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Boards Prep: Ocular Disease: Book Flashcards

1
Q

Trauma: Chemical Burns

  1. Epidemiology?
  2. Symptoms? (6)
  3. Signs?
  4. Pathophysiology?
  5. Common Alkali Agents (Worse one)?
  6. Common Acidic Agents?
  7. Normal pH of Tears?
  8. Sign of ISCHEMIA?
A
  1. Exposure to chemical/thermal agents. ~66% occur in industrial settings.
  2. Normal/decreased vision, Pain, FBS, Photophobia, Tearing, BLEPHAROSPASM
  3. Mild SPK to Sloughing of Epithelium. Conj. Injection, Chemosis, Ciliary Injection, AC RxN, Conj Hemes, Scleral and LIMBAL BLANCHING (Limbal = BAD: Eye will SCAR = COMPLETE BLINDNESS). SEVERE BURNS can INCREASE IOP.
  4. ALKALI Burns = WORSE Px d/t raising pH = breakdown of FAs = Faster Penetration. 2x’s more common than ACIDIC BURNS.
  5. MORE DANGEROUS (Most Common: CALCIUM HYDROXIDE); Ammonia. lye, magnesium hydroxide, lime (plaster, mortar, cement, mouthwash), Airbag residue.
  6. Hydrofluoric Acid, Sulfuric Acid, Nitric Acid, Chromic Acid, PAVA spray.
  7. 7.45
  8. Limbal Blanching
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2
Q

Trauma: Corneal Abrasion

  1. Epidemiology?
  2. Symptoms? (4-6)
  3. Signs?
A
  1. Hx of Trauma
  2. Sharp pain (esp after blinking); FBS, Photophobia, Tearing, Blurred vision; maybe AC RxN and Miotic pupil.
  3. Corneal defect. Stains w/Fluorescein w/NO SEI!
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3
Q

Trauma: Conjunctival Abrasion

  1. Epidemiology?
  2. Symptoms?
  3. Signs?
A
  1. Hx of Trauma
  2. Pain, FBS, Tearing
  3. Maybe Conj Injection, or Subconj Heme.
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4
Q

Trauma: Corneal and Conjunctival Superficial FBs.

  1. Epidemiology?
    a. Most common Non metallic FBs?
  2. Symptoms?
  3. Signs?
    a. Metallic FBs usually have what surrounding them?
  4. Upper EYELID FBs: usually cause what?
  5. Algar BRUSH will NOT GO THRU what?
A
  1. Hx of Ocular Trauma;
    a. Vegetable matter, cloth particles, cilia, stone, glass.
  2. FBS, Tearing, Redness, Photophobia, decreased vision.
  3. FB w/ or w/o Sterile Infiltrate. Corneal Edema and Mild AC RxN can occur.
    a. RUST RING.
  4. Linear, Vertical, Corneal Scratches.
  5. thru the STROMA!
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5
Q

Trauma: Ruptured Globe and Penetrating Ocular Injury

  1. Epidemiology:
    a. Hx?
    b. Common more in whom?
  2. Symptoms?
  3. Signs?
  4. What Test should u perform and how do u perform it?
A
  1. a. Recent trauma
    b. Males (3:1) esp. young to middle-aged males.
  2. Blurred Vision, Pain, Photophobia, Redness, Tearing.
  3. Full thickness laceration, SEVERE Conj Heme, EOM Restriction, Leakage of intraocular contents, LOW IOP. POSITIVE SEIDEL’s SIGN, HYPHEMA, COMMOTIO RETINAE, Choroidal Rupture, Tractional RD.
  4. Seidel’s Test: want to know if a wound leak is present. Take Fluorescein Strip, put it at the wound site, and u will see what looks black and gel like stuff leaking out.
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6
Q

Trauma: Hyphema

  1. Epidemiology/Hx?
  2. Pathophysiology/Dx
    a. Main cause d/t?
    b. What 2 tests should NOT be performed and why?
    c. What test is INDICATED?
  3. Symptoms?
  4. Signs?
    a. 8 Ball hyphema?
    b. Microhyphemas?
  5. Other possible Signs?
  6. What can occur in LATE STAGES of HYPHEMA?
  7. If there’s a significant increase in IOP, what should the pt do?
A
  1. Hx of blunt/penetrating trauma, Systemic Dx (sickle-cell retinopathy, clotting dz, etc), Idiopathic.
  2. a. Trauma to IRIS and/or CB.
    b. Gonioscopy or Scleral Depression; Wait at least 1 month to prevent rebleeding, which is usually worse than original presentation.

c. B-SCAN if it’s occluding view of fundus or if u think there might be an RD.
3. Pain, Blurred Vision

  1. Blood in AC.
    a. Black Hyphema that covers the entire AC (B-Scan; and Goldmann, but NO Gonio or Scleral Depression)

b. RBCs suspended in AC, seen with Slit Lamp.
5. Iris sphincter tears, Iridodialysis, cataract, lens subluxation, VOSSIUS RING (Pigmen ring) on Anterior lens capsule, Commotio Retinae, ANGLE RECESSION (60% of cases –> HIGH RISK for GLAUCOMA).
6. CORNEAL BLOOD STAINING. (~5% of pts: usually seen w/LARGE HYPHEMAS, rebleeds, elevated IOP, compromised Corneal endothelial cells)
7. Elevate their head ~30 degrees so RBCs can settle inferiorly and hopefully not continue to block TM.

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7
Q

Trauma: Idiopathic Hyphema

  1. Number 1 Cause?
  2. Always ask pt about the use of what meds?
  3. Consider ordering what blood tests?
  4. Sickle Cell and/or Clotting diseases should be considered in what ethnicities?
A
  1. TRAUMA
  2. Blood thinners (aspirin, NSAIDs, etc)
  3. CBC, Prothrombin time/partial thromboplastin time (PT/PTT), Sickle cell screen.
  4. AA, and Mediterranean Pts.
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8
Q

Trauma: Intraocular FB

  1. Epidemiology
  2. Symptoms
  3. Signs?
  4. Intraocular FBs
    a. Types that can cause Major Inflammation?
    b. Types that can stay in the eye for long periods of time w/o causing inflammation?
A
  1. Hx of Trauma. Consider Intraocular FB if injury from metal striking metal or if an object was flying at high speed towards the eye. DO NOT ORDER MRI if u suspect METALLIC FB.
  2. Decreased VA, Pain.
  3. FB seen on CT scan, B Scan; Iris Transillumination Defects, Distorted pupil, Hyphema, Cataract, Decreased IOP, + Seidel’s TEST. Microcystic Edema of Peripheral Cornea.
  4. a. Iron (BBs), Steel, Copper, Vegetable Matter
    b. Glass, Stone, Precious Metals, Plastic.
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9
Q

Trauma: Orbital Fracture

  1. Epidemiology?
  2. Pathophysiology?
  3. Symptoms?
  4. Signs?
  5. What 4 things should you look for when u suspect this?
  6. What 2 tests should you not perform and for how long should you wait?
  7. Tell Pts not to do what?
A
  1. Hx of Trauma from a large object
  2. Usually Orbital Blow Out Fractures d/t MAXILLARY BONE in Posterior Medial Floor breaking.
  3. Pain, Binocular Diplopia, CREPITUS (crackling when blowing nose) and on palpation of medial orbital area.
  4. Depends. Subconj Heme, Enophthalmos, diplopia, step-off fracture of the orbital rim, globe ptosis, infraorbital hypesthesia, asymmetric monocular PDs (>3 mm difference), Hyphema, Angle Recession, etc.
  5. TRAPPED IR, damage to INFRAORBITAL NERVE (causes Hypoesthesia), + Forced Duction Test, PERIORBITAL CREPITUS (Orbitla Emphysema)
  6. Gonio and Scleral Depression; Wait at least 4 WEEKS after trauma.
  7. To not BLOW their nose w/in 48 hrs of trauma to limi risk of orbital infection.
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10
Q

Trauma: Commotio Retinae

  1. Epidemiology
  2. Pathophysiology?
  3. Symptoms?
  4. Signs?
A
  1. Hx of Recent Trauma
  2. Disruption of RPE and Photoreceptor Outer Segements. Usually resolves w/o Sequelae w/in 24-48 hrs. Permanent vision/VF loss can happen.
  3. Usually Asymptomatic. May have Acute Vision loss if trauma happens w/in the macula.
  4. Gray-White Discoloration in the retina; Called BERLIN’s EDEMA when found w/in the MACULA. May see Retinal Hemes or a Choroidal Rupture.
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11
Q

Trauma: Iridodialysis

  1. What is it?
  2. What does it look like on SLE?
    a. Best seen with that technique?
  3. Monitor Pts for what? Cause?
A
  1. Disinsertion of Iris Root from CB. (Weakest point of attachment)
  2. Peripheral Iris Hole
    a. Retroillumination
  3. Angle Recession Glaucoma; TM may be damaged secondary to trauma.
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12
Q

Trauma: Vossius Ring

  1. What is it?
  2. Cause?
A
  1. Pigment Ring on Anterior Lens Surface

2. d/t contact w/the Posterior Pigmented Iris Epithelium during Trauma

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13
Q

Trauma: Purtscher’s Retinopathy

  1. Retinopathy associated with what?
  2. What signs do we normally see with it? (3)
A
  1. ACUTE CHEST-COMPRESSION TRAUMA

2. Diffuse Retinal Hemes, Exudates, CWS

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14
Q

Trauma: Choroidal Rupture

  1. Occurs in what % of Blunt Ocular Trauma?
  2. Most common presentation?
  3. Associated with what risk?
A
  1. 5%
  2. single area or multiple areas of Subretinal Hemes, usually w/in TEMPORAL POSTERIOR POLE w/Crescent Shaped Tears Concentric to the ONH.
  3. Long Term Risk of CNV at margins of the TEAR (happens in ~5-10% of Pts)
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15
Q

Trauma: Eyelid Ecchymosis

  1. What is it?
A
  1. Bruise or Black Eye. d/t Leaking BVs in SUBCUTANEOUS TISSUE that’s likely d/t Trauma.
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16
Q

Trauma: Conjunctival and Corneal Lacerations

  1. What is it?
  2. What test should be done to see if an open globe wound is present?
  3. Px?
  4. What else can result from TRAUMA?
A
  1. Tear in corneal or Conj tissue, usually d/t Trauma
  2. Seidel’s Test
  3. Good; Unless laceration is in the Visual Axis.
  4. OPTIC NEUROPATHIES. Disc pallor seen several weeks later.
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17
Q

Prolapsed Orbital Fat

  1. Why does this occur as we age?
  2. What does it look like?
  3. Possible issues with it?
A
  1. d/t weakening of the Orbital Septum –> Extraconal fat to prolapse.
  2. Outpouching of skin in upper and lower lids
  3. Can cause lid malposition, exposure keratopathy d/t lid malposition; Ocular irritation, redness, tearing, blurred vision, etc.
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18
Q

Preseptal Cellulitis

  1. Epidemiology?
  2. Pathophysiology?
    a. Ocular Infection
    b. Systemic Infection
    c. Skin Trauma
  3. Signs?
A
  1. Young adults and children during WINTER. More common than orbital cellulitis.
  2. Infection ANTERIOR to ORBITAL SEPTUM
    a. Acute Hordeolum (most common), Dacryocystitis
    b. URI or Middle Ear Infection
    c. Puncture wound, insect bite
  3. Eyelid Edema, Erythema, Ptosis, Warmth. Hard bump on eyelid. No pain. Maybe mild tenderness.

NO SIGNS of Orbital Congestion

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19
Q

Orbital Cellulitis

  1. Epidemiology
  2. Pathophysiology
    a. Sinus Infection
    b. Orbital Infection
    c. 2 other causes?
  3. Most common cause in Adults?
    a. In Children?
  4. Symptoms?
  5. Signs?
  6. Prognosis?
A
  1. **Leading cause of Exophthalmos in Kids. Ask about Fever, Recent Sinus or dental infections, Trauma
  2. a. ETHMOID SINUSITIS is the most common. From here, infection can spread thru the Lamina Papyracea (Very thin)
    b. Dacryoadenitis, Dacryocystitis, progression of Preseptal Cellulitis
    c. Orbital Fracture, Dental Infection
  3. Staph Aureus
    a. H. Influenzae
  4. Red eye, pain, decreased vision, HA, fever, general malaise, reduced color vision, APD, PROPTOSIS, DIPLOPIA w/PAIN on Eye movement (d/t EOM RESTRICTIONS)
  5. Eyelid Edema and Redness
  6. Can cause Cavernous sinus thrombosis, Brain Abscess, and/or MENINGITIS;

**Diabetics and immunocompromised Pts can get MUCORMYCOSIS (BAD!!!)…Fungal infection…life-threatening…Pt’s get “BLACK ESCHAR (Necrotic Tissue)”

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20
Q

Orbital vs. Preseptal Cellulitis

  1. Pts w/Orbital Cellulitis will have the following, while Preseptal Pts will not…(5)
A
  1. Decreased Vision, Proptosis, FEVER, Pain on Eye Movement, EOM Restrictions.
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21
Q

Thyroid Eye Disease (Graves’ Ophthalmology)

  1. Epidemiology
  2. Pathophysiology
  3. Symptoms?
  4. Signs?
A
  1. Females (8:1); 4th-5th decade of life; STRONGEST RISK FACTOR for developing TED: SMOKING (2-9x’s greater risk)
  2. AI: TSH Receptor Antibodies –> Cause major inflammation to EOMs and Orbital Tissue –> Thickening EOMs –> ON Compression. Hyperthyroidism. TED in 30-70% of PTs w/Graves’
  3. Prominent Eyes; Chemosis, FBS, Tearing, Photophobia, Pain, Diplopia, Decreased Vision, Color Vision Loss, Etc.
  4. U/L or B/L PROPTOSIS, UPPER LID RETRACTION, APD, Eyelid Erythema and Edema, Conj and Caruncle Injection, Decreased Color Vision; IOP can be increased in Primary and UPGAZE.

**MOST Common cause of U/L or B/L Proptosis in Middle-Aged Peeps

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22
Q

Thyroids: NO SPECS grading system

A
  1. N: No signs or symptoms
  2. O: Only signs but no symptoms. (DALRYMPLE’s SIGN: Stare appearance)
  3. S: Soft Tissue involvement (lid edema; Conj Chemosis)
  4. P: Proptosis
  5. E: EOM Involvement –> Diplopia. INFERIOR RECTUS affected first, then > MR > SR > LR
  6. C: Corneal Involvement (Punctate Keratitis, SLK, Ulceration)
  7. S: Sight loss d/t ON Compression. Enlarged EOMs at orbital apex –> Compressing the Optic Nerve –> Disc Edema, APD, Reduced Color Vision, VF Loss. Decreased VAs.
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23
Q

Signs

  1. Von Graefe’s Sign
  2. Kocher’s Sign
  3. Dalrymple’s Sign
A
  1. Upper Eyelid lag during Downgaze
  2. Globe lag compared to lid movement when looking up
  3. Lid retraction which gives a Stare Appearance.
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24
Q

Thyroid Eye Dz

  1. Diagnosis? (5)
A
  1. a. Forced Ductions to detect EOM Restrictions
    b. CT/MRI to detect enlargement of the EOMs
    c. Exophthalmometry to measure proptosis
    d. VFs detect ON Compression
    e. Blood Work (T3/T4/TSH)
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25
Q

Thyroid Eye Dz: Hertel Exophthalmometry Norms for Adults

  1. Caucasians?
  2. Asians?
  3. AAs?
  4. What’s considered Abnormal?
A
  1. 12-22 mm
  2. 12-18 mm
  3. 12-24 mm
  4. Abnormal if HIGHER OR presence of >3 mm asymmetry.
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26
Q

Carotid Cavernous Fistula (CCF)

  1. Cause?
  2. Most Commonly results from what?
  3. What happens?
  4. TRIAD?
A
  1. D/t abnormal communication b/w Arterial and Venous Systems
  2. Closed Head Trauma. Can happen spontaneously d/t Ruptured Carotid Aneurysm.
  3. High Pressure blood from carotid artery builds up in the cavernous sinus. Prevents return of venous blood back to the cavernous sinus.
  4. Leads to CHEMOSIS, OCULAR BRUIT, and PULSATILE PROPTOSIS
    * Any of the CN Palsies could potentially be affected.
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27
Q

Orbital Tumors

  1. Most common BENIGN tumor in adults?
    a. Epidemiology?
    b. Signs?
  2. Most Common BENIGN tumor in KIDS?
    a. Epidemiology?
    b. Signs?
  3. Most common PRIMARY Pediatric Orbital MALIGNANCY?
    a. What happens?
    b. Dx’d around what age?
  4. Most common SECONDARY Pediatric Orbital Malignancy?
    a. What happens?
  5. Most COMMON INTRINSIC TUMOR of the OPTIC NERVE?
    a. WHat happens?
    b. Associated with what?
  6. Most common BENIGN BRAIN TUMOR?
    a. Epidemiology?
    b. Cause?
  7. Dermoid Cyst
    a. Most common location?
    b. What happens?
A
  1. Cavernous Hemiangioma
    a. 4th-6th decade; Females
    b. Painless, progressive U/L Proptosis. Usually starts Posterior to the GLOBE w/in the MUSCLE CONE.
  2. Capillary Hemiangioma
    a. Dx’d by 6 Mos usually.
    b. Proptosis, and DEPRIVATION AMBLYOPIA; Rapid Growth; Spontaneous Involution, usually by Age 7.
  3. Rhabdomyosarcoma
    a. Destroys the bones pretty quickly. Get progressive U/L Proptosis
    b. by Age 7.
  4. Neuroblastoma
    a. Usually comes from a tumor in the ABDOMEN!, mediastinum, or neck (Horner’s may be seen as well.) 2nd most common overall malignancy after Rhabdo.
  5. Optic Nerve GLIOMA
    a. Symptoms usually seen in 1st decade of life. (2-6 y/o)
    b. Neurofibromatosis Type 1.
  6. Meningioma
    a. Middle aged women
    b. Sphenoid ones come from Sphenoid bone; Most common Intracranial Tumor to invade the orbit
  7. a. Sup/Temp Quadrant.
    b. Usually congenital, causes Proptosis. CT Scan shows well-defined mass.
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28
Q

Orbital Tumors (2)

  1. Most commonly seen in PTs 50-70 y/o. Get an APD, Progressive Proptosis, Vision Loss. 60% have a 5 year survival rate. What is it?
  2. Neurofibroma
    a. Epidemiology
    b. What is it?
    c. Usual location?
    d. Can be associated with what?
  3. Neurilemmoma (Schannoma)
    a. What is it?
    b. Epidemiology?
    c. Usual Location?
    d. Usually starts to affect what CN as it develops?
    e. Signs?
A
  1. Lymphoma
  2. a. young/middle aged peeps.
    b. Benign, Y-W Tumor of ASTROCYTES
    c. Superior Orbit.
    d. Neurofibromatosis
  3. a. Benign tumor of SCHWANN CELLS
    b. Young/Middle Aged Adults
    c. Superior Orbit
    d. CN 5
    e. Painless, progressive proptosis.
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29
Q

Most orbital tumors have what signs?

A

Progressive vision loss, Proptosis, diplopia, and an APD.

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30
Q

Orbital Pseudotumor (Orbital Inflammatory Dz)

  1. Epidemiology
  2. Pathophysiology?
  3. Symptoms
  4. Signs
A
  1. Rare; Acute, Recurrent, or Chronic, Young/Middle-Aged Peeps. 3rd MOST COMMON ORBITAL problem in ADULTS.
  2. IDIOPATHIC. Inflammatory. Can hit the Soft tissue. Can look anywhere from T.E.D. to Orbital Cellulitis.
  3. Acute onset; U/L Pain, Red Eye, Diplopia, Decreased Vision. Kids: can be B/L and 1/2 of those can have Fevers, Nausea, and Emesis
  4. PROPTOSIS, EOM restrictions, Chemosis, Periorbital Swelling, Lacrimal Gland Enlargement, Lid Ptosis, Hyperopic Shift, ON Swelling, Increased IOP on one side. Reduced Corneal Sensation (CN V1 involvement), etc.
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31
Q

Chemosis

  1. Usually seen with what?
    a. If it’s not seen along with this, what should u suspect?
A
  1. w/Allergic Symptoms

a. Start thinking IDIOPATHIC Inflammatory condition esp if the Pt is young/Middle Aged.

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32
Q

Idiopathic Orbital Inflammation

  1. Inflammation seen where?
  2. What should be done to help Dx it?
A
  1. widespread. in all of the orbit, INCLUDES EOMs tendons.

2. CT/MRI…can see enlarged EOMs/Tendons

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33
Q

Tolosa Hunt Syndrome

  1. What is it?
  2. Presentation?
  3. CN most commonly affected?
  4. what else can be seen?
A
  1. Rare, Idiopathic, Orbital Inflammation that can hit the CAVERNOUS SINUS and SOF.
  2. ACUTE and PAINFUL exophthalmoplegia; Diplopia d/t I/L Palsies of CNs 3,4,6.
  3. 3
  4. V1 and V2 can be affected too, so u can see decreased sensory innervation in their respected areas.
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34
Q

If a PT has B/L ORBITAL PSEUDOTUMORS, what should you be thinking they have?

A

Systemic Vasculitis (Wegener’s, Polarteritis Nodosa) or Lymphoma.

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35
Q

What is Phthisis Bulbi? Associations?

A

Shrinkage/Atrophy of Globe d/t Trauma, Infection, Sx, Advanced Dz.

Associations: Inflammtion, Hypotony, Blind Eye

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36
Q

What is Enophthalmos?

A

Retraction of the globe w/in the Orbit, usually d/t Ocular Trauma

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37
Q
  1. Enucleation: Define
  2. Evisceration: Define
  3. Exenteration: Define
A
  1. Removal of GLOBE
  2. Removal of INNER Contents of the eye; Sclera and other oribtal stuff still there.
  3. Removal of EVERYTHING: includes EOMs and Orbital Fat.
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38
Q

Ocular Rosacea

  1. Epidemiology
  2. Pathophysiology
  3. Symptoms
  4. Signs
    a. Facial Flushing w/rosacea associated with what?
A
  1. Middle Aged Northern Europeans. WOMEN > Men. Men get more severe version though. 10% of population affected w/50% having Acne Rosacea
  2. Affects SEBACEOUS GLANDS –> Chronic Ocular Surface Dz.
  3. Redness, Burning, FBS, Ocular Irritation
  4. Papules on Cheek and Forehead w/TELANGIECTASIA, RHINOPHYMA (sebaceous gland hyperplasia of the nose) and FACIAL FLUSHING (butterfly rash)
    a. Alcohol, Exertion, Spicy Foods, Caffeine, More sun exposure
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39
Q

Ocular Rosacea

  1. Causes what kinds of lid diseases?
    a. This results in what?
A
  1. Inspissated MGs, Blepharitis, Hordeola, Chalazia

a. Ocular Surface Dz (Phlyctenules, Staph marginal Keratitis, SPK, Corneal Neo (greatest inferiorly), DES).

