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Clinical Medicine > eye lecture 9 > Flashcards

eye lecture 9 Flashcards

1
Q

strabismus causes

A

congenital vs acquired

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2
Q

accommodative esotropia

A
  • child has hyperopia

- focus so hard that eye turns in (esotropia)

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3
Q

what is the most common cause of strabismus?

A

hyperopia (far-sightedness)

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4
Q

intermittent exotropia

A

-a convergence error

Focus harder and bring eye in but eye will drift out sometimes

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5
Q

what medical conditions cause strabismus?

A
  • Down’s syndrome
  • Cerebral palsy
  • Stroke – if stroke affects the nerve that causes an eye turn
  • Head injury
  • Prematurity and low birthweight
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6
Q

what is the problem in hypertropia?

A

CN IV palsy

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7
Q

how do people with hypertropia accommodate?

A

head turn/head tilt

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8
Q

what is worse, vertical diplopia or horizontal diplopia?

A

vertical

-person will start to function with using one eye only

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9
Q

txt of hyperopia

A
  • Lenses
  • Prisms (no more diplopia)
  • Vision therapy
  • Surgery – eye turns are too big to train them to fuse together
  • Botulinum toxin – take the muscle that is over acting and put some botox in them and help the eyes align again
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10
Q

amblyopia

A

Condition where have one eye that isn’t functioning properly (e.g., exotropia) and brain suppresses it -> amblyopia (eye stops functioning)
-affects one in every 40 children

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11
Q

why don’t miss children with strabismus?

A

b/c associated with retinoblastoma

-20% of retinoblastoma have strabismus

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12
Q

what does a new onset strabismus/diplopia in adult mean?

A

aneurysm until proven otherwise

-EMERGENCY!!!

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13
Q

where does aneurysm occur with new onset strabismus/diplopia in adults?

A

posterior communicating artery (of circle of willis)

-pushes on CN3 - pushes eye down and out -> diplopia

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14
Q

what does gradual onset diplopia mean?

A

intracranial tumor - need MRI

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15
Q

what does transient or persisting diplopia mean?

A

temporal arteritis - HA, jaw claudication, scalp tenderness (painful to brush hair)
-seen in >50 y.o

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16
Q

what tests do you run for transient or persisting diplopia?

A

erythrocyte sedimentation rate or C-Reactive protein

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17
Q

variable diplopia seen in what?

A

myasthenia gravis - fatigue

  • 2 forms: ocular and systemic
  • starts with ocular and w/in 3 years can turn into systemic
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18
Q

what layer of the cornea results in a scar?

A

2nd lays - bowman’s layer

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19
Q

what side is most common for pterygium?

A

nasal side

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20
Q

what does pterygium start as in terms of symptoms?

A

Starts asymptomatic, but proceeds to dry eye, burning, gritty sensation

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21
Q

pathogenesis of pterygium

A
  • Benign fibro-vascular proliferation and basophilic degeneration of corneal collagen
  • Matrix metalloproteinase (enzymes responsible for degradation of extracellular matrix proteins) show signs of necrosis (surface of eye is changing and also starting to die)
  • Destroys Bowman’s layer and superior layer of stroma of the cornea
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22
Q

what part of the pterygium is comprised of blood vessels?

A

body/tail

not cap or head

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23
Q

what is a pterygium a result of?

A

UV light exposure, dust, smoke, and low humidity

SURFERS EYE

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24
Q

diff dx of pterygium

A

Pannus

  • Contact lens over wear
  • Trauma to limbal stem cell area (stem cells that grow at edge of cornea)

Phlyctenular keratitis
-Delayed sensitivity – pt is experiencing hypersensitivity d/t staphylococcus (most common) or TB

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25
Q

txt of pterygium

A

-sunglasses/hats
-topical lubricants/mild steroid
-surgical:
Bare sclera – reoccurs
Auto graft from other area of eye
Amniotic membrane grafting
Mitomycin C and Beta irradiation – prevents growing of tissue

