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Adult/Ped Medicine Cumulative Final > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

When does normal vision develop?

A

During infancy and childhood

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2
Q

Focused visual stimuli are critical to:

A

Normal sight developmentEarly detection and correction of vision problems

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3
Q

Visual Development-a) Newborns follow:b) By 2-3 months infants follow:c) By 4-6 months:

A

a) Facesb) Lights and high contrast objectsc) Visual system matures (20/40)

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4
Q

Symptoms of Potential Eye Problems

A

Rubbing the eyesShutting or covering one eyeTilting or turning headSquintingInability to see distant objects clearlyBumping into walls or objectsHolding objects close to seeCrossing of eyes

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5
Q

Red Reflex

A

Screen for posterior segment (RETINA) abnormalities or corneal opacities

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6
Q

3 Categories of Visual Impairment

A

Neurological abnormalities that mimic vision impairmentVision impairment with NystagmusVision impairment without Nystagmus

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7
Q

Neurological Abnormalities mimicking visual impairments

A

Developmental delay or autism - poor visual fixation

Poor occulomotor control - cerebral palsy or congenital motor apraxia

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8
Q

define Nystagmus:

A

rhythmic oscillation of the eyes

usually horizontal, but can be vertical or rotatory

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9
Q

Visual Impairment with Nystagmus

A

any disorder of the **bilateral anterior visual pathways (cornea to geniculate body) **that affects the visual acuity under the age of 2 almost always results in nystagmus

ex: Congeital cataracts, anterior segment anomalies, retinal degenertation/dystrophy, optic nerve anomalies

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10
Q

Visual Impairment without Nystagmus is (almost always) caused by-

A

cortical visual impairment or delayed visual maturation

abnormality of the posterior visual pathways

  • Hypoxia
  • Hemorrhage
  • Cerebral malformations
  • Metabolic disorders
  • Infections
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11
Q

define Amblyopia:

A

lazy eye - loss of one eye’s ability to see details

in the absence of proper visual input from the visual pathway the brain “shuts down” the vision in the affected eye

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12
Q

Amblyopia causes

A

prolonged abnormal visual experience

  • distortion of normally clear retinal image (cataracts, refractive difference between eyes)
  • abnormal binouclar interaction (Strabismus)
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13
Q

Amblyopia treatment

A

address refractive errors

visual rehabilitation - patching eyes, fogging the good eye with chemicals or lenses

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14
Q

define Strabismus:

A

misalignment of one eye relative to the other in one or more positions of gaze

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15
Q

Manifest Strabismus (Tropia)

A

occurs spontaneously

may be constant or intermittent

examiner cannot induce it

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16
Q

Latent Strabismus (Phoria)

A

apperent only when single binocular vision is disrupted (Cover Test)

can be induced by examiner

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17
Q

Comitant Strabismus

A

misalignment is the same in all positions of gaze

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18
Q

Incomitant Strabismus

A

misalignment is apperent in only certain positions of gaze

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19
Q

Testing for Strabismus

A

corenal light reflexes

cover test

extraocular rotations

red reflex

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20
Q

define: Esotropia

A

visual axes of the eyes are convergent

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21
Q

Congential (Infantile) Esotropia

A

onset in first year of life

large, obvious deviation

treatment: surgery

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22
Q

Accomodative Esotropia

A

cuased by excessive focusing due to normal accomodation in uncorrected hyperopia

intermittent intially and gradually becomes constant

age of onse ~2 years (6m -7y)

managment: glases, amblyopia treatment, surgery

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23
Q

Nonaccomodative (Aquired Esotropia)

A

caused by unequal refractive errors, cataracts, corneal scarrring

treat underlying condition

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24
Q

define: Exotropia

A

visual axes of the eyes are divergent

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25
Q

Exotropia

A

begin intermittently after age 2

child often closes one eye in bright sunlgiht

more noticeable when fatigued or ill

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26
Q

Color Blindness

A

80% of white-males have some red-green deficiency

familial

tested using Ishihara tests

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27
Q

Retinoblastoma

A

most common childhood occular tumor

can be hereditary (bilateral) or sporadic (unilateral)

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28
Q

Occular Tumors: Congenital Cataracts

A

can be secondary to trauma or inherited

can be unilateral or bilateral

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29
Q

Retinopathy of Prematurity

A

common in infants

incomplete retinal vascularization, can lead to retinal detachment

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30
Q

define: Emmetropia:

A

Visual condition in which an infinitely distant fixated object is imaged sharply on the retina (without an accommodative response)

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31
Q

What vision does this diagram represent?

A

Emmetropia

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32
Q

Refraction:

A

Altering of the pathway of light from its original direction, result of passing from one medium to another

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33
Q

Ametropia:

A

Refractive condition in which parallel rays do not focus on the retina; a deviation from emmetropia (abnormal vision)

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34
Q

define Myopia:

A

Refractive condition in which parallel rays of light entering the eye, focus in front of the retina; nearsightedness

Corrected using LASIK surgery

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35
Q

What vision does this diagram represent?

A

Myopia

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36
Q

Lenses for myopia

A
  • Minus
  • Concave
  • Diverging
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37
Q

define Hyperopia:

A

Refractive condition in which parallel rays of light entering the eye f_ocus behind the retina_; farsightedness

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38
Q

What vision does this diagram represent?

A

Hyperopia

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39
Q

Lenses for hyperopia

A
  • Plus
  • Convex
  • Converging
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40
Q

define: Astigmatism

A

Refractive condition in which rays emanating from a single point are focused as two line images (blurry vision at all distances), generally at right angles to each other; due to unequal refraction of the incident light in different meridians

Eye becomes astigmatic when any of its refracting surfaces assumes a toroidal shape

Eye is not perfectly round (ex: football shaped not basketball shaped)

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41
Q

What type of asitgmatism is this?

A

compound myopic astigmatism

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42
Q

What type of astigmatism is this?

