Sebaceous Cell Carcinoma

Cardinal Signs:

- Eyelash involvement: madorosis, poliosis, thick red lid margin inflammation

- Lid adenopathy common

Poor Px:

- Sx > 6 months

- size > 2mm

- poor differentiation

- local vascular or lymphatic inflitration

Squamous Cell Carcinoma

• second most common eyelid tumor BUT 40-50x less common than BCC
• usually on lower lid with margin involvment
• FASTER GROWTH THAN BCC
• Px varies depending on tumor size, degree of differentiation, underlying etiology, and dept of tumor invastion

Basal cell carcinoma

• older adults with male predilection
• lower lid usually but can appear subsequently on upper lid
• locally invasive but rarely metastatic

Keatoacanthoma

• found in sun exposed areas with a central ulcerated, keratin killed crater and hyperkeratotic margins
• older adults

Ceftriaxone; Cephalosporin family

Dosage:

If cornea is involved: 1g IV q12-24hrs (duration of tx depends on clinical response (3-5days usually)

If cornea is NOT involved, 1g IM

Mucocutaneous lymph node syndrome

• children < 5 yo
• Japanese more common
• Dx based on 5/6 criteria

1. fever (> 5 days)
2. bilateral conjunctivitis
3. strawberry tongue (oral mucosal changes)
4. peripheral extremity changes (edemia, erythema)
5. cervial lymphadenopathy

F.  Non granulomatous uveitis

"Fat old crone skipping down a cobblestone road"

• SKIP lesions in GI tract with rectal sparing
• ulcers and fistulas, COBBLESTONE mucosa
• wall thinkening
• infectioous

1) Crohn's Disease

2) Ulverative Collitis

Ulcerative Colitis

• Colon = RECTAL INVOLVEMENT
• granulomatous uveitis
• pseudopolyps abscess and ulcers
• mucosal inflammation, colorectal carcinomas, stenosis, toxic megacolon

d/t failure of coppor to enter circulation in form of ceuloplasmin 

Kayser-Fleisher Ring

Signs: tremor of wrise, basal ganglia degene, cirrhosis, corneal deposits, carcinoma, dementia

Tx: Pencillamine (Cuprimine): chelating agent that binds Cu.  Many SE (OMG, pemphigoid, optic neuritis)

inflammation of gall bladder lining d/t cholesterol stones

Fat, Fertile Females over Forty

(+) Murphy's sign = pain on inspiration when the examiner's finger are placed under the rgiht costal region  next to the rectus abdominalis.  Think: "Black Swan"

Cholingergic Antagonist used as a muscle relaxant prior to SX

CONTRAINDICATED in intraocular SX d/t rapid increase in IOP and expulsion of intraocular contents

1) Polymyxin: not used along because very limited activity.  Gram (-) coverage only; affects cells MEMBRANE

2) Neomycin: toxic to ocular surface? affects PROTEIN SYNTHESIS

VANCOMYCIN

Red Man Syndrome is a reaction to the drug vancomycin. Patients typically develop symptoms within 5 or 10 minutes of receiving the drug, and they experience itching and flushing of the face, neck, & torso. They may also experience swelling of the lips, face, or eyes and/or a drop in blood pressure, but this is less frequent. Red Man Syndrome is not a true allergy, even though the symptoms look similar to an allergic reaction. 

When signs of red man syndrome appear, the first step is often to stop the vancomycin infusion. Some patients may receive antihistamine medications before the drug is restarted. It is common practice to infuse the vancomycin at a slower rate thereafter. If the drug is given again, Red Man Syndrome can usually be avoided by pre-treating the patient with antipyretic and antihistamine medications (like acetaminophen and diphenhydramine) and infusing the drug at the slower rate.

Choloramphenicol

• works on 50S subunit in protein synthesis
• rarely Rx'd d/t S/E: irreversible aplastic anemia, optic neuritis, Grey Baby Syndrome

Which drugs are safe during a pregnancy?

Which drugs are harmful? <-- These drugs are also the main BROAD spectrum drugs

Which drugs can you eat on an empty stomach?

" You never say FAT to a pregnant woman because they are just PACking a baby." 

