don't properly form stria vascularis


Congenital conduction deafness:

-Persistence of meatal plug (seen in first arch syndrome)
-Fixation of footplate of stapes
-Abnormalities of malleus and incus often involved in first arch syndrome



Arrested development of optic vesicle; globe is small, lens does not form



Arrested development of optic vesicle early in 4th week, usually accompanies severe craniocerebral defects.


Congenital glaucoma

Cloudy cornea from abnormally high intraocular pressure, usually from malformed drainage apparatus.

Genetic abnormalities account for 85% of cases and Rubella for rest

Cupping of eye exam.


Persistent hyaloid artery or pupillary membrane

failure of either structure to completely dissolve during development.

Hyaloid artery: normal regression around 11 weeks and is complete by 8 months. Generally little or no visual defect if persists

Pupillary membrane: may interfere with visual acuity


CHARGE syndrome

Coloboma, heart defects, atresia of choanae, retarded growth/development, genital hypoplasia, ear abnormalities


Congenital Ptosis

Does not affect vision and correctable via surgery by tightening LPS

Autosomal dominant trait

Can result from birth trauma, myasthenia gravis, abnormal CN III development, or dysgenesis of LPS


Nasolacrimal groove atresia

Results in canalization failure, infection is common, and newborn may have constant tearing/mucuous drainage, and subsequent chapping of periocular skin


Macular degeneration

Degeneration of RPE leading to blurry vision and loss of central vision first


Vitamin A defeciency

Night blindness due to loss of 11-Cis-Retinal


Marcus Gunn pupil or relative afferent pupillary defect (RAPD)

Monocular defect in cranial nerve 2 afferent for pupillary response. No consensual or ipsilateral pupillary constriction on affected eye, but consensual and ipsilateral reaction when testing normal eye.


Argyll Robertson pupils

bilateral small pupils that reduce in size when the patient focuses on a near object (they “accommodate”), but do not constrict when exposed to bright light (they do not “react” to light). They are a highly specific sign of neurosyphilis, and might also be a sign of diabetic neuropathy


Temporal Bone Fracture (hearing loss)

Post trauma

Ssx: Headache, vertigo, SNHL, CHL, facial nerve paralysis, CSF leak

RX: CT --> Neurosurgical


Acoustic Neuroma

Ssx: asymmetric SNHL, vertigo, facial nerve paralysis, aural fullness, trigeminal numbness, diplopia

Dx: MRI of IACs w/ contrast

Rx: Observation vs. Surgery vs Radiation



Illusion of movement. Commonly epidsodic



Sense of poor coordination with erect posture or movement, usually continuous



Implies orthapedic or neuro problem



All-encompassing term (i.e. light-headed, orthostatic, hypoglycemic, inability to concentrate)


Meniere's Disease

Ssx: Fluctuating SNHL, Tinnitus, Episodic vertigo (min-hr), often totally asymptomatic between spells.

Rx: R/O stroke, tumor, infx, trauma, hypothyroid. Salt restriction.

Ppy: believed to be inflammatory


Vestibular Neuronits

Ppy: viral infection of the vestibular nerve

SSx: Vertigo lasts hours to days w/o hearing loss

May last weeks to months and preceded by URI

Rx: Meclizine, benzos, antiemetics



Grade I: Ear is slightly smaller than normal; surgery not needed

Grade II: Auricle is half sized; surgery is sometimes beneficial

Grade III: Small cartilage present; surgical repair at age 5-6.


Lop Ear

Most common external abnormality.

Absence of antihelical fold.

Cosmetic surgery offered


Preauricular pits and fistulas

Frequently infected pits in front of ear

Rx with antibiotics and incision and drainage.

Frequently bilateral


Auricular appendages

Ppy: Arrested development of fusion of the Hillocks of His. Growth that contains cartilage and skin.

Rx: Elective excision

Note: facial nerve is quite superficial in infants and toddlers.


Relapsing Polychondritis

Autoimmune disease of external ear that is episodic and inflammatory.

Dx: elevated ESR and IgG

Rx: Steroids and NSAIDS

DDx: between cellulitis


Nodularis Chornicus Helicus

Very painful benign growth on helix of old patients.

Rx: Excisional biopsy


Keloids of the ear

Avoid piercing.