A

Compound hyperopic astigmatism

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43
Q

What type of astigmatism is this?

A

Mixed astigmatism

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44
Q

define Presbyopia:

A

Reduction in accommodative ability occurring normally with age and necessitating a plus lens addition for satisfactory seeing at near
Amplitude decreases from childhood to age 75

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45
Q

Presbyopia

A

affects 100% of people

treat with reading glasses

corrected surgically using: Conductive Keratoplast or Scleral Spacing Procedure (FDA trial)

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46
Q

define Accommodation:

A

Ocular adjustment for vision at various distances, by changes in shape (steepening) of the crystalline lens

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47
Q

define Diplopia:

A

Condition in which a single object is perceived as two objects rather than as one; double vision

  • usually results from EOM imbalance
  • monocular: persists when fellow eye is covered
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48
Q

define: Anisometropia:

A

Condition of unequal refractive state for the two eyes, one eye requiring a different lens correction from the other

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49
Q

Six Elements or Major Categories of Eye History

A
  1. chief complaint
  2. medical history
  3. medications/ hypersentitivities
  4. visual and occular history
    • last eye exam
    • galsses or contacts
  5. family eye and medical history
    • cataracts, glaucoma, macular degneration
  6. vocational and recreational demands
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50
Q

VISUAL Symptoms of Ocular Discomfort

A
  • Blurred vision
  • Diplopia
  • Distortion
  • Vertigo
  • Glare/light sensitivity
  • Spots before eyes
  • Light flashes
  • Loss of vision
  • Halos around lights
  • Loss of visual field
  • Night blindness
  • Movement of field
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51
Q

OCULAR Symptoms of Ocular Discomfort

A
  • Itching or burning
  • Tenderness, soreness
  • Pain, foreign body sensation
  • Excessive lacrimation
  • Change in blink rate
  • Warm, hot, tired feeling
  • Twitching of lids
  • Mattering of eyelids
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52
Q

REFERRED Symptoms of Occular Discomfort

A
  • Headache
  • Fatigue
  • Stress
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53
Q

Physical Exam

A

Visual Acutiy: Snellen

Pupils: size, shape, equality; reaction to light (PERRLA)

Extra-ocular muscles: movements of eyes into 6 cardinal positions (H test)

Visual field: confrontation testing

Anterior Segment Exam: slit lamp or pen light look at - lids, lashes, lacrimal gland, cornea, conjuntiva, iris, lens

Direct Ophthalmoscopy: media - cornea, lens, vitreous, disc, macula, vessels

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54
Q

Physical Exam: Visual Acuity

A
  • Patients will usually get some letters correct and some incorrect as the letter size approaches their threshold
  • Non-conventional methods: Near/Tumbling E/Pictures
  • Pg. 66 Mosby’s Record line in which they miss NO letters….(Evan)
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55
Q

Four Cardinal Eye Complaints

A
  1. Changes in Vision
  2. Changes in Appearance
  3. Pain or Discomfort
  4. Trauma
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56
Q

Cardinal Changes: Change in Vision

A
  • Painless or Painful
  • Extent of Vision Loss
  • One or Both Eyes:
  • Bilateral: neurologic etiology, not a primary problem

• Flashes or Floaters

  • Multiple – retinal tear, vitreous hemorrhage
  • Single – benign

• Rate of Onset

  • Rapid deterioration: vascular cause
  • Gradual loss: cataracts
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57
Q

Cardinal Changes: Pain or Discomfort

A
  • Pain or no pain?
  • Foreign body sensation
  • Excessive tearing
  • Itching or burning
  • Light sensitivity
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58
Q

Cardinal Changes: Trauma

A
  • Tetanus immunization state
  • Fluid or chemical exposure
  • Blunt or penetrating injury
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59
Q

Special Tests: Sit-Lamp Examination

A

Highly magnified views of: anterior segment and posterior segment

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60
Q

Special Tests: Intraocular Pressure

A

Analogous to systemic blood pressure

IOP – 8 to 21 mm Hg

Glaucoma screening

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61
Q

Emergent Conditions (immediate referral)

A

o Sudden Vision Loss
o Retinal Artery Occlusion
o Chemical Burns
o Acute Angle-Closure Gluacoma

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62
Q

Urgent Conditions

(referal with 1 day or less)

A

o Acute glaucoma
o Orbital cellulitis
o Hyphema
o Corneal Ulcer
o Retinal Detachment

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63
Q

Implantable Collamer Lens (ICL)

A

used in patients who cannot have lasik (too nearsighted)

in surgery - cut the limbus, insert the ICL next to the patient’s lens

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64
Q

Occular Maturity

A

often occurs at age 18

vision change of less than +or- 0.75 within 1 year

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65
Q

Cataract

A

natural clouding (or darkening) of lens

age dependent

typically affects older adults (60+), can occur in infants or children - rarely

Leading cause of preventable blindness world wide

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66
Q

Cataract Surgery

A

Entry Incision

Capsulorhexis (cutting the lens)

Phacoemuslification (use ultrasound to destroy lens)

Lens placement (standard, multifocal, accomodative lens types)

Corneal Arcuate Incisions (correct astigmatism if needed)

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67
Q

Keratoconus

A

Cone-shaped cornea

Progressive blinding disease

No good treatment - corneal transplant, Collagen Cross-Linking (Clinical Trial)

