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KMK Ocular Disease > KMK Ocular Disease > Flashcards

KMK Ocular Disease Flashcards

1
Q

Sclerotic scatter

A

Evaluate corneal clarity.
illuminate a parallelepiped beam 60 on temporal limbus.

Observe with naked eye.
When someone is naked, people scatter!

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2
Q

Specular reflection

A

Evaluate corneal endothelium and lens surfaces.

1mm wide beam, Oculars should be set directly in front of patient and beam should be at 45-60 degree away. Set the beams at equal incidences.

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3
Q

Indirect illumination

A

Used to evaluate non-opaque corneal lesions such as micro cysts.

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4
Q

Good way to detect fleisher rings in KCN

A

Use cobalt blue filter without dye

Will appear black

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5
Q

Alkali burns are __x more common than acidic

-Common agents

A

2x

Alkali: Ammonia, fertilizer, cleaning agents, lye, drain cleaners, magnesium hydroxide, fireworks, lime, cement, airbag residue,

Acidic: Glass polisher, rust remover, battery acid, PAVA spray.

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6
Q

Most common cause of alkali burns

A

Calcium Hydroxide

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7
Q

K defect with no SEI

A

Corneal abrasion

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8
Q

Vossius ring

A

pigment ring on the anterior lens capsule due to trauma. iris smacks lens. Likely will see this with hyphema.

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9
Q

Examples of positive forced ductions

A

Graves
Browns
Duanes
Orbital floor fracture

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10
Q

Commotio retinae

A

Disruption of RPE and outer segments of PR cells

Resolves within 3-6 weeks

Berlins edema in macula

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11
Q

Iridodialysis difference from angle recession

A

Iridodialysis- Disinsertion of the iris root from the CB
Appears as peripheral iris hole on retro
Monitor for angle recession glaucoma due to possible TM damage secondary to trauma

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12
Q

What can occur if orbital cellulitis is not treated?

A

Cavernous sinus thrombosis, brain abscess or meningitis.

Diabetics and immunocompromised can develop mucormycosis, an aggressive fungal infection. Black necrotic tissue in mouth and nose.

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13
Q

TED is related to what other systemic conditions

A

MG

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14
Q

What do these mean in TED

  • Von Grafes sign
  • Dalrymple’s sign
  • Kocher’s sign
A
  • Von Grafes sign: Upper eyelid lag during downgaze.
  • Dalrymple’s sign: Staring appearance
  • Kocher’s sign: Globe lag compared to lid movement when looking up.
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15
Q

Hertel Exophthalmometry norms

A

Asians: 12-18
Caucasians: 12-22
AA: 12-24

No more than 3mm asymmetry.

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16
Q

Most common benign orbital tumor in children

A

Capillary hemangioma

Rapid growth and spontaneous involution

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17
Q

Most common benign orbital tumor in adults

A

Cavernous hemangioma
4th-6th decade, females
Progressive, painless, unilateral proptosis.
Tumor usually arises in the muscle cone.

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18
Q

Yellow/white tumor of astrocytes

A

Neurofibroma

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19
Q

Optic nerve glioma/juvenile pilocytic astrocytoma

A

Most common intrinsic tumor of the ONH
Common ages 2-6
NF type 1

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20
Q

Most common benign brain tumor

A

Meningioma

Middle age women

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21
Q

Most common primary and secondary pediatric orbital malignancy

A

Rhabdomyosarcoma

Neuroblastoma- most commonly arises from tumor in the abdomen, mediastinum, or neck (associated horners)

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22
Q

Orbital pseudotumor/idiopathic orbital inflammatory syndrome

A

Rare, may be acute, recurrent or chronic.
Young to middle age patients.
Impacts any soft tissue in the orbit. Appearance can vary significantly depending on the orbital tissue involved.

Acute onset of unilateral pain, red eye, diplopia, and decreased vision.

Chemosis without itching 
Increased IOP 
Swelling of tendons and muscles 
Hyperopic shift 
Lacrimal gland and sac inflammation

Bilateral? Lymphoma or systemic vasculitis (wegener’s, PAN)

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23
Q

Chemosis without itching? think

A

Think orbital cause.

Cavernous sinus fistula or IOIS

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24
Q

Tolosa Hunt

A

Idiopathic orbital inflammation that can affect the cavernous sinus and SOF

Acute and painful exophthalmoplegia due to ipsilateral palsies of CN 3, 4, and 6.
Loss of sensory innveration may also occur since V1 and V2 travel thru the SOF.

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25
Q

Anophthalmos

A

Absence of ocular tissue within the globe

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26
Q

Enucleation, evisceration, and exentration

A

Removal of globe

removal of inner contents of the eye- leave sclera

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

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27
Q

Signs of rosacea

A

Papules on the cheek and forehead with telangiectasia and rhinopehyma (sebaceous gland hypertrophy of the nose) and facial flushing.

Facial flushing may occur with triggers such as alcohol, exertion, spicy foods, caffeine and increased sun exposure.

can cause ocular rosacea- inspissated meibomian glands, phlyctenules, staph marginal keratitis, SPK corneal neo and dry eye

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28
Q

Medications that can cause contact dermatitis

A 
Aminoglycosides- Tobragent30 
Trifluridine 
Cycloplegics 
Glaucoma meds
Preservatives

PERIORBITAL swelling

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29
Q

When do you see periorbital swelling

A

Contact dermatitis

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30
Q

Ocular cicatricial pemphigoid

A

65 year old female subacute onset
Idiopathic mucous membrane disorder that commonly affects the oral and ocular mucous membranes
Type II hypersensitivity due to autoantibodies targeting conj basement membrane.
Can be induced by timolol, epinephrine or pilocarpine.
Sym/ankyloblepharon
Entropion and trichiasis with ulceration, neo, and keratinization.

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31
Q

SJS

A

Type 3 or 4 hypersensitivity that affects mucous membranes.

Due to sulfa drugs, penicillin, aspirin, barbiturates, tetracyclines, NSAIDs or infections (herpes, adenovirus)

Acute phase 2-4 weeks, can be chronic.

Prodrome, diffuse erythema or bullseye lesions, papule on the palms of hands and feet.

Severe, bilateral conjunctivitis with pseudomembranes.

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32
Q

Which 2 syndromes cause symblepharon

A 
Steven Johnsons (type 3 or 4) 
Ocular Cicatricial pemphigoid (type 2)
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33
Q

2 types of blepharitis

A

Staph and seborrheic
Seborrheic is associated with less lid inflammation, more oily, greasy scales with flaking and more eyelash loss.

Patients often asymptomatic, but may report vision that clears after blinking, burning, itching or foreign body sensation.

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34
Q

Milia

A

Due to occlusion of sweat pores or pilosebaceous units

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35
Q

Ectropion most common causes and signs

A 
Age related (involutional- Loss of muscle tone of the orbicularis oculi) 
Bells palsy

Signs- exposure keratopathy, epiphora, brow ptosis

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36
Q

Entropion signs and causes

A
  1. Involutional
  2. Cicatricial:
    Trachoma- leading cause of blindness world wide
    SJS
    OCP
    Chemical burns

Mild punctate keratitis to corneal ulceration and panes

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37
Q

Floppy eyelid syndrome

A

Loss of elasticity in the tarsal plate, poor CT. Face down sleeping at night.
Mechanical trauma to arsal plate.

