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NBEO Part 1 > Ocular Disease > Flashcards

Ocular Disease Flashcards

1
Q

Sclerotic Scatter

A

Get it aligned and then look with naked eye

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2
Q

Optic section

A

Depth

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3
Q

Conical beam

A

Dark adaption

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4
Q

Specular reflection

A

Oculars and beams at equal angel

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5
Q

Indirect illumination

A

Look off to the side

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6
Q

Is blanching in chemical burns bad or good?

A

Bad. Indicates ischemia.

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7
Q

Which is the most bad ocular burn?

A

Alkali. More prevalent too.

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8
Q

Corneal erosion

A

Can have mitotic pupil and mild anterior chamber reaction

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9
Q

Commotion Retina

A

Bruising of the retina OS. White. Resolves in 24-48 hours.

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10
Q

Berlins edema

A

Commotion retina in the macula

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11
Q

Can you do gonio on a hyphema?

A

No. Wait 1 month post injury to avoid re bleed.

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12
Q

Vossius ring

A

Pigment on lens due to lens hitting iris. Trauma.

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13
Q

Iriodialysis

A

Breaking at iris root. Will see a wide band of CB. Monitor for angle recession glaucoma due to damage of TM.

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14
Q

Orbital fracture

A

Most common to occur in maxillary bone in posterior medial. Crepitus, pain, diplopia, restriction. infraorbital hypesthesia, angle recession, etc.

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15
Q

Gonio and orbital fracture

A

None for 4 weeks

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16
Q

Blowing nose and orbital fracture

A

don’t do it for 48 hours after trauma.

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17
Q

Purtscher’s Retinopathy

A

Occurs with CPR or strangulation. Diffuse retinal hemorrhages, exudates, and cotton wool spots.

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18
Q

Choroidal rupture

A

Temporal to ON. Concentric to ONH. Risk of CNVM. Occurs with trauma.

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19
Q

Preseptal cellulitis

A

Most common. Occurs secondary to skin trauma like bug bites or acute hordeolum. no pain to mild tenderness, eyelid edema, no orbital congestion, ptosis, warmth.

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20
Q

Orbital Cellulitis

A

An infection posterior to septum. Can occur from a sinus infection. Will have diplopia, EOM restriction, APD, eye pain, malice, reduced color vision, diplopia.

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21
Q

What can orbital cellulitis cause

A

meningitis or cavernous sinus thrombosis

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22
Q

What can diabetics and immunocompromised get?

A

mucormycosis.

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23
Q

How to tell if preseptal or septal.

A

Preseptal will not have decreased VA, Pain on eye movements, fever, proptosis, EOM restriction.

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24
Q

Thyroid Eye Disease (Graves)

A

Females. MG correlation. TSH receptor antibodies attacking EOMs and can also affect thyroid gland. Tendon sparing. IM SLO.

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25
Q

Signs with TED

A

Unilateral or bilateral proptosis, upper lid retraction, edema. Decreased color vision, EOM restriction, APD.

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26
Q

What is the most common cause of proptosis in middle aged patients

A

Graves

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27
Q

Greatest risk factor for the development of Graves?

A

Smoking

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28
Q

Grading system for TED

A

NOSPECS. No signs or symptoms. Only signs but no symptoms (Dalrymple’s side-lid retraction), Soft tissue involvement (such as lid edema and conj. chemosis) Proptosis EOM involvement. Corneal involvement, Sight loss due to EOM compression.

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29
Q

Von Graffe sign

A

Lid delay on down gaze

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30
Q

Where does the thyroid patient have difficulty looking?

A

No looking up. The IR must relax.

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31
Q

Lochner’s Sign

A

Globe lag compared to lid movement when looking up

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32
Q

Normal exopthalmetry for adults

A

12-22 caucasians. 12-18 Asians. 12-24 African americans.

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33
Q

Carotid Cavernous Fistula

A

Abnormal communication between arterial and venous system. Common with closed head trauma. Build up of venous fluid with bruit, pulsatile proptosis, ocular bruit. Can also have loss of facial sensation or CN 3,4,6 palsy.

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34
Q

What goes through cavernous sinus

A

3,4,6V1,V2. V3 and 7 do not go through.

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35
Q

Cavernous Hemangioma

A

Most common benign orbital tumor in adults

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36
Q

Capillary hemangioma

A

Most common benign orbital tumor in kids

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37
Q

Rhabdomyosarcoma

A

Most common primary pediatric orbital malignancy

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38
Q

Neuroblastoma

A

Most common secondary malignancy. From abdomen.

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39
Q

Optic nerve glioma

A

Most common intrinsic tumor of the ON. NF type 1.

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40
Q

Mengingioma

A

Most common benign brain tumor

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41
Q

Dermoid cyst

A

Often in ST quadrant. Will have proptosis.

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42
Q

Neurofibroma

A

Tumor of astrocytes. Associated with NF.

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43
Q

Neurilemmoma (schwannoma)

A

A benign tumor of Schwann cell

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44
Q

What is seen with orbital tumors commonly

A

Progressive vision loss, APD, proptosis, diplopia.

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45
Q

Idiopathic Orbital inflammatory syndrome (orbital Pseudotumor)

A

Young to middle aged. Inflammatory process that can affect anything in the eyes. Have acute unilateral red eye, diplopia, or decreased vision. Can have fever, nausea, and vomiting. Proptosis or EOM restrictions, perioribital swelling, CHEMOSIS, lacrimal gland enlargement, increased IOP, decreased corneal sensation. Tendons WILL be inflamed.

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46
Q

Chemosis

A

Typically with allergic symptoms. However, if no itching and uliateral consider Idiopathic orbital inflammatory syndrome

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47
Q

Tolasa hunt syndrome

A

idiopathic orbital inflammation that affect cavernous sinus or SOF. Acute and painful exopthlamplegia to ipsilateral palsies on CN 3,4,6. Loss of sensory can also occur.

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48
Q

What do you suspect with bilateral orbital psuedotumor?

A

Systemic vasculitis.

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49
Q

Ocular Rosacea

A

Affects sebaceous glands (meiobomian). Has telengectasia. Can cause Ocular surface disease (phlyctenules, SPK, corneal neo, staph marginal keratitis) and dry eye syndrome.

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50
Q

Contact dermatitis

A

Type 4 reaction. Acute periorbital swelling, redness, and itching. 24-72 hours.

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51
Q

Ocular Cicatrical Pemphigoid

A

Type II reaction. Cell-mediated. Old female. conj. basement membranes are attacked. Symblepharon (bulbar to palpebral), ankyloblepharon, conj fibrosis and scaring. Destroys meiobomina, goblet, and accessory lacrimal gland=severe ocular surface disease.

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52
Q

What drugs can cause OCP

A

Pilocarpine, epinephrine, Timolol (PET)

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53
Q

Stevens-Johnson Syndrome

A

Type III hypersensitivity. Affects mucus membranes. Drugs (sulfa) or infectious agents can cause.

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54
Q

Stevens-Johnson Syndrome Acute signs/symptoms.