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68
Q

Identify this condition and describe the treatment:

pt reports - burning, gritty sensation that gets worse in the evenings

A

Dry Eyes

common with aging, F >M, often worse when reading

exposure: Bell’s palsy, Thyroid eye disease, scarred or malpositioned lids

may be associated with: rheumatological disorders, Stevens-Johnson, systemic meds

tx: artificial tears, lubricating ointment, punctal plug, Restasis, lid taping

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69
Q

Identify this condition and describe the treatment:

red, swollen lids and skin

normal: vision, pupils, occular motility, conjunctiva

A

Anterior (preseptal) cellultis

cause: trauma, URI, sinusitis, otitis
tx: cool compresses, systemic antibiotics

hospitalize if a child < 3

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70
Q

Identify this condition and describe the treatment:

spontaneous blood red eye, with normal vision, no pain and no discharge

A

Subconjunctival Hemorrhage

tx: resolves in 2-3 weeks on own

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71
Q

Identify this condition and describe the treatment:

localized or diffuse redness, deep red, pain

pt: history of RA

A

Episcleritis/Scleritis

scleritis - deep red, pain, can be vision threatening

idiopathic may have rheumatologic/autoimmune associations

tx: refer to ophthalmologist

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72
Q

Identify this condition and describe the treatment:

red eye, watery discharge, foreign body sensation, dendrite branching

A

Viral Keratitis

cause: Herpes Simplex Virus (type 1)
refer: STAT

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73
Q

Identify this condition and describe the treatment:

thick, red lid margins with crusting, some loss of eye lashes

A

Blepharitis

staphylococcal, seborrheic (meibomian gland dysfunction)

tx: warm compress, lid hygiene, topical antibiotics ung (ointment), oral antibiotics

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74
Q

Identify this condition and describe the treatment:

watery discharge with stringy mucus, itching

pt is an asthmatic

A

Allergic Conjunctivitis

ITENSE ITCHING

hx: allergy, ashtma, atopic/allergic disease
tx: topical antihistamines, mast cell stablizers

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75
Q

Causes of this condition

hint: pt was born at 0730

A

Neonatal Conjunctivitis

Staph, strep, h.flu

N. gonorrhea - refer to ophthalmologist, systemic antibiotics and topical

Chlamydial - topical and oral erythromycin

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76
Q

Identify this condition and describe the treatment:

pain, tearing, foriegn body sensation, photophobia, blurred vision

fluroscein exam:

A

Corneal Abrasion

tx: cycloplegic drops, oral analgesics with codiene; topical antibiotics; pressure patch 24 hours
refer: if not healed in 24-48 hours

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77
Q

Identify this condition and describe the treatment:

red, painful decreased vision with purulent discharge

A

Bacterial Keratitis

refer STAT

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78
Q

Identify this condition and describe the treatment:

pt was at work in a lab and got something in his eye

A

Chemical Injury

tx: immediate irrigation for 15 minutes, further irrigate until pH is normal

Alkali causes more damage

refer: STAT

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79
Q

Identify this condition and describe treatment:

localized or diffuse lid cellulitis, tenderness

A

Hordeola/chalazia

inflammed lid glands due to obstructed orifces

tx: warm compress, topical antibiotic ung (ointment)

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80
Q

Identify this condition and describe the treatment:

severe eye pain, blurred vision, halos around lights, nausea and vomiting

exam: mid-dilated pupil, redness, cloudy cornea, hard eye

A

Acute Glaucoma

cause: dim lights, drugs, emotional stress
refer: STAT

81
Q

Identify this condition and describe the treatment:

purulent discharge

A

Bacterial Conjunctivitis

cause: Staph, Steph, Hemophilus Influenzae
tx: warm compress, topical antibiotics, fluroquinolones

if Neisseria gonorrhea systemic antibiotics and hyperpurulent discharge

82
Q

Identify this condition and describe the treatment:

circumcorneal redness, pain, photophobia, decreased vision, small pupil

A

Iritis/Uveitis

idiopathic, infectious, sarcoidosis, autoimmune disorders, trauma

refer

83
Q

Identify this condition and describe the treatment:

watery, serous discharge, tender preauricular nodes

A

Viral Conjunctivitis

cause: Adenoviral, highly contagious
tx: no effective therapy (will clear in 1-2 weeks)
refer: pain, decreased vision, photophobia

84
Q

Identify this condition and describe the treatment:

swollen, red lids and conjuncitva; proptosis; impaired occular motility and painful movement; decreased vision; afferent pupillary defect; optic disc edema

A

Posterior (orbital) cellulitis

tx: hospitalization, CT scan, blood cultures IV antibiotic

often a fungal infection in immunocompromised

can lead to cavernous sinus thrombosis, meningitis

85
Q

Vision Threatening Red Eye Disorders

these need to be refered to ophthalmologist ASP!

A

orbital cellulitis

scleritis

chemical injuries

corneal infection

hyphema

iritis

acute glaucoma

86
Q

Identify this condition and describe the treatment:

inflamamtion and irritation

pt has job exposure to sun, wind and dust

A

Pinguecula (top photo)/Pterygium (bottom photo)

tx: artifical tears, topical NSAIDs
refer: severe inflammation, or if pterygium is actively growing

87
Q

Identify this condition and describe the treatment:

pt recieved a blow to the face, reports decreased vision and pain

A

Hyphema

blood in anterior chamber

refer STAT

88
Q

Identify this condition and describe the treatment:

tearing and discharge

A

Nasolacrimal Duct Obstruction

infected tear sac (Dacryocystitis)

Congenital tx: daily massage, antibiotics if infected, refer if no resolution 6-8 months

Aquired tx: systemic antibiotics if infected, refer if chronic

89
Q

Identify this condition and describe the treatment:

furuncle that points onto the conjunctival surface of the lid, examination shows involvement of the meibomian gland

A

Stye (Internal Hordeolum)

meibomian gland involvement

can be on the upper or lower lid

can lead to generalized cellulitis

tx: warm compresses, topical antibiotics, may need I&D if conservative treatment fails

watch for cellultiis, may lead to a chronic inflammatory lesion

90
Q

Identify this condition and describe the treatment:

pt reports foreign body sensation, burning sensation, lid crust, also has a problem with dandruff exam: no ulcerations