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26
Q

complications of pterygium

A
  • Irritated, gritty eyes
  • Cosmetic appearance – most of eye will be white except for pterygium that will be inflamed
  • Contact lens intolerance
  • Astigmatism – changes shape of cornea and makes it more of a football shape and get induced stigmatism
  • Decrease vision
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27
Q

nuclear cataract

A
  • Sits in center of lens
  • most likely congenital (occurs while being developed)
  • Can be due to infections that affect the mother or toxins (e.g., fetal alcohol syndrome)
  • Usually so small that barely affect vision; usually not noticed until routine eye exam
  • Typically don’t progress
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28
Q

when do you start to have difficulty seeing?

A

around 40 years old

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29
Q

why is nuclear cataract usually congenital?

A

b.c nucleus of lens is the first part of the lens that forms during fetal development

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30
Q

cortical cataract

A

spokes that come through from the side of the lens into the visual access
aka peripheral cataract

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31
Q

posterior capsular cataract

A
  • Forms at the back of the lens (back surface on capsule)
  • Looks like dirty smudge on lens, reflects bright colors
  • Most visually devastating and grows fast
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32
Q

types of cataracts

A
  • congenital
  • age related (as you get older)
  • secondary
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33
Q

what is the most common cause of cataract in adults?

A

secondary cataracts

34
Q

what causes secondary cataracts

A

smoking, diabetes, steroids

35
Q

when do congenital cataracts need to be removed?

A

first 4-5 days of life

-b/c nerves for sight won’t develop correctly if not removed

36
Q

causes of congenital cataracts

A
  • toxic

- infection

37
Q

what happens when cataract get more mature?

A

pupil can become white (but doesn’t always mean it’s a cataract - could mean retinal detachment or tumor)

38
Q

symptoms of cataracts

A
  • Light is scattering in all directions and causes glare

- Can wash out colors: see more yellow and less blue

39
Q

txt of cataracts

A
  • treat before lose license (vision at 20/40)
  • New glasses prescription as the cataract forms
  • Sunglasses for glare
  • Surgery
40
Q

cataract complications

A

Hyper-mature cataract

  • Decreased vision
  • Riskier surgery – Cataracts harden the lens and make the lens harder to remove – makes surgery hard to do and complication rates are much higher
41
Q

normal pressure in eye?

A

15-20mmHg

42
Q

glaucoma

A
  • group of diseases that damage the optic nerve of the eye and results in vision loss
  • Associated with increased eye pressure (production exceeds drainage)
43
Q

types of glaucoma

A
  • primary open angle glaucoma
  • congenital glaucoma
  • secondary glaucoma
  • angle closure glaucoma
44
Q

is primary open angle glaucoma dependent on angle of eye?

A

NO!, but IOP is high

-maybe imbalance with fluid production and drainage

45
Q

secondary glaucoma types

A

neo-vascular or steroid response

46
Q

neo-vascular glaucoma

A
  • secondary glaucoma

- new vessels that form and obstruct the trabecular meshwork and fluid can’t flow out of it

47
Q

steroid response glaucoma

A
  • secondary glaucoma
  • sometimes people that use steroids respond with increased in the IOP and it gives them glaucoma or makes their glaucoma worse – steroids don’t have to be PO, can be topical (eye drops) or creams
48
Q

what is the HALLMARK symptom of angle closure glaucoma?

A

PAIN

49
Q

onset of angle closure glaucoma

A
  • occurs suddenly

- eye pressure increases, eye becomes very red, cornea becomes steamy and pacified, very painful

50
Q

pseudoexfoliatoin glaucoma

A

trabecular meshwork is clogged up

51
Q

what can happen to patient with glaucoma over time?