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40
Q

Contact Dermatitis

  1. Type of RxN?
    a. Main Causes?
    b. Medications that can cause it?
  2. Symptoms?
  3. Signs?
A
  1. Type 4 Hypersensitivity RxN: DELAYED (24-72 hrs later)
    a. Cosmetics: anything really.
    b. Aminoglycosides (Gentamicin, Tobramycin), Trifluridine, Cycloplegics/Mydriatics, Glaucoma Meds (like Timolol, Alphagan, Trusopt), and Preservatives (Thimerosol, BAK)
  2. Acute Periorbital Swelling, Redness, Itching, Tearing
  3. U/L or B/L Erythema and crusting of the lid and periorbital tissues and lots of CONJUNCTIVAL CHEMOSIS
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41
Q

Ocular Cicatricial Pemphigoid

  1. What is it?
  2. Epidemiology?
  3. Pathophys?
  4. Symptoms?
  5. Signs?
  6. Prognosis?
A
  1. Mucus Membrane Disorder!
  2. Rare. Females > Males (2:1), Avg Dx Age: 65; can get B/L blindness after ~10-30 yrs after Dx.
  3. Chronic, SYSTEMIC, IDIOPATHIC mucous membrane disorder. Usually hits ORAL and OCULAR mucous membranes (CONJ, Mouth, Esophagus). Can be Drug induced (TIMOLOL!, Epinephrine, Pilocarpine)
  4. Sub-acute onset of nonspecific symptoms: Redness, Dryness, FBS, Decreased Vision
  5. Conj Fibrosis and Scarring (fine white Striae), B/L SYMBLEPHARON (Palp Conj sticks to Bulbar Conj), Ankyloblepharon (Lids stick together).
  6. Destroys Goblet Cells, Meibomian Glands, Krause and Wolfring, Ducts of Main Lacrimal Gland –> SEVERE OCULAR SURFACE DISEASE.

Late Stage can also show Entropion, Trichiasis, Corneal Ulceration, Neo, Keratinization

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42
Q

Stevens-Johnson Syndrome

  1. Pathophys?
  2. Acute Signs?
  3. Acute Symptoms?
  4. Chronic Signs/Symptoms
    a. Eyelid Pathologies?
    b. Conj Pathologies?
    c. Corneal Pathologies?
A
  1. Type 3 Hypersensitivity RxN (Mucous membrane issue); DRUG INDUCED (SULFONAMIDE most common), Phenytoin, Penicillin, Aspirin, Barbiturates, Isoniazid, Tetracyclines, NSAIDs, Immunizing Vaccinations);

Also can be caused by INFECTIOUS AGENTS (HSV, Mycoplasma Pneumoniae, Adenovirus, Streptococcus)

*Acute Phase (often self-limiting w/in 2-4 wks) which can lead to a chronic phase

  1. Skin Lesions (diffuse erythema, or “bull’s Eye” lesions, papules on the palms of hands and soles of feet.)
    a. Ocular Lesions: Severe, B/L Diffuse Conjunctivitis w/Pseudomembranes
    b. Bacterial Conjunctivitis can lead to Endophthalmitis in severe cases
  2. PRODROME: Fever, Malaise, HA, Nausea, Vomiting
  3. a. Entropion, Ectropion, Trichiasis, MG damage
    b. SYMBLEPHARON, fornices shorten, Conj Keratinization, Limbal Stem Cell Damage –> more corneal pathologies.

c. Ulcers, Neo, Scars, Perforation.

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43
Q

Dermatochalasis

  1. Epidemiology?
  2. Patho?
  3. Advanced cases can do what?
A
  1. Common in Old Peeps.
  2. Redundant Upper Eyelid Skin from WEAKENED ORBITAL SEPTUM –> Eyelid Ptosis, Pseudoptosis, and a loss of distinct eyelid creases.
  3. Can cause an apparent Superior VF Loss. (Lid Droop, Fat Prolapse)
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44
Q

Blepharitis

  1. 2 types?
    a. Both can cause what?
  2. Symptoms?
  3. Seborrheic Blepharitis is frequently associated with what?
A
  1. STAPHYLOCOCCAL BLEPHARITIS and SEBORRHEIC BLEPHARITIS (Thick Crusting; Greasy; Easy Loss of Lashes)
    a. Ant and/or Posterior Bleph (Meibomitis)
  2. Usually Asymptomatic; Can report that vision clears after blinking, burning, itching, FBS, Tearing, Crusting (esp in morning), and Mild Discharge
  3. w/Seborrheic Dermatitis. Associated w/Less lid inflammation, more oily, greasy scales with flaking, more eyelash loss (Madarosis) and/or misdirected growth compared to Staph Blepharitis.
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45
Q

Chalazion

  1. Epidemiology
  2. Pathophys
  3. Signs/Symptoms?
  4. Recurrent chalazions: What should u do?
A
  1. Hx of recurrent lesions; Ask about ACNE ROSACEA and Seborrheic Dermatitis
  2. Chronic, localized, STERIL INFLAMMATION of a Meibomian Gland d/t retention of normal secretions. 25% resolve w/o Tx.
  3. Hard, Painles, immobile nodule w/o redness. Usually on Upper eyelid. Usually Asymptomatic.
  4. Eval for SEBACEOUS GLAND CARCINOMAS
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46
Q

Hordeolum

  1. Epidemiology
  2. Pathophys
    a. Internal Hordeolum
    b. External Hordeolum
  3. Signs/Symptoms
A
  1. Hx of recurrent infections (like chalazia) that are successfully self treated. Ask about Acne Rosacea and Sebborheic Dermatitis
  2. Acute Staphylococcus Infection of Eyelid Glands.
    a. Hits Meibomian Glands (White Blister)
    b. Hits Zeis or Moll. (Aka STYE)…looks like a pimple
  3. Tender, Red, Warm area of Focal Swelling on the lid.
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47
Q

Eyelid Cysts

  1. What are they?
  2. Inclusion Cyst
  3. Milia
  4. Dermoid Cyst
  5. Sebaceous Cyst
A
  1. Benign lesions from epithelium of epidermis and dermal tissues associated with meibomian, sebaceous, and sweat glands of eyelids.
    * No issues w/VA, No Pain, unless they rupture…can cause inflammatory RxN. Main complaint is POOR COSMESIS
  2. Congenital or acquired lesion (trauma or Sx) on lid…usually white d/t accumulation of Keratinous Debris
  3. Acquired Lesion on lid and surrounding Adnexal tissue. Can Look White d/t Occlusion of Sweat Pores or Pilosebaceous Follicles
  4. Congenital lesion. Firm, immobile. Usually on Superior Temporal or Superior Nasal Eyelid
  5. Fluid retention in Glands of Zeis or debris retention in Meibomian Glands. Solitary, Smooth lesions….Yellow or Opaque.
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48
Q

Ectropion

  1. Patho
    a. Causes
  2. Big Complaint?
  3. Signs/Symptoms?
A
  1. Eversion of lid. Most commonly d/t Involutional (age-related) loss of MUSCLE TONE of ORBICULARIS OCULI.
    a. Mechanical (Tumor-related), Cicatricial (Scar tissue), Paralytic (CN 7 Palsy), Congenital (rare)
  2. TEARING.
  3. EXPOSURE KERATOPATHY; Epiphora, Brow Ptosis
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49
Q

Entropion

  1. Patho
    a. Causes?
  2. Signs
  3. Trichiasis
  4. Distichiasis
  5. Many cases of blindness in TRACHOMA are d/t what?
A
  1. Inversion of eyelid.
    a. Involutional (age-related), Cicatricial (TRACHOMA, OCP, STEVENS-JOHNSON, Chemical burns, Trichiasis, etc), Congenital
  2. Mild Punctate Keratitis to Corneal Ulcers and Pannus
  3. Lashes grow inward
  4. 2nd row of lashes
  5. Corneal ulcers from Entropion and Trichiasis
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50
Q

Floppy Eyelid Syndrome

  1. Epidemiology?
  2. Patho?
  3. Symptoms?
  4. Signs?
  5. Systemic Dz associations?
A
  1. OBESE peeps w/OBSTRUCTIVE SLEEP APNEA
  2. Reduced elastin in Tarsal Plate. Usually in FACE-DOWN Sleepers. Mechanical trauma to Tarsal plate.
  3. Chronic, B/L (78%) red eyes in the morning, mild mucous discharge
  4. Chronic Papillary Conjunctivitis w/loose upper eyelids that evert easily; Punctate Epithelial Keratopathy (50%) and Keratoconus
  5. Obstructive Sleep Apnea, HTN, DM, Hyperthyroidism
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51
Q

Benign Essential Blepharospasm (BEB)

  1. Epidemiology
  2. Symptoms
  3. Signs
  4. Patho?
  5. What is MEIGE’s SYNDROME?
  6. Tx?
A
  1. Age: 50-70; F > M (2:1)
  2. Repetitive B/L twitching and/or forceful closing of the eyelids…less common during sleep. Involuntary
  3. Spasms of Orbicularis Oculi, Procerus, and Corrugator Muscles
  4. IDIOPATHIC; 50% of Pts have an Ocular Surface disorder (usually DES) that can be exacerbating symptoms.
  5. BEB AND Lower Facial Abnormalities (can’t chew right, jaw spasms, jaw pain, etc). 50% of Pts with BEB have MEIGE’s SYNDROME.
  6. BOTOX
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52
Q

Myokymia

  1. What is it?
  2. Main causes?
A
  1. U/L TWITCHING of Orbicularis Oculi ONLY.

2. Sleep deprived, lots of caffeine intake, stress.

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53
Q

Basal Cell Carcinoma

  1. Epidemiology
  2. Pathophysiology
  3. Signs
A
  1. MOST COMMON Skin cancer. M > F (2:1); MOST COMMON EYELID CANCER (90%). Fair skin, UV Exposure (UV-B (290-320 nm)). Chronic Lesion that does not Heal
  2. Malignancy of Basal Cell Layer of the Epidermis. Minimally Invasive.
  3. SHINY, FIRM, PEARLY NODULE w/SUPERFICIAL TELANGIECTASIA. Progression –> CENTRAL ULCERATION (RODENT ULCER). Usually on LOWER EYELID and MEDIAL CANTHUS
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54
Q

Squamous Cell Carcinoma (SCC)

  1. Epidemiology
  2. Pathophys
  3. What’s the most common Precancerous skin lesion, and is a precursor to SCC?
    a. What does it normally look like?
    b. % that develop into SCC?
  4. SCC is more likely to do what than BCC?
  5. Signs?
A
  1. M > F (2:1); 2nd most common eyelid cancer; 40-50x’s less common than BCC
  2. Malignancy of Stratum Spinosum layer of the Epidermis; UV Exposure (esp. UV-B); ACTINIC KERATOSIS, fair skin; prior radiation; burn scars; chemical exposure (smoking); forms of chronic irritation.
  3. ACTINIC KERATOSIS
    a. Elevated, usually pink or red, scaly lesion that does not heal.
    b. 25%
  4. to Metastasize
  5. similar to BCC but NO TELANGIECTASIA. Usually: Erythematous plaque that looks rough, scaly, and/or ulcerated, may be flat or elevated. usually on Lower eyelid/lid margin.
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55
Q

Keratoacanthoma

  1. Where are they found?
  2. What do they look like?
  3. How fast do they grow?
  4. Tx?
A
  1. Sun exposed areas
  2. Usually a Central Plaque or Ulcer like BCCs or SCCs
  3. Very fast: Size: 1-2 cm
  4. None. Slowly shrink and usually resolve spontaneously.
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56
Q

Sebaceous Gland Carcinoma

  1. Epidemiology
  2. Pathophys
  3. Signs
A
  1. Rare…about the same as SCC. ELDERLY FEMALES; Hx of Chronic U/L Blepharitis or Recurrent Chalazia
  2. Neoplasm of Sebaceous Glands (MEIBOMIAN GLANDS and Glands of ZEIS); may be associated w/prior radiation therapy; POOR Px. Lid Lesion is GREATER THAN 2cm, Mortality: 60%; Symptoms MORE than 6 MONTHS, mortality is 38%. Overall Mortality is 10%.
  3. Tumor: HARD and YELLOW; Madarosis, Thickened Red Lid Margins (usually on UPPER EYELID). LYMPHADENOPATHY
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57
Q

Malignant Melanoma

  1. Epidemiology
  2. Pathophys
  3. Signs
A
  1. RARE (<1% of all eyelid malignancies); Most LETHAL PRIMARY SKIN CANCER
  2. Malignancy of MELANOCYTES. Risk Factors: Age, Skin color, FHx, Repeated irritation, Sun Exposure
  3. ABCDE; Depth of Invasion and LESION SIZE = 2 most IMPORTANT Prognostic Factors for this.
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58
Q

Dacryoadenitis

  1. Epidemiology
  2. Pathophys
  3. Signs/Symptoms
    a. Acute
    b. Chronic
A
  1. Children and Young adults mostly
  2. Inflammation of Lacrimal Gland
  3. Swelling of OUTER 1/3rd of TEMPORAL Upper Eyelid
    a. S-SHAPED PTOSIS, Temporal upper eyelid pain, redness, swelling, preauricular lymphadenopathy, occasional fever, elevated WBC Count

b. Temporal upper eyelid swelling w/less redness, swelling, and pain compared to acute dacryadenitis. Can lead to inferonasal globe displacement and proptosis.

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59
Q

Canaliculitis

  1. Pathophys
    a. Most common Cause?
  2. Symptoms
  3. Signs
A
  1. Inflammation of Canaliculi d/t Bacterial, Viral, or Fungal Infections; **PUS OUT OF CANALICULI
    a. ACTINOMYCES ISRAELI (Yellow Sulfur Granules)
  2. Smoldering, U/L red eye that’s unresponsive to Antibiotic Tx. usually misdiagnosed as Recurrent Conjunctivitis
  3. Tenderness of Nasal Part of Upper or Lower Eyelid, SWOLLEN PUNCTA (POUTING PUNCTA), Mucopurulent Discharge w/palpation of lacrimal sac region
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60
Q

Dacryocystitis

  1. Epidemiology
  2. Pathophys

a. common causes?
b. Characterized by what?

  1. Symptoms
  2. Signs
  3. Chronic Cases should make u suspect what?
  4. How do u tell the difference b/w this and Canaliculitis?
  5. Tx?
A
  1. Ear, Nose, Throat infections
  2. LACRIMAL SAC INFECTION d/t Obstruction in Lacrimal Drainage System –> Backflow of bacteria in lacrimal sac from the lacrimal lake.
    a. Staph Aureus, Staph Epidermidis, Pseudomonas, H. Influenzae in children
    b. Swelling below medial canthal tendon. Swelling ABOVE medial canthal tendon, think Lacrimal Sac Tumor
  3. Pain, crusting and tearing, occasional fever
  4. Prominent edema and tenderness over the lacrimal sac area.
  5. Epithelial Carcinomas and Malignant Lymphomas. Carcinomas can express blood into the Tear Film with palpation of the lacrimal Sac.
  6. this usually has more swelling, tenderness, and pain.
  7. DONT refer for Surgery or try to irrigate the lacrimal system during an ACUTE Infection. Tx should be done FIRST.
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61
Q

Punctal Stenosis

  1. Acquired: What is it?
    a. Most commonly associated with what?
  2. Most common Symptom?
A
  1. Narrowing or Occlusion of Puncta of the upper and/or lower lids.
    a. Older Age
  2. EPIPHORA
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62
Q

Nasolacrimal Duct Obstruction

  1. Epidemiology
  2. Pathophys
    a. Involutional Stenosis
    b. Membrane Blockage at Valve of Hasner
  3. Symptoms
  4. Signs
  5. Secondary Dacryocystitis can occur in what?
A
  1. Congenital/Acquired. Acquired more often seen in FEMALES
  2. a. Most common cause of NLDO in OLDER Pts. Other etiologies in older patients: Chronic Sinus Dz, Dacryocystitis, and Naso-Orbital Trauma
    b. Most common cause of Congenital NLDO. seen in ~30% of newborns; Spontaneous opening usually after 1-2 months after birth. IF not, digital massage can be performed.
  3. U/L Tearing, discharge, crusting, and recurrent conjunctivitis
  4. Epiphora, Mucous reflex from the puncta after compression of the lacrimal sac, medial lower eyelid erythema, and mild to no redness or tenderness around the puncta
  5. in Congenital NLDO d/t Stagnant tears in the lacrimal sac.
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63
Q
  1. Jones 1 Test

2. Jones 2 Test

A
  1. Tests Patency of system. Fluorescein instilled in Inferior Fornix…Should drain w/in 5 minutes.
    + Test: means PATENT SYSTEM
  2. Irrigation with SALINE. Reflex of Fluid thru the same punctum = OBSTRUCTION in UPPER or LOWER CANALICULUS (proximal to common canaliculus)

Retrograde flow thru Opposite canaliculus and punctum: means NASOLACRIMAL BLOCKAGE (Obstruction distal to Common Canaliculus)

Pt Tastes saline or has Gag reflex, Obstruction has been cleared

Jones Test II FAILS to open Nasolacrimal drainage system, a DACRYOCYSTORHINOSTOMY (DCR) is the best Treatment Option.

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64
Q

Conjunctival Lesions

  1. Conjunctival Cyst: What is it?
    a. AKA?
  2. Conjunctival Concretions: What are they?
    a. AKA?
    b. Symptoms?
  3. Conjunctival Nevus: What is it?
    a. Main Location and presentation?
    b. Most common location?
  4. Primary Acquired Melanosis (PAM)
    a. What is it?
    b. Location?
    c. Characteristics?
A
  1. Common, benign, fluid-filled sac on conjunctiva. Can cause irritation.
    a. Inclusion or Retention Cyst
  2. Superficial, whitish-Yellow deposits of mucous secretions and epithelial cells in the palpebral conjunctiva.
    a. Ocular Lithiasis.
    b. Usually Asymptomatic, but may experience a FBS.
  3. Rare, Benign proliferation of Melanocytes that start around puberty or early adulthood. Size and darkness can increase in puberty.
    a. U/L, Solitary, Flat, Freely Mobile, sometimes non-pigmented. INCLUSION CYSTS w/in lesion are diagnostic for this.
    b. JUXTALIMBAL AREA, then Plica, then Caruncle
  4. a. Rare, U/L, Acquired Pigmentation. Usually in Old Caucasians
    b. Anywhere.
    c. Flat, INDISTINCT MARGINS. Benign, but has a PREMALIGNANT POTENTIAL (30% progress to MALIGNANT MELANOMA)
    * *Increased vascularity to it, or an increased growth rate…suspect possible Malignancy.
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65
Q

Conjunctival Lesions (2)

  1. Conjunctival Melanomas
    a. Secondary to what?
    b. Seen mainly in whom?
    c. Color and arise from what?
    d. Most important prognostic indicator for progression to malignancy?
    e. Most common site of metastasis?
  2. Conjunctival Intraepithelial Neoplasia (CIN)
    a. Rare but most common what?
    b. AKA?
    c. What does it look like?
    d. Presentation?
A
  1. a. to uncontrolled proliferation of melanocytes
    b. Caucasians (around age 50)
    c. Pigmented and Non-pigmented. usually come from PAM.
    d. THICKNESS of LESION
    e. LIVER
  2. a. Most COMMON CONJUNCTIVAL MALIGNANCY
    b. Bowen’s Dz or Conjunctival Squamous Dysplasia
    c. U/L, PREMALIGNANT condition. Can progress to SCC (risk is low though).
    d. Elevated, gelatinous mass w/neo. ~10% have Leukophakia (Keratinization). 95% found at limbus w/in Interpalpebral Fissure. Can progress onto the Cornea.
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66
Q
  1. PAM can progress to what?