A

Will have a systemic prodrome of fever, malaise, and vomiting. Followed by skin lesions and ocular lesions (pseudomembranes, bilateral conj, endopthalmitis)

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55
Q

Chronic Steven-johnson

A

Entropion, ectropion, trichiasis, Mebomian gland damage, symblepharon, conj. keratinization. Ulcers, neo, scars.

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56
Q

Seborrheic vs. staph belph

A

Seborrheic has less lid inflammation, more oily, greasy scales, and more eyeglash loss and misdirected growth.

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57
Q

Chalazian

A

Chronic, steril inflammation of meiobomian gland. Ask about acne rosacea or seborrheic dermatitis

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58
Q

Hordeolum

A

Acute and hot. Ask about acne rosacea and seborrhea dermatitis. An acute staph infection of the eyelids

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59
Q

Internal hordeolum

A

meiobmoian glands

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60
Q

External hordolum

A

Glands of Zeiss or moll

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61
Q

Floppy Eye Lid Sydrome

A

Associated with Sleep apnea, NAION, normotensive glaucoma

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62
Q

Benign Essental Belpharospasm

A

Both eyes. Orbitularis, procures, and corregatio.

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63
Q

Meige syndrome

A

BEB and lower facial abnormalities

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64
Q

Myokymia

A

orbicular oculi only. Unilateral.

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65
Q

Basal Cell Carcinoma

A

Telengectasia. Rodent ulcer. Most common. Lower and medial most common

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66
Q

Squamous cell carcinoma

A

Comes from actinic keratosis. No telengectasia. More likely to metastasize

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67
Q

Order of most likely to metastastize

A

Malik mel–>Sebaceous gland–>squamous–>basal

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68
Q

Keratocanthoma

A

Look like BCC or SCC but will grow and then shrink.

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69
Q

Sebaceous gland carcinoma poor prognosis

A

Greater than 2mm

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70
Q

Dacroadentitis

A

Acute–>staph. Chronic–>sacred. S-shaped ptosis in acute. Can have swelling of preauricaular lymphadopenathy.

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71
Q

Canaliculitis

A

Pouting punch. Most common culprit is Actinomyces isralies (yellow sulfur granules). Will have a smoldering red eye. Will have pus or blood with palpitation.

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72
Q

Dacryocystitis

A

Lacrimal sac infection. Often occurs with nasolacrimal duct obstruction (kids) or involutional stenosis (aging). Selling below the medical canthal tendon. More pain and swelling than with cannaliculitis.

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73
Q

What to do with dacryocystitsi

A

Do not refer for treatment or irrigate. Start treatment first.

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74
Q

Nasolacrimal duct stenosis. M or F.

A

More common in females

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75
Q

Jones 1 testing

A

Put in dye and should drain out. Positive=patent=good.

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76
Q

Jones 2 testing

A

Nasolacrimal irrigation with saline following a negative Jones 1 test.

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77
Q

Conj. cyst

A

common benign fluid filled sac on conj.

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78
Q

Conj concretions

A

Superficial deposits in conj.

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79
Q

Conjunctival nevus

A

Presents puberty or early adulthood. Inclusion cysts are diagnosis for conj. nevus.

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80
Q

PAM (primary acquired melanosis)

A

Older patient. Flat and indistinct. Premalignant tendencies.

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81
Q

Conj. melanomas

A

happen in caucasians. Come from PAM. Thickness of lesion is prognosis. Metas. to liver.

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82
Q

Conjunctival intraepithelial neoplasm

A

Most common conj. malignancy. Can progress to squamous cell carcinoma.

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83
Q

PAM vs. CIN

A

PAM goes to melanoma. CIN goes to squamous cell carcinoma.

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84
Q

Conj. squamous cell carcinoma

A

Rare and slow growing. Comes from CIN. Caucasians.

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85
Q

Conj. Granuloma

A

Inflamed area within the conj. stroll tissue. Occurs with retained FB etc. Symptomatic or FB symptoms

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86
Q

Types of bacterial conjunctivitis

A

Simple bacterial conjunctivitis or Gonococcal

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87
Q

Cause of simple bacterial conjunctivitis in kids

A

h. influenza

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88
Q

Cause of simple bacterial conjunctivitis in adults

A

s. aureus or s. epidermis

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89
Q

Simple bacterial conjunctivitis

A

Acute onset of redness that usually begins in one eye and become bilateral. Eyelids stuck together upon wakening. Symptoms typically subside in 10-14 days without treatment. Discharge is typically mucopurulent. Corneal signs and pre auricular lymphadenopathy are rare.

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90
Q

Among all age groups what is the most common cause of simple bacterial conjunctivitis

A

S. aureus.

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91
Q

Gonococcal conjunctivities

A

hyper acute purulent discharge. conj. chemises with pseudomembrane, papillary reaction, pre auricular lymphadenopathy, and tender and swollen eyelids. Also evaluate for chlamydial infection.

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92
Q

How is gonorrohea conjunctivitis different than simple bacterial conjunctivitis?

A

G. has pseudomembrane and pre auricular lymphadenopathy.

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93
Q

Adenoviral conjunctivititis

A

Include Acute nonspecific follicular conjunctivitis, pharyjgoconjunctival fever, and epidemic keratoconjuntivitis. Most common from upper respiratory tract infections. Highly contagious for 12-14 days.

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94
Q

Acute non-specific follicular conjunctivitis

A

Most common. Diffuse red eye, follicles and mild discomfort. Mild cold.

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95
Q

Pharyjgoconjunctival Fevere (PCF)

A

Swimming pool conj. Very contagious. Follicular conj, mild low grade fever, and sore through. Corneal rarely involved.

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96
Q

Epidemic Keratoconjunctivitis

A

Most serous. Pain and corneal involvement occurs. Clinical symptoms occur 8 days after exposure. SPK is common during acute phase and Supepitelial infiltrates are common in the 3rd week when the active portion of the disease has stopped. Pre auricular lymphadenopathy is present and almost always has pseudomembranes.

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97
Q

What is pathognomonic for EKC

A

Palpable node in patient suspected of adenovirus. Will also has pseudomembranes.

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98
Q

Molluscum Contagiosum

A

Rare. DNA Pox virus. Umbilicate waxy nodules. If see multiple think HIV.

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99
Q

Allergic Conjunctivitis

A

Type 1 hypersensitivity (both seasonal and perennial). Chemises, papillae, itching, tearing.

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100
Q

Vernal Keratoconjucntivitis

A

Very rare and affects males under the age of 10. Occurs 2-10 years before resolving around pubutery. Those predisposed to atopic conditions. Seasonal outbreak with warm month.

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101
Q

Classic signs with Vernal

A

prominent papillae on limbus (truants dots) or upper conj (cobblestone). Can also have corneal involvement that begin the SPK and eventually coalesce into late erosion with shield ulcers.

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102
Q

Atopic keratoconj. vs. vernal

A

VKC prominently on conj and cornea. Allergic on outer eyelids and skins.

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103
Q

Atopic Keratoconj.

A

Common in young to middle age adults with a history of atopic conditions. AKC in not seasonal. Type 1 + 4. Prominent outer eyelids, dennie’s line (extra crease under eyes), and atopy shiners. Papillae are classically more inferiorly. Keratinous more common.

