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(PA school) CAM I > Ophthalmology II > Flashcards

Ophthalmology II Flashcards

1
Q

Open Globe/Ruptured Globe:
1) Define this condition
2) Full thickness break of the eye wall includes what 2 things?

A

1) Blunt or penetrating trauma to the eye, usually from a sharp object or projectile.
2) Sclera and cornea.

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2
Q

Open Globe/Ruptured Globe: how is it treated?

A

1) Requires emergent Ophthalmic consultation
LEAVE THE EYE ALONE
Can apply eye shield for protection
Do not put anything in the eye
Avoid any pressure on the globe or eye exam procedures
Avoid topical meds
2) CT scan of orbits
3) IV antibiotics per ophthalmology
-Typically Vancomycin + Ceftazidime

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3
Q

What condition is more common in young males and is generally caused by assaults, MVCs, or being struck by a ball in the face/eye?

A

Orbital Fractures

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4
Q

Orbital “Blowout” fracture
1) Who is at risk? What pt of the orbit is involved?
2) What are the Sx?
3) How is it diagnosed?

A

1) History of small, round, high-speed object (ex: baseball) strikes the eye/orbit.
In one study, half of all orbital fractures involved the inferior wall or floor of the orbit.
2) Bruising and soft tissue swelling, pain
3) CT imaging

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5
Q

Orbital “Blowout” fracture
1) How is it treated?
2) What a significant consequence of Fx of orbital floor?
3) Ischemia and subsequent loss of muscle function may occur bc of one of what two things? Which is more likely in adults

A

1) Requires ophthalmology referral + hospitalization
2) Entrapment of the inferior rectus muscle and/or orbital fat.
3) Entrapment of muscle within the fracture fragment (more likely in children)
-or as the result of edema and hemorrhage of muscle that have prolapsed through the fracture into the maxillary sinus (more likely in adults)

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6
Q

Chemical ocular injury:
1) Eye contact with what two things requires emergency evaluation and treatment to prevent permanent vision loss?
2) Which of these usually causes more severe damage? Which should you assume if unknown?

A

1) Acids or alkalis
2) Alkaline substances(can eat through the eye in minutes); assume alkali if unknown

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7
Q

Chemical ocular injury: Are alkaline substances a true medical emergency? What should you do prior to pt leaving office?

A

Yes, true ocular emergency; referral to ophthalmology prior to patient leaving office

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8
Q

Chemical ocular injury:
1) How does it typically present?
2) What is the Tx?
3) What is commonly used in the emergency dept?

A

1) Decreased vision, moderate-to-severe pain, conjunctival redness, inability to open eyelids, and photophobia
2) Profuse continuous irrigation with water or saline (until neutral pH is achieved, takes approx. 30-60 mins for most injuries)
3) Morgan lens (anesthetize first)

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9
Q

1) What is retinopathy a complication of?
2) What is it?
3) What does it involve the abnormal growth of?
4) What is it the leading cause of?

A

1) HTN or DM
2) Damage to the blood vessels at the light-sensitive tissue at the back of the eye (retina)
3) Blood vessels in the retina
4) Preventable blindness

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10
Q

What is the most common cause of vision loss ages 20-74 in many countries?

A

Retinopathy

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11
Q

What condition contributes to the importance of regular eye exams, especially for those with risk factors?

A

Retinopathy

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12
Q

What are the Sx of retinopathy?

A

Blurred vision
Floaters
Dark or empty areas of vision
Fluctuating vision

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13
Q

Diabetic Retinopathy:
1) Define this condition and describe how it happens
2) How does it present? What are the stages?

A

1) A microvascular complication of diabetes mellitus (DM)
-Damage to retinal blood vessels leads to retinal ischemia and edema
2) Asymptomatic until late stages; visual impairment that may progress to blindness
Nonproliferative (early) and proliferative (late)

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14
Q

Microaneurysms (red dots), leaking capillaries that can then become occluded, are characteristic of what?

A

Diabetic retinopathy

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15
Q

What are the retinal findings of diabetic retinopathy?