2. CIN can progress to what?

A
  1. CONJUNCTIVAL MELANOMA

2. SCC

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67
Q

Conjunctival Lesions (3)

  1. Conjunctival Squamous Cell Carcinoma
    a. What is it?
    b. Seen in whom?
    c. most commonly coming from what?
    d. Usually associated with what?
    e. Main Location?
    f. Usually has what with it?
A
  1. a. Rare, Slow-growing, Malignant tumors.
    b. Eldery Caucasian Males
    c. from CIN
    d. UV Radiation and HPV
    e. at LIMBUS and may involve the adjacent cornea.
    f. a FEEDER VESSEL
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68
Q

Conjunctival Lesions (4)

  1. Pyogenic Granuloma
    a. What is it?
    b. Results from what?
  2. Conjunctival Granuloma
    a. What is it?
    b. Location?
    c. Cause?
    b. Symptoms?
A
  1. a. Pedunculated, Benign, Red, VASCULAR LESION of the Palpebral Conjunctiva
    b. Trauma, Surgery, Chalazion, or other sources of Chronic Irriation
  2. a. Inflamed area (White, Yellow, translucent, or brown)
    b. w/in Conjunctival Stromal Tissue
    c. Retained Foreign Bodies, Surgery, Trauma, Infections (Parinaud’s Oculoglandular Syndrome) or associated systemic conditions (Sarcoidosis)
    d. Can be Asymptomatic or have Ocular Irritation and FBS.
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69
Q

Bacterial Conjunctivitis: Simple

  1. Epidemiology
  2. Pathophys
  3. Symptoms
  4. Signs
  5. Most frequent cause of bacterial conjunctivitis worldwide? Why?
A
  1. Children > Adults
  2. H. INFLUENZAE (Gram - ROD)…Most common cause in young kids. Adults: S. Epidermidis and S. Aureus
  3. ACUTE ONSET of REDNESS usually one eye, then goes B/L. FBS, Eyelids stuck together when they wake up. Symptoms usually go away after ~10-14 days w/no Tx.
  4. DISCHARGE (Mod to Severe), starts SEROUS then becomes more MUCOPURULENT (most common) or purulent. Rare Corneal signs and rare Lymphadenopathy.
  5. S. Aureus. D/T high association w/BLEPHARITIS
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70
Q

Bacterial Conjunctivitis: Gonococcal

  1. Epidemiology
  2. Pathophys?
  3. Diagnosis: What’s used?
  4. Symptoms?
  5. Signs?
  6. Systemic Symptoms
    a. Men?
    b. Women?
  7. All Pts should be evaluated for what?
  8. N. Gonorrhea is the only bacterial Conjunctivitis that COMMONLY CAUSES what?
A
  1. STD…Young adults. Multiple sex partners. Can be passed to infants via birth canal.
  2. N. Gonorrhea most COMMON cause. (Gram - intracellular diplococci)
  3. THAYER-MARTIN AGAR
  4. HYPERACUTE ONSET of SEVERE PURULENT DISCHARGE. Redness, FBS, Eyelids stuck together when they wake up. U/L then becomes B/L usually
  5. SEVERE PURULENT DISCHARGE, Conjunctival Chemosis (usually w/PSEUDOMEMBRANES), MARKED PREAURICULAR LYMPHADENOPATHY. Tender and swollen lids.
    * Severe Cases: N. Gonorrhea can invade intact corneal epithelium and cause an ULCERATION
  6. a. Purulent URETHRAL Discharge after ~3-5 days of intubation
    b. ~50% are asymptomatic. Discharge less common.
  7. for CHLAMYDIAL SYSTEMIC INFECTION (co-infection)
  8. PREAURICULAR LYMPHADENOPATHY and PSEUDOMEMBRANES which are usually associated with Viral Conjunctivitis.
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71
Q

Viral Conjunctivitis: Adenoviral

  1. Epidemiology
  2. Pathophys
  3. 3 most common Syndromes?
A
  1. Adults > Children
  2. usually d/t URTI’s. ~1/3 of serotypes are associated with ocular infections. Transmission = Direct Contact. Highly Contagious for 12-14 days.
  3. Acute, Nonspecific Follicular CONJUNCTIVITIS, Phayngoconjunctival Fever (PCF) and Epidemic Keratoconjunctivitis (EKC)
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72
Q

Viral Conjunctivitis: Adenoviral: Syndromes

  1. Acute Nonspecific Follicular Conjunctivitis
    a. Comes from what Serotypes?
    b. Presentation?
  2. PCF
    a. Serotypes?
    b. AKA?
    c. Affects whom more?
    d. TRIAD of what signs/symptoms?
  3. EKC
    a. Serotypes?
    b. What is most commonly associated with this type?
    c. Symptoms and signs?
    d. What is almost always present in these patients?
A
  1. a. 1-11 and 19 = Most common type.
    b. Diffuse Red Eye, Conjunctival FOLLICLES in INFERIOR FORNICES, Tearing, Mild Discomfort; Rare corneal involvement
  2. a. 3-5 and 7.
    b. SWIMMING Pool Conjunctivitis
    c. Children. Highly Contagious
    d. Acute Follicular Conjunctivitis (Red Eye); Mild low grade Fever; Pharyngitis (sore throat). Rare corneal involvement
  3. a. 8, 19, 37. MOST SERIOUS FORM of Adenoviral Conjunctivitis.
    b. PAIN and CORNEAL INVOLVEMENT
    c. seen after 8 days from exposure. SEIs seen in 3rd week when pt is NO LONGER CONTAGIOUS
    d. PREAURICULAR LYMPHADENOPATHY. May also have pseudomembranes.
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73
Q

Viral Conjunctivitis: Adenoviral (3)

  1. Symptoms
  2. General Signs
  3. SEIs can be one of 2 things?
  4. What is almost always pathognomonic for EKC?
A
  1. Rapid onset of redness, tearing, mild discomfort, PREAURICULAR LYMPHADENOPATHY. Starts U/L, then spreads…B/L.
  2. ACUTE FOLLICULAR CONJUNCTIVITIS (follicles in Inferior Fornices), Conjunctival Injection, PSEUDOMEMBRANE FORMATION, PREAURICULAR LYMPHADENOPATHY (Classic for EKC) and Diffuse Keratitis (esp in EKC)
  3. Infectious (viral, chlamydial, bacterial) or Noninfectious (Graft rejection, solution hypersensitivity, hypoxia)
  4. PALPABLE NODE.
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74
Q

Viral Conjunctivitis: Molluscum Contagiosum

  1. Epidemiology
  2. Pathophys
  3. Signs/Symptoms
A
  1. Rare; Usually in places w/POOR HYGIENE; Children and Young Adults
  2. Chronic Infectious skin condition d/t DNA POX VIRUS spread via Direct Contact. Multiple nodes seen…suspect HIV
  3. Single or multiple dome-shaped, umbilicated, waxy nodules on Lid or LID Margin. Asymptomatic usually. Rupture –> chronic follicular conjunctivitis and superficial pannus.
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75
Q

Viral Conjunctivitis: Herpes Simplex

  1. How does it usually present?
A
  1. U/L Follicular Conjunctivitis w/Watery Discharge
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76
Q

Allergic Conjunctivitis

  1. Seasonal: Cause?
  2. Perennial: Cause?
  3. Signs/Symptoms?
A
  1. Type 1 Hypersensitivity (airborne allergens)
  2. less common type 1 hypersensitivity…Household allergies (dust mites, animal dander, etc)
  3. Conjunctival Chemosis, PAPILLAE, itching, tearing, watery discharge
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77
Q

VKC

  1. How common is it?
  2. Epidemiology?
  3. When does it come on?
  4. Patho?
  5. Symptoms?
  6. Signs?
    a. Signs are mainly found in what 2 areas of the eye?
A
  1. RARE
  2. young males; Hot, dry climates. resolves usually by puberty
  3. Seasonal. ex: 8 y/o male. Asthma. Huge Papillae on lid eversion each spring.
  4. pt is PREDISPOSED to ATOPIC SYSTEMIC CONDITIONS (rhinitis, asthma, etc). SEASONAL OUTBREAKS…WARM MONTHS!
  5. INTENSE ITCHING, Photophobia (most common Complaint), Ptosis, THICK MUCOUS DISCHARGE. INITIAL OUTBREAK MOST SEVERE
  6. PROMINENT PAPILLAE on Limbus (TRANTAS DOTS) or upper palpebral Conjunctiva (COBBLESTONE PAPILLAE). Cornea: starts w/Punctate Epithelial Keratitis –> coalesces to LARGE EROSION –> Plaque Formation –> LOCALIZED ULCERATION (SHIELD ULCER).
    a. Conjunctiva and Cornea
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78
Q

AKC (Atopic)

  1. Epidemiology
  2. What is ATOPIC DERMATITIS?
  3. Patho?
  4. Symptoms?
  5. Main Signs?
  6. What else can cause an ALLERGIC CONJUNCTIVITIS w/a FOLLICULAR REACTION?
A
  1. RARE; Young to middle aged adults (40s). Hx of Atopic conditions, especially ATOPIC DERMATITIS
  2. Chronic Eczema (Early infancy). 60% w/in first year of life. Pruritis, Rash. Can get a CATARACT b/w 15 and 30.
  3. NOT SEASONAL. KID will ITCH like CRAZY. (Type 1 and Type 4 Hypersensitivity RxN)
  4. B/L ITCHING of EYELIDS. watery discharge, redness, photophobia, pain.
  5. DENNIE’s LINES (extra crease under lower lid d/t periorbital edema); Atopy Shiners (bags under eyes from constant rubbing). Prominent outer eyelid. Periorbital involvement.
    * Papillae: usually INFERIORLY (Superior Papillae in VKC and GPC). Conj signs can be mild.
    * Corneal NEO, KERATOCONUS and Cataracts more common in AKC
    * Symblepharon Formation of Inferior Fornices in severe cases
  6. TOXICITY to Topical Medications or CL solutions.
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79
Q

Papillae vs. Follicles

  1. Papillae: What are they?
    a. Main cause?
  2. Follicles
    a. What are they?
    b. Main cause?
    c. Cells w/in it?
A
  1. inflamed, elevated Conjunctiva w/a Central vessel that’s the source of infiltration of Eosinophils, mast cells, neutrophils, and lymphocytes.
    a. Allergies and Bacteria, but NON-SPECIFIC.
  2. a. Avascular, white-gray nodules..usually in Tarsal and Fornix Conjunctiva. FIRM.
    b. Chlamydia, Toxic, or Viral Infections
    c. Immature lymphocytes and macrophages in it.
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80
Q

GPC

  1. How common?
  2. Epidemiology?
  3. Patho?
  4. Symptoms?
  5. Signs?
A
  1. Extremely Common
  2. 95%: CL Wear; exposed sutures, glaucoma filtering blebs, scleral buckles, ocular prosthetics. EW SCLs main cause. AWT: 8 months before it starts; or as early as 3 wks.
  3. Non-Infectious inflammation…usually d/t MECHANICAL TRAUMA and IMMUNE RESPONSE to CL surface deposits or environmental factors.
  4. Itching. Early: some mucous discharge; Late: Ropy mucous discharge. Photophobia.
  5. Mild-severe papillae in upper conjunctiva. ptosis; mucous in eye.
    * Papillae >0.3 mm diameter. Giant Papillae (>1.0 mm)…neighboring papillae coalesce after prolonged inflammation.
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81
Q

CL Disorders…

  1. Solution Hypersensitiity/Toxicity: Severe RxN usually d/t solutions with what 2 preservatives?
  2. Corneal Neo: Look out for what?
  3. Corneal Warpage: With what kind of lenses?
    a. Symptoms/signs?
  4. Superior Limbic Keratoconjunctivitis (SLK): Cause?
    a. Signs?
  5. Deposits
    a. GP lens
    b. Hydrogel?
  6. Tight-lens Syndrome (TLS)
    a. What is it?
    b. Symptoms?
    c. Signs
  7. Classic example of a lens that rides too high?
  8. Classic example of a lens that rides too low?
  9. Superior Epithelial Arcuate Lesion (SEAL): What is it?
  10. Dimple Veiling: What is it?
A
  1. Chlorhexidine or Thimerosal….Conj. Injection and diffuse SPK.
  2. Superior Pannus. Corneal neo more than 1.5 mm is a concern.
  3. long-term PMMA wearers, GP wearers w/poor fitting lens.
    a. Vision clear in CL but blurry in glasses. Ghost images and diplopia. *refit and not wearing for a while will fix the problem.
  4. CL Hypersensitivity reaction (esp Thimerosal) or Poor CL fit
    a. Sup Bulbar and upper tarsal conjunctival injection. Papillary reaction and corneal filaments uncommon.
  5. a. look like PLAQUES
    b. look like JELLY BUMPS
  6. CL doesn’t move w/blinking. Usually High myopes (>-8.00D), hyperopes and aphakes. Lenses too steep or have OAD 15.00 mm.
    b. Redness. Worsens after lens is removed, hazy vision, halos, dyness.
    c. mild-severe corneal edema. corneal blebs. injection around limbus.
  7. Corneal Warpage
  8. 3 and 9 o’clock staining
  9. EW Hydrogel lenses fit too tight. Poor lens wettability. 30% asymptomatic. FBS, Irritation, underlying corneal infiltrates (40%)
  10. small bubbles trapped under CL (RGP). pushes bubble onto cornea –> divot for fluorescein to pool.
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82
Q

List things that could cause Keratoconjunctivitis?

A
  1. Bacterial/Viral Infections, HSV, HZV, Fungal Infections, Atopy, Allergic, Vernal, Toxic Reactions, Factitious Dz.
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83
Q

Adult Inclusion Conjunctivitis: Chlamydial

  1. Epideimology
  2. Patho (Starts w/a D, ends w/a K)
  3. Symptoms
  4. Signs
  5. What is Ophthalmia Neonatorum?
A
  1. Rare. Sexually active young adults. Most common STD in US.
  2. Urogenital disease d/t Chlamydia serotypes D-K. Direct spread. See signs 5-14 days after inoculation. Active Genital Infection.
  3. ACUTE FOLLICULAR CONJUNCTIVITIS…gets to be CHRONIC. Starts U/L then goes B/L.
  4. FOLLICLES (limbal or palpebral) usually in INFERIOR PALPEBRAL CONJUNCTIVA and FORNICES. Preauricular lymphadenopathy. Scant mucopurulent discharge. matting of lids. Cornea: punctate keratitis, superior pannus, SEIs usually more peripheral than EKC.
  5. Acute Cojunctivitis in newborns (HSV, Gonorrhea, chalmydia)…CHLAMYDIA leading cause in US.
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84
Q

Trachoma Conjunctivitis: Chlamydia

  1. Epidemiology
  2. Patho
  3. Signs/Symptoms
    a. Early
    b. Late
A
  1. Most prevalent b/w ages 1-5. LEADING CAUSE of PREVENTABLE BLINDNESS WORLDWIDE. Poor hygiene. Direct spread.
  2. Chlamydia Serotypes A-C. ALMOST ALWAYS B/L.
  3. a. FOLLICULAR CONJUNCTIVITIS on sup. tarsal conj. mucopurulent discharge, MILD SUPERIOR PANNUS.
    b. ARLT LINES (white scarring on sup. tarsal conj.) and HERBERT’s PITS (depression on limbal conj. after resolution of limbal follicles); *Blindness d/t Corneal ulceration from tarsal conjunctival scarring.
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85
Q

Superior Limbic Keratoconjunctivitis (SLK)

  1. Epidemiology
  2. Patho
    a. Keratoconjunctivitis Sicca
    b. Thyroid Disease
    c. CL Wearers
  3. Symptoms
  4. Signs
A
  1. Uncommon; Females (3:1); Mean Age: 50. Hx: Recurrent episodes
  2. Chronic inflammation reaction associated with Keratoconjunctivitis Sicca (25%), thryroid Dz (20-50%) and CL wear.
    a. Drying b/w upper eyelid and Bulbar Conj –> more friction –> turnover and replacement of mature sup. conj. cells does not happen.

b. continual friction of sup. palpebral conj on sup. bulbar conj d/t tight apposition from exophthalmos
c. increased friction –> increased risk of SLK
3. Redness, FBS, frequent blinking, NO DISCHARGE. SYMPTOMS WORSE THAN SIGNS.
4. Thickened, red SUPERIOR Bulbar CONJ prominent at LIMBUS and is B/L usually. w/Adjacent SPK and Filamentary Keratitis. Upper tarsal conj can look velvety d/t diffuse papillary hypertrophy.

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86
Q

Phlyctenular Keratoconjunctivitis

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
  5. Conjunctival Phlyctenules
  6. Corneal Phlyctenules
A
  1. Teenage; Females; similar eye infections in the past. History of TB.
  2. Type-4 HYPERSENSITIVITY RxN to STAPHYLOCOCCUS (Blepharitis most common culprit), tuberculoprotein, and Acne Rosacea.
  3. Tearing, FBS, Itching, Conj and Corneal Phlyctenules; Photophobia common w/Corneal Phlyctenules.
  4. Phlyctenules on Conj or Cornea.
  5. at LIMBUS…look pink, fleshy nodules w/Conj injection
  6. Near limbus. Small, White (lymphocytic) nodule w/adjacent conj. Injection.
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87
Q

Ligneous Conjunctivitis

  1. Epidemiology
  2. Patho
  3. Signs
  4. Symptoms
A
  1. Rare; Childhood
  2. Ocular signs of Systemic problem; Associated w/Systemic PLASMINOGEN deficiency. Can affect mucous membranes in the body.
  3. Thick, White, “woody” membranous plaque of the superior tarsal conjunctiva
  4. Chronic tearing, FBS, photophobia; constant discomfort and cosmetic concerns in advanced disease.
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88
Q

Parinauds’ Oculoglandular Syndrome

  1. Epidemiology
  2. Patho
    a. Cat-Scratch Fever
    b. Tularemia
    c. Other causes?
  3. Symptoms
  4. Signs
A
  1. Rare; Exposure to cats, dogs, rabbits, squirrels, ticks
  2. a. Most common cause; Bartonella Henselae. Cat scratch to eye or thru flea bites to eye.
    b. ticks, rabbits, squirrels
    c. TB and Syphilis
  3. Red eye, FBS, mucopurulent discharge
  4. U/L, GRANULOMATOUS, follicular, palpebral conjunctivitis. SWOLLEN PREAURICULAR/SUBMANDIBULAR LYMPHADENOPATHY. Could have Fever and Rash
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89
Q

Phthiriasis Palpebrarum (Pediculosis Ciliaris)

  1. Patho
  2. Symptoms
  3. Signs
A
  1. from Phthirus Pubis (Crab louse) from hair in genital area. Infection of Eyelashes, eyebrows, facial hair via direct contact w/infected peeps or clothing or linen. Can be U/L or B/L.
  2. Mild itch to Imflammation w/Burning, itching, tearing, blurred vision
  3. Transparent lice and white nits (eggs) on eyelashes; Blood-tinged debris on lids and lashes. Mild-Severe Chronic Follicular Conjunctivitis. Preauricular Lymphadenopathy.
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90
Q

Subconjunctival Heme (COMMON)

  1. What is it?
    a. Causes?
  2. Order what?
A
  1. Blood under conj.
    a. VALSALVA; Meds (Aspirin, Coumadin), HTN, Blood Clotting disorder (sickle cell)
  2. CBC, PT/PTT, sickledex for idiopathic and recurrent cases esp in African or Mediterranean descent.
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91
Q

Pterygium/Pingueculum

  1. What causes it?
  2. Pingueculum
  3. Pterygium
A
  1. Degeneration of collagen fibrils w/in Conj. Stroma.
  2. Y-W (raised) deposit adjacent to Limbus but not on cornea.
  3. Triangular fibrovascular growth of Bulbar Conj. Extends onto cornea. DESTROYS BOWMANs MEMBRANE –> ATR Astigmatism. STOCKER’S LINE (IRON DEPOSIT) can be present at ANTERIOR edge of PTERYGIUM.
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92
Q

Episcleritis

  1. Causes: Systemic Dzs
    a. Collagen Vascular/Inflammatory Dzs
    b. Spirochectes
    c. Viruses
    d. Metabolic Dzs
    e. Vasculitis Dzs
    f. Dermatological Dzs
  2. Epidemiology
  3. Patho
  4. Symptoms
  5. Signs
A
  1. a. RA, Lupus, Ulcerative Colitis, Crohn’s Dz, Reactive Arthritis, AS, Psoriatic Arthritis
    b. Syphilis, Lyme Dz
    c. Herpes Zoster, HSV, Mumps
    d. Gout
    e. Temporal Arteritis, Wegener’s, Behcet’s Dz, Polyarteritis Nodosa
    f. Acne Rosacea
  2. Young adults; Frequent Recurrences
  3. Benign, self-limiting inflammation; IDIOPATHIC usually; associated with systemic Dzs though.
  4. Acute, U/L Red Eye; maybe mild pain
  5. Sectoral Injection (70%); Simple (80%), Nodular (20%); Can move the nodule w/a Cotton tip applicator (way to Differentiate from Scleritis)
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93
Q

Scleritis (RARE)

  1. Epidemiology
  2. Non-Necrotizing (85%)
    a. Diffuse (60%)
    b. Nodular (25%)
  3. Necrotizing (15%)
    a. w/Inflammation (5%)
    b. w/o Inflammation (10%)
A
  1. Females; 98% are Anterior Scleritis;
  2. a. MOST COMMON TYPE. Most BENIGN form. Least Severe Systemic Conditions. DIFFUSE HYPEREMIA
    b. DEEP, Focal, Painful, Injected, Immobile Nodule
  3. a. WORST FORM; 33% die w/in a few years d/t severe AI Dz. Many lose Vision; Many have ocular or systemic problems (Ant Uveitis, Sclerosing Keratitis, Peripheral Corneal Melt, Scleral Thinning, Cataracts, Glaucoma)
    b. aka SCLEROMALACIA PERFORANS. usually d/t CHRONIC RA. LACK OF SYMPTOMS. Asymptomatic; maybe GRAY-BLUE PATCHES d/t SCLERAL THINNING (uvea exposed)
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94
Q

Scleritis (2)

  1. Patho
  2. Symptoms
  3. Signs
A
  1. Granulomatous Inflammation of Sclera w/1/2 having some systemic Dz. 30% d/t a Collagen vascular Dz (RA being most common, then WEGENER’s Granulomatosis)
  2. SEVERE, BORING, OCULAR PAIN. Wakens pt in night. Radiated pain. Gradual onset of Redness and Decrease in Vision (except for Scleromalacia perforans)
  3. Sectoral or diffuse inflammation. Can’t be moved w/Cotton swab. THIN SCLERA. usually B/L
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95
Q

What are Hyaline Plaques?

A

Benign, Oval shaped areas of SCLERAL THINNING that happen w/Age.

