Written Flashcards

1
Q

Define lagophthalmos and the most common cause?

A

Incomplete closure of the eyelid, most common cause is the 7th nerve palsy.

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2
Q

Define ptosis

A

The eye lid covers more than 2mm if the cornea.

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3
Q

Explain how thyroid eye disease (TED) affects the eye

A

The volume of the extraocular muscles, retro-bulbar connective and adipose tissue is increased, due to inflammation and accumulation of hyaluronic acid, in these tissues.

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4
Q

Give the manifestations for thyroid eye disease (TED).

A

injection, hyperemia and conjunctival edema (chemosis) especially in the earl y acute phase in conjunctiva.

Eye lid shows lid retraction, incomplete closure of eyelids, lid lag and staring look.

Impaired extraocular motility causing diplopia.

Proptosis: exophthalmos, which can cause corneal exposure and corneal ulcers

Optic neuropathy: visual acuity, color vision and field vision should be assessed.

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5
Q

Enumerate the assessment of severity in thyroid eye disease (TED) chart.

A

The severity ranges from 0 to VI. (NOSPECS)

  • Class 0-No symptoms or signs.
  • Class I-Only signs, no symptoms
  • Class II - Soft tissue involvement.
  • Class III -Proptosis.
  • Class IV -Extraocular muscle involvement.
  • Class V-Corneal involvement
  • Class VI - Sight loss (optic nerve involvement) .
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6
Q

Discuss the treatment of the thyroid eye disease (TED).

A

1) Restoration of the euthyroid state In case of hyperthyroidism by antithyroid drugs, radioactive Iodine, or thyroidectomy.

2) Protection of the cornea by lubricants day and night.

3) Systemic steroids in severe acute stage.

4) Orbital decompression and extraocular muscle surgery may be needed.

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7
Q

Give investigations needed for proptosis

A

CT scan and MRI of the orbit

Thyroid function tests and thyroid antibodies should be requested if TED is suspected

In case of tumors, a surgical biopsy is taken for pathological diagnosis

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8
Q

Define acute hordeolum, causes and treatment,

A

Acute inflammation of a hair follicle or meibomian gland

Predisposing factors are usually eye fatigues from lack of sleep or eye strain or systemic disease like diabetes. Infection is caused by staphylococcus.

Control predisposing factor
Give oral and topical antibiotics and hot foments.

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9
Q

Define chalazion

A

Chronic inflammation of meibomian gland possibly due to their blockage

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10
Q

Define blepharitis

A

Chronic inflammation of lid margin and the meibomian gland orifices

Two types: Seborrheic and ulcerative blepharitis

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11
Q

Enumerate the causes of the ptosis

A

Congenital: most common cause due to dystrophy of the levator muscle.

Paralytic: occurs in 3rd nerve palsy and in Horner’s syndrome due to sympathetic denervation

Neuromuscular ptosis: occurs in myasthenia gravis

Aponeurotic: occurs usually in old age may be caused by trauma or following surgery due to weak or stretched levator aponeurosis

Mechanical: due to increase weight of upper eye lid

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12
Q

Give the examinations for the diagnosis of ptosis

A
  1. Degree of ptosis: is judged by the lid margin-corneal reflex distance (MRD), normally 4- 5mm. In ptosis, this is decreased.
  2. Levator action: is measured by the difference in the width of the palpebral fissure between extreme downgaze and upgazed, normally it is 12 nm
  3. Other extraocular muscle are examined to exclude 3rd nerve palsy.
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13
Q

Explain the treatment of ptosis

A

Congenital ptosis is generally treated surgically. Severe or unilateral ptosis requires early intervention whereas in mild cases the surgery may be postponed till school age.

If there is good levator action, the treatment is by levator muscle resection. If the ptosis is severe and the levator action is poor, a frontalis suspension surgery is done.

Other types of ptosis are treated according to the cause.

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14
Q

Define Epiphora

A

Overflow of tears over the lower lids due to failure of drainage. It is managed surgically because the cause is obstruction in the lacrimal drainage system.

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15
Q

Define chronic dacryocystitis. Give the main symptom and the complications.

