Ocular Disease: anterior

Question 1

Which is associated with vitritis, choroiditis or retinitis

Answer 1

Retinitis

Question 2

All posterior uveitis presents with vitritis, T or F?

Answer 2

F

Question 3

Inflammation of the retina

Answer 3

Breakdown of blood retinal barrier, resulting in WBCs in the vitreous. Patients may complain of floaters and/or decreased vision

Vitritis

Question 4

Inflammation of the choroid

Answer 4

Does NOT affect the blood retinal barrier and will NOT present with vitritis

Question 5

Most common cause of posterior uveitits

Answer 5

Toxoplasmosis

Question 6

Pathophysiology of toxoplasmosis

Answer 6

Parasitic infection caused by toxoplasma gondii, an obligate intracellular parasite. May be congenital or acquired

Question 7

Which is the most common form of toxoplasmosis

Answer 7

Congenital

Question 8

In what ways can congenital toxoplasmosis occur

Answer 8

Only if the mother contracts it during pregnancy. If she has it before pregnancy, it will not transfer to the fetus

Question 9

Of congential toxoplasmosis, what are the possible outcomes

Answer 9

90%-baby will be fine, recurrence in early adulthood with chorioretinal scar at birth

10% mentally handicapped: triad of convulsions, CEREBRAL CALCIFICAITON, and retinochoroiditis

Question 10

How do you get acquired toxoplasmosis

Answer 10

Inhalation of the parasite in cat feces and/or through eating undercooked meat

Question 11

Typical characteristics of toxoplasmosis

Answer 11

• young health patient with redness, photophobia, floaters, uveitits, vitritis, and decreased vision
• focal, fluffy, yellow-white retinal lesion adjacent to an old inactive scar with an overlying vitritis (Headlights in the fog)

Question 12

Headlights in the fog appearance

Answer 12

Toxoplasmosis

Question 13

Difference between toxoplasmosis and histoplasmosis

Answer 13

Histoplasmosis: FUNGAL infection that causes CHOROIDITIS that does NOT lead to vitritis. Results in multifocal “punched out” lesions in the periphery with associated peripapilllary atrophy and maculopathy, including CNVM

Toxo: retinovitritis, parasite, univocal, young and healthy, vitritis

Question 14

Less common causes of posterior uveitits

Answer 14

Sarcoidosis
Syphilis
CMV

Question 15

Posterior uveitis in sarcoidosis

Answer 15

Granulomatous panuveitis 
Retinal vitritis (cotton ball opacities)
Retinal vasculitis (candle wax drippings)

Question 16

Ocular findings in sarcoidosis

Answer 16

• Chronic dacryoadenitis
• dry eye disease
• chronic, bialteral, anterior granulomatous uveitits
• CN VII palsy
• retinal vasculitis
• vitritis
• optic nerve disease (unilateral optic disc edema, papilledema)

Question 17

CMV: posterior uveitis

Answer 17

• most common ocular infection and cause of blindness in AIDS
• white patches of necrotic retina with hemorrhagic retinitis and vascualr sheathing

Question 18

When does someone get CMV retinitis in AIDS

Answer 18

CD 4 counts less than 50

Question 19

Difference between CMV retinitis and toxoplasmosis

Answer 19

CMV has more intravitreal hemorrhages and less vitritis than toxo

Question 20

Difference between PORN and CMV

Answer 20

PORN has minimal amounts of vitritis (similar to CMV) and hemorrhages (less than CMV)

Question 21

Causes of iris coloboma

Answer 21

Incomplete closure of the embryonic fissure

Question 22

Most common place of iris coloboma

Answer 22

Inferior nasal

Question 23

Iris coloboma associations

Answer 23

Coloboma of

• CB
• zonules
• choroidal
• retinal
• ON

Question 24

What layer are iris melanomas found

Answer 24

Stroma

Question 25

Iris melanoma is an abnormal proliferation of

Answer 25

Melanocytes in the iris stroma

Question 26

Signs of iris melanoma

Answer 26

``` Pigmented or amelanotic Iris stromal tissue Inferior quadrant Feathery margins >3mm in diameter ```

Question 27

Iris lesions in younger patients (<40)

Answer 27

Any iris lesion found in younger patients (<40 years of age) with high risk characteristics, including associated hyphema, ectropion uvea, angle involvement, inferior iris location, and diffuse feathery edges, should be evaluated for potential iris melanoma

Question 28

Dellen

Answer 28

◦ An area of the cornea that wets poorly, leading to stromal dehydration and corneal thinning, with resulting pooling of NaFL within the affected area; seen adjacent to areas of elevation such as pterygia, filtering blebs, tumors, and poor fitting RGP lenses ◦ Patients may be asymptomatic or complain of an occasional FB sensation and other dry eye symptoms

Question 29

Exposure keratopathy

Answer 29

Due to abnormal CN 7 or orbicularis oculi function

Question 30

CN 7 issues and exposure keratopathy

Answer 30

Bell’s Palsy (idiopathic CN 7 palsy), cerebrovascular accident, aneurysm, MS, HSV, HZV

Question 31

Orbicularis oculi issues and exposure keratopty

Answer 31

eyelid surgery causing ectropion, thyroid eye disease, nocturnal lagophthalmos, floppy eyelid sybdrome

Question 32

Number one cause of exposure keratopathy

Answer 32

Lag ophthalmos

Question 33

Symptoms of exposure K

Answer 33

redness, FB sensation and burning; symptoms are typically worse in the AM

Question 34

Signs of exposure K

Answer 34

vary from mild SPK (commonly in the inferior 1/3 or intrapalpebral region of the cornea) to corneal ulceration. Decreased corneal sensitivity is common

Question 35

When is exposure K worse for the pt

Answer 35

AM

Question 36

Most common cause of filamentary keratitis

Answer 36

Keratoconjunctivits sicca

Question 37

What are the filaments composed of in filamentary keratopathy

Answer 37

Degenerated epithelial cells and mucous Stain with NaFL

Question 38

What generally causes filamentary keratitis

Answer 38

Chronic inflamamtion and friction

Question 39

Early sign of filamentary keratitis

Answer 39

Coma shaped SPK

Question 40

Treatment for filamentary keratitis

Answer 40

Acetylcistein (mucomyst)

Question 41

Histroy of thygesons

Answer 41

Most common in the 2nd-3rd decade. Patients often have a history of recurrent episodes with similar symptoms. There is no sex predilection

Question 42

Pathophysiology/Dx of Thygesons

Answer 42

unknown etiology although may be viral or AI. The condition has no known associations with ocular or systemic diseases

Question 43

Symptoms of Thygesons

Answer 43

FB sensation, photophobia, tearing, and occasional blurred vision. Overal lthe eye is relatively quiet with no anteiror chamber reaction or conjunctival injections. Symptoms are typically chronic and almost always bilateral

Question 44

Signs of Thygesons

Answer 44

bilateral (90%), small, multiple, asymmetric gray-white clusters of superficial intraepithelial raised corneal lesions (avg 15-20). The condition is characterized by periods of exacerbation of remissions without serious sequelae over a period of 10-20 years before It permanently resolves. ‣ Acute attacks (exacerbation)-last 1-2 months (if untreated) before resolving; lesions will stain lightly with NaFL. Exacerbations often recur within 6-8 weeks ‣ Remissions: periods of inactive disease in between acute attacks; lesions do not stain with NaFL during remission

Question 45

Where are the corneal lesions in Thygesons

Answer 45

Intraepithelial

Question 46

Pathophysiology of neurotrophic keratopathy

Answer 46

trigeminal nerve neuropathy (CN V1) that results from damage to sensor nerve supply anywhere from the trigeminal nucleus to the corneal nerve endings. This condition results in decreased corneal sensitivity and a subsequent decline in corneal regeneration and wound healing

Question 47

Common causes of neurotrophic keratopathy

Answer 47

‣ Common causes that directly affect CN V1 include herpes simplex, herpes zoster, diabetes, LASIK, CL wear, conditions that cause chronic corneal epithelial injury, surgeries, and medications

Question 48

Damage to CN 7 and neurotrophic keratopathy

Answer 48

‣ Damage to CN 7 can also results in neurotrophic keratitis due to impaired reflex tearing. Tumors, CVA, Bell’s palsy, surgeries or other conditions that damage CN 7 prevent reflex tearing, which results in chronic damage to the ocular surface and disruption of CN V1

Question 49

Neurotrophic is damage to which nerve

Answer 49

Nasocilairy branch of V1

Question 50

Symptoms of neurotrophic keratopathy

Answer 50

redness, tearing, decreased vision, FB sensation, and swollen eyelids. Corneal findgins are often worse than what the symptoms indicate

Question 51

Signs of neurotrophic keratopthy

Answer 51

decreased corneal sensitivity (hallmark of the condition). Early signs include SPK with associated perilimbal injection. Late signs include a sterile inferior oval ulcer (often with an associated iritis) without signs of significant inflammation ‣ This condition is characterized by non-healing epithelial defects; if not treated appropriately, the corneal defects will ulcerate, which may lead to corneal perforation

Question 52

Big ulcer, little pain

Answer 52

Neurotrophic keratopathy

Question 53

When does RCE occur

Answer 53

In the morning upon awakening

Question 54

Causes of RCE

Answer 54

Corneal abrasion (any trauma, especially from organic matter like wood or fingernails) Corneal dystrophies, most commonly EBMD

Question 55

Symptoms of RCE

Answer 55

recurrent episodes of acute pain that most often occur in the morning upon awakening. Additional symptoms include lacrimation, photophobia, and blurred vision.

Question 56

What wavelengths cause thermal/UV keratitis

Answer 56

Below 300

Question 57

What parts of the cornea absorb UV light below 300

Answer 57

Epithelium and bowmans

Question 58

Pathophysiology of UV keratitis

Answer 58

recall that the epithelial and bowmans membrane absorb wavelengths below 300nm; excessive absorption of this short wavelength light can result in hyperactivation of K+ channels, with resulting loss of intracellular K+ and cell death

Question 59

Symptoms of UV keratitis

Answer 59

ocular pain, photophobia, and blurred vision. Symptoms are typically worse 6-12 hours after the incident

Question 60

When is UV keratitis the worst for the patient

Answer 60

6-12 hours after the incident

Question 61

Signs of UV keratitis

Answer 61

SPK within the intrapalpebral region of the cornea that stains with NaFL

Question 62

DEW dry eye def

Answer 62

according to the international Dry Eye Workshop (DEWS), dry eye is a “multifactorial disease of the tears and ocualr surface that results in symptoms of discomfort, visual disturbance, and tear film instability with potential damage to the ocular surface.”

Question 63

Who gets dry eye the most

Answer 63

Post menopausal women

Question 64

Medications associated with dry eye

Answer 64

* Atropine, scopolamine, homatropine, cyclopentolate, tropicamide (STopACH) * ANTIhistamines: diphenhydramine, brompheniramine, chlorpheniramine, promethazine * ANTIpsychotics: chlorpromazine, thioridazine * ANTIdepressants: TCAs (amitriptyline, imipramine), MAOI (phenelzine), SSRIs (fluoxetine, excitalopram) * ANTIanxiety: diazepam * Muscle relaxant: cyclobenzaprine * Ipratropium (via muscarinic blockade)

Question 65

When are dry eye symptoms typically worse

Answer 65

End of the day

Question 66

TBUT and dry eye

Answer 66

<10s

Question 67

Is tear osmolarity increased or decreased in dry eye

Answer 67

Increased

Question 68

Aqueous deficient dry eye signs

Answer 68

thin tear meniscus (<0.2mm in height is abnormal), decreased Schrimer findings, and decreased phenol red thread test

Question 69

Evaporative dry eye signs

Answer 69

‣ Decreased TBUT (<10s) | ‣ Poor expression of the meibomian glands or toothpaste consistency of meibum, meibomian gland atrophy on meibography

Question 70

Schirmer I testing

Answer 70

Performed without anesthetic. Measures the basal, emotional, and reflex tearing

Question 71

Normal on Schirmer I

Answer 71

>10mm wetting in 5m Borderline: 5-10mm wetting in 5m Abnormal: <5mm wetting in 5m

Question 72

Schirmer II testing

Answer 72

Performed with anesthetic. Measures only basal tearing

Question 73

Normal Schirmer II

Answer 73

>5mm wetting in 5m

Question 74

Normal phenol red thread

Answer 74

>10mm of wetting after 15s

Question 75

What do rose bengal and lissmine green stain

Answer 75

Dead and devitalized conjunctival and corneal cells, as well as cells that have lost their mucous covering.

Question 76

Two mechanisms behind dry eye disease

Answer 76

Increased Tear osmolarity | Tear film instability

Question 77

Increased tear osmolarity and dry eye

Answer 77

results in inflammatory cascade that damages the ocualr surface and releases inflammtory mediators into the tears. Aqueous deficient dry eye and evaporative dry eye can cause tear hyperosmolarity

Question 78

TearLab

Answer 78

TearLab technology measures tear osmolarity and may become a new gold standard in the dx of dry eye syndrome because of its high level of sensitivity and specificity. A tear osmolarity >308 mOsm/L or >8mOsm/L difference between the eyes is considered diagnostic for dry eye disease

Question 79

Tear film instability and dry eye

Answer 79

can arise secondary to tear hyperosmolarity, or can be the initiating event in the disease process (reduces lipid layer in meibomian gland disease)

Question 80

How does aqueous tear deficient dry eye result in increased tear osmolarity

Answer 80

• Aqueous tear deficient dry eye results in increased tear osmolarity- even though water evaporates form the ocular surface at a normal rate, there is a reduces aqueous layer of the tears

Question 81

What are the two main categories of dry eye

Answer 81

Aqueous deficient | Evaporative

Question 82

What are the categories of aqueous deficient dry eye

Answer 82

Sjogrens - primary: dry eye and dry mouth - secondary: dry eye, dry mouth, and autoimmune disease (usually RA) Nonsjogrens - primary lacrimal gland deficiency (age related) - secondary lacrimal gland deficiency (inflammatory disease, surgery, CL)

Question 83

Types of evaporative dry eye

Answer 83

Intrinsic -MGD, lid position disroders, low blink rate Extrinsic -ocular surface disease (vit A), CL wear,

Question 84

Difference between MGD and posterior blepharitis

Answer 84

• Posterior blepharitis and meibomian gland dysfunction (MGD) are often used interchangeably in medical practice, but this is an incorrect use of clinical terminology. Posterior blepharitis is a general term that refers to inflammatory conditions of the eyelid and may be caused by several conditions. In the latera stages of MGD, if inflammatory signs are present, an MGD-related posterior blepharitis is the appropriate diagnosis.

Question 85

Low blink rate and evaporative dry eye

Answer 85

A low blink rate resutls in poor expression of meibum from the meibomian glands. The terminal meibomian gland ducts hyperkeratinize=obstruction of the ducts=intraductal HTN due to build up of meibum=dilation of the ducts=meibomian gland atrophy

Question 86

Vitamin A and dry eye

Answer 86

Vitamin A is essential for goblet cell and glycocalyx development. Vit A deficiency can also result in aqueous tear deficient dry eye as a result of lacrimal gland acinar damage. It is associated with Bitots spots on the conjunctiva.

Question 87

What staining is used in dry eye

Answer 87

Lissamine green | -inferior and 3 and 9 o’clock

Question 88

When does keratoconnus start

Answer 88

Puberty

Question 89

Inheritance of keratoconnus

Answer 89

Sporadic but can be AD

Question 90

Pathophysiology of keratoconnus

Answer 90

non-inflammatory progressive and degenerative disease of unknown etiology that initally damages bowmans membrane. The condition results from the following ‣ Stromal collagen fibril displacement due to a loss of adhesion between fibrils, which resutls in corneal thinning and protrusion due to degradation of the fibrils by MMPs

Question 91

What is keratoconnus associated with

Answer 91

Eye rubbing Atopy CL wear Ocular and systemic diseases

Question 92

Ocular conditions that may be assoacited with keratoconnus due to eye rubbing

Answer 92

Allergic causes -VKC, AKC, floppy eyelid syndrome CT abnormalities -fuches ED, PPMD, granular dystrophy, lattice dystrophy Hereditary causes (poor vision causing eye rubbing) -aniridia, RP, Lebers, ROP, cone dystrophy

Question 93

Systemic conditions associated with keratonncus

Answer 93

T-DOME - Turners - Down’s syndrome - Osteogensis imperfecta - Marfans - Ehlers-Danlo’s Also atopic dermatitis and mitral valve prolapse

Question 94

Which corneal Ectasias can have hydrops

Answer 94

All three of them

Question 95

Signs of keratoconnus

Answer 95

classical clinical signs include inferior, central, or paracentral stromal thinning that is typically bilateral, asymmetric, and progressive. As the condition progresses, irregular astigmatism occurs and is poorly corrected with glasses or SCL

Question 96

Early signs of keratoconnus

Answer 96

Fleischer’s ring (iron deposits at the base of the cone that is best seen with a cobalt blue filter (appears dark)), scissors reflex on retinoscopy, irregualr mires on keratometry, and inferior steepening on topography

Question 97

Late signs of keratoconus

Answer 97

Vogt’s striae (vertical lines in deep stroma), Munson’s sign (lower lid protrusion on downgaze), RIzzuti’s sign (conical reflection on the nasal cornea when a light is shown from the temporal side), and hydrops (tears in descemets membrane that result in edema and rupture of the epithelium). 53% of patients with moderate to severe keratoconnus develop corneal scarring in one or both eyes

Question 98

Mild keratoconus

Answer 98

Less than 48D

Question 99

Moderate keratoconus

Answer 99

48-54D

Question 100

Severe keratoconnus

Answer 100

>54D

Question 101

When does PMD present

Answer 101

Early adulthood

Question 102

Pathophysiology of PMD

Answer 102

unknown; researches believe collagen abnormalities result in a thin, weakened area of the cornea in a crescent shaped distribution inferiorly. IOP causes the cornea to protrude right above the area of thinning (not WITHIN the area of thinning, as with keratoconnus)

Question 103

Signs and symptoms of PMD

Answer 103

patients typically do not experience pain. Characterized by bilateral, inferior corneal thinning (4-8 o’clock) 1-2mm from the limbus that leads to high amounts of ATR astigmatism. Classic corneal topography findings include “kissing doves” or “Crab claws”

Question 104

Difference between PMD and keratoconnus

Answer 104

PMD vs Keratoconnus: unlike keratoconnus, there is no cone, no Flieshcers ring, not Vogt’s striae found in PMD. However, patients in PMD can develop sudden vision loss from hydrops (although it is less common than keratoconnus). Corneal scarring is also more common in keratoconnus

Question 105

When does keratoglobbus present

Answer 105

Birth

Question 106

Pathophysiology of keratoglobus

Answer 106

associated with Ehlers-Danlo’s syndrome, blue sclera, and Leber’s congenital amaurosis

Question 107

Signs of keratoglobus

Answer 107

diffuse corneal thinning most concentrated in the periphery, resulting in a globular appearance. Can result in acute corneal edema due to rupture of Descemet’s membrane; corneal perforation can occur with only minor trauma

Question 108

What are the anterior corneal dystrophies

Answer 108

EBMD Meesmans Reis-Bucklers

Question 109

Pathophysiology of EBMD

Answer 109

Excess basement membrane

Question 110

Inheritance of all EBMD

Answer 110

AD

Question 111

Signs of EBMD

Answer 111

characterized by negative staining of map-lines, dots, and/or finger prints of the corneal epithelium (best seen with retro)

Question 112

EBMD and RCE

Answer 112

10% of patients with EBMD develop RCE. 50% of patients with RCE will have EBMD

Question 113

Signs of Meesmans dystrophy

Answer 113

Anteiror corneal dystrophy characterized by extensive (100s), bilateral, clear intraepithelial cysts that are diffusely spread across the entire cornea (most dominant in the intrapalpebral region)

Question 114

Reis Buckler Syndrome

Answer 114

Anteiror corneal dystrophy Reports pain early in life Bowmans replaced with collagen RCE that decreases with age Signs: bialteral, symmetric, sub-epithelial Gray reticular opacities that are most concentrated in the central cornea and spare the peripheral cornea; these opacities typically get worse with age

Question 115

What is the most severe stromal dystrophy

Answer 115

Macular dystrophy

Question 116

Which stromal dystrophy is AR

Answer 116

Macular dystrophy

Question 117

Symptoms of macualr dystrophy

Answer 117

Stromal dystrophy progressive vision loss and episodes of irritation and photophobia (secondary to RCE); severe vision loss occurs by the age of 20-30

Question 118

Signs of macular dystrophy

Answer 118

characterized by diffuse, superficial, central haze between 3 and 9 years of age. Progression results in diffuse stromal opacification (cloudy cornea), stromal thinning, and multiple gray-white opacities (mucopolysaccharide deposits) with irregular borders that are present in all layers of the cornea and extend to the limbus

Question 119

What accumulates in macular dystrophy

Answer 119

Mucopolysaccharides

Question 120

What accumulates in granular dystrophy

Answer 120

Hyaline

Question 121

Signs/symptoms of granular dystrophy

Answer 121

small, snowflake granules (hyaline deposits) in the central stroma. The deposits eventually spread towards the epithelium and deep stroma, becoming confluent and resulting in decreased visual acuity. RCE are rare

Question 122

Rare variant of granular dystrophy that is characterized by granular and lattice deposits within the central stroma

Answer 122

Avellino dystrophy

Question 123

What accumualtes in lattice dystrophy

Answer 123

Amyloid

Question 124

Signs and symptoms of lattice dystrophy

Answer 124

anterior stromal haze with branching, refractile, lattice-like lines (amyloid deposits). Patients typically report decreased acuity (in 3rd decade) resulting from significant corneal scarring and haze. RCE common

Question 125

What are granular, lattice, and avellino dystrophies assocaited with

Answer 125

mutation in the transforming growth factor beta 1 (TGFB1) gene

Question 126

What accumualtes in schnyders dystrophy

Answer 126

Cholesterol

Question 127

Pathophysiology of schnyders dystrophy

Answer 127

the condition has a strong association with hyperlipidemia, xanthelasma, and corneal arcus, and is typically non-progressive

Question 128

How to remember the types of deposit in the corneal stromal dystrophies

Answer 128

Marilyn Monroe Got Hers in LA - Macular=Mucopolysaccharides - Granular=hyaline - Lattice=amyloid -Schnyders=cholesterol

Question 129

What are the posterior corneal dystrophies

Answer 129

Fuchs | PPMD

Question 130

Epidemiology of Fuchs

Answer 130

AD inherited condition. Female predilection, mroe common in patients over 60 years old (post menopausal women). 30% of patients have a positive family histroy of the condition

Question 131

Pathophysiology of Fuchs endothelial Dystophy

Answer 131

recall that descemets membrane consists of an anterior lamina (produced in the embryo) and a posterior lamina (secreted by the endothelium throughout life). In Fuch’s dystrophy, the posterior lamina is produced in excess and is seen as clumps (guttata) of BM on Descemet’s membrane with an assoacited decrease in endothelial cell density (hallmark of Fuch’s)

Question 132

Symptoms of Fuchs endothelial dystrophy

Answer 132

most patients remain asymptomatic until later in life; progression resutls in blurred, hazy vision that is worse in the AM with pain and glare

Question 133

Signs of Fuchs endothelial dystrophy

Answer 133

often apparent early in life. Characterized by decreased endothelial cell density associatd with pleomorphism (shape) and polymegathism (size), endothelial guttata that have a “beaten metal” appearance, and thick pachymetry findings

Question 134

Primary concern in Fuch’s endothelial dystrophy

Answer 134

The primary concern in this condition is stromal edema, which develops when the endothelial cell pumps are no longer able to maintain the proper osmotic balance. Stromal edema most commonly occurs when endothelial cell counts are less than 500 cells/mm2. As the condition progresses, stromal edema can spill over into the epithelium, leading to painful bullae (within the epithelial layer of the cornea) and scarring

Question 135

What kind of pumps does the endothelial have that get lost in Fuchs endothelial dystrophy

Answer 135

NAK

Question 136

Cataract surgery and Fuchs endothelial dystrophy

Answer 136

Cataract surgery can increased endothelial cell loss and accelerate the condition, especially in cell counts <1000 cell/mm2.

Question 137

Kids endothelial cell count

Answer 137

3000-4000 cells/mm2

Question 138

Endothelial cell count age 80

Answer 138

1000 cells/mm2

Question 139

What is the minus number of endothelial cells needed to prevent corneal edema

Answer 139

Between 400-700 cells/mm2

Question 140

Epidemiology of PPMD

Answer 140

AD inherited condition that occurs within the 2-3rd decade of life, although it may manifest as a cloudy cornea at birth.

Question 141

Symptoms of PPMD

Answer 141

typically slowly progressive or non-progressive and most patients are asymptomatic; thus most patients with PPD are not identified with the condition until 30-50 years of age. Decreased vision secondary to cornea edema is the most common symptom in patients with PPD

Question 142

Signs of PPMD

Answer 142

characterized by bilateral, but often asymmetric, findings that occur at the level of Descemet’s membrane and the endothelium. Findings include subtle patches of vesicle (hallmark), band lesions (linear “Tran track lesions”) and diffuse opacities. In severe cases, corneal edema and bullae lead to painful vision loss

Question 143

What is the main concern in PPMD

Answer 143

PPD results in metaplasia of endothelial cells and an epithelial like endothelium. These endothelial cells have the potential to spread over the iris and angle architecture, resulting in angle closure glaucoma from PAS formation. ALWAYS DO GONIO FOR PPD

Question 144

What layer of the cornea is being effected in PPMD

Answer 144

Descemets (and endothelial)

Question 145

Megalocornea

Answer 145

