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NBEO Part 1 > Ocular Disease > Flashcards

Ocular Disease Flashcards

1
Q

Arlt’s line

A

Scarring on upper cornea
* in trachoma

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2
Q

Signs of trachoma

A
  1. Art’s line (scarring on upper cornea)
  2. Herbert’s pits (follicles on/around limbus)
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3
Q

Testing for preseptal cellulitis

A
  1. Optic nerve (no involvement)
  2. EOMS (no restrictions, if there is pain/restrictions=orbital cellulitis)
  3. Proptosis exophthalometer
  4. Fever and headaches
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4
Q

Tx for EKC

A

Cold compress
Good hygiene + pt education
* epidemic keratoconjunctivitis self resolving 2-3 weeks
* caused by adenovirus, transmitted via secretions (respiratory, ocular)

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5
Q

Which disease causes s-shaped ptosis?

A

Acute Dacryocystitis
* infection and/or inflammation of the lacrimal gland and can result in acute swelling and discomfort in upper lateral eyelid

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6
Q

Infectious agent of canaliculitis

A

Actinomyces Israeli

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7
Q

What is the estimated percentage of chemical ocular burns that occur in industrial settings?

A

66%

This statistic highlights the prevalence of chemical burns in occupational environments.

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8
Q

Name three symptoms of chemical burns.

A
  • Normal or decreased vision
  • Pain
  • Foreign body sensation

Additional symptoms may include photophobia, tearing, and blepharospasm.

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9
Q

What are some signs of corneal damage in chemical burns?

A
  • Mild superficial punctate keratitis (SPK)
  • Sloughing off of the entire epithelium
  • Conjunctival injection
  • Chemosis
  • Ciliary injection
  • Anterior chamber reaction
  • Conjunctival hemorrhages
  • Scleral and limbal blanching

Severe burns may also increase intraocular pressure (IOP).

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10
Q

True or False: Alkali burns have a better prognosis than acidic burns.

A

False

Alkali burns raise tissue pH, leading to more severe damage.

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11
Q

Fill in the blank: Alkali burns are ______ compared to acidic burns because they raise tissue pH.

A

worse

This is due to the breakdown of fatty acids in cell membranes.

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12
Q

What are common alkali agents that can cause chemical burns?

A
  • Ammonia
  • Lye
  • Magnesium hydroxide
  • Lime
  • Airbag residue

These substances are often found in household or industrial products.

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13
Q

List two common acidic agents that can cause chemical burns.

A
  • Hydrofluoric acid
  • Sulfuric acid

Other examples include nitric acid, chromic acid, and PAVA spray.

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14
Q

What is a notable characteristic of alkali burns regarding penetration?

A

Faster penetration (often less than 1 minute)

This rapid penetration contributes to the severity of the injury.

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15
Q

What symptom may indicate severe chemical burns?

A

Increased intraocular pressure (IOP)

Severe burns can lead to complications affecting eye pressure.

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16
Q

Limbal blanching is a sign of _____ and is most common in alkali burns

A

Ischemia
* alkali injuries are more dangerous than acidic injuries

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17
Q

Symptoms of corneal abrasion

A
  • Sharp pain (esp. after blinking)
  • FBS
  • photophobia
  • tearing
  • blurred vision
  • mild anterior chamber reaction
  • miotic pupil
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18
Q

Epidemiology of corneal abrasion

A

History of trauma (fingernail, tree branch)

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19
Q

What is retinoblastoma?

A

The most common primary intraocular malignancy in children

It represents about 3-4% of all childhood cancers.

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20
Q

What percentage of childhood cancers does retinoblastoma represent?

A

About 3-4%

This indicates its relative frequency among childhood cancers.

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21
Q

What is the incidence rate of retinoblastoma?

A

Occurs in about 1 in 17,000 live births

This statistic highlights its rarity.

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22
Q

At what age do most children present with retinoblastoma?

A

Before the age of 3

About 80% of diagnosed cases occur before this age.

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23
Q

Is an initial diagnosis of retinoblastoma over the age of 6 common?

A

Extremely rare

This underscores the typical age range for diagnosis.

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24
Q

What is the most common intraocular malignancy in adults?

A

Melanoma

This contrasts with retinoblastoma, which is primarily seen in children.

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25
Q

What is phacomorphic glaucoma?

A

An acute secondary angle-closure type of glaucoma caused by antero-posterior growth and anterior movement of the crystalline lens

This leads to increased iridolenticular contact, pupillary block, and iris bombe.

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26
Q

What are the consequences of untreated phacomorphic glaucoma?