A

Chronic inflammation of the lacrimal sac secondary to nasolacrimal duct obstruction

main symptom is epiphora with recurrent mucoid discharge with positive regurge test

Complications are recurrent conjunctivitis, acute dacryocystitis on top and endophthalmitis.

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16
Q

Define Acute Dacryocystitis

A

Acute exacerbation of chronic dacryocystitis caused by infection with virulent organisms such as Staphylococcus aureus or Streptococcus . The sac is swollen, red, and very painful. Regurge is absent.

Treatment is by antibiotics, hot foments, an d sometimes incision and drainage.

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17
Q

Discuss the causes of dry eye

A
  1. Deficiency of aqueous tears the most common causes are collagen diseases such as rheumatoid arthritis, and an idiopathic form in old age, Treatment is by artificial tears eye drops.
  2. Mucin deficiency: occurs when there is widespread loss of goblet cells of the conjunctiva as in severe vitamin A deficiency, chronic trachoma. The severe form is called ocular xerosis. Treatment is also by artificial tears
  3. Eye dryness may be secondary to eyelid diseases such as ectropion or lagophthahnos.
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18
Q

What are the clinical picture of dry eye?

A

Symptoms of eye irritation such as burning and grittiness or foreign body sensation

Signs: Tear film debris may be noticed on slit lamp examination

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19
Q

Discuss the special tests in dry eye disease.

A

Schirmer’s filter paper strip test: number of mm wetted is measured as an indication of tear production.

Decrease tear film break up time as demonstrated by fluorescein staining of the tear film and observing the time that passes before dry corneal islands become visible

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20
Q

Discuss diagnosis of astigmatism

A

1) The patient may only identify some signs and miss others in the same line of the visual acuity chart.

2) Retinoscopy.

3) Keratometry is used to detect corneal astigmatism.

4) Corneal topography (see later in keratoconus).

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21
Q

Define anisometropia

A

a condition in which the refractive error of both eyes is significantly different. In children, it can result in amblyopia

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22
Q

Define aphakia

A

is the absence of crystalline lens from the visual axis often due to cataract surgery or trauma

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23
Q

Define cataract and give the most common cause

A

Opacity of crystalline lens and it is the leading cause of reversible blindness. The most common cause of cataract is aging.

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24
Q

Discuss the symptoms of cataract

A

Gradual painless progressive diminution of vision is the classic symptom (frequent change of eyeglasses, glare, day-blindness)

First symptom may be glare and/ or haloes around the light

Patient may notice improvement of near vision (second sight) due to index myopia.

Mature cataract should be hand motion and immature cataract should be counting fingures.

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25
Q

Discuss the signs of cataract

A
  • Cataract can be directly visualized by the penlight when it is mature and by the slit lamp and/or the red reflex if it is immature.
  • In a mature cataract where there is no fundus visibility, the projection of light and the ability to discriminate colors help to give an idea about the retinal and optic nerve functions.
  • Special attention should be given to the anterior chamber (AC) depth in order not to miss an intumescent cataract which causes a shallow AC.
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26
Q

Treatment of cataract

A

No medical treatment all surgical.

Phacoemulsification: use of ultrasound waves to emulsify the cataract to extract it from a small, often sutureless, incision. An intraocular lens (IOL) is then implanted.

Conventional extracapsular cataract extraction (ECCE) i.e. the nucleus and cortex are removed while the posterior capsule is kept

Intracapsular cataract extraction (ICCE) i.e. the whole cataractous lens is removed within its capsule.

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27
Q

Mention possible Lens complications of blunt trauma to the eye

A

Symptoms: Blurring of vision, monocular diplopia

Signs: Astigmatism is always present. In mild cases, the crystalline lens is completely present in pupillary space; may be gone in severe cases.

Complications: Both subluxation and dislocation may be complicated by cataract, uveitis or glaucoma.

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28
Q

Enumerate the causes of corneal opacity

A

Corneal edema: The most important physiological factor for corneal clarity is its dehydration,

Disturbances of the regular stromal structure: Scarring due to trauma or inflammation/ulceration causing loss of regular arrangement of collagen fibers

Defective corneal epithelium: disturbances in bowman’s membrane can be caused by diabetes

Tear film abnormalities: severe prolonged dry eye results in keratinization and loss of transparency

Deposition of abnormal material in corneal stroma and corneal dystrophies.