A

Seborrheic Blepharitis

associated with seborrheic dermatitis invovlement often of scalp, lashes, eyebrows and ears

tx: chronic condition, lid hygiene

91
Q

Identify this condition and describe the treatment:

young infant, parents report excessive tearing

A

Nasolacrimal Duct Obstruction and Dacryocystitis

may devleop an infection

tx: massage over nasoalcrimal sac, cleanse the lids if infected use topical antibioitcs, may resolve on its own, or surgical treatement - probing of the duct

92
Q

Exposure Keratitis

A

similar to dry eyes

cause: incomplete lid closure during blinking and sleep

may result from: Bell’s palsy, malpositioned eyelids, thyroid exopthalmos

tx: lubricating solutions, mechanical measures to help close lid

93
Q

define Blepharospasm:

A

eyes closed, lid spasms, may also have facial twitches

94
Q

Identify this condition and describe the treatment:

hard, nontender swelling, conjunctiva - red and swollen, chronic granulomatous inflammation

A

Chalazion

chronic granulomatous inflammation of a meibomian gland

may follow an internal hordeolum

vision may or may not be blurred in addition to the other symptoms listed

tx: warm compresses refer: if persistent, ophthamologist may incise and curettage or corticosteroid injections

95
Q

define Lid Retraction

A

eye bigger, appears to stare, upper lid pulled up, lower lid pulled down (Grave’s Disease)

96
Q

Identify this condition and describe the treatment:

localized, painful lid swelling, furuncle on the eyelid margin

A

STYE (Acute Hordeloum- External)

usually a staphylocoocal infection

involves lash follicle and gland Zies or Moll

tx: warm moist compresses, topical (or oral) antibiotics, may spontaneously drain or resolve, I&D if conservative treatment fails

97
Q

define Blepharoptosis:

A

upper lid droop, excess skin

98
Q

Identify this condition and describe the treatment:

exam shows lids are hyperemic with telangiectasis, inflammation of the meibomian glands

A

Posterior Blepharitis -

inflammation of meibomian glands can be bacterial (staphylococcal) or glandular dysfunction association with acne rosacea

99
Q

define Entropion:

A

eyelid flipped in, lashes and skin against the eye

100
Q

define Trichiasis:

A

normal lid position; lashes directed posteriorly

101
Q

define Dermatochalasis

A

baggy eyelids

102
Q

Identify this condition and describe the treatment:

pt reports foreign body and burning sensations and matting of the lashes exam: lid crusting, red-rims, discharge, some loss of lashes

A

Staphylococcal Blepharitis

can be intially asymptomatic, may also observe loss of lashes (ulceration) chronic condition

tx: lid hygiene, topical antibiotics for staph

103
Q

define Ectropion:

A

eyelid flipped out, conjunctiva exposed

104
Q

Identify this condition and describe the treatment: pt reports foreign body sensation, dryness, burning, exam shows lack of corneal and conjuctival luster, punctate erosions, stringy discharge

A

**Dry Eye **

Keratitits Sicca

Keratoconjunctivitis Sicca

deficiency in tear production, symptoms worsen as the condition progresses may be releated to autoimmune disorder, secondary to systemic drugs

tx: lubrication with artificial tears or ointment (Lacrilube)

105
Q

What is the macula?

A

area of the retina responsible for detailed, fine central vision - made of rods and cones

106
Q

What is the fovea?

A

the center of the macula

high density of CONES, NO rods

107
Q

Describe Microaneurysms

A

saccular out pouching at the site of capillary degeneration

earliest ophthalmoscopic manifestation of diabetic retinopathy

108
Q

Describe Macular Edema

A

breakdown of the inner blood-retinal barrier - allowing leakage of fluid and plasma constituents into the surrounding retina

can occur in non-proliferative and proliferative diabetic retinopathy

109
Q

Macular Edema Treatment

A

LASER

  • zaps leaking microaneurisms - no treatment of foveal avascular zone
  • marked absorption of fluid and lipids
  • lipids take longer to disappear by macrophages

Intraocular Steroid Injections

  • stabilizes endothelial cells and blood-retinal barrier
  • reduces immune and inflammatory response

VEGF Inhibitiors

  • inhibits vascualar endothelial growth factor - reudcing neovascualrizaation
110
Q

Changes in NON-PROLIFERATIVE diabetic retinopathy

A
  • macular edema
  • changes result due to retinal ischemia and capillary obliteration
  • COTTON WOOL SPOTS
  • acute swelling of axons
  • intra-retinal microvascular abnormalities - dilation and duplication of the capillary bed
  • venous beading (irregular diameter of retinal venules)
  • capillary closure and dropout - increases Foveal Avascular Zone
111
Q

Non-Surgical Means of Managing

Non-Proliferative Diabetic Retinopathy

A

Tight glycemic control

Rx hyperlipidemia

Control hypertension

112
Q

Disease states in which vascular changes are seen:

A

CVO - central retinal vein occlusion

BVO - branching retinal vein occlusion

Sickle Retinopathy

Coats’ Disease

Hypertension

Sarcoidosis

Radiation Retinopathy

Hyperviscosity Syndromes

Collagen Vascular Disorders

113
Q

Pathogeneis of Prolfierative Retinopathy

A
114
Q

Nevoascularization Elsewhere

A

occurs with

  • severe venous beading
  • intraretinal hemorrhages
  • can occur anterior to the retina and into vitreous humor (which can apply traction to the NVE)
115
Q

Nevoascularization of the Disc (NVD)

A
  • pre retinal hemorrhage (anterior to retina and into the vitreous)
  • larger fibrous component
  • can cause traction of the retina
  • can also be present with clinically signficant macular edema
116
Q

Outcomes of Proliferative Retinopathy

A

traction retinal detachment

vitreous hemorrhage

neovascular glaucoma

117
Q

Pathophysiology of traction retinal detachment and vitreous hemorrhage

A
  1. neovascularization anterior to the retina
  2. the posterior cortical vitreous contracts

this may induce hemorrhage - the blood will collect in the subvitreous space or vitreous cavity