Friction –> papillary conjunctivitis

think LOW O2. this can lead to NTG, NAION

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38
Q

Meige’s syndrome

A

Benign essential blepharospasm + lower face abnormalities

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39
Q

Most common precancerous skin lesion

A

Actinic keratosis, precursor to squamous cell
Elevated, pink or red. Scaly lesion on sun-exposed skin that does not heal.
25% develop in SCC

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40
Q

Main difference in appearance between basal and squamous cell

A

Basal cell has telangiectasia, squamous cell does not.

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41
Q

Keratocanthoma lifespan

A

Sun exposed areas with early appearance similar to BCC and SCC (central plaque)
Grow very quickly and then slowly shrink- spontaneously resolve.

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42
Q

Sebaceous gland carcinoma. If greater than 2mm, mortality rate is

A

60%

Overall is 10%

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43
Q

Once a malignant melanoma has been diagnosed, the two most important prognostic factors are

A

Depth of invasion and size of lesion

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44
Q

Dacryoadenitis

What causes the acute and chronic presentations? Which is more common

A

Acute- infection

Chronic- inflammatory disorders such as sarcoid, TB, graves. This is more common

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45
Q

S shape ptosis

A

Dacryoadenitis

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46
Q

How to know if actinomycetes israellii caused canaliculitis

A

Yellow sulfur granules after expression

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47
Q

What causes conj concretions

-other name

A

Ocular lithiasis

Friction of mucous and epithelium + calcium

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48
Q

Primary Acquired Melanosis PAM

A

Precursor to malignment melanoma, 30% progress.
Unilateral acquired pigmentation with indistinct margins
on the conj
Common in elderly white people

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49
Q

1 precursor to conjunctival melanoma

A

PAM

Primary acquired melanosis

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50
Q

Conjunctival intraepithelial neoplasia (CIN)
AKA Bowens
AKA Conjunctival squamous dysplasia

A

Most common conj neoplasia
premalignant to squamous cell carcinoma (risk is low if BM remains intact)
Elevated, gelatinous mass with neo and keratinization.
95% at the limbus within the interpalpebral fissure.

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51
Q

Most common conj neoplasia

A

CIN

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52
Q

What is premalignant to squamous cell carcinoma

A

CIN

Conjunctival intraepithelial neoplasia

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53
Q

Pyogenic granuloma

A

Pedunculated, benign, red, vascular lesion of the palpebral conj due to surgery, trauma, or infection.

Pyro think red= pyromaniac

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54
Q

What bacteria causes simple bacterial conjunctivitis in adults and kids

A

Kids- H influenza (gram negative)

Adults- Staph aureus (gram, catalase, coagulase positive)

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55
Q

Most adenovirus infections result from what

A

Upper respiratory tract or nasal mucous infection.

There are over 45 serotypes 1/3 are associated with eye infections

Transmission occurs from direct contact, ocular secretions, equipment.

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56
Q

All 3 adenoviral syndromes are associated with

A

Follicles, pseudomembranes, and diffuse conjunctival hyperemia.
Most follow from a systemic viral infection.

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57
Q

Toxic causes of follicles

A

Molluscum, parinauds catscratch, phthiriasis palpebraum (public lice)

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58
Q

Acute non specific follicular conjunctivitis

-serotypes

A

1-11 and 19
Most common
-Diffuse red eye, inf follicles, tearing, mild discomfort

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59
Q

PCF viral conjunctivitis

-Common serotypes

A 
Pharyngoconjunctival fever 
3-5 and 7 
More commonly affects children 
HIGHLY contagious 
Triad: Fever, follicles, pharyngitis (sore throat) 
Rare corneal involvement
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60
Q

EKC

-serotypes

A

Most serious form of adenovirus conjunctivitis.
8,19,37
Pain and corneal involvement !!!!!! Other 2 types of viral conjunctivitis do not have corneal involvement (80%)
pre-auricular lymphadenopathy

Serotype 8, 80% corneal involvement, symptomatic 8 days after exposure, 8 days after that –> SEI’s, non contagious.

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61
Q

Presence of a palpable node in a patient with suspected adenoviral infection is always pathognomonic for ___

A

EKC

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62
Q

2 types of allergic conjunctivitis

A

Seasonal and perennial (less common type 1 rxn. Year round response to household allergens like dust)

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63
Q

VKC

A

8 year old boy with asthma or eczema.
Seasonal outbreaks during warm months
Superior HUGE cobblestone papillae that can cause a shield ulcer on the cornea. May also see truants dots- papillae on the limbus.

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64
Q

AKC is what type of hypersensitivity reaction

A

1 and 4

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65
Q

do follicles or papillae contain a central vessel

A

Papillae
serves as the source of infiltration of eosinophils, mast cells, neutrophils and lymphocytes.

Associated with allergies, bacteria, and friction. q

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66
Q

GPC is most likely to occur with which CL material

GPC can occur due to what other sources?

A

SiHy due to high amount of protein deposits.

But can also occur due to sutures, blebs, scleral buckle, prosthetic.

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67
Q

CL solution reactions. What are the two most toxic types

A

Thimerosal and chlorhexadine

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68
Q

3 causes of SLK

A

CL
Dry eye
Thyroid

** all related to friction ***

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69
Q

Classic complication of CLs that ride too high

Classic complication of CLs that ride too low

A

High- Corneal warpage

Low- 3 and 9 o clock staining

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70
Q

SEAL: Superior epithelial arcuate lesion

A

Superior corneal staining

secondary to tight extended wear hydrogel CLs

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71
Q

Keratoconjunctivitis

A

Implies simultaneous inflammation of the cornea and conj.

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72
Q

Adult inclusion chlamydia is due to serotypes ___

How do you treat?

A

D-K
1000mg 1 dose
Doxycycline

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73
Q

3 conditions with swollen pre-auricular nodes

A

Gonnorhhea
Chlamydia
EKC

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74
Q

Signs of adult inclusion conjunctivitis

A 
Inferior follicles + some papillae. 
Chronic, lasting 3-12 months. 
May spread bilaterally. 
Sub epi infilatrates. 
Pain with urination 
Node inflammation
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75
Q

Trachoma serotypes and symptoms

A 
A-C trAChoma 
Bilateral 
Superior follicles + some papillae 
Arlt's line and herberts pits 
Pannus 
Node involvement 
3rd world country, poor country
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76
Q

Leading cause of preventable blindness worldwide

A

Trachoma

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77
Q

Phlyctenules
due to what
-location
-what is it made of

A

Type 4 hypersensitivity reaction to staph
-bleph is the most common culprit

Ask if they have a history of Tb

Can be on the conj or cornea.

Made of lymphocytes

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78
Q

Common cause of parinauds ocularglandular syndrome

-Symptoms

A

Cat scratch fever is the most common cause- caused by bartonella henselae.
“paranoid about cats”
Unilateral granulomatous, swollen nodes, conjunctivitis.