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29
Q

Discuss the treatment of corneal opacities

A

It is surgical. The opaque cornea is totally or partially exchanged in keratoplasty (corneal transplantation)

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30
Q

The 3rd cranial nerve (oculomotor) is the motor nerve supply of all the extraocular muscle except two which are

A

Superior oblique muscle which is supplied the 4th cranial nerve (trochlear)

Lateral rectus muscle supplied by the 6th cranial nerve (abducent)

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31
Q

Enumerate 5 risk factors for primary open-angle glaucoma

A
  1. Ocular hypertension.
  2. Positive family history.
  3. Wide optic disc cup .
  4. Myopia.
  5. Steroid responsiveness
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32
Q

Discuss the symptoms of primary open angle glaucoma

A

It is asymptomatic in the beginning stages as it affects peripheral vision first which is not noticeable. Symptoms of visual fields defects occur late in the disease; hence OAG is known as the theft of sight. Glaucoma should be routinely measured for in patients all above 40 years.

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33
Q

Discuss the signs of primary open angle glaucoma

A

Elevation of IOP: above 21 is suspicious

Fundus examination: Different cup/disc ratio in the eyes.

Glaucomatous cupping: refers to an increase in the size of the optic cup in relation to the optic disc. The increase in the cup is due to the loss of nerve fibers in the optic nerve

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34
Q

Describe the advanced glaucomatous cupping

A

Appears excavated and the retinal vessels passing over the disc are seen to bend at the overhanging edge of the cup and appear as if interrupted

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35
Q

Discuss the visual field changes in glaucoma

A
  • The most crowded fibers at the optic nerve are the temporal fibers above and below the macula and this explains why the earliest glaucomatous field defects occur in this zone.
  • The least crowded are the macular fibers and this explains the relative sparing of visual acuity until the late stages of the disease.
  • No fibers from the upper half of the retina enter through the lower half of the disc and vice versa, and this explains why glaucomatous field defects respect the horizontal meridian.
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36
Q

Discuss the first choice anti-glaucoma medications

A

Prostaglandin analogues: effective medications that increase aqueous uvea-scleral outflow

Beta-blockers: blocks sympathetic beta-receptors, which play role in aqueous secretion.

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37
Q

Second choice medications for glaucoma

A

Alpha agonist: reduce aqueous humor production

Carbonic anhydrase inhibitor: inhibit aqueous formation in ciliary body

Miotics: stimulate ciliary muscle pulling on trabecular meshwork and increasing the aqueous outflow

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38
Q

Give the systemic treatments for glucoma

A

Systemic Carbonic Anhydrase Inhibitors (CAIs): very effective medications but have a lot systemic side effects such as paresthesia.

Surgical treatment: Sub scleral trabeculectomy to create a canal for exit of aqueous humor.

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39
Q

Discuss the causes of Secondary Open Angle Glaucoma

A
  1. Lens induced glaucoma: lens proteins leak through the lens capsule.
  2. Glaucoma secondary to iridocyclitis: The plasmoid aqueous obstructs the pores of trabecular meshwork and decreases the aqueous outflow.
  3. After blunt trauma: Hyphema and angle recession glaucoma after blunt trauma due to fibrous changes at level of drainage channels
  4. Corticosteroid induced Glaucoma
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40
Q

Causes of Secondary Angle Closure Glaucoma

A

Lens induced: glaucoma occurs with in which the lens increase size which causes pupillary block resulting in angle-closure.

Neovascular Glaucoma: due to abnormal blood vessels growing from the iris surface to the angle of the anterior chamber secondary to retinal ischemia

Glaucoma secondary to iridocyclitis

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41
Q

Define myopia and give the two causes

A

Myopia is the state of refraction in which the non-accommodating eye has excessive refracting power and focuses parallel light rays in front of the retina

Higher than normal refracting power of the cornea or lens

A longer than normal axial length of the eye

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42
Q

Enumerate the complications of myopia

A

Retinal complications

Primary open angle glaucoma

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43
Q

Discuss the complications of keratoconus

A

Blurring of vision which starts at adolescence and progresses gradually

Increase myopia (especially myopic astigmatism)

Marked central corneal thinning

44
Q

Define Heterophoria (latent squint) and discuss its clinical picture

A

It is the tendency of the eye to deviate

Usually asymptomatic, may cause eyestrain (asthenopia) after visual exertion or fatigue. This can cause headache, ocular pain, blurring of vision and feeling of tiredness.