A

patient will lose vision and can become completely blind (usually takes about 20 years to be end-stage)

52
Q

main treatment of glaucoma

A

STABILIZE PRESSURE

53
Q

1 treatment for glaucoma

A

prostaglandins

  • increase uveoscleral outflow by dilating the blood vessels
  • will make patients eyes red (know drugs are working)
  • make eye lashes grow
54
Q

surgical options for glaucoma

A

trabeculoplasty, cyclophotocagulation

-laser shit

55
Q

medications associated with angle closure glaucoma

A
  • cholinergic meds (salagen)
  • anti-cholinergic meds (SSRI, anti-histamines)
  • adrenergic agonists (epi, amphetamines)
56
Q

other medications for txt of glaucoma

A

beta-blockers, alpha-adrenergic agonists, carbonic anhydrase inhibitors, motifs (pilocarpine)

57
Q

treatment of narrow angle glaucoma

A

LASER Peripheral Iridotomy – laser burn in iris that will equalize the pressure between the anterior chamber of the eye and the posterior chamber of the eye -> fluid flows naturally

58
Q

treatment for acute angle closure glaucoma

A

medications

59
Q

normal tension glaucoma

A
  • Unusually fragile optic nerve

- Reduced blood flow to the optic nerve (Damages optic nerve that it loses axons)

60
Q

2 types of macular degeneration

A

dry and wet

61
Q

dry macular degeneration

A

an atrophic condition where retinal receptors die off and leaves the eye dry and atrophic and affects vision

62
Q

wet macular degeneration

A

almost same process as dry, but at some stage the VEGF factors send new blood vessels to try to fix eye and then get explosion of new blood vessels under macula that are weak and leak fluid into bottom of eye

63
Q

risk factors of dry macular degneration

A
  • age (drusen spots -white spots)
  • fam hx
  • caucasian
  • smoking
  • obesity
  • CVD
64
Q

what is the HALLMARK SIGN of dry macular degeneration?

A

drusen spots - white spots

65
Q

symptoms of dry macular degeneration

A

blurry, distorted vision

-blind spot

66
Q

is there a cure for dry macular degeneration?

A

NO

  • eat fatty fish and fruits and veggies
  • take vitamins
67
Q

wet macular degeneration management

A

Anti-VEGF injection into eye (prevents blood vessels from growing)
-ranibizumab, bevacizumab, pegaptanib, alifbercept

68
Q

other wet macular degeneration management

A
  • photodynamic therapy (verteporfin)

- photocoagulation (laser thermal burn)

69
Q

what is arteriosclerosis caused by?

A

elevated blood pressure of >140/>90

70
Q

signs of HTN retinopathy

A

elschnig spots, siegrist streaks, retinal hemorrhages, cotton wool spots, exudates, papilledema

  • widerning of arteriole light reflex
  • arteriovenous crossing signs
  • copper or silver wire arteries
71
Q

papilledema occurs from?

A

malignant HTN, >180/120

-MEDICAL EMERGENCY

72
Q

symptoms of HTN retinopathy?

A
  • blurry vision
  • spots or floaters
  • dark spot in vision
  • difficulty seeing well at night
73
Q

diabetic retinopathy

A

Damage to small blood vessels of the eye by sugar in the blood

74
Q

treatment for diabetic retinopathy

A
  • Tight control of blood sugar and blood pressure
  • Anti-VEGF injections
  • Steroid injections/implants
  • LASER
  • Vitrectomy
75
Q

when is an eye exam recommended for pt with diabetes?

A

when first diagnosed and annually thereafter

76
Q

how much is risk of retinopathy reduced by if tightly control blood sugar?

A

50%

77
Q

classification of diabetic retinopathy?

A

non-proliferative and proliferative

78
Q

proliferative retinopathy?

A

new blood vessels are formed on the retina and in the angle of the eye in response to ischemia

  • they are prone to leakage and bleeding
  • can also form diabetic macular edema (also occurs in non-proliferative stage)
79
Q

what is the goal of diabetic retinopathy txt?

A

control blood pressure and blood sugar

80
Q

what can diabetic retinopathy lead to?

A

retinal detachment -> blind

Clinical Medicine (11 decks)

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