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104
Q

What is interesting about the papillae in Atopic keratconj.

A

Inferior more common.

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105
Q

Papillae

A

Occur with allergies, bacteria, and nonspecific reaction. PAPILLAE. is vascular.

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106
Q

Follicues

A

Lymphocytes. CHAT. Chlamydia, Herpes, Aden, Toxic.

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107
Q

GPC

A

Contact lens wear. Mechanical trauma and immune response to contact lens deposits. Symptoms more severe when remove lenses.

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108
Q

GPC is characterized by papillae that are ____

A

> 1 mm for giant papillae by >0.3 mm in GPC

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109
Q

Corneal Neovascularization

A

Chronic hypoxia. Watch for superior panned.

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110
Q

Corneal neovasculaization are larger than _____ mm

A

1.5

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111
Q

Corneal warpage

A

Alteration in corneal shape due to cl.

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112
Q

Superior limbic keratoconjunctibitis

A

occurs with CL, CL hypersentivitity, and TED. Papillary reaction and corneal filaments are rare when due to CL hypersensitivity to solution vs. TED.

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113
Q

3 and 9 o’clock staining

A

Most common complication of CL wear. Due to low riding cl.

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114
Q

Complication of low riding cl

A

3 and 9 staining

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115
Q

complication of high riding cl

A

corneal warpage

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116
Q

Superior Epithelial Arcuate Lesion (SEAL)

A

Too tight CL.

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117
Q

Chlamydial Adult Inclusive Conjunctivitis

A

Rare. D-K. Chronic smoldering. 5-14 days after inoculation. Have acute follicular conj that become chronic. Can persist a year if not treated. Have follicles and inferior palpebral conjunctivitis. Pre auricular lymphadenopathy. Corneal involvement can also occur.

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118
Q

Ophthalmia Neonatorum

A

Acute conj in newborns from any source. Chalmydia is the most common cause

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119
Q

Chlamydial Trachoma Conjunctivitis

A

Serotype A-C. Trachoma is the leading cause of blindness. Early have follicular conjunctivitis on the superior tarsal conjunctiva, lymphadenopathy, and mild superior pants. late they have arlt line (white scarring of the superior lid) and herberts pits (depression on the Limbal conj after resolving gimbal follicles) Leads to distortion of the lids and ulceration due to trichiasis.

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120
Q

Phlyctenular Keratoconjunctivitis

A

Common in teenage years and females. Type 4 hypersentivitiy. Tearing foreign body sensation, and itching occurs. Can be located on conj (pink and fleshy and near limbs) or cornea (near limbs and white and fleshy with adjacent conj injection).

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121
Q

What conditions should you ask about with phlyctenual keratoconjunctivitis

A

TB, Blepharitis, or cane rosacea.

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122
Q

Ligenous Conjunctivitis

A

Rare. Starts in childhood. Associated with systemic plasminogen deficiency. Thick, white, woody membrane plaques. Plasminogen does the breakdown of fibrin.

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123
Q

Parinaud’s Oculoglandular SYndrome

A

Cat scratch fever is number one. Tularemia, TB, and Syphilis too. Red eye, foreign body, Unilateral granulomatous follicular palpebral conj with pre auricular and submandibular lymphadenopathy.

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124
Q

Why is Parinaud’s oculoglandar syndrome easy to catch?

A

It is unilateral granulomatous uveitis and very swollen lymph nodes.

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125
Q

Phthiriasis Palpebrarum

A

Crab louse on lash. Unilateral or bilateral. Range from mild itching to blurred vision. Mild to severe chronic follicular conjunctivitis and preauriciular lymphadenopathy.

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126
Q

How to tell lice from demodex

A

Lice on lash. Demodex in lash.

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127
Q

Pterygium/Pinguculum

A

UV and chronic dryness are number one cause.

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128
Q

Pingueculum

A

yellow-white deposit adjacent to the limbus

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129
Q

Pterygium

A

Fibrovascular growth of bulbar conj that extend into the cornea and destroys Bowmans. Lead to WTR astigmatism.

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130
Q

Stocker’s line

A

Iron deposits on leading edge of ptergyium.

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131
Q

Episcleritis

A

Normally sectoral. Recurrence is common. Unilateral. Can get with UCRAP or Idiopathic. Mild discomfort.

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132
Q

Scleritis

A

F>M. Divided into necrotizing and non-necrotizing. Very painful. Thin sclera. Frequently bilateral.

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133
Q

Non-necrotizing

A

Diffuse: most common. Nodular: deep focal painful injected immobile nodule

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134
Q

Nectortizing with inflammation

A

Worst kind. Occurs with severe autoimmune disease.

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135
Q

Nectrozing w/o inflammation

A

Slceromalcia Perforano. Occurs in patients with RA. Complete lack of symptoms.

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136
Q

Scleritis vs. episcleritis

A

Scleritis is more serious. Episcleritis doesn’t have much pain. Scleritis has a blue hue. Scleritis is bilateral and diffuse. Scleritis is much less common.

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137
Q

How to differ scleritis from epi with phenylephrine

A

2.5% phenyl will blanch with conj. with episcleritis. 10% will blanch the superficial episcleral vessels (episcleritis less red). Scleritis will still be red.

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138
Q

Axenfeld’s nerve loop

A

Congenital abnormality where ciliary nerve loops are visible in sclera.

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139
Q

Acute vs. chronic uveitis

A

Acute is 3 weeks or less. Chronic is greater than 3 weeks.

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140
Q

What do worry about with uveitis

A

Cataracts, CME, PS, PAS.

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141
Q

Early what will happen with the IOP

A

decreased

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142
Q

What else can you have in uveiis

A

hypopyon, keratin precipitates.

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143
Q

What suggests granulmoatous

A

Mutton fat KPs and iris stroll nodules

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144
Q

Mutton Fat Kps

A

collection of macrophages and look greasy

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145
Q

Koeppe Nodules

A

WBC at pupillary margins. Granulomatous and non

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146
Q

Buscacca nodules

A

WBC within any part of stroma. Granulomatous.

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147
Q

Common Cause of granulomatous uveitis

A

Sarcoid, TB, Rarely sphyllis

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148
Q

Common cause of non-granulomatous uveitis

A

idiopathic, UCRAP.

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149
Q

Cyclic Membranes

A

Can be present in chronic uveitis. Fibrovascular membranes that extend into the ciliary body into the posterior chamber and involve lens

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150
Q

Common cause of posterior uveitis

A

toxo. Unlit.

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151
Q

Interstitial keratitis

A

stromal inflammation without primary involvement of the epithelium or endo. Get neo in stroma. Can get ghosting in late.

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152
Q

Causes of IK

A

syphyllis, tuberculosis, herpes simplex (SHiT)

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153
Q

Congenital trid

A

hutingtons teeth, deafness, IK.

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154
Q

Pars planitis

A

chronic intermediate uveitis characterizes by inflammation over the pars plans (snow banking). Not associated with systemic conditions.

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155
Q

Does posterior uveitis have to have WBC?

A

NO.

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156
Q

Most common cause of posterior uveitis

A

Toxo

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157
Q

If mother gets pregnant after infected by toxo will baby be infected?