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79
Q

Signs of Phthiriasis palpebrarum

A

Pubic lice- transparent lice and white nits attached to the eyelashes. Blood tinge debris on lids and lashes
Pre-auricular lymphadenopathy

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80
Q

pinguecula/pterygium

  • Etiology
  • What does it do to the conj/K
A

UV light exposure or chronic dryness
Degeneration of collagen fibers.
Damages Bowman’s membrane on the cornea, leading to WTR astigmatism.
stockers line (iron deposits) may be present at the leading edge

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81
Q

Stockers line is seen when

A

Pterygium

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82
Q

Causes of episcleritis and presentation

A

70% idiopathic
Other causes: Collagen vascular/inflammatory diseases (RA, SLE, UCRAP)

Unilateral, sectoral injection, 80% simple 20% nodular,

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83
Q

Groupings of scleritis

A
  1. Necrotizing (15%)
    - Necrotizing with inflammation (5%)
    - Necrotizing without inflammation (10%)(scleromalacia perforans)
  2. Non-Necrotizing (85%)
    - Diffuse (60%)
    - Nodular (25%)
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84
Q

Most common form of scleritis

A

Diffuse scleritis

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85
Q

Worst form of scleritis
33% die within a few years due to autoimmune disease
Signs

A

Necrotizing with inflammation

May cause peripheral K melt, keratitis, scleral thinning, anterior uveitis, cataracts, secondary glaucoma.

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86
Q

Necrotiazing without inflammation is due to

A

Chronic RA

Asymptomatic, gray-blue patches of scleral thinning due to exposure of underlying uvea

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87
Q

Episcleritis and scleritis

  • Unilat or bilat
  • causes
  • Onset
A

Episcleritis is unilateral

  • 70% idiopathic, other causes due to collagen vascular diseases like RA, SLE, or UCRAP.
  • acute

Scleritis is bilateral.

  • 50% due to systemic autoimmune conditions like vascular disease (RA) or Wegener’s Granulomatosis.
  • Gradual onset
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88
Q

What a seg infection has severe, boring pain that radiates to forehead and awakens pt at night

A

Scleritis

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89
Q

Axenfeld loop

A

LPCN from nasocil (LINES)

Congenital anomaly. Focal, pigmented, elevated area.

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90
Q

What occurs secondary to the breakdown in blood aqueous barrier

A

Uveitis

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91
Q

50% of patients with uveitis are __ positive

A

HLA-B27
70% if the condition recurs.
Usually related to ankylosing spondylitis.

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92
Q

HLA-B27

A 
U ulcerative colitis- IBD
C Chrons 
R Reiters 
A Ankylosing 
P psoriatic arthritis
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93
Q

Acute anterior uveitis is less than __ duration

A

3 month

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94
Q

Why does anterior uveitis cause pain?

A

Congestion and irritation of the anterior ciliary nerves.

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95
Q

Anterior uveitis is based on the presence of

A

White blood cells in the anterior chamber

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96
Q

Anterior uveitis main threats to vision

A

PS, PAS, CME, cataracts (PSC)

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97
Q

Granulomatous uveitis presenttion

A

Mutton fat KPs- macrophages
Koeppe nodules- granulomatous AND non granulomatous
Busacca nodules

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98
Q

Stellate KP’s are found in what diseases

A

Fuch’s heterochromic iritis

Herpetic uveitis

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99
Q

Bechet’s is common in who

A

Young adults of asian and middle eastern descent.

Hypopyon, mouth ulcers, genital ulcers.

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100
Q

Glaucomatocyclitic crisis/Posner-Schlossman

A

Unilateral
Mild iritis with recurrent, self limiting episodes of elevated IOP
Secondary to traubeculitis

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101
Q

3 major conditions that will present with unilateral cells in the anterior chamber with acute elevated IOP (30-50)

A

Posner Schlossman
Herpes zoster / simplex
Fuch’s

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102
Q

Chronic granulomatous uveitis is usually associated with

A

Sarcoid- AA females, abnormal chest scan, elevated ACE levels.

TB- Positive PPD test, abnormal chest x ray, night sweats.

Herpes simplex/zoster- Stellate KPs

Syphilis: may have interstitial keratitis (stromal inflammation without primary involvement), maculopapular rash

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103
Q

Most common cause of interstitial keratitis

A

Congenital syphilis, TB, and herpes simplex.

Stromal inflammation WITHOUT primary involvement of epithelium or endothelium.

Acute stromal edema and neo

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104
Q

Congenital syphilis triad

A

Hutchinson’s teeth (small, widely spaced), deafness and IK

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105
Q

Why does posterior uveitis sometimes result in WBCs in the vitreous and sometimes not?

A

Inflammation of retina–> breakdown in blood retinal barrier –> WBC in vitreous. Pts may have floaters and decreased VA.

Inflammation of the choroid without significant involvement of the retina (like histoplasmosis) does not affect blood retinal barrier and pt will not have a vitritis.

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106
Q

Most common cause of posterior uveitis in the US

How do they contract it

A

Toxoplasmosis
90% contracted through transplacental transmission if the mother contracts it during pregnancy. May result in convulsions, cerebral calcifications, and retinochoroiditis. Most cases are mild and just have chorioretinal scar.

10% acquired from cat feces and/or undercooked meat.

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107
Q

Most common scenario of toxoplasmosis recurrence

A

Recurrence of an old, stable, congenital lesion is the most common cause of infectious retinitis.

at 25 years old, pt will have unilateral redness, photophobia, floaters, uveitis, vitritis, and decreased VA.

Focal fluffy retinal lesion adjacent to old inactive scar with overlying vitiritis (HEADLIGHT IN THE FOG)

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108
Q

headlight in the fog

A

Toxoplasmosis

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109
Q

Sarcoid panuveitis findings

A

Cotton ball opacities (retinitis)
Candle wax drippings (vasculitis)

Others: 
Dacryoadenitis 
Dry eye 
Chronic, bilateral, granulomatous uveitis 
CN VII palsy 
ON disease !!!!!!!!!!!!!
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110
Q

Iris coloboma usually located in which quadrant

A

Inferior nasal

May see coloboma elsewhere- CB, zones, choroid, retina, ON

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111
Q

Iris malignancy

-What layer of the iris, what location and what are concerning signs

A

Stroma, inferior, feathery margins, greater than 3mm

Can be pigmented or amelanotic

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112
Q

Dellen

A

Area of cornea that wets poorly, leading to stromal dehydration and corneal thinning.

Dye will POOL

Adjacent to areas of elevation

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113
Q

Exposure keratopathy is due to which 2 things

A

CN 7- bells, CVA, aneurysm, MS, herpes

Orbicularis oculi- eyelid surgery, TED, nocturnal lagophthalmos, floppy eyelid

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114
Q

Most common cause of filamentary keratopathy

A

Dry eye

Composed of degenerated epithelial cells and mucous

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115
Q

How does UV keratitis cause damage to the K?

A

Excessive absorption below 300nm can cause hyperactiviation of K+ Channels (very sensitive to pH)

Loss of intracellular K+ results in cell death

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116
Q

Which 2 tests are diagnostic for evaporative dry eye

A

Meibomography, expression of meibomian glands.