" You PAT an empty stomach"

 Safe drugs (PAC)

- Penicillin

- Azithromycin/Erythromycin

- Cephalosporins

Harmful drugs (FAT)

- Flouroquinolone

- Aminoglycosides

- Tetracyclin

Drugs on Empty stomach (PAT)

-  Penicillin

- Azithromycin

- Tetracycline

Which two drugs are given in IV form for an orbital cellulitis?

Naficillin; Penicillin family; penicillase resistant

Ceftriaxone: Cephalosporin; IV x 1 week

Combo Drugs

What are the components of these drugs?

1) Polytrim

2) Polysporin

3) Neosporin

4) Tobradex

1) Polytrim: Polymixin B (cell membrane) and Trimethroprim (folate metabolism)

2) Polysporin: Polymixin B (cell membrane) and Neosporin (30S Protein Synthesis--> Aminoglycoside)

3) Neosporin: Neomycin (30S protein synthesis-->aminoglycosides) , Gramicidin (cell membrane), Polymixin B

4) TobraDex: Tobramycin (30S--> aminoglycosides) + Dexamethasone 0.1% 

1) As Cephalosporins go from 1st --> 4th generation, it starts with more gram (+/-) coverage to more gram (+/-) coverage

2) As FQ go from 1st --> 4th generation, it starts with more gram (+/-) coverage to more gram (+/-) coverage

1) (+) --> (-)

2) (-) --> (+)

Prescribing Tetracyclines for...

1) Meibomianitis

2) Acne Rosacea

3) Chlamydia Conjunctivitis

4) RCE

1) Meibomianitis: Doxycycline 100 mg PO bid x 1 month, then taper to qd x 3-6 mo

2) Acne Rosacea: Doxy 100mg PO BID (x until sx are relieved), then taper 100mg PO qd x several weeks after.  Long term tx: Periostat (20mg Doxy) tablet po qd

3) Chlamydia Conjunctivitis: Doxy 100mg PO bid x 10days 

OR

1g Zpack (Azithromycin) but this question doesn't warrant this answer

4) RCE: Doxy 50 mg bid x 2 months

Tx choice #1:

• 1 gtt Viroptic opth soln 9x/day (q2hr) until leasion heals (usually 5-7days), then taper to 5x/day x 5-7 days

FAV

Famcyclovir: 250mg TID x 7 days

Acyvlovir: 400mg 5x/day x 7 days

Valacyclovir: 500mg TID x 7 days

Prophylactically

F: 125 mg bid

A: 400mg bid

V: 250mg bid

** all BID and 1/2 dosage of acute HSV, except for Acyclovir which is same dosage

1) Sulfonylureas: Glipizide (Glucotrol), Glyburide (Diabeta, Micronase), Chloropropamide (Diabenase), Tolbutamide (orinase)

-- increase secretion of insulin by beta cells, decrease glucagon release, increase sensitivity to insulin

2) Biguanides: Metoformin (glucophage): decreases liver glucose production, increases glucose uptake

3) The Zones: Thiazolidendiones (all end in -zones)

4) Juanuvia (commercials)

whorl keratopathy (corneal verticillata): inevitable at 400mg/day

ASC lens deposits: >600mg/day after 6 mo of tx (in 50% of cases)

Mucomyst 10-20% = Acetylceysteine 

What are the indications of this drug ophthalmically, even though this is a respiratory drug?

severe DES, especially when filametns are present

also Tx for corneal burns

inhibits T-cell ativation by stopping hte production of interleuki-2

Dosage: q12hrs or BID

S/E: stinging upon instillation

1) Bromocriptine (Parlodel) : also for Parkinsons and prolactic secreting pituitary adenoma

2) Immunosuppressive agents: Cyclosporine (Sandi-immune), Azathiprine (Imuran)

How to tx these following dz's with systemic steroids

1. Scleritis

2. GCA

3. Toxoplasmosis

4. Thyroid eye dz (optic neuropathy)

1. 60-100mg qd x 1 week, then taper to 20mg qd x 2-3wks

2, IV methylprednisolone x 3 days, then PO 800-1000 qd x 2-4 wks until sx resolve or ESR normal

3. 20-40mg qd - initiated 24-48 hrs after starting Ab therapy

4. 100mg qd x 2-14 days

uthoff's sign

vision worse when body temperature raises

ddx - MS, congestive heart failure, pulmonary problems

1. Lid fatigue - have pt look upwards and fixate a target held in your hand. If your hand gets tired before they do, the test is negative. Impt  not to have pt blink, therefore administer a drop of proparicane prior to the test