A

NO

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158
Q

Toxo presentation

A

Will commonly have one chorioretinitiis scare with overlying vitritis. Headlights in fog.

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159
Q

Histo presentation

A

Fungal infection. Choroiditis with no vitritis. Multifocal punched out lesions in periphery, peripapillary maculopathy. NO VITRIFIES.

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160
Q

Stellate KP’s

A

Fuch’s heterochromic iritis and hepetic uveitis

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161
Q

Sarcoidoisis

A

Granulomatous uveitis. Diffuse vitiates with retinal vasculitis (cotton ball droppings)

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162
Q

Cytomegalovirus

A

Ocular infection in HIV. White patches of necrotic retina with hemorrhagic retinitis and vascular sheathing.

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163
Q

CMV vs. toxo

A

CMV has less vitirits and more intravitral hemorrhage.

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164
Q

SE of Sarcoidosis

A

dacryadentisis, DED, Bells, vasculitis and vitritis, and ON disease.

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165
Q

Coloboma

A

Most often IN. Failure of embryonic tissue to close.

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166
Q

Where do iris malignancy occur?

A

Melanocytes in the strma

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167
Q

Dellen

A

Dehydrated stroma. Due to elevated tissue next to it.

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168
Q

Filamentous Keratopathy

A

Mucus and epithelial cells. Caused by prolonged inflammation and DED>

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169
Q

SPK

A

BAK causes. Non specific inflammation of he cornea. Basically everything causes

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170
Q

Pathophysiology behind SPK

A

With the epi pump the K senses when 78% water is not in stroma. The Na is pumped out, K to the A, and Cl with water out. Loss of much of K can lead to cell death and SPK.

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171
Q

Thygeson’s superficial punctate keratopathy

A

20 year old with FB sensation but quiet eye. Have bilateral central opacities that look like bread crumbs and are intraepithelial and raised (also with Herpes). May be viral. Attacks and resolutions. Lasts for 10-20 years.

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172
Q

Neurotrophic keratatitis

A

Damage to V1. Big ulcer with no pain. V1 is not telling epithelium to regenerate.

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173
Q

RCE

A

Due to past abrasion or EBMD. Pain worse upon waking up.

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174
Q

Thermal keratopathay

A

SPK 6-12 hours after exposure to Vitamin C (less than 300). Affects epithelium and bowman.

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175
Q

Most common type of DED

A

Evaporative intrinsic

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176
Q

Aqueous deficiency dry eye

A

Sjogrens or non-sjogrens.

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177
Q

Sjogrens

A

Can be primary or secondary (triad)

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178
Q

Non-sjogrens dry eye

A

Can be primary (caused by age and ducts just not working as well) or secondary (something else affecting ducts like pemphigoid)

179
Q

Criteria of DED

A

Hyperosmality (<308) and TF instability with symptoma

180
Q

Tests for aqueous defiency

A

Schirmer, Lacrimal lake evaluation, phenol red

181
Q

Schirmer one

A

No anesthetic. Looks at main and accessory tears. Normal is >10 mm in 5 minutes.

182
Q

Schirmer two

A

Anesthetic so only looks at basal tears. Normal >5 mm in 5 minutes.

183
Q

Phenol red test

A

Use a phenol red string. A normal result is >10 mm of wetting after 15 seconds.

184
Q

Flurzscene vs. lissamine/rose bengal

A

Flurzscene pools in epithelial defects. Lissamine and bengal stain dead and devitalized tears

185
Q

Evaporative DED

A

More common. Can be intrinsic or extrinsic

186
Q

Intrinsic Evaporative DED

A

Due to MGD

187
Q

Extrinsic Evaproative DED

A

Due to seoncdary causes damaged MG. i.e. cl wear or vitamin A deficiency.

188
Q

Vitamin A deficiency

A

Need for glycocalyx so cause Evaporative DED and can cause Bitots spot on the conj

189
Q

Keratoconus

A

Corneal ectasia. + family history with AD. Begins around puberty. Damage to bowman layer and corneal thinning. Results in stroll collagen fibril displacement and corneal thinning and protrusion (due to MMP). T-DOME associated.

190
Q

What ring do you get with Keratoncus

A

Fleisher

191
Q

Vogt’s striae

A

Late in keratoconus. Vertical lines deep in stroma

192
Q

Munson’s sign

A

lower lid protrusion with downsize with Keratoconus.

193
Q

Rizzuti’s sign

A

Conical reflection on the nasal cornea when light shown temporally with keratoconus.

194
Q

Hydrops

A

Tears in descemets. Occurs with all corneal ecstaias.

195
Q

Pellucid Marginal Degeneration

A

Less symptoms. Doves on cornea. High ATR astigmatism. Can also get hydrops

196
Q

Keratoglobus

A

Thinning of the cornea present at birth

197
Q

Names for Epithelial Basement membrane dystrophy

A

Map-dot, Cogans, Fingerprint, ABMD.

198
Q

What is the most common anterior dystrophy

A

EBMD.

199
Q

EBMD

A

Most commonly. Slightly more common in F. Abnormal epithelial adhesion with excessive BM production which causes maturing epi to become trapped below. Will have negative staining (around elevation) of map-lines, dots, and/or fingerprints.

200
Q

Meerman’s Dystrophy

A

AD. Rare. Extensive clear intraepithelial cysts.

201
Q

Reins-Buckler Dystrophy

A

Affects Bowmans development and replacement with collagen. Bilateral sub-epithelial gray opacities that are more central.

202
Q

Why is Macular dystrophy Unique

A

Only AR corneal dystrophy

203
Q

Macular dystrophy

A

Stromal dystrophy. AR. Have mucopolysaccharide deposits in stroma and progresses to all of cornea.

204
Q

Granular Dystrophy

A

AD. Stromal dystrophy. Hyaline deposits. Rarer erosions.

205
Q

Avellino dystrophy

A

Rare granular dystrophy variant. Granular and lattice deposits.

206
Q

Lattice Dystrophy

A

AD stromal dystrophy. Amyloid deposits in stroma.

207
Q

What do granular, avenillo, and late dystrophies have in common

A

All are a result of TGFB1 mutation. Macular is NOT.

208
Q

Schneider’s Dystrohy

A

Stromal dystrophy. Correlated with high cholesterol.

209
Q

Fuchs Endothelial Dystrophy

A

AD. More common in old females. Posterior lamina is produced excessively (guttate) and results in decrease in endo cell density and pleomorphism and polymegthism. If less than 500 cells will get stroll edema with chance of bullae.

210
Q

Posterior Polymorphous Dystrophy

A

AD. Metaplasia of endocells where they can migrate into the angle and cause glaucoma. Can have vesicles (hallmark) band lesions, and diffuse opacities.

211
Q

Characteristics of Dystrophies

A

bilateral, symmetric, central, no neo, associated family history

212
Q

Anterior Dystrophies

A

Cogans (EBMD), Messman’s, Reis Buckler

213
Q

Stromal Dystrophies

A

Macular (AR), Granular (Avellino), Lattice. TGFB1 associated last three. Schneider’s.

214
Q

Posterior Dystrophies

A

Fuchs, Posterior polymorphic dystrophy.