45
Q

Define Asthenopia

A

Eyestrain

46
Q

Enumerate the causes of paralytic strabismus (squint)

A

i. Lesions of the motor nerve nucleus.
a. Congenital absence of the nucleus.
b. Inflammations such as encephalitis
c. Degenerative and vascular lesions.

d. Neoplastic (brain tumors).
ii. Lesions of nerve trunk
a. Trauma by direct injury or by pressure.
b. Systemic diseases such as diabetic neuropathy.

iii. Lesions of the muscle
a. Congenital absence or mal-development of the muscle.
b. Direct injury.
c. Myopathy.

47
Q

Discuss the clinical picture of 3rd nerve palsy

A

Complete paralysis presents with ptosis together with the limitation of upwards, downwards, and inwards movements . The eye adopts the abducted and slightly downward position, and the pupil is dilated and fixed, with accommodation completely lost. Since there is complete ptosis, there is no diplopia.

48
Q

Enumerate 5 causes of 3rd nerve palsy

A

Intracranial aneurysm (most common cause)

Trauma

Cerebral herniation

Brain tumor

Microvascular disease: diabetes and hypertension

49
Q

Compare between conjunctival injection and ciliary injection

A
50
Q

Define Acute bacterial conjunctivitis and give its clinical picture

A

It is inflammation of the conjunctiva caused by gram-positive bacteria such as Staphylococci and Streptococcus pneumoniae and viridans and gram-negative bacteria such as Hemophilus influenzae, Neisseria gonorrhoeae.

Lid edema, Hyperemia of conjunctiva, mucopurulent discharge, foreign body sensation

51
Q

Discuss the fate and complications of Acute bacterial conjunctivitis

A

Spontaneous cure may occur within 1 or 2 wks much shorter with treatment. Can turn chronic. Secondary keratitis with possible corneal ulceration

Treatment: Standard infection control, broad spectrum antibiotic drops of Quinolone family. Antibiotic ointments higher concentration, used only at bed. Systemic antibiotics not needed only indicated in gonorrheal or chlamydial infections

52
Q

Give etiology Acute viral conjunctivitis and give the clinical symptoms and signs

A

Most common causative viral agents are adenoviruses. Viral infections are well known to occur in epidemics hence the name: epidemic keratoconjunctivitis (EKC) . Herpes simplex and Herpes Zoster are the second most common causes.

Symptoms: Hyperemia, watery eye

Signs: Palpebral conjunctival follicles, punctate epithelial keratitis, Lid vesicles in herpetic cases.

53
Q

Discuss the treatment and fate of acute viral conjunctivitis

A

Fate: Self-limiting, resolving in 7-14 days, involvement of other eye often occurs.

Infection transmission precautions must be followed.

No topical or systemic antivirals are effective in adenoviral infections; symptomatic treatment with cold compresses and artificial lubricants is the only regimen

54
Q

Define Phylctenular Keratoconjunctivitis

A

Phlyctens are single or multiple greyish-yellow elevated inflammatory lesions at conjunctiva surrounded by intense injection of blood vessels. Occurs commonly in children and young adults as a result of hypersensitivity to microbial agents.

55
Q

Enumerate 4 predisposing factors for bacterial keratitis

A

Epithelial damage due to trauma

Poor general resistance (immune-compromised patient)

Xerosis (vitamin A def)

Exposure of cornea due to proptosis

56
Q

Complications of corneal ulcer:

A

In its acute phase, the most dreaded complication of a corneal ulcer is perforation. The most serous complications are endophthalmitis and secondary glaucoma.

57
Q

Discuss the treatment of corneal ulcer.