A

Significantly elevated intraocular pressure and severe damage to the optic nerve

Immediate treatment is crucial to prevent optic nerve damage.

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27
Q

What triggers phacolytic glaucoma?

A

High molecular weight proteins leaking into the anterior chamber from a hypermature cataractous crystalline lens

These proteins obstruct the trabecular meshwork.

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28
Q

What is the result of obstruction in phacolytic glaucoma?

A

Significant elevation in intraocular pressure and eventual optic nerve damage

Efficient and effective treatment is necessary.

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29
Q

What characterizes Posner-Schlossman syndrome?

A

Recurrent acute attacks of anterior uveitis with elevated intraocular pressure

Presumed to be due to acute trabeculitis.

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30
Q

What is phacoanaphylactic uveitis?

A

An autoimmune reaction secondary to proteins leaking from a lens with a ruptured capsule

This condition can lead to inflammation and other complications.

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31
Q

Fill in the blank: Phacomorphic glaucoma is considered an acute secondary _______ type of glaucoma.

A

angle-closure

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32
Q

True or False: Phacolytic glaucoma can occur due to the leakage of low molecular weight proteins from the lens.

A

False

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33
Q

What morphological changes contribute to phacomorphic glaucoma?

A

Antero-posterior growth and anterior movement of the crystalline lens

These changes increase iridolenticular contact.

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34
Q

Fill in the blank: In Posner-Schlossman syndrome, elevated intraocular pressure is presumed to be due to _______.

A

acute trabeculitis

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35
Q

What can happen if phacolytic glaucoma is not treated efficiently?

A

Optic nerve damage

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36
Q

ROP occurs due to?

A

Infants exposed to high oxygen concentrations
* causes vasoconstriction of immature peripheral retinal blood vessels
* subsequent removal of oxygen leads to hypoxic state in retinal periphery and proliferation of new, abnormal, leaky blood vessels (neovasc)

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37
Q

What is scleritis?

A

An inflammation of the sclera that generally occurs as a result of a systemic condition, usually of collagen vascular origin, most commonly rheumatoid arthritis.

Scleritis can also be induced post-surgically or occur secondary to infections such as corneal ulcers or trauma.

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38
Q

What are the two types of scleritis?

A

Diffuse scleritis and nodular scleritis.

Anterior necrotizing scleritis is another variant, which can be with or without inflammation.

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39
Q

What are the common symptoms associated with scleritis?

A

Ocular injection and pain, extreme ocular pain, and mild symptomology in some cases.

Pain may radiate to the jaw, brow, and forehead.

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40
Q

Describe the pain experienced in anterior necrotizing scleritis with inflammation.

A

Extreme ocular pain that may awaken the patient at night; described as boring and may radiate to the jaw, brow, and forehead.

This type of scleritis has significant inflammation.

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41
Q

What is scleromalacia perforans?

A

A form of anterior necrotizing scleritis without inflammation where patients may report only mild symptoms.

It is characterized by scleral thinning.

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42
Q

What clinical sign is associated with diffuse scleritis?

A

Sectoral or diffuse inflammation of the episcleral, conjunctival, and scleral vessels with distortion of the scleral vasculature.

This indicates a widespread inflammatory response.

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43
Q

What characterizes nodular scleritis?

A

Presents with a scleral nodule that is typically inflamed and non-moveable.

Nodules are a key feature of this type of scleritis.

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44
Q

What happens to the scleral vasculature in anterior necrotizing scleritis with inflammation?

A

The scleral vasculature may become necrotic, leading to ulcerated conjunctiva.

Over time, the uvea becomes more visible through areas of thinned sclera.

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45
Q

What is a potential complication of severe scleral thinning?

A

A staphyloma may form.

This is a bulging of the sclera that can occur due to weakness in the scleral structure.

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46
Q

What is the most severe form of scleritis?

A

Anterior Necrotizing Scleritis With Inflammation

This form has a higher mortality rate than other types due to its association with autoimmune diseases.

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47
Q

How does scleritis typically present?

A

Bilateral, but may also be unilateral

Most cases of scleritis are bilateral.

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48
Q

What should be evaluated in the sclera during an examination?

A

A blue hue, indicating previous episodes and scleral thinning

The sclera should be examined in natural light and in all fields of gaze.

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49
Q

What is the significance of a dilated fundus exam in scleritis?

A

To rule out posterior pole involvement

This exam is critical for assessing potential complications.

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50
Q

What may extend to the uvea in scleritis?