A

Dot and blot hemorrhages
Hard exudates
Cotton-wool spots
Diabetic macular edema (DME)

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16
Q

Describe the 2 stages of diabetic retinopathy

A

1) Nonproliferative – early stages – the walls of the blood vessels weaken, and blood can leak into the retina
2) Proliferative – late stages, needs urgent treatment – abnormal new vessels grow onto the retina

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17
Q

Diabetic Retinopathy: When should you screen for it with each type of diabetes?

A

Type 1 DM: initial screening @ 5 years after diagnosis
Type 2 DM: initial screening @ time of diagnosis, then yearly or PRN

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18
Q

What are the risk factors for diabetic retinopathy?

A

1) Diabetes obviously
2) Poor glycemic control
3) HTN
4) CKD with proteinuria or anemia

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19
Q

What are the potential treatments for diabetic retinopathy?

A

1) Optimize blood glucose control
2) Intraocular anti-vascular endothelial growth factor (anti-VEGF)
3) Injections (Ranibizumab, bevacizumab)
4) Peripheral photocoagulation (laser)
5) Surgery

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20
Q

Hypertensive Retinopathy:
1) Define this condition
2) How does it present?

A

1) Retinopathy related to arteriolar sclerosis and chronic elevated blood pressure leading to ischemia
2) Asymptomatic until late stages when vision is impaired

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21
Q

What are the retinal findings with Hypertensive Retinopathy?

A

1) Copper/silver wiring
2) Exudates – stellate configuration referred to as “macular star”
3) Flame-shaped hemorrhages
4) Subretinal edema, optic disc swelling
5) AV nicking
6) Cotton wool spots

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22
Q

List and describe the 3 stages of hypertensive retinopathy

A

1) Mild: arteriolar narrowing, AV nicking, copper wiring
2) Moderate: retinal hemorrhages (blot, dot, flame-shaped hemorrhages), cotton wool spots, exudates
3) Severe: moderate retinopathy findings plus swelling of the optic disc (papilledema)
-Often involves acute changes in increased blood pressure

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23
Q

What are the 2 treatments for hypertensive retinopathy?

A

1) Control blood pressure and lipids
2) Laser treatment

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24
Q

List 2 types of retinopathy

A

Diabetic retinopathy and hypertensive retinopathy

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25
Q

Name a risk factor for diabetic retinopathy

A

Diabetes mellitus

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26
Q

Describe the visual pathway

A

1)Light must follow an unhindered path from the front to the back of the eye, traveling through the cornea, aqueous humor, lens, and vitreous humor to the retina.

2) Refracted by cornea and lens (+also by glasses/contact lenses), light is focused onto the retina & turned into an electrochemical signal by photoreceptors and supporting cells.

3) Signal is transmitted via the optic nerve thru visual pathways to occipital lobes.

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27
Q

Optic neuritis:
1) Define it
2) What kind of vision loss? Explain why
3) Sx?
4) Most common cause?

A

1) Acute inflammation and demyelination of the optic nerve which results in acute monocular vision loss and pain with eye movement (stretching the optic nerve at posterior aspect of eye)
2) Monocular vision loss; caused by an ocular issue anterior to the optic chiasm (one eye or optic nerve)
3) Acute onset of monocular vision loss/blurred vision and pain in affected eye
4) Most common cause is Multiple Sclerosis (MS)

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28
Q

Describe the results of an optic neuritis exam

A

Documented newly impaired vision, fundoscopy (blurred optic disc):
1) Presents with a relative afferent pupillary defect (RAPD, also called Marcus Gunn Pupil)
-A condition in which pupils respond differently to light stimuli shone in one eye at a time due to unilateral disease of the retina or optic nerve.
2) Swinging flashlight test: Pupil dilates instead of constricts when light is swung to the eye
3) MRI to confirm demyelination of optic nerve

29
Q

How is optic neuritis treated?

A

IV methylprednisolone, referral to Neurology

30
Q

Papilledema
1) Define papilledema. Bilat or unilat?
2) What are the Sx?
3) Tx?

A

1) Swelling of the optic disc secondary to increased intracranial pressure; classically bilateral
2) No early symptoms, generally asymptomatic (vision often minimally impaired)
-May have symptoms of increased intracranial pressure (headache, dizziness, N/V)
3) ID & treat the underlying cause to decrease intracranial pressure

31
Q

1) What is the testing for Papilledema?
2) What are potential causes?