A

bacterial corneal ulcer is a vision-threatening condition that demands prompt treatment by eradication of the causative bacteria

Specific: Topical antibiotics combined with therapy of broad spectrum antibiotics to cover both gram +ve and -ve

Nonspecific: Cycloplegic drugs like 1% atropine eye drops and systemic analgesics and anti-inflammatory drugs.

Physical: patching of eye with ulcer help relieve the pain caused by increased sensitivity. Hot fomentation gives heat comfort, reduces pain and causes vasodilation.

58
Q

Discuss the manifestation and treatment of herpes keratitis

A

The manifestation is a dendritic corneal ulcer or a geographic ulcer

Treatment is topical acyclovir 3%, 5 times/day until epithelial healing occurs. Should be discontinued after 10-14 days to avoid toxic keratopathy. Supportive therapy and physical and general measures.

59
Q

Define Herpes Zoster Opthalmicus and define Hutchinson’s rile

A

an infection of the Gasserian ganglion of the fifth cranial nerve by the varicella-zoster virus. It is neurotropic in nature,

Hutchinson’s rule: ocular involvement is frequent if the patient presents with vesicles on the side or tip of the nose

60
Q

In herpes zoster Opthalmicus, the frontal nerve is more frequently affected than the lacrimal and nasocilary nerves.

A

True

61
Q

Discuss the symptoms and signs of Herpes zoster opthalmicus

A

Symptoms: onset of illness sudden fever, severe neuralgic pain along the course of the affected nerve

Cutaneous lesion in the area of distribution of the involved nerve. Redness–>vesicle formation—-> pustules–> burst and become crusting ulcers

Signs: Ocular complications occur at appearance of the skin eruptions and manifest as: conjunctivitis and zoster keratitis (micro dendritic ulcers {different than regular dendritic ulcer less define shape}), ulcers more severe than HSV, diminution in corneal sensation.

62
Q

Treatment of herpes zoster opthalmicus

A
  1. Oral antiviral drugs: the treatment should be started immediately after the onset of the rash Acyclovir for 10 days.
  2. Analgesics.
  3. Systemic steroids may be given under the cover of systemic antivirals.

II. Local therapy for ocular lesions

a) Topical acyclovir 3% eye ointment for about 2 weeks.

b) Topical steroid eye drops 4 times/day.

63
Q

T/F this case is threatening to vision and shows discharge

A

False, non threating to vision, no discharge

This is episcleritis

64
Q

Define Photophthalmia

A

It is inflammation of the cornea and conjunctiva due to exposure to intense light of short wavelength as in exposure to an ultraviolet lamp or arc welding

65
Q

Discuss the mechanism of acute angle closure glaucoma

A
66
Q

Enumerate the predisposing risk factors for angle closure glaucoma

A

Small (hypermetropic) eye

Shallow anterior chamber (due to length growth later in life)

Being female

Moderate pupillary dilation during emotional excitement

Staying in the dark for long time

Application of mydriatics

67
Q

Discuss the signs of acute angle closure glaucoma

A
  • Red eye characterized by ciliary injection.
  • Severe corneal edema and haze.
  • Very shallow AC (Fig. 7-22).
  • Semi-dilated irreactive (fixed) pupil that is frequently vertically oval (Fig. 7-22).
  • Rapid drop of vision
  • The optic disc may not be visualized due to loss of corneal clarity (corneal edema)
68
Q

Discuss the treatment of acute angle closure glaucoma

A

Hospitalization

Hyperosmotic agents: draw water of eye lowering IOP

Carbonic anhydrase inhibitors

Topical miotics: pilocarpine 2-4%, every 15 min then every 30 min until pupil constricts: This is effective in pulling iris away from the angle.