``` Males Bilateral Diameter >13mm Highly myopic Glaucoma ```

Question 146

Microcornea

Answer 146

Unilateral or bilateral Diameter <10mm Hyperopic Risk of angle closure

Question 147

Cornea plana

Answer 147

- cornea and sclera equal curvature (pathognomonic) - assocaited with sclerocornea and microcornea - bilateral flat corneas (<38D) - hyperopia, shallow angles, increased risk of angle closure glaucoma

Question 148

Aniridia

Answer 148

Bialteral Partial or complete Associated with corneal lesions, lenticular changes, post seg abnormalities

Question 149

Haab’s striae

Answer 149

- congenital glaucoma | - horizontal cracks in descemets (forceps trauma are vertical)

Question 150

Axenfeld-Rieger syndrome

Answer 150

Condition characterized by a continuum of disorders, including posterior embryotoxon, axenfeld anomaly, Rieger anomaly, and Rieger syndrome. They suffer from anterior segment developmental abnormalities that affect the AC angle. Appx 50% of patients with axenfeld-Rieger syndrome develop glaucoma

Question 151

Posterior embryotoxon (PE)

Answer 151

anteriorly displaced Schwalbes line. Hallmark of Axenfeld-Rieger syndrome

Question 152

Axenfeld anomaly

Answer 152

PE + angle anomalies + increased glaucoma risk ‣ Angle anomalies include prominent iris processes that travel to the level of the PE, often obscuring the scleral spur

Question 153

Rieger anomaly

Answer 153

PE + angle anomalies + increased glaucoma risk + iris stromal abnormalities ‣ Iris stromal abnormalities include a displaced pupil (corectopia) and iris hypoplasia with resulting holes within the iris tissue (polycoria)

Question 154

Rieger syndrome

Answer 154

PE + angle abnormalities + increased glaucoma risk + iris stromal abnormalities + systemic abnormalities ‣ Systemic abnormalities include mental retardation, dental, craniofacial, genitourinary, and skeletal abnormalities

Question 155

Peters anomaly

Answer 155

- Rare condition in which patients are born with central white corneal opacities (leukoma) with iris adhesions. 80% of cases are bialteral - Although some consider the condition to be part of axenfeld-Riger syndrome continuum, peters anomaly rarely occurs in conjunction with these disorders; it is best to consider the condition separately. 50-70% develop secondary glaucoma. Patients may also develop corneal edema and cataracts

Question 156

Limbal dermoid

Answer 156

Normal dense CT with hair follicles and sebaceous glands that is displaced to an abnormal location; most commonly located at the inferotemporal limbus

Question 157

Sclerotic scatter

Answer 157

Corneal clarity | Naked eye

Question 158

Optic section

Answer 158

Angle depth

Question 159

Conical beam

Answer 159

Dark adapted | Cells and flare

Question 160

Specular reflection

Answer 160

Endothelium | Angles of incidence

Question 161

Indirect illumination

Answer 161

Adjacent | EBDM

Question 162

Cobal blue filter + NaFL

Answer 162

Better visualization of corneal and tears film integrity. Use the filter without NaFL to see iron rings appear black (Fleischer rings in Kones)

Question 163

Which is worse, red or white eye with chemical Brian

Answer 163

White | Limbal blanching not good

Question 164

Which is worse, alkali or acidic burns

Answer 164

Alkaline

Question 165

Alkali burns

Answer 165

Alkali injuries are more dangerous than acidic injuries; calcium hydroxide is they most common cause of alkali burns. Remember, limbal blanching is an indicator of inschemia and is most common in alkali burns Basic Burns Bad Penetrate faster and deeper to cell membrane White chemical burn us bad=ischemia Hydroxide=base

Question 166

Why do we use doxycycline when there is injury to the cornea

Answer 166

Decrease MMPs=increased healing

Question 167

What can a patient get once they have a healed injury on their cornea

Answer 167

RCE

Question 168

Signs of ruptured globe

Answer 168

full thickness laceration, severe conjunctival hemorrhage, EOM restriction, leakage of intraocular contents, low IOP, positive Seidel’s sign, hyphema, commotio retinae, choroidal rupture, and tractional retinal detachmen

Question 169

Siedels test

Answer 169

◦ Siedel’s test is used to determine if a wound leak exists. If a leak exists (a positive seidels sign), the NaFL dye will appear as a black stream (diluted by the aqueous) within the green dye of the tears; cobalt blue filter should be used

Question 170

Pathophysiology of hyphema

Answer 170

condition typically results from trauma to the iris and/or CB

Question 171

What should you not do to someone with a hyphema

Answer 171

DO NOT perform gonioscopy or scleral depression on these patients until 1 month post injury to avoid rebleeding. Rebleeds tend to be worse than the principal presentation.

Question 172

Microhyphema

Answer 172

RBCs suspended in the AC that can only be viewed with a slit lamp

Question 173

Signs of hyphema

Answer 173

Additional signs include iris sphincter tears, iridodialysis, cataract, lens subluxation, pigment ring (Vossius ring) on the anterior lens capsule, commotio retinae, and angle recession Iridodialysis: truama, iris root (thin) is pulled from CB Vossius Ring: trauma, back of iris hits the lens, pigment on the front surface of the lens Trauma is the number one cause of subluxatio

Question 174

Number one cause of lens subluxation

Answer 174

Trauma

Question 175

Idiopathic hyphema

Answer 175

In idiopathic hyphema, always inquire about the use of blood thinners (aspirin, reversible NSAIDs, warfarin, clopidogrel) and consider ordering a CBC, PT/PTT, and sickle cell screen. Sickle cell and/or clotting diseases should be considered in these cases, especially in AA and Mediterranean patients. Idiopathic-think sickle cell and NSAIDs

Question 176

IOP and hyphema

Answer 176

Increases bc TM getting blocked by RBCs and debris Patients should elevate their head (30 degrees), allowing RBCs to settle inferiorly

Question 177

FBs that cause significant inflammation

Answer 177

iron, steel, copper, or vegetable matter

Question 178

FBs that do not cause a lot of inflammation

Answer 178

Glass, stone, precious metals, and plastic are inert materials and may stay in the eye for prolonged periods of time without causing inflammation

Question 179

Most common site of orbital fracture

Answer 179

Orbital floor | Maxillary bone is the weakest (posterior medial)

Question 180

Things to look for in orbital fracture

Answer 180

In orbital wall fractures, look for a trapped inferior rectus or inferior oblique (limiting upgaze, downgaze, or both), damage to the infraorbital nerve (causing hypoesthesia of the cheek), positive forced ductions, and peripheral crepitus

Question 181

What not to do after orbital fracture

Answer 181

Do not perform gonio or scleral depression until 4 weeks after the trauma, patients should not blow their nose within 48 hours of trauma in order to limit the risk of an orbital infection

Question 182

Forced duction test and orbital fracture

Answer 182

Orbital floor fractures are associated with a positive forced duction test. Remember that during forced duction testing, the clinical attempts to move the anesthetize eye in the direction of gaze of the affected EOM by using forceps to grasp the conj ‣ Positive: eye cannot be physically moved. EOM restriction ‣ Negative: can be physically moved. Cranial nerve muscle palsy

Question 183

Pathophysiology of commotio retina

Answer 183

trauam causes disruption of the RPE and PR outer segments. Although the condition usually resolves without sequelae within 3-6 weeks, permanent vision, VF loss may occur ◦ Vitreous smacks into the PR outer segments. Gone in 72 hours

Question 184

Symptoms of commotio retina

Answer 184

Usually asymptomatic

Question 185

Berlins edema

Answer 185

Macular edema in commotio retinae

Question 186

• disinsertion of the iris root from the CB ; appears as a peripheral iris hole that’s is best seen with retroillumination

Answer 186

Iridodialysis Carefully monitor for angle recession glaucoma

Question 187

Vossius ring

Answer 187

• a pigment ring on the anterior lens surface that retuslt from contact with the posterior pigmented iris epithelium during trauma

Question 188

Associated with acute chest compressing truama and acute pancreatitis

Answer 188

Purtchers retinopathy

Question 189

Chorodial rupture

Answer 189

* occurs in 5-10% of cases of blunt ocular trauma. Most commonly appears as a single area or multiple areas of subretinal hemorrhage, usually with the temporal posterior pole, with crescent shaped tears concentric to the optic nerve head. Choroidal rupture is assocairted with a long term risk of development of CNVM at the margins of the tear, occurring in an estimated 5-10% of patients * Rupture always between the disc and the macula

Question 190

What should be performed when there is a conjunctival or corneal laceration

Answer 190

Siedels test

Question 191

ONH and trauma

Answer 191

Optic neuropathies can also resutls from trauma, disc pallor often takes weeks to appear

