Eye disorders Flashcards

ENT

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1
Q

How does Dacryocystitis present?

A

persistent tearing and discharge and swelling in the medial portion of the eye

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2
Q

Acute or chronic infection resulting in inflammation of the lacrimal sac is caused by …

A

Dacryocystitis can be either an acute or chronic stasis of tears leading to infection resulting in inflammation of the lacrimal sac

S. aureus and streptococcus are commonly associated with acute Dacryocystitis

Pneumococcus, H. influenza and Pseudomonas are commonly associated with chronic Dacryocystitis.

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3
Q

Besides infectious, what is another cause for Dacryocystitis?

A

congenital

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4
Q

How is congenital dacryocystitis managed?

A

The diagnosis is clinical but can be supported with syringing or probing

The treatment starts with massage, followed by stenting, then dacryocystorhinostomy.

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5
Q

How does acute Dacryocystitis present?

A

Erythema, edema, warmth, and significant pain below the medial canthus of the eye
Pressure on the swelling causes pain and purulent discharge from the punctum.
Epiphora
Fever (may be present)

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6
Q

How is acute Dacryocystitis managed?

A

Diagnosis is clinical but can be supported with a pus culture. Blood cultures may be indicated in patients with systemic symptoms (fever).

Treatment is symptomatic, using warm compresses, NSAIDs. If necessary, systemic antibiotics such as Oral clindamycin, IV or oral amoxicillin + clavulanic acid, or IV vancomycin can be used empirically. Culture-specific antibiotics are used once the report is ready. Incision and drainage if lacrimal sac abscess occurs. Dacryocystorhinostomy (treatment of the NLD obstruction): after treating the infection

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7
Q

How does chronic Dacryocystitis present?

A

Persistent epiphora
Mucopurulent discharge from the punctum
No signs of acute inflammation; no fever

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8
Q

How is chronic Dacryocystitis managed?

A

Antibiotics (culture-specific)

DCR (to prevent recurrence)

Children < 12 months old with chronic dacryocystitis: Nasolacrimal duct probing

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9
Q

When would advanced diagnostics be indicated for Dacryocystitis?

A

A Dacryocystography (DCG) can be used in advanced diagnostics where a contrast imaging of the lacrimal sac and NLD but is mainly performed in patients with dacryostenosis secondary to trauma (altered anatomy) or suspected tumors (to locate the tumor).

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10
Q

What is a major complication of Dacryocystitis?

A

Preseptal cellulitis

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11
Q

localized, tender, erythematous, pus-filled nodules at the distal lid margin

A

Hordeolum (Stye)

A common acute inflammation of the tear gland or eyelash follicles (Zeis or meibomian glands), most commonly due to S. aureus. Presents as a painful, erythematous, and tender pus-filled nodule on the eyelid.

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12
Q

A patient describes seeing this, what are the likely causes?

A

Age-related macular degeneration

Optic neuritis

Open-angle glaucoma: Peripheral vision loss, disc cupping on fundoscopy.

Central retinal artery occlusion: Acute painless vision loss, cherry-red macula.

Retinal detachment: Acute vision loss with a “curtain falling” sensation.

Cataracts: Gradual vision dimming with glare and opacified red reflex.

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13
Q

What is the leading cause of blindness in individuals over 65 years of age in developed countries?

A

Age-related macular degeneration (AMD).

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14
Q

What are the two major forms of macular degeneration, and what is their prevalence?

A

“Dry” and “Wet”

Dry AMD (nonexudative or atrophic): ~90%.
Wet AMD (exudative or neovascular): ~10%.

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15
Q

What is the pathophysiology of Dry AMD?

A

Deposition of drusen (lipid and protein deposits) under the retinal pigment epithelium (RPE) and Bruch’s membrane, leading to slow progressive atrophy of the retina.

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16
Q

What is the pathophysiology of Wet AMD?

A

Choroidal neovascularization between the RPE and Bruch’s membrane, resulting in leakage of fluid and blood, leading to rapid vision loss and potential retinal detachment.

17
Q

What are the primary clinical features of AMD?

A

Dry AMD: Gradual, progressive vision loss over decades.
Wet AMD: Sudden or insidious vision loss over weeks to months.

Painless central or pericentral visual impairment with reduced acuity.
Metamorphopsia: Straight lines appear wavy (detected via Amsler grid).
Scotomas: Central blind spots.

18
Q

What findings on fundoscopy are diagnostic of Wet AMD?

A

Grayish-green retinal discoloration.
Retinal and subretinal hemorrhages or exudates.
Serous detachment of the retina and RPE.

19
Q

What findings on fundoscopy are diagnostic of Dry AMD?

A

Drusen: Yellow-white deposits under the retina.
RPE atrophy and mottling.

20
Q

What tools are used to diagnose AMD?

A

Amsler grid for visual distortion.

Fundoscopy:
Dry AMD: Drusen, RPE atrophy, and mottling.
Wet AMD: Retinal hemorrhages, serous detachments, and exudates.

Fluorescein angiography: Identifies neovascularization in wet AMD.
Optical coherence tomography (OCT): Detects fluid accumulation or retinal thinning.

21
Q

What are the risk factors for AMD?

A

Advanced age.
Family history/genetics.
Smoking.
Cardiovascular disease.
Obesity.

22
Q

How does the clinical presentation of Wet AMD differ from Dry AMD?

A

Dry AMD: Gradual vision loss due to retinal atrophy.
Wet AMD: Rapid vision loss due to choroidal neovascularization and fluid leakage.

23
Q

What treatments are available for Dry AMD?

A

Supportive care:
Patient education and visual aids (e.g., magnifying glass).
Lifestyle modifications: Avoid smoking, improve diet with antioxidants (vitamins A, C, E, and zinc).

No curative treatment available.

24
Q

What is the first-line treatment for Wet AMD?

A

Intravitreal injection of VEGF inhibitors (e.g., bevacizumab, ranibizumab, pegaptanib) to inhibit neovascularization.

25
Q

What are second-line treatments for Wet AMD if VEGF inhibitors are contraindicated?

A

Laser coagulation for direct thermal ablation of neovascularization.
Photodynamic therapy with laser-activated dyes to destroy abnormal vessels.

26
Q

What is the prognosis for AMD?

A

Dry AMD: Slowly progressive vision loss, no effective treatment.

Wet AMD: Poor prognosis without treatment; early VEGF inhibition can significantly slow progression.

Complete central vision loss is rare but possible in advanced cases.

27
Q
A