118
Q

Treatment of Proliferative Retinopathy

A

Viterectomy

Pantretinal Photocoagulation

VEGF Inhibitiors

119
Q

Treatment of Proliferative Retinopathy:

Viterectomy

A

indications:

  • tractional retinal detachment threatens the macula
  • non-clearing vitreous hemorrhage
120
Q

Treatment of Proliferative Retinopathy:

Panretinal Photocoagulation

A

may induce the regression of fibrovascular tissue - therefore decrease the likelihood of

  • traction detachment
  • vitreous hemorrhage
  • neurovasuclar glaucoma
121
Q

** Epidemiology **

as the duration of diabetes increases

  • the rate of proliferative diabetic retinopathy ________
  • the occurance of macular edema ________
A

increases

increases

122
Q

Glycemic Control in Diabetic Retinopathy

A
  • cannot completely prevent the occurance of retinopathy
  • reduction in the rate of progression
  • 35-45% reduction in risk of retinopathy progression for every 10% decrease in HbA1C
123
Q

Other Risk factors for Diabetic Retinopathy (4)

A

Hypertension

Hyperlipidemia

Pregnancy

Anemia

124
Q

Age-Related Macular Degeneration

A
  • leading cause of severe central visual acuity loss
  • chronic disease
  • 2 types - Non-Exudative (Dry) and Exudative (Wet)
125
Q

Risk Factors for AMD

A

age

hyperopia

smoking

low HDL and high LDL

familial history (parents > sibling)

126
Q

Features of Non-Exudative (dry) AMD

A

drusen

focal hyperpigmentation

retinal pigment epithelieum atrophy

127
Q

Drusen

A

small or large, round, yellow lesions - between the retinal pigment epithelium basement membrane and Bruch’s membrane

128
Q

AERDS Supplementation in AMD

A

greatest reduction in conversion to advanced AMD

  • lutein/zeaxanthine
    • recommend AREDS 2 over AREDS 1
  • anti-oxidants + zinc + copper
  • zinc + copper alone
  • anti-oxidatnts alone
129
Q

Management of Non-Exduative (Dry) AMD

A

40-64: 2 year exam

>65: 1-2 year exam

Daily Amsler Grid Monitoring

AREDS 2 Eye Vitamins - Vitamin C, E, Lutein/Zeaxanthine, Zinc, and Copper

Lifestyle modification - smoking cessation, optimize diet, exercise

130
Q

What is being monitored for, using the Amsler Grid?

A

sudden decreased vision

Metamorphosia: distorted vision in which a grid of straight lines appears wavy

Sctoma: shadows of missing areas of vision

Blurring

131
Q

Features of Exudative (wet) AMD

A

chorodial neovascularization

break in Bruch’s membrane that allows new blood vessels to grow into the sub-RPE space

the vessels leak fluid, lipid, blood under the RPE and subretinally

can cause subretinal fibrotic scar formation

132
Q

Management of Exudative (Wet) AMD

A

Anti-VEGF Drugs - Ranibizumab, Aflibercept (+PIGF)

Older therapies that have fallen out of favor: laser photocoagulation, photodynamic therapy

133
Q

Anti-VEGF treatment

A

recombinant humanzied antibody fragments

one of the first therapies to stabilize and improve vision: can gain 6-9 letters instead of losing 23 letters

134
Q

8 Point Occular Examination

A
  1. Visual Acutiy
  2. External adnexa (lids, brow, nodes)
  3. Alignment and motility
  4. Visual fields
  5. Pupilary exam
  6. Anterior Segment (conjunctiva, cornea, Anterior Chamber)
  7. Posterior Segment (retina, choroid, optic nerve)
  8. Intraocular Pressure
135
Q

Identify this condition and describe the treatment and management:

patient is a cotton-headed-ninny-muggins and forgot to wear his lab goggles

A

Chemical Injury

(pH is important determinate of extent of injury - alkali is worse)

immediately: IRRIGATE!!!

topical anesthesia: proparacaine

cycloplegia (to prevent iris scarring)

prophylactic antibiotic

REFER STAT

136
Q

Identify this condition and describe the treatment and management:

pt is a football player who was tackled on the turf, he is complaining of pain, increased tearing and foriegn body sensation - see photo

A

Occular Surface Foreign Bodies

Removal Techniques: flushing, cotton tipped applicator, needle, spud

tx: patching, topical antibiotic ointment, cycloplegia, oral anaglesics
refer: prolonged healing, infilitrate, increased pain, decreased vision

***metal foreign bodies - toxic precipitate corenal breakdown, incites inflammatory response leads scarring and neovascualrization - refer because Burr required to remove rust ring

137
Q

Signs of a Perforating Occular Injury

A

Corneal Scleral Laceration

Irregular Pupil

Subconjunctival Hemorrhage

Uveal Prolapse

Lens opacity or disolocation

Hyphema

138
Q

Describe the treatment of a perforating occular injury

A

Shield Eye and Refer

no pressure applied - no patching

no topical meds

NPO

beware of narcotics for pain - can cause nausea and emesis - give an anti-emetic with narcotics

139
Q

Identify this condition and describe the treatment and management:

pt was playing raquetball and got hit in the face

A

Hyphema

cycloplegia, rest, fox shield to prevent manipulation

shield eye and refer as a ruptured globe until proven otherwise

**important to know vascular status - especially for sickle cell

140
Q

Identify this condition and describe the treatment and management:

pt was hit in the face during a fight

physical exam shows: enophthalmos, restrictive diplopia, and hypothesia over the lower lid, ala of the nose, and the upper lip, teeth and gums

see CT scan:

A

Orbital Fractures

associated features: orbital hemorrhage, orbital emphysema, traumatic optic neuropathy, globe injury

tx: antibiotics, mucosal decongestents, corticosteroids, postural drainage, protection
abstience: aspirin, NSAIDs, noseblowing

surgical indications: enopthalmos (2mm or greater), restrictive diplopia, defect of >50% of orbital wall