Question 192

Pathophysiology of preseptal cellulitis

Answer 192

``` Infection anterior to the orbital septum Most commonly from -ocular infection (horeodlum) -systemic infection -skin trauma ```

Question 193

Signs of preseptal cellulitis

Answer 193

eyelid edema, erythema, ptosis, warmth, no pain to mild tenderness, hard bump on eyelid. WILL NOT see signs of orbital congestion, as in orbital cellulitis

Question 194

One of the leading causes of exophthalmos in kids

Answer 194

Orbital cellulitis

Question 195

What to ask about when a kid has orbital cellultiis

Answer 195

Fever, recent dental infections or recent trauma

Question 196

Pathophysiology of orbital cellultiis

Answer 196

an infection posterior to the orbital septum. Most commonly results from the following ◦ 1. Sinus infection-specially ethmoid sinusitis (the infection can easily spread through the very thin lamina papyracea) ◦ 2. Orbital infection - dacryoadenitis, dacryocystitis, progression of preseptal cellulitis ◦ 3. Orbital fracture ◦ 4. Dental infection

Question 197

Most common bacterial culprits of orbital cellultiis

Answer 197

Staphylococcus aureus=adults haemophilis influenzae=kids

Question 198

Symptoms of orbital cellulitis

Answer 198

red eye, pain, decreased vision, HA, fever, general malaise, reduced color vision, an afferent pupillary defect (APD), proptosis, and diplopia with pain on eye movement due to EOM restrictions

Question 199

Prognosis of orbital cellulitis

Answer 199

◦ Orbital cellulitis is a serious infection that can results in a cavernous sinus thrombosis, brain abscess, and/or meningitis if not caught early and managed appropriately ◦ Diabetics and immunocompromised patients with orbital cellulitis can develop mucormycosis, an aggressive fungal infection that can be life threatening; these patients have a characteristic “black eschar” (black necrotic tissue) in their mouth and nose

Question 200

Preseptal vs orbital cellulitis

Answer 200

◦ Preseptal vs orbital cellulitis: patients with preseptal cellulitis will NOT have decreased vision, proptosis, fever, pain on EOM, or EOM restrictions, all of which are common in orbital cellulitis

Question 201

What is something that can occur with TED

Answer 201

MG

Question 202

What is the strongest risk factor for the development of TED

Answer 202

Cigarette smoking (2-9x greater)

Question 203

Pathophysiology of TED

Answer 203

autoimmune disorder characterized by thyroid stimulating (TSH) receptor ABs directed against the EOMs and orbital tissue, causing fibroblast proliferation and significant inflammation and thickening of the EOMs that results in ON compression in the last stage of the disease ◦ Abs may also affect the thyroid gland, most commonly causing hyperthyroidism. TED occurs in 30-70% of patients with Graves’ thyroid disease

Question 204

Symptoms of TED

Answer 204

prominent eyes, chemosis, FB sensation, tearing, photophobia, pain, diplopia, decreased vision, and color vision loss (non exhaustive list)

Question 205

Signs of TED

Answer 205

unilateral or bilateral (often asymmetric) proptosis, upper lid retraction, Elemis erythema and edema, conjunctival/ caruncle injection and edema, decreased color vision, EOM restrictions, and an APD. IOP may be elevated in primary and upgaze

Question 206

Most common cause of unilateral OR bialteral proptosis in middle aged patients

Answer 206

TED

Question 207

NOSPECS grading system for TED

Answer 207

◦ N: no signs or symptom ◦ O: only signs but no symptoms. Examples include upper lid retraction (stare appearance); this is referred to as Dalrymple’s signs ◦ S: soft tissue involvement such as lid edema and conjunctival chemosis ◦ P: proptosis ◦ E: EOM involvement, resulting in diplopia; inferior rectus is typically affected first, followed by the medial, superior, and lateral recti (IMSLOW) ◦ C: corneal involvement (SPK, SLK, ulceration) ◦ S: sight loss due to ON compression

Question 208

What is the greates threat to vision in TED

Answer 208

Compression of the ON ◦ Enlarged EOMs and inflamed orbital fat at the orbital apex can compress the ON, causing optic disc edema, and APD, reduced color vision, and visual field loss. ON compression is the greatest threat to vision due to thyroid eye disease, and occurs in 5% of patients

Question 209

Von graefes sign

Answer 209

Upper eyelid lag during downgaze | TED

Question 210

Kochers sign

Answer 210

Globe lag compared to lid movement when looking up

Question 211

Dalrymple’s sign

Answer 211

Lid retraction resulting in stare appearance

Question 212

Dx for TED

Answer 212

◦ forced duction to detect EOM restrictions ◦ CT/MRI to detect enlargement of the EOMs (tendons will be spared) ◦ Exophthalmometry to measure proptosis ◦ VF to detect ON compression ◦ Blood work (T3/T4/TSH) to measure thyroid function

Question 213

Normal exophthalmometry

Answer 213

‣ 12-22mm for caucasians ‣ 12-18mm for Asians ‣ 12-24mm for AA ‣ Abnormal titer if higher OR presence of >3mm asymmetry. Make sure to record the base

Question 214

Carotid Cavernous Fistuals result from

Answer 214

Abnormally communication between the AV systems

Question 215

Most common cause of cavernous sinus fistula

Answer 215

◦ Most commonly results from closed head trauma (77% of cases). CFFs may also develop spontaneously (classically from a ruptured ICA aneurysm) or from cavernous sinus pathology

Question 216

Signs of cavernous sinus fistula

Answer 216

◦ High pressure blood from the carotid artery builds up in the cavernous sinus and impedes the return of venous blood back to the cancerous sinus; this leads to a build up of pressure posterior to the globe and the unique classic triad of chemosis, pulsatile proptosis, and an ocular bruit. ◦ Additional signs include episcleral venous congestion, periorbital tissue swelling, elevated IOP, diplopia secondary to CN 3,4, or 6 palsies, and loss of lid /face sensation on the affected side due to a CN 5 palsy

Question 217

Most common benign orbital tumor in children. Almost all cases are diagnosed by 6m of ge

Answer 217

Cap hemangioma

Question 218

What can cap hemangioma cause

Answer 218

proptosis and deprivation amblyopia if the visual axis is blocked. Characterized bu rapid growth and spontaneous involution (70-75% of lesions gradually involuted by age 7)

Question 219

Most common benign tumor in adults

Answer 219

Cavernous hemangioma 40-60 year old females

Question 220

Signs of cavernous hemangioma

Answer 220

progressive, painless, unilateral proptosis as the tumor most commonly arises posterior to the globe within the muscle cone

Question 221

Dermoid cyst

Answer 221

commonly located within the superior/temporal quadrant.l often congential and diagnosed in early childhood as a result of noticeable proptosis. A CT scan will show a well defined mass

Question 222

Neurofibroma

Answer 222

a benign, yellow-white tumor of astrocytes that is most common in young to middle aged adults. A CT scan shows a well defined mass that is usually located int he superior orbit it can be isolated, multiple, unilateral, or bilateral. May be associated with NF

Question 223

Neurolemmoma (scwhannoma)

Answer 223

a benign tumor of the Schwann cells that is mot common in young to middle aged adults. Typically located in the superior orbit, as the tumor develops within the first division of CN 5. Patients report a gradual onset of painless, progressive proptosis

Question 224

Most common intrinsic tumor of the optic nerve

Answer 224

Optic nerve glioma | Usually in the first decade of life. Associated with NF1

Question 225

Most common benign brain tumor

Answer 225

Meningiomas Sphenoid meningiomas are the most common intracranial tumor to invade the orbit

Question 226

Malignant orbital tumors

Answer 226

Rhabdomyosarcoma neuroblastoma Lymphoma

Question 227

Most common primary pediatric orbital malignancy

Answer 227

Rhabdomyosarcmoa

Question 228

Rapid bone destructing tumor thar causes progressive unilateral proptosis with an average age of 7

Answer 228

Rhabdomyosarcoma

Question 229

Most common secondary pediatric orbital malignancy

Answer 229

Neuroblastoma

Question 230

Where does a neuroblastoma arise from

Answer 230

The abdomen, they may have horners

Question 231

Orbital lymphoma

Answer 231

most common in patients 50-70 yo. Characteristic signs include an APD and insidious progressive proptosis and vision loss. 30-50% of patients have orbital disease develop systemic involvement, of which 60% have a 5 year survival rate

Question 232

Most common problems that result from orbital tumors

Answer 232

Progressive vision loss Proptosis Diplopia APD

Question 233

Who gets orbital pseudotumor

Answer 233

Young to middle aged patients

Question 234

Pathophysiology of orbital pseudotumor

Answer 234

Idiopathic inflammatory process that can impact any soft tissue component of the orbit

Question 235

Symptoms of orbital pseudotumor

Answer 235

Acute onset of unilateral pain, red eye, diplopia, and or decreased vision. Bilateral involvement may occur in kids. 50% of kids will have additional symptoms of fever, nausea, vomitting

Question 236

Signs of orbital pseudotumor

Answer 236

``` ‣ Lid ptosis ‣ Periorbital swelling ‣ Lacrimal gland enlargement ‣ Conjunctival chemosis ‣ Reduced corneal sensation (due to CN V1 involvement) ‣ Increased IPO on the involved side ‣ ON swelling (if posterior) ‣ EOM restrictions (causing external ophthalmoplegia) and proptosis due to inflammation of the orbital contents ```

Question 237

If someone has chemosis unilaterally and not associated with allergies

Answer 237

Be certain to include idiopathic orbital inflammation in the list of differentials

Question 238

Difference between TED and orbital pseudotumor

Answer 238

TED will not have EOM tendon inflammation and orbital pseudotumor will

Question 239

Rare type of idiopathic orbital inflammation that can affect the cavernous sinus and the superior orbital fissure

Answer 239

Tolosa hunt syndrome

Question 240

Patient presentation of tolosa hunt syndrome

Answer 240

Acute and painful exophthalmoplegia and diplopia due to ipsilateral palsies of CN 3,4,6,V1,V2 Loss of sensory innervation to V1 and V2 areas as well

Question 241

What nerves pass though the cavernous sinus

Answer 241

3,4,6,V1,V2

Question 242

Bilateral orbital pseudotumor in adults

Answer 242

Raise suspicions for systemic vasculitis (wagners, polyartertitis nodosa) or lymphoma

Question 243

shrinkage and atrophy of the globe as a result of trauma, infection ,surgery, and advanced disease. Typically associated with inflammation, hypotony, and a blind eye

Answer 243

Phthisis Bulbi

Question 244

absence of ocular tissue within the globe; primary cases are very rare

Answer 244

Anophthalmos

Question 245

small globe, congential in nature

Answer 245

Microphthalmos

Question 246

retraction of the globe within the orbit; often results from ocular trauma

Answer 246

Enophthalmos

Question 247

Removal of the globe

Answer 247

Enucleation

Question 248

Removal of inner contents of the eye; scleral and other orbital contents remain

Answer 248

Evisceration

Question 249

Exteneration

Answer 249

Removal of all contents of the orbit, including EOMs and orbital fat

Question 250

Who gets ocular rosacea

Answer 250

most common in middle aged adults of norther European ancestry. Women are affected more than men, but men often have more severe disease. Affects appx 10% of the population, including an estimated 50% with acne rosacea

Question 251

Pathophysiology of ocular rosacea

Answer 251

condition affects the sebaceous glands (including meibomian glands of the eyelids), resulting in chronic ocular surface disease

Question 252

Symptoms of ocular rosacea

Answer 252

redness, burning, FB sensation, ocular irritation

Question 253

Signs of ocular rosacea

Answer 253

characterized by papules on cheek and forehead with telangiectasia, rhinophyma, and facial flushing ‣ Facial flushing with rosacea is associated with triggers such as alcoholic beverages, exertion, spicy food, caffeine, and increased sun exposure

Question 254

What can ocular rosacea lead to

Answer 254

lid diseases (inspissated meibomian glands, blepharitis, hordeola, chalazion), which results in ocualr surface disease (phlyctenules, staph marginal keratitis, SPK, corneal neo (greatest inferiorly), and dry eye syndrome

Question 255

What type of HS reaction is contact dermatitis

Answer 255

Type 4 HS reaction

Question 256

What causes contact dermatitis

Answer 256

‣ Cosmetics: makeup, shampoo, soaps, hairspray, fingernail polish, perfumes, jewelry, poison ivy, CL solutions ‣ Medications: aminoglycosides (gentamicin, tobramicin), trifluridine, cycloplegic/mydriatics, glaucoma meds, preservatives

Question 257

Symptoms of contact dermatitis

Answer 257

acute periorbital swelling redness, itching, tearing

Question 258

Signs of contact dermatitis

Answer 258

unilateral or bilateral erythema and crusting of the lid and periorbital tissues and significant conjunctival chemosis.

Question 259

Who gets ocular cicatricial pemphigoid

Answer 259

rare condition that affects females more than males. The average age of Dx is 65y; a significant number of these pateitns develop bilateral blindness an estimated 10-30 years after dx

Question 260

Pathophysiology of ocular cicatricial pemphigoid

Answer 260

chronic AI idiopathic mucous membrane disorder that most commonly affects the oral and ocular mucous membranes (conjunctiva, mouth, esophagus, and less commonly the vagina and skin). Recent research suggests OCP is caused by a type II HS reaction involving auto Abs directed against the conjunctival BM. OCP can also be drug induced from timolol, epinephrine, and pilocarpine.

Question 261

What type of HS reaction is ocular cicatricial pemphigoid

Answer 261

Type II HS

Question 262

What is a common drug that can cause ocular cicatricial pemphigoid

Answer 262

Timolol

Question 263

Symptoms of ocular cicatrial pemphigoid

Answer 263

sub-acute onset of nonspecific symptoms including redness, dryness, FB sensation, and/or decreased vision

Question 264

Signs of ocular cicatricial pemphigoid

Answer 264

conjunctival fibrosis and scarring (seen as a fine white striate), bilateral symblepharon, ankyloblepharon, and stretched inferior fornices due to shortening of the conjunctival tissue.

Question 265

Prognosis of ocular cicatricial pemphigoid

Answer 265

progression of the diseases results in the destruction of the goblet cells, meibomian glands, and the glands of krausse and wolfring, and the ducts of the main lacrimal gland, resulting in severe ocular surface disease. Additional late stage findings include entropion and trichiasis, with resulting corneal ulceration, neo, and keratinization

Question 266

Pathophysiology of SJS

Answer 266

SJS is a severe progression of a type 3 or type 3 HS reaction that affects mucous membranes (typically oral and ocualr mucous membranes). It is most commonly drug induced (sulfonamide) or from an infectious agent

Question 267

Acute signs and symptoms of SJS

Answer 267

systemic prodrome of fever, malaise, HA, nausea, vomitting. The prodrome is followed by the development of skin lesions ( diffuse erythema, classic target or bulls eye lesions, and papules on the palms of the hand and soles of the feet). Ocular lesions also occur in this phase and include ‣ Severe, bilateral, diffuse conjunctivitis associated with pseudomembranes ‣ Bacterial conjunctivitis can progress to endophthalmitis in severe cases

Question 268

Chronic signs and symptoms of SJS

Answer 268

‣ Eyelid pathology: entropion, ectropion, trichiasis, meibomian gland damage ‣ Conjunctival pathology: symblepharon, foreshortening of the fornices, conjunctival keratinization, and limbal stem cell damage, which leads to subsequent corneal pathology ‣ Corneal pathology: ulcers, neo, scars, and in some cases, perforation

Question 269

* common condition in the elderly. It is characterized by redundant upper eyelid skin that results from a weakened orbital septum, often causing eyelid ptosis, pseudoptosis, and a loss of typical distinct eyelid creases. * Advanced cases may cause an apparent superior VF loss

Answer 269

Dermatochalasis

Question 270

Two types of blepharitis

Answer 270

Staph and seborrheic

Question 271

Symptoms of blepharitis

Answer 271

• Patients are often asymptomatic, but may report vision loss that clears after blinking, burning, itching, FB sensation, tearing, crusting (especially in the AM), and mild discharge.

Question 272

Seborrheic bleph is assoacited with

Answer 272

Seborrheic dermatitis

Question 273

Seborrheic blepharitis

Answer 273

◦ Seborrheic blepharitis is assocaited with less lid inflammation, more oily, gresasy scales with flaking, and more eyelash loss (madarosis) and/or misdirected growth compared to staph blepharitis

Question 274

Anterior and posterior lids are separated by

Answer 274

The gray line (muscle of riolan)

Question 275

Who gets chalazion

Answer 275

often have a history of similar recurrent lesions. Ask about acne rosacea and seborrheic dermatitis

Question 276

Pathophysiology of chalazion

Answer 276

chronic, localized, sterile inflammation of a meibomian gland due to retention of normal secretions. 25% of chalazion resolve spontaneously without treatment

Question 277

Signs and symptoms of chalazion

Answer 277

characterized by a hard, painless, immobile nodule without redness that is most commonly located on the upper eyelid. Patients are typically asymptomatic

Question 278

Recurrent chalazia

Answer 278

warrant an evaluation for possible malignancies (sebaceous gland carcinoma

Question 279

Difference between hordeolum and chalazion

Answer 279

◦ Both chalazia and internal hordeola affect the meibomian glands. Internal hordeola are caused by infection, and chalazia are caused by non-infectious inflammation

Question 280

Who gets hordeolum

Answer 280

often have a history of similar recurrent infections (similar to chalazia) that are successfully self treated. As with chalazia, ask about acne rosacea and seborrheic dermatitis

Question 281

Pathophysiology of hordeolum

Answer 281

An acute staph infection of the eyelid glands

Question 282

Internal hordeola

Answer 282

Meibomian glands

Question 283

External hordeolum

Answer 283

Affects the glands of zeiss and moll. Also known as a stye

Question 284

Signs and symptoms of hordoelum

Answer 284

Tender, red, warm area of focal swelling on the lid

Question 285

• benign lesions that develop from the epithelium of the epidermis and dermal tissues and are often associated with the meibomian, sebaceous, and sweat glands of the eyelids

Answer 285

Eyelid cysts • Does not affect VA or cause pain, unless rupture of the cyst leads to an inflammatory reaction. The most common patient complaint is poor cosmesis

Question 286

Decreased vitamin A

Answer 286

Bitot spots

Question 287

Decreased B1

Answer 287

Thiamine | Wernicke-Korsakoff syndrome

Question 288

a congenital or acquired lesion (secondary to trauma or surgery) found on the lid and surrounding adnexal tissue that often appears white due to the accumulation of kertinous debris

Answer 288

Inclusion cyst

Question 289

acquired lesion found on the lid and the surrounding adnexal tissue that may appear white and is due to occlusion of sweat pores or pilosebaceous follicles

Answer 289

Milia

Question 290

a congenital lesion that is firm and immobile and usually located on the superior temporal or superior nasal eyelid

Answer 290

Dermoid cyst

Question 291

characterized by retention of fluid int he glands of zeiss or retention of debris in the meibomian glands. They are usually solitary, smooth lesions that are yellow or opaque

Answer 291

Sebaceous cyst

Question 292

eversion of the Lid away from the globe of the eye. The most common cause is age related (involutional) loss of muscle tone of the orbicularis oculi muscle. Other causes include mechanical, cicatricial, paralytic, and congential. • Signs/symptoms: exposure keratopathy, epiphora, brow ptosis

Answer 292

Ectropion

Question 293

inversion of the eyelid against the globe, causes include age related (involutional) (most common), cicatricial (trachoma), and congenital. Can result in pseudotrichiasis

Answer 293

Entropion

Question 294

eyelashes grow posteriorly from their site of origin

Answer 294

Trichiasis

Question 295

a second row of eyelashes arises from the meibomian gland openings

Answer 295

Distichiasis

Question 296

Signs of entropion

Answer 296

range from mild punctate keratitis to corneal ulceration and pannus (in chronic and severe cases)

Question 297

Blindness due to trachoma are due to

Answer 297

corneal ulceration secondary to entropion and trichiasis

Question 298

Who gets floppy eyelid syndrome

Answer 298

most common in obese men with obstructive sleep apnea

Question 299

Pathophysiology of floppy eyelid syndrome

Answer 299

associated with significant reduction in elastin within the tarsal plate; this occurs predominantly in face down sleeping and is thought to result from mechanical trauma to the tarsal plate from chronic lid to pillow contact ◦ During sleep, spontaneous lid eversion exposes the superior tarsal subconjunctival to the bedding, causing a papillary conjunctivitis due to friction ◦ Systemic disease associations include obstructive sleep apnea, diabetes melliutus, hyperthyroidism, and HTN

Question 300

Symptoms of floppy eyelid sybdrome

Answer 300

chronic, bilateral red eyes in the morning upon wakening, often with mild mucus discharge

Question 301

Signs of floppy eyelid sybdrome

Answer 301

chronic papillary conjunctivitis with loose upper eyelids that every easily; punctate epithelial keratopathy (50%) and keratoconnus are noteworthy corneal associations

Question 302

Ocular conditions that most often cause red eye in the AM

Answer 302

floppy eyelid syndrome, RCE, and exposure keratopathy

Question 303

Who gets BEB

Answer 303

most common in ages 50-70, with a mean age of onset of 56 years. Women are affected 2x more commonly than men

Question 304

Symptoms of BEB

Answer 304

involuntary, sustained, repetitive bilateral twitching and/or forceful closing of the eyelids that is less common during sleep

Question 305

Signs of BEB

Answer 305

spasm of the orbicularis oculi, procerus, and corrugator musculature

Question 306

Pathophysiology of BEB

Answer 306

most commonly idiopathic, although can be a result of corneal or conjunctival irritation. 78% of patients with BEB initially Jane random episodes of increased blinking that last seconds to minutes, with eventual progression to involuntary spasms with eyelid closure ◦ Over 50% of patients have an ocular surface disorder (most commonly dry eye) that may be exacerbating the spasms

Question 307

Meige’s syndrome

Answer 307

characterized by BEB AND lower facial abnormalities (difficulty chewing, and opening the mouth, jaw spasms, jaw pain, etc) appx 50% of patients with BEB have Meige’s syndrome