215
Q

Megalocornea

A

X linked. Males. 13 mm or greater HVID

216
Q

Microcornea

A

Less than 10 mm HVID. Almost always hyperopic.

217
Q

Cornea plana

A

Very flat cornea.

218
Q

Haab’s Striae

A

horizontal lines that form due to cracks in descemets with congenital glaucoma.

219
Q

Posterior Embryotoxon

A

Anterior displaced Schwalbe’s line.

220
Q

Axenfeld Anomaly

A

PE+ angel abnormalities + increased glaucoma risk

221
Q

Rieger anomaly

A

PE + angle anomalies + increased glaucoma risk + iris stromal abnormalities

222
Q

Rieger Syndrome

A

PE + angle abnormalities + increased glaucoma risk + Iris stromal abnormalities + systemic abnormalities

223
Q

Peters Anomaly

A

Rare condition where patients are born with white central corneal opacities with iris adhesions

224
Q

What is an ulcer

A

Epithelial defects with SEI

225
Q

How to tell sterile from infectious ulcer

A

Sterile will have very small stain. Bacterial will stain entire lesion.

226
Q

Bacterial Keratitis

A

Most common infeciotus keratitis. Common with CL wear.

227
Q

Pseudomonas Aeuruginosa

A

The most common gram - associated with bacterial keratitis. Has a thick green discharge, hypopyon, a dense stromal infiltrate, and can perforate the cornea within 24 hours.

228
Q

Who can invade an intact cornea epithelium

A

CNHL. Corynebacterium diphtheria, Neisseria Gonorrhea and meningitides, Haemophilus, and Listeria.

229
Q

How will an infectious corneal ulcer stain with fluorescent

A

1:1.

230
Q

How will a sterile corneal ulcer stain with fluorescne

A

Less than 1:1

231
Q

Fungal Keratitis

A

Trauma with vegetative matter.

232
Q

Agar for fungal

A

Sabouraud’s agar. SO MUCH FUN ON MY SAB.

233
Q

Candida

A

Normal floral. If see an infection think immunocompromised or chronic corneal disease. Similar appearance to bacterial ulcer.

234
Q

Aspergillus and Fusarium

A

Culprit with vegetative trauma. Feathery borders with starlight lesion.

235
Q

Acanthamoeba Keratitis

A

Rare parasitic infection associated with inadequate contact lens hygiene. Can invade if epithelium is damaged. Culture performed with non-nutrient agar with heat killed E. Coli. Starts with intense pain with barely any signs and then can have radial keratoneuritis with a ring ulcer.

236
Q

Chocolate agar plates

A

For Haemophils and Niseria

237
Q

Herpes Simplex Virus

A

Can affect the epithelium, Stroma, or Endo

238
Q

Epithelial disease due to HSV

A

Due to direct invasion of corneal epithelial cells by HSV. Can have corneal vesicles (SPK like), Dendritic ulcers, Geographic ulcers (similar to dendritic ulcer but wider), and marginal ulcers (close to limbus).

239
Q

Dendrite staining in HSV

A

Edges stain with rose bengal. Flurzscene pools in dendrite.

240
Q

Neurotrophic Keratophaty

A

Also occurs with HSV. Can have a neurotrophic ulcer as well. Differed from geographic as it has smooth borders and inferior.

241
Q

Stromal disease with HSV

A

IK (also with SHiT Syphilis and TB). Infiltrate in stroma with diffuse neovascularization, an immune rings, stomal thinning, and scaring. No involvement of the epi or endo.

242
Q

Necrotizing Stromal keratisi

A

Rare keratitis from direct invasion of stroma. Results in severe inflammation in stroma and perforation.

243
Q

Endothelium disease with HSV

A

Disciform Keratisis. Secondary stromal edema due to immune reaction within endo. Focal, disc-shaped, stromal edema with overlying keratic precipitates. No neovascularization in stroma.

244
Q

Herpes Zoster Virus

A

Chickenpox is first infection.

245
Q

Pre-zosters

A

Prodrome. Want to tx here so less chance of post.

246
Q

Active zosters

A

Does not cross the midline. Have a pseudo dendrite. Uveitis. Hutchinson’s sign.

247
Q

Post Zosters

A

Pain that lasts one month after Zosters.

248
Q

Staining in HSV and HZV

A

HSV will stain the entire dendrite with flurzscene and edges with lissamine. HZ with stain borders only as it is elevated.

249
Q

Mooren’s Ulcer

A

Rare condition. Older Men. No systemic disease associated. Typically uliateral. Painful vasculitis of the gimbal blood vessels that leads to necrosis and peripheral ulcerative keratitis that goes around. Associated with hepatitis C viral infection or hookworms. Classic presentation is unilateral peripheral crescent shaped gray infiltrate that progresses to an ulcer.

250
Q

Staph Marginal Keratitsi

A

Very common. Due to body attacking staph aeurus. on lids. Type III hypersentitivy. Will have infiltrates at 2,4,8,10.

251
Q

Collagen Vascular Disorders

A

Peripheral marginal ulcers or thinking due to collagen vascular disorders like RA, Lupus. ETC.

252
Q

Fleshier ring

A

Iron at base in keratoconus

253
Q

Hudson Stahli line

A

Iron found at the junction between the middle and lower third of cornea

254
Q

Stocker’s line

A

Iron on the leading edge of ptergium

255
Q

Ferry’s line

A

Iron with bleb

256
Q

Band keratophaty

A

Calcium deposits within Bowman’s layer

257
Q

Terrin’s marginal dystrophy

A

30 year old male. SN bilateral thinning with vascular that can lead to perforation. Idiopathic.

258
Q

Salzman

A

60 YOF. Wearing a blue bowtie. Blue nodules on bowman. Hyaline deposits.

259
Q

Band Keratopathy

A

Calcium deposit in bowmans. Can be due to uveitis, DED, trauma, gout, and hyper calcium, sarcoidosis, and renal failure. Normally asymptomatic. Swiss cheese pattern.

260
Q

Unilateral arcus

A

Rare and associated with carotid disease on the side WITHOUT the Arcus.

261
Q

Crocodile Shagreen

A

Can be in Descents or Bowmans.

262
Q

Corneal Farinata

A

Flour dust in the cornea. Due to aging or AD.

263
Q

How many does do sCL wearer need to be out of their lenses before surgary

A

3-14 days

264
Q

How long do topic soft and rigid CL need to be out of their lenses before surgery

A

14-21 days

265
Q

how many um per Diopter

A

15

266
Q

How much stromal bed should be left after LASIK

A

250

267
Q

Conductive Keratopathy

A

Used to shrink collagen with presbyopia, low hyperopia, and residual astigmatism after other surgeries. Must be repeated in 3 years.

268
Q

Infections with refractive surgery

A

typically frame + or mycobacteria.

269
Q

Complications in steep corneas

A

button holes

270
Q

complications in flat corneas

A

free caps

271
Q

When can you fit patients in CL after refractive surgery

A

8-12 weeks

272
Q

Diffuse Lamellar Keratitis (DLK or Sands of the Sahara)

A

fine, granular sand like parties between the flap and stroma.

