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Ocular Disease III > Optic Neuropathies Part III > Flashcards

Optic Neuropathies Part III Flashcards

1
Q

Compressive optic neuropathy can have a progressive onset, vision loss and central VF involvement, dyschromatopsia, +/- ______, +/- optic nerve _____, +/- optic nerve ______

A

APD; edema; pallor

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2
Q

You won’t see edema with _____

A

pallor; nerves have died off

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3
Q

non neoplastic compressive optic neuropathy can deal with ____ eye disease, aneurysm due to _____, anterior cerebral artery, or ophthalmic artery aneurysm.

A

thyroid; ICA

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4
Q

neoplastic compressive optic neuropathy can be intracranial due to:

A
  1. sphenoid wing meningioma
  2. pituitary adenoma
  3. metastases
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5
Q

neoplastic compressive optic neuropathy can also be involved with your optic nerve due to:

A
  1. optic nerve sheath meningioma

2. optic nerve glioma

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6
Q

optic nerve sheath meningioma is mainly in _____. F >M, seen in the fourth decade. It presents with _____ , optic nerve collateral vessels, and gradual VA loss

A

adults; pallor

treated with radiation therapy

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7
Q

what two conditions cause shunt vessels

A
  1. glaucoma

2. CRVO

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8
Q

in neuroimaging, optic nerve meningioma presents with a train track appearance bc?

A

meninges are thickened by the tumor

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9
Q

Optic nerve ______ is seen in children, usually seen before age ____, and 50% have _____.

A

glioma; 20; NFI

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10
Q

what is NFI

A

genetic disorder due to nervous system tumor, most tumors are benign in children, but high mortality in adults.

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11
Q

neurofibromas are _____ nerve tumors

A

peripheral

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12
Q

optic nerve sheath meningioma think:

A

adults, collateral shunt vessels and ON pallor

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13
Q

optic nerve glioma think:

A

kids, proptosis, NF1.

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14
Q

glioma in adults you have to ________

A

neuroimaging.

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15
Q

compressive optic neuropathy can also be due to _______ adenoma which is seen in mainly adults. F > M in the 4th or 5th decade. It is a slow growing epithelial tumor and can be due to ______

A

pituitary; hyperpituiatrism

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16
Q

What can hyperpituitarism cause?

A
  1. cushing syndrome due to excess ACTH: excessive cortison, moon face, big trunk,
  2. acromegaly due to excess growth hormone; prominent brows, and jaw
  3. prolactinoma: amenorrhea, galactorrhea, infertility, decreased libido
  4. hyperthyroidism: goiter
  5. Excess LH/FSH: precocious puberty in children and decreased libido in adults
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17
Q

A ______optic neuropathy will usually be due to trauma and will cause a forceful backward dislocation of optic nerve from scleral canal bc of blunt force. Optic nerve avulsion will be ______

A

laminar; irreversible

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18
Q

An _____orbital trauma will be due to a penetrating foreign body, displaced fracture or bone fragment, or compression by hematoma. What will it appear like?

A

intra orbital

usually direct injury to CRA and disc edema

In this case order a CT scan cause it will tell you if its in the orbit or globe and show hematomas.

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19
Q

_______ trauma is the most common intracanalicular trauma. It occurs with/without fracture. Optic nerve appears normal initially but pallor develops _____weeks later, if its direct injury it will be from damage from bone fragments. Indirect injury is because of tearing of _____ blood vessels or shearing of axons or edema

A

Intracanalicular; 4-6; pial

20
Q

In a traumatic optic neuropathy VA will be typically poor immediately after trauma, and you will have a + _______as well as VF defects

A

RAPD

21
Q

Why is it useful to document VF defects in a traumatic optic neuropathy

A

return of vision or progression of VF loss

22
Q

how do you manage traumatic optic neuropathy

A
  1. mega dose corticosteroids to decrease edema

2. optic nerve decompression done if there is continuous deterioration or no improvement in vision.

23
Q

What bacteria can cause infectious optic neuropathy

A
  1. bartonella henselae: cat scratch
  2. TB
  3. Trepenoma pallidum (STD)
  4. Lyme (tick bite)
24
Q

A fungal infection is usually rare but may be due to DM or immunocompromised patients (AIDS) - cryptococcal meningitis, or mucucormycosis which is extension of _____.

A

sinusitis

25
Q

A virus infection is due to:

A
  1. HZV
  2. Measles
  3. Mumps
  4. Chickenpox
26
Q

A parasitic infection is due to

A
  1. toxoplasma

2. toxocara

27
Q

If you have a swollen nerve with some exudates and sort of inflammation, that points to an _____

A

infection

28
Q

an infectios optic neuropathy presents with sudden or gradual (a few days) VA loss in one or both eyes. It may present with _____, lymphadenopathy, RAPD, macular edema, or anterior uveitis/vitritis/vasculitis, and swollen optic disc

A

fever

29
Q

Stellate ______usually deals with the macula and deals with inflammation of the nerve and retina.

A

neuroretinitis; star appearance around macula

30
Q

How do you manage a pt with infectious etiology

A

urgent referall to PCP for bloodwork.

  • CBC with differential
  • ESR (GCA)
  • CRP (GCA)
  • Bartonella henselae titers
  • Lyme titers
  • RPR-VDRL
31
Q

_______ optic neuropathy is usually painless, slowly progressive, bilateral, symmetric vision loss. VA ranges from 20/50 - _____. You will see characteristic VF loss and ONH pallor

A

nutritional; 20/200;

32
Q

Exam findings for nutrional optic neuropathy include ____ ONH pallor, centro cecal VF defects (extends from ONH to macula), dyschromatopsia, and no _____

A

temporal; RAPD (bilateral, and symmetric)

33
Q

Vitamin ____ must be ingested and converts carbs into glucose. Vitamin _____ helps with serotonin, norepineprine, and myelin formation. Vitamin ____ is critical for cell growth and metabolism. Vitamin ____ is critical for RBC formation and nerve function.

A

B1; B6, B9; B12

34
Q

Vitamin B12 deficiency is usually due to pernicious anemia which is due to decrease in RBC due to poor absorption of B12. It is an autoimmune condition. Neurologic symptoms include peripheral neuropathy, numbness, tingling ,and decreased deep tendon reflexes. B12 deficiency is also due to _____ surgery bc B12 absorption is imparied

A

GI

35
Q

With alcoholics, they have poor intake of B1 and B12, and poor absorption of it. Improves with _______Tobacco-alcohol amplyopia is ______ optic nerve toxicity

A

vitamin supplementation synergistic

36
Q

how do you manage nutritional optic neuropathy

A
  1. Lab studies: CBC with differential, B1, B12, folate, RPR-VDRL, and Lyme
  2. ERG to rule out rod/cone dsytrophy
  3. B12 injections q1 mo x few months
  4. multivitamin supplements.
37
Q

Toxic optic neuropathy can be due to medications, or ____ ingestion. Name some meds or toxic