Question 308

Overview of BEB

Answer 308

``` Bilateral Idiopathic 3 muscles involved -orbicularis -procerus -corrugator ```

Question 309

Myokimia

Answer 309

* characterized by unilateral twitching (NOT eyelid closure) of the orbicularis oculi; does not affect the procerus or corrurgator muscles * Commonly caused by sleep deprivation, too much caffeine, or stress

Question 310

Overview of myokimia

Answer 310

One eye One muscle (orbicularis) Triggers

Question 311

List of malignant eyelid tumors from most deadly to least concerning

Answer 311

Melanoma SGC SCC BCC This is also the order from rarest to most common

Question 312

BCC epidemiology

Answer 312

the most common skin cancer in the US. Affects males more than females. BCC is the most common eyelid cancer, accounting for over 90% of all eyelid malignancies. It is asooiciated with fair skin and UV exposure, especially in the UV-B range. Patients often report a chronic lesion that occasionally bleeds and will not heal

Question 313

Pathophysiology of BCC

Answer 313

malignancy of the basal cell layer of the epidermis. Increases sun exposure in childhood and adolescent years is a critical risk factor for the development of BCC later in life ‣ BCC is minimally invasive; the incidence of metastasis is less than 0.1%

Question 314

Signs of BCC

Answer 314

varies in appearance. Most commonly presents as a shiny, firm pearly nodule with superficial telangiectasia. If not recognized and treated at an early stage, progression occurs and central ulceration develops (“rodent ulcer”). Most commonly located on the lower eyelid (50-66%) and the medial canthus

Question 315

Shortened version of BCC

Answer 315

Telangiectasia Early pearly Late=rodent ulcer

Question 316

Epidemiology of SCC

Answer 316

more common in males. SCC is the second most common eyelid cancer, but it is 40-50x less common than BCC

Question 317

Pathophysiology of SCC

Answer 317

malignancy of the stratus spinosum layer of the epidermis. Associated with UV exposure (especially in the UV-B range of 290-320nm), actinic keratosis, fair skin, prior radiation, burn scars, chemical exposure (smoking), and other forms of chronic irritation

Question 318

Main differnece between SCC and BCC

Answer 318

SCC has NO telangiectasia

Question 319

Most common precancerous skin lesions and is a precursor to SCC

Answer 319

Actinic keratosis -It is an elevated, commonly pink or red, scaly lesion on sun exposed skin that does not heal. 25% of cases of actinic keratosis develop into squamous cell carcinoma

Question 320

Signs of SCC

Answer 320

variable presentation; often appears similar to BCC but WITHOUT surface telangiectasia. Classically described as an erythematous plaque that appears rough, scaly, and/or ulcerated, and may be flat or elevated. Most commonly located on the lower eyelid or lid margin

Question 321

What range of UV light causes malignant eyelid tumors

Answer 321

UV-B

Question 322

SCC and BCC

Answer 322

‣ SCC and BCC are both associated with chronic exposure to sun light; they can appear very similar, but SCC rarely contains surface vascularization

Question 323

Keratoacanthoma

Answer 323

usually found in sun-exposed areas and has an early appearance (often a central plaque or ulcer) that is similar to BCCs and SCCs. Keratoacanthoma tumors grow very quickly to a large size (1-2 cm) before they slowly shrink and often sponataneously resolve

Question 324

Who gets SGC

Answer 324

rare, with a similar incidence to SCC. More common in elderly females. Patients may have a History of chronic unilateral blepharitis or recurrent chalazia

Question 325

Pathophysiology of SGC

Answer 325

neoplasm of the sebaceous glands of the eyelids (meibomian glands and glands of zeiss) that may be assocaited with prior radiation therapy. Sebaceous gland carcinoma has a poor prognosis; if the lid lesion is greater than 2cm, the mortality rate is 60%. If symptoms have been present longer than 6 months, the mortality rate is 38%. The overall mortality rate is 10%

Question 326

Signs of SGC

Answer 326

varies. The tumor is often hard and yellow. It is associated with madarosis, thickened and red lid margins (most common on the upper eyelid), and lymphadenopathy

Question 327

Epidemiology of malignant melanoma

Answer 327

rare (<1% of all eyelid malignancies) but most lethal primary skin cance r

Question 328

Pathophysiology of malignant melanoma malignancy of melanocytes, the cells that produce pigment within the skin. Risk factors include age, skin color, family Hx, repeated irritation, and sun exposure

Answer 328

malignancy of melanocytes, the cells that produce pigment within the skin. Risk factors include age, skin color, family Hx, repeated irritation, and sun exposure

Question 329

Signs of malignant melanoma

Answer 329

``` characteristics that increase suspicion for a malignant melanoma include the following: ‣ A: asymmetry ‣ B: border irregularity ‣ C: color differences (uneven) ‣ D: large diameter ‣ E: elnalrgement of the lesion ```

Question 330

Most important prognostic factors for malignant melanoma

Answer 330

Depth of invasion and size of the lesion

Question 331

Who gets dacryoadenitis

Answer 331

more common in children and young adults. Ask if acute or chronic symptoms and if there is any history of a recent fever or systemic infection

Question 332

Pathophysiology of dacryoadenitis

Answer 332

inflammation of the lacrimal gland that can be acute or chronic in nature ‣ Acute infections: most commonly a result of an infection by bacteria (staphylococcus aureus, neisseria gonorrheae, streptococci) or viruses (mumps, mono, influenza, HSZ) ‣ Chronic infections: more common than acute infections. Results from inflammatory disroders including sarcoidosis, TB, graves, and idiopathic orbital inflammation; 25% of patients with idiopathic orbital inflammation will have lacrimal gland involvement

Question 333

Signs and symptoms of dacryoadenitis

Answer 333

swelling of the outer 1/3rd of the temporal upper eyelid region (near the lacrimal gland). Signs may vary in acute and chronic presentations ‣ Acute: classically presents with a S shaped ptosis, temporal upper eyelid pain, redness, and swelling, preauricular lymphadenopathy, an occasional fever, and an elevated WBC count ‣ Chronic: presents as temporal upper eyelid welling with less redness, swelling, and pain. May have inferonasal globe displacement

Question 334

Pathophysiology of canaliculitis

Answer 334

inflammation of the canaliculi that can be caused by bacterial, viral, or fungal infections. The most common culprit is actinomyces israelii (streptothrix), which is characterized by yellow sulfur granules after expression of the canaliculi ‣ Other culprits include staphylococcus aureus, Candida albicans, aspergillus, nocardia asteroides, HSV, HZV ‣ Canaliculitis May also occur after surgery, trauma, and secondary to neoplastic disorders

Question 335

Most common cause of canaliculitis (bacteria)

Answer 335

Actinomyces Israelis

Question 336

Symptoms of canaliculitis

Answer 336

smoldering, unilateral red eye that is often unresponsive to abx treatment; often misdiagnosed as recurrent conjunctivitis

Question 337

Signs of canaliculitis

Answer 337

tenderness over the nasal portion of the upper or lower eyelid, a swollen puncta (pouting puncta), dacryoliths, and mucopurulent discharge that occurs with palpation over the lacrimal sac region

Question 338

Epidemiology of dacryocystitis

Answer 338

ask about concomitant ear, nose, or throat infections

Question 339

Pathophysiology of dacryocystitis

Answer 339

lacrimal sac infection that occurs when the lacrimal drainage system is obstructed (NLDO) resulting in a back flow of bacteria from the nasolacrimal duct into the lacrimal sac ‣ Common causative agents include staph aureus, staph epidermidis, pseudomonas, and H. Influenzae in kids ‣ Characterized by swelling below the medial canthal tendon: note that swelling ABOVE the medial canthal tendon should raise suspicion for a lacrimal sac tumor

Question 340

Chronic cases of dacryocystitis

Answer 340

should raise suspicion for epithelial carcinomas and malignant lymphomas, unfortunate pathology that are often overlooked; carcinomas can express blood into tear film with palpation of the lacrimal sac

Question 341

Symptoms of dacryocystitis

Answer 341

pain, often with crusting and tearing, occasional fever

Question 342

Signs of dacryocystitis

Answer 342

prominent edema and tenderness over the lacrimal sac area

Question 343

Differnece between dacryocystitis and canaliculitis

Answer 343

Dacryocystitis has more swelling, tenderness, and pain

Question 344

Treating dacryocystitis

Answer 344

‣ DO NOT refer for surgery or attempt to irrigate the lacrimal system during an acute dacryocystitis infection. Treatment should be initiated first

Question 345

Punctal stenosis

Answer 345

◦ Acquired punctal stenosis is defined as a narrowing or occlusion of the puncta of the upper or lower eyelids. It is commonly associated with older age, where progressive narrowing and occlusion of the puncta occur

Question 346

Symptoms of punctal stenois

Answer 346

◦ The most common symptom is epiphora, although patients may also report nonspecific complaints of ocular irritation

Question 347

NLDO

Answer 347

Congenital or acquired, more common in females

Question 348

Older patients; NLDO

Answer 348

Involutional stenosis most commo ncause

Question 349

Young patients: NLDO

Answer 349

Most commonly caused by membranous blockage of the valve of hasner, occurs in 5-30% of newborns. Spontaneous opening occurs 1-2 months after birth. Gentle massage

Question 350

Symptoms of NLDO

Answer 350

unilateral tearing, discharge, crusting, and recurrent conjunctivitis

Question 351

Signs of NLDO

Answer 351

epiphora, mucus reflex from the puncta after compression of the lacrimal sac, medial lower eyelid erythema, and mild to no redness to tenderness around the puncta

Question 352

Secondary dacryocystitis in cases of congenital NLDO

Answer 352

‣ A secondary dacryocystitis is not uncommon in cases of congenital NLDO due to the stagnant tears in the lacrimal sac

Question 353

Tests to evaluate the ability of the tears to pass through the lacrimal drainage system

Answer 353

Jones I and II

Question 354

Jones I

Answer 354

Tests the patency of the system - NaFL in 5minues - positive=patent. Confirmed by the presence of NaFL in the back of the patient’s throat or by having them blow theirn nose and seeing NaFL on the tissue

Question 355

Jones II

Answer 355

Irrigation with saline following a negative jones I ◦ Reflex of fluid through the same punctum indicates an obstruction within the upper and lower canaliculus (proximal to the common canaliculus) ◦ Retrograde flow though the opposite canaliculus and punctum indicates nasolacrimal blockage (obstruction distal to the common canaliculus) ◦ If the patient tastes the saline, performs a gag reflex, or if the fluid is recovered from the nose, the obstruction has been cleared ◦ If the Jones II test fails to open the nasolacrimal drainage system, a DCR is the best treatment option

Question 356

A common benign, fluid filled (typically clear) sac on the conjunctiva that may cause irritation. Also referred to as an inclusion or retention cyst

Answer 356

Conjunctival cyst

Question 357

Superficial, white yellow deposits of mucous secretions and epithelial cells in the palpebral conjunctiva. Conjunctival concretions are also known as ocular lithiasis ◦ Patients are typically asymptomatic, but may experience a FB sensation

Answer 357

Conjunctival concretions

Question 358

Conjunctival nevus

Answer 358

◦ Rare benign proliferation of melanocytes that presents around puberty or early adulthood (within the first two decades of life). During puberty it is not uncommon for the size and darkness of the nevi to increase ◦ Conjunctival nevi are typically unilateral, solitary, flat, freely mobile, and are occasionally non-pigmented. Inclusion cysts within the lesion ar diagnostic for a conjunctival nevus ◦ The most common location for a conjunctival Venus is the juxtalimbal area, followed by the plica and caruncle

Question 359

PAM is a precursor for

Answer 359

Malignant malanoma of the conjunctiva

Question 360

PAM

Answer 360

◦ Unilateral acquired pigmentation with indistinct margins that is more common in elderly white patients ◦ The patches, which can be located anywhere on the conjunctiva, are usually flat with indistinct margins. Although PAM can be benign, it also has premalignant potential; 30% of cases progress to malignant melanoma. Nodular lesions with increase vascualrity and/or increased growth are suspect for possible malignancy. A biopsy is warranted to determine whether the lesion is malignant.

Question 361

Conjunctival melanoma

Answer 361

◦ Secondary to the uncontrolled proliferation of melanocytes. They are found almost exclusively in whites and usually develop around age 50 ◦ Malignant melanomas of the conjunctiva can be pigmented or non pigmented and most commonly arse from PAM (50-75% of cases), less commonly from a pre-existing nevus (33% of cases), and rarely be novo ◦ The most important prognostic indicator for progression to malignancy is the thickness of the lesion. The most common site of metastasis is the liver.

Question 362

Conjunctival intraepithelial neoplasia (CIN) is a precursor for

Answer 362

SSC

Question 363

CIN

Answer 363

◦ Although rare, CIN is the most common conjunctival neoplasia in the US. It is also known has Bowen’s disease or conjunctival squamous dysplasia ◦ CIN is a unilateral, premalignant condition that can progress to SSC (although the risk is low as the BM most often remains intact). Risk factors for development include UV-B exposure, smoking, exposure to petroleum derivatives, fair skin, xeroderma pigmentosa, HIV, and HPV. ◦ Presentation can vary, but the most common appearance is an elevated, gelatinous mass with neovascularization; appx 10% of cases exhibit leukoplakia (keratinization) 95% of cases are found at the limbus within the interpalpebral fissure. CIN can progress onto the cornea. ◦ Studies have suggested that toluidine blue 0.05% staining may be used as a diagnostic tool for benign vs malignant or premalignant lesions, although the PPV is only 41% and the NPV is 88%. It does not distinguish between premalignant and malignant conjunctival lesions.

Question 364

◦ A pedunculated, benign, red, vascular lesion of the palpebral conjunctiva that results from trauma, surgery, a chalazion, or other sources of chronic irritation.

Answer 364

Pyogenic granuloma

Question 365

``` Inflamed area (white, yellow, translucent, brown) located within the conjunctival stromal tissue that results from retained FB, surgery, trauma, infections, or associated systemic conditions Patients may be asymptomatic or complain of ocular irritation and FB sensation ```

Answer 365

Conjunctival granuloma

Question 366

Simple bacterial conjunctivitis culprits

Answer 366

- kids | - H influenza most common in kids, S epi and S aureus most common in adults

Question 367

Symptoms of simple bacterial conjunctivitis

Answer 367

acute onset of redness that usually begins in one eye and becomes bialteral. Additional symptoms include FB sensation and eyelid stuck together upon wakening. Symptoms typically subside in 10-14 days, even without treatment

Question 368

Signs of simple bacterial conjunctivitis

Answer 368

variable discharge (typically moderate to severe) that is often initially serous before becoming mucopurulent (most common) or purulent. Corneal signs and preauricular lymphadenopathy are rare.

Question 369

What is the most commonly isolated organism in simple bacterial conjunctivitis

Answer 369

S aureus

Question 370

Pathophysiology of gonococcal conjunctivitis

Answer 370

neisseria gonorrhoeae is the most common causative agent. The Thayer Martin agar (chocolate agar) is used for diagnosis. Gram stain for N. Gonorrhea will show gram negative intracellular diplococci

Question 371

Thayer martin (Chocolate agar)

Answer 371

Neisseria gonorrhea and Haemophilus influenzae Hershey’s and Nestles CHOCOLATE

Question 372

Symptoms of gonococcal conjunctivitis

Answer 372

characterized by hyperacute onset of severe purulent discharge. Aspirational symptoms include redness, FB sensation, and eyelids that are stuck together upon awakening; condition usually begins in one eye and becomes bilateral over time

Question 373

Signs of gonococcal conjunctivitis

Answer 373

severe purulent discharge, conjunctival chemosis (often with pseudomembranes), a severe papillary reaction, marked preauricular lymphadenopathy, and tender, swollen eyelids. remember that N. gonorrhea can invade an intact corneal epithelium and may result in peripheral corneal ulceration in severe cases.

Question 374

Systemic complications and gonococcal conjunctivis

Answer 374

* Men: purulent urethral discharge that occurs after 3-5 day incubation period * Women: discharge is less common; appx 50% of patients are asymptomatic

Question 375

All patients with a gonococcal conjunctivitis should be tested for

Answer 375

Chlamydia

Question 376

What kind of bacterial conjunctivitis causes preauricular lyhmpadenopathy and pseudomembranes

Answer 376

N gonorrhea

Question 377

Hallmark of adenoviral conjunctivitis

Answer 377

Follicles

Question 378

Pathophysiolgoy of adenoviral conjunctivitis

Answer 378

most adenoviral infections result from upper respiratory tract or mucosal infections. Appx 1/3 of serotypes are associated with ocular infections. Transmission occurs from direct contact (e.g. respiratory or ocular secretions, contaminated towels, equipment) and is highly contagious for 12-14 days. Classic adenovirus syndromes include acute nonspecific follicular conjunctivitis, pharyngoconjunctival fever (PCF), and epidemic keratoconjunctivitis (EKC

Question 379

What are adenoviral syndromes assocaited with

Answer 379

follicles, pseudomembranes, and diffuse conjunctival hyperemia and will follow from a systemic viral infection

Question 380

Acute nonspecific follicular conjunctivitis

Answer 380

results from serotypes 1-11 and 19 and is the most common type of adenoviral infection • Presents with a diffuse red eye, conjunctival follicles in the inferior fornices, tearing, and mild discomfort; corneal involvement is rare No lymphadenopathy

Question 381

PCF

Answer 381

results from serotypes 3-5 and 7. It is also referred to as “swimming pool conjunctivitis.” PCF more commonly affects chidlren and is highly contagious • Diagnosis of PCF is based on a triad of acute follicular conjunctivitis (occasionally hemorrhagic), mild, low grade fevere, and pharyngitis. Corneal involvement is not common Fever, follicles, pharyngitis

Question 382

EKC

Answer 382

most serious form of adenoviral conjunctivitis and results from serotypes 8, 19, and 37. This condition is well known for pain and corneal involvement (80% of cases) • Clinical symptoms classically occur 8 days after initial exposure to the virus. Superficial keratitis is common during the acute phase (1-2 weeks), while subepithelial infiltrates (SEIs) commonly occur after the 3rd week, after the active portion of the disease has subsided (patient no longer contagious) • Preauricular lymphadenopathy is almost always present in EKC patients. They may also have pseudomembranes. Lymphadenopathy, pain, corneal invovlemt

Question 383

Rules of 8 for EKC

Answer 383

caused by serotypes 8, symptoms occur 8 days after exposure, and SEIs occur 8 days after the onset of symptoms.

Question 384

Symptoms of adenoviral conjuncgitis

Answer 384

rapid onset of redness, tearing, mild discomfort, and preauricular lymphadenopathy. The condition typically starts in one eye before spreading to the other

Question 385

Signs of adenoviral conjunctivitis

Answer 385

acute follicular conjunctivitis (follicles are most common in the inferior fornices), marked conjunctival injection, pseudomembrane formation, preauricular lymphadenopathy (classic for EKC), and diffuse keratitis (particularly in EKC)

Question 386

What is virtually always pathognomonic for EKC

Answer 386

Palpable node in a patient with suspected adenoviral infections

Question 387

Molluscum contagiosum

Answer 387

- areas of poor hygiene - chronic infectious skin condition caused bu the DNA pox virus that is spread through direct contact. If multiple molluscum nodules RA present, consider HIV or other immunodeficiency conditions - characterized by single or multiple dome-shaped, umbilicated, waxy nodules located on the loud or lid margin. Patients are usually asymptomatic but may complain of a mild mucus discharge. Rupture of the molluscum nodules may lead to an associated chronic follicular conjunctivitis and superficial pannus.

Question 388

Viral conjunctivitis with unilateral follicular conjunctivitis with a watery discharge

Answer 388

Herpes simplex

Question 389

Seasonal allergic conjunctivitis is a _____ hypresentivity reaction

Answer 389

1

Question 390

Signs and symptoms of allergic conjunctivitis

Answer 390

conjunctival chemosis, papillae, itching, tearing, watery discharge

Question 391

VKC

Answer 391

- very rare condition. Classically affects young males under the age of 10 that live in hot, dry climates. The condition occurs for 2-10 years before resolving around puberty - VKC occurs in patients predisposed with atopic systemic conditions; 40-75% of patients with VKC have eczema or asthma, and 40-60% of patients have a family history of atopy. Seasonal outbreaks during the warm months are common, although patients may have symptoms year round. - intense itching and photophobia (most common complaints), ptosis, thick mucus discharge. The initial outbreak is the most severe; symptoms decrease in intensity over time - the classic sign is bilateral prominent papillae, either on the limbus (horners trantas dots) or the upper palpebral conjunctiva (cobblestone papillae). Can also have corneal involvement that begins with punctate keratitis that eventually coalesces into larger erosions, leading to plaque formation and localized ulceration (shield ulcer)

Question 392

Classic signs of VKC

Answer 392

Cobble stone papillae Shield ulcer Horner trantas dots

Question 393

VKC signs are predominantly in the

Answer 393

Conjunctiva and cornea | The eyelid margin and skin of the outer eyelids is rarely affected

Question 394

AKC

Answer 394

- no asthma, not seasonal, chronic eczema on face, rubbing lids=Dennie’s lines, small papillae inferiorly - atopic dermatitis - type 1 and 4 HS - bilateral itching of the eyelids (the main symptom). Other common associated symptoms include watery discharge, redness, photophobia, and pain

Question 395

Signs of AKC

Answer 395

‣ Prominent outer eyelid (scaly, thickened, swollen) and periorbital involvement, including Dennie’s lines (an extra crease under the lower lid due to periorbital edema), and “atopy shiners” (bags under the eyes from constant eye rubbing) ‣ Papillae are classically more prominent inferiorly (as compared to superior papillae in VKC and GPC), although signs may be very mild, causing the inferior conjunctival to appear featureless ‣ Corneal neo, cataracts, and keratoconnus common ‣ Symblepharon formation of the inferior fornices may occur in severe cases and mimic ocular cicatricial pemphigoid

Question 396

Atopic dermatitis

Answer 396

type of chronic eczema that starts in early infancy (within the first two years of life). 60% of patients are diagnosed within the first year of life. Hallmark signs include pruritis and a rash. An estimated 25-42% of patients with atopic dermatitis have ocular involvement. 10% of patients with severe AD develop a cataract between the ages of 15 and 30

Question 397

Toxicity to topica;l medication or CL solutions can easily result in an ______ that is characterized by _____

Answer 397

Allergic conjunctivis | Follicular reactions

Question 398

What conditions get follicles

Answer 398