A

Inflammation, causing associated anterior uveitis

Persistent uveitis can lead to complications like cataract, glaucoma, or macular edema.

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51
Q

What is Scleromalacia Perforans?

A

Anterior Necrotizing Scleritis Without Inflammation

Patients typically do not experience pain or inflammation.

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52
Q

How does scleromalacia perforans typically present?

A

Typically bilateral with patches of thinned sclera

The patches are surrounded by non-inflamed tissue.

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53
Q

What happens to the underlying uvea in scleromalacia perforans?

A

Becomes progressively more visible with increasing coalescence of necrotic tissue

This condition is commonly observed in patients with rheumatoid arthritis.

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54
Q

What is the risk of perforation in scleromalacia perforans?

A

Rare

Although staphyloma formation may occur, perforation is uncommon.

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55
Q

What are the first-line treatments for diffuse and nodular scleritis?

A

Oral NSAIDs such as indomethacin, flurbiprofen, or ibuprofen

Indomethacin is typically 25 mg t.i.d., flurbiprofen 100 mg t.i.d., and ibuprofen 400-600 mg q.i.d.

56
Q

What may be prescribed if NSAIDs are ineffective?

A

Oral steroids such as prednisolone

Prednisolone is often prescribed at 40-80 mg q.d., tapered over weeks to months.

57
Q

What is occasionally required in the treatment of scleritis?

A

Concurrent use of lower-dose oral steroids and oral NSAIDs

This combination may be necessary for effective management.

58
Q

What are the initial treatment options for necrotizing scleritis?

A

Oral steroids, oral NSAIDs, or a combination of the two

59
Q

What may be necessary if oral steroids prove to be ineffective in treating necrotizing scleritis?

A

IV corticosteroids

60
Q

What type of therapy may be required for very severe cases of necrotizing scleritis that do not respond to steroids?

A

Immunosuppressive therapy, such as methotrexate, cyclosporine, azathioprine, or cyclophosphamide

61
Q

When might a patch graft be required in the treatment of necrotizing scleritis?

A

If there is a risk of perforation

62
Q

Are topical steroids generally effective in treating necrotizing scleritis?

A

No, they are generally ineffective

63
Q

Why are subtenon steroid injections typically contraindicated in necrotizing scleritis?

A

Due to the increased risk of perforation from tissue thinning

64
Q

What should be attempted in patients with diffuse anterior scleritis?

A

Determine if there is a systemic cause associated with the scleritis

65
Q

Name three common causative conditions for diffuse anterior scleritis.

A
  • Rheumatoid arthritis
  • Systemic lupus erythematosus
  • Relapsing polychondritis
66
Q

What are other conditions that frequently develop anterior diffuse scleritis?

A
  • Inflammatory bowel disease
  • Ankylosing spondylitis
  • Reiter’s syndrome
67
Q

List two infectious causes associated with anterior diffuse scleritis.

A
  • Herpes zoster
  • Syphilis
68
Q

What granulomatous disease is associated with anterior diffuse scleritis?

A

Sarcoidosis

69
Q

What metabolic diseases are commonly associated with anterior diffuse scleritis?

A
  • Diabetes mellitus
  • Gout
70
Q

What should be done to reduce the risk and/or severity of future manifestations of scleritis?

A

Treat the underlying systemic cause

71
Q

True or False: Recurrences of scleritis are uncommon.

A

False

72
Q

What is important to refer patients with diffuse scleritis for?

A

Systemic work-ups

73
Q

What are optic disc hemorrhages commonly associated with?

A

Normal tension glaucoma

Optic disc hemorrhages are typically found at the margin of the optic nerve in patients with normal intraocular pressures.

74
Q

Where do Drance hemorrhages typically appear?

A

At the edge of the optic disc

Drance hemorrhages extend onto the nerve fiber layer.

75
Q

In which quadrant of the optic nerve head are optic disc hemorrhages most often found?

A

Infero-temporal quadrant

This location is common for the occurrence of these hemorrhages.

76
Q

What is thought to cause optic disc hemorrhages in patients with normal intraocular pressures?

A

Vascular insufficiency or low systemic blood pressure

These conditions can lead to decreased ocular perfusion pressure.

77
Q

What may manifest several months after an optic disc hemorrhage?

A

Nerve fiber layer defect and/or visual field defect

These defects correspond to the location of the previous hemorrhage.

78
Q

True or False: Optic disc hemorrhages are more commonly observed in individuals with elevated intraocular pressures.

A

False

They are more commonly observed in individuals exhibiting normal intraocular pressures.

79
Q

Fill in the blank: Optic disc hemorrhages typically extend onto the _______.