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117
Q

All types of dry eye are characterized by which of the following?

A

Tear hyperosmolarity, tear film instability.

AKA increased tear osmolarity, decreased TBUT

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118
Q

Hydrops vs bullae. What layer are they in?

A

Hydrops is due to KCN. Tears in descent’s membrane that results in edema and rupture of the epithelium.

Bullae is edema in the epithelium due to due Fuchs.

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119
Q

Three types of tearing.

How does Schirmer testing isolate them?

A

Reflex, basal, emotional

Schirmer 1 is WITHOUT anesthetic and measures all three types of aqueous secretions. Normal is >10mm in 5 mins.

Schirmer 2 is WITH anesthetic and only measures the basal aqueous secretions. Normal is >5mm in 5 minutes.

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120
Q

How does an increased in tear hyperosmolarity contribute to dry eye?

A

Results in an inflammatory cascade that damages the ocular surface and releases inflammatory mediators into the tears.

Both types of dry eye cause hyperosmolarity.

Abnormal: Greater than 308 or 8 difference between each eye.

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121
Q

Prolopased orbital fat vs prolapsed SOOF

A

Steatoblepharob

Malar bags

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122
Q

Pt who wear soft CL and RGPs should discontinue CL wear how many days before surgery

A

soft Cl- 2 week

RGPs- 3 weeks

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123
Q

An axial length change of 1mm corresponds to how many diopters?

124
Q

What drops can be used pre and post op to decrease the risk of CME

125
Q

Hemolacria

A

blood in tears

126
Q

Bulbar conj salmon patch

A

Conj Lymphoma

127
Q

What % of the population has physiologic aniso

128
Q

Primary and secondary sjogrens

A

Primary- Dry eye, dry mouth, dry eyes.

Secondary- triad + another autoimmune disease.

129
Q

Non sjogrens aqueous deficient dry eye

A

Primary lacrimal gland deficiencies-
Age related, the most common type of non-sjogrens dry eye.

Secondary lacrimal gland deficiencies- Think ABC!

A- Attacked glands due to inflammation infiltration: Sarcoid, lymphoma, AIDs
B- Blocked: Trachoma, pemphigoid, thermal burns.
C- Cut nerves: Damage to CNV1 or VII due to CL wear, diabetes, bells palsy.

130
Q

Two forms of evaporative dry eye

A
  1. Intrinsic:
    - MGD
    - Lid structure: Proptosis, nocturnal lagophthalmos
    - Low blink rate: Intense concentration, Parkinson’s
  2. Extrinsic:
    - Ocular surface disease: Vitamin A deficiency, topical anesthetics, topical preservatives.
    - CL wear.
131
Q

How many patients with KCN have it by AD inheritance?

When do symptoms appear

A

10%

Condition begins around puberty

132
Q

KCN etiology

A

Non-inflammatory, progressive and degenerative disease of unknown etiology

Stromal collagen fibril displacement due to loss of adhesion between fibrils, which results in corneal thinning and protrusion due to DEGRADATION OF THE FIBRILS BY MMPS!

133
Q

Ocular conditions associated with KCN

A

Allergic- VKC, AKC, floppy eyelid

Connective tissue- Fuchs, PPMD, granular dystrophy, lattice

Hereditary- conditions that cause eye rubbing to stimulate vision. Aniridia, RP, Lebers, ROP, cone dystrophy.

134
Q

Systemic conditions associated with TDOME

A 
T- Turners 
D-Down syndrome
O- Osteogenesis imperfecta 
M- Marfans 
E- Ehler's Dalos
135
Q

Early and late signs of KCN

A

Early- Fleisher’s ring, scissor reflex on retinoscopy, irregular mires on keratometry, and inferior steepening on topography.

Late signs- Vogt’s Striae (vertical lines in the stroma that disappear with pressure), munson’s sign, Rizzuti’s sign (conical reflection on the nasal cornea when a light i shown from the temporal side), and hydros (tears in descemets)

136
Q

pellucid marginal degeneration

A

Most commonly presents in early adulthood (20-40 years)

Collagen abnormalities that begins in a crescent-shape inferiorly, usually at 4 and 8 o clock. IOP causes the cornea to protrude right above the area of thinning (not within the area of thinning like in KCN)

Pt usually asymptomatic, ATR astig.

137
Q

Similarities and differences of KCN and PMD

A

PMD- Does not have Fleisher’s ring or Vogt’s stream.

Both can develop hydrops, which are tears in descent’s membrane.

138
Q

Keratoglobus

A

Onset at birth.

Associated with Ehler’s dances syndrome, blue sclera, an leber’s

Diffuse corneal thinning from limbus to limbus.

139
Q

EBMD / Cogans

A

Excessive basement membrane dystrophy

Abnormal epithelial adhesion and excessive BM production

Typically asymptomatic. But can be pain, photophobia, and vision loss.

Charactertized by negatives staining. Too much BM underlying epithelium. Fluorescene slides off.

140
Q

3 main groupings of dystrophies:

Anterior
Stromal
Endothelial/posterior

A

Anterior:

  • EBMD
  • Meesman’s (snail track) A multitude of ruptured cysts or RCE
  • Reis Buckler (replaces bowman with collagen)

Stromal: Marilyn Monroe got hers in LA

  • Macular
  • Granular
  • Lattice
  • Schnyders

Endothelial/posterior:

  • Fuchs
  • PPMD
141
Q

Meeseman’s

A

Multitude of intraepithelial cysts, bilaterally, that spread across the entire cornea.
AD

142
Q

Reis Bucklers Dystrophy

A

Replaces Bowmans with collagen

Bilateral, symmetric, sub epithelial grey opacities.

143
Q

Least common but most severe stromal dystrophy that will affect vision much earlier.

A

Macular dystrophy

144
Q

Signs of macular dystrophy

A

Diffuse, superficial, central strombe haze between 3-9 years of age.

Progresses to a cloudy cornea with mucopolysaccharide deposits with irregular boarders that are present in all layers of the cornea. Extend limbus to limbus.

145
Q

Most common dystrophies due to the TGFB1 gene

A

Granular- hyaline deposits (snowflake like) in the stroma.

Avelllino Dystrophy is a rare variant of granular that has granular and lattice like deposits.

Lattice- Amyloid deposits (Branching, lattice like)

146
Q

Fuch’s

What % have a positive family history

A

30%

AD, female predilection, more common in 60+

147
Q

Do Fuch’s patients have a thick or thin pachymetry findings?

A

Thick because K edema

148
Q

Concerning endothelial cell count number

A

500
400-700 required to prevent edema.

Kids have around 3-4k
By 80 years old, down to 1-2k

149
Q

PPMD

Posterior polymorphous dystrophy

A

Patch of vesicles that create a band (train track lesions) on descent’s and the end.

Metaplasia of the endothelial cells. They have an endothelium that acts like an epithelium. These cells may spread into the angle and cause glaucoma

150
Q

Megalo cornea

A

X linked
Males
13mm horizontal diameter
Steep Ks

May have Marfans, Ehler’s Danlos, or osteogenesis imperfecta.