A

1) Fundoscopy followed by MRI and perhaps lumbar puncture; MRI to determine underlying cause
2) Tumor
Brain bleed
Cerebral edema (infection, trauma, bleed)
Obstruction of CSF flow (hydrocephalus)
Idiopathic (pseudotumor cerebri, elevated intracranial pressure without mass lesion)

32
Q

List 5 common causes of blindness

A

1) Cataracts
2) Uncorrected refractive errors
3) Glaucoma
4) Age-related macular degeneration
5) Diabetic retinopathy

33
Q

Define uncorrected refractive errors and give examples

A

1) Refractive errors that could be corrected with glasses but have not been
2) Myopia, hyperopia, astigmatism, presbyopia

34
Q

Chronic vision loss:
1) Define
2) 3 major causes?

A

1) Chronic vision impairment in the elderly
2) Glaucoma, cataracts, age-related macular degeneration

35
Q

Glaucoma:
1) Define it
2) What are the 2 main types?

A

1) An abnormality in the drainage system of aqueous humor, causing fluid to build up and leading to increased intraocular pressure in the eye.
2) Acute angle-closure glaucoma and chronic open-angle

36
Q

Acute angle-closure glaucoma
1) Define
2) Risk factors?

A

1) Sight-threatening medical emergency due to increased intraocular pressure (IOP) which is the fluid pressure in the eye
2) Age, family hx, black race, increased IOP

37
Q

Acute angle-closure glaucoma
1) Describe the Sx
2) Give the classic triad on exam

A

1) Acute, unilateral, onset of severe ocular pain, impaired vision (colored halos or rainbows around light), red teary eye, headache, N/V
2) Red eye; hazy cornea; fixed, dilated pupil

38
Q

Chronic open-angle glaucoma:
1) Define
2) Is it more or less common than acute angle?

A

1) Impaired outflow of aqueous humor through diseased trabecular meshwork resulting in a gradual increase in IOP with insidious progressive optic nerve damage leading to peripheral visual field loss
2) Common ~ 90% of glaucoma cases

39
Q

Chronic open-angle glaucoma:
1) Describe the presentation and Sx
2) How can it be diagnosed?

A

1) Risk factors are same as acute angle-closure; asymptomatic
2) During routine IOP screening and fundoscopic exam demonstrating optic nerve damage

40
Q

Differentiate between glaucoma and macular degeneration

A

1) Progressive peripheral vision loss > central vision loss = glaucoma
2) Progressive central > peripheral vision loss = macular degeneration

41
Q

Acute glaucoma:
1) How do you measure IOP? What is normal IOP?
2) When does screening begin?

A

1) Measure IOP using a Tonopen; ~10-21mmgHg
Commonly performed in ER when indicated
2) Annual screening ~ 40 years old

42
Q

For screening purposes of chronic open-angle glaucoma, measurement of______ is not valuable and the best indicator relies on elevated cup : disc ratio seen in fundoscopy
Fundoscopic exam: cupping of the optic nerve
Optic cup: disc ratio > 0.5 is suggestive

A

1) IOP; elevated cup

43
Q

Acute angle-closure glaucoma:
1) When must it be treated? Why?
2) What is the focus of Tx?
3) What medications are given?
4) What is the definitive Tx?

A

1) Must be treated within hours to avoid irreversible damage to optic nerve
Focus on decreasing IOP via decreased aqueous humor production
Pressure-lowering topical and systemic agents are administered
Topical B-blocker (Timolol) – decreases IOP via decreased AH production without affecting visual acuity
Miotics/cholinergic (pilocarpine) – affect vision
Definitive treatment is laser peripheral iridotomy (performed same day by ophthalmologist) – holes in iris

44
Q

Chronic open-angle glaucoma:
1) Is it reversible?
2) What does Tx focus on?
3) Describe 3 ways to treat

A

1) Irreversible disease – management focuses on slowing progression and preserving quality of life
2) Focus on reducing IOP and maintaining normal ocular pressure
3) Prostaglandin analogs (Latanoprost) – increase AH outflow
-Topical B-blocker (Timolol) decrease production of AH
-Smoking marijuana (cannabis) can lower IOP – however not clinically indicated because it does not change the course of the disease, is short-acting, and has other adverse effects