2. Pseudo lid retraction - the other eye may look retracted d/t retrievable of equal innervation. Manually close the ptotic eye and see if the retracted eye comes done

3. Orbicularis weakness

4. Sleep test - for 30 mins

5. Ice pack test  - cold temperatures inhibit the action of AchE, therefore increasing Ach --> less pitied

1. Tensilon test  in adults, Prostigmine in kids

2. Blood tests

• AchR for MG dx
• TSH to rule out autoimmune thyroid dz

ANA to rule out autoimmune dz such as RA

3. Mediastinal imaging bc 23% have thymomas

4. Electrophysiologic testing

kids -think neoplasm

30 yo - MS

elderly - CVA

GUNN'S SIGN

stare appearance found in graves disease

think: "It is not kosher to stare at people"

both discrete and confluent white to yellow dots

stationary night blindness

contracted visual field

markedly reduced ERG

1. Best disease

2. Pattern dystrophy

egg yolk or glial scar, central scotoma, rpe changes c Neovascular changes

abn EOG, normal ERG

CONE DYSTROPHY

CONE ROD DYSTROPHY

TAMOXIFEN TOXICITY

CHLOROQUINE

HYDROXYCHLOROQUINE

You injected Tensilon into a patient's arm and they experience SLUD. You immediately think of administering this in office drug to help counter the effects of this drug.

The patient later arrives at the hospital in which they will administer which IV drug?

percentages of MG pts with...

1. a thymoma

2. Thyroid disease

3. Initially presenting with OMG

4. Presenting with OMG at some point in their lives

1. 10

2. 5

3. 75

4. 90

Think: disc at risk (very small) c buried drusen

- Nerves that are very small

- anomolous vascular branching patterns c multiple bifurcations and trifurcations

- Drusen may be a result of this small nerve.  This occurs d/t the prelaminar stasis of axoplasmic flow that results from crowding of axons as they pass through the narrowed scleral canal

- Drusen laetr makes the nerve look lumpy bumpy, which further confuses the clinician from TRUE papilledema

MAJOR DISTINGUISHING FACTOR for ONH Drusen and Papilledema = Autofluressence and B scan U/S.  Drusen will Autoflluress, show calcific changes in B scan ultrasound

Also Pseudopapilledema has...

1) swelling in the middle of the nerve (True Papilledema is swelling around the borders of the nerve)

2) large disc vessels arise from a central cone and there is little to no physiologic cups.  Multiple trifurcations and bifurcations, but no real changes in microvasculature

3) (+) SVP intact

4) no flame hemes around the disc

5) Familial trait...family members will have similar looking nerves

• subnormal # of axons in the ON
• Disc: smaller disc, Peripapillary halo, Double ring sign (inner ring: where ON head, Outer ring: where RPE ends)
• VA range from normal to severe
• VF can be anything
• CV: deficient
• Nystagmus (not always)
• Midline defects (absence of corpus collosum, septum pelludcidum, poorly developed nose bridge
• Fetal Alcohol Syndrome

Morning Glory Syndrome

What condition is associated with it?

• Unilateral, Dysplastic disc that resembles the morning glory flower
• characterized by an excated funnel shape, spoke like vessels
• elevated chorioreitnal pigmentary disturbance

Tilted Discs

- Characteristics

- It's VF defect mimics which disease process? 

Characteristics:

• oval shape, situs inversus, scleral crescent (usually IT or IN)
• high myopic oblique astigmatism
• causes amblyopia with guarded Px

T or F: 

Vascular lesions respect the midline of a VF

Compressive lesions can involve both sides of a VF

Chiasmal Syndrome

Si/Sx

Sx: unilateral, asymmetric, or bilateral painless, progressive vision loss, HA (due to stretching of the diagphrama sella), and DIPL (if involvement of the cranial nerves)

Si: VF defect, Optic atrophy, APD, CV defect, Endocrine Dysfunction

Band pallor, diffuse palor

Chiasmal Syndrome

Etiology

Name the 4 most common types of Neoplasms as well as the other causes

1. Neoplasms:

• Pituaitary Adenoma
• Most common 10% of all chiasmal; can be hormone secreting and non-hormone secreting, attacks chiasm from below
• Craniopharygioma: attacks chiasm from above, benign, but can cause papilledema
• Glioma: most impt infiltrative tumor in kids
• Meningioma: looks like a pitutitary adenoma but with a less hyperintense signal