At risk of developing glaucoma

151
Q

Microcornea

A

AD inheritance
Less than 10mm horizontal K diameter
Hyperopic
Shallow angle –> Glaucoma

152
Q

Cornea Plana

A

Corneal curvature equal to the scleral curvature

Bilateral flat Ks, less than 38D

Associated with sclerocorneo (due to bilateral scleralization- opacification and vascularization) and micro cornea.

153
Q

Complications due to aniridia

A

Autosomal dominant

Corneal lesions
Lenticular changes- cataracts 
Glaucoma !!!!!! 75% 
foveal hypoplasia 
disc hypoplasia
154
Q

Axenfeld-Rieger Syndrome

A

Continuum of disorders where patient suffer from anterior seg developmental abnormalities that affect the anterior chamber.

50% develop glcuaom

155
Q

PE
Axenfeld anomaly
Reiger anomaly
Reiger Syndrome

A

PE- 15% of normal people have. Does not put you at risk for glaucoma.

Axenfeld anomaly- PE + angle abnormalities + glaucoma risk

Reiger anomaly- PE + angle abnormalities + glaucoma risk + iris stromal abnormalities (corectopia, iris hypoplasia)

Reiger Syndrome- PE + angle abnormalities + glaucoma risk + iris stromal abnormalities + systemic abnormalities (mental retardation, skeletal abnormalities)

156
Q

Peter’s Anomaly

A

Patients are born with central white corneal opacities with iris adhesions.
Bilateral.

70% develop secondary glaucoma..

157
Q

An infiltrate without an overlying defect means what

A

An infiltrate is a sign of your bodies immune system attacking an antigen via antibodies. But no defect means there is no sign of infection.

Sterile infiltrate

158
Q

Define

Sterile infiltrate
Sterile ulcer
Infectious ulcer

A

Sterile infiltrate- Infiltrate without epi defect (sign of immune system attacking an antigen with antibodies. Immune mediated, no infection)

Sterile ulcer- infiltrate with epi staining less than infiltrate size.

Infectious ulcer- infiltrate with epi staining the same size as the infiltrate. (bugs attacking K)

159
Q

What 2 scenarios would cause fungal keratitis

What is the most common fungus

A
  1. Trauma with veg matter
  2. Immunocompromised
    Both caused by candida
160
Q

Culture fungi on what agar

A

Sabouraud’s agar.

It’s fun to drive a subaru !

161
Q

appearance of a fungal keratitis with aspergillum/fusarium vs candida

A

aspergillum/fusarium– Epi defect with underlying grey-white corneal infiltrate with feathery edges

candida- Similar appearance as bacterial ulcer.

162
Q

How to culture acanthamoeba

A

Non-nutrient agar with heat killed E-coli

163
Q

Early and late signs of acanthamoeba

A

early- barely any SPK. Severe pain.

late- Radial keratoneuritis (inflammation of the corneal nerves) and patchy stromal infiltrates that progress to form a ring ulcer.

164
Q

Only type of scleritis associated with glaucoma

A

Necrotizing with inflammation

165
Q

Other name for phthiriasis palpebrarum

A

pediculosis ciliaris

166
Q

After a thermal/UV burn, symptoms get worse how many hours after the event?

A

6-12 hours

167
Q

Lab test to run for Sjogrens

A

Anti SSA, SSB

168
Q

Tumor that pt might have with
Sjogrens
MG

A

Sjogrens: Non Hodgkin’s Lymphoma
MG: Thymoma

169
Q

Corneal ectasias

A

KCN
PMD
Keratoglobus

170
Q

1 disease associated with a CRVO

A

POAG
CRVO occurs because the vein is able to cork on itself. Usually veins are held in place by a thick, strong RNFL. In POAG, the RNFL weakens and the vein is able to cork on itself.

171
Q

Emboli and thrombus. Which is associated with vein and artery occlusions?

A

Thrombus= Clot that stays where it was formed. Vein occlusion.

HTN/DM –> artery compresses vein –> thrombus

Embolus= Clot moves from where it was formed. Artery occlusion, GCA.

HTN sets pt up for CRVO, BRVO, CRAO, BRVO

172
Q

DR VOS

-All can lead to what 3 things?

A

Proliferative retinopathy

DM 
ROP
Vein occlusion 
OIS
Sickle Cell

Worried about tractional RD, vitreous hemes, and VEGF getting into the angle

173
Q

Types of epithelial diseases in HSK

A

Corneal vesicles/punctate keratopathy: Small lesions that represent earliest epithelial signs related to HSK

Dendritic- most common presentation. Boarder stains pink, center stains green.

Geographic- Wider

Marginal ulcer- Located near limbus. SEI + epi defect + limbal injection

174
Q

How can HSK affect the eye

A
  1. Bleph
  2. Conjunctivitis
  3. Neurotrophic
  4. Epithelium- vesicles, dendrite, geographic, marginal.
  5. Stroma- IK, necrotizing
  6. Endothelium- Disciform
175
Q

Types of stromal diseases due to HSK

A
  1. IK- Inflammation that began in the stroma without primary involvement of the epi or endothelial.
    Infiltrate + diffuse neo + stromal thinning + stromal scar + wessley ring (Immune ring)
  2. Necrotizing. could occur due to IK or infiltration of the stroma by epi or endo HSK. May lead to thinning and perforation.
176
Q

Types of endothelial diseases due to HSK

A

Dendritic
Focal, disc shaped stromal edema overlying KPs stuck on the endothelium.

Focal, no neo, no infiltrate, disc shape

177
Q

Difference between IK and Disciform

A

IK:
Stroma
Diffuse infiltrate
Diffuse neo

Disciform:

  • KP on the endothelium
  • No infiltrate
  • No neo
  • Overlying focal stromal edema
  • Disc shape
178
Q

What conditions have prodromes

A

Zoster

Migraine

179
Q

How do dendrite and pseudodendrites stain

A

Dendrite:
Rose stains boarders
Fluorescein stains inside

pseudodendrite:
Rose stains entire thing
Fluorescein does not stain well

Pseudodendrite has stuck on appearance, no end bulbs

180
Q

Zoster eyelid signs

A 
Trichiasis 
Entropion
Ectropion
Madarosis 
Poliosis
181
Q

Ocular signs of HZV

A

Could develop episcleritis, scleritis, 40% have uveitis, trabeculitis, cataracts, ARN, optic neuritis, cranial nerve palsies (leads to poor EOM innervation)

182
Q

Post herpetic neuralgia

A

Pain persisting beyond 1 month after rash onset or rash resolution.

Most common complication post zoster.

Affects 7%

183
Q

What is a macular star

A

Exudate in Henle’s layer

184
Q

What is exudate

A

Lipoprotein and macrophages leaking out of the deep capillary network

185
Q

retinal edema or exudate first?

A

Pre existing condition –> Hypoxia –> edema –> exudate

Some type of retinal/vascular compromise breaks down the retinal capillary system and leads to liberation of blood contents.

see exudate? know edema has been there a while.