141
Q

Identify this condition and describe other common clinical forms:

pt reports hitting his head and now has loss of visual acutiy and field, ipsilateral affarent pupillary defect, and dyschromatopsia (disorder of color vision)

A

Traumatic Optic Neuropathy

occurs in closed head injury patients and midfacial frature patients

clinical forms:

  • indirect trauma optic neuropathy
  • penetrating foreign body or fractures
  • diffuse orbital hemmorrhage
  • optic nerve avulsion/transection
  • localized orbital hemorrhage (hematoma)
  • optic nerve sheath hematoma
  • tension (stage IV) orbital emphysema
142
Q

Laceration Danger Zones of the Eyelid (3)

A
  1. Eyelid Margin
  2. Lacrimal System
  3. Lid Retractors
143
Q

describe the treatment and management:

animal bites to the eyelid

A

causative agents: cat (pasturella multocida), dogs (capnocytophaga)

tx: irrigate, debride nonviable tissue, early cloasure, antibiotics (amoxacillin, calvulnic acid)

144
Q

Identify this condition and describe the treatment and management:

pt has proptosis, conjunctival edema (chemosis)

exam shows: reduced visual acuity, afferent pupillary defect, reduced occular motility

systemically toxic

A

Orbital Cellulitis

this is an emergency even with antibiotics mortality rate is 2% in the general population and 11% in newborns

start on systemic antibiotics

145
Q

Identify this condition and describe the treatment and management:

pt reports ocular pain, headache located over the eyebrow, halos around lights and nausea

signs: steamy cornea, mid-dilated, fixed pupil and high IOP

A

Acute Glaucoma

tx: IV acetazolamide, topical pilocarpine, laser iridotomy

**emergent **

146
Q

Identify this condition and describe the treatment and management:

pt reports painless vision loss, cherry red spot, chalky retina, attenuated vasculature

A

Central Retinal Artery Occlusion

emergency

lay patient flat, occular massage, high concentration of inhaled oxygen, IV acetazolamide and anterior chamber paracentsis

147
Q

Identify this condition and describe the treatment and management:

pt reports pain less altitudinal visual field loss (loss of vision above or below the midline - see pic)

on opthalmascope exam: optic nerve swelling, flame hemorrhages

A

Ischemic Optic Neuropathy

can be arteritic AION (giant cell arteritis) or non-arteritic (NAION)

if caused bt giant cell arteritis - high dose systemic corticosteroid

admit and monitor closely

refer emergently

148
Q

Identify this condition and describe the treatment and management:

painless sectoral vision loss

patient reports a “curtain-falling” of vision loss

A

Retinal Detachment

refer urgently

during transport postion pateint so retina will fall back into place with the assistance of gravity

photocoagulation surgery

149
Q

Afferent Pupil

A

Releative Afferent Pupil Defect (RAPD) if defect in the “in” information

CN 2 (Optic Nerve)

150
Q

Efferent Pupil

A

Anisocoria (unequal pupils) if defect is in the “out” signal

CN 3

Parasympathetic constricts

Sympathetic dilates

151
Q

Near Triad

A

Miosis

Convergence

Accomodation

152
Q

Pupillary Responses

A

Direct

Consensual

Accomodative

153
Q

Relative Afferent Pupillary Defect (RAPD)

Marcus-Gun Pupil

A

objective measure of the afferent light input of one eye compared to the other

signifies asymmetric pre-geniculate damage - examples: retinal lesions, ispsilateral optic nerve, optic tract

tested by Swinging Flashlight Test

no anioscoria, not due to cataracts or corneal opacity

154
Q

In an abnormally large pupil anisocoria is greatest in ____________?

In an abnormally small pupil - anisocoria is greatest in ____________?

A

abnormally large pupil - anisocoria greatest in light

abnormally small pupil - anisocoria greatest in dark

155
Q

Identify this condition and describe the treatment and management:

abnormally large pupil, vermiform movement of iris, sgemental/sector sphincter palsy

A

Adie’s Pupil

etiology: infection, inflammation, ischemia, local anesthesia, surgery, laser, trauma, autonomic

tonic pupil causes: diabetes, chronic alcoholism, encephalitis

treatment: increase biofocal strength, pilocarpine

156
Q

Identify this condition and describe the treatment and management:

absent deep tendon reflexes, hyperthermia, syncopal episodes, dysgeusia, chronic GI motlity, tonic pupils

A

Adie’s Syndrome

refer for a neurology consult

157
Q

Pharmacologic Mydriasis

A

large dilated pupil

does not react to light or near

does not react well to miotics

exposure to :

  • dilating drops
  • parsympatholytic agents (Atropine, Asthma medicine)
  • plants (Belladonna, Jimson Weed)
  • pesticides
158
Q

Cranial Nerve III Palsy

A

Associated with ptosis +/- EOM abnormality

Pupil involving a third nerve palsy - is an anerusym until proven otherwise

Causes: PCA aneurysm, trauma, brain tumor, microvascular ischemia

Isolated dilated pupil - not likely to be thrid nerve palsy

159
Q

Pharmacologic Miosis

A

small pupil - poor reaction to light and near stimuli

exposure to:

  • acetycholinesterases
  • tick and flea collars
  • pilocarpine and topical parasympathomimetics
160
Q

Aberrent Reinnervation

A

third nerve palsy with smaller pupil

does NOT react well to light

light-near disocciation

clincial features: unilateral miosis which accompanies eye movement may also have lid elevation/retraction with eye movement

161
Q

Horner’s Syndrome Symptoms

A

Ptosis

Miosis

Anhydrosis

162
Q

Etiology of Horner’s Syndrome

A

Congenital - affected eye may be lighter, likely from birth trauma

Acquired - cartoid dissection, carotid aneurysm, apical lung tumor (Pancoast tumor), occult neuroblastoma

163
Q

Pharmacologic Diagnosis of Horner’s Syndrome

A

Cocaine Testing - confirms - nothing enstilled in eye before, Horner’s pupil dilates less than normal one

Apraclonidine - little or no effect on a normal pupil

Localization of Horner’s Syndrome - Hydroxyamphetamine Testing: done 48 hours after cocaine test

164
Q

Glaucoma

A

chronic progressive ocular disease that toleads to progressive damage to the optic nerve and subsequent loss of visual field

major risk factor: increased IOP

165
Q

Classification of Glaucoma

A

Based on Etiology

  • Primary: open angle closure, congential
  • Secondary: due to other ocular or systemic disease (inflammatory or lens induced glaucoma)

Based on Mechanism

  • open angle glaucoma
  • angle closure glaucoma
166
Q

What is normal intraocular pressure?