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96
Q

Differentiating b/w Episcleritis and Scleritis

  1. Onset
  2. Characteristics
  3. 2.5% Phenylephrine BLANCHING in which Pt?
  4. Findings?
  5. More common? More likely to have an underlying Systemic Disorder?
  6. DDx for SEVERE OCULAR PAIN?
A
  1. Scleritis: Gradual, but SEVERE OCULAR PAIN and more severe complications.
  2. Scleritisi: BLUISH-HUE
    Episcleritis: RED appearance
  3. EPISCLERITIS; still red: 10% phenylephrine will blanch superficial vessels…so EPISCLERITIS will look less red.
  4. Scleritis: B/L w/Diffuse Injection
    Episcleritis: U/L w/Sectoral Injection
  5. Episcleritis; Scleritis
  6. Scleritis, Uveitis, Acute ACG, Corneal Pathology (abrasions, erosions, ulcers)
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97
Q

Axenfeld’s Nerve Loop

  1. What is it?
  2. What nerve is it?
A
  1. Focal, Pigmented, Elevated area.

2. Posterior Ciliary Nerve loops visible in sclera.

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98
Q

Anterior Uveitis

  1. Epidemiology
  2. Patho
  3. Spondyloarthropathies
  4. HLA-B27..doesn’t tell u CRAP!
A
  1. 15/100,000/yr; 45,000 new cases/yr in US. YOUNG ADULTS; Rare in peeps over 70 (if seen, think Toxoplasmosis or HERPES ZOSTER!)
  2. 2ndary breakdown to Blood-Aq Barrier. 50% w/Acute Anterior Uveitis have HLA-B27 (70% if recurs);
    50% new onset acute Anterior Uveitis: ASSOCIATED SPONDYLOARTHROPATHY w/80% having AS.
  3. IBD (Crohn’s, Ulcerative Colitis), Reactive Arthritis (Reiter’s Syndrome), AS, Psoriatic Arthritis
  4. Crohn’s, Reactive arthritis, AS, Psoriatic
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99
Q
  1. Majority of Uveitis Cases are what?
A
  1. 75% Anterior (Iritis, Iridocyclitis), 8% intermediate (pars planitis) and 17% Posterior or Panuveitis
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100
Q

Anterior Uveitis

  1. Acute: Length of time?
  2. Chronic?
  3. Most common type seen?
A
  1. Less than 3 MONTHS
  2. Lasts for more than 3 MONTHS
  3. Acute Anterior U/L Nongranulomatous Uveitis
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101
Q

Anterior Uveitis

  1. Symptoms
    a. If Chronic?
  2. What causes PAIN in this?
A
  1. PAIN, REDNESS, PHOTOPHOBIA, lacrimation, maybe decreased vision.
    a. can be Asymptomatic; or have blurred vision or a dull ache.
  2. d/t CONGESTION and irritation of ANTERIOR CILIARY NERVES
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102
Q

Anterior Uveitis

  1. Signs
  2. Main threats to vision?
  3. Other possible Signs?
  4. Granulomatous..think what?
A
  1. Presence/Absence of WBCs in AC.
  2. PS, PAS, Cystoid Macular Edema (CMS), CATARACT FORMATION (usually PSC)
  3. Flare, Hypopyon, Circumlimbal inj, decreased IOP (early stages), Keratic Precipitates (KPs on Endothelium)
    * Decreased IOP d/t CB Inflammation. Increased IOP d/t eye gets better, Trabeculitis, PS (Acute angle closure), PAS (chronic Angle closure), lots of inflammation, Steroid Tx, Chronic TM Damage.
  4. Infectious (TB, Syphilis) (signs…Mutton Fat KPs and Iris Stromal Nodules….granulomatous)
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103
Q

Anterior Uveitis: Granulomatous

  1. Mutton Fat KPs
  2. Koeppe Nodules
  3. Busacca Nodules
  4. Most common Corneal finding in Ant Uveitis?
  5. What is seen most commonly in Fuch’s Heterochromic Iritis and sometimes Herpetic Uveitis?
A
  1. Macrophages w/Greasy appearance; usually in Middle/Lower cornea
  2. Pupillary margin; seen in both gran and non-gran uveitis
  3. any part of IRIS STROMA…just not pupillary margin…GRANULOMATOUS etiology.
  4. KPs
  5. STELLATE KPs
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104
Q

Anterior Uveitis: Systemic Conditions (Acute Non-Granulomatous Anterior Uveitis)

  1. Inflammatory Bowel Disease
  2. Reactive Arthritis
  3. Ankylosing Spondylitis
  4. Psoriatic Arthritis
  5. Behcet’s Dz
  6. Lyme Dz
  7. Glaucomatocyclitic Crisis
A
  1. B/L w/Posterior Uveitis component. Chronic, intermittent Diarrhea w/alternating episodes of constipation. Uveitis: RARE (2.4%). More common w/Ulcerative Colitis (5-10%)
  2. Young Males; URETHRITIS, POLYARTHRITIS, and CONJUNCTIVITIS (w/IRITIS)
  3. MALES (3:1), 30s; LOWER BACK PAIN; Symptoms improve w/Exercise
  4. Asymmetric, Peripheral, Small Joint Pain, and Psoriatic Lesions on Knees, Elbows, and Scalp
  5. Young adults: Asian and Middle Eastern Descent; Acute, Recurrent Hypopyon Iritis and Mouth and Genital Ulcers; Can be associated w/Retinal Vasculitis, Cataracts, and Glaucoma
  6. Hx of Tick bites, Skin Rash, and/or Arthritis
  7. aka Posner-Schlossman Syndrome: Mild Iritis w/RECURRENT, self limiting episodes of Elevated IOP (30-40s) secondary to Trabeculitis, fine KPs and Open angle on Gonio.
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105
Q

Anterior Uveitis: Systemic conditions: Chronic Granulomatous

  1. Sarcoidosis
  2. TB
  3. Herpes Simplex/Zoster
  4. Syphilis
    a. Interstitial Keratitis
  5. Most common Causes of Interstitial Keratitis
  6. CONGENITAL SYPHILIS TRIAD?
A
  1. Females; AAs; Uveitis: B/L: Posterior or Panuveitis; Abnormal Chest X-Ray; Increased ACE Levels
    • PPD; Abnormal Chest X-ray; NIGHT SWEATS; can have Posterior or Panuveitis
  3. Increased IOP in involved eye. Stellate KPs, Corneal Edema, Maybe epithelial defects; Zoster: Vesicles on Affected Dermatome
  4. May have Interstitial Keratitis; Maculopapular Rash (palms/Soles); +VDRL or RPR; and + FTA-ABS or MHA-TP
    a. Stromal Inflammation W/O Primary involvement of Epithelium or Endothelium
    * IK: Chracterized by Acute Stromal Inflammatory Edema and Neo; Progresses to Diffuse stromal Neo.
    * Late Stages of IK: Stromal vessels partially clear, leads to Ghost vessels, Corneal scarring, and Irregular Astigmatism
  5. CONGENITAL SYPHILIS (90%), TB and Herpes Simplex;
    * Stromal Keratitis: Most common sign of Late Congenital Syphilis
    * ACQUIRED SYPHiliS: rarely causes keratitis; if seen, usually U/L and less severe than Congenital.
  6. HUTCHINSON’S TEETH (small, widely spaced), DEAFNESS, and INTERSTITIAL KERATITIS! May also have saddle-nose deformity and Frontal Bossing (Prominent Forehead)
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106
Q

Anterior Uveitis: Chronic, Non-Granulomatous: Systemic

  1. JIA
  2. Fuch’s Heterochromic Iridocyclitis
  3. What 3 big Drugs can cause Anterior Uveitis?
  4. What is Pars Planitis?
A
  1. Most common cause for Uveitis in KIDS; B/L uveitis in young Girls; NEGATIVE RF factor, but + ANA
  2. More common in BLUE EYES; U/L (90%) mild uveitis w/FINE, Stellate KPs, Angle Neo, Iris Heterochromia. Associated w/Glaucoma (15%) and Cataracts (70%). Usually ASYMPTOMATIC.
  3. RIFABUTIN, SYSTEMIC SULFONAMIDES, and CIDOFOVIR.
  4. Chronic, Intermediate Uveitis; Inflammation of Pars Plana (SNOWBANKING) and Peripheral retina. NOT ASSOCIATED w/SYSTEMIC CONDITIONS.
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107
Q

Posterior Uveitis

  1. Cause?
  2. Ask about what?
A
  1. Breakdown of Blood Aq. Barrier –> WBCs w/in VITREOUS. Pts: Complain of FLOATERS and/or DECREASED VISION
  2. Rash, tick bites, risk factors for AIDS, breathing problems, Recent travel to Ohio-Mississippi River Valley
108
Q

Posterior Uveitis: Systemic Conditions

  1. Toxoplasmosis
    a. Epidemiology
    b. Patho
    c. Congenital
    d. Acquired

e. Signs/Symptoms
f. Characterized by what?

A
  1. a. MOST common cause in US
    b. PARASITIC INFECTION by Toxoplasma Gondii (Obligate intracellular Intestinal Parasite). Congenital or Acquired

c. Transplacental Transmission; Most common form (90% of cases); 40% transferred if mother gets an ACUTE FORM during Pregnancy; Infected PRIOR to pregnancy, baby WILL NOT BE INFECTED.
10%: TRIAD: Convulsions, Cerebral Calcifications; Chorioretinitis. Most are mild w/insignificant chorioretinal scars

d. Inhaling parasite in CAT FECES and/or eating UNDERCOOKED MEAT.

e. Most common cause of infectious Retinitis: recurrence of old, stable, congenital ocular toxoplasmosis lesion;
* Young Healthy Pt; recent Onset of U/L Redness, Photophobia, floaters, uveitis, vitritis, decreased vision. Recurrences: ~age 25.

f. Focal, Fluffy, Yellow-white retinal lesion adjacent to an OLD INACTIVE SCAR w/overlying VITRITIS.
* Lesion usually hard to see cleary d/t dense vitritis. (HEADLIGHTS in the FOG)…basically…active lesion w/WBCs floating in front of it.

109
Q
  1. What does HISTOPLASMOSIS cause?
  2. Does it lead to Posterior Uveitis?
  3. What does it look like?
A
  1. Choroiditis
  2. NO
  3. Multifocal, “punched out” yellow-white lesions in PERIPHERY w/Peripapillary atrophy and maculopathy. Common in Ohio-Mississippi River Valley. FUNGUS
110
Q

Posterior Uveitis: Systemic Conditions: Less common causes

  1. Sarcoidosis
  2. Syphilis
  3. CMV
  4. CMV vs. PORN
    a. CMV
    b. PORN
A
  1. Granulomatous Panuveitis w/RETINAL VITRITIS (Cotton-Ball OPACITIES: white, fluffy opacities in INFERIOR VITREOUS);
    and/or
    RETINAL VASCULITIS: sheathing around retinal veins and yellow-white exudates d/t Periphlebitis (CANDLE-WAX DROPPINGS)
  2. 2ndary syphilis can cause ACUTE MULTIFOCAL chorioretinitis w/Vitritis or Panuveitis
  3. Most common Ocular Infection and leading cause of blindness in AIDS; White Patches of Necrotic retina w/Hemorrhagic retinitis and vascular sheathing. CD4 LESS THAN 50! DDx from TOXOPLASMOSIS and PORN
  4. a. More intravitreal Hemorrhage and less vitritis than Toxoplasmosis
    b. Minimal amts of Vitritis (similar to CMB) and Hemorrhage (less than CMV)
111
Q

Iris Coloboma

  1. Patho
  2. Signs
  3. Complete Iris Coloboma
  4. Incomplete Coloboma
  5. Iris Colobomas are usually associated w/other Coloboma types things…such as…?
A
  1. Local defect/Notch in iris: INCOMPLETE CLOSURE of EMBRYONIC FISSURE of OPTIC VESICLE during gestation
  2. usually in INFERIOR NASAL QUADRANT (where embryonic fissure is w/in optic vesicle)
  3. Full thickness defect; can go from Pupillary margin to Peripheral Cornea (KEY HOLE PUPIL). or involve only pupillary margin (OVAL SHAPED PUPIL)
  4. Partial thickness defect: visible as IRIS TRANSILLUMINATION DEFECT on Retroillumination
  5. CB, Zonular, Choroidal, Retinal, or ON Coloboma
112
Q

Iris Malignancy

  1. Patho
  2. Signs
A
  1. Malignant Tumor. D/t abnormal proliferation of melanocytes w/in iris stromal tissue. Most are though to come from Iris Nevi (2% of cases w/in 5 years)
  2. Iris melanomas may be pigmented or amelanotic and are located w/in iris stromal tissue in INFERIOR QUADRANT in 80% of cases. Irregular “Feathery” margins and a diameter greater than 3 mm = classic sign.
113
Q

Cornea/Refractive Surgery: Miscellaneous Keratopathies

  1. Dellen
  2. Exposure Keratopathy
    a. Patho
    b. Symptoms
    c. Signs
A
  1. Area of cornea that wets poorly –> stromal dehydration, corneal thinning w/POOLING of FLUORESCEIN w/in that area. (near pterygia, filtering blebs, tumors, poor fitting RGP lenses). Pts: Asymptomatic or occasional FBS.
  2. WORSE in the MORNING
    a. Abnormal/INCOMPLETE LID CLOSURE d/t Bells Palsy, Eyelid Sx, CVA, Aneurysm, MS, HSV, HZV, TED, FES, etc.
    b. Redness, FBS, Burning

c. Mild SPK (usually inferior 1/3 or Interpalpebral region of cornea) to Corneal Ulceration. Common DECREASED CORNEAL SENSITIVITY

114
Q

Cornea/Refractive Surgery: Miscellaneous Keratopathies

  1. Filamentary Keratopathy
    a. Epidemiology
    b. Patho
    c. Symptoms
    d. Signs
A
  1. a. Chronic irritation/dryness.
    b. Chronic inflammation of cornea. ex: KERATOCONJUNCTIVITIS SICCA (most common cause), SLK, Corneal abrasions, erosions, CL overwear, Neurotrophic Keratopathy, etc.

c. Mild-Severe FBS w/Photophobia, epiphora, blurred vision and Blepharospasm
d. DEGENERATED EPITHELIAL CELLS and MUCOUS that remain attached to Epithelial surface. Size: 0.5-10 mm. Short, long, or stringy. Filaments stain w/Fluorescein

115
Q

Cornea/Refractive Surgery: Miscellaneous Keratopathies

  1. SPK (Superficial Punctate Keratitis)
    a. Patho
    b. Signs/Symptoms
  2. Thygeson’s SPK
    a. Epidemiology
    b. Patho
    c. Symptoms
    d. Signs
A
  1. a. Non-Specific inflammation of Corneal Epithelium d/t CL wear, infections, DES, Blepharitis, etc…tons and tons of reasons. Allergic response to meds, trichiasis, distichiases, FES, FBs, UV exposure, LASIK
    b. Pinpoint defects in corneal epithelium that stain w/Fluorescein. Asymptomatic, or have blurred vision, irritation, FBS, Photophobia, redness, tearing.
  2. a. RARE; ex: 30y/o FBS B/L corneal lesions, minimal inflammation, frequent episodes

b. Unkown. Viral or AI. Soft Steroid FEELS REALLY GOOD.
c. FBS, Photophobia, tearing, blurred vision. Chronic, B/L, asymmetric.

d. B/L, small, multiple, asymmetric Gray-white clusters of Superficial, intraepithelial, raised CENTRAL Corneal lesions (~15-20). Comes and goes w/o serious sequelae for ~10-20 years before finally resolving.
a. Acute Attacks (exacerbations): 1-2 months if untreated then resolves. lightly stain w/fluorescein. recurs w/in 6-8 wks
b. Remissions: inactive b/w acute attacks. Don’t stain w/Fluorescein during remission

116
Q

Cornea/Refractive Surgery: Miscellaneous Keratopathies

  1. Neurotrophic Keratopathy
    a. Epidemiology
    b. Patho
    c. Causes?

d. Symptoms
e. Signs?

A
  1. a. Past Sx procedures, CL wear, systemic Dzs, medications

b. CNV1…damage to sensory nerve supply. DECREASED CORNEAL SENSITIVITY. decline in Corneal regeneration and wound healing.
c. Common: HSV, HZV, Diabetes, LASIK, CL wear, RCEs, corneal dystrophies.
Less common: Tumors (Acoustic neuroma), CVA, meds (Timolol, Betaxolol, Diclofenac Sodium). Surgery: Maxillary fracture repair, trigeminal neuralgia.

d. Redness, tearing, decreased vision, FBS, Swollen eyelids. CORNEAL FINDINGS are WORSE than SYMPTOMS. (should feel a lot worse)
e. DECREASED CORNEAL SENSITIVITY; SPK w/Perilimbal injection. Inferior OVAL ULCER (late sign)

117
Q

Cornea/Refractive Surgery: Miscellaneous Keratopathies

  1. RCE
    a. Patho
    b. Symptoms
    c. Signs
A
  1. a. Poor Hemidesmosome Attachments to BM; d/t SUPERFICIAL TRAUMA (Corneal abrasions), Corneal Dystrophies (MOST COMMONLY EBMD) and/or Age-related thickening or reduplication of BM. Risk increases for RCE if previous abrasion d/t Organic etiology (wood, fingernail, etc)
    b. Recurrent episodes of ACUTE PAIN…usually in MORNING AFTER WAKING UP. Lacrimation, photophobia, blurred vision.
    c. Corneal abrasion.
118
Q

Cornea/Refractive Surgery: Miscellaneous Keratopathies

  1. Thermal/UV Keratopathy
    a. Epidemiology
    b. Patho
    c. Symptoms
    d. Signs
A
  1. a. Prolonged sun exposure, welding, skiing, sunlamp w/o protective eye wear
    b. Epithelium and Bowman’s layer absorb wavelengths below 300 nm; Excessive absorption –> Hyperactivation of K+ channels –> Loss of intracellular K+ –> Cell death
    c. Ocular pain, photophobia, blurred vision. usually worse 6-12 hours after incident.
    d. Confluent SPK w/in interpalpebral region of cornea that stains w/fluorescein.
119
Q

DES: DEWS study

  1. Epidemiology
  2. Medications
    a. Anticholinergic Effect drugs?
    b. What else? (multiple)
  3. Systemic Dzs
  4. Environmental Factors
  5. Classic Lissamine Green Staining?
A
  1. More common w/Aging; Postmenopausal women.
  2. a. Atropine, Scopolamine, TCAs
    b. Antihistamines, Chlorpromazine, Thioridazine, Isotretinoin, B-Blockers, Oral Contraceptives, Hormone Replacement Therapy, ADHD meds, Diuretics
  3. TED, Collagen Vascular Dzs (RA, Sjogrens, SLE)
  4. Ceiling fans, dusty places, low humidity.
  5. Inferior and at 3 and 9 o’clock
120
Q

DES: DEWS study

  1. Schirmer 1 Testing
    a. What does it do?
    b. Normal?
    c. Borderline?
    d. Abnormal?
  2. Schirmer 2 Testing
    a. What does it do?
    b. Normal?
  3. Phenol Red Test (PRT)
    a. Normal?
A
  1. a. w/o Anesthetic; Measures BASAL and Aq. Tear Secretions
    b. >10 mm wetting in 5 min
    c. 5-10 mm wetting
    d. 5 mm wetting in 5 minutes.
  2. Assesses Aq. Tear Production by using Cotton thread w/pH sensitive Phenol red.
    a. >10 mm of wetting (thread turns red) after 15 seconds
121
Q

What do Rose bengal and lissamine green stain?

A

DEAD and DEVITALIZED CONJUNCTIVAL and CORNEAL CELLS, and cells that have lost mucous covering.

Fluorescein: pools w/in epithelial defects and aqueous part of tears. useful for evaluating thickness of the tear meniscus.

122
Q

DES: DEWS study: Mechanisms behind Dry Eye Dz.

  1. TEAR HYPEROSMOLARITY
  2. Tear Film instability
A
  1. causes inflammatory cascade–> damages ocular surface –> releases inflammatory mediators into TEARS. Aq. tear-deficient Dry eye and Evaporative dry eye can cause this.
  2. 2ndary to tear hyperosmolarity or starting event in the disease process. (reduced lipid layer in MGD).
123
Q

DES: DEWS study: Aqueous Tear Deficient Dry Eye (ADDE)

  1. Sjogren’s Syndrome
    a. Primary
    b. Secondary
  2. Secondary: Classic Triad
A
  1. a. Aq. Deficient w/symptoms of Dry mouth, decreased salivary secretion. 95% w/this Dry eye are FEMALE.
    b. Primary Sjogren’s w/AI CT Dz (RA, SLE, Polyarteritis Nodosa, Wegener’s). ~50% of Dry Eye Syndrome
    * Sjogrens: 2nd more common AI Rheumatologic Dz (RA is the first)
  2. DRY Eyes, Dry Mouth, and AI Dz (usually RA)
124
Q

DES: DEWS study: Aq. Tear Deficient Dry Eye: Non-Sjogren’s Syndrome Dry Eye

  1. Cause?
  2. Primary Lacrimal Gland Deficiencies
  3. Secondary Lacrimal Gland Deficiencies
A
  1. Lacrimal Gland Dysfunction
  2. AGE-RELATED DRY EYE SYNDROME: Most common type. Increased age –> Stenosis, Acinar Cell Atrophy, Ductal Fibrosis. (~5-30% of peeps over 50 years of age)
  3. Inflammatory infiltration of lacrimal gland (sarcoidosis, lymphoma, AIDS, Graft vs. host Dz)
    * Obstruction of Lacrimal Gland Ducts (Trachoma, Pemphigoid, Erythema multiforme, chemical and thermal burns)
    * Reflex Hyposecretion (CL wear, diabetes, CN7 damage, systemic drugs, Neurotrophic keratitis, infection, corneal surgery (LASIK, PRK, RK)
    * ~50% of CL wearers have Dry Eye Symptoms
125
Q

DES: DEWS study: Evaporative Dry Eye

  1. Cause?
A
  1. Excessive Water loss in presence of normal lacrimal secretory function. Intrinsic and Extrinsic types.
126
Q

DES: DEWS study: Evaporative: Intrinsic Causes

  1. MGD
  2. Difference b/w Posterior Blepharitis and MGD?
  3. Lid Position Disorders
  4. Low Blink Rate
A
  1. Most common CAUSE; MG obstruction –> too much evaporation.
  2. a. Posterior Bleph: general term. refers to Inflammatory condition of eyelid. Can be cause by many things.
    b. MGD: late stages –> Inflammatory signs (redness) are present, MGD-related Posterior Bleph is the right diagnosis
  3. Proptosis (TED, Creaniostenosis), Nocturnal Lagophthalmos
  4. Intense Concentration, Parkinson’s.
127
Q

DES: DEWS study: Evaporative: Extrinsic Causes

  1. Ocular Surface Dz
  2. CL Wear
  3. VIT A: Purpose
A
  1. VIT A DEFICIENCY (Xerophthalmia), Topical Anesthetics, Topical Preservatives
  2. Can decrease number and length of meibomian glands. CL w/a lower overall water content are usually more comfortable for Pts w/DES.
  3. Goblet cell and Glycocalyx development. Lack of it –> Aq. Tear deficient DES d/t lacrimal gland ACINAR DAMAGE. Associated w/BITOT’s SPOTS on the CONJUNCTIVA.
128
Q

Keratoconus: CLEK Study **usually starts around puberty

  1. what did CLEK study say?
  2. Patho
    a. Stromal Collagen Fibril displacement: Cause
    b. Corneal Thinning and Protrusion: Cause
  3. Associations?
    a. Associated Ocular Conditions
    b. Associated Systemic Conditions (T-DOME)
A
  1. 53% of patients reported a history of ATOPY
  2. Non-inflammatory, progressive, degenerative Dz. Cause: unknown. Starts by damaging Bowman’s membrane.
    a. d/t loss of Adhesion b/w Fibrils
    b. Ezymatic (MMPs) degradation
  3. Eye rubbing, Atopy, CL wear, Ocular and systemic conditions
    a. VKC, AKC, FES, Fuch’s, Other Dystrophies, RP, Leber’s, ROP, Cone, Granular, Lattice Dystrophies. Aniridia

b. Turner syndrome, Downs syndrome, Osteogenesis imperfecta, Marfan’s syndrome, Ehler-danlos syndrome; also, ATOPIC DERMATITIS and MITRAL VALVE PROLAPSE are additional associated conditions