``` CHAT Chlamydia Herpes Adenovirus Toxic (molluscum) ```

Question 399

Conditions that get papillae

Answer 399

pABillae - allergies - bacterial - non specific inflammation (friction)

Question 400

GPC

Answer 400

can results from silicone hydrogel CL, exposed sutures, glaucoma filtering blebs, scleral buckles, and ocular prosthetics. Environmental factors are the second most common cause of GPC (severe allergies). Although GPC can occur with any type of CL, it is most commonly associated with extended wear SCL. ‣ Obtain a detailed CL histroy (replacement schedule, cleaning system, recent switch to silicone hydrogel lens?). Risk factors for hydrogel lenses include extended wear, high watyer0ionic lenses, higher modulus of elasticity, and poor replacement compliance. ‣ The average length of time with soft lenses before development of GPC is 8 months, although it may develop as early as 3 weeks depending on the type of lens wearing schedule, etc,

Question 401

Pathophysiolgoy of GPC

Answer 401

Friction causing inflammation

Question 402

Symptoms of GPC

Answer 402

itching, scant mucus discharge (early), ropy mucus discharge (late), decreased Cl wearing time, photophobia. Symptoms are often more severe after removing CL

Question 403

Signs of GPC

Answer 403

mild to severe papillae of the upper (tarsal) conjunctiva and eyelid, ptosis, and mucous throughout the eye and/or on the CL ‣ GPC is characterized by papillae > 0.3mm in diameter. Giant papillae (>1mm) form when neighboring papillae break down septa’s and coalesce together after prolonged inflammation

Question 404

CL solutions hypersensitivity/toxicity

Answer 404

patients may have very subtle complaints and no signs to very obvious signs and symptom that most commonly occur after a recent switch to a new CL cleaning system. Severe reactions are most often in reasons to solutions containing chlorhexidine or thimerosol, although newer solutions may also cause reactions • Symptoms: redness and burning upon CL insertion after cleaning, solution change weeks to months prior with chronic redness and discomfort, reduced CL wear time due to dryness or discomfort • Signs: follicular conjunctivitis, diffuse conjunctival injection, and diffuse SPK

Question 405

If a previously asymptotic patients complains of increased dryness throughout the day, and no signs or symptoms of dryness are present without the CL,

Answer 405

Remember to ask about a recent change in CL solution

Question 406

Corneal neo and CL

Answer 406

results from chronic hypoxia; watch for superior pannus. According to the FDA, corneal neo larger than 1.5mm is abnormal and or course; stromal scarring and hemorrhage are uncommon but can occur

Question 407

Corneal warpage

Answer 407

alteration in corneal shape due to the CL material that is classically seen in long term PMMA wearers o GP wearers with poor fitting CL; in rare cases it can be seen with SCL ‣ Initially, patients often report that vision is clear in CL but blur in classes. They also note ghost images and diplopia ‣ Irregular astigmatism, which can mimic keratoconnus, is evident on topography. A high riding CL classically causes inferior steepening of the cornea over time.

Question 408

Corneal warpage vs keratoconnus

Answer 408

corneal warpage will not have other corneal findings consistent with keratoconnus and will improve with discontinuing/refitting of the CL

Question 409

SLK due to CL

Answer 409

CL hypersensitivity or a poor CL fit ‣ Signs include: superior bulbar and upper tarsal conjunctival injection. Papillae reaction and corneal filaments are uncommon, unlike SLK in thyroid disease

Question 410

Causes of SLK

Answer 410

CL Thyroid Dry eye

Question 411

Contact lens deposits

Answer 411

common in CL abusers who are not replacing lenses on schedule or who are not cleaning their lenses properly. ‣ If deposits are located on ONLY the back surface of the CL, the patient may be digitally cleaning the lenses incorrectly. Re-instruct the patient to use the finger and palm of the hand for digital cleaning ‣ A stronger cleaner or a weekly enzyme cleaner should be considered for diffuse deposits on GP contact lenses

Question 412

Deposits on HP will be ______ deposits on SCL will be ______

Answer 412

Plaques | Jelly bumps

Question 413

Tight lens syndrome

Answer 413

occurs when a CL is fitting too tight, resulting in poor movement with the blink (appears stuck on to the cornea) ‣ More common in high myopes (>-8D), CL that are fit too steep, or an abnormally small (<13mm) or large (>15mm) OAD. It is less commonly seen in hyperopes and aphakes ‣ symptoms: redness that worsens after the CL is removed, hazy vision, halos, dryness ‣ Signs: injection or indentation around the limbus and distorted keratometry mires that clear with blinking • Severe cases may result in mild to severe corneal edema or corneal blebs and an AC reaction • A corneal abrasion may occur when the CL is removed from the eye

Question 414

3 and 9 staining with CL

Answer 414

the most common implication associatd with GP CL wear ‣ Classically due to low riding GPCLs that do not adequately cover the cornea, resulting in poor spreading of the tears across he exposed corneaal surfaces ‣ Patients may be asymptomatic or complain of horizontal redness ‣ Chronic 3 and 9 staining may lead to dellen formation, pseudopterygia, and corneal vascularization

Question 415

Classic complication of a CLthat ride too high is ____ and too low ____

Answer 415

Corneal warpage | 3 and 9 staining

Question 416

SEAL

Answer 416

characterized by an arcuate shape of superior corneal staining within 1mm of the limbus ‣ SEAL most often occurs secondary to tight extended wear hydrogel CL. Loose CL that chafe or contact lenses with poor wettability may also cause SEAL ‣ An estimated 30% of cases are symptomatic. Symptoms include FB sensation, irritation, and corneal subepithelial infiltrates

Question 417

Dimple veiling

Answer 417

characterized bu small depression within the cornea that pool NaFL. Caused by small gas bubbles that become trapped underneath a CL (most often GCL

Question 418

Chlamydia-adult inclusion conjunctivitis pathophysiolgoy

Answer 418

adult inclusion conjunctivitis is the ocular manifestation of urogenital disease and is caused by chlamydia serotypes D-K. It is most commonly spread via direct inoculation, although there have been reported cases of tranmission through contaminated swimming pool water or shared cosmetics; ocular manifestation begin appx 5-14 days after inoculation. 54% of men and 74% of women will have an active genital infection

Question 419

Symptoms of chlamydia conjunctivitis

Answer 419

acute follicular + papillary conjunctivitis that becomes chronic (this prompt patients to seek medical attention); most infections begin unilaterally, but bilateral involvement often develops. The infection can persist for 3-12 months if not treated

Question 420

Signs of chlamydia conjunctivitis

Answer 420

follicles (limbal or palpebral) AND papillae that are most concentrated in the inferior palpebral conjunctiva and fornices, preauricular lymphadenopathy, scant mucopurulent discharge, and matting of the lids. Corneal involvement occurs in 30-85% of patients and includes punctate keratitis, superior pannus, and subepithelial infiltrates (more peripheral in location compared to EKC)

Question 421

Leading cause of ophthalmia naonatorum in US

Answer 421

Chlamydia

Question 422

Trachoma epidemiology

Answer 422

most prevalent between the ages of 1 and 5. Trachoma is the leading cause of preventable blindness worldwide (3rd most common cause of blindness worldwide after cataract and glaucoma). The primary risk factor is living in a community with poor hygiene. Most infections spread directly from eye to eye, but fomites, flies, and shared cosmetics are other routes of transmission

Question 423

Pathophysiolgoy of trachoma

Answer 423

caused by chlamydia serotypes A-C. Presentation begins in early childhood with a follicular and papillary conjunctivitis of the superior tarsal conjunctiva that ultimately spreads throughout the entire conjunctiva. It is almost always bialteral

Question 424

Signs and symptoms of trachoma

Answer 424

‣ Early: follicular conjunctivitis predominantly on the superior tarsal conjunctiva, mucopurulent discharge, lymphadenopathy, and mild superior pannus ‣ Late: Artl’s Lines (white scarring of the superior tarsal conjunctiva) and Herbert’s Pits (depression on the limbal conjunctiva after resolution of limbal follicles); progressive tarsal conjunctival scarring can lead to distortion of the eyelids and subsequent corneal ulceration from trichiasis

Question 425

Things that cause preauricular lymphadenopathy

Answer 425

``` Gonorrhea Chlamydia EKC Parinauds Phthisis palpebrum ```

Question 426

SLK epidemiology

Answer 426

uncommon condition that most often affects females with a mean age dx of 50. History likely to include recurrent episodes

Question 427

Pathophysiology of SLK

Answer 427

chronic inflammatory reaction most commonly associated with keratoconjunctivitis sicca, thyroid disease, and CL wear. The exact etiology is unknown. SLK is characterized by flare ups and remissions that eventually cease over time

Question 428

Causes of SLK

Answer 428

‣ Keratoconjunctivitis sicca-drying effect between the upper eyelid and bulbar conjunctiva enhances friction and creates an environment where natural turnover and replacement of mature superior bulbar conjunction cells does not occur ‣ Thyroid disease-may results from continual friction of the superior palpebral conjunctiva against the superior bulbar conjunctiva as a result of tight apposition from exophthalmos ‣ CL wearers and those with tight upper eyelids also have increased friction and thus have an increased risk of SLK

Question 429

Symptoms of SLK

Answer 429

redness, FB sensation, frequent blinking, no discharge. Symptoms are often worse than the signs; in these cases, instillation of a vital dye (NaFL, rose bengal, lissmine) can reveal prominent staining and pathology that is otherwise difficult to visualize on clinical examination

Question 430

SLK is best seen with

Answer 430

Lissamine green

Question 431

Signs of SLK

Answer 431

characterized by thickened, red, superior bulbar conjunctiva that is most prominent at the limbus and is often bilateral, with adjacent SPK and inflamamtory keratitis. The upper tarsal conjunctiva can have a velvety appearance as a result of diffuse papillary hypertrophy

Question 432

Friction on the cornea leads to

Answer 432

Papillae and filaments

Question 433

Number one cause of phlyctenules

Answer 433

Staph

Question 434

Epidemiology of phlyctenules

Answer 434

most common in teenage years with a higher occurrence in females. Ask if the patient has had simialr eye infections in the past and whether he/she has a histroy of TB

Question 435

Pathophysiolgoy of phylectenules

Answer 435

most commonly a result of type 4 HS reaction to staphylococcus (blepharitis is the most common culprit), tubuerculoprotein, and acne rosacea

Question 436

Symptoms of phlyctenules

Answer 436

tearing, FB sensation, and itching associated with conjunctival and corneal phylctenulea; significant photophobia is common with corneal phlyctenules

Question 437

Signs of phlyctenules

Answer 437

phlyctenules can be located on the conjunctiva or cornea ‣ Conjunctival phlyctenules most commonly occur at the limbus and classically appear as pink, fleshy nodules with conjunctival injection ‣ Corneal phlyctenules most commonly occur near the limbus as a small, white (lymphocytic) nodule with adjacent conjunctival injection

Question 438

When should a PPD test be read

Answer 438

48-72 hours

Question 439

Ligneous conjucntiis

Answer 439

◦ Epidemiology/Hx: rare, starts during childhood ◦ Pathophysiology/Dx: ocualr manifestations of a systemic disorder; is associated with systemic plasminogen deficiency. May affect mucous membranes throughout the body ◦ Signs: thick, white, “woody” membranous plaques of the superior tarsal conjunctivitis ◦ Symptoms: chronic tearing, FB sensation, photophobia; constant discomfort and cosmetic concerns are typical in advanced disease

Question 440

Plasmin

Answer 440

derived from plasminogen) catalyze the breakdown of fibrin, which drops unwanted clot formation within healthy vessels throughout the body

Question 441

Parinaud’s oculoglandular syndrome

Answer 441

◦ Epidemiology/Hx: rare, ask about contact exposure to cats, dogs, rabbits, squirrels, and ticks ◦ Pathophysiology/Dx: common cause include the following ‣ Cat scratch fever (most common cause)-caused by bartonella henselae, which can be transmitted by a cat scratch to the eye or through cat flea bites to the eyes ‣ Tularemia-typically transmitted via ticks, rabbits, and squirrels ‣ TB and syphilis-other noteworthy causes ◦ Symptoms: red eye, FB sensation, mucopurulent discharge ◦ Signs: unilateral, granulomatous, follicular, palpebral conjunctivitis, visibly swollen preauricular/submandibular lymphadenopathy. May also have a fever and rash Unilateral Granulomatous Swollen nodes

Question 442

Phthiriasis palpebrum

Answer 442

◦ Pathophysiology/Hx: results from phthisis pubis, know as the crab louse, found in the hair follicles of the genital area. Infection of the eyelashes, eyebrows, and facial hair may occur trough direct contact with infected individuals or infected clothing or linen. May be unilateral or bilateral ‣ Differs from demodicosis, a common parasitic mite hair follicle infectio nassociated with blepharitis that classically causes sleeving of the base of the eyelashes ◦ Symptoms: range from mild itching of the eyelids to marked inflammation with resultant burning, itching, tearing, and blurred vision ◦ Signs: transparent lice and white nits (egg sacs) attached to the eyelashes, blood tinged debris on lids and lashes, mild to severe chronic follicular conjunctivitis, and preauricular lymphadenopathy

Question 443

Subconjunctival hemorrhage

Answer 443

◦ Blood underneath the conjunctiva that typically results from valsalva, medications, hypertension, or a blood clotting disorder ◦ Remember to consider ordering a CBC, PT/PTT, and sickledex for idiopathic and recurrent cases, especially in patients of African or Mediterranean descent

Question 444

Pterygium/pingeucula

Answer 444

◦ Epidemiology/Hx: associated with environmental exposure and UV radiation; common in individuals who work outdoors ◦ Pathophysiology/Dx: UV exposure (leading cause) and chronic dryness are believed to cause degeneration of collagen fibrils within the conjunctival stroma ◦ Symptoms: range from asymptomatic to irritation, redness, and decreased vision (depending on the location of the pterygium) ◦ Signs: both conditions are typically located at 3 and 9 o’clock ‣ Pingueculum: yellow-white (typically raised) deposit adjacent to the limbus (but not on the cornea) ‣ Pterygium-triangular fibrovascular growth of bulbar conjunctiva that extends onto the cornea, destroying Bowman’s membrane and often leading to WTR astigmatism due to flattening of the horizontal meridian. Stocker’s line (iron deposits) can be present at the anterior (leading edge) of the pterygium

Question 445

Most common cause of pterygia/pingeula

Answer 445

UV radiation

Question 446

Pterygium affects what layer

Answer 446

Bowmans

Question 447

Sign of pterygium

Answer 447

Stockers line

Question 448

Epicleritis

Answer 448

• epidemiology/Hx: most common in young adults (2nd-4th decade). History of frequent recurrences (60-67%) is common • pathophysiology/dx: benign, self limiting inflammation of the episclera; often idiopathic, but can be associated with systemic diseases, including the following ◦ Collagen vascular/inflammatory diseases-RA, ulcerative colitis, crohn’s disease, reactive arthritis, ankylosing spondylitis, psoriatic arthritis ◦ Spirochetes- syphillis, Lyme ◦ Viruses- herpes zoster, herpes simplex, mumps ◦ Metabolic diseases- temporal arteritis, Wegner’s granulomatosis, Behcet’s diseases, polyarteritis nodosa ◦ Dermatological diseases- acne rosacea • Symptoms: acute unilateral red eye, occasional mild pain • Signs: injection that is typically sectoral (70%). The condition can be simple (80%) or nodular (20%); the nodule can be moves slightly with a cotton tip applicator (unlike scleritis)

Question 449

What vessels are affected in episcleritis

Answer 449

ACA

Question 450

Types of scleritis

Answer 450

Necrotizing | Nonnecrotizing

Question 451

Necrotizing scleritis types

Answer 451

``` Inflammatory (worst kind) Non inflammtory (scleromalacia perforans) ```

Question 452

Types of nonnecrotizing scleritis

Answer 452

Diffuse (#1) and nodular

Question 453

Who gets scleritis

Answer 453

female predilection (peak incidence in the 4th-6th decades). Scleritis is much less common than episcleritis. Anterior scleritis occurs in 98% of cases (2% of cases are posterior). Anterior scleritis can be divided into non-necrotizing and necrotizing scleritis

Question 454

Diffuse scleritis

Answer 454

Non necrotizing scleritis 60%): most common type of anterior scleritis and the most benign form of the disease; associated with the least severe systemic conditions. Characterized by diffuse hyperemia.