A

10 to 21 mm Hg

167
Q

Pathophysiology of IOP causing Optic Nerve damage

A

Mechanical Compression of Optic Nerve

Obstruction of blood supply and death of nerve fibers - causes hollowing of the optic nerve (cupping)

168
Q

Eye Examination for Glaucoma

A

Check Vision

Refraction

Pupils (RAPD)

Measure IOP (Applanation, Tonopen, Schiotz, Pneumatonometer or palpation)

Gonioscopy

Examine Optic Nerve

Perimetry and Visual Fields - can do confrontation testing, or Humphrey Field Analyzer or Goldmen Perimetry

Imaging

169
Q

ISNT Rule

A

“if it isn’t ISNT then it isn’t”

Rim width - distance between border of disc and position of blood vessel bending

Inferior > Superior > Nasal > Temporal

170
Q

Characteristic Field Defects

A

Arcuate Defects

Nasal Step

Paracentral Defect

Annular Scotomas

Temporal Wedge

Tunnel Vision with temporal Island

Enlargment of Blind Spot

171
Q

ACUTE VISION LOSS - - - REFER IMMEDIATELY

A

Acute Glaucoma

Keratitis

Endophthalmitis

Vitreous or Retinal Hemorrhage

Retinal Detachment

Acute Maculopathy

Retinal Vessel Occlusions

Optic Neuritis

Ischemic Optic Neuropathy

Cortical Infart

172
Q

CHRONIC VISION LOSS - - - REFER NON-URGENTLY

A

Refractive Error

Media Disturbances in the tear film, cornea, lens or vitreous

Lesions of the nueral visual pathway from the retina to the visual cortex

173
Q

Open Angle Glaucoma

A

usually no symptoms

identified on routine eye exams

some patients compalin of decreased peripheral vision

prognosis: depends on stage at time of diagnosis and ability to reduce and manage IOP

174
Q

Managment of Chronic Glaucoma

A

establish a baseline

set a reasonable goal for IOP

lower the pressure

continue to observe patient, modifiy if necessary

175
Q

Prostoglandin Analogs for Glaucoma

A

Xalatan, Travatan, Lumigan

  • increase uveo-scleral outflow, reducing IOP
  • administered once a day
176
Q

ß Adgrenergic Antagonists

A

Timpotic, Betoptic S, Betagan

  • reduces the production of aqueous humor by inhibiting cAMP, reduces IOP
  • adminstered 1-2x a day
  • side effects: corneal anesthesis, ptosis, hypotony, burining, superficial punctate keratitis, dry eye
  • systemic: psychosis, fatigue, BRADYCARDIA, syncope, alopecia, nausea, impotence, ASTHMA, altered response to hypoglycemia, heart failure, tinnitus, depression, anxiety, hallucinations, dysarthria, CVA
177
Q

Sympathomimetics

A

Epinephrine, Dipivefrin (Propine)

  • reduces aqueous humor production, increases outflow through trabecular meshwork
  • twice a day
  • side effects: local irritation, pigmentation, corenal damage, macular edema, HTN, cardiac failure

Alpha Agonists: Iopidine, Alphagan

  • reduce production of aqueous humor, possibly increases outflow
  • 3x a day
  • side effects: local allergy, dry nose and mouth, fatigue, trachyphylaxis
178
Q

Parasympathomimetrics

A

Pilocarpine, Carbachol, Echothiophate

  • increases outflow facility, reduces IOP
  • 2x a day for echo, 4x a day for pilo
  • side effects: browache, headache, occular allergy, pupillary constriction, RD, ocular inflammation
  • parasympathetic effects
179
Q

Carbonic Anydrase Inhibitors

A

Topical: Drozolamide (Trusopt), Brinzolamide (Azopt) - twice a day

Oral/Parenteral: Acetazolamide (Diamox), Methazolamide (Neptazane) - 2-4 x a day

  • reduces production of aqueous humor by inhibiting carbonic anydrase
  • side effects: fatigue, parestheisas, metallic taste, electrolyte imbalance, acidosis, kidney stones, cardiovascualr and respiratory depressions, topical drops may cause local allergy
180
Q

Hyperosmotic Agents

A

Oral: Glyercol, Isosorbide

IV: Mannitol

  • reduce vitreous volume to lower IOP
  • rapid effect to lower pressure within minutes
  • side effects: nausea, vomiting, diuresis, cardiovascular overload, hyperglycemia in diabetics
181
Q

Current Medical Treatments to Lower IOP

A
  1. Prostaglandin
  2. ß-Adrenergic Antagonists (ß-Blockers)
  3. Adrenergic Agonists (Sympathomimetrics)
  4. Carbonic Anhydrase Inhibitors
  5. Cholinergic Agonists (miotics)
182
Q

Surgical Treatments of Glaucoma

A

Laser - iridectomy

Trabeculectomy - guarded opening in the sclera

Glaucoma Drainage Device

183
Q

Describe the presentation of congenital glaucoma:

A
  • Epiphora – watering eyes
  • Photophobia
  • Blepharospasm
  • Buphthalmos – enlargement of the eye
  • Haab’s Striae - Horizontal breaks in Descemet’s membrane
184
Q