129
Q

Keratoconus:

  1. Symptoms
  2. Signs
    a. Early

b. Late Signs

  1. Classification
    a. Mild
    b. Moderate
    c. Severe
A
  1. Progressive decreased vision, photophobia, glare, monocular diplopia, ghost images. Acute vision loss and pain from Hydrops
  2. Inferior, central, or paracentral stromal thinning. B/L. Asymmetric. Progressive. Irregular Astigmatism. Poor glasses and SCL correction.
    a. FLEISCHER’s RING (iron deposits at base of cone best seen w/Cobalt Blue filter…looks dark), Scissors reflex on ret, Irregular mires on Keratometry, inferior steepening on Topography
    b. VOGT’s STRIAE (vertical lines in DEEP STROMA), MUNSON’s SIGN (lower lid protrusion on downgaze), RIZZUTI’S SIGN (conical reflection on nasal cornea), HYDROPS (tears in descemet’s that causes in edema and rupture of epithelium). 53% of pts w/Mod to severe keratoconus develop corneal scarring in one or both eyes.
  3. a. Less than 48D
    b. 48-54D
    c. More than 54D
130
Q

PMD

  1. Epidemiology
  2. Patho
  3. Signs/Symptoms
  4. Difference b/w this and Keratoconus
A
  1. Early Adulthood.
  2. Thinnest area of cornea is a CRESCENT SHAPE distribution INFERIORLY; Corneal protrusion occurs right above this area and not w/in the area of thinning as w/Keratoconus.
  3. No pain; B/L, inf corneal thinning (4-8 o’clock) 1-2 mm from limbus that leads to high amts of ATR Astigmatism. Corneal Topography: KISSING DOVES or CRAB-CLAWS pattern of inferior thinning.
  4. No cone, no fleisher ring, no Vogt striae. Can get sudden vision loss from Hydrops though. (Less common tho). Corneal scarring also less common than in KCN.
131
Q

Keratoglobus

  1. Epidemiology
  2. Patho
  3. Signs
A
  1. Rare; Onset: BIRTH; Congenital inheritance (AR) MOST COMMON; can be acquired from advanced keratopathy, trauma, or exophthalmos
  2. Associated w/Ehlers Danlos Syndrome, Blue sclera, and Leber’s Congenital Amaurosis
  3. Diffuse corneal thinning mostly in PERIPHERY causing a GLOBULAR SHAPE. can cause Acute corneal edema d/t rupture of Descemet’s, Corneal perforation can happen w/minor incidents of TRAUMA.
132
Q

Anterior Corneal Dystrophies

  1. EBMD (Map-Dot, Fingerprint, ABMD, Cogan’s Microcystic Dystrophy)
    a. Epidemiology
    b. Patho
    c. Symptoms
    d. Signs
  2. % of Pts w/ABMD that get RCEs?
  3. % of pts w/Corneal erosions that have ABMD?
A
  1. a. Most common type. AD; Females > Males
    b. Abnormal epithelial adhesion and EXCESSIVE BM production –> trapped corneal epithelial cells under BM
    c. Asymptomatic; Usually not progressive; Vision loss, pain, photophobia can happen d/t central corneal changes or RCEs.
    d. NEGATIVE STAINING of Map-lines, dots, and/ot fingerprints of corneal epithelium. (best seen w/Retroillumination)
  2. 10%
  3. 50%
133
Q

Anterior Corneal Dystrophies

  1. Meesman’s Dystrophy
    a. Epidemiology
    b. Symptoms
    c. Signs
A
  1. a. Rare, AD. usually seen w/in 1st year of life
    b. Asymptomatic; Symptoms can come from ruptured cysts or RCEs (usually not before middle age)
    c. Extensive (100s), B/L, clear intraepithelial cysts diffusely spread across entire cornea (mostly in Interpalpebral Region)
134
Q

Anterior Corneal Dystrophies

  1. Reis-Buckler Dystrophy
    a. Epidemiology
    b. Patho
    c. Symptoms
    d. Signs
A
  1. a. Rare, AD. Dx’d early in life d/t OCULAR PAIN
    b. ABNORMAL development and replacement of BOWMANS LAYER w/COLLAGEN
    c. Painful d/t RCEs esp in early life; fewer as you age.
    d. B/L, Symmetric, Sub-epithelial gray reticular opacities mostly concentrated in Central cornea, and that spare the peripheral cornea; opacities get worse with age.
135
Q

Stromal Corneal Dystrophies

  1. Macular Dystrophy (Mac-Daddy…different…RARE)
    a. Epidemiology
    b. Symptoms
    c. Signs
A
  1. a. Rare. AR. Least COMMON, MOST SEVERE.
    b. Progressive vision loss. Irritation and Photophobia d/t RCEs; Severe vision loss by 20-30.
    c. Diffuse, superficial, central stromal haze b/w 3 and 9 years of age. Progression causes stromal opacification (cloudy cornea), Stromal thinning, multiple gray-white opacities (MUCOPOLYSACCHARIDE DEPOSITS) w/irregular borders that are seen in all layers of the cornea and extend to the limbus.
136
Q

Stromal Corneal Dystrophies

  1. Granular Dystrophy
    a. Epidemiology
    b. Signs/Symptoms
  2. What is AVELLINO DYSTROPHY?
A
  1. a. AD. Onset: 1st decade. Loss of vision in middle age
    b. Small snowflake granules (HYALINE DEPOSITS) in Central stroma. Deposits spread to epithelium and deep stroma. Become confluent. causes decreased VA. RCEs are RARE!
  2. Rare variant of Granular dystrophy. Has Granular and LATTICE-LIKE DEPOSITS w/in Central stroma. AKA Granular-Lattice Dystrophy
137
Q

Stromal Corneal Dystrophies

  1. Lattice Dystrophy
    a. Epidemiology
    b. Signs/Symptoms
  2. Causes of this?
A
  1. a. AD
    b. Ant stromal haze w/branching, refractile, lattice-like lines (AMYLOID DEPOSITS). Decreased acuity in 3rd decade d/t major corneal scarring and haze. RCEs are COMMON!
  2. Transforming Growth Factor Beta 1 (TGFB1) gene (aka BIGH3) gene mutation causes granular, lattice, and avellino dystrophies. DOES NOT CAUSE MACULAR STROMAL DYSTROPHY though.
138
Q

Stromal Corneal Dystrophies

  1. Schnyder’s Dystrophy
    a. Epidemiology
    b. Patho
    c. Signs/Symptoms
A
  1. a. VERY RARE AD. Ask about current/past HIGH CHOLESTEROL
    b. Strong association w/Hyperlipidemia, Xanthelasma, Corneal Arcus. Non-Progressive.
    c. Fine Yellow-white ring of stromal crystals w/haze in central stroma. Usually Asymptomatic.
139
Q

Pneumonic to remember types of deposits for Stromal Dystrophies:

  1. Marilyn Monroe Got Hers in Los Angeles
A
  1. Macular-Mucopolysachharide.

Granular- Hyaline

Lattice-Amyloid

140
Q

What are the most common symptoms associated with Anterior/Stromal Corneal Dystrophies?

A
  1. DECREASED VISION, and PAINFUL RCEs
141
Q

Posterior Corneal Dystrophies

  1. Fuch’s Endothelial Dystrophy
    a. epidemiology
    b. Patho
    c. Symptoms
    d. Signs
A
  1. a. AD. Females. Over 60. 30% have + FHx
    b. Descemets: Anterior Lamina (made in embryo) and Posterior Lamina (secreted thru life). Posterior Lamina produced in excess…clumps up. Decreased Endothelial Cell Density

c. Asymptomatic until later on. Blurred hazy vision that’s worse in morning w/pain and glare. (sign for surgery talk). Muro128 buys time.
d. seen early in life (30-40). DECREASED ENDOTHELIAL CELL DENSITY w/Pleomorphism and Polymegathism, Endothelial Guttata w/BEATEN METAL appearance w/Thick Pachymetry findings.

Stromal Edema usually happens when cell count is 500 cells/mm2 or less. Can spill over into Epithelium –> PAINFUL BULLAE and Scarring.

*Cataract surgery can increase Endothelial cell loss, esp if it’s less than 1000 cell/mm2.

142
Q

Endothelial cell count

  1. Kids
  2. By age 80?
  3. Minimum needed to prevent corneal edema?
A
  1. 3k-4k cells/mm2
  2. 1k-2k cells/mm2
  3. 400-700 cells/mm2
143
Q

Posterior Corneal Dystrophies

  1. Posterior Polymorphous Dystrophy
    a. Epidemiology
    b. Symptoms
    c. Signs
  2. What does PPD do to Endothelial cells?
A
  1. a. AD; 2nd-3rd decade. Can be seen at birth but rare…cloudy cornea.
    b. Slow progressive/Non-progressive and most are asymptomatic. Usually Dx’s b/w 30-50. Decreased vision secondary to corneal edema = most common symptoms
    c. B/L, Asymmetric. At Descemet’s and Endothelium. Patches of VESICLES (hallmark); Band Lesions (linear TRAIN TRACK LESIONS) and diffuse opacities.

Rare: Severe cases: Corneal edema and Bullae –> Painful vision loss.

  1. Metaplasia of endothelial cells and gives an epithelial like endothelium. Can spread over IRIS and Angle, causing angle-closure glaucoma from PAS.
144
Q

Congenital Anterior Segment Anomalies

  1. Megalocornea
    a. Epidemiology
    b. Signs
    c. Patho
    d. Associations
  2. Microcornea
    a. Epidemiology
    b. Signs
    c. Associations
A
  1. a. Rare, X-linked. Mostly Males
    b. B/L Corneal Horiz. Diameter of 13 mm or MORE. Highly Myopic w/Steep Cornea. Usually have good acuity w/Correction.
    c. Ocular tissue stretching –> Lens subluxation, angle abnormalities –> Glaucoma
    d. Marfan’s Syndrome, Ehlers-Danlos Syndrome, Osteogenesis Imperfecta, etc.
  2. a. Very rare AD or AR. U/L or B/L
    b. H diameter of LESS than 10 mm
    c. HYPEROPIC; Risk for Angle closure d/t shallow AC.
145
Q

Congenital Anterior Segment Anomalies

  1. Cornea Plana
    a. Epidemiology
    b. Patho
    c. What is SCLEROCORNEA
    d. Signs
A
  1. a. Rare; AD or AR
    b. Corneal Curvature equal to Scleral curvature is pathognomonic for this. Associated w/Sclerocornea and Microcornea

c. B/L Scleralization (opacification and Vascularization) of Peripheral and/or central cornea. 80% association w/Cornea Plana.
d. B/L Flat Corneas (LESS than 38D or as low as 20-30D). Hyperopia, Shallow ACs, Increased risk for Angle-closure glaucoma

146
Q

Congenital Anterior Segment Anomalies

  1. Aniridia
    a. Epidemiology
    b. Signs
  2. Haab’s Striae
    a. Cause?
A
  1. a. Rare, B/L. AD. Partial to total loss of iris tissue.
    b. Corneal lesions (opacity, microcornea, pannus), Lenticular changes (cataract, lens subluxation), Posterior segment abnormalities (Glaucoma in ~75% of cases, Foveal hypoplasia, disc hypoplasia, choroidal colobomas)
  2. a. CONGENITAL GLAUCOMA. Horizontal Cracks (clear parallel lines) in Descemet’s form increased IOP.
147
Q

Axenfeld-Rieger Syndrome

  1. What is it?
  2. Posterior Embryotoxin
  3. Axenfeld Anomaly
  4. Rieger Anomaly
  5. Rieger Syndrome
A
  1. Several disorders. They have Anterior Segment developmental abnormalities that affect AC angle. ~50% w/this get Glaucoma
  2. Anteriorly displaced Schwalbe’s line. ~15% healthy eyes have PE. No increased risk of Glaucoma
  3. PE + Angle abnormalities + Increased Glaucoma risk. (Prominent iris processes that travel to level of PE, usually obscuring SS)
  4. PE + angle abnormalities + Increased Glaucoma Risk + Iris Stromal Abnormalities
    * Iris Stromal issues: Displaced Pupil (Corectopia) and Iris Hypoplasia causing holes w/in Iris Tissues (Polycoria)
  5. PE + Angle abnormalities + Increased Glaucoma Risk + Iris Stromal Abnormalities + Systemic Abnormalities
    * Systemic: Mental retardation, Dental, Craniofacial, Genitourinary, and Skeletal abnormalities.
148
Q

Peter’s Anomaly

  1. What is it?
  2. % that develop secondary glaucoma? Pts may also develop what 2 things?
A
  1. Rare; Born w/CENTRAL WHITE OPACITIES (leukoma) w/Iris Adhesions. 80% are B/L.
  2. 50-70%; Corneal edema and Cataracts.
149
Q

Limbal Dermoid

  1. What is it?
  2. Most common location?
A
  1. Normal dense CT w/hair follicles and sebaceous glands that’s displaced to an abnormal location.
  2. Inferotemporal Limbus
150
Q

Keratitis: Infectious

  1. Risk Factors?
A

CL Wear, Dry Eye, Exposure Keratopathy, Neurotrophic Keratopathy, Trauma, Lid abnormalities, and Bullous Keratopathy

151
Q

Keratitis: Bacterial

  1. Epidemiology
    a. Most Common MICROBES?
  2. Patho?
  3. Symptoms?
  4. Signs?
A
  1. Most common for INFECTIOUS KERATITIS; CL wear (EW) is most common predisposing factor.
    a. PSEUDOMONAS AERUGINOSA; Staph (epidermis and aureus), H. Influenzae, Moraxella Catarrhalis
  2. Most bacteria need an epithelial defect for invasion and corneal ulceration.
  3. SEVERE PAIN, Red eye, Photophobia, Decreased Vision
  4. CORNEAL ULCER = corneal infiltrates w/overlying epithelial defect (Have to have both to have an ulcer…)??
152
Q
  1. Pseudomonas Aeruginosa
    a. Most common type of what pathogen?
    b. Characteristics?
    c. Can perforate the cornea in how many hours?
A
  1. a. of GRAM (-) pathogen in severe bacterial keratitis.
    b. TONS of THICK Mucopurulent Discharge (usually green), Hypopyon, Dense stromal infiltrate, and Rapid Progression
    c. w/in 48 hrs.
153
Q

What are bacteria that can INVADE an INTACT EPITHELIUM of the cornea?

(Canadian National Hockey League)

A
  1. Corneyobacterium diphtheriae

Neisseria Gonorrhea and meningitidis

Haemophilus

and

Listeria

154
Q

How do you tell the difference b/w Corneal infiltrates and Corneal Ulcers (2 things)

A
  1. FLUORESCEIN STAINING: 1:1 Ratio if corneal ulcer.
    Corneal infiltrates: staining area is less than the lesion size.
  2. CORNEAL ULCERS: MODERATE to SEVERE PAIN w/Mild AC RxN, and DIFFUSE Conj injection.

Infiltrates: Less painful w/multiple lesions, no AC RxN, Sectoral Injection

155
Q

Fungal Keratitis

  1. Epidemiology
  2. Patho
    a. Most common culprits after Vegetable MATTER TRAUMA (2)?
    b. Fungi culture done w/what agar?
  3. What is part of the normal human flora but is deadly in immunocompromised pts?
  4. Symptoms
  5. Signs
A
  1. Most common type after Traumatic Corneal injury, esp from VEGETABLE MATTER
  2. CANDIDA INFECTIONS in eyes w/Chronic Corneal Dz (Chronic Dry Eye, Herpes Keratitis, Exposure Keratopathy), IMMUNOCOMPROMISED or severely debilitated pts.
    a. Aspergillus and Fusarium Species more common culprits after VEGETABLE MATTER TRAUMA.
    b. SABOURAUD’s AGAR
  3. CANDIDA
  4. Pain, Photophobia, Tearing, decreased vision
  5. Epithelial defect w/gray-white corneal infiltrate with FEATHERY EDGES and may Surrounding SATELLITE INFILTRATES (classic for Aspergillus and Fusarium). Presentation similar to Bacterial corneal ulcer (Classic for CANDIDA). Maybe AC RxN and Hypopyon.
156
Q

Acanthamoeba Keratitis (I Can’t Believe ya’d war CL’s/wash CL’s in Water and wear them in a HOT TUB)

  1. Epidemiology
  2. Patho
    a. Culture?
  3. Symptoms
  4. Signs
    a. Early
    b. Late
A
  1. Rare. Parasitic; Poor CL hygiene.
  2. Most common Protozoa in soil. Found in water and oral cavity in humans. Corneal Epithelium compromised –> It invades Corneal Epithelial and Stromal TIssues. Slow infection progress. Usually misdiagnosed in early Tx.
    a. Non-nutrient Agar w/Heat-Killed E. COLI

3 Blurred vision, pain, minimal discharge

  1. a. Punctate/pseudodendritic epithelial defects (can confuse w/HSK) associated with SEVERE PAIN out of PROPORTION TO THE SIGNS
    b. Radial Keratoneuritis (corneal nerve inflammation), Patchy Anterior Stromal Infiltrates that progress to a RING ULCER
157
Q

Smears and Cultures for Infectious Keratitis

  1. Gram Stain (smear)
  2. KOH or Giemsa Stain (smear)
  3. Sabaroud’s Agar culture plate
  4. Chocolate Agar culture plate
  5. Thioglycolate culture broth
  6. Non-nutrient agar culture plate w/E. Coli overlay
A
  1. Bacteria
  2. Fungi/Yeasts
  3. Fungi
  4. Haemophilus and Nisseria
  5. Aerobic and Anaerobic Bacteria
  6. Acanthamoeba
158
Q

HSV

  1. Epidemiology
    a. Primary Exposure
    b. Recurrent HSV Infections
  2. Patho
  3. Symptoms
  4. Signs
  5. Primary Exposure
    a. Usually causes what 2 things?
    b. Blepharitis
    c. Conjunctivitis
A
  1. DNA Virus; young patients; Hx of past episodes and Cold sores
    a. Children (6 mos to 5 years). Usually asymptomatic

b. Reactivation in TRIGEMINAL GANGLION. Trigger: Physical or emotional stress, sun exposure, fever, etc.
3. Tissue Damage: direct invasion from virus, neurotrophic mechanisms, or by immune system response to HSV
4. DECREASED CORNEAL SENSITIVITY
5. a. Blepharitis and/or Conjunctiviits
b. Focal vesicular lesions w/crusting on eyelids and periorbital area
c. Acute U/L Follicular Conjunctivitis w/Watery Discharge and Preauricular Lymphadenopathy

159
Q

HSV: Recurrent Infections (1)

  1. Epithelial Disease
    a. Corneal Vesicles
    b. Dendritic Ulcers
    c. Geographic Ulcers
    d. Marginal Ulcers
A
  1. a. Small epithelial lesions referred to as PUNCTATE EPITHELIAL KERATOPATHY. Represents earliest epithelial signs of reactivated HSV.
    b. Most common HSV Keratitis. Edges stain well with ROSE BENGAL; Center ulceration stains WELL with FLUORESCEIN
    c. Like dendritic ulcer but WIDER (not longer linearly); usually d/t previous use of TOPICAL STEROIDS
    d. Close to limbus; looks like Stromal infiltrate w/overlying epithelial defect and associated limbal injection
160
Q

HSV: Recurrent Infections (2)

  1. Neurotrophic Keratopathy
    a. Cause?
    b. Happens in pts who have had what?
    c. Neurotrophic ulcer looks like what?
    d. Main ulcer location?
A
  1. a. REDUCED CORNEAL INNERVATION, decreased tear secretion, poor wound healing.
    b. Infectious epithelial keratitis; not immune-mediated or infectious
    c. OVAL defect with smooth borders. Usually preceded by Punctate epithelial erosions that then form an ulcer.
    d. Inferior.
161
Q

HSV: Recurrent Infections (Stromal Disease)

  1. % of initial HSV disease?
  2. % of recurrent HSV disease?
  3. Interstitial Keratitis?
    a. cause?
  4. Most patients are born with IK as a result of WHAT?
  5. Necrotizing Stromal Keratitis
  6. Main concerns for HSV STROMAL KERATITIS?
A
  1. 2%
  2. 20-48%
  3. Infiltrate with DIFFUSE NEO, immune ring (WESSLEY RING), Stromal thinning, and subsequent scarring
    * IK: Stromal inflammation W/O Primary involvement of epithelium or endothelium.

a. Antigen-Antibody complement cascade against a live virus or viral antigen w/in Corneal stroma.
4. of CONGENITAL SYPHILIS (90%).
5. RARE; Direct Invasion into STROMA. SEVERE STROMAL INFLAMMATION w/NECROSIS –> Corneal Thinning and Perforation
6. Can cause major Stromal Scarring and Decreased Acuity

162
Q

HSV: Recurrent Infections

  1. Endotheliitis (Disciform Keratitis)
    a. Cause?
  2. Disciform Endotheliitis
    a. Most common what?
    b. Characteristics?
  3. What are present in IK, that are NOT seen in Disciform Endotheliitis?
A
  1. a. 2ndary stromal edema d/t Immune RxN to a VIRAL ANTIGEN or live virus w/in Corneal Endothelium
  2. a. form of endotheliitis.
    b. Focal, Disc-Shaped, Stromal Edema overlying keratic precipitates. Mild to moderate IRITIS
  3. Stromal Infiltrates and NEO.
163
Q

HZV

  1. Epidemiology
  2. Patho
  3. Main peeps affected?
  4. Signs?
    a. Pre-Zoster
    b. Active-Zoster
A
  1. 95% of kids by age 5 in US. Chickenpox.
  2. Transported to Trigeminal Ganglia and other neural cell bodies. Dormant. OLDER AGE, trauma, Neurodegeneration, or IMMUNOSUPPRESSION –> reactivation of virus –> HZV infection.
  3. Old peeps. Seen in younger than 50, think immunocompromised or pregnant women.
  4. Varies. More severe in immunocompromised Pts. U/L INFECTION
    a. PRODROME (tingling, malaise, fever)
    b. Skin involvement that respects Dermatomes and DOES NOT CROSS MIDLINE. Vesicles form on LID MARGIN –> BLEPHAROCONJUNCTIVITIS; Episcleritis is common.
164
Q

HZV (2): HZO

  1. Corneal Signs in what %?
  2. Common Signs?
  3. Less Common Signs?
A
  1. 65% w/active HZO
  2. Punctate Epithelial Keratitis, Pseudodendritic Keratitis, Anterior Stromal Keratitis, Keratouveitis/Endotheliitis, Neurotrophic Keratopathy
  3. Exposure Keratopathy, Disciform Keratitis, IK
165
Q

HZV: HZO (2)

  1. HZV Keratitis: Starts how?
  2. UVEITIS: What % of Pts?
    a. What kind?
  3. Other Findings?
A
  1. Small, stellate lesions –> PSEUDODENDRITES (tapered ends, NO TERMINAL BULBS) w/”Stuck on” Appearance. Entire lesion stains with ROSE BENGAL. Don’t stain well with Fluorescein.
  2. 40% w/Acute HZO
    a. Gran or Non-Gran. Significant KPs, Corneal Edema, PS.
  3. Trichiasis, Ectropion, Entropion, Madarosis, Poliosis, Episcleritis, Scleritis, Retinitis, Vasculitis, Optic Neuritis, CN Palsies, Glaucoma, Cataracts
166
Q

HZV: HZO (3)

  1. Post-Zoster
    a. PHN
    b. Severe PHN
A
  1. a. Pain that lasts for more thant 1 month after rash onset or rash resolution. Most common complication of HZV and hits 10-30% of Pts.
    b. 7% of Pts. Leading cause of suicide in Pts over 70 years of age with CHRONIC PAIN
167
Q

Peripheral Ulcerative Keratitis
(PUK)

  1. Mooren’s Ulcer
    a. Epidemiology
    b. Benign (Typical or Limited) Mooren’s Ulcer
    c. Malignant (Atypical) Mooren’s Ulcer
A
  1. a. RARE; MEN and Older Pts (40-70; can occur at all ages tho).
    b. 75%; U/L; Old. Mild-Mod symptoms; Responds well to Tx.
    c. B/L; Younger pts (esp Black males); SEvere symptoms, Responds POORLY to Tx; Relentless.
168
Q

Peripheral Ulcerative Keratitis
(PUK) (2)

  1. Patho
  2. Symptoms
  3. Signs
A
  1. Painful, Progressive, Chronic vasculitis of Limbal BVs –> Ischemic Necrosis and PUK!
    a. Mooren’s Ulcer: Idiopathic in nature. Occurs INDEPENDENT of any diagnosable Systemic Disorder that could be responsible for the Progressive Corneal Pathology.
    b. Associated w/Systemic Hep C or Hookworm
  2. PAIN (SEVERE usually), Redness, tearing, photophobia. Decreased vision d/t Irregular astigmatism or Iritis, or if ulcer is central.
  3. U/L PERIPHERAL CRESCENT SHAPED GRAY INFILTRATE –> progresses to ulcer. Ulcer is concentric to limbus.
169
Q

Staphylococcal Marginal (Peripheral) Keratitis

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
A
  1. Common. Hx of similar recurrent acute episodes
  2. TYPE 3 HYPERSENSITIVITY to Staph Aureus. See it in Pts w/Chronic Staph Blepharitis.
  3. Asymptomatic; or Acute Photophobia, pain, tearing, redness, decreased vision
  4. Corneal Stromal Infiltrates (multiple and B/L) in PERIPHERY; Usually at 2,4,8,10 o’clock.
    Probably Chronic if: Residual thinning, Superficial Neo, and Peripheral scarring
170
Q
  1. An Infiltrate is a sign of what?
A
  1. that the Pt’s immune system is attacking the infection via ANTIBODIES (esp in Staphylococcal Marginal Keratitis…sign of attacking the Staph).

