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optho clinical Flashcards

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1
Q

what sort of patients get optic neuritis?

A

young white women

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2
Q

patient presents with:

  • Pain with eye movement
  • Unilateral decrease in vision developing over 1-2 weeks
  • Relative afferent pupillary defect (RAPD)
  • Optic disc may be swollen
A

optic neuritis

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3
Q

what patterns of visual field defects can you see in optic neuritis

A

o May be altitudinal
o May be central scotoma
o May be cecocentral pattern (central scotoma that has expanded to include the blind spot)

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4
Q

retrobulbar neuritis

A

describe optic neuritis that occurs in the portion of the optic nerve posterior to the globe
o Optic neuritis with a normal appearing optic disc
o Associated with multiple sclerosis
o Vision ranges from okay (> 20/40) to terrible (< 20/200)

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5
Q

patients with optic neuritis should have a brain MRI to assess for?

A

multiple sclerosis

-would see enhancement of optic nerve and white matter lesions

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6
Q

Treatment of patients with optic neuritis who have…

1) brain evidence of MS
2) no brain evidence of MS

A

1) IV corticosteroids +/- IFNb
2) no treatment, will resolve on it’s own
* do not treat with oral corticosteroids (will make optic neuritis worse)

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7
Q

papilledema

A

o Elevation of the optic nerve is more marked than in retrobulbar neuritis and is bilateral
o Due to increased intracranial pressure
o Normal visual acuity
o Normal pupillary response
o Intact visual field, with the exception of an enlarged blind spot in each eye

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8
Q

who gets non-arteritic ischemic optic neuropathy?

A
  • Typical age of onset is 50s-60s
  • Risk factors include hypertension, atherosclerosis, diabetes, hyperlipidemia, smoking and sleep apnea
  • Predisposing factors include reduced cup-to-disc ratio, optic nerve drusen and increased intraocular pressure
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9
Q

what is the mechanism of vision loss in non-arteritic ischemic optic neuropathy?

A

• Results from occlusion of the posterior ciliary arteries (in the lamina cribrosa area, behind the optic nerve head)

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10
Q

clinical presentation of non-arteritic ischemic optic neuropathy

A
  • Sudden, painless, unilateral loss of vision (often occurs upon awakening)
  • Swollen optic nerve with disc edema occurs within 24 hours after the onset of visual symptoms
  • It is NOT NAION if the optic nerve isn’t swollen
  • The contralateral eye will have a small, crowded disc
  • Visual defects tend to be altitudinal, with inferior defects being worse than superior defects
  • NO prodrome
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11
Q

clinical course and managment of non-arteritic ischemic optic neuropathy

A

clinical course:
• The loss of vision stays stable and generally does not progress
• Some visual recovery may occur

management: assess and treat underlying d/o, smoking cessation

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12
Q

Who gets temporal arteritis (arteritic ischemic optic neuropathy)?

A

• Exclusively in persons over 55 years of age (incidence increases with age)

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13
Q

what is the mechanism of disease in temporal arteritis (arteritic ischemic optic neuropathy)?

A

• Related to autoimmune response to internal elastic lamina of medium size arteries, caused by ulcerated atherosclerotic plaques

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14
Q

what is the clinical presentation of temporal arteritis (arteritic ischemic optic neuropathy)?

A
  • May have sudden, severe, initially unilateral loss of vision which can quickly become bilateral
  • Headache or pain over the temporal arteries
  • Jaw claudication – facial muscle pain with chewing (most sensitive and specific finding)
  • Weight loss, fever of unknown origin, anemia
  • Polymyalgia rheumatica
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15
Q

what lab values would you expect in temporal arteritis?

what do you need for a definitive diagnosis?

A
  • High ESR (always order Westergren ESR method)
  • High C-reactive protein
  • Thrombocytopenia

Temporal arterial biopsy (>2cm sample)
• Ordered within 2 weeks of presentation
• But do NOT wait for the results before initiating therapy
• If a biopsy is negative, repeat the biopsy in the contralateral temporal artery

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16
Q

what is the clinical course and treatment of temporal arteritis?

A

clinical course:
• Visual loss tends to be permanent
• If diagnosis is missed at early presentation in a single eye, it can often lead to bilateral blindness within hours to days

treatment:
• Immediate, high dose corticosteroids (IV methylprednisone, followed by oral prednisone)
• Do NOT wait for biopsy results; treat empirically and immediately if there is clinical suspicion!!!
• Steroids are given long term and tapered very slowly, under the management of a rheumatologist

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17
Q

what is the most common cause of unilateral or bilateral proptosis in adults?

A

thyroid related orbitopathy

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18
Q

what is the mechanism of disease in thyroid orbitopathy?

A

o Autoimmune disease where antibodies are formed against components in the orbit, especially (but not only) the extraocular muscles
• Tendons are spared
• Antibody deposition results in secondary edema
• In addition, cellular inflammatory response causes additional edema and eventual fibrosis

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19
Q

what do you need for the diagnosis of thyroid orbitopathy?