Exudate is found in the OPL or can spread throughout the inner 1/3 from ILM to ELM

186
Q

Where is acute and diffuse edema located

A

Acute- INL and OPL

Diffuse- ILM to RPE

187
Q

What occurs before/after CWS

A

Significant ischemic event –> CWS –> neo

188
Q

3 conditions that exclusively cause PUK

A

Mooren’s Ulcer
Staph marginal keratitis
Collagen vascular disorders

189
Q

Mooren’s Ulcer

A 
Need more info !! Idiopathic. No systemic disease! 
70 year old male
Unilateral peripheral infiltrate
Mild to moderate symptoms 
Could be associated with hep C

Vasculitis of the limbal blood vessels –> ulcer on the peripheral cornea that spreads circumferentially. Grey, crescent shape. Ulcer has a huge over hanging edge

190
Q

Ulcer at the limbus that has a huge, over hanging edge

191
Q

Staphylococcal marginal keratitis

A

Causes PUK
Sterile ulcer (due to bugs hanging out, staining is less than infiltrate)
Immune system over reacts to staph wherever lid touches eye (2,4,8,10)
Type III hypersensitivity response

192
Q

Collagen vascular disorder

A

PUK due to RA, SLE, PAN, or Wegeners.

Mild symptoms

193
Q

Terrien’s Marginal Degeneration

A

Stuck up 30 year old male (bilateral thinning SN, ATR astigmatism)
No ulcer, idiopathic, non inflammatory.

May lead to perforation. Associated with panus. The rest of the eye is quiet- no AC reaction or conj injection or epi defect.

**mooren’s ulcer (causes PUK) is similar but it has an overlying epithelial defect. Terriens does not have an epi defect, just infiltrate.

194
Q

Salzmann’s Nodular Degeneration

A

Mrs. Salzmann, a 60 year old women walking around with a blue bowtie, bowing to people. And she’s very happy. Very beat up women, maybe homeless.

-blue grey nodules in bowmans layer composed of hyaline.

Signifiant corneal inflammatory disease- MGD, trachoma, phlycentulosis, VKC, dry eye, IK. but can be asymptomatic.

195
Q

Band keratopahty

  • What layer
  • what causes it
A

High serum calcium or phosphorus levels (grout0 and hypercalemia (hyperparathyroidism), renal failure.
After trauma
Uveitis(common in JIA pts) dry eye, exposure keratopathy

196
Q

Arcus begins on what layer of K and moves where

A

Begins on Descemets–> bowmans –> stroma

197
Q

When is Arcus concerning

A

Unilateral- carotid disease on the side without Arcus.

Younger than 50

198
Q

What 2 layers can crocodile shagreen be on?

A

Descemets (posterior) or bowmans (anterior)

199
Q

Corneal Farinata

A

Bilateral flour dust deposits in the aroma.

AD

200
Q

Signs of stromal rejection after a K graft

A

Krachmer’s spots

SEIs after graft surgery

201
Q

Signs of endothelial rejection after K graft

A

Khodadoust lines

WBCs on the endothelium in a line

202
Q

Absolute CI of refractive surgery

A

Under 18
Unrealistic expectations
KCN, active herpes, CL warpage on K
CT disease (keloids), collagen vascular disease, immunocomp (on systemic steroids)

203
Q

Keratotomy

Keratectomy

A

Keratotomy - knife making incisions

Keratectomy- removal of tissue with laser

204
Q

Main SE from radial keratotomy

A

Progressive hyperopic shifts

205
Q

PRK

Photorefractive keratectomy

A

Corneal epi, bowmans, and superficial stromal tissue is REMOVED.
Excimer laser applied.
400 residual K required after.
1-2 week healing because K epi must regrow.

206
Q

Benefits to PRK

A

Painful and poor vision for 1-2 weeks after BUT

better for people who might damage flap (athletes, boxers) 
Less risk of ectasia 
Less aberrations 
less dryness 
Cheaper
207
Q

Main differences after PRK and LASIK

A

After PRK- missing bowmans, 400 residual required, pain and slow healing
After LASIK- thinner stroma, flap, 250 residual required, less pain and fast healing

208
Q

LASIK stands for

A

Laser- assisted in situ keratomileusis

209
Q

Conductive keratoplasty

A

Used to tx presbyopia and low hyperopia

using radio frequencies

210
Q

Refractive surgery allowed with KCN

A

Intrastromal corneal rings (intacs)

PMMA rings inserted into stroma to flatten the K

211
Q

Clear lens extraction

A

Cataract surgery but no cataract.
Remove clear lens and put in an IOL to reduce the refractive error.
No residual accommodation remains.

212
Q

Astigmatic keratotmy

A

K incisions made with diamond blades to relax the cornea in steep mer.
Similar to RK but just in astig meridians.

213
Q

Most common SE of LASIK

A

Dry eye since corneal nerves are severed

214
Q

LASIK side effects

A 
Pain in 24 hours 
Serious infection (usually gram positive) 
Flap complications
Corneal ecstasies 
Residual refractive error 
Glare 
Dry eye 
Diffuse lamellar keratitis or sands of sahara (fast and furious, 2-3 days PO) 
Epithelial ingrowth (slow, 1 month PO)
Corneal haze
215
Q

Diffuse lamellar keratitis (sands of the sahara)

A 
Fast and furious 
Shows up 2-3 days PO 
Inflammatory, non infectious reaction that occurs between the K flap and stroma. 
Fine, sand like infiltrate 
May be response to toxins (blade debris)
216
Q

Epithelial ingrowth after LASIK

A

Slow growth, 1 month PO
Faint grey line within 2mm of flap edge.
Asymptomatic.
Not tx unless progression or visual axis obstructed.

217
Q

Most common LASIK complication after an enhancement

A

Epithelial ingrowth

218
Q

What 2 measurements are used to calculate the appropriate IOL power

A

Axial length by A scan and keratometry

219
Q

Average axial length is ____

If the calculation is off by 1mm, that corresponds to how many D

A

average is 24

1mm difference is 3D error in the calculated IOL power

220
Q

3 classes of medication of concern before cat surgery

A

Anticoagulants, alpha blockers, prostaglandins

221
Q

Etiologies of CRVO

A 
Oral contraceptive pills
POAG (40-60%) 
Protein S, C, antithrombin III deficiency 
Antiphospholipid antibody syndrome 
Collagen vascular disease 
AIDS
222
Q

Signs of vein occlusion

A 
Retinal hemes 
Collaterals
dilated tortuous veins 
CWS
Optic disc edema
223
Q

What are collaterals

A

Veins that become visible over several weeks-months after vein occlusion.
Often on the disc.
Permit blood flow between the retinal and choroidal circulations, help drain blood and retinal edema into the choroid circulation.

224
Q

What is the leading cause of vision in ischemic and non-ischemic CRVOs

A

Macular edema

225
Q

2 types of CRVO

A

Ischemic (33%) - Vision is worse than 20/200, poor prognosis. 10DD or more of non-perfusion.

Non ischemic (67%)

226
Q

60% of BRVO occur in what quadrant

A

ST at AV crossing since they both share adventitia

**If it does not occur at an AV crossing, consider a vascular disorder.

227
Q

CRAO has what acuity

A

20/400

UNLESS cilioretinal artery is present to spare the macula (present in 15-30% of patients)

228
Q

Which condition has a cherry red spot

229
Q

How will the retina appear after the patient has a CRAO/BRAO

A

The edema and whitening will resolve in weeks, but the retinal tissue remains non-functional and the patient will have permanent visual field defect.