In isolation, immune-mediated response is NOT a sign of infection

171
Q

Collagen Vascular Disorders

  1. Types that can cause Peripheral corneal thinning and/or ulcers (kind of like Mooren’s ulcer but now we know what’s causing it)
  2. Symptoms
  3. Signs
A
  1. RA, SLE, Polyarteritis Nodosa, Wegener’s Granulomatosis.
  2. Asymptomatic, or lots of pain, redness and decreased vision
  3. Peripheral corneal thinning/ulcers w/or w/o inflammation. U/L or B/L. Ulcers can progress to encompass entire peripheral cornea. Findings: Associated w/Scleritis, Episcleritis, and KERATOCONJUNCTIVITIS SICCA.
172
Q

Corneal Deposits

  1. Whorl Keratopathy
  2. Fleischer’s Ring
  3. Rust Rings
  4. Hudson Stahli Lines
  5. Stocker’s Line
  6. Ferry’s Line
  7. Kayser-Fleischer Ring
  8. Band Keratopathy
A
  1. Seen in FABRY’s Dz, and use of Chloroquine, Hydroxychloroquine, Amiodarone, Indomethacin, and Tamoxifen
  2. Iron Ring at base of cone in KCN
  3. From metallic FBs.
  4. Elderly; Iron deposits b/w middle and lower third of cornea; No symptoms and no clinical significance.
  5. Iron Deposits on leading edge of Pterygium
  6. Iron Deposits on leading edge of Filtering Bleb
  7. Copper accumulation in pts w/Liver issues, esp WILSONS DISEASE
  8. CALCIUM deposits w/in Bowman’s Layer (swiss-cheese pattern…white spots)
173
Q

Corneal Degenerations: Terrien’s Marginal Degeneration

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
  5. What presents like Terrien’s? What’s the difference?
A
  1. Rare. Men (3:1); 20-40 y/o
  2. Idiopathic; Inflammatory; Degenerative; Slow, progressive PERIPHERAL STROMAL THINNING. Perforates in 15% of cases
  3. Asymptomatic; Progression can cause ATR and decreased acuity.
  4. SUPERONASAL, B/L, asymmetric, slow, progressive peripheral thinning w/Vascularized Pannus. Usually no AC RxN, No Conj Injection, no overlying epithelial defects.
  5. Mooren’s ulcer, but has an OVERLYING DEFECT (mooren’s)
174
Q

Corneal Degenerations: Salzmann’s Nodular Degeneration

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
A
  1. Rare; Females; by 6th decade
  2. Degenerative; after episodes of keratitis; SIGNIFICANT CORNEAL INFLAMMATORY DZ, w/MGD, Trachoma, Phlyctenulosis, VKC, KJS, IK, Idiopathic.
  3. Asymptomatic; Pain if RCEs start over the nodule.
  4. HYALINE PLAQUE DEPOSITS b/w Epithelium and Bowman’s Membrane, usually mid-peripheral, elevated BLUE-GRAY or Yellow-white nodular lesions. U/L or B/L; Single or multiple nodules. Nodules usually adjacent or w/in OLD CORNEAL SCAR or CORNEAL PANNUS
175
Q

Corneal Degenerations: White Limbal Girdle of Vogt

  1. Epidemiology
  2. Signs/Symptoms
A
  1. Age; over 80, ~100% pts affected

2. B/L Chalk-like linear opacities of Nasal Limbus (usually 3 and 9 o’clock). Pts are asymptomatic.

176
Q

Corneal Degenerations: Band Keratopathy

  1. Patho
    a. Ocular Conditions
    b. Systemic Conditions
    c. Also after what?
  2. Symptoms
  3. Signs
A
  1. a. ones that cause Chronic Inflammation and Ocular Surface Dz (uveitis, DES, Exposure Keratopathy)
    b. Increased Serum Calcium or Phosphorous levels, (GOUT (uric acid levels), HYPERCALCEMIA, Sarcoidosis, Renal Failure (BUN and Creatinine)
    c. TRAUMA (like tons of eye sx’s)
  2. Asymptomatic cuz Calcium Plaques are peripheral at 3 and 9 o’clock. Plaques could move centrally causing an FBS and decreased vision
  3. Calcium deposits on Ant Surface of Bowman’s membrane or Sub-epithelial space…look like White Spots w/”Swiss Cheese Pattern” usually w/in interpalpebral region of cornea
177
Q

Corneal Degenerations: Arcus Senilis

  1. Epidemiology
  2. Patho
  3. Signs
  4. What is it’s U/L?
A
  1. Most common Peripheral corneal opacity. Old peeps. 100% over age 80. Males and AAs
  2. AGING and HIGH CHOLESTEROL. Lipid deposition on Descemet’s and subsequently deposited on Bowman’s Layer before extending into the stroma.
  3. B/L, Symmetric; Circumferential 1mm band w/in Peripheral cornea w/clear zone of separation to the limbus
  4. RARE. Associated with CAROTID Dz on the SIDE W/O the ARCUS! In Pts younger than 50, they have an increased risk of CAD. LIPID PROFILE is WARRANTED.
178
Q

Corneal Degenerations: Crocodile Shagreen

  1. Signs
  2. Symptoms
A
  1. B/L, Gray-White, Polygonal Stromal Opacities (Cracked ice appearance) near Bowman’s (ANT crocodile Shagreen) or near Descemet’s (Posterior Crocodile Shagreen). D/T irregular arranged folds of collagen.
  2. Asymptomatic and Benign.
179
Q

Corneal Degenerations: Corneal Farinata

  1. What is it?
A
  1. B/L “Flour Dust” deposits usually in CENTRAL DEEP STROMA. Could be d/t aging or AD condition. Usually Asymptomatic.
180
Q

Corneal Graft Rejection

  1. Cause?
  2. Epithelial Rejection
  3. Stromal Rejection
  4. Endothelial Rejection Line
A
  1. Type 4 HYPERSENSITIVITY to donor cornea. 30% of pts have rejection w/in 1 year. Decreased vision, mild pain, redness, photophobia
  2. Rare; Looks like elevated, irregular epithelium
  3. SEIs (KRACHMER’s SPOTS)
  4. WBCs on Endothelium…form KHODADOUST LINE.
181
Q

Refractive Surgery

  1. Absolute CIs (4)
  2. Relative CIs (5)
  3. Soft CLs: Out of lenses how many days PRIOR to Sx?
  4. Soft Toric and RGP: Out of lenses how many days prior?
A
  1. a. Younger than 18 w/unstable RE w/in last year
    b. Unrealistic Expectations: reduce dependence on glasses (but NOT glasses free). Post-op glare and dryness.
    c. KCN, Active HSK, CL Warpage
    d. CT Dz (Keloid formers), Collagen Vascular Dz, Immunocompromised Dz (Chronic Steroid Use)
  2. a. Bleph, DES, Chronic eye rubbing, Ocular surface Dz, Large Pupils
    b. DM
    c. POAG
    d. Pregnancy
    e. Retinal Thinning/Lattice Degeneration can increase risk of Retinal tears.
  3. 3-14 days prior
  4. 14-21 days prior
182
Q

RK (Radial Keratotomy)

  1. How is it done?
  2. Problem with it?
A
  1. Radial Incisions w/Diamond Knife. Flatten Peripheral Corneal Stroma.
  2. Better options out there. Hard to Titrate. Leads to PROGRESSIVE HYPEROPIC SHIFTS
183
Q

PRK (Photorefractive Keratectomy)

  1. How is it done?
  2. Tx Range?
  3. How much residual cornea is needed after Tx?
  4. Healing time?
  5. Stromal Haze risk highest w/Higher Rx’s. How can we reduce this risk?
A
  1. Epi, Bowman’s, and Superficial stromal tissue are removed…No Flap…Excimer laser applied directly to CENTRAL CORNEA (Myopia) or Mid-peripheral Cornea (HYPEROPES)
  2. -8D to +4D; up to 4D cyl
  3. 400 um
  4. 1-2 wks. Very poor vision and pain right after. (NSAIDs and BCL help control this)
  5. use Mitomycin C during the procedure.
184
Q

LASIK (Laser-Assisted in situ keratomileusis)

  1. What is done?
  2. Treatment Range
  3. Thickness Requirements (3)
  4. Healing time?
  5. What should be the total thickness?
  6. Femtosecond Laser Flap: What is it?
  7. Laser Epithelial Keratomileusis (LASEK or E-LASIK): What is it?
  8. Epi-LASIK: What is it?
A
  1. Epithelial Flap made w/Microkeratome; Excimer Laser is applied to ANTERIOR STROMAL BED…and the flap is then reattached.
  2. -10D to +4D; up to 5D cyl. Can do CLEAR LENS EXTRACTION if Pts exceed these.
  3. 250 um under flap; Flap has to be 160-200 um thick. Ablation Depth is 15 um/Diopter
  4. 1-2 days, less pain, less post-op haze.
  5. 250 um: Total Pach minus flap thickness (160-200 um) minus ablation depth (15 um/diopter) = at least 250 um.
  6. Same as LASIK but flat is made with this laser instead. Flap is thinner…so more tissue can be ablated. Removes risk of mechanical malfunction of the microkeratome. Less Post-op dry eye.
  7. Same as LASIK but flap is made w/DILUTE ALCOHOL instead of a microkeratome
  8. Blunt plastic blade creates the flap.
185
Q

CK (Conductive Keratoplasty)

  1. Purpose?
  2. How is it down?
  3. Regression after how many years?
  4. Can Sx be repeated?
  5. Tx range?
A
  1. Tx of Presbyopia, Low Hyperopia, Residual Astigmatism after other surgeries.
  2. Radio Frequency energy…shrinks collagen fibers in Peripheral Corneal Stroma…lets central cornea steepen.
  3. ~2-3 years.
  4. Yes
  5. +0.75D to +3.00 D w/less than 0.75D of astigmatism
186
Q

Intrastromal Corneal Rings (Intacs)

  1. What is done?
  2. Approved for what Dz?
  3. Tx range?
A
  1. PMMA rings–>Insert into Stroma. Flattens the cornea; rings can be removed or exchanged.
  2. KERATOCONUS
  3. -0.75D to -3 D; No HYPEROPES.
187
Q

Clear Lens Extraction (CLE)

  1. What is it?
  2. Tx Range?
A
  1. Cataract Sz w/o a Cataract. IOL is selected that reduced RE.
  2. Large.
188
Q

Phakic IOL (Implantable CL)

  1. What is it?
  2. Requires what?
  3. Can be used to treat what?
A
  1. IOL in a PHAKIC EYE.
  2. Peripheral Iridotomy
  3. A Larger range or REs compared to Corneal Sx and the IOL is removable.
189
Q

Astigmatic Keratotomy (AK)

  1. What is it?
A
  1. Corneal incisions w/Diamond blades to relax the cornea in the steepest meridian.
190
Q

Wave-Front Guided, Custom Corneal Surgery

  1. What does this do?
  2. Done with what surgeries?
A
  1. Reduces Higher order Aberrations (coma, spherical, etc) as well as correcting RE (Lower order aberrations ~90% of all aberrations)
  2. LASIK and PRK
191
Q

LASIK Complications (1)

  1. Pain in first 24 hrs
  2. Serious Infection
  3. Flap Complications
A
  1. d/t Corneal wound. Severe pain = dislocation of flap.
  2. usually in first 1-3 days. (Gram + or Mycobacteria)
  3. Free Caps, button holes, flap folds, irregular flaps, etc.
192
Q

LASIK Complications: Flap Complications (2)

  1. Button Holes
  2. Free Caps
  3. Flap Folds
  4. Flap dislodment
A
  1. hole in flap. more common w/VERY STEEP corneas and deep set eyes
  2. No hinge made. Common w/FLAT CORNEAS and d/t not enough cornea in the ring.
  3. 1/2 w/in first hour; 95% w/in first week.
    Flap Folds are MACROSTRIAE if they’re Full-thickness.

MICROSTRIAE: Fine, irregular, multi-directional folds in Bowman’s. usually resolve on their own.

  1. more often seen w/Keratome flaps than w/Femtosecond laser flaps. d/t accidental touch to eye or eyelid.
193
Q

LASIK Complications (3)

  1. Corneal Ectasia
  2. Residual RE
  3. GLARE
  4. Dry Eye
  5. DLK (Sands of Sahara) Diffuse Lamellar Keratitis
  6. Epithelial Ingrowth
  7. Corneal Haze
A
  1. Anterior protrusion d/t thinning. High myopes, KCN, or Forme Fruste are at high risk.
  2. Pt may be over or under-corrected or have regression after Sx (usually RE >-8D)
    * Can fit PTs w/RGPs or reverse geometry lenses after ~8-12 wks.
  3. Large pupils, monovision correction, Higher REs, and Small ablation zones.
  4. Most common SE from LASIK; Severed Corneal Nerves
  5. Rare; Inflammatory, Non-infectious RxN at Lamellar Interface (b/w Corneal flap and Stroma). Fine Granular sand-like infiltrate usually w/in 2-3 days after Sx.
  6. Rare; Usually after 1 month. Faint gray line, or white milky deposits w/in 2mm of flap edge. Usually Asymptomatic. Most common issue w/LASIK enhancement.
  7. Long-term Haze: 0.1% w/LASIK and PRK: 1% w/REs less than 6D.
194
Q

LASIK: Re-treatment

  1. Earliest time?
  2. Preferred time to retreat?
  3. Astigmatism
  4. RE
  5. Uncorrected VA of what?
A
  1. 3 mos
  2. 6 mos
  3. > 0.75D w/Symptoms
  4. > or equal to 0.75D
  5. 20/30 or worse
195
Q

LASIK: Long-Term

  1. IOP readings…False high/low?
  2. Gonio and Retinal Evals in what pts?
  3. Pts should wear what?
A
  1. Falsely low. d/t thin corneas
  2. w/Hx of High Hyper/Myopia repectively….
  3. Eye protections in contact sports.
196
Q

Cataracts

  1. Nuclear Sclerosis
  2. Cortical Cataract
  3. Ant Subcapsular Cataract
  4. PSC
    a. What can Mild PSCs do?
  5. Infant Cataracts
  6. What’s a CERULEAN CATARACT?
A
  1. Most common; myopic shift (ATR)
  2. Radial spoke-like opacities…Hyperopic Shift
  3. Directly underneath Ant Lens Capsule
  4. Directly in front of PL Capsule. messes with NEAR VISION > Distance. d/t SYSTEMIC or TOPICAL STEROIDS and X-RAYs
    a. Significant reduction in acuity. associated w/Worse glare compared to other cataracts
  5. Associated: Galactosemia and Rubella. Most common type: Lammellar (zonular) cataract: Lens opacity around the Embryonic Nucleus
  6. Congenital; Rarely affects VA. Tiny dot-like or flake-like white or bluish-green opacities
197
Q

Cataracts (2)

  1. Presenile (MAD Wilson, Lacks Calcium)
  2. Traumatic
  3. Toxic
  4. Secondary
  5. What are Epicapsular Stars?
A
  1. Assoc: DM, Myotonic Dystrophy (PSC Christmas Tree cataracts), Wilson’s, Hypocalcemia, Atopic Dermatitis
  2. Rossette catracts. looks for a Vossius ring
  3. Ant Subcapsular effects: Chlorpromazine (Stellate Cataracts), Amiodarone (deposits), Miotics Vacuoles), Gold Salts (Gold Deposits)

Post Subcapsular: Corticosteroids

  1. Chronic Ant Uveitis (most common), High Myopia, RP, Gyrate Atrophy
  2. Residual remnants of tunica vasculosa lentis and looks like small, star-shaped, pigmented deposits on ant capsule of the lens.
198
Q

Cataract Testing

  1. PAM
  2. BAT
  3. Axial Length: determined by what?
  4. B-Scan Ultrasound
  5. Axial Length?
A
  1. determines impact on acuity d/t lens changed. predicts VA post-op
  2. tests glare disability
  3. A-Scan. Helps determine IOL Power needed
  4. Used to look for Post seg abnormalities w/a person w/a Dense Cataract
  5. 24 mm; 1 mm error in length = 3 D error in calculated IOL power.
199
Q

Cataract Considerations

  1. Cataract: Monocular
  2. Pt is Monocular
  3. Pre-operative Eval: Look for what?
  4. Ocular Conditions to consider before referral?
  5. FLOMAX: what is it, what can it cause?
A
  1. Age of pt…determine if it would affect Accommodative status for pt.
  2. Severity of Cataract vs. risk/benefit ratio to the pt.
  3. Meds: ANTICOAGULANT (Coumadin), ALPHA BLOCKERS (Flomax), PROSTAGLANDINS
  4. Hx of Acute/Chronic Uveitis, Severe Bleph, Fuch’s, Pseudoexfoliation
  5. Alpha Blocker; FLOPPY IRIS SYNDROME
200
Q

Cataract Sx

  1. Intracapsular Cataract Extraction (ICCE)
  2. Extracapsular Cataract Extraction (ECCE)
  3. Phacoemulsification
  4. Femtosecond Laser
A
  1. Lens and capsule removed; Lg incision; Aphakia; Need CATARACT GLASSES; Higher risk of RD. Needs a Peripheral Iridotomy to prevent Vit Prolapse and Pupillary Block
  2. Lens removed; Still large incision; IOL inserted;
  3. Type of ECCE; Fragment lens w/Ultrasound then remove; Smaller incision.
  4. Newer Tx; Use: Corneal incisions, Anterior Capsulorhexis, and Lens fragmentation
201
Q

Post-op Complications: Cataracts

  1. Striate Keratopathy
  2. Acute-Post Op Bacteral Endophthalmitis (worst)
  3. Delayed Post-OP Bac Endophth.
  4. Toxic Ant Seg Syndrome (TASS)
  5. Lens Subluxation
  6. Post Capsular Opacification (PCO)
  7. Cystoid Macular Edema (CME)
  8. What are some other complications after Sx?
A
  1. Corneal edema. Descemet folds; resolved w/in a few days;
  2. Rare; 1/1000; 50% become blind; Symptoms: w/in 2-4 days; 70% Gram (+): Staph Epidermidis (most common), staph aureus;
  3. Symptoms: 1 wk to 1 month after; FUNGAL Post-op is usually a delayed complication.
  4. STERILE INFLAMMATORY REACTION –> Toxic Damage to Ant Seg Structures. Cause: Chemical Exposure during surgery. Usually 12-48 hrs after. NO VITRITIS, INCREASED IOP.
  5. Rare. PXF/Marfans: D/t Pupillary capture and Poor capsular support. Trauma: Most common cause.
  6. Most common Complication after CATARACT Sx. ELSCHNIG PEARLS is a type of PCO is most common in children w/Cataract Extraction.
  7. MOST COMMON REASON for decreased acuity after Cataract Sx. IRVINE-GASS SYNDROME (buzz word for Post-Cataract Sx w/CME). Peak Incidence: 6-10 WEEKS. Usually resolves w/Tx in 6 mos.
  8. RD, Wound Leak, Suprachoroidal Heme, Increased IOP, Corneal Edema, Diplopia, Ptosis, UGH (Uveitis, Glaucoma, Hyphema Syndrome), Induced Corneal Astigmatism, and Iritis.
202
Q

What can CME occur in?