A 
•	Eyelid retraction + 1 of the following:
•	Thyroid dysfunction
•	Exophthalmos
•	Optic nerve dysfunction
•	Extraocular motility involvement
OR
•	Thyroid dysfunction + 1 of the following:
•	Exophthalmos
•	Optic nerve dysfunction
•	Extraocular movement involvement
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20
Q

treatment of thyroid orbitopathy

A

o 1st-line systemic treatment for INFLAMMATORY PHASE is oral corticosteroids
• Considered a short-term, temporizing measure for patients in the inflammatory phase of thyroid-related orbitopathy
• Corticosteroids have little effect on the exophthalmos or on the lid retraction

o 2nd-line systemic treatment for INFLAMMATORY PHASE is low dose radiotherapy
• Radiotherapy is given to the retro-orbital region

o In cases of severe involvement of the optic nerve, intravenous pulse therapy with methyprednisone has been shown to help (short-term)

o For severe optic neuropathy with visual loss and proptosis, surgery is preferred
• Orbital decompression
• Strabismus surgery
• Eyelid surgery

o Local treatment of thyroid-related orbitopathy includes supportive measures to prevent corneal exposure, such as the following:
• Topical lubricants
• Moisture chambers
• Tarsorrhaphy

o Diplopia can be helped with prisms and occlusion

o Urge smoking cessation! (smoking makes thyroid-related orbitopathy worse)

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21
Q

what is the mechanism of disease of idiopathic inflammatory orbital pseudotumor

A

diffuse inflammation involving any structure of the eye (including tendons! vs thyroid orbitopathy)

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22
Q

frequent cause of proptosis in adults

A

orbital psuedotumor

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23
Q

clinical presentation of orbital pseudotumor

A

o Usually sudden
o Usually accompanied by severe pain
o In adults, it is typically unilateral
o In children, it can be bilateral and associated with systemic symptoms (e.g. fever malaise), mimicking bacterial orbital cellulitis
o In some cases, “orbital apex syndrome” can be present and vision can be decreased because of compression
o Although infrequent, it can affect the paranasal sinuses
o There is a rare sclerosing variant can lead to blindness and necessitate orbital exenteration

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24
Q

clinical course and treatment of orbital pseudotumor

A

clinical course:
• Clinical Course
o Recurrences are very common
o Long-term sequelae can include any of the following: Diplopia, Exophthalmos, Visual loss

Treatment:
o Oral prednisone, with slow tapering over several weeks
• The response to corticosteroids is extremely dramatic, with the patient often feeling better after a single dose!
o If pseudotumor continues to recur, low-dose radiation should be considered

25
Q

what tests can you do to confirm the diagnosis of myasthenia gravis?

A

o Edrophonium injection
• Provides a quick response in positive patients
o Applying an ice pack over a ptotic eyelid will provide temporary resolution of the ptosis is myasthenia gravis is the causative etiology
o Note: acetylcholine receptor antibodies are negative in up to 50% of patients who only have ocular myasthenia gravis
o If acetylcholine receptor antibody test is negative and suspicion, a single fiber EMG can be performed
o If diagnosis is confirmed, a chest CT should be performed, to check for a thymoma

26
Q

what is the treatment for myasthenia gravis?

A

o Pyridostigmine (acetylcholinesterase

27
Q

key features of conjunctivitis

A

moderate discharge
no pain
no decreased vision
normal pupil

28
Q

key features of keratitis

A 
=inflammation of cornea
\+/- discharge
\+ pain
\+decreased vision
nl pupil
29
Q

key features of iritis

A 
=inflammation b/t lens and cornea
- discharge
\+ pain
\+ dec. vision
smaller pupil
30
Q

key features of glaucoma

A 
(acute angle closure)
- discharge
\++pain
\++ dec vision
dilated and fixed pupil
31
Q

Pt presents with red eyes. There is watery discharge, tender palpable preauricular node. The patient recently recovered from a URI

A 
viral conjunctivitis (highly contagious, spread hand to eye)
-tx:  cool compresses and drops
32
Q

Pt presents with red eyes. There is bilateral itching of eyes. There is a stringy mucous discharge. He has a hx of asthma

A

allergic conjunctivitis

tx: cool compresses, topical or systemic antihistamines, NSAIDS, mast cell stabilizers

33
Q

patient presents with red eyes and purulent discharge of the eyes.

A

bacterial conjunctivitis

tx: quinolones for broad spectrum coverage including psuedomonas, (cipro, ofloxacin, levofloxacin, moxifloxacin)

34
Q

patient presents with a red eye, that is painful and sensitive to light. He wears contacts. You also notice a white spot on the cornea (corneal epithelial defect).