273
Q

What is the most common complication of LASIK

A

Epithelial ingrowth

274
Q

Epithelial ingrowth

A

Occurs 1 month post op. Faint gray line or deposits near the flap.

275
Q

Retreatment

A

Occurs in 3-6 months post. 0.75D or more in an unhappy patient or worse than 20/30

276
Q

Nuclear Sclerotic

A

Most common aging cataract. Can cause a myopic shift (helps with near vision)

277
Q

Cortical cataract

A

Radial spoke like opacities that commonly induce a hyperopic shift.

278
Q

Anterior sub capsular cataract

A

Directly under the anterior lens capsule

279
Q

Posterior sub capsular cataract

A

located directly in front of the posterior lens capsule. Affects near vision worse than distance. Occurs with systemic or topical steroids.

280
Q

Infant cataracts

A

rubella and galctosemilia

281
Q

Early cataracs

A

MAD wilson. Myotonic dystrophy, atopic dermatitis, DM. Wilson.

282
Q

Epicapsular stars

A

Residual remnants of the tunica vasculosa lentil and are small star shaped pigment deposit on the anterior lens capsule.

283
Q

Potential Acuity Meter (PAM)

A

Look at how much the acuity is affected by cataracts

284
Q

Brightness Acuity Testst (BAT)

A

Look at glare and cataracts

285
Q

Average axial length

A

24 mm

286
Q

How much RE does 1 mm correspond to

A

3D

287
Q

What meds should you report before cataract surgery

A

Flomax, anticoagulants, prostaglandins.

288
Q

Intracapsule cataract extraction

A

All of cataract and capsule. Must wear very large glasses to correct.

289
Q

Extracapsule cataract extraction

A

Remove lens and keep capsule. Put lens back in. Need a big inceision

290
Q

Acute Post-operative Endophthalmitis

A

Very serious. Most are staph epidermis.

291
Q

Delayed Post-operative Endopthalmitis

A

Within a week to a month after surgery. Fungal is commonly delayed.

292
Q

Toxic anterior segment syndrome

A

A sterile inflammatory rections due to chemical exposure during surgery. 12-48 hours after surgery. Must rule out endopthalmitis.

293
Q

Most common SE in cataract surgery

A

PCO, and CME.

294
Q

Posterior Capsule Opaciciciation (PCO)

A

Commonly occur 2-6 months post. Due to equatorial epithelial cells migrate to the posterior capsule

295
Q

Elshnig Pearls

A

The PCO seen in children

296
Q

Irvine-Gas’s Syndrome

A

CME due to cataract surgery. 6-10 weeks following surgery.

297
Q

CME on FA

A

petaloid leakage.

298
Q

Elevated IOP in Cataract sugery

A

Due to retained viscoelastic or steroid responder.

299
Q

3 mirror lens

A

Only reversed.

300
Q

D mirror

A

Angle

301
Q

Trapezoid

A

Equator

302
Q

Square

A

Ora

303
Q

Asteroid Hyalosis

A

Normal with aging. Does not affect the Vision. Calcium-phosphate in the vitreous.

304
Q

Synthesis Scintillians

A

Rare and occurs after vitreous hemorrhage, surgery, or uveitis. Unilateral golden brown cholesterol crystal.

305
Q

Posterior Vitreous Detachment

A

Vitreous syneresis causes vitreous to detach from retina. Can cause ERM, vitreomacular traction, macular hole, weiss ring, retinal heme, retinal breaks (atrophic hole or tractional tear).

306
Q

Shafer’s sign

A

retinal pigment epithelium in the vitreous after a retinal tear.

307
Q

Causes of PVD

A

Age, DM, Myopia

308
Q

Pre-retinal/Viteral hemorrhage

A

Can occur with pre-retinal neovascularization with a PVD. Ask about DM and HTN. Do a B-scan if the vitreous cannot be seen.

309
Q

CRVO

A

Risk with HTN, diabetes, cardiovascular disease, open angle glaucoma. The artery compresses the vein and cause turbulent blood and a thrombus forms. Will have painless unilateral vision loss. Will then release VEGF and can cause neovasclarization in the angle (90 day glaucoma)

310
Q

CRVO and POAG

A

If get a CRVO the NFL is poor and will be poor in the other eye. Check the other eye for POAG.

311
Q

Collateral Veins

A

Occur several weeks to months. Help to get blood out of the eye.

312
Q

Threatens to vision with CRVO

A

macular disease and neovascular glaucoma.

313
Q

Ischemic and non-ischemic CRVO

A

Ischemic is 10 disc diameters

314
Q

Where are BRVOs most common

A

ST.

315
Q

What do you do if BRVOs occur at areas that are not AV crossings

A

Evaluate for vasculitis.

316
Q

CRAO

A

Amaurosis fugal-unilateral vision loss. Common from the heart.

317
Q

Which does CRAO come from

A

Embolis

318
Q

Where does CRVO come from

A

Thrombus

319
Q

Which emboli is worse

A

Calcific. It is bigger so obstructs more and more likely and from the heart.

320
Q

Hollenhurst

A

Cholesterol emboli. From carotid arty and smaller so not as scary as calfic.

321
Q

What tests should you run on a patient with CRAO or BRAO

A

Carotid doppler and EKG.

322
Q

Giant cell arteritis

A

Can also cause a CRAO.

323
Q

Cilioretinal artery

A

Can save vision with a CRAO.

324
Q

Signs with CRAO

A

Superficial whitening of the inner retinal layers with a cherry red spot and an APD. Will return to normal color after perfusion is restored.

325
Q

When do you get irreversible damage

A

After 90 minutes.

326
Q

Do you get 90 day glaucoma with CRAO

A

no as retina is dead so doesn’t release VEGF

327
Q

BRAO

A

patient will have a permament VF loss.

328
Q

When to see a patient with no diabetic retinopathy

A

1 year

329
Q

Mild to moderate retinopathy when do you see back

A

6-12 months

330
Q

NPDR or PDR

A

Repeat every 2-4 months

331
Q

What is the greatest risk factor for patient with type I diabets

A

Duration of disease

332
Q

Risk of Mild progressing to PDR

A

5%

333
Q

Risk of Moderate progressing to PDR

A

15%

334
Q

Risk of severe processing to PDR

A

50%

335
Q

Rules for Severe NPDR

A
  1. 4 quadrants of dot blot hemes. Venous needing in 2 quadrants. 1 quadrant of IRMA. Must meet one of the criteria.
336
Q

Very severe NPDR

A

75% chance of progression. Two or more of the criteria in 4.2.1 rule. 4 dot blot heme quadrant, 2 venous needing, 1 IRMA.

337
Q

High risk for vision loss with PDR

A

Neo of the disc greater than 1/4 within 1 DD, NED or NEA with sub retinal or intravitreal heme.

338
Q

Threats to vision with diabetic retinopathy

A

macula or neo.

339
Q

Macular disease with DR

A

Can have ischemia or edema. Send for FA to differentiate

340
Q

CSME criteria

A
  1. retinal thickening with 500 um 2. hard exudates within 500 um with adjacent thickening 3. 1 DD of thickening within 1 dd
341
Q

Threats to vision with Neovascularization with DR.