Topical B-blockers: reduce aqueous formation

Topical steroids for inflammation

Analgesics

Gonioscopy after: if more than 50% of angle is open then laser iridotomy; if less then trabeculectomy. Surgery is the actual end goal treatment

69
Q

Discuss the complications of Acute Iridocyclitis (Anterior Uveitis)

A

Uveitic glaucoma: cells and exudates in the anterior chamber can clog the angle

Posterior synechiae: fibrin will cause adhesions between the two adjacent surfaces (back of iris and anterior lens surface)

Ring synechia: adhesions between the back of the pupil and anterior lens preventing passage of aqueous from the posterior to the anterior chamber pushing the iris forward (IRIS BOMBE)

70
Q

Enumerate the most common causes of acute red eye

A

Conjunctivitis

Corneal ulcer

Iridocyclitis

Acute Glaucoma

71
Q

Define Endophthalmitis and Panophthalmitis

A

Endophthalmitis: Inflammatory condition of intraocular cavities

Panophthalmitis: Inflammation of all coats of the eyes together with intraocular structure

72
Q

Define Orbital cellulitis. Give its symptoms, treatment and complications

A

inflammation of the soft tissue posterior to the orbital septum, usually caused by pre-existing sinus infection

Patients may have proptosis, decreased ocular mobility, ocular pain, and tenderness in eye movement

Hospitalization, IV antibiotics and drainage of abscess if present

Complications include localized abscesses, intracranial extension causing intracranial abscess, meningitis, cavernous sinus thrombosis

73
Q

T/F this condition is dangerous and is often spontaneous

May be caused by Valsalva maneuver

Can occur due to skull base fracture

A

It is often spontaneous T
It is dangerous F
T
T

74
Q

Discuss the signs of Vernal Keratoconjunctivitis (Spring Catarrhal)

A

Symptoms: It is 2:1 in males. Severe itching and copious mucoid discharge. With corneal involvement, there may be photophobia and blurring of vision.

Signs
Limbal VKC: There is a thickened, fleshy appearance to the limbus.

Palpebral VKC: Conjunctival hyperemia and chemosis associated with diffuse papillary hypertrophy are more prominent on the upper tarsus. In more severe cases, the papillae can enlarge giving rise to giant ‘cobblestone’ papillae. These may cause mechanical ptosis.

Corneal involvement: Keratopathy includes punctate epithelial erosions and pannus

75
Q

Discuss the complications of Spring Catarrhal (Vernal Keratoconjunctivitis)

A

It is bilateral chronic inflammation of the conjunctiva

Severe allergic conjunctivitis is associated with keratoconus.

Steroid-induced glaucoma may occur secondary to long-term topical steroid use

76
Q

Define Trachomatous Conjunctivitis (Egyptian Ophthalmia) and give the symtpoms

A

is the world’s leading cause of preventable blindness of infectious origin. It is caused by Chlamydia trachomatis.

  1. Mild irritation and foreign body sensation is often present.
  2. Mild chronic discharge.
  3. In the chronic stage, the cornea is involved causing pain, lacrimation and photophobia.
77
Q

Discuss the WHO classification for Trachomatous conjunctivitis

A

TF: Trachomatous follicles in beginning of the infection with 5 or more follicles

TI: The eye is irritated and highly infectious. Papillary hypertrophy and inflammatory thickening of the upper tarsal conjunctiva

TS: Presence of scaring in the tarsal conjunctiva

TT: Trichomatous tricharis: Lashes turn and rub into cornea

CO: Corneal opacity continual inflammation and scratching from rubbing lashes lead to clouding of cornea

78
Q

Discuss the complications of Trachoma (cornea)

A

Corneal: Herbet’s pits caused by herbert’s rosettes. Pannus (superior superficial epithelial vascularization). Corneal ulcers at lower edge of pannus leading

79
Q

Discuss the complications of trachoma (Lid complications and Lacrimal system)

A

Lid complications: Ptosis, Trichasis due to local scarring around the lid margin, Cicatricial entropion due to conjunctival shrinkage.

Lacrimal system: Obstruction of puncti by fibrosis, chronic dacrycocytitis, chronic canaliculitis with epiphora

80
Q

Define Pterygium

A

an abnormal wedge-shaped growth of degenerated fibrovascular conjunctiva that extends progressively over the cornea, usually from nasal side. Usually occurs in patients living in hot climates with excessive exposure to ultraviolet rays from the sun.