Question 455

Nodular scleritis

Answer 455

Non necrotizing | 25%): characterized by a deep, focal, painful, injected immobile nodule

Question 456

Necrotizing scleritis with inflammation

Answer 456

5%): the worst form of scleritis, as 33% of patients may die within a few years as a result of severe AI disease. 40-82% of patients will lose vision; 60% have ocular or systemic complications, including anterior uveitis, scleroising keratitis, peripheral corneal melt, scleral thinning, cataracts, and secondary glaucoma

Question 457

Necrotizing scleritis without inflammation

Answer 457

scleromalacia perforans) (10%): typically a result of chronic RA. The condition is characterized by almost complete lack of symptoms and minimal injection; asymptomatic, large, gray-blue patches of scleral thinning (due to exposure of the underlying uvea) my be seen

Question 458

What type of scleritis is assocaited with the most severe ocular signs

Answer 458

Necrotizing scleritis | peripheral cornel melt, sclerosing keratitis, scleral thinning, anterior uveitis, cataracts, and secondary glaucoma

Question 459

Pathophysiology of scleritis

Answer 459

granulomatous inflammation of the sclera in which 50% of cases are assocaited with an underlying systemic disease; 30% of the cases that result from systemic disease are caused by collagen vascular disease; RA is the most common, followed by Wegner’s granulomatosis.

Question 460

Symptoms of scleritis

Answer 460

severe, boring ocular pain (hallmark for scleritis) that can radiate to the ipsilateral forehead, brow, or jaw and awaken the patient during the night. Additional symptoms include a gradual onset of redness and a decrease in vision (except for scleromalacia perforans!)

Question 461

Signs of scleritis

Answer 461

sectoral or diffuse inflammation of the large, deep vessels that cannot be moved with a cordon swab. Edematous or thin sclera with a classic bluish hue under natural light. Signs are frequently bilateral (compared to unilateral signs of episcleritis)

Question 462

Hyaline plaques

Answer 462

benign, oval shaped areas of scleral thinning that occur with age and allow underlying visibility of the uvea

Question 463

What is associatd with scleromalacia peroforans

Answer 463

RA

Question 464

Things that can cause severe pain in the eye

Answer 464

Corneal pathology Antererio uveitis Scleritis Angle closure

Question 465

Episcleritis vs scleritis

Answer 465

◦ Scleritis is typically gradual in onset, unlike the acute nature of episcleritis, but results in more significant ocular pain and more severe ocular complications ◦ Scleritis often has a characteristic bluish hue under natural light (due to scleral thinning), as compares to the red appearance of episcleritis ◦ 2.5% phenylephrine will result in conjunctival blanching in a patient with episcleritis. It will NOT blanch the deep episcleral vessels (scleritis will remain injected. ◦ Scleritis findings are frequently bilateral and diffuse injection is more common; episcleritis signs are typically unilateral and sectoral injection is more common ◦ Scleritis is much less common than episcleritis and is more commonly associated with an underlying systemic disease

Question 466

a congenital anomaly characterized by a focal, pigmented, elevated area where the posterior ciliary nerve loops are visible in the sclera; can be painful

Answer 466

Axenfelds Nerve loop

Question 467

Epidemiology of anterior uveitis

Answer 467

affects 15/100,000 per year; there are 45,000 new cases per year in the US. Anterior uveitis frequently occurs in young adults (peak incidence in the second-fourth decade of life); it rarely locusts in individuals older than 70 (common causes in this age group are toxoplasmosis and herpes zoster)

Question 468

Blood aqueous barrier

Answer 468

Schlemms Iris vessels NPCE

Question 469

Pathophysiolgoy of anteiror uveitis

Answer 469

uveitis occurs secondary to breakdown in the blood aqueous barrier. 50% of patients with acute anterior uveitis are HLA-B27 positive (70% if the condition recurs). 50% of new onset acute anteiror uveitis cases have an associated spondyloarthropathy; 80% of these patients have anylosing spondylitis

Question 470

HLA-B27 conditions

Answer 470

UCRAP | Ulcerative Colitis, Crohn’s disease, Reactive arthritis, Ankylosing spondylitis, Psoriatic arthritis

Question 471

Terminology for anterior uveitis

Answer 471

acute, chronic, or recurrent, and classified by cell type (granulomatous vs non), location (anteiror, intermediate, posterior, pan), and laterality ◦ 75% of uveitis cases are anterior (iritis, iridocyclitis), 8% are intermediate (pars planitis), and 17% of cases are posterior or panuveitis

Question 472

Acute anteiror uveitis definition

Answer 472

self limiting disease of less than 3 months duration; it may b characterized by recurrent attacks. Chronic uveitis persists for more than 3 months; it may have periods of exacerbation, but nerve fully resolves

Question 473

Symptoms of anterior uveitis

Answer 473

pain, redness, photophobia, lacrimation, and mildly decreased vision (especially with CME). Patients with chronic anterior uveitis may be asymptomatic or report blurred vision or a dull ache

Question 474

What is the pain from in anteiror uveitits

Answer 474

congestion and irritation of the anterior ciliary nerves

Question 475

Grnaulomatous antieror uveitis causes

Answer 475

Sarcoidosis | TB

Question 476

Nongranulmatous causes of anteiror uveitis

Answer 476

Idiopathic (70%) | UCRAP (30%)

Question 477

Signs of anterior uveitis

Answer 477

diagnosed based on the presence or absence of white blood cells in the anterior chamber (or elsewhere for other locations of uveitis) ◦ Main threats to vision include posterior synechiae (PS), peripheral anterior synechiae (PAS), CME, and cataract formation (most commonly PSC and assocaited with chronic cases) ◦ Other prominent anterior segment signs include flare, hypopyon, circumlimbal injection of the conjunctival vessels, decreased IOP in the involved eye (in early stages), and keratic precipitates (collection of white blood cells) on the endothelium ‣ Note that although IOP is decreasing during the early stages of uveitis due to ciliary body inflammation, IOP may also be elevated in the later stages from a variety of factors (e.g. the eye getting better, trabeculitis, PS (Leading to acute angle closure), PAS (leading to chroninc angle closure), significant inflammation, topical steroid use, chronic TM damage) ◦ Fine KPs are characteristic of non granulomatous etiology ◦ A granulomatous etiology, in comparison to non granulomatous, is more commonly infectious (TB, syphilis) and chronic in course with an increased predilection for the posterior chamber. Mutton Fat KPs and iris stromal nodules (Koeppe, Bussaca) are highly suggestive of a granulomatous etiol

Question 478

Cyclitic membranes and uveitis

Answer 478

• Cyclitic membranes may be present in chronic uveitis; they are fibrovascular membranes that extend from ciliary body into the posterior chamber and may involve the lens

Question 479

Types of KPs

Answer 479

``` Mutton fat -granulomatous Fine -nongranulomatous (UCRAP) Stellate -herpes and fuches ```

Question 480

Koeppe nodules

Answer 480

Collection of WBC located on pupillary margin | Granulomatous and non granuloamtous

Question 481

BUsacca nodules

Answer 481

WBC on any part of the iris stroma expect the pupillary margin

Question 482

Most common corneal findgin of antieror uveitis

Answer 482

KPs

Question 483

Inflammatory bowel disease

Answer 483

usually bilateral with a posterior uveitis component. Characterize by chronic intermittent diarrhea with alternating episodes of constipation. Uveitis is rare in Crohn’s disease, but is more common with ulcerative colitis Acute non granulomatous anterior uveitits

Question 484

Reactive arthritis

Answer 484

young makes with urethritis, polayarthritis, and conjunctivitis Acute anterior non granulomatous uveitiis

Question 485

Ankylosing spondylitis

Answer 485

more commonly affects males in the 3rd decade. Characterized by lower back pain; symptoms improve with exercise Acute, anterior non granulomatous uveitis

Question 486

Psoriatic arthritis

Answer 486

characterized by asymmetric, peripheral, small joint pain and psoriatic lesions on the knees, elbows and scalp Acute antieror non gran uveitis

Question 487

Behçet’s disease

Answer 487

most common in young males of middle eastern and Asian descent. Characterized by acute, recurrent hypopyon iritis and mouth and genital ulcers. May also be assocaited with retinal vasculitis, cataracts and glaucoma Acute anteiror nongran uveitis

Question 488

Lyme disease

Answer 488

patients may have a history of tick bites, a skin rash, and/or arthritis. Note that Lyme disease may be assoacited with non-granulomatous or granulomatous uveitis

Question 489

Glaucomatocyclitic crisis

Answer 489

Posner-Schlossman syndrome. Unilateral condition characterized by mild iritis with recurrent, self limiting episodes of elevated IOP (30-40) secondary to trabeculitis, fine KPs, and open angle. rare to mild cells in the AC, normal corneal sensitivity, absence of a vesicular rash, normal angle anatomy (no NVA or PAS) Unilateral iritis, increased IOP, trabeculitis

Question 490

3 major conditions that will present with unilateral cells in the AC with acutely elevated IOP (30-50mmHg)

Answer 490

poster-schlossman syndrome HSV or HZV trabeculitis Fuch’s heterochromic idirocyltiis

Question 491

HSV or HZV trabeculitis

Answer 491

reduced corneal sensitivity, concurrent corneal edema, concurrent dendrite or psuedodendrite, vesicular rash along dermatome that respects vertical midline Unilateral cells in the AC with acuity elevated IOP

Question 492

Fuch’s heterocyclic iridocyclitis

Answer 492

Unilateral cells in the AC with acute elevated IOP rare to mild cells in the AC, normal corneal sensitivity, NVA is often present on gonio, significant iris atrophy and cataracts.

Question 493

Chronic granulomatous anterior uvetiis mate be assocaited with the following conditions

Answer 493

Sarcoidosis TB HSV/HZV Syphilis

Question 494

Sarcoidosis and anteiror uveitis

Answer 494

Chronic, granulomatous -more common in females and AA. Uveitis is typically bilateral and may be posterior or panuveitis. Patients typically have an abnormal chest radiograph and increased ACE (angiotensin converting enzyme) levels.

Question 495

TB and anteiror uveitis

Answer 495

Chronic granulomatous | positive PPD test, abnormal chest X ray, night sweats. May have posterior or panuveitis.

Question 496

Number one symptom or TB

Answer 496

Night sweats

Question 497

HZV and HSV uveitits

Answer 497

Chronic granulomatous OR nongranu associated with increased IOP in the involved eye. May have stellate KPs, corneal edema, and/or epithelial defects. Zoster will present with vesicles along the affected dermatome

Question 498

Syphilis and uveitis

Answer 498

Chronic and can be gran or non gran may have an associated interstitial keratitis. Characterized by a maculopapular rash (on the palms and soles), a positive VDRL or RPR, and a positive FTA-ABS or MHA-TP ‣ Interstitial keratitis is a stromal inflammation without primary involvement of the epithelium or endothelium. • IK is characterized by acute stromal inflammatory edema and neo. Progression results in diffuse stromal neo that often spares the line of sight • During the late stages of IK, stroma vessels may partially clear, leading to ghost vessels, corneal scarring, and irregular astigmatism.

Question 499

stromal inflammation without primary involvement of the epithelium or endothelium.

Answer 499

Interstitial keratitis • IK is characterized by acute stromal inflammatory edema and neo. Progression results in diffuse stromal neo that often spares the line of sight • During the late stages of IK, stroma vessels may partially clear, leading to ghost vessels, corneal scarring, and irregular astigmatism.

Question 500

The most common cause of IK

Answer 500

Congenital syphilis

Question 501

Acquired syphilis and IK

Answer 501

Not common

Question 502

Congenital syphilis triad

Answer 502

Hutchinson’s teeth (small widely spaced teeth), deafness, and interstitial keratitis. Additional signs of congenital syphilis include saddle-nose deformity and frontal bossing (prominent forehead)

Question 503

Chronic non gran anterior uveitis

Answer 503

JIA | Fuchs heterochromic iridocyclitis

Question 504

JIA and anteiror uvetiits

Answer 504

Chronic non gran most common known caused of uveitis in chidlren. Classic presentation is a bialteral uveitis in young girls. Patients typically have a negative RF and positive ANA

Question 505

Fuchs heterochromic iridocyclitis and antieror uveitis

Answer 505

Chronic non gran more common in patients with blue eyes. Characterized by a unilateral mild uveitis with fine, stellate KPs, angle neo, and iris heterochromia. Assocaited with glaucoma (15%) and cataracts (70%); patients are often asymptomatic

Question 506

a chronic intermediate uveitis characterized by inflammation over the pars plana (known as snowbanking) and peripheral retina; it is NOT associated with systemic conditions

Answer 506

Pars planitis

Question 507

Risk factors for corneal infectious keratitis

Answer 507

CL wear, dry eye, exposure keratopathy, neurotrophic keratopathy, trauma, lid abnormalities, and bullous keratopathy

Question 508

Epidemiology of bacterial keratitis

Answer 508

bacterial keratitis is the most common etiology for infectious keratitis. Cl wear, especially extended wear, is a commmon predisposing factor for bacterial keratitis. Consider bacterial etiolgoy first with any corneal infection associated with Cl wear ‣ The most common microbes invovled are pseudomonas aeruginosa, stap epi, staph aureus, haemophilus influenzae, and moraxella catarrhalis

Question 509

Pseudomonas and keratitis

Answer 509

Pseudomonas is the most common gram negative pathogen found in severe bacterial keratitis. It is characterized by significant thick mucopurulent discharge (often green in color), hypopyon, and dense stromal infiltrates, and rapid progression )can perforate the cornea within 48 hours)

Question 510

Pathophysiolgoy of bacterial keratitis

Answer 510

remember that most bacterial rewuire an epithelial defect for invasion and subsequent infectious corneal ulceration. Noteworthy bacterial that can invade an intact corneal epithelium ‣ “Canadian national hockey league”-Crynebacterium, Neisseria gonorrhea and meningitis, Haemophilus influenzae, and Listeria

Question 511

Bacterial that can invade an intact corneal epithelium

Answer 511

Canadian national hockey league”-Crynebacterium, Neisseria gonorrhea and meningitis, Haemophilus influenzae, and Listeria

Question 512

Symptoms of bacterial keratitis

Answer 512

severe pain, rede eye, photophobia, and decreased vision

Question 513

Signs of bacterial keratitis

Answer 513

a corneal stromal infiltrate with and overlying epithelial defect (infectious corneal ulcer

Question 514

Corneal infiltrate

Answer 514

sign of your body’s immune system attacking an antigen via Ab. An infiltrate without an overlying epithelial defect is an immune mediated repsosne and is NOT a sign of infection

Question 515

Corneal ulcer

Answer 515

corneal infiltrate with an overlying epithelial defect. Cornal ulcers may be infectious or non infectious. A non infectious (sterile) corneal ulcer may result from a sterile infiltrate that erodes through the corneal epithelium, leading to a small overlying epithelial defect

Question 516

Infectious corneal ulcers

Answer 516

NaFL staining are to lesion ratio of 1:1. They classically present with moderated to severe pai nwith a mild anterior chamber reaction and diffuse conjunctival injection

Question 517

Sterile corneal ucler

Answer 517

NaFL staining area to lesion ratio of less than 1:1 with less pain and injection compared to an infectious corneal ulcer. (Staph marginal keratitis)

Question 518

Sterile infiltrate

Answer 518

NOT stain with NaFL (there is no overlying epithelial defect); they commonly present as multipl leasions with mild pain, sectoral conjunctival injection, and no anteiror chamber reaction

Question 519

Epidemiology of fungal keratitis

Answer 519

the most common type of corneal ulcer after traumatic corneal injury, especially from vegetable matter.

Question 520

Pathophysiology of fungal keratitis

Answer 520

‣ 1. Candida infections often occur in eyes with chronic corneal disease or in immunocompromised patients ‣ 2. Aspergillus and Fusarium species are more commonly the culprit after vegetable matter trauma ‣ Culture of fungi should be performed on a Sabaroaud’s agar

Question 521

What kind of culture is used for a fungal infection

Answer 521

Sabarouds agar

Question 522

When is candid harmful

Answer 522

Immunocompromised

Question 523

Signs of fungal keratitis

Answer 523

‣ 1. Aspergillus/Fusraium: classically prestn as an epithelial defect with an underlying gray white corneal infiltrate with feathery edges and possible surrounding satellite infiltrates ‣ 2. Candida classically presents with a similar appearance as a bacterial corneal ulcer ‣ Additional signs include an aC reaction and hypopyon

Question 524

Epidemiology of acanthamoeba keratitis

Answer 524

rare parasitic infection associated with inadequate CL hygiene

Question 525

Pathophysiolgoy of acanthamoeba keratitis

Answer 525

acanthamoeba is one of the most common Protozoa found in soil and is also frequently found in water and within the oral cavity of humans. Compromise of the corneal epithelium allows acanthamoeba to invade the corneal epithelium and stromal tissues. Infections progresses slowly and are often misdiagnosed early in management. Culture should be performed with a non nutrient agar with heat killed E. coli.

Question 526

Signs of acanthamoeba keratitis

Answer 526

‣ Early=punctate or pseudoendritic epithelial defects (may be confuse with HSV) associated with severe pain out of proportion to the signs ‣ Late=radial keratoneuritis(inflammation of the corneal nerves) and patchy anterior stromal infiltrates that progress to ring ulcer

Question 527

Gram stain

Answer 527

Bacterial

Question 528

KOH or Giemsa

Answer 528

Fungi and yeasts

Question 529

Sabarouds

Answer 529

Fungi

Question 530

Chocolate agar

Answer 530

Haemophilus and N gonorrhea

Question 531

Thioglycate

Answer 531

Aerobic and anaerobic bacteria

Question 532

Non nuretient agar with E. coli

Answer 532

Acanthamoeba

Question 533

Epidemiology of HSV

Answer 533

DNA virus that is mot common in young patients. Ask about previous history of cold sores

Question 534

Primary exposure of herpes simplex

Answer 534

occurs in young kids age 6m to 5 years. Patients are mot commonly asymptomatic but they may experience mild virus-type symptoms

Question 535

Recurrent HSV infections

Answer 535

resutls from reactivation of a latent infection in the trigeminal ganglion. Can be triggered by physical or emotional stress from sun exposure, fever, and immunosuppression

Question 536

Pathophysiology of HSV

Answer 536

tissue damage in HSV occurs either by direct invasion from the virus, neurotrophic mechanisms, or by immune system repsosne to HSV

Question 537

Symptoms of HSV keratitis

Answer 537

decreased corneal sensitivity is common in these patient

Question 538

Primary exposure of HSV reuslts in

Answer 538

‣ 1. Blepharitis-focal vesicular lesions with crusting located not he eyelids and periorbital area (usually UL if dendrite is present) ‣ 2. Conjunctivitis-acute unilateral follicular conjunctivitis with watery discharge and preauricular lymphadenopathy

Question 539

Recurrent HSV infections reuslts in

Answer 539

Epithelial disease Neurotrophic keratitis Stromal disease Endotheliitis

Question 540

Epithelial disease from HSV

Answer 540

• Includes corneal vesicles, dendritic ulcers, geographic ulcers, and marginal uclers. Due to direct invasion of the corneal epithelial cells by HSV ◦ Corneal vesicles-small epithelial lesions often referred to as punctate epithelial keratopathy. Represent the earliest epithelial sign of reactive HSV ◦ Dendritic ulcers-most common presentation of HSV keratitis. The edges of the HSV dendrite (active viral cells) stain well with rose bengal; the center of the ulceration stains well with NaFL ◦ Geographic ulcers: similar to a dendritic ucler but wider in appearance; assocaited with previous use of topical steroids ◦ Marginal ulcers: located close to the limbus; presents as a stromal infiltrate with an overlying epithelial defect and assocaited limbal injection

Question 541

Neurotrophic keratitis from HSV

Answer 541

• Reuslts from reduced corneal innervation (V1) and decreased tear secretion, leading to poor wound healing (big ulcer, no pain) ◦ Occurs in patients who have had infectious epithelial keratitis; unique because etiolgoy is not immune mediated or infectious ◦ A neurotrophic ucler appears as an oval defect with smooth borders, it is often preceded by punctate epithelial erosions that then progress to form an ulcer

Question 542

Appearance of neurotrophic keratitis

Answer 542

Neurotrophic ulcers are typically inferior in location and oval in appearance with smooth borders, geographic ulcers result in irregular epithelial defects with scalloped borders

Question 543

Stromal disease (interstitial K) from HSV

Answer 543

Accounts for only 2% of initial epidoses of ocular HSV disease but 20-40% of recurrent ocular HSV disease. There are several types of stromal disease in HSV keratitis ◦ Interstitial keratitis (IK)-characterized by an infiltrate with diffuse neo, an immune rings (Wesley ring), stromal thinning, and subsequent scarring ‣ In herpetic disease, IK is thought to result from an Ag-Ab complement cascade against a live virus or viral antigen retained within the corneal stroma ‣ By definition, IK I stromal inflammation without primary injury to the epithelium or endothelium ◦ Necrotizing stromal keratitis-rare keratitis that results from direct virus invasion into the stroma. Results in severe stromal inflammation with necrosis that can lead to corneal thinning and perforation

Question 544

Why is HSV interstitial keratitis concerning

Answer 544

it may lead to significant stromal scarring and decreased acuity

Question 545

Endotheliitis from HSV

Answer 545

Secondary stromal edema due to an immune reaction against a viral antigen or live circus within the corneal endothelium ◦ Disciform endotheliitis-most common form of endotheliitis. Characterized by focal, disc shaped, sotrmal edema overlying KPs. Often accompanied by a mild to moderate iritis.

Question 546

Differnece between IK and endotheliitis

Answer 546

stromal infiltrates and neo are not present in disciform endotheliitis

Question 547

Additional findings in HSV K

Answer 547

Acute unilateral anterior granulomatous uveitis Trabeculitis (unilateral mild to no cells in the AC with acutely elevated IOP and often concurrent corneal edema Acute retinal necrosis

Question 548

Epidemiology of HZV

Answer 548

varicella zoster virus (VZV) is the initial invading organism, affecting 95% of children by the age of5 in the US. After the primary infection (chickenpox), VZV is transported to the trigeminal ganglia and other neural cell bodies, where it becomes dormant. Older age, trauma, neurodegeneration, or immunosupression may contribute to reactivation of the virus and resulting herpes zoster infection

Question 549

Who gets HZV most

Answer 549

‣ HZV primarily affects the elderly and is rarei n kids to young patients. If HZV occurs in patients younger than 50, consider a medical eval to determine if the patient is immunocompromised. HZV is contagious for those who have not had chickenpox

Question 550

Signs of HZV

Answer 550

vary depending on invovlemt of the cornea. Symptoms are more severe in immunocompromised patients. HZV is unilateral and follows the affected dermatomes

Question 551

Pre zoster

Answer 551

cluster of warning signs known as prodrome

Question 552

Active zoster

Answer 552

vesicular rash that respects the dermatomes and does not cross the midline. Vesicles can form on the lid margin, resulting in blepharoconjunctivitis

Question 553

HZO

Answer 553

◦ Activation along the ophthalmic branch of the trigminal ganglion leads to ophthalmic manifestations and is referred to as herpes zoster ophthalmicus

Question 554

Eyelid signs of HZO

Answer 554

* Trichiasis * Ectropion * Entropion * Madarosis * Poliosis

Question 555

Corneal signs of HZO

Answer 555