A

Worry about Pre-retinal/vitreal heme, neo glaucoma, or tractional RD.

342
Q

Stage 1 of Hypertensive Retinopathy

A
  1. mild to moderate diffuse narrowing of retinal arteries.
343
Q

Stage 2 of hypertensive retinopathy

A

stage 1 plus focal constrictor al retinal vasculature (nicking) and exaggeration of the ALR

344
Q

Stage 3 of hypertensive retinopathy

A

Stage 2 plus CWS, retinal hemes, hard exudates (star) and retinal edema

345
Q

Stage 4 hypertensive retinopathy

A

Papilledema (malignant HTN)

346
Q

Elschnig Spots

A

choroidal infarcts that occur in severely hypertensive patients

347
Q

Secondary HTN conditions

A

Diabetes, Vein occlusion, NAION, N. palsy, macroanyrusm.

348
Q

Retinal Macroanarysm.

A

Unilateral focal area of dilation in a retinal with multilevel hemorrhages from a ruptured aneurysm with surround exudates.

349
Q

Macular star

A

Exudates around the macula in a star pattern with HTN.

350
Q

Ocular Ischemic Syndrome vs. Venous Stasis in REtinoapty

A

OIS is if the front of the eye is also affected. Venous stasis retonpathy if the back of the eye is only affected.

351
Q

OIS

A

Occlusion of the ICA or ophthalmic artery secondary to atherosclerosis or GCA. Symptoms include granular vision loss, dull pain, amaurosis fugal. Will see unilateral dot blot hemorrhages int he mid periphery with dilated non-tortious retinal veins. Can have possible neo of the dic or anterior segment. Associated with systemic HTN, DM, and cardiac disease. Will have gradual VA loss in one eye.

352
Q

Hyper viscosity REtinopathy

A

An increased resistance to blood flow secondary to elevated levels of plasma. Most common cause is hyperglobulinema.

353
Q

Interferon Retinopathy

A

Looks similar to DR. patients getting interferon. Follow every 4-6 months patients on interferon.

354
Q

Vascular sheathing

A

An inflammation of vessels. Characterized by exudates around the vessels. Occurs with syphyllis and sarcoidosis.

355
Q

Idiopathic Juxtafoveal Retinal Telengectsia

A

Idiopathic abnormal perivofeal capillaries in the JXF region.

356
Q

Coats’ disease

A

Males less than 20 years old. idiopathic peripheral retinal disease. Will progress to a total exudative retinal detachment. Will have decreased vision, leukocoria, strabismus. Will have marked hard exudates (diagnostic). Dilated telengectasia of vessels that have a lightbulb appearance and can progress to neovascular glaucoma.

357
Q

Leukocoria

A

white reflex secondary to fibrovascular scaring secondary to tractional RD with ROP

358
Q

Retinoblastoma

A

Most common intraocular malignancy in kids. Bilateral is heritable. Unilateral is non-heritable.

359
Q

Differentials for leukocoria

A

Call the retina rude. Coat’s disease, toxo, ROP, RB.

360
Q

Malignant choroidal nevus

A

TFSOMUHHD. Thickness (>2 mm), fluid (sub retinal), orange pigment, Margins, Ultrasound hallow, halo absent, diameter large.

361
Q

Risks for ARMD

A

white, older, smoking, hyperopia, hypercholesterimia.

362
Q

Nonexudative ARMD

A

Sick RPE with druse and RPE abnormalities (modeling). Worry about geographic atrophy. Could get PED due to build up of druse.

363
Q

Risk of going from nonexudative to wet AMRD

A

Multiple soft drusen, hyper pigmentation, smoking, HTN.

364
Q

wet macula edema

A

neovascularization. Can be blood under the RPE (Sub-RPE heme) can be blood under the Retina (sub retinal heme). Can be plasma under the RPE (Pigment epithelial detachment) or plasma under the retina (serous retinal detachment).

365
Q

Type of CNVMs

A

Classic: well defined membrane. Occult: not well defined

366
Q

What are more CNVMS

A

Predominately classic.

367
Q

Central Serous Choroidopathy

A

Young middle aged males with type A personality. Localized macular serous detachment. Will have a smokestack appearance. Can also have a hyperopic shift. Improve in 1-3 months.

368
Q

Histo

A

Chorioditis, multiple lesions, periparpillary, macula. No VITRITIS>

369
Q

Pathological Myopia characterization

A

<6 or 26

370
Q

Lacquer cracks

A

Streaks from the macula.

371
Q

Epiretinal membrane

A

Occur from a PVD when glial cells are lost behind on the ILM.

372
Q

MILD vs sever epirretinal membrane

A

mild=celophane Sever=macular pucker

373
Q

Who is more effected by macular hole

A

Women.

374
Q

Stages of Macular hole

A
  1. impending hole with loss of foveal depression and a yellow spot or ring around the fovea 2. round, small, full thickness hole with psuedooperculum 3. Large full thickness hole with operculum. Watzke allen sign. 4. PVD occurs.
375
Q

Macular photostress test

A

Normally less than 60 seconds.

376
Q

Albinism

A

Mutation in genes that make melanin. Foveal hypoplasie.

377
Q

What is the most common retinal dystrophy

A

RP

378
Q

RP

A

Progressive loss of RPE. Night blindness and peripheral vision loss.

379
Q

RP triad

A

Retinal bone spicules, arterial attenuation, waxy nerve pallor.

380
Q

Stargardt’s Dystrophy

A

AR. Kid ARMD. Have VA loss worse than what is seen in the back of the eye. Will have pisiform yellow flecks bilateral. Late stages will have bulls eye and salt and pepper changes.

381
Q

Choroidermeia

A

X linked recessive. Deficiency in rap gernyl-geranyl transference. Have night blindness and peripheral vision loss. Have progressive atrophy of the RPE and choriocapillariis.

382
Q

What could night blindness be due to

A

RP, CHoridoremia, or gyrate dystrophy.

383
Q

Cone Dystrophy

A

Slowly progressing central vision loss. Late can have bull’s eye macular appearance etc.

384
Q

Things with bulls eye maculopathy

A

Stars can’t handle the color. Starboard’s, chloroquine, hydroxycholorquine, thiadizein, cone dystrophy

385
Q

Lukocoria

A

Call the retina rude. Coats, toxo, ROP, RB.

386
Q

Best’s Disease

A

AD. Due to accommodation of material in the RPE. Patient will have big retinal signs with mild VA loss (opposite to stargardts)

387
Q

Stage 1 bests

A

Pre-vitelliform. Abnormal EOG with normal funds in symptomatic patients

388
Q

Stage 2 bests

A

Vitelliform. Egg yolk macular lesion apprear

389
Q

Stage 3 bests

A

Pseudohypopyon. Lesion can become absorbed with little to no effect on vision

390
Q

Stage 4 bets

A

Vitelliruptive. The eye yolk starts to break up and a scrambled egg appearance results. Mild vision loss expected

391
Q

Stage 5 bests

A

End stage. Moderate to severe vision loss due to choroidal neo, hemorrhage, atrophy, or macular scarring.