Early Rx: Steroids

Late Rx: Excision


Auricular Hematoma

Caused by trauma.

Rx: Incison, drainage, and BOLSTER; if untreated results in cauliflower


Cellulitis of the pinna

Key organisms: Staph, Strep, Psuedomonas



Benigh projections in canal that is more common in norweigians. Linked to cold water exposure.

Surgical removal is rarely indicated

Looks like cholesteatoma


Carcinoma of Ear Canal

Painful, bleeding, soft tissue mass in canal. Needs Biopsy.

Rx: Excision and radiation. Can metastasize and kill.


Otitis externa

Sx: Very painful red swollen canal with purulence. Painful to rotate or palpitate external ear.

Risk factors: swimmers, Q tip users, diabetics, immunocompromised.

Rx: AB drops and systemic ABs w/ topical suctioning and debridement (sever cases)

Causative agents: Pseudomonas, E coli, Staph corynebacter. Also Candida and other fungal

Hearing may be affected.


Herpes Zoster Oticus

Sx: purulent ulcers in and around ear, decresed hearing, SEVERE pain, Facial nerve paralysis

Rx: Antiviral and pain relief

Risk factor: immunocompromised


Otorrhea (Ear drainage)

Ddx: Otitis media, otitis externa, allergy, trauma, CSF leak

Dx: culture, GM stain, beta 2 transferrin for CSF


Ear canal stenosis

Can be congenital or secondary to trauma and infx. Small amt of cerumen clogs ear.

Rx: canalplasty



Sx: itching painful ear drainage w/ decreased hearing. Secondary to antibiotic rx.

Rx: Antifungal drops, pills, pain relief, debridement


TM perforation

Ppy: Secondary to Otitis media, trauma, slag burns, indwelling PE tubes, etc.

Rx: keep ear dry and consider tympanoplasty in severe or persistent cases. Often heal on own.


Bullous myringitis

Inflamed TM w/ serous bullae. Associated w/ virus of mycoplasma post URI.

Sx: otalgia, otorrhea, hearing loss

Rx: analgesia, ABs, decompression of vesicle, steroids


Dermoid Cyst

Cysts consist of squamous cell epithelium containing epidermal appendages.

Several possible locations: fronto-temporal region, orbital region, or nasoglabellar region.


Naso Encepahlocele

Extracranial protrusions of meninges, CSF fluid, and neural tissue.

Meningoceles present similarly w/o herniation of brain tissue.

Dx: CT scan

(Looks like Jhonny!)


Nasal Glioma

Congenital neoplasm on the nose. Varying theories on origin.


Nonallergic Rhinitis

Rhinitis caused by virus, occupational exposures, abuse of antihistamines, and more.


Sinusitis (Rhinosinusitis)

Complex group of disorders with inflammation as the major universal finding

Affects almost 15% of US pop.

Ppy: Bacterial: S. aureus, M Cat, H Influ --> biofilms
Fungi, Allergic

Dx: Head CT (gold standard) to visualize paranasal sinuses. Nasal endoscopy


Chronic Sinusitis

Inflammatory not infectious sinusitis. Treatment = nasal saline lavage.


Hoarse Voice

Many causes. The big ones that we can control are smoking, drinking, DM, GERD, and overuse.

Other rarer causes such as tumors that can be ruled out via scoping.



Opacity of the normally clear lens caused by age, metabolic disorder (hyperglycemia, hypergalactosemia etc.), trauma, or hereditary. Generally painless and bilateral.

Indications for surgery: severity of visual loss, functional needs of patients, need to improve view of posterior eye to care for occular pathology

Risk factors: age, smoking, EtOH, sunlight, DM, classic galactosemia, galactokinase deficiency, trauma, infx.

Rx: Cataract surgery and lens replacement


Dry Macular Degeneration

Degeneration of macula. Causes central vision loss (scotomas) that is slow, due to fat deposits and causes gradual decrease in vision.

Age Related if after 50; usually over 70

Eye exam = Drusen around macula and atrophy of retina

Rx: quit smoking, nutritional recommendations, AREDS (antioxidants and zinc in high levels) supplements, manage systemic diseases


Wet (exudative) Macular Degeneration

Defects in deep retinal layers. Degeneration of macula. Causes central vision loss (scotomas) that is rapid due to neovascularization, edema, and hemorrhage.