A
  1. DR
  2. RVOs
  3. Uveitis
  4. RP
  5. ARMD
  6. ERM
  7. Retinal Vasculitis (Sarcoidosis, Behcet’s)
  8. Coat’s Dz
203
Q

Fundoscopy Utilizing Auxillary Lenses

  1. Hruby Lens
    a. Indications
    b. Interpretation
  2. 3-Mirror
    a. Indications
    b. Interpretation
    c. Trapezoidal Mirror
    d. Square Mirror
    e. Bullet Mirro
  3. 78 and 90D Lens
    a. Indications
    b. Interpretation
  4. BIO
    a. Indication
    b. Interpretation
A
  1. a. Noncontact exam of Optic Disc, Macula, Posterior Pole, Central Vitreous
    b. Stereoscopic, Erect, Magnified image
  2. a. Retina exam: Optic disc to Ora Serrata. Peripheral concerns, Hx of blunt trauma, risk or with symptoms of Retinal Break/Detachment
    b. Stereoscopic, reversed, magnified image, 180 degrees from mirror position
    c. 73 degrees from corneal plane; EQUATOR
    d. 67 degrees; ANTERIOR Equator and Ora Serrata
    e. 59 degrees; AC angle and Ora serrata
  3. a. Routine Post Seg eval. Easier than Hruby lens and 3 mirror. FOV directly proportional to Pupil diameter and Dioptric power of the lens.
    b. Real, inverted, reversed magnified image.
  4. a. indications: look at 3 mirror.
    b. real image; Magnifiied, reversed and inverted.
204
Q

Vitreous

  1. Asteroid Hyalosis
    a. Epidemiology
    b. Symptoms
    c. Signs
  2. Synchysis Scintillans
    a. Patho
    b. Signs
A
  1. a. age
    b. Asymptomatic
    c. tons of small, yellow-white, refractile particles (Calcium-Phosphate Soaps) attached to collagen fibrils in normal vitreous. U/L in 3/4 of cases.
  2. a. Rare; happens after: Chronic Uveitis, Vit Heme, trauma
    b. U/L, Golden Brown, Refractile CHOLESTEROL CRYSTALS. usually settle inferiorly
205
Q

Vitreous

  1. PVD:
    a. Epidemiology
    b. Patho
    c. Symptoms
    d. Signs
    e. What can happen d/t VITREOUS TRACTION during a PVD?
A
  1. a. Females > Males; older = more likely. Earlier in Myopes; Risk Factors: DM, Sx, Inflammation, Vit Heme, Trauma
    b. Liberated collagen contracts –> Posterior Hyaloid to detach from retina. Pockets of Liquefaction
    c. Acute floaters, photopsia, decreased vision.
    d. WEISS RING; Possible Vit Heme/Tobacco dust/Shafer’s sign.
    e. Epiretinal Membrane, Macular Holes, Vit and Retinal Hemes, Retinal Breaks.
206
Q

Vitreous

  1. Preretinal/Vit Heme
    a. Epidemiology
    b. Patho
    c. Causes?
    d. Symptoms
    e. Signs (3)
A
  1. a. Trauma, Ocular and Systemic Dzs (DM and HTN are big ones)
    b. d/t Trauma or from other things that cause NEO.
    c. DR, RVO, Sickle cell retinopathy, ROP, OIS. NEO is PRERETINAL in ALL OF THESE.
    d. Pre-Ret Heme: Asymptomatic unless macula is involved. Vit Heme: Sudden, Painless Vision Loss and/or Black Spots
    e. PRERETINAL HEME; VIT HEME; B-Scan is INDICATED if fundus can’t be seen thru the Vit Heme.
207
Q

Retina/Choroid

  1. CRVO
    a. Epidemiology
    b. RISK FACTORS?
    c. Ocular Dz most commonly Assoc w/CRVOs?
    d. Other Possible Etiologies in CRVO and BRVO?
    e. Patho
    f. Symptoms
    g. Signs

h. Where do we normally start to see COLLATERAL VEINS?
i. What could develop w/in first 3 mos of diagnosis?
j. Leading cause of Vision loss in Ischemic and Non-ischemic (67% of CRVOs are non-ischemic) CRVOs?
k. Define Ischemic CRVO

A
  1. a. CRVOs: 3rd most common vascular cause of VISION LOSS (DR is most common).
    b. HTN (big one), DM, Cardiovascular Dz, Open-Angle Glaucoma
    c. Glaucoma
    d. BIRTH CONTROL, Deficiencies in protein S/C/Antithrombin 3, Factor 12, Collagen vascular Dz, AIDS
    e. CRVOs: Compression of artery on a vein –> turbulent BF, venous vessel wall damage –> THROMBUS FORMATION usually at or near Lamina Cribosa.

f. Sudden, U/L, Painless vision loss (90% > 50 y/o pts)
g. Thrombus –> Ischemia –> release of VEGF –> ret hemes, collaterals, dilated tortuous veins, CWS, Optic Disc Edema
h. on disc. seen wks-mos after CRVO. Help increase drainage of excessive fluid.
i. NEO GLAUCOMA
j. MACULAR EDEMA
k. 10 DD or more of non-perfusion on FA. 90% have VA of 20/200 or worse. Poor Px.

208
Q

Retina/Choroid: BRVO

  1. Epidemiology
  2. Risk Factors
  3. Patho
  4. Evaluate for what if BRVO isn’t at an AV crossing?
  5. Symptoms
  6. Signs
  7. Vision Threatening Complications (2)
A
  1. MOST COMMON RVOs.
  2. HTN, Cardiovascular Dz, Increased BMI at 20 yrs, OAG.
  3. d/t THROMBUS after artery compression on a vein at AV crossing. MAIN LOCATION: SUP/TEMP QUADRANT!
  4. VASCULITIS
  5. Sudden, U/L, Painless VF Loss. Blurred vision OR no symptoms
  6. Dilated tortuous retinal veins, CWS, Collateral Vessels, and Intraretinal Hemes
  7. MACULAR Dz (ischemic, edema, intramacular hemes) and NEO (–> Preretinal and Vit Hemes)
209
Q

Retina/Choroid: CRAO

  1. Epidemiology
  2. Risk Factors
  3. Consider what Etiologies in young pts w/CRAOs
  4. Patho?
  5. Work up?
  6. Other possible causes?
  7. Symptoms
  8. Signs
A
  1. Transient Vision loss (AMAUROSIS FUGAX); Old peeps; 10% risk of it happening in other eye.
  2. HTN, DM, COD. Cardiac valve dz.
  3. IV drug use, Birth control
  4. a. CALCIFIC EMBOLI (large, dangerous from calcified heart valves)
    b. CAROTID EMBOLI (small cholesteol plaques: aka, HOLLENHORST PLAQUES).
  5. Carotid Doppler (Carotid Artery), EKG/Echo (cardiac dz)
  6. GCA, ACUTE increased IOP, Collagen vascular Dzs, IV drug use, Sickle-cell dz, Syphilis.
  7. Acute, major VA loss, unless CILIORETINAL ARTERY is there. VA is LP or worse…consider Ophthalmic Artery Occlusion
  8. whitening of inner retinal layers; CHERRY RED SPOT in FOVEOLA. APD.
210
Q

Retina/Choroid: BRAO

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
A
  1. Similar to CRAO
  2. 90% d/t Retinal Emboli (Hollenhorst Plaques (most common), Calcium, Fibrin, Platelet emboli)
  3. Asymptomatic. Maybe VF defect or sudden U/L Vision loss w/no pain.
  4. Whitening of retina in affected area. (90% are temporal vessels). PERMANENT VF DEFECT
211
Q

Retina/Choroid: DR

  1. Indications for Diabetic Retinal Exam? (4)
  2. Epidemiology
    a. Dx before 30: % for developing DR each year?
    b. after 7 yrs?
    c. after 25 yrs?
  3. Patho
A
  1. a. 1st exam w/in 3-5 YEARS of Dx of Type 1, and AT TIME of Dx for Type 2.
    b. No DR, repeat exam every year
    c. Mild-Mod DR: exam every 6-12 mos
    d. Severe NPDR or PDR: exam every 2-4 mos.
  2. DR: Leading cause of new blindness in US. DURATION OF DZ = MOST IMPORTANT RISK FACTOR
    a. 2%
    b. 50% will have DR
    c. 90% will have DR
  3. D/t Loss of pericytes and damage to Retinal capillary BM –> breakdown of Blood-retinal barrier.
212
Q

Retina/Choroid: DR: NPDR

  1. Risk of Progression to PDR?
    a. Mild
    b. Mod
    c. Severe
  2. Severe NPDR: Pt has 1 of the following 3: ( 4-2-1 RULE?)
  3. Very Severe NPDR?
A
  1. a. 5%
    b. 15%
    c. 52%
  2. a. Severe Ret HEMES in 4 QUADRANTS
    b. Venous beading: 2 Quadrants
    c. IRMA: 1 Quadrant
  3. 75% risk to getting PDR. Pt has 2 or more of the 4-2-1 rule.
213
Q

Retina/Choroid: DR: PDR

  1. Happens in what % of pts w/DR?
    a. Dx’d based on presence of what?
  2. High RISK CHARACTERISTICS for vision loss risk?
  3. Symptoms
  4. Signs
A
  1. 5%
    a. NEO
  2. a. NEO (NVD) more than 1/4 of DD w/in 1 DD of ON.
    b. Any NVD or NVE w/an associated Vit or Preretinal Heme
  3. Pts: usually asymptomatic. May have Blurred vision and Metamorphopsia
  4. Numerous signs of DR. Most important: MACULAR Dz and NEO
214
Q

Retina/Choroid: DR: PDR: Macular Dz

  1. Macular Ischemia
  2. Macular Edema
  3. What are the 3 criteria for CSME
  4. NEO
    a. 3 Threats to vision
A
  1. FA can differentiate b/w Ischemia and Edema. (Ischemia: looks like an enlarged foveal avascular zone)
  2. Most common cause of legal blindness in DR. Any stage of DR. CSME: based on 3 criteria.
  3. a. Retinal thickening w/in 500 um of Foveal center
    b. Hard exudates w/in 500 um of foveal center w/adjacent retinal thickening
    c. Retinal thickening at least 1 DD in size w/in 1 DD of the center of the fovea.
  4. a. Preretinal/Vit Heme (Most common)
    b. NEO Glaucoma
    c. Tractional RD
215
Q

Retina/Choroid: HTN Retinopathy

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
    a. Stage 1
    b. Stage 2
    c. Stage 3
    d. Stage 4
  5. Numerous SECONDARY CONDITIONS
  6. What are ELSCHNIG SPOTS?
A
  1. 60 million; AA
  2. Retinal arteries autoregulate diameter based on BP.
  3. Asymptomatic; Possible Macular edema (macular star), Papilledema, Serous RD, Vein occlusion
  4. B/L; Asymmetric
    a. Mild-mod diffuse narrowing of retinal arteries

b. Stage 1 + focal constriction of the retinal vasculature (AV Nicking) and exaggerated ALR.
c. Stage 2 + Ret Hemes, CWS, Hard exudates (star) w/in OPL, Retinal edema
d. Stage 3 + PAPILLEDEMA (MALIGNANT HTN); Pts w/this have to be hospitalized immediately d/t a HIGH RISK of STROKE. BP is usually >220/120
5. Vascular Occlusions, Retinal Macroaneurysm, NAION, OMN Palsies, Diabetes.
6. Choroidal Infarcts that happen in SEVERE HYPERTENSIVE RETINOPATHY

216
Q

Retina/Choroid: Retinal Artery Macroaneurysm

  1. Epidemiology
  2. Symptoms
  3. Signs
A
  1. Elderly women w/HTN or Atherosclerosis
  2. Asymptomatic; maybe gradual vision loss d/t Macular Edema or Sudden VL from Vit Heme.
  3. U/L Focal area of dilation in a retinal artery w/multi Hemes from a RUPTURED ANEURYSM w/surrounding circinate exudates; usually at an AV crossing.
217
Q

Retina/Choroid: Venous Stasis Retinopathy/OIS

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
  5. AMAUROSIS FUGAX: What is it?
A
  1. Men. 50-80.
  2. d/t occlusion of ICA/Ophthalmic Artery, secondary to ATHEROSCLEROSIS; can also happen d/t GCA
  3. GRADUAL VL (90%), dull periorbital pain or HA (40%), Amaurosis Fugax
  4. U/L (80%) dot/blot Hemes in MIDPERIPHERAL FUNDUS, dilated non-tortuous retinal veins, narrowed retinal arteries, and possible neo of the disc.
    a. VENOUS STASIS RETINOPATHY: Has these findings and CAROTID ARTERY OBSTRUCTION and NO ANT SEGMENT SIGNS.
    b. Post and Ant Segment Signs and Symptoms = OIS.
  5. Transient Monocular VL (seconds to minutes). Vision then returns to normal. Carotid Artery Embolus is the most common cause.
218
Q

Retina/Choroid: Hyperviscosity Retinopathy

  1. Patho
  2. Most common cause?
  3. Signs
A
  1. increase in resistance to BF 2ndary to elevated plasma proteins, RBCs, and/or WBCs –> decreased BF –> vessel walls damaged.
  2. HYPERGLOBULINEMIA. (found in Multiple myeloma, RA, SLE, HIV, Waldenstrom’s Macroglobulinemia)
  3. Retinal venous dilation, Ret hemes, CWS, Exudates
219
Q

Retina/Choroid:

  1. Interferon Retinopathy
  2. Talc Retinopathy
A
  1. looks like DR; usually seen w/in 3-5 mos after starting Interferon. Resolves w/o Tx once stopped. F/u every 4-6 mos
  2. B/L in IV drug users using talc as a filler. Gets stuck in Retinal Capillaries. –> Capillary Occlusion and Retinal Ischemia
220
Q

Retina/Choroid:

  1. Vascular Sheathing/Periphlebitis
A
  1. Inflammatory; Exudates around vessels; Retinal edema, ischemia, Hemes. Vessel walls stain on FA. CAUSEs: SYPHILIS, SARCOIDOSIS (Candle wax drippings), Pars Planitis, Sickle Cell Dx.
221
Q

Retina/Choroid: Idiopathic Juxtafoveolar Retinal Telangiectasis

  1. Patho
  2. U/L Congenital Form
  3. U/L Idiopathic Form
  4. B/L Acquired Form
  5. Symptoms
  6. Signs
A
  1. abnormal perifoveal capillaries w/in Juxtafoveal region.
  2. men; 4th decade; VA: 20/25-20/40
  3. Middle-aged men; 20/25 or better
  4. Equal sex distribution in 5th or 6th decades. Poor visual Px.
  5. Decreased vision
  6. Right Angle Venules and Dilated Tortuous Vessels, Hemes, varying degrees of exudate, w/in or nearby the fovea, macular edema, and/or CNVM.
222
Q

Retina/Choroid: Coats’ Dz

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
A
  1. Males; under 20. 2/3: Onset at age 10. Rapid progression if starts under age 4. Can look like Retinoblastoma
  2. Idiopathic peripheral vascular dz. untreated –> total exudative RD.
  3. Decreased vision, Strab, leukocoria.
  4. U/L, telangiectatic dilated vessels (“Lightbulb” appearance), Progression can lead to MARKED HARD EXUDATES, intraretinal hemes, exudative RD, Neo glaucoma, etc.
223
Q

Retina/Choroid: ROP (Retrolental Fibroplasia)

  1. Epidemiology
  2. Patho
  3. Signs
  4. Area of Retinal Most likely to be affected?
A
  1. Premature infants (under 36 wks) or Low bw infants who got O2 therapy.
  2. Immature BVs vasoconstrict and stop developing d/t high O2 concentration –> Proliferative retinopathy. Vision threats: Preretinal/Vit Hemes and Tractional RD
  3. Leukocoria, strab, vitreoretinal traction, PRERETINAL/VIT HEMES, and TRACTIONAL RD
  4. ANTERIOR TEMPORAL RETINA (last to get mature vascular development)…NEO and Tractional RDs here.
224
Q

Retina/Choroid: Retinoblastoma

  1. Epidemiology
  2. Patho
    a. Heritable Retinoblastoma
    b. Non-Heritable
  3. Signs/Symptoms
A
  1. Most common intraocular Malignancy in KIDS, 2nd most common of all age groups (choroidal melanoma MOST COMMON)
  2. tumor made form retinoblasts d/t mutation of Rb tumor suppressor gene.
    a. 40%: All B/L and some U/L cases are hereditary. 50% chance of passing it on to each child
    b. 85% U/L are this. Won’t pass on to their offspring.
  3. LEUKOCORIA, STRABISMUS, intraocular inflammation, decreased Vision.
225
Q

Differentials for LEUKOCORIA? (4)

A

Coats’ Dz, Toxocariasis, Retinoblastoma, ROP

226
Q

Retina/Choroid: CHRPE: Congenital Hypertrophy of the RPE.

  1. Epidemiology
  2. Signs
A
  1. Congenital.
  2. Benign, Pigmented, non-progressive lesions. Sharp borders. Central Hypopigmented Lacunae

If B/L and Multifocal…associated w/GARDNER’s SYNDROME

227
Q

Retina/Choroid: Choroidal Nevus

  1. Epidemiology
  2. Patho
  3. To Find Smal Ocular Melanomas, Use Helpful Hints
  4. Signs
  5. Most common PRIMARY INTRAOCULAR MALIGNANCY?
A
  1. Rare. Whites
  2. Benign focal accumulation of melanocytes w/in Choroid.
3. Thickness (elevation >2mm)
Fluid (subretinal)
Symptoms (blurred vision, floaters)
Orange Pigment (lipofuscin on surface of lesion)
Margins (irregular borders)
UH: Ultrasonographic hollowness
Halo Absence

Diameter more than 4DD or 6mm or close to ON…then send it out.

  1. Flat or slightly elevated, less than 5 mm in size w/overlying drusen.
  2. Choroidal Melanoma.
228
Q

Retina/Choroid: ARMD

  1. Framingham Eye Study
  2. Risk Factors
A
  1. 6.4% of pts 65-74 and 19.7% >75 y/o had signs of ARMD
  2. Age, Caucasians, + FHx, Light iris color, cigarette smoking, Hyperopia (>0.75D), HTN, Hypercholesterolemia, Female, Cardiovascular Dz
229
Q

Retina/Choroid: Nonexudative ARMD

  1. % of ARMD cases?
  2. Characterized by what?
  3. Main Symptoms?
  4. % that develop severe vision loss? Major reason for this VL?
  5. MACULAR PHOTOCOAGULATION STUDY GROUP: 4 Main risk factors that increase risk of progression from dry to wet ARMD?
A
  1. 85-90%
  2. DRUSEN; RPE abnormalities (Mottling, granularity, focal hyperpigmentation)
  3. Metamorphopsia, gradual VL (months to years), Blurred vision
  4. 12%; GEOGRAPHIC ATROPHY
  5. a. MULTIPLE SOFT DRUSEN
    b. FOCAL HYPERPIGMENTATION
    c. HTN
    d. SMOKING
230
Q

Retina/Choroid: Exudative ARMD (wet ARMD)

  1. % of legal blindness caused by this form?
  2. Main Symptoms?
  3. Characterized by what?
  4. 4 Potential presentations of wet ARMD?
A
  1. 88%
  2. Metamorphopsia, Central Scotoma, Rapid VL
  3. DRUSEN associated w/signs of CNVM. They can leak BLOOD or Plasma into 2 major places (Sub-RPE or Subretinal space)
  4. a. SUBRETINAL HEME
    b. SUB-RPE HEME
    c. SUBRETINAL DETACHMENT (Serous RD) (Plasma under the retina)
    d. Sub-RPE Detachment (Plasma under RPE aka PIGMENT EPITHELIAL DETACHMENT (PED))
231
Q

Retina/Choroid:: ARMDS

  1. PEDs: can happen in Dry ARMD as well. Why?
  2. FA can tell us 2 things about CNVMs
  3. Risk for B/L wet ARMD?
A
  1. d/t build-up of confluent soft drusen on Bruch’s membrane. Creates a space b/w RPE and choroid. It’s a Sub-RPE detachment called DRUSENOID PED
  2. a. CLASSIC CNVM: well defined membrane that fills w/dye during early phases of FA.
    b. OCCULT CNVM: poorly defined membrane w/LATE appearing and less intense leakage.
  3. It’s fairly high.
232
Q

Retina/Choroid: CSR (central serous choroidopathy)

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
  5. Are RPE changes permanent?
A
  1. young/middle-aged men; Type A; Stress, pregnancy, steroid use, hypochondriasis, HTN
  2. Unknown. Causes RPE/Choroidal Dysfunction –> submacular serous fluid.
  3. U/L sudden onset of blurred vision (20/20 to 20/200), Metamorphopsia, and Relative scotoma can happen.
  4. Localized MACULAR SEROUD DETACHMENT; FA: Gradual pooling into PED (90%) or SMOKESTACK appearance (10%); OCT to Dx/monitor. Can have HYPEROPIC SHIFT and loss of FLR.
  5. Yes. w/in macula. Most improve w/o Tx in 1-3 MONTHS. 94% get 20/30 or better acuity.
233
Q

Retina/Choroid: Histoplasmosis

  1. Epidemiology
  2. Patho
  3. Recurrences?
  4. Symptoms
  5. Signs
A
  1. Rare in AA. Ohio-Mississippi River VALLEY.
  2. d/t Histoplasmosa Capsulatum…FUNGUS in soil and in BIRD or BAT DROPPINGS
  3. happen in preexisting Histo Spots
  4. Asymptomatic unless Maculopathy develops. Earliest symptom is Metamorphopsia.
  5. CHOROIDITIS; Clinical triad of Peripapillary Atrophy of ON, Multifocal lesions in the periphery, and Maculopathy (including CNV). Vitreous is always clear in Histoplasmosis
234
Q

Retina/Choroid: Pathological Myopia

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
  5. LACQUER CRACKS
  6. PAVINGSTONE DEGENERATION
A
  1. Genetic. 2% of US pop. WOMEN in young adulthood.
  2. RE >-6.00 D w/axial length >26 mm –> Scleral thinning and Choroidal Atrophy
  3. Asymptomatic or decreased vision and metamorphopsia
  4. POSTERIOR STAPHYLOMA (hallmark)…POSTERIOR bulging of Weakened sclera. Other signs: Oblique insertion of Optic Disc, Fuch’s Spots, LACQUER CRACKS, macular holes, premature cataracts (NS and PSC), extensive vitreous syneresis, PVD, Peripheral retinal degenerations (lattice, snail-track, pavingstone), retinal breaks, RDs
  5. ~5% of high myopes; Fine, yellow, irregular lines = Large breaks in BRUCH’s. Choroidal neo can happen –> Severe VL. usually young males.
  6. Discrete, circular areas of yellow-white chorioretinal atrophy in retinal periphery. AKA Cobblestone degeneration. Predisposing for RD.
235
Q

Retina/Choroid: ERM/Macular Pucker

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
A
  1. Females (3:2), Age; 2% older than 50, 20% older than 75.
    a. Idiopathic; can be d/t PVDs, retinal breaks, cataract or other Sxs. Trauma.
  2. GLIAL CELL PROLIFERATION on ILM. Can be d/t Vitreal traction from Posterior Hyaloid (back of vitreous) on ILM.
  3. Asymptomatic or have decreased vision and/or metamorphopsia
  4. Mild ERMs: Fine, glistening membrane (cellophane maculopathy). Advanced ERM: Thick, gray-white membranes w/associated retinal folds (Macular Pucker)
236
Q

Retina/Choroid: Macular Hole

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
    a. Stage 1
    b. Stage 2
    c. Stage 3
    d. Stage 4
  5. Macular Photostress Test
A
  1. most d/t aging. WOMEN
  2. d/t Posterior vitreous traction on macula. Idiopathic (age), Trauma, surgery, CME, inflammation can cause them. B/L onset in 1/4.
  3. Decreased vision and/or metamorphopsia. Full thickness macular holes associated w/20/20 or worse acuity
  4. Round, red, well-delineated spot in macula.
    a. Impending hole w/loss of foveal depression and a YELLOW SPOT or ring at the fovea.

b. Round, small, full-thickness hole w/Pseudo-operculum
c. Large, Full-thickness hole w/an Operculum. Pts report POSITIVE WATZKE-ALLEN SIGN (shine light on macula…missing part of the light/line)
d. Stage 3 PLUS PVD
5. Pt has BCVA; Shine bright light 10 seconds at 2 cm from pt. See how long it takes to get to one line less than his/her BCVA. Normal recovery time: 60 seconds.