392
Q

Gyrate Atrophy

A

AR. Bilateral chorioretinal degeneration due to orinithin aminotransferase deficiency. Will have night blindness (RP and CHoriodremia too).

393
Q

Rhegmatogenous RD

A

Caused by a retinal break (hole or tear) that allows vitreous into the sub retinal space.

394
Q

Risk factors for rehmatogenous RD

A

Myopia and lattice degernation and PVD

395
Q

Atrophic holes

A

Round or small full thickness defects that are NOT associated with vitreoretinal traction and therefore have a low risk for subsequent detachment. Holes are caused by chronic atrophy of the sensory retina. Most likely to be temporal.

396
Q

Retinal tears

A

Caused by vitreous traction. Can be flap tears or percolated.

397
Q

Flap tears

A

The flap is present because of uneven vitreous traction and the vitreoretinal traction persists so greater risk of detachment.

398
Q

Operculate tears

A

The initial vitreoretional traction results in an even and symmetrical tear. No longer traction.

399
Q

Acute RD

A

Convex wavy retina with clear sub retinal fluid that does not shift with body position. Shafter’s sign may be present.

400
Q

Chronic RD

A

Pigment demarcation line will be present.

401
Q

Most common location for retinal breaks and BRVO

A

Superior temporal.

402
Q

Lattice degeneration

A

Educate about RD. Lateral is an area of peripheral thinning. Inner portion is atrophic and outer has an adhesion to the vitreous. More commonly ST.

403
Q

Non-rhegmatogenous RD

A

Not caused by a break in the retina. Can be serous (exudative) and tractional.

404
Q

Exudative RD non-Rhegmatogenous RD

A

Caused by subregional disorders (CH BALA) that damage the RPE and allow fluid to accumulate under the retina.

405
Q

Tractional Non-rhegmatogenous RD

A

Caused by Dr. VOS.

406
Q

Age related retinoschisis

A

splitting of the OPL and INL. Most commonly IT. Have an absolute field defect. Outer wall breaks are more dangerous.

407
Q

Angoid Streaks

A

Breaks in bruch by PEPSI. Occur at the disc.

408
Q

Toxocariasis

A

Will have optic nerve edema, RD, vitrifies, endopthlamitis, subretinoal granulomas.

409
Q

Central Areolar Choroidal Dystrohpy

A

AD condition with bilateral large areas of geographic atrophy in the macula.

410
Q

Acute Posterior Mulitofcal Placoid Pigment Epitheliopathy

A

Occurs after a viral infection. bilateral, yellow sub retinal lesions. Disc edema and RD can occur. resolves in a few weeks.

411
Q

Ocular hypertension

A

IOP greater than 21 on consecutive visits in a patient without glaucomatous optic neuropathy.

412
Q

Risks for Ocular Hypertension conversion to POAG

A

Age, race, family history, thin corneas, IOP (only one we can control)

413
Q

POAG

A

glaucomatous ON damage that occurs with IOP greater than 21 with VF defects and an open angle.

414
Q

What rim does glaucoma typically damage first?

A

The vertical rims.

415
Q

Pseudo exfoliative Syndrome

A

Secondary open angle glaucoma. Abnormal white flaky deposits all over in body and in eye. Can have sampaolesi line due to pigment released when deposits rub on posterior iris epithelium (also with pigment dispersion). Associated with poor pupil dilation and increased risk of lens sublimation.

416
Q

Pigmentary Dispersion Glaucoma

A

more common in caucasians, myopes, and males. Higher anterior chamber pressure that cause iris to bow back and rub against zonules. Cause pigment shedding. Will have transillumination defects in mid periphery, kruckenberg’s spindle, and samploswi line.

417
Q

Angle Recession glaucoma

A

Due to trauma. Have a wide open angle with a recessed iris and wide ciliary body band.

418
Q

Normal Tension Glaucoma

A

POAG where IOP is normal. Females have a greater risk. Also higher risk with vascular disorders.

419
Q

Who is dance hemes most common with

A

Normal tensive POAG.

420
Q

Who gets exfoliative glaucoma

A

Myopes and males. Caucasions

421
Q

What race is more likely to get psuedoexfoliative and pigment dispersion glaucoma

A

Caucasians.

422
Q

Primary angle closure glaucoma

A

Occurs as a result of posterior pressure pushing the peripheral iris anteriorly into contact with the TM.

423
Q

Who gets pupillary block most common

A

Hyperopes. Asians and Eskimos

424
Q

When are patients at greatest risk for pupillary block

A

When pupil reaches mid position of dilation.

425
Q

Plateau Iris

A

Anterior positioned ciliary processes push iris forward into contact with the TM. Slit lamp and gone show o flat iris plane, a normal anterior depth, but a convex peripheral iris.

426
Q

Sub acute Angle closure

A

Get a closure of the angle without symptoms as occludes and then opens Should expect with PAS and progressive ON damage and VF loss

427
Q

Acute angle closure

A

Is angle closure causing an acute elevation in pressure and patient symptoms. Can have pain, vomiting, hazy cornea, glacuomflecken, corneal edema.

428
Q

Glucomflecken

A

Anterior sub capsular opacities from high IOP causing epithelial cell death

429
Q

Greatest threat to vision with angle closure

A

CRAO.

430
Q

Mixed method glaucaom

A

Patients that suffered an acute angle closure are more likely to have POAG now

431
Q

Neovascular glaucoma

A

DR VOS. Recognize with rubeosis of the iris. The fibrosis tissue with the neo is what causes glaucoma. Can block TM or pull iris into contact with TM

432
Q

Uveitis Glaucoma

A

Caused by PAS (iris to TM) or PS (iris to lens). PS will only cause an elevation if there is an iris bombe (360 degrees) and pupillary block which move iris anterior into contact with TM.

433
Q

Congenital glaucoma

A

Bilateral and males. Development abnormality in TM.

434
Q

Bupthalmos

A

Enlarged eye as a result of congenital glaucoma.

435
Q

ICE syndromes (iridocorneal endothelial) syndromes

A

Disorders characterized by abnormal corneal endothelium that grows onto the iris or in the angle. More common in Females

436
Q

Essential Iris Atrophy

A

Iris thinning with resulting heterochromia, polycoria, correctopia, and ectropion uvea.

437
Q

Chandler’s syndrome

A

The corneal endo with have a beaten metal appearance with corneal edema and correctopia

438
Q

Iris-Nevus Syndrome (rogan reese)

A

Nodules will be present on anterior iris surphase

439
Q

Glaucomatocylitic Crisis

A

Posner-Schlossmai syndrome. Acute trabeculitis that result in an acute elevation. There will be few cells in the anterior chamber and gonio will have an open angle.

440
Q

Fuchs’ Heterochromic Iridocylctitis

A

Chronic, non-gram, low grade anterior units and stellate keratin precipitates. Will have iris heterochrima and iris/angle neo. Patient have an increased risk of glaucoma and cataracts.

441
Q

Photolytic glacuoma

A

Occurs when hyper mature cataract leaks material into the anterior chamber and result in blockage of aqueous outflow through the TM.

442
Q

PSD

A

Absolute value. Higher means more vision oss

443
Q

MD

A

Lower means more general depression.

NBEO Part 1 (17 decks)

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