81
Q

Compare rods and cons in location, optimal light conditions, visual acuity, color sensitivity, type of vision and abundance

A
82
Q

Diabetic Retinopathy (DR) predisposing factors

A

In insulin-dependent diabetes mellitus (IDDM, type 1), more than 20% of patients develop retinopathy after 5 years of onset of their DM, and 80 % develop retinopathy
after 15 years of onset

Systemic hypertension: the association between DM and hypertension is know to predispose to blinding complications

83
Q

Discuss the type of DR

A

Background diabetic retinopathy (Non proliferative): Microaneurysm, Dot and blot hemorrhages.

Severe non-proliferative diabetic retinopathy: Increase in retinal ischemia, soft exudates, Intra-retinal microvascular abnormalities and segmental dilation of retinal veins

Proliferative diabetic retinopathy: Ischemic retinal tissue release vascular endothelial growth factor (VEGF), which causes new abnormal fragile vessels

Advanced diabetic eye disease: Massive vitreous hemorrhage, tractional retinal detachment and neovascular glaucoma.

84
Q

Discuss the grades of the hypertensive retinopathy Grade IV

A

Grade I: Slight or moderate narrowing of the retinal arterioles with an arterial: venous ratio of > 1:2.

Grade II: Moderate to severe narrowing of retinal arterioles with an arterial : venous ratio <1:2, or arteriovenous nicking.

Grade III: Soft exudates and flame-shaped hemorrhages

Grade IV: Grade III changes and bilateral optic nerve edema (Fig. 8-22).

85
Q

Discuss the causes of Retinal venous occlusions

A

Most common cause is hypertension/atherosclerosis which cause the artery to compress the vein at lamina cribosa of the optic disc.

Less common causes are increased blood coagulation diseases

Ocular hypertension and open angle glaucoma are risk factors for venous occlusion

86
Q

Give the treatment of the Retinal vein occlusion

A
  1. In the acute stage, monthly injections of anti-VEGF into the vitreous for up to 6 months for the macular edema.

II. If NVI develops, pan-retinal laser photocoagulation is done to prevent neovascular glaucoma.

87
Q

Central retinal artery occlusion (CRAO) and symptoms

A
  1. In the elderly the most common is thrombosis.

II. In the young, embolization is more common.

a) The most typical presentation is sudden painless complete loss of vision.

b) If the occlusion is temporary there will be loss of vision for a few minutes.

c) Loss of upper or lower half field of vision in branch artery occlusion.

88
Q

Signs of Central Artery Occlusion and treatment

A

The fundus showing attenuated arteries. If occlusion presists for a few to several hours, the central retina becomes milky white due to coagulative necrosis and in contrast, the thin fovea looks cherry-red.

For treatment to be effective, it must be tried within minutes, before retinal damage is permanent. Emergency treatment includes marked lowering of intraocular pressure.

89
Q

Define Choroidal neovascular membrane and discuss the causes

A

Central retina, especially fovea, maybe infiltrated by the abnormal growth of neovessels from the choroid into the subretinal space.

Age-related
Idiopathic
Degenerative myopia
Trauma
Rarely iatrogenic; secondary to intense laser burn

90
Q

Discuss the risk factors of Primary (Rhegmatogenous) RD

A

High myopia

Aphakia and pseudophakia

Trauma (blunt or perforating)

Family history of RD or history of RD in fellow eye

91
Q

Clinical Picture of RD (Symptoms and Signs)

A

Symptoms:

  1. Flashes of light (photopsia) due to mechanical stimulation of photoreceptors due to traction by the vitreous.
  2. Floaters (musca volitantes) are caused by a shower of minute red-colored or dark spots usually indicating vitreous hemorrhage secondary to the tearing of a peripheral retinal blood vessel
  3. A black curtain of loss of vision coming from one side.
  4. Loss of central vision when the fovea becomes involved.

Signs: Greyish reflex from the fundus instead of the normal red reflex. Retinal breaks which appear red.