``` occur in 65% of patients with acute HZO and include • Punctate epithelial keratitis • Pseudodendritis keratitis • Anterior stromal keratitis • Interstial keratitis • Endotheliitis • Keratouveitis • Neurotrophic keratitis • Exposure keratopathy ```

Question 556

How does HZV start on the cornea

Answer 556

begins with small, stellate lesions that can progress to pseudodenrites (tapered ends with no terminal bulbs) with a “stuck on” appearance. The entire lesion stains with rose bengal (compared to just the edges in HSV) HZV lesions DO NOT stain well with NaFL (unlike HSV)

Question 557

Other eye findgins in HZO

Answer 557

‣ Episcleritis/scleritis ‣ Uveitis occurs in up to 40% of patients with acute HZO • Can be granulomatous or non and typically assocaited with significant KPs, corneal edema, and PS ‣ Trabeculitis (acutely elevated IOP with minimal to no cells in the AC and likely corneal edema) ‣ Cataracts ‣ Acute retinal necrosis ‣ Optic neuritis ‣ Cranial nerve palsies

Question 558

Hutchinson’s sign

Answer 558

• Hutchinson’s sign is a rash on the tip of the nose as a result of reactivation of the virus along the terminal branch of the nasocilairy nerve (V1). It indicates a high risk of ocualr involvement

Question 559

Post zoster

Answer 559

characterized by PHN and depression ‣ PHN-defined as pain persisting beyond 1 month after rays onset or rays resolution. Most common complication of herpes zoster and affects 10-30% of patients ‣ Severe PHN affects about 7% of patients. The leading cause of suicide in patients over 70 years of age with chronic pain

Question 560

Epidmiolgoy of mooren’s ucler

Answer 560

rare condition that is more common in men and older patients (40-70, although may occur at all ages). The classification of mooren’s ulcer ‣ 1. Benign (typical or limited) mooren’s ucler (75%)-unilateral, affects the elderly, mild to moderate symptoms, responds well to treatment - 2. Malignant (atypical) Mooren’s ulcer-bilateral, affects younger patients (especially black males), severe symptoms, responds poorly to treatment, and progresses relentlessly

Question 561

Pathophysiology of mooren’s ulcer

Answer 561

painful, progressive, chronic vasculitis of the limbal blood vessels that leads to ischemic necrosis and peripheral ulcerative keratitis ‣ Mooren’s ulcer is idiopathic in nature, but is likely autoimmune mediation. By definition, the condition occurs idendpent of any diagnosable systemic disorder that could be responsible for the progressive corneal pathology ‣ Associatd with systemic hepatitis C viral infection or hookworm infestation

Question 562

Symptoms of mooren’s ulcer

Answer 562

the most common symptoms is pain, which is often severe. Additional symptoms include redness, tearing, and photophobia. Decreased vision can result from irregular astigmatism, associated iritis, or if the ucler is central in location

Question 563

Signs of mooren’s ucler

Answer 563

the classic presentation is an unilateral peripheral crescent shaped gray infiltrate in an older patients that progresses to an ulcer. The ulcer is concentric to the limbus and has a unique overhanging edge. The ulceration may be self limiting Ir may spread circumferentially and/or centrally in the late stages of the condition

Question 564

Epidemiology of staph marginal keratitis

Answer 564

Most common PUK | common condition. Ask about a similar recurrent acute episode

Question 565

Pathophysiolgoy of staph marginal keratitis

Answer 565

type III HS response to staph aureus; typically occurs in patients with chonric staph blepharitis. Recurrences are common unless the underlying blepharitis is treated appropriately

Question 566

Symptoms of staph marginal keratitis

Answer 566

patients may be asymptomatic or complain of acute photophobia, pain, tearing, redness, and decreased visio

Question 567

Signs of staph marginal keratiits

Answer 567

corneal stromal infiltrates (usually multiple and bilateral) located in the periphery; classically occur at 2, 4, 8, and 10 o’clock positions where the lid margin makes contact with the limbus. Look for assoacited phlyctenules, signs of bleph, and/or acne rosacea. Residual thinning, superficial neo, and peripheral scarring are common

Question 568

What is a corneal infiltrate

Answer 568

infiltrate is a sign of your patients immune system attacking the staph antigens via antibodies. In isolation, it is an immune mediated repsosne and not a sign of an infectio

Question 569

Collagen vascular disorders (PUK)

Answer 569

◦ Recall that collagen vascular disorders such as RA, SLE, polyartertiis nodosa, and Wegner’s granulomatosis can cause peripheral corneal thinning and/or uclers ◦ Patients can be asymptomatic or may report significant pain, redness, and decrease in vision ◦ Corneal findings include peripheral corneal thinning/uclers with or without inflammation. The condition may be unilateral or bilateral. The uclers may progress to encompass the entire peripheral cornea. Corneal findings may be associated with scleritis, episcleritis, and keratoconjunctivitis sicca

Question 570

Appearance of corneal deposits

Answer 570

may be pigmented, refractile, metallic, or non pigmented in color. They can occur within any layer of the cornea, from the surface epithelium to Descemets membrane

Question 571

Whork K causes

Answer 571

seen in Fabry’s disease and with the use of chloroquine, hydroxychloroquine, amidoarone, indomethacin, tamoxifen

Question 572

Fleischers ring cause

Answer 572

iron ring in the base of the cone in keratoconnus

Question 573

Rust ring causes

Answer 573

Metallic FB

Question 574

Hudson Stahli line

Answer 574

common in the elderly, iron deposits found at the junction between the middle and lower third of the cornea

Question 575

Stocker’s lines

Answer 575

iron deposits on the leading edge of a filtering bleb

Question 576

Kaiser Fleischer ring cause

Answer 576

accumulation of copper that occurs in patients with certain liver disorders, Wilson’s disease

Question 577

Band keratophy cause

Answer 577

calcium deposits within Bowmans layer

Question 578

Types of corneal degenerations

Answer 578

``` Terriens marginal degeneration Salzmanns nodular degeneration White limbal girdle of Vogt Band keratopathy Arcus senilis Crocodile shagreen Corneal farinata ```

Question 579

Terriens marginal degeneration

Answer 579

``` Superior nasal thinning ATR Bilateral 30 yo male idiopathic non-inflammtory degeneration that reuslts in slowly progressive peripheral stromal thinning. Perforation occurs in appx 15% of cases ```

Question 580

Symptoms of terriens

Answer 580

often asymptomatic, although progressing can lead to irregular astigmatism (classically ATR) and decreased acuity

Question 581

Signs of terriens

Answer 581

characterized by superonasal, bilateral (asymmetric), slowly progressive peripheral thinning with an associated vascularized pannus. In most cases, there is no AC reaction, no conjunctival injection, and no overlying epithelial defects