237
Q

Retina/Choroid:: Choroidal Folds

  1. What are they?
  2. Characterized by what?
  3. Macular involvement symptoms?
  4. Main causes
A
  1. waves w/in choroid, bruch’s membrane, and RPE that form d/t mechanical stress on or w/in the choroid.
  2. Alternating light and dark striations w/in the fundus.
  3. Metamorphopsia and reduced VA.
  4. Ocular or systemic conditions that cause mechanical stress on the choroid.
238
Q

Retina/Choroid: Albinism

  1. Patho
  2. Signs
  3. Symptoms
  4. can be associated with what?
A
  1. Mutation of genes that make MELANIN. Affect skin and eyes (oculocutaneous albinism) or eyes only (ocular albinism)
  2. Hypopigmentation of skin and fundus, iris translucency, FOVEAL HYPOPLASIA, nystagmus, strabismus, mis-routing of temporal optic nerve fibers thru optic chiasm.
  3. Photophobia and reduced VA.
  4. Severe systemic conditions: Hermansky-Pudlak and Chediak-Higashi Syndrome
239
Q

Hereditary Fundus Dystrophies: RP

  1. Epidemiology
  2. What is USHER’s?
  3. Patho?
  4. Symptoms
  5. Signs
  6. How to Dx?
A
  1. MOST COMMON Retinal Dystrophy. USHERS SYNDROME (5%). Avg Dx: 9-19 y/o
  2. AR w/CONGENITAL HEARING LOSS
  3. Rods and cones involved. Rods more damaged. varied presentation
  4. NIGHT BLINDNESS; PERIPHERAL VL (in dim light in early stages). Takes years or decades for symptoms to develop. at 30 years, ~75% are asymptomatic
  5. Bone Spicules, VESSEL ATENNUATION, Waxy Optic Disc Pallor. Other signs: PSC, Optic Disc Drusen, Macular Changes, KCN, Myopia, Progressive contraction of VF. Annular Scotomas –> central VL.
  6. ERG (Early stages, SCOTOPIC ERG is REDUCED), but Photopic ERG is fairly normal.
240
Q

Hereditary Fundus Dystrophies: Stargardt’s Dz

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
  5. ERG?
A
  1. MOST COMMON HEREDITARY MACULAR DYSTROPHY. Onset: 1st-2nd decade of life; AR; M = F
  2. Fundus Flavimaculatus and Stargardt’s Dz are considered variants of the same disorder.
    a. Fundus Flav: No Macular dystrophy signs. Later in life (4th-5th decade); Asymptomatic.
  3. Fast VL, Color Vision abnormalities; Level of decreased vision is usually worse than fundus findings. Acuity: 20/200 by 3rd Decade, stable/slowly progressive after this.
  4. B/L yellow flecks in Pisciform (fish-tail) configuration in Posterior Pole and Mid-Periphery. Non-Specific RPE mottling of the macula can be apparent.
    Late Stages: Classic “Beaten Bronze” macular appearance (bull’s eye maculopathy), Salt and Pepper pigmentary changes in periphery.
  5. Normal in early stages of dz, then gets abnormal.
241
Q

Hereditary Fundus Dystrophies: Choroideremia

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
  5. DDx for NIGHT BLINDNESS?
A
  1. X-LINKED RECESSIVE. 1st decade
  2. lack of Rab Geranyl-Geranyl Transferase (enzyme for membrane metabolism)
  3. Night-blindness and Peripheral VL. Night-blindness: early on then goes to total night-blindness w/in 10 years. Good vision until 50-60 y/o. Females: Benign and non-progressive.
  4. B/L; Progressive; Atrophy of RPE and Choriocapillaris –> Sclera exposure. Macula…affected in late stages. Optic Disc and Retinal BVs are normal.
  5. RP, GYRATE ATROPHY, and CHOROIDEREMIA
242
Q

Hereditary Fundus Dystrophies: Cone Dystrophy

  1. Epidemiology
  2. Symptoms
  3. Signs
    a. Early
    b. Late
  4. DDX for BULL’s EYE MACULOPATHY
A
  1. Onset: 1st-3rd decade. Usually AD inheritance
  2. Slow, progressive decrease in Central Vision; Severe: Photophobia and Color VL. Worse during day. VA: 20/400 by 4th decade
  3. a. Normal fundus; Abnormal Cone function on ERG
    b. Central geographic atrophy of RPE w/Bull’s Eye Maculopathy, Vessel attenuation, Temporal Pallor of Optic Nerve (like RP) w/Severe DEUTAN-TRITAN color defects; Abnormal Photopic ERG and fine nystagmus
  4. Stargardt’s Dz, Progressive Cone Dystrophy, Chloroquine, Hydroxychloroquine Toxicity, THIORIDAZINE Toxicity
243
Q

Hereditary Fundus Dystrophies: Best’s Disease (Vitelliform Dystrophy)

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
  5. Stages
    a. Stage 1 (Pre-vitelliform)
    b. Stage 2 (Vitelliform)
    c. 3 (Pseudohypopyon)
    d. 4 (Vitelliruptive)
    e. 5 (End-Stage)
  6. ERG
  7. Adult Foveomacular Vitelliform Dystrophy
A
  1. AD; Early childhood. (Child, Mild VL, BID MACULAR SIGNS)
  2. d/t abnormal accumulation of material (maybe lipofuscin) in RPE
  3. little to no symptoms. Eventually it’s Decreased vision
  4. B/L, Yellow, round, subfoveal (egg-yolk) lesion.
  5. a. Abnormal EOG w/Normal fundus in Asymptomatic pt
    b. Egg yolk macular lesion; Age: 3-15
    c. Lesion can become absorbed w/little to no effect on vision
    d. Egg yolk starts to break up and looks more like “scrambled egg” appearance. Mild VL expected
    e. Mod-Severe VL d/t Choroidal Neo, Hemes, Atrophy, and/or Macular Scarring
  6. Normal ERG, ABNORMAL EOG
  7. Onset: 30-50; Similar to Best’s Dz. Px is better. Normal EOG and ERG; maybe small Tritan color defect
244
Q

Hereditary Fundus Dystrophies: Gyrate Atrophy

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
A
  1. AR; Symptoms by age 10
  2. B/L Choroiretinal Degeneration d/t deficiency in Mitochondrial Enzyme (ORNITHINE AMINOTRANSFERASE) High Ornithine blood plasma levels.
  3. Nyctalopia, Decreased Vision, Constricted VF
  4. Several, well-defined, scalloped areas of peripheral chorioretinal atrophy; Lesion starts in Midperiphery then coalesces to covering the entire PP w/Macula spared until 4th-7th decade. PSC, High Myopia and Astigmatism associated.
245
Q

Hereditary Fundus Dystrophies: Rhegmatogenous RD

  1. Epidemiology
  2. Risk Factors? (6)
  3. Patho
  4. Atrophic Holes
  5. Retinal Tears
    a. Flap Tears
    b. Operculated Tears
  6. Symptoms
  7. Signs
    a. Acute RD
    b. Chronic RD
A
  1. Males; Over 45.
  2. Previous Ocular Sx; PVD; Trauma; FHx; Myopia; Lattice Degeneration
  3. D/t RETINAL BREAKS (full-thickness). Vitreous goes into Subretinal space –> separation of sensory retina from RPE. (Atrophic holes, and vitreo-retinal traction tears)
  4. small, full-thickness, round. Not d/t Vitreoretinal traction. Low risk for detachment. d/t CHRONIC ATROPHY of sensory retina. Most often seen in TEMPORAL RETINA (Sup > Inf)
  5. d/t VITREOUS TRACTION
    a. d/t UNEVEN VITREOUS TRACTION which continues -> higher risk of RD.
    b. Symmetrical vitreoretinal traction. After tear is formed, Vitreous pulls away, and traction is gone. Lower risk for RD.
  6. Floaters, Photopsia, Curtain or veil over vision, decreased acuity.
  7. a. Convex undulating retina w/clear subretinal fluid that doesn’t shift with body position. Shafer’s sign can be seen. Maybe Mild Iritis, and Lower IOP in the affected eye.
    b. PIGMENT DEMARCATION LINE. Intraretinal Cysts (takes a year to form), Fixed folds, and/or subretinal precipitates.
246
Q

Hereditary Fundus Dystrophies: Lattice Degeneration

  1. % of Pts that have it?
  2. Risk?
  3. What is it?
  4. Characteristics?
  5. Types of Pts that can have Lattice like lesions?
  6. What are Vitreoretinal Tufts?
A
  1. 6-10% of population.
  2. 20-33% of RRD pts have it. only 1% of pts w/Lattice actually get an RD.
  3. Peripheral retinal thinning. Usually circumferential (cigar-shaped) and concentric w/the Ora Serrata
  4. inner part: Atrophic; Outer margins: firm adhesion to vitreous. Most do not have a criss-cross pattern of white sclerosed vessels (classic appearance). B/L and usually Temporal and Superior. 25% have Atrophic holes.
  5. Marfan’s, Stickler, Ehlers-Danlos syndromes.
  6. Small focal areas of Vitreous traction in periphery. 2nd most common peripheral retinal lesion associated w/RDs.
247
Q

Hereditary Fundus Dystrophies: Non-RRDs.

  1. Types?
  2. Exudative RD
  3. Traction RD
A
  1. Serous (exudative) RDs and Traction RDs. These are NOT CAUSED by RETINAL BREAKS.
  2. d/t subretinal disorders that damage RPE and let fluid accumulate under the retina. ex: ARMD (most common), inflammatory stuff, Vascular stuff, neoplasms, and others. Usually Asymptomatic.
  3. usually d/t PDR, ROP, and Proliferative Sickle Cell Retinopathy. Rarely complain of flashes and floaters. Maybe decreased vision or progressive VF defects
248
Q

Age Related Degenerative Retinoschisis

  1. Epidemiology
  2. Patho
  3. Symptoms
  4. Signs
  5. Other noteworthy things…
A
  1. 4-7% of pop. usually 40 or older
  2. Split of OPL and INL –> elevation of inner retina. Looks like an RD.
  3. Asymptomatic. Rare VL.
  4. Dome-shaped bullous elevation in Inf/Temp most likely. Retina won’t move. B/L. Absolute VF defect corresponds to area of elevation.
  5. Most are Hyperopes; Snowflake or Frosting and sheathed retinal vessels in elevated retinal layer; Inner and outer wall breaks can happen. Outer wall breaks are more DANGEROUS (look “Pockmarked on scleral depression). Sometimes laser Tx done to prevent RD.
249
Q

Angiod Streaks

  1. Patho
  2. Systemic Causes: PEPSI
  3. Symptoms
  4. Signs
A
  1. Large breaks in Bruch’s d/t damage of elastic core of Bruch’s. 50% idiopathic. Rest d/t Systemic Dzs.
  2. PSEUDOXANTHOMA ELASTICUM (most common), Ehlers-Danlos, Paget’s Dz, Sickle-Cell Dz, and Idiopathic (50%)
  3. Asymptomatic or major VL d/t Choroid Neo (CNVM). Most will have some form of VL.
  4. Spoke-like around Optic Disc; Linear, Well-demarcated red/orange or brown lines w/in elastic core of Bruch’s membrane
250
Q

Toxocariasis

  1. Patho
  2. Symptoms
  3. Signs
  4. What is CHORIORETINITIS?
    a. Examples?
A
  1. Toxara Canis or Cati; Children/Young Adults from eating dirt, vegetables, meat, water, or infected cats/dogs; Larvae penetrate intestinal wall and travel to various organs.
  2. Floaters and Blurred Vision
  3. Ocular infections –> U/L Inflammatory response –> Optic Nerve Edema, RD, Vitritis, Endophthalmitis, Subretinal Granulomas. Large, White Chorioretinal scars seen after active infection is gone.
  4. Type of Post. Uveitis. Inflammation of Choroid and Retina.
    a. Toxoplasmosis, Toxocariasis, Sarcoid, Syphilis, CMV, Serpiginous Choroidopathy, Birdshot Chorioretinopathy, Tb, and Onchocerciasis.
251
Q

Acute Posterior Multifocal Placoid Pigment Epitheliopathy

  1. Epidemiology
  2. Chracteristics
  3. Tx?
A
  1. YA, usually after a Viral illness
  2. B/L, Yellowish, Flat, Subretinal Lesions. Disc Edema and RD can also occur.
  3. Resolves w/o Tx in a few wks.
252
Q

Central Areolar Choroidal Dystrophy

  1. Epidemiology?
  2. Characteristics?
  3. Senile Choroidal Atrophy
A
  1. AD
  2. B/L. Lg areas of Geographic Atrophy in Macula. VL by 4th-5th decade. Poor Px.
  3. Choroidal Thinning. Can look like Exaggerated TIGROID FUNDUS appearance d/t increased visibility of choroidal vasculature.
253
Q
  1. What is a Port Wine Stain? What’s it associated with?
A
  1. Vascular birthmarks. High Association with IPSILATERAL GLAUCOMA (45%). Rarely associated w/Systemic stuff. but most common is Sturge-Weber Syndrome (~5%)
254
Q

Secondary Open Angle Glaucoma: Pseudoexfoliation Syndrome

  1. What is it?
  2. Characterized by what?
  3. Signs?
  4. Signs on Gonio?
  5. PXF associations?
  6. Main presentation?
A
  1. Age-related SYSTEMIC CONDITION. Caucasians, Scandinavian descent. Most common identifiable cause of Elevated IOP
  2. ABNORMAL, WHITE, FLAKY DEPOSITS (TM).
  3. Deposits on Pupillary margin. Lens Capsule (BULL’s EYE PATTERN), on Lens Zonules, and TM.
  4. SAMPAOLESI’s LINE d/t accumulation of pigment from rubbing on Post Iris Epi. (Basically, an increased pigmentation ant to Schwalbe’s Line).
  5. Poor pupil dilation, risk of lens subluxation, Cataract Sx complications d/t weak lens zonules.
  6. U/L or B/L asymmetric Pseudoexfoliative Glaucoma. Risk: 15% w/in 10 years of getting glaucoma.
255
Q

Secondary Open Angle Glaucoma: Pigmentary Dispersion Glaucoma

  1. Epidemiology
  2. Symptoms
  3. Presentation/Patho.
  4. Signs
  5. Glaucoma risk?
A
  1. Caucasians, Young, Myopes.
  2. Asymptomatic; Maybe blurred vision and halos around lights after exercising or pupil dilation.
  3. B/L. Higher AC Pressure –> Excessive BOWING of the IRIS POSTERIORLY –> more contact b/w iris and lens zonules.
  4. TIDs, Krukenberg’s spindle (vertically oriented pigment lines on Corneal Endothelium), pigment on Ant Capsule of lens and Iris surface, and TM hyperpigmentation.
  5. 5 years: 10%; 15 years: 15%
256
Q

Secondary Open Angle Glaucoma: Angle Recession Glaucoma

  1. What is it?
A
  1. Wide open angle w/Recessed Iris and Widened CBB. U/L and d/t Blunt Trauma. Even w/Wide angle, TM is damaged –> Increased risk of glaucoma over time.

10% of pts develop it if 2/3 of angle is recessed.

257
Q

NTG

  1. What is it?
  2. Epidemiology
  3. Before Dx’ing, what should you do?
  4. Signs
A
  1. type of POAG. NFL damage at lower pressures. (IOP < 21).
  2. Females; Japanese; Vascular disorders = higher risk (Raynaud’s, Migraines, LBP, Sleep Apnea, Hypercoagulation, Taking BP meds before bed…can decrease Ocular perfusion pressure)
  3. Take diurnal IOP readings.
  4. DRANCE HEMES more common in NTG. VF defects start out as FOCAL usually but more dense. Closer to fixation d/t Temporal and inferotemporal rim tissue being more commonly affected first compared to POAG.
258
Q

Primary Angle Closure Glaucoma

  1. Epidemiology
  2. Causes
  3. Pupillary Block
  4. Plateau Iris Syndrome
  5. Sub-acute
  6. Acute Angle Closure
  7. What’s Glaucomflecken?
  8. Biggest threat to vision in Acute Angle Closure?
  9. Drug that treats migraines, weight loss, and epilepsy can cause acute 2ndary angle closure?
A
  1. Acute/Intermittent; d/t Post pressure in PC pushing Peripheral iris Anteriorly into contact w/TM.
  2. PUPILLARY BLOCK and PLATEAU IRIS SYNDROME (less common)
  3. Anatomically narrow angles (hyperopes) when aq. flow thru pupil is blocked (usually d/t lens). MOST AT RISK after pupil hits mid position after coming down from dilation. (Risk: Hyperopes, ADVANCING CATARACTS, Asians, Eskimos, Lens subluxation).
  4. Anteriorly positioned ciliary processes that push the peripheral iris forward into contact w/the TM. SLE: flat iris plane, normal central AC depth, convex peripheral iris.
  5. partial angle closure –> increased IOP w/o Symptoms. More common. Chronic angle closure expected w/an Occludable Angel. PAS, Progressive ON damage
  6. Angle closure (No TM seen) –> Increased IOP (50-100 mmHg) and Pt Symptoms (emesis, eye pain, HAs, Nausea, VL). Signs: Hazy cornea, mid-dilated pupil w/poor response to light, ciliary flush, Glaucomflecken.
  7. AC opacities d/t Lens epithelial cell ischemia and necrosis 2ndary to high IOP.
  8. CRAO (IOP higher than PP of CRA).
  9. TOPAMAX (topiramate). usually w/in 1st month of use or if dosage is increased.
259
Q
  1. Most common causes of NVG? (2)
  2. Less common causes of NVG (2)?
  3. Most important sign?
  4. Tx?
A
  1. CRVO (1st) then PDR
  2. CAD and CRAO
  3. RUBEOSIS of the IRIS
  4. Anti-VEGF; then PRP.
260
Q
  1. When will a PS cause elevation in IOP?
A
  1. If there’s 360 degrees of attachment b/w Iris and Lens. (IRIS BOMBE and Pupillary Block, moving Iris anteriorly into contact w/TM).
261
Q

Congenital Glaucoma

  1. Epidemiology
  2. Patho
  3. What is Buphthalmos?
A
  1. Birth to 3 months onset. B/L. Males.
  2. Abnormal AC development
  3. enlarged eye w/corneal diameter >13mm. d/t elevated IOP.
262
Q

ICE (Iridocorneal endothelial) Syndromes

  1. Group of disorders: characterized by…
  2. Signs
  3. epidemiology
  4. Essential Iris Atrophy
  5. Chandler’s Syndrome
  6. Iris-Nevus Syndrome (Cogan-Reese Syndrome)
A
  1. Abnormal Corneal endothelium that grows on iris or in angle, increases risk for glaucoma.
  2. Corneal edema, iris atrophy, PAS, angle closure.
  3. Females. Pts age 20-50.
  4. Iris thinning. causes Hetereochromia, polycoria, corectopia, and Ectropion Uvea
  5. Corneal endothelium has “beaten Metal” appearance w/Corneal edema and corectopia
  6. Nodules on Anterior iris surface
263
Q

Inflammatory Glaucoma

  1. Glaucomatocyclitic Crisis
  2. Fuch’s Heterchromic Iridocyclitis
  3. Phacolytic Glaucoma
A
  1. AKA: Posner-Schlossman Syndrome. ACUTE TRABECULITIS –> Acute IOP increase (40-60 mmHg). Some cells in AC. Gonio: OPEN ANGLE. Young-middle aged. RCEs that burn out over time
  2. Chornic, Non-granulomatous, low grade anterior uveitis w/Stellate Keratic Precipitates. Iris Heterochromia and Iris/Angle Neo. Increased GLAUCOMA RISK d/t chronic TM damage and CATARACTS d/t Chronic Inflammation
  3. HYPERMATURE CATARACT that leaks lens material into AC –> Aq flow blockage in TM. Cells, Flare, Iridescent lens particles in AC.
264
Q

Dx Tests for glaucoma

  1. GDx
  2. OCT
  3. HRT
A
  1. uses scanning laser polarimetry to detect thinning of RNFL
  2. optical coherence tomography
  3. confocal scanning laser ophthalmoscopy for a topographical evaluation of ON and Peripapillary retina.
265
Q

VF (perimetry)

  1. SAP: Static Automated Perimetry
  2. SWAP: Shor Wavelength Automated Perimetry
  3. FDT: Frequency Doubling Technology
  4. Blindspot location and size
A
  1. Humphrey VF most popular
  2. Yellow background w/blue stimuli to detect early damage in glaucoma that cant be seen with SAP
  3. fast screening w/Sinusoidal gratings as stimulus.
  4. 15 degrees temporal and ~7.5 degrees in diameter

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