A

nerve fiber layer

This extension characterizes Drance hemorrhages.

80
Q

What are conjunctival follicles?

A

Discrete, pale yellowish-white, round elevations in the conjunctival fornices

Follicles typically range from 0.5 to 2.0mm in diameter and are associated with various conjunctival conditions.

81
Q

What is the typical size range of conjunctival follicles?

A

0.5 to 2.0mm in diameter

The size can vary depending on the severity and duration of the disease.

82
Q

What conditions commonly feature a follicular response?

A
  • Viral conjunctivitis
  • Chlamydial conjunctivitis
  • Parinaud’s oculoglandular syndrome
  • Hypersensitivity reactions to topical medications

These conditions may trigger the formation of conjunctival follicles.

83
Q

Where are conjunctival papillae typically located?

A

Areas where the conjunctiva is attached to the deeper fibrous layer, like the tarsal conjunctiva and limbal bulbar conjunctiva

Papillae are distinct from follicles due to their location.

84
Q

What do smaller micropapillae look like?

A

Polygonal, elevated, red dots less than 1mm in size

They form a mosaic pattern.

85
Q

What is a key structural feature of conjunctival papillae?

A

Central fibrovascular core that arborizes as the vessel reaches the surface

This core distinguishes papillae from follicles.

86
Q

What can lead to papillary reactions in the conjunctiva?

A
  • Allergic conjunctivitis
  • Bacterial conjunctivitis
  • Contact lens wear
  • Chronic blepharitis
  • Superior limbic keratoconjunctivitis
  • Floppy eyelid syndrome

These factors can stimulate the formation of papillae.

87
Q

True or False: Conjunctival follicles contain a vascular core.

A

False

Follicles do not contain a vascular core; blood vessels sweep over their surface.

88
Q

Fill in the blank: Conjunctival papillae are typically found where the conjunctiva is attached to the __________.

A

[deeper fibrous layer]

This attachment is crucial for the formation of papillae.

89
Q

What is metamorphopsia?

A

A type of visual distortion where perceived linear images appear wavy or broken

Commonly occurs in macular diseases such as macular degeneration, clinically significant macular edema, and central serous retinopathy

90
Q

How do clinicians typically test for metamorphopsia?

A

Using an Amsler Grid

The Amsler Grid is a tool used to detect visual distortions and changes in central vision

91
Q

What is micropsia?

A

A type of visual distortion where images appear decreased in size

Caused by the spreading apart of foveal cones

92
Q

What is macropsia?

A

A perceived increase in image size

Results from a crowding together of foveal cones

93
Q

Are micropsia and macropsia common visual symptoms?

A

No, they are very uncommon

Both conditions are rare visual distortions

94
Q

What is photopsia?

A

A perceived flash of light

Can be associated with traction of the retina in cases of a retinal break, tear, or detachment, or most commonly, a posterior vitreous detachment

95
Q

What are scotomas?

A

Areas of the visual field where vision is partially or entirely degenerated

Scotomas can vary in size and shape and can be caused by various ocular conditions

96
Q

In general, how is IOP affected in patient with idiopathic anterior uveitis?

A

IOP is typically decreased
* because ciliary body decreases its production of aqueous when inflamed

BUT if TM gets blocked by cells and flare it can increase IOP

97
Q

Which organism is the MOST frequent to cause CL-associated keratitis?

A

Pseudomonas aeruginosa
*must treat quickly, enzymes can easily liquefy cornea in 1-2 days time

98
Q

What is epidemic keratoconjunctivitis (EKC)?

A

A very common and contagious infection of viral etiology

99
Q

What virus causes epidemic keratoconjunctivitis?

A

Adenovirus, particularly serotypes 8 and 19

100
Q

What is the ‘Rule of 8s’ in relation to EKC?

A

Serotype 8 is the type most frequently isolated and symptoms appear on the 8th day

101
Q

What is the typical progression of symptoms in EKC?

A

Diffuse superficial punctate keratitis on day 8, followed by sub-epithelial infiltrates on day 16

102
Q

When is a patient with EKC considered no longer contagious?

A

Once sub-epithelial infiltrates (SEIs) are present

103
Q

What are common signs of EKC?

A

Follicular conjunctivitis, positive lymphadenopathy, mild lid edema

104
Q

What are some additional symptoms that may be present in EKC?

A

Small sub-conjunctival hemorrhages, pseudo-membranes, and iritis

105
Q

What is the general treatment approach for EKC?