Question 582

Difference between mooren’s ucler and terriens

Answer 582

Mooren’s has an overlying epithelial defect and terriens does not

Question 583

Salzmanns nodular degeneration

Answer 583

``` 60 yo female Really bad dry eyes Blue gray nodules Bowmans Hyaline ```

Question 584

Symptoms of salzmanns nodular

Answer 584

typically asymptomatic, although patients may experience pain if RCE develop in epithelial cells overlying the nodule; vision may be reduced if the nodule is located within the visual axis

Question 585

Signs of salzmanns nodular

Answer 585

hyaline plaque deposits located between the epithelium and bowmans membrane that classically appear as midperoheral, elevated blur gray or yellow white nodular lesions. May be unilateral or bilateral and single or multiple in number. Nodules are often located within or adjacent to an old corneal scar or corneal pannus

Question 586

White limbal girdle of Vogt

Answer 586

Older patients (common) Bilateral chalk like linear opacities of nasal limbus Asymptomatic

Question 587

Base keratopathy pathophtysiolgoy

Answer 587

reuslts from the following ‣ Ocular conditions that cause chronic inflammation and ocular surface disease ‣ After trauma ‣ Systemic conditions that cause increased serum Ca++ or phosphorous levels, including gout, hypercalcemia, sarcoidosis, and renal failure

Question 588

Symptoms of band keratopathy

Answer 588

patients are often asymptomatic because the calcium plaques are usually located in the periphery at 3 and 9 o’clock positions. Although uncommon, the plaques may move centrally and cause a FB sensation and decreased vision

Question 589

Sign of band keratopty

Answer 589

calcium deposits on the anterior surface of Bowmans membrane or in the sub-epithelial space that appear as white splits with a Swiss cheese pattern; usually concentrated with in the intrapalpebral region of the cornea

Question 590

Arcus senilis epidemiology

Answer 590

most common peripheral corneal opacity. Arcus is prominent in the elderly and affects almost 100% if patients over the age of 80. Higher incidence in males and AA

Question 591

Pathophysiolgoy of arcus senilis

Answer 591

associated with aging and high cholesterol. Lipid deposition begins on descemets membrane and is subsequently deposited on bowmans layer before extending into the stroma

Question 592

Signs of arcus senilis

Answer 592

usually bialteral and symmetric circumferential 1mm band within the peripheral cornea, with a clean zone of separation to the limbus

Question 593

When is arcus concerning

Answer 593

‣ Arcus is typically of little concern, unless • Unilateral arcus is rare and is assocaited with carotid disease on the side without the arcus • Arcus in patients younger than 50 is assocaited with an increased risk of coronary artery disease; a lipid profile is warranted in these cases

Question 594

Crocodile shagreen

Answer 594

bilateral, gray white, polygonal stromal opacities (Cracked ice) either near bowmans layer (anterior crocodile shagreen) or occasionally near descemets membrane (posterior crocodile shagreen). Opacities are caused by irregularly arranged folds of collagen ◦ Symptoms: usually asymptomatic and benign

Question 595

Corneal farinata

Answer 595

◦ Bilateral flour dust deposits that are most commonly located in the central deep stroma. May be due to aging or an AD condition. Patients are typically asymptomatic

Question 596

Corneal graft rejection

Answer 596

• type 4 HS reaction to the donor cornea. 30% of patients will have rejection within one year. Characterized by decreased vision, mild pain, redness, and photophobia ◦ Epithelial rejection: rare; appears as an elevated, irregualr epithelium ◦ Stromal rejection-assocaited with subepithelial infiltrates known as Krachmer’s spots ◦ Endothelial rejection line-characterized by WBCs on the endothelium that form a Khodadoust line

Question 597

an elective procedure that modifies the refractive status of the eye by lenticular or corneal modifications.

Answer 597

Refractive surgery

Question 598

Absolute contraindications for refractive surgery

Answer 598

‣ Younger than 18 with an unstable refractive error within the last year ‣ Unrealistic expectations-will reduce dependence on glasses (but NOT glasses free), will experience post op glare and dryness ‣ Keratoconnus, active herpes simplex keratitis, contact lens warpage ‣ Connective tissue disease, collagen vascular disease, immunocompromised disease

Question 599

Relative contraindications for refractive surgery

Answer 599

‣ Blepharitis, DED, chronic eye rubbing, ocular surface disease, large pupils ‣ DM-fluctuating blood sugar levels can change the refractive error, which makes the amount of treatment needed unclear ‣ POAG (if not well controlled)-IOP elevates during placement of the suction cup during surgery, which could be dangerous if a patient already has uncontrolled or advanced glaucoma ‣ Pregnancy ‣ Retinal thinning/lattice degeneration May increase the risk of retinal tears during or after surgery. Although a clear link has not been establishes, caution should be taken

Question 600

How long do spherical SCL wearers need to be out of CL before refractive surgery

Answer 600

3-14 days

Question 601

How long do toric and RGP lens wearers need to be out of their CL before their refractive surgery

Answer 601

14-21 days

Question 602

Radial keratotomy

Answer 602

* radial incisions are made with a diamond knife it flatten the perierhal corneal stroma; the normal IOP then pushes the weakened peripheral cornea outward, causing the central cornea to flatten to reduce myopia * No longer performed due to better options. RK was difficult to titrate, caused significant instability in the refractive error, and led to progressive hyperopic shifts

Question 603

PRK

Answer 603

* the corneal epithelium, Bowmans, and superficial stromal tissue are removed (no flap) and excimer laser is applied directly to the central cornea (for myopia) or mid periphery (steepens the cnetral cornea to correct for hyperopia) * Treatment range: -8D to +4D, up to 4D of astigmatism * 400um residual cornea is required after treatment * PRK requires longer healing time (1-2 weeks) compared to LASIK because the entire corneal epithelium must regrow. Patients will experience extremely poor vision and pain (controlled with NSAIDs and BLC) in the immediate post op period * The risk of stromal haze is greatest with higher Rxes and can be reduced by using MMC during the procedure

Question 604

Benefits of PRK

Answer 604

◦ PRK is ideal for patients who are at risk of trauma because there is no risk of flap complications. PRK is also associated with less risk for corneal ectasia, less induction of higher order aberrationsm les post op dryness, requires less corneal thickness, and is cheaper compared to LASIK

Question 605

LASIK

Answer 605

* an epithelial flap is made with a micokeratome, an excimer laser is applied to the anterior stromal bed, and the flap is then reattached * Treatment range: -10D to +4D, up to 5D of cyl. Clear lens extraction can be performed on patients who exceed LASIK refractive error requirements * LASIK patients heal faster (1-2 days), experience less pain, and have less post op corneal haze compared to PRK patients

Question 606

Thickness requirements for LASIK

Answer 606

◦ 250um must remain under the flap to maintain a corneal integrity ◦ The flap itself is approximately 150um thick (determined by intraoperative pachymetry) ◦ Ablation depth is appx 12 um/Diopter

Question 607

Total pachymetry for LASIK

Answer 607

‣ Total pachymetry minus the flap thickness (160-200um) minus the ablation depth (15um/diopter) should be at least 250um

Question 608

Femtosecond laserflap for LASIK

Answer 608

the same procedure as LASIK but the flap is made with a femtosecond laser instead of a micorkeratome. A femtosecond laser flap is thinner, leaving behind more tissue to ablate. It also removes the risk of mechanical malfunction of the microekratome and is assoacited with less post op dry eye

Question 609

LASEK

Answer 609

same procedure as LASIK, but the flap is made with dilute alcohol instead of a microkeratoma

Question 610

Epi-LASIK

Answer 610

this is another version of LASIK where a blunt plastic blade is used to create the epithelial flap rather than a microkeratome

Question 611

Conductive keratoplasty

Answer 611

* used to treat presbyopia, low hyperopia, and for treating residual astigmatism after previous surgeries * Uses radio frequency energy to shrink the collagen fibers in the peripheral corneal stroma, allowing the central cornea to steepen. Regression is expected after about 2-3 years; the surgery can be repeated * Treatment range: +0.74D-+3D with less than 0.75D cyl

Question 612

Intratromal corneal rings

Answer 612

* PMMA rings are inserted into the peripheral stroma to flatten the cornea (shortens the corneal arc length); rings can be removed or exchanged * Approved fro use with keratoconus * Treatment range: -0.75D to -3D; does not treat hyperopia

Question 613

Clear lens extraction

Answer 613

* essentially cataract surgery without a cataract. The IOL that is selected reduces the refractive error * No residual accommodation remains unlesss a multifocal or accommodating IOL is used * Large treatment range

Question 614

Phakic IOL (implantable CL)

Answer 614

* intraocular lens implantation in a phakic eye. The lens implanted to alter the total power of the eye * The IOL is angle supported, iris supported, or sulcus supported. Rewuire a peripheral iridotomy * Can be used to treat a larger range of refractive errors compared to corneal surgery and the IOL is removable. Also preserves natural accommodation (unlike clear lens extraction)

Question 615

Astigmatic keratotomy (AK)

Answer 615

• corneal incisions are made with a diamond blade to relax the cornea in the steepest meridian

Question 616

Wavefront guided, custom corneal surgery

Answer 616

* reduces higher order aberrations in addition to correcting the refractive error. * Can be done with LASIK or PRK and theoretically resutls in better quality vision with improved contrast and acuity and less glare

Question 617

Refractive surgery success

Answer 617

In refractive surgery, success is generally considered 20/40 VA or better. In those with low refractive error, about 90-99% achieve this level. About 75% achieve 20/25 or better

Question 618

Potential LASIK complications

Answer 618

1. Pain in the first 24 hours 2. Serious infection 3. Flap complications 4. Corneal ectasia 5. Residual refractive error 6. Glare 7. Dry eye 8. DLK 9. Epithelial ingrowths 10. . corneal haze

Question 619

Serious infection after LASIK

Answer 619

◦ Typically occurs day 1-3. Can lead to corneal melting, irregular astigmatism, and scarring ◦ Bacteria are usually gram + or mycobacterium ◦ Risk with PRK=1/1000 to 1/35000 ◦ Risk with LASIK=1/5000

Question 620

Flap complications from LASIK

Answer 620

Free caps, button holes, flap folds, irregualr flaps, corneal perforation, and flap subluxation Flap displacement is more common with keratome flaps than with femtosecond laser flaps and is usually due to accidental touch to the eye or eyelid. Dislodged flaps can be repositioned

Question 621

Types of flap complications after LASIK

Answer 621

‣ Button holes (cap perforation, a hole in the flap) are more common with very steep corneas or deep et eyes. The steep cornea can buckle in the suction ring, causing a hole as the keratome moves across the cornea ‣ Free caps (no hinge made) are more common with very flat corneas and are the result of an inadequate amount of cornea in the ring, causing the blade to cut off the hinge ‣ Flap folds occurs in 56% of cases at day 1 (usually within the first hour), and 95% of cases within 1 week

Question 622

Microstriae and macrostriae flap folds after LASIK

Answer 622

* Flap folds are called macrostriae if they are full thickness with undulating, parallel stromal folds; they result from slippage or malpositioning during surgery. They typically require treatment of the flap by lifting and reposition * Microstriae are fine, irregular, multi0directional folds in bowmans layer that typically resolve on their own; they are treated only if they are visual significant

Question 623

Corneal ectasia after LASIK

Answer 623

◦ Anteiror protrusion of the cornea due to thinning. Patients with high myopia, undetected keratonnus, or forme fruste keratoconnus are more at risk. Corneal ectasia may occur at any time following the surgery

Question 624

Residual refractive error after LASIK

Answer 624

◦ Patients may be over or under-corrected or may have regression after surgery (more common if >8D) ◦ Patients can be fit with GPS or reverse geometry lenses after appx 8-12 weeks. Refractive surgery enhancement may also be considered

Question 625

Glare after LASIK

Answer 625

◦ Worse glare is expected with small ablation zones, large pupils, monovision correction, and higher refractive errors

Question 626

Dry eye after LASIK

Answer 626

◦ The most common side effect of LASIK; occurs in up to 33% of all refractive surgery patients ‣ Corneal nerves are severed during LASIK, resulting in decrease in corneal sensitivity resulting in decreased neural feedback to the lacrimal gland. Resolves 1-2 months

Question 627

DLK after LASIK

Answer 627

rare, inflammtory non infectious reaction that occurs at the lamellar interface (between the corneal flap and stroma). It is characterized by fine, granular, sand like infiltrate that typically presents within 2-3 days after surgery. The etiology is poorly understood, but may be a response to toxins (glad debris). DLK is less common with dispoasalbe microkeratomes maybe be asymptomatic or experience photophobia, blurred vision, FB sensation, and pain. Can lead to vision loss (from corneal scarring and corneal melt) if not properly managed

Question 628

Epithelial ingrowths after LASIK

Answer 628

Rare, less than 3% of surgical cases ‣ Last pos op LASIK complication that is most commonly observed at the one month post op visit as a faint gray line or white, milky despots within 2mm of the flap edge interface ‣ The pattens is typically asymptomatic and the condition is not treated unless progression is documented, the visual axis is obstructed, greater than 2mm of ingrowth occurs from the flap edge, or resutls in corneal astigmatism

Question 629

Most common complication associated with LASIK enhancement

Answer 629

Epithelial ingrowths

Question 630

Corneal haze after LASIK

Answer 630

◦ The prevalence of lone term haze with LASIK is 0.1% and with PRK is 1% in those with refractive errors below 6D. The risk increases with higher refractive errors ◦ Remember, corneal haze is normally present for severeal weeks after PRK

Question 631

Retreatment criteria for enhancement in refractive surgery

Answer 631

◦ The earliest time for retreatment is 3 months, but 6 months is preferred to allow the refractive error to stabilize. Criteria for enhancement include the following ‣ Astigmatism >0.75D causing symptoms ‣ RE> or equal to 0.75D from target in an unhappy patient ‣ Uncorrected VA of 20/30 or worse in an unhappy patient

Question 632

Long term management of LASIK

Answer 632

◦ IOP realigns will always be falsely low due to thin corneas ◦ Gonio and retinal evals are still necessary in patients with a history of high hyperopia and myopia, respectively ◦ Patients should wear eye protection during contact sports to avoid dislodging the corneal flap and to block UV radiation

Question 633

AOA definition of cataract

Answer 633

opacification of the lens that leads to measurably decreased VA and/or some functional disability as perceived by the patient. An estimated 20.5 million Americans older than 40 have them

Question 634

Nuclear sclerosis

Answer 634

most common aging cataract. Typically causes myopic shift, elderly patients often report “second sight” because of thei improved abiltiy to read without spectacles

Question 635

Cortical cataract

Answer 635

radial spoke like opacities that commonly induce a hyperopic shift

Question 636

Anteiror subcapsular cataracts

Answer 636

located directly underneath the anterior lens capsule

Question 637

Posterior subcapsular cataracts

Answer 637

located directly in front of the posterior lens capsule; often affects near vision more than distance vision and is commonly a result of systemic or topical steroids and X rays.

Question 638

Mild PSC

Answer 638

can cause significant reduction in acuity and are typically associated with worse glare compared to other cataracts

Question 639

Infant cataracts

Answer 639

associated with galactosemia and rubella. The most common type of congenital or infantile cataract is a lamellar (zonular) cataract that consist of a lens opacity that surrounds the embryonic nucleus

Question 640

Cerulean cataract

Answer 640

type of congenital cataract that rarely affects VA. It appears as tiny dot like or flake like white or bluish green opacities

Question 641

Presenile cataracts

Answer 641

assoacited with DM, myotonic dystrophy (PSC Christmas tree), Wilson’s disease, hypocalcemia, and atopic dermatitis

Question 642

Traumatic cataract

Answer 642

rosette cataracts, also look for a Vossius ring

Question 643

Toxic anterior subcapsular cataract

Answer 643

chlorpromazine (stellate cataract), amiodarone (deposits), miotics (vacuoles), and gold salts (gold deposits)

Question 644

Toxic posterior subcapsular cataract

Answer 644

Corticosteroids

Question 645

Secondary cataract

Answer 645

common causes include chronic anterior uveitis (most common), high myopia, retinitis pigmentosa, and gyrate atrophy

Question 646

Epicapsular stars

Answer 646

‣ Residual remnants of the tunica vasculopathy lentos and appear as small, star shaped, pigmented deposits on the anterior capsule of the lens

Question 647

Testing for catracts

Answer 647

PAM BAT A scan B scan

Question 648

PAM

Answer 648

can help determine how much the lenticular changes are impacting acuity in order to better predict post op VA

Question 649

BAT

Answer 649

asses glare disability

Question 650

Axial length for catracts

Answer 650

A scan or IOL master; axial length and keratometry measurements are used to calculate the appropriate IOL power based on the desired final refractive error

Question 651

B scan and cataracts

Answer 651

helps to determine if posterior segment abnormalities are present when cataracts are so dense that the fundus cannot be viewed

Question 652

Axial length and IOL power

Answer 652

‣ The average axial length us 24mm; a 1mm error in axial length measurement corresponds to a 3D error in the calculated IOL power

Question 653

If the cataract is monocular

Answer 653

before referring for surgery consider the age of the patient’s and whether lens removal would impact accommodation status and post op refraction

Question 654

If the patient is monocular, before cataract surgery

Answer 654

consider the severity of the cataract and discuss the risk/benefit ratio with the patient’s

Question 655

Preop by PCP before catract surgery

Answer 655

◦ Each patient’s should have a careful preop eval by their medical doctor prior ro cataract surgery; medications should also be reviewed carefully-anticoagulants, A blockers, and PGs are of particular concern

Question 656

Alpha blockers for BPH and cataract surgery

Answer 656

‣ Flomax is an alpha blocker that can cause floppy iris syndrome, which is characterized by poor preop pupil dilation, iris billowing and prolapse, and progressive intraoperative miosis. This occurs in up to 90% of pateitns who are currently on the medication or have been at any time in the past

Question 657

Ocular conditions to consider before cat sx

Answer 657

◦ Ocular conditions should be considered prior to referral, including history of acute or chronic uveitis, severe bleph, Fuchs endothelial dystrophy, and pseudoexfoliation

Question 658

Types of cataract surgeries

Answer 658

intracapsular cataract extraction (ICCE) Extracapsular cataract extraction (ECCE) Phacoemulsifcation Femtosecond laser

Question 659

Intracapsular cataract extraction (ICCE)

Answer 659

◦ the entire lens and capsule is removed, requiring large incision ◦ Resulted in aphakia and the need for cataract glasses (+12D) with caused distortion of images, secondary IOLs could be implanted with a second surgery ◦ ICCE was associated with a higher risk of RD. It also required a surgical peripheral iridotomy to prevent vitreous prolapse and pupillary block ◦ This surgery has been replaced by newer and safer techniques ◦ ICCE=ICE age, not done anymore

Question 660

Extracapsular cataract extraction (ECCE)

Answer 660

◦ The lens is removed by the lens capsule remains. The incision must still be large because the lens is removed as a while. An IOL is typically inserted into the capsule

Question 661

Phcaoemulsification

Answer 661

◦ A form of ECCE where the lens is fragmented with ultrasound before removal. Allows for a much smaller incision that rarely requires sutures, as the aqueous will push against the corneal flap to close it ◦ Typical utilizes a clean cornal incision for lens removal

Question 662

Femtosecond laser for cataract surgery

Answer 662

◦ A fairly new addition to the traditional cataract surgery performed by some surgeons. It is used for corneal incisions, anterior capsulorhexis, and lens fragmentation

Question 663

Types of IOLs

Answer 663

Toric (4D), aspheric, multifocal/bifocal, accommodating, monovision

Question 664

Design of IOLS

Answer 664

Foldable, rigid, injectable

Question 665

Placement of IOLS

Answer 665

AC, iris fixed, ciliary sulcus fixed, scleral fixed, or in the capsular bag (most common

Question 666

Post op complications (cat surgery)

Answer 666

``` Striate keratopathy Acute post op endophthlmitis Delayed post op endophthalmitis Toxic anterior seg syndrome Lens subluxation PCO CME RD Wound leak Suprachoroidal hemorrhage Elevated IOP Corneal edema Diplopia Ptosis UGH syndrome Induced cornea astigmatism Iritis ```

Question 667

Striate keratopathy after cataract surgery

Answer 667

post op corneal edema and folds in descemets membrane; typically resolves without treatment within days

Question 668

Acute post op endophthalmitis: cataract surgery

Answer 668

rare complication that occurs in 1/1000 cases; however, even with early treatemnt, 50% of eyes become blind ‣ Stmptoms occur within days (2-4) of the procedure and include progressively decreased vision, redness, and increasing eye pain ‣ 70% of cases are gram + bacteria, including staph epi and staph aureus. The normal bacterial flora from the eyelids and conjunctiva are the most likely sources of infection ‣ Signs include a significant AC reaction that can be accompanied by hypopyon, vitritis, chemosis, eyelid edema, fibrous exudate, mucous discharge, corneal edema, and reduced red reflex

Question 669

Delayed post op endophthalmitis: catract

Answer 669

symptoms occur within a week to one month after the procedure. Vision loss is insidious and pain gradually worsens. Fungal post op endophthalmitis is also commonly a delayed complication

Question 670

Toxic anterior segment syndrome (TASS)

Answer 670

sterile inflammtory reaction that leads to toxic damage to the AC structures. Typically a result of chemical exposure during surgery ‣ Typically presents 12-48 hours pos op with decreased vision, no to mild pain, diffuse limbus corneal edema, hypopyon, fibrous membrane, no vitritis, and increased IOP ‣ MUST rule out infectious endophthalmitis

Question 671

Lens subluxation after cataract surgery

Answer 671

rare in cataract surgery. Caused by pupillary capture and poor capsular support, findings are common common in PXF or Marfans syndrome ‣ Trauma is the number one cause of lens subluxation ‣ Systemic conditions that cause lens subluxation include: Marfans, Ehlers-Danlos, Weill-Marchesani syndrome, and homocystinuria

Question 672

Difference between OI and ehlers danlos

Answer 672

• Ehlers Danlos and OI cause similar effects including keratoconus, blue sclera, megalocornea; ehlers danols differs in that it can also cause lens subluxation. In marfans, RDs are common and are the most serious ocular complication

Question 673

PCO after cataract

Answer 673

the most common post op complication following cataract surgery. Also referred to as a secondary cataract ‣ Equatorial epithelial cells migrate to and proliferate over the posterior capsule, resulting in opacification most commonly within 2-6 months after surgery ‣ Elschnig Pearls are a type of PCA that is most common in children who undergo cataract extraction

Question 674

Most common post op complication from cataract surgery

Answer 674

PCO

Question 675

CME after catract surgery

Answer 675

one of the most common reasons for decreases acuity after cataract surgery. The surgical trauma results in inflammation; with the disruption of the lens/vitreous interface, inflammatory cells have an easier time getting to the posterior pole to cause inflammation ‣ The most common cause of CME is post cataract surgery (Irvine Gas’s syndrome). Remember that CME develops within the OPL (Henles) ‣ Peak incidence is within 6-10 weeks following cataract surgery. CME is common on FA but only about 1.5% of patients have significant and symptomatic CME with modern surgical procedures. FA will show hyperfluroescent leakage within the macula (petaloid pattern) and around the ON ‣ Most cases resolve with treatemtn around 6 months

Question 676

When can CME occur

Answer 676

after intraocular surgery or in DR, retinal vein occlusion, uveitits, RP, ARMD, ERM, retinal vasculitis, and Coat’s

Question 677

Wound leak after cataract surger

Answer 677

occurs early in the post op period and may be initiated by valsalva maneuver, trauma, or suture failure ‣ Signs include a positive Seidel signs, hypotony, iris prolapse (will point towards the wound), choroidal detachement (fluid accumualtes in the suprachorodial space) and a shallow AC ‣ Patients with an open wound are at risk for endophthalmitis and should be promptly treated

Question 678

Suprachoroidal hemorrhage after cataract surgery

Answer 678

Super chorodial hemorrhage: rare complication characterized by the accumulation of blood between the choroid and sclera during surgery. This is a devastating complication that is mroe common in the elderly and has an unknown etiolgoy

Question 679

Elevated IOP after cataract surgery

Answer 679

make be caused by retained viscoelastic, steroid response, inflammtory debris or RBC clogging the TM, pupillary block, or retinae lens material

Question 680

Corneal edema after cataract surgery

Answer 680

typically an early complication characterized by folds in Descemets membrane, bullae, and/or Microcysts that slowly resolve. Potential causes ‣ High IOP-can cause microsystic edema ‣ Low IOP- can cause descemets folds ‣ Surgical trauma-causes edema due to the shock waves from phacoemulsification. This is less common with the intraoperative use of viscoelastic material ‣ Pre-existing corneal Disease predisposes patients to corneal edema ‣ Bullous keratopathy (occurs later in life in the post op period) is more common in aphakia and with AC IOLs ‣ Haptic rubbing on the endothelium can cause damage and edema

Question 681

Ptosis after cataract

Answer 681

permanent ptosis can be due to levator dishiscence by the lid speculum. A temporary ptosis may be due to spot op swelling or use of local anesthetic

Question 682

UGH syndrome

Answer 682

Uveitits, glaucoma, hyphema Syndrome (UGH): most likely due to an ill fitting AC IOL that rubs the Iris, causing hyphema and uveitis. The accumulation of RBC in the TM causes an elevated IOP. Very uncommon complication now that AC-IOLs are less commonly used

Question 683

Iritis after catraact surgery

Answer 683

secondary to surgical trauma, retained lens material (will appear as fluffy, white material behind the iris), endophthalmitis, or occurs in an eye that is predisposed to uveitis and is then aggravated again by surgery