230
Q

High risk characteristics of developing PDR

A

NNV > 1/4 DD
NVD associated vitreous or pre retinal heme
NVE associated vitreous or pre retinal heme

231
Q

How does macular ischemia appear

A

Enlarged foveal avascular zone (hypo fluorescent)

232
Q

Macular edema can occur at any stage of diabetic ret.

What are the criteria for CSME

A

**based on the presence of retinal thickening within the fovea

  1. Retinal thickening within 500 micrometers (1/3DD) of the fovea
  2. Hard educates within 500 micrometers of the fovea with adjacent retinal thickening
  3. Retinal thickening at least 1DD within 1DD of the fovea

**pt only needs to meet one of these criteria to have CSME

233
Q

A CRAO causes tremendous damage to the retina. How will the Erg of a person who suffered from a CRAO be affected?

A

A wave will remain since this is the PR supplied with blood by the choroid

The B wave will disappear since this is the bipolar & muller cells that are supplied with blood from the CRA

234
Q

Normal diurnal fluctuation in patients with and without glaucoma

A

With- variation of 10mmHg

without- 2-5mmHg variation

235
Q

Difference between PAS and AS

A

PAS- Iris and TM

AS- Iris and K

236
Q

Layers of the lens

A

Nucelus- Embyronic, fetal, juvenile, adult
Cortex
Capsule

237
Q

Fuch’s spots

A

RPE hyperplasia and may be associated with CNV in pathological myopia.

238
Q

Elschnig’s spots in the retina

A

Areas of chorioretinal necrosis due to local occlusion of choriocap

seen in pts with HTN

239
Q

An enlarged blind spot is associated with

A

Papilledema or peripapillary atrophy

240
Q

Two types of primary angle closure glaucoma are :

What causes secondary angle closure?

A

Pupillary block
Plaeeau iris

Secondary angle closure glaucoma is due to mechanisms that push or pull the angle closed such as neo or phagomorphism

241
Q

ORBSCAN studies in patients with KCN show

A

Steepening of the posterior K

KCN is characterized by anterior central or paracentral corneal stromal thinning.

242
Q

Glaukomflecken

A

ASC opacities that develop secondary to necrosis and ischemia of the lens after an acutely elevated IOP

243
Q

Vitreous condition that is pathognomonic for blunt trauma?

A

Vitreous base avulsion

244
Q

Central retinal problems in pathological myopia

A 
Fuch's spots 
Laquert cracks 
ERM 
macular hole
Pavingstone degeneration
245
Q

Most common cause of mortality rate in OIS?

A

Cardiac disease

246
Q

HTN associated secondary conditions

A 
Vascular occlusions (artery pressing on vein --> turbulent blood flow --> thrombus --> CRVO) 
Macroaneurysm 
NAION 
Ocular motor nerve palsies 
Worsening of diabetes
247
Q

What layers of the retina are affected in macro aneurysms

A

Multi level- sub retina, intraretina, preretinal and or vitreous heme
surrounding exudate in a ring
Usually located at AV crossing

248
Q

Symptoms of venous stasis ret/OIS

A

Gradual vision loss
Dull periorbital painm
Amaurosis Fugax
Signs: UNILATERAL dot blot hemes in mid-periph, dilated non-tortuous veins, narrow arteries, NVD/NVE

249
Q

Amaurosis Fugax

A

Type of TIA characterized by transient MONOCULAR vision loss that typically lasts seconds to minutes.
Vision returns to normal
Common cause: carotid artery embolus

250
Q

TIA

A

Temporary neurologic defect due to transient loss of blood flow to the brain
Perfusion restored in less than 24 hours (but usually 15 minutes)

251
Q

Most common cause of hyper viscosity retinopathy

A

Hyperglobulinemia (excess immunuglobulins in blood) making blood more viscous.
This condition is found in Wadenstrom’s macroglobulinemia

252
Q

Interferon retinopathy occurs within ___ months after interferon has started.
Patient without retinopathy should be followed how often?

A

retinopathy will occur within 3-5 months of starting
Follow patient every 6 months
Retinopathy will resolve after treatment is discontinued

253
Q

3 forms of macular telangiectasia

A

Mac Tel Type 1: Congenital and unilateral. May be a variant of coat’s- looks very similar with exudate and hemes.

Mac Tel Type 2: Acquired and bilateral. Middle age and elderly. No exudation. Dilated vessels begin temporal to the macula and may progress to atrophy or macular holes.

Mac Tel Type 3: Occlusive vascular disease

254
Q

Another name for ROP

A

Retrolental fibroplasia

255
Q

ROP occurs in who

What part of the retina is most susceptible

A

premature (32 weeks) or low birth weight (less than 1,500g) who receive oxygen therapy.
Temporal retina- usually finishes development during the 9th month gestation

256
Q

Retinoblastoma

  • What causes it
  • Hereditary?
  • Signs
A

Mutation in Rb tumor suppressor gene
All bilateral cases are hereditary, 20% of unilateral cases are hereditary
Bilateral cases have 50% chance of passing mutation to children

Leuko, strab

257
Q

Leukocoria DDX

A

Coats, toxocariasis, retinoblastoma, ROP

258
Q

Another name for abnormal CHRPE that are associated with FAP

A

RPE hamartomas
Multifocal, bilateral, tear drop shape
70% of people with FAP have RPE hamartomas

259
Q

Orange pigment on a suspicious nevus. What is it and what do you think

A

It is accumulation of lipofuscin. Sign that nevus has progressed to melanoma

260
Q

Size and depth of nevus that is sus

A

Greater than 2mm elevation and 6mm in diameter or close to ONH

Not sus- overlying drusen

261
Q

Risk factors of AMD

A 
75+ 
Female 
White 
Fam Hx 
Light iris 
cig use (2.5x)
Hyperopes (2.5x more risk of exudative AMD)
262
Q

AMD pathogenesis

A

Nutritional factors and light toxicity

263
Q

% of dry vs wet/exudative AMD

A

90% dry, 10% wet

264
Q

Dry AMD

  • Accounts for what % of AMD
  • Appearance
  • What % of people go blind
A

90% of AMD
Characterized by the presence of drusen and RPE abnormalities (mottling, granularity, focal hyperpigmentation)

Most patients do not have severe vision loss but 12% will lose vision due to geographic atrophy

265
Q

4 main risk factors that increases the risk of progression from dry to wet AMD

A

Multiple soft drusen (esp. if confluent)
Focal hyperpigmentation
HTN
Smoking

266
Q

Exudative/wet AMD

  • Accounts for % of AMD cases
  • Common symptoms
  • Characterized by what
  • Incidence of involvement of the fellow eye with wet AMD is estimated to be
A

10% of AMD
Metamorphopia, central scotoma, rapid vision loss
Characterized by CNV that leak blood or plasma sub retinal or sub RPE. PEDs can occur in dry and wet.
After 5 years, risk of condition becoming bilateral is 40-85%

267
Q

How can a PED present in both dry and wet AMD

A

Dry- presents as drusenoid PED

Wet- Serous fluid under RPE

268
Q

Classic vs occult CNV during IVFA patterns

A

Classic is well defined. Fills space during early phases of FA
Occult is not well defined.