A

Palliative treatment including ocular lubrication, topical vasoconstrictors, cool or warm compresses, topical NSAIDs, and sunglasses

106
Q

What off-label treatment is sometimes used for EKC?

A

Betadine® (5%) in office treatment

107
Q

Why is the use of steroids in EKC controversial?

A

EKC and Herpes simplex virus (HSV) can initially present similarly, and steroid use on HSV can lead to corneal damage

108
Q

When are topical steroids effective in EKC?

A

If the patient suffers from visually debilitating sub-epithelial infiltrates

109
Q

What is vernal conjunctivitis?

A

A severe form of allergic conjunctivitis observed in young males with atopy

110
Q

What is the main symptom of vernal conjunctivitis?

A

Severe itching

111
Q

How does bacterial conjunctivitis typically present?

A

Starts in one eye and can spread to the other via self-inoculation

112
Q

What type of discharge is commonly associated with bacterial conjunctivitis?

A

Mucopurulent discharge

113
Q

Does bacterial conjunctivitis affect the pre-auricular nodes?

A

No, except in hyperacute bacterial conjunctivitis caused by N. gonorrhoeae

114
Q

What is phlyctenulosis?

A

A hypersensitivity reaction to microbes or their by-products

115
Q

What commonly causes phlyctenulosis?

A

Staphylococcus exotoxins

116
Q

What is the presentation of phlyctenulosis?

A

A pink elevated nodule of tissue on the conjunctiva or cornea

117
Q

What symptoms do patients with phlyctenules typically complain of?

A

Pain and irritation

118
Q

Do pre-auricular nodes get involved in phlyctenulosis?

A

No, they remain uninvolved

119
Q

What is oculoglandular syndrome?

A

A condition that typically presents as unilateral follicular conjunctivitis along with lymphadenopathy on the same side as the affected eye.

120
Q

What are common etiologies of oculoglandular syndrome?

A
  • Cat-scratch disease
  • Tularemia
  • Syphilis
  • Tuberculosis
  • Sporotrichosis
  • Mononucleosis
  • Coccidioidomycosis
  • Sarcoidosis
  • Hansen’s disease
  • Mumps
  • Actinomycosis
  • Listeria
  • Herpes simplex
121
Q

What is the most common cause of oculoglandular syndrome in children?

A

Cat-scratch disease.

122
Q

How can cat-scratch disease be verified in a child?

A

By asking if the child had recently been scratched by a cat and performing the Hanger-Rose skin test.

123
Q

How is coccidioidomycosis contracted?

A

Through exposure to a fungus found in soil and vegetables via an opening in the skin.

124
Q

Who is most likely to contract coccidioidomycosis?

A

Gardeners, farm workers, or botanists.

125
Q

Do diabetes, measles, and toxoplasmosis correlate with the development of oculoglandular syndrome?

A

No, they do not display a correlation.

126
Q

Fill in the blank: Oculoglandular syndrome typically presents as a unilateral follicular conjunctivitis along with _______.

A

lymphadenopathy on the same side as the affected eye.

127
Q

True or False: Oculoglandular syndrome can be caused by a single organism.

A

False.

128
Q

What is apoptosis?

A

The process of programmed cell death

Apoptosis is a natural process that helps regulate cell populations and can prevent tumor formation.

129
Q

What is necrosis?

A

Premature death of living cells and tissues

Necrosis is usually caused by external factors like infection, trauma, or toxins.

130
Q

What are the typical causes of apoptosis?

A

Natural processes within the body

Apoptosis is generally a beneficial process for tissue health.

131
Q

What are the typical causes of necrosis?

A

External factors such as infection, trauma, or toxins

Necrosis is detrimental to tissue health.

132
Q

How does apoptosis affect tumor formation?

A

It can prevent tumor formation by balancing cell death rate and mitosis rate

This balance is crucial for maintaining healthy tissue homeostasis.

133
Q

What is a characteristic feature of necrosis?

A

Results in inflammation of surrounding tissues

This inflammation can become chronic, leading to further tissue damage.

134
Q

What is autolysis?

A

Destruction of a cell by means of its own enzymes

Commonly known as self-digestion.

135
Q

What is phagocytosis?

A

The process by which a cell engulfs a particle, forming a phagosome

This process is crucial for immune response and cellular cleanup.

136
Q

True or False: Apoptosis is detrimental to tissue.

A

False

Apoptosis is generally regarded as beneficial to tissue health.

137
Q

Fill in the blank: Necrosis is caused by _______ factors.

A

external

These factors can include infection, trauma, or toxins.

NBEO Part 1 (15 decks)

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