- MOST SEVERE HA ever

- subarachnoid hemorrhage

- DIPL

- poor thermal regulation d/t disruptions in cortisol levels

- EXTREME MEDICAL EMERGENCY

- enlarging pituitary gland becomes necrotic --> internal hemorrhage with rapid expansion of tumor 

- mechanism: the gland becomes strangulated by the diaphragma sella --> chokes off blood supply --> necrosis --> hemorrhage --> rapid expansion of tumor

1. Smallest of all cranial nerves

2. Only cranial nerve to decussate dorsally from the brainstem

3. Longest  intracranial course

4. Only nerve to completely decussate

Pt c/o DIPL greater while reading.  

Pupils: No consensual or direct response.  (-) Anisocoria.  Near response intact.  Eyelids are retracted

Motilities: Vertical Gaze Palsy, Convergence Retraction Nystagmus

Ant seg: unremarkable

Post Seg: Papilledema

What does this pt have? What should you r/o?

Dorsal Midbrain Syndrome (this is a CN IV palsy!)

R/O:

Pineal gland tumor (Neuroimage)

Tentorial Meningioma (Neuroimage)

DM, HTN for vasculopathic age group (CBC/ESR)

• definition: any neuro-ophthalmic presentation that involves more than one structure contained within the cavernous sinus
• Cavernous Sinus: located lateral to the sella turcica.  It is a blood filled channel that completely surround intracvernous portions of the cranial nerves and the cartoid artery
• Structures involved: ICA, CN III, IV, VI, V-1, Oculosympaththeics

multiple cranial nerve pareses (CN 3, 4, V1, V2, 6, and sympathetic involvement (may have Horner's syndrome)

1. Aneurysm (rare because fortunately as aneurysm expalns, it is surrounded by the tough, dural walls of the sinus which prevents rupture)

2. Carotid Cavernous Fistula - see next slide

3. Neoplasm

4. Infection

5. Inflammation

• multiple cranial nerve pareses (CN 3, 4, V1, V2, 6, and sympathetic involvement (may have Horner's syndrome)
• d/t rupture of ICA or one of its branches within the cavernous sinus
• think: trauma or rupture of a pre-existing aneurysm
• Result: arterial blood from a high pressure source empties into a low pressure venous structure --> extends into superior and inferior ophthalmic veins --> congestion of orbit --> pulsating proptosis, chemosis, epibulbar injection, and vascular tortuosity, increased IOP
• PULSATING PROPTOSIS, AUIDBLE BRUIT = HIGH FLOW FISTULA

In medicine, a fistula (pl. fistulas or fistulae) is an abnormal^[1] connection or passageway between two epithelium-lined organs or vessels that normally do not connected

high pressure arterial blood is emptying into the low pressure system --> causes retrograde flow

most impt cause of cavernous sinus inflammation

• granulomatous, idiopathic, PAINFUL ophthalmoplegia that results from dramage to the cranial nerves by the granulomatous inflammation
• optic nerve can be compromised when the process occurs at the orbial apex
• ptosis (d/t CN III involvement)
• no proptosis because no pressure on CS like in carotid cavernous sinus fistula
• rapidly respsonsive to high dose corticosteroids

What is the calling card of a 6NP?

Horizontal DIPL greater at distance than near

Ipsi abduction deficit

6NP - Where is the lesion located?

contralateral hemiglegia

ipsilateral facial palsy

ipsi facial analgesia

ipsi Horners

nystagmus. or ipsi hearing loss

Brainstem

(Nucleus and Fascicles of pons) of abducen's nerve

6NP - Where is the lesion located? What are you suspecting as an etiology?

Bilateral 6NP

Papilledema

Subarachnoid

Clivus lesion d/t...

1. neoplasm
2. compression
3. severe head trauma
4. meningitis
5. increased ICP!

6NP - Where is the lesion located? What is another name of this condition?

Ipsi facial palsy

Ipsis facial pain

Otitis media (middle ear infection)

Subarachnoid

Petrous Apex

Gradenigo's Syndrome

6NP - Where is the lesion located?