269
Q

Histo and toxoplasmosis differences

A

Histo- bilateral, multifocal, due to bird or bat droppings (fungus), choroiditis. No vitritis.
Toxo- Unilateral, single lesion due to undercooked meats or cat poop (parasite). Retinitis and vitritis present.

270
Q

Define pathological myopia based on rx and axial length

A

Rx: Greater than -6.00D

Axial length: greater than 26.5

271
Q

4 stages of macular hole

A

1- impending hole with loss of foveal depression. Yellow spot at fovea.
2- Round, small, full thickness hole with pseudo-operculum.
3- Large full thickness hole with operculum. + Watzke-Allen sign
4- Stage 3 + PVD

272
Q

Signs and symptoms of albinism

A 
Hypopigmentation 
Foveal hypoplasia 
ONH hypoplasia 
MicroK
Nystagmus 
Strab 
Misrouting of the temporal ON fibers through the chiasm

Symptoms: Photophobia, reduced BCVA

273
Q

Most common retinal dystrophy

274
Q

RP
Most common inheritance pattern
most common associated systemic condition

275
Q

Most common hereditary macular dystrophy

A

StargARdt’s
Onset early in life
Autosomal recessive

276
Q

Signs of Stargardts

A

Bilateral yellow flecks
Bulls eye maculopathy (beaten bronze)
Salt and pepper
Acanthameoba of the retina

277
Q

What causes Stargardts

A

AR condition due to a mutation the ABCA4 gene that is a protein responsible for moving all trans retinal from the photoreceptor disc lumen to the cytoplasm.
This leads to degeneration of the PR and RPE.

Variant of same disorder- Fungus Flavimaculatas.

278
Q

Choroidermia

A

X linked recessive
Deficiency in RGG transferase, enzyme used in membrane metabolism.
Progressive, diffuse atrophy of the RPE and choriocap, exposing the underlying sclera.
Night blindness and peripheral vision loss

279
Q

5 stages of Bests

A
  1. Pre vitelliform. No symptoms but abnormal Arden ratio (below 1.8) on EOG.
  2. Vitelliform. 2 egg yolk macular lesions
  3. Pseydohypopyon.
  4. Vitelliruptive. Scrambled egg
  5. End stage. CNV

*Normal ERG, abnormal EOG.

280
Q

Difference between Best’s and adult vitelliform

A

Bests: Onset in childhood

Adults: Onset at 30-50 years. Signs may be similar, but prognosis is better. Minimal metamorphosis, mild acuity loss.

281
Q

Gyrate Atrophy

A

Symptoms by age 10
Bilateral chorioretinal degeneration due to a deficiency in the mitochondrial enzyme ornithine aminotransferase. The ornithine levels in the body become high, damaging choroid/retina.

282
Q

Most common cause of rhegmatogenous retinal detachment

A

Myopia

40% of RRD’s occur in myopic eyes

283
Q

Risk factors for rheg RD

A 
Previous ocular surgery 
PVD 
trauma
Family hx 
lattice 
**Myopia 40%
284
Q

Rheg is defined as

A

Retinal BREAK due to atrophic holes or tractional tears

285
Q

What causes atrophic holes

A

Round, small, full thickness defect not associated with traction.
Chronic atrophy of the retina usually located ST
Poor nutrition, common in high myopes with long eyeballs.

286
Q

Retinoschisis

-2 types and appearances

A

Occurs in 4-7% of the population, bilateral

Bullus elevation is most common
Unlike RD, the retina is immobile 
Absolute VF defect 
Most pts are hyperopes
Shethed retinal vessels occur in the elevated retinal layer of retinoschisis

Typically asymptomatic
Inner and outer wall breaks can occur. Outer breaks are more dangerous and can cause RD.

287
Q

Angioid streak cause

A

Angiod streaks from the disc
Due to damage of the elastic core of bruch’s
50% idiopathic, other causes are systemic

Pseudoxanthoma elastic 
Ehlers dances 
Pagets 
Sickle cell 
Idiopathic 50%
288
Q

APMPPE

A

Acute posterior multifocal placoid pigment epitheliopathy
Viral posterior uveitis
Good prognosis, resolves.

289
Q

Central areolar choroidal dystrophy

A

AD condition with bilateral large areas of geographic atrophy in the macula. Will cause vision in the 4-5th decades. Poor prognosis

290
Q

Senile Choroidal atrophy

A

Choroidal thinning and may cause an exaggerated tigroid fungus appearance as you can see more of the choroidal vasculature.

291
Q

Most common source of optic neuropathy

292
Q

Leading cause of irreversible blindness world wide

293
Q

Risk factors for conversion of ocular HTN to POAG

A 
High IOP 
Race- AA 4x more likely 
Family Hx 
Age 90% over 55 
Thin K
294
Q

Glaucoma risk based on CCT

A

High risk if under 555

Low risk is over 585

295
Q

PXE syndrome demographics

A

Caucasians, Scandinavian descent

296
Q

PDS is common in what demographics

A

Bilateral, caucasians, males, myopes, 30s

297
Q

How can angle recession cause glaucoma

A

Recessed iris and widened CB. Usually due to blunt trauma.

Although angle is wide open, the TM is damaged and can cause glaucoma.

298
Q

NTG

  • What is it
  • Demographics
  • Risk factors
  • SIgns
A

Type of POAG in which NFL is damaged at lower pressures
IOP less than 21 with open angles and glaucomatous nerve damage.

Females, japanese at higher risk

Other risk factors: Vascular disorders: Raynauds, migraines, Low BP, sleep apnea, taking Bp meds before bed (may decrease ocular perfusion pressure)

Pressure on the high end of normal, drance hemes are more common, dense VF defects closer to fixation.

299
Q

Examples of primary and secondary angle closure glaucoma

A

Primary- Pupillary block or plateau iris
Secondary- neovascular, uveitic, congenital, ICE, inflammatory (Fuch’s, posner schlossman, phacolytic hypermature cataract)

300
Q

Plateau iris

A

Anteriorly positioned ciliary processes that push peripheral iris forward into contact with the TM
Convex peripheral iris.
PI will not help

301
Q

Greatest threat to vision during acute angle closure

A

CRAO

IOP is higher than the perfusion pressure of the CRA

302
Q

Topamax/Topiramate is used for what

What can it cause

A

Migraines, weight loss, epilepsy.

Causes choroidal effusion and can cause bilateral angle closure

303
Q

Buphthalmos

A

Enlarged eye, K diameter greater than 12mm.
Occurs in patients with congenital glaucoma
Congenital glaucoma and increased IOP —> enlarges eye

304
Q

ICE syndromes

A

Abnormal corneal endothelium that grows into the angle, causing secondary open angle glaucoma.

Essential iris atrophy-
Chandler’s Syndrome
Iris-Nevus Syndrome (Cogan Reese)

Also abnormal pupil

305
Q

Extent of normal VF

A

100 degrees temporal, 60 superior and nasal, 70 inferior

KMK Ocular Disease (1 decks)

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