Eye exam = neovascularization, edema, hemorrhage, and eventual scarring and vision loss.

Age Related if after 50; usually over 70

Rx: quit smoking, nutritional recommendations, AREDS (High amounts of zinc and antioxidants) supplements, manage systemic diseases. And conventional laser, photodynamic therapy, anti-vegf drugs.


Open Angle Glaucoma

Increased ocular pressure causes optic nerve loss. Can be multifactorial. Caused by obstructed outflow (i.e. canal of schlemm) Painless with slow onset.

More common over age 40

Risk factors: Age, African American, and myopia

Treatment: Decrease production, increase outflow. Beta blockers, acetazolamide, prostaglandin analogs, topical cholinergic agonists, and topical alpha agonists and irodotomy surgery putting hole in iris.

Eye exam: Monitor cupping and cupping ratio. 0.3 is the normal average (varies greatly between patients so progression is more important than numbers)


Closed Angle Glaucoma

Increased ocular pressure causes optic nerve loss. Can be multifactorial. Obstruction of flow between iris and lens leading to pressure buildup behind iris.

Symptoms: Red eye, +/- nausea, very painful, decreased vision, rock-hard eye (touch it!) frontal headache.

Opthalmologic emergency! Give pilocarpine, acetazolomide, oral glycerine or isosorbide. Get to optho ASAP for laser iridotomy.


Nonproliferative diabetic retinopathy (NPDR)

PPY: Diabetic induced vascular damage leading to neovascularization and other symptoms below.

Eye exam: Blot hemorrhages, Cotton wool spots, microaneurysms, macular edema, hard exudates.

Prevention by controlling blood sugars (use this as a motivator! Also can reverse minor retinopathy w/ sugar control. Steroid injection can be short term fix as well.

Treat early and aggressively!


Proliferative Diabetic Retinopathy (PDR)

PPY: Diabetic induced vascular damage leading to neovascularization and other symptoms below.

Eye exam: Neovascular vitreoretinopathy with vietrous hemorrhage.

Prevention by controlling blood sugars (use this as a motivator! Also can reverse minor retinopathy w/ sugar control. Steroid injection can be short term fix as well.

Treat early and aggressively!

Treatment: Panretinal Photocoagulation


Hypertensive Retinopathy

Ppy: Narrowing and sclerosis of arterioles (sliver wired arterioles on eye exam) leading to flame hemorrhages within retina, cotton wool spots, and optic nerve edema

Rx: Treat blood pressure! If significant occlusions and ischemia can use panretinal photocoagulation (PRP)


Amuaurosis Fugax

Sudden loss of vision in one eye that lasts only minutes. Painless.

Generally due to vascular insufficiency, so cardiac workup before optho work up.


Retinal Cholesterol Emboli

Non occlusive emboli seen in occular vessels that is a warning sign of future disaster in vascular system.

Workup with carotid ultrasound and echocardiogram.


Opthalmic Migraine

Scintillating scotoma is hallmark (visual aura)

Symptoms: painless and temporary, involves both eyes causing temporary hemianopsia. Time is key =20-30 min.

Etiology: spasm of arteriole in occiptial cortex



Retinal Arterial Occlusion

Sx: sudden severe loss of vision in one eye. Painless. Usually permanent unless caught quick!

CHERRY RED SPOT on eye exam with pale retina.

Treatment protocol: rebreathing CO2, Timolol, IV acetazolamide, massaging globe, refer to optho!


Retinal Vein Occlusion

Central (CRVO), or Branch (BRVO) Symptoms are SQUASHED TOMATO on eye exam.

Risk factors: HTN, DM


Temporal Arteritis (Giant Cell Arteritis)

Sx: Headache and extreme scalp tenderness. Fever, weight loss, jaw claudication, polymyalgia rheumatica. Vision loss secondary to inflammatory vaso-occlusion.

Vision loss can be severe involving one or both eyes. Often permanent.

Dx: STAT ESR and CRP. Biopsy of artery.

Rx: Start high dose steroids IMMEDIATELY.
Pale and swollen optic nerve (acutely ischemic)


Visual CVA

Sudden painles loss of vision causing bilateral hemianopsia. Usually involves occipital cortex.