6NP with reduced tearing ispilaterally

possible favial pain (facial nerve involvment)

Subarachnoid 

Middle Cranial Fossa 

1) Management of Isolated 6NP in ...

- children

- 15-40 yo

- >40yo

2) Is neoplasm a common cause of 6NP?

1)

• children: neuro consult, monitor q2-6 weeks, r/o brainstem glioma and infection
• 15-40: MRI, lumbar puncture, r/o trauma, idiopathic, ifectious, demyelinating dz (MS)
• older adults: ischemia (ATH, GCA), increased ICP, infection, neoplasm

Neuroimage! Contrast enhanced MRI is test of choice.

If petrous apex disease is suspected (Facial pain/palsy, otitis media), CT scan is test of choice because it will detect bony erosion

increase ICP

OUTSIDE brainstem (Clivus) 

papilledema

Think: MENINGEAL DISEASE! MUST NEURP-IMAGE

Important causes of Horner's Syndrome

What do you suspect in First Order Lesions?

First order lesions = "Central" Sympathathtics in the hypothalamus

Therefore, suspect...

• Brainstem disease (tumor, trauma, infection, hemorrhages)
• ALWAYS has associated neurological signs such as CNP

Second Order = "Preganglionic" = Spinal Cord (Cervical), Neck, and ICA

Therefore, suspect...

• Spinal cord injuries
• apical lung tumor!! RARE and very unlikely in the absense of arm or axillary pain
• neck injury/SX

Third Order = "Post-Ganglionic" = IVA, Cilary ganglion, Cavernous Sinus, Ear

Therefore, suspect...

• Cavernous sinus disease (tumor, aneurysm, inflammation, infection)
• Cluster HA
• Otits media

1st order: ipsi body

2nd order: ipsi face and neck

3rd order: ipsi brow

• Dilated pupil
• LND 
• Sector paralysis - under slit lamp, areas of intact (innervated sphincter) can be visualized
• Sluggish near response c slow redilation
• Irregular pupil - d/t flattening of the pupillary margin from the denervated iris
• Impaired accommodation (can't relax acc)

1) Local tonic pupils: d/t truama, infection, CE

2) Neuropathic tonic pupils: bilateral.  DM!! Syphillis and chronic alcoholism

3) Adies's or Idiopathic Tonic Pupil:  most likey, idiopathic, healthy pts.  reduced or absent tendon reflexes

Where is the lesion?

- Adies

- Argyl Robertson

- Dorsal Midbrain Syndrome

- APD

Adies: Ciliary Ganglion, Ciliary nerves, or iris sphincter

Argyl Roberston: Prectal Oculomotor tract

Dorsal Midbrain: Posterior Commisure

APD: Optic tract, nerve

1. in retinoschisis, the surface is very taut and typically does not move with eye movements (RD, undulates freely with eye movements).  Reason = the cavity of the retinoschisis is thought to be filled with hyaluronic acid

2. honeycomb appearance in RS d/t to the inner and outer layer breaks

3. RS usually does not have a pigmented line of demarcation (probably because the split is no where near the RPE)

4. RS ALWAYS has an area of cystoid degneration btw PRS (Peripheral RS) and Ora

5. Choroidal features are visible but dim in RS, but totally obscured in RD.  (This is bc in RS, you get a very thin splitting of the retina, wheareas RD you get a complete thick separation of sensory retina from RPE)

Pt presents with facial paralysis of the entire half of the face.  

Ant Seg: SPK, Exposure Keratitis

1) What do you suspect?

2) Where is the lesion?

3) How to Tx?

4) How to manage as an OD

1. Bells Palsy

2. Peripheral, Isolated facial nerve lesion.  May be d/t ischemia involving the vasa nervorum or inflammatory dz but Dx'd by EXCLUSION

3. Possible help from corticosteroids

4. Ocular lubricants, patching, moisture chambers, tarsorrhaphy, eyelid weight implant

Pt presents with paralysis of the lower facial muscles.  

Ant seg: normal

You suspect a facial nerve palsy and run the battery of tests.  You find the frontal muscls, orbicularis occuli are all functioning appropriately.  

What is the Dx? Where is the lesion? 

Pt comes in complaining of DIPL.  