45
Q

List the categories of glaucoma meds

A

1) Cholinergic agents
-Pilocarpine
2) Prostaglandin analogs
-Xalatan (latanoprost)
3) Beta blockers
-Timolol
4) Alpha agonists
-Brimodine
5) Carbonic anhydrase inhibitors (CAIS)
-Acetazolamide

46
Q

Glaucoma meds:
1) How do cholinergic agents lower IOP?
2) How do beta blockers lower IOP?
3) Give examples of beta blockers

A

1) Increasing aqueous outflow (drainage) through the trabecular network
2) Decreasing production of fluid in the eye (reduces formation of aqueous humor by the ciliary body)
3) Timolol, Betaxolol, Careolol

47
Q

Glaucoma meds:
1) How do prostaglandin analogs lower IOP?
2) Give examples of prostaglandin analogs

A

1) Increasing outflow of fluid from the eye (drainage)
2) Xalatan (latanoprost, now available in generic)
-Lumigan (bimatoprost), Travatan (travaprost), Zioptan (tafluprost)

48
Q

Glaucoma meds:
1) How do alpha agonists lower IOP? Give 2 examples of meds in this group
2) How do Carbonic anhydrase inhibitors (CAIS) lower IOP?

A

1) Both decrease production of fluid AND increase drainage
-Alphagan P (brimodine); Iopidine
2) Decreasing the production of intraocular fluid (aqueous humor)

49
Q

1) Leading cause of blindness worldwide is what?
2) What are the Sx of this condition?

A

1) Cataracts
2) Opacity of the lens, causes blurring or distorted vision.
-Painless; progression highly variable

50
Q

Cataracts:
1) Risk factors
2) How does it present?

A

1) Age (usually > 70 yrs. old), smoking, ETOH, UV exposure, diabetes, metabolic syndrome, prolonged drug use (glucocorticoids, statins), HIV/AIDS, and radiation.
2) Slowly progressive visual impairment

51
Q

Cataracts:
1) What would you see during an exam?
2) What is the Tx?

A

1) Diminished red reflex, may note clouding of lens, difficulty seeing retina and posterior structures
2) Generally, very successful treatment with surgical removal.
-Initial treatment can include activity modification and observation

52
Q

Cataracts:
1) What do they do to the eye?
2) What are some potential vision changes?

A

1) Cataracts causes an opacity/clouding of the lens
2) Cloudy/blurry
-Can’t see well at night
-Double vision
-Halos around lights
-Lamps, headlights seem too bright

53
Q

1) Why are cataracts so common?
2) How common are they?
3) Can they be treated easily?
4) What do you need to ensure is not the cause?

A

1) Lens grows throughout life – increased cortical fibers increases thickness
2) Age-related: most persons over the age of 70 will have some degree of cataracts
3) One of the most successfully treated conditions in all of surgery
4) Glaucoma, retinopathy, or macular disease

54
Q

Age-related Macular degeneration (AMD):
1) Is the leading cause of what?
2) What are the Sx?
3) What are the 2 types?

A

1) Visual impairment and vision loss in developed countries
2) Gradual vision loss, blurry vision, mostly affecting central vision, so that things in the center look blurry.
3) Dry and Wet AMD

55
Q

Age-related Macular degeneration (AMD):
1) Risk factors?
2) Tx?

A

1) Aging (>65 yrs. old), smoking is the strongest modifiable risk factor for developing AMD
2) Special combination of vitamins and minerals (AREDS formula), smoking cessation (slows progression)
-Patients with wet AMD can be treated with anti-VEGF drugs
(which have developed significantly in past two decades)

56
Q

Age-related Macular degeneration (AMD): describe the two types and how common they are

A

1) Dry AMD: more common (85-90%), more chronic, lose vision slowly
2) Wet AMD: less common (10-15%), more acute, vision loss can happen quickly

57
Q

Macular degeneration:
1) What is it related to?
2) Describe how it usually presents
3) Is central or peripheral vision loss worse?