Describe Diabetic Retinopathy

A

leading cause of blindness in patients 20-64 years

prevelence increases with duration of diabetes and age of patient

185
Q

Describe the retinal capillary changes in diabetic retinopathy (4)

A
  1. microaneurysms
  2. leakage of blood and fluid
  3. poor blood supply/ischemia
  4. growth of new abnormal blood vessels
186
Q

Identifity the condition and describe the treatment:

pt is a type 2 diabetic of 10 years

opthalamoscopic examination shows: microaneurysms, nerve fiber layer infarcts (cotton wool spots) and macular edema hard exduates

A

**Non-Proliferative **Diabetic Retinopathy

Treatment:

  • tight glycemic control
  • Rx hyperlipidemia
  • control hypertension

other microvascular changes are confined to the retina

  • capillary non-perfusion
  • IRMAs
  • dot-and-blot intraretinal hemorrhages
  • dialtion and bleeding of retinal veins
187
Q

What is a microaneurysm?

A

pericyte loss - local structural weakness within the vessel wall

NO vision changes result

188
Q

What are hard exudates?

A

Extracellular lipid which has leaked from abnormal retinal capillaries

fluid in the macula = blurry vision

189
Q

Describe Macular Edema

A

most common cause of vision loss from diabetes

considered clinically signifiicant if close to the fovea or large area

diagnosis: exam, optical coherence tomography, fluroescein angiography
treatment: focal laser (zap microanuerysms), anti-VEGF, intra-ocular steroid

190
Q

Severe Non-Proliferative Diabetic Retinopathy

4:2:1 Rule

A

4 Quadrants of diffuse intraretinal hemorrhages and microaneurysms

2 Quadrants venous beading

1 Quadrant IRMAs

15% chance of progessing to proliferative diabetic retinopathy within 1 year

191
Q

Identify the condition and describe the pathophysiology and treatment

ophthalmoscopic exam shows neovascularization elswehere, decreased red reflex and vitreous hemorrhage;

pt reports increasing floaters, hx of type 1 DM

A

Proliferative Diabetic Retinopathy

retina is so ischemic that it responds by growing new blood vessels that break through the retina and bleed

  • if growth off of the disc = NVD
  • if growth off of the retina = NVE

this new growth can cause vitreous hemorrhage (floaters)

decreased red reflex

recurrent bleeding leads to fibrosis

treatment:

  • virectomy
  • panretinal photocoagulation
192
Q

4 Common Diabetic Nerve Problems

A
  1. Diabetic Retinopathy
  2. Transient refractive errors
  3. Higher incidence of cataract
  4. Neovascular glaucoma
    • neovascularization of iris and closure of the angle
193
Q

Identify the condition and descirbe the treatment:

ophthalmoscopic examination shows: microaneurysms, arterial venous nicking, flamed shaped hemorrhages, and Elscnig Spots

A

Hypertensive Retinopathy

clinical features: microanerusysms, IRMA’s, blot hemorrhages, hard exudates, venous beading, Elschnig spots- nonperfusion of choriocapillaries

Acute: associated with preeclampsia, eclampsia, pheochromocytoma or renal hypertension

Severe: flame-shaped hemorrhages, blurring of the disc marginas, exudates

aterial venous nicking - related to vascular sclerosis - see the image on the left

194
Q

Identify this condition and describe the treatment:

ophthalmoscopic examination shows cotton-wool spots in a sector of the retina

patient reports vision loss, no pain

A

Branch Retinal Vein Occlusion

superficial hemorrhages, retinal edema, cotton-wool sports in a sector of the retina drained by the affected vein

if macula is affected - painless vision loss

occurs most commonly at arteriovenous crossing

risk factors: hx systemic hypertension, cardiovascular disease, increased BMI at age 20, hx of glaucoma

tx: anti-VEGF, sector photocoagulation

195
Q

Identify this condition and describe the treatment:

ophthalmoscopic examination shows: retinal hemorrhages in all 4 quadrants

A

Central Retinal Vein Occlusion

retinal hemorrhages in all 4 quadrants

dilated, toruous retinal veins

can be ischemic which leads to neovascularization

tx: anti-VEGF, panretinal photocoagulation

196
Q

Identify this condition and describe the treatment:

pt reports: sudden painless vision loss in his left eye

physical exam findings: RAPD, decreased visual acutiy

ophthalmoscopic examination: cherry red spot, retinal edema

A

Central Retinal Artery Occlusion

****irreversible vision loss within 90 minutes

tx: ocular massage, reduce IOP via needle or drops, hyperbaric oxygen - none have great evidence

poor prognosis

central occlusion due to artherosclerotic disease, emboli, vascultitis, coagulopathy (branch - emobli)

boxcarring of retinal vessels

197
Q

Identify this condition and describe the treatment:

pt reports - painless vision loss in her right eye, but vision has since returned

A

Carotid Stenosis Related Eye Diseases

Amaurosis fugax - painless transient monocular vision loss

descriptors: “curtain” coming down over the eye, blindness, dimming, fogging, or blurring

may see Hollenhorst plaque

**can be an emboli from the heart; patient is at high risk for a stroke

198
Q

Identify this condition and describe the treatment:

pt reports transient vision loss, scalp tenderness, arthralgia, and recent weight loss

exam shows: tenderness over temproal artery, thickened temproal artery, bruits

A

Giant Cell Arteritis =

Temporal Arteritis

medium vessel vasculitis in older people (>65)

scalp tenderness, tender over temporal artery, jaw claudication, fever, weight loss, joint pain

transient vision loss, double vision, sudden marked vision loss from ischemic optic neuropathy

tx: high dose steroids to save the other eye

199
Q

Other Causes of Retinal Vascular Disease/Ischemia

A
  • Radiation
  • Congenital AV malformations of the retina
  • Lupus
  • Bechet
  • IBD
  • Sarcoidosis
  • Sickle Cell Disease

Adult/Ped Medicine Cumulative Final (6 decks)

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