(+) ipsi horizontal gaze palsy to the right

(+) contralateral hemiparesis to the left

(+) difficulty abducting to the right (6NP) with facial analgesia

You suspect?... (there are 2 right answers)

Where is this lesion? (There are 2 right answers)

Facial Nerve palsy or 6NP

Lesion = (1) Brainstem or (2) Cerebellopontine Angle

Orbicularis oculi: ask pt to squeeze eyelids shut.  Look for inability to bury lashes or incomplete closure

Frontalis: raise and scrunch eyebrows

Orbicularis oris: smile then whistle

Buccinator: fill cheeks with air

Stapedus: if hear things louder on side of palsy

 What is a nasal step?  Why do we see it in GL?

nerve fibers from the optic nerve spread out across the retina.  They stop on the temporal side of the optic nerve at the horizontal midline of the retina.  Therefore, damage above or below what is called the horizontal raphe produces asymmetric loss at the nasal mid-horizontal line. 

[image]

What do these terms mean?

- plegia?

- paresis?

- palsy?

- plegia = paralysis

- paresis = weakness

- palsy = paralysis of a body part, often accompanied by loss of sensation and tremor

CN III palsy with choreiform movements, temor, ataxia

1) Where is the lesion?

2) If this pt had hemiplegia on one side, what syndrome are you thinking of?

3) If this pt had hemiparesis on one side, now what syndrome are you thinking of?

CNIII Palsy:

1) Location: Fascicular in the red nucleus, sup.cereballar peduncl, cerebral peduncle

2) Weber's Syndrome (Think: if you are caught in a Web you will be unable to move and will be paralyzed)

3) Benedict's Syndrome: (Think: if you do not eat your egg's benedict in the morning, you will have muscle weakness)

How do you treat Lyme Dz

Doxy 100mg BID x 3 weeks

Refer to infectious dz

• caused by Bartonella henselae
• Ocular conditions:
• Parinaud Oculoglandular Syndrome: unilateral conjuncitivitis, (+) PAN
• Neuroretinitis: stellate macular star and disc edema

AD, Phakomatosis

• buttery malar rash
• cyst on toenails
• ash leaf spots
• reinal astrocytic hamartomas that start as noncalcified lesions and becomes calcified
• mulberry lesion: bc multilobulated surface with intralesional calcium --> exudative RS or hemmorhhage
• DDx: Retinoblastoma 
• to differentiate, note that TS has smooth surface, not exophytic growth, no viteous seeding, or any vascular abnormalities

Leber's Congenital Amaurosis 

Presentation, AR or AD?,

VA?

CV?

VF?

ERG/ EOG?

Tx?

• Nystagmus one to the 5 A's
• AR hereditary disorders onset at birth or early childhoos
• SEVERE visual impairment.  Think: EVERYTHING is wrong
• sluggish pupils
• nyctalopia
• light sensitivity
• nystagmus
• high hyperopia
• keratoconus, PSC, high HYP, salt and pepper fundus, vasculopathy, attenuation, macular colobomas, chorioretinal atrophy
• Systemic: MR, deafness, seizures, skeletal abnormalities, renal musclar abormalities

Salzmann nodular degeneration

blue/white elevated, midperipheral, subepithelial hylanie nodule

associated with trachoma, chronic DES/Bleph

- Cyclo

- PF 1% QID with slow taper

- Trifluridine 1% TID to QID OR Acyclovir 400mg BID

** Acyclovir po alone will not resolve the stromal keratitis!

Common causes of Angiod Streaks

PEPSI

Pseudoelasticum xanthoma

Ehler Danlos

Pagets

Sickle Cell 

Idiopathic (50%)

. “To Find Small OcularMelanomas, Use Helpful Hints.” 

1. Thickness (elevation) > 2mm
2. Fluid - any subretinal fluid
3. Symptoms 
4. Orange Pigment (lipofuscin on the surface of the tumor)
5. Margins
6. Ultrasonographic Hollowness (on B-scan)
7. Halo absence

This is a superficial brown to black tumor that has a "stuck-on" appearance and a cobble-stone surface. 
Unlike squamous carcinomas of the eyelid, seborrheic keratosis does not typically cause inflammation around its edges nor does it have a smooth reddened scaly surface. If it does become inflammed it can be mistaken for a basal or squamous cell carcinoma. 

BENIGN!

Emboli! 

Causes CRAO, BRAO