92
Q

Define papilledema and give its causes

A

Papilledema is passive non-inflammatory swelling of the optic nerve head (optic disc) that is usually secondary to increased intracranial tension (ICT)

Intracranial causes: Space occupying lesions, Idiopathic hypertension, Inflammatory causes such as meningitis, Vascular causes such as cavernous sinus thrombosis

Systemic causes: Diseases such as anemia and polycythemia

93
Q

Discuss the clinical picture of papilledema

A

Symptoms: Asymptomatic with normal visual acuity and color vision. Transient attacks of blurring of vision due to sudden block of axonal fluid. Associated symptoms due to increase ICT such as headache and vomiting. Late is gradual painless loss of vision

Signs: Optic disc is hyperemic with blurred edges. Retinal veins become congested and tortuous. Field of vision may show enlargement of blind spot.

94
Q

Discuss the investigations of papilladema

A

Field of vision

Neuroimaging: CT scan, MRI

Lumbar puncture may be done in case of Increase Intracranial Hemorrhage to evaluate CSF

95
Q

Complications of papilledema

A

Post-papilledemic optic atrophy: The optic disc becomes flat and greyish with ill defined edges

96
Q

Enumerate the causes of leukocoria (white pupil)

A
  1. Cataract, the most cotntnon.
  2. Retinoblastoma, the most serious.
  3. Tractional retinal detachment; most importantly retinopathy of prematurity (ROP), history of NICU.
  4. Coats’ disease.
  5. Endophthalmitis.
97
Q

Discuss the clinical features of Retinoblastoma

A
  1. Leukocoria: white pupillary reflex, accounts for 65%> of cases.
  2. Strabismus (squint): if the tumor affects the macular area.
  3. Secondary glaucoma.
  4. Proptosis due to extraocular extension, with an occasional red and painful eye .
  5. Accidental discovery on routine
    examination or screening of babies for families with a positive history of retinoblastoma.
  6. Spread of the tumor is via the optic nerve.
  7. An inflamed angry eye
98
Q

Discuss the causes of congenital glaucoma

A

Almost always primary due to maldevelopment of the angle caused by Barkan’s membrane. Less common it may be 2ndry to ocular diseases such as retinoblastoma.

99
Q

What are the signs and symptoms of retinoblastoma?

A

In early stages: watery eye, photophobia, frequent rubbing of eyes

Late stage: Large cornea and deep anterior chamber

Advanced stage: cornea turns opaque due to stretch and rupture of Descemet’s membrane

Signs: Normal IOP for infants and young children is 10-12 mmHg

100
Q

Discuss the treatment of hyphema

A

Most cases resolve spontaneously with bed rest in a semi-sitting position . No miotics or mydriatics need to be used. Topical steroids
may be given to control iritis if present. Daily monitoring of the lOP should be done.

Surgical evacuation of the blood is indicated if the hyphema is massive or if there is high lOP in order to prevent blood staining of the
cornea.

101
Q

Discuss the types of trauma that can happen in the iris and the pupil

A

1) Traumatic iritis.

2 ) Traumatic miosis or more often mydriasis secondary to damage of the sphincter pupillae muscle.

3) Iris sphincter tears : small defects in the constrictor pupillae muscle at the pupillary border (Fig. 12-1 0).

4) Iridodialysis: separation of the root of the iris fron1 the ciliary body (Fig. 12-11 ). The pupil is typically D-shaped. Monocular diplopia 1nay occur which necessities surgical repair.

102
Q

Define hypopyon

A

Pus present in the anterior chamber of the eye

103
Q

Enumerate 7 causes for Miosis

A

Extremities of age
Opium toxicity
Acute iridocyclitis
Trauma
Homer’s syndrome
Pontine hemorrhage
Irritative stage of cerebral compression

104
Q

Enumerate four causes of Mydriasis

A

Acute glaucoma
Trauma
3rd nerve palsy
Paralytic stage of cerebral compression

105
Q

Discuss the treatment of spring catarrhal (Vernal keratoconjunctivitis)

A

Topical vasoconstrictors for symptomatic relief

Topical antihistaminic, topical mast cell stabilizers (start 2 wks before allergy begins)

Topical steroids are for severe exacerbations

Oral antihistamines especially if associated rhinitis

106
Q

Discuss the types of Entropion and Ectropion

A

Age related Entropion or Ectropion: Due to the horizontal laxity of lid tissues and ligaments with age

Cicatricial: In Entropion, there is conjunctival fibrosis, while in Ectropion there is fibrosis of skin following burn or surgery