A

bacterial ulcer

1) mild-moderate (peripheral): topical fluoroquinolones
2) moderate-severe (central): topical fortified antibiotics (tobramycin/gentamycin + cefazolin/vancomycin)

35
Q

A patient presents with red eye accompanied by moderate pain. You do a topical fluorescein stain and notice a tree branching area of staining

A

HSV keratitis

  • aggravated by topical steroids (don’t give!)
  • tx with topical or oral antivirals
  • tends to recur, may result in permanent scarring
36
Q

Iritis

A

signs/sx: circumcorneal injection, photophobia secondary to blunt trauma, keratitis
-assoc/ w/ systemic diseases (sarcoidosis, CT conditions) or idiopathic

37
Q

Topical anesthetics assoc/ w/

A

severe corneal infections/ulcerations

never perscribe!

38
Q

topical steroids in eye assoc w/

A

complications including glaucoma, cataracts, enhancing HSV infection

39
Q

chlamydia conjunctivitis

A

neonates=systemic disease
sexually active adults
tx: systemic erythromycin, tetracycline, azithromycin

40
Q

blepharitis

A

inflammation of eyelid margin, assoc w/ dry eyes

-tx: warm compress, eyelid scrub, antibiotic gel/ointment, systemic tetracylclines

41
Q

opthalmia neonatorum (neonatal conjunctivitis) DDX

A
  1. chemical conjunctivitis (silver nitrate prophylaxis)
  2. chlamydia
  3. gonococcus
  4. staph, strep, pseudomonas, HSV

prophylaxis is erythromycin ointment

42
Q

contact lens complications

A
  1. giant papillary conjunctivitis
  2. tight contact lens syndrome
  3. toxic/allergic rxn to chemicals in contact lens solution
  4. bacterial corneal ulcers (esp. pseudomonas)
  5. acanthamoeba keratitis
43
Q

Red eye danger symptoms

A
  • dec. vision
  • pain
  • photophobia
44
Q

Red eye danger signs

A
  • corneal fluorescein staining
  • corneal edema
  • circumcorneal injection
  • abnormal pupil size or reaction (abnormal eye pressure)
45
Q

urgent red eye conditions

A
  • corneal infection
  • iritis
  • acute angle closure glaucoma
  • orbital cellulitis
  • trauma: hypema (blood in anterior chamber) or laceration
46
Q

one way to differentiate optic neuritis vs papilledema

A

papilledema has bilateral swelling of optic disc vs optic neuritis is unilateral

47
Q

which drug increases the risk of recurrent optic neuritis

A

oral prednisone

48
Q

patients with optic neuritis and brain MRI findings should be treated with

A

IV methylprednisone

49
Q

older patient with hypertension, diabetes, and atherosclerosis develops monocular, sudden, painless visual loss. There is evidence of disc edema. Dx?

A

non-arteritic ischemic optic neuropathy
no effective treatment
-some visual function can be recovered

50
Q

patient (age>55) presents with sudden, severe, unilateral vision loss and jaw claudication

A

arteritic ischemic optic neuropathy
tx is immediate, high dose corticosteroids (don’t delay b/c can lead to bilateral vision loss quickly)
-visual loss tends to be permanent

51
Q

treatment of myasthenia gravis

A

pyridostigmine

52
Q

what is the leading cause of vision loss in diabetics?

A

macular edema

sx: blurred or distorted vision and poor night vision

53
Q

describe diabetic retinopathy

A

microvascular disease; early histo findings include capillary damage characterized by thickening of basment membrane and pericyte dropout mediated by VEGF

54
Q

what would you see in mild non-proliferative diabetic retinopathy? What about severe?

A 
mild:
o	Microaneurysms
o	Dot and blot hemorrhages
o	Hard exudates
o	Cotton wool spots (small retinal infarctions)
o	Macular edema
moderate:
o	Increased hemorrhages
o	Dilated and beaded veins
o	Macular ischemia
o	Intraretinal microvascular abnormalities
55
Q

what happens in proliferative diabetic retinopathy?

A

o Capillary nonperfusion leads to neovascularization
o Fragile new vessels tend to bleed
o Fibrous tissue grows along new vessels→touches vitreous body→vitreous hemorrhages→Floaters, traction retinal detachment (lead to blindness)

56
Q

risk factors for presence of diabetic retinopathy?

A 
o	Duration of disease
o	Age of onset
o	Glycemic control
o	BP control
o	Serum lipid levels
57
Q

medical management of diabetic retinopathy

A

o Excellent glycemic control (HbA1c<130/85

58
Q

surgical treatment of diabetic retinopathy

A

o Laser treatment—panretinal photocoagulation
o Intravitreal injection of triamcinolone (can cause cataracts and glaucoma so reserved for patients with worst vision and unresponsive to other therapy)
o Vitrectomy surgery: remove vitreous and fibrovascular tissue; indicated in non-clearing vitreous hemorrhage and traction retinal detachment

neuro.psych.optho (8 decks)

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