A

1) Age-related
2) Painless loss of central vision
Decreased as wavy or distorted vision
Difficulty driving and reading
3) Central > peripheral vision loss

58
Q

Macular degeneration:
1) What would you see on otoscopy?
2) What test do you use to screen for it?
3) What is the the most common cause of in the elderly?

A

1) Areas of retinal depigmentation and presence of yellow retinal deposits (drusen)
2) Amsler Grid test
3) Central visual loss and permanent blindness

59
Q

Giant Cell Arteritis, also known as Temporal Arteritis:
1) Define
2) Risk factors?
3) What are 2 diagnostic studies? Are they required?

A

1) Inflammation of the lining of the arteries near your temples.
2) Age (> 60-70 years old) and strong correlation with Polymyalgia Rheumatica (PMR)
-Never occurs in individuals under 50 years of age
3) Elevated ESR (sed rate) and CRP levels; can be Dx’d clinically

60
Q

Giant Cell Arteritis:
1) Sx?
2) Is the visual loss binocular or monocular? Transient or permanent?
2) What can happen if left untreated?
3) Tx?

A

1) New onset headaches, scalp tenderness, claudication (jaw pain), unexplained fever, and vision problems
2) Transient or permanent monocular vision loss
3) Can cause blindness
4) IV steroids (methylprednisolone), hospital admission for temporal artery biopsy

61
Q

Retinal detachment:
1) Define
2) Risk factors?

A

1) Medical emergency in which thin layer of tissue at the back of the eye pulls away from its normal position. Separates retinal cells from the blood vessels that provide oxygen and nourishment to the eye.
2) Myopia (nearsightedness), aging (> 50 years old), family history, previous eye surgeries

62
Q

Retinal detachment: what is the hallmark presentation?

A

1) Flashes of light (photopsia)
2) Floaters: sudden appearance of many floaters
3) Painless, sudden vision loss
-A curtain-like shadow descending over the visual field

63
Q

Retinal detachment:
1) Why does this happen?
2) What does it often present with?

A

1) Mostly spontaneous
2) A peripheral field defect

64
Q

Retinal detachment:
1) What happens the longer it goes untreated?
2) What are 2 ways to test for it?

A

1) The longer is goes untreated, the greater the risk of permanent vision loss in the affected eye.
2) Fundoscopy and ultrasound

65
Q

Retinal detachment:
1) Tx?
2) How should you position the pt?

A

Ophthalmologic emergency:
1) Surgery: pneumatic retinopexy (cryoretinopexy followed by an injection of air bubble)
2) Keep patient supine, head turned toward side of detached retina.

66
Q

Retinoblastoma:
1) Define
2) Who’s it most commonly found in?
3) Who should be screened?
4) What is seen on PE?

A

1) Rare malignant eye cancer that forms in the back of the eye (retina)
2) Children
3) Anyone with family history
4) Absent red reflex or if pupil appears white (when light is shined upon it); refer any kids who come in w this

67
Q

List and describe the 3 types of retinal detachment. Which is most common?

A

1) Rhegmatogenous: most common subtype, slowly pulls away
2) Traction: fibrosis prolif. leads to tissue that pulls
3) Serous: fluid behind retina leads to detachment

68
Q

List the 9 Steps For Evaluation The Red Eye

A
  1. Visual acuity: normal or not?
  2. Visual inspection– pattern of redness
    Subconjunctival hemorrhage, conjunctival hyperemia, ciliary flush, etc.
  3. Presence of conjunctival discharge
    Profuse or scant? Purulent, mucopurulent, serous?
  4. Detect corneal opacities with pen light, transilluminator, or slit lamp
    Corneal ulcer, corneal abrasion, irregular corneal reflection
  5. Fluorescein stain cornea for disruption
  6. Anterior chamber: Estimate depth as normal or shallow
    -Detect layered blood (hyphema) or pus (hypopyon)
  7. **Assess pupils for size, symmetry, response to light
  8. If elevated IOP suspected and reliable tonometer available, measure IOP**
    -Omit if obvious external infection
  9. Detect the presence of proptosis, eyelid malfunction, or any EOM limitations
69
Q

When a pt has vision loss, what’s a good first question to ask?

A

Painless or painful?

(PA school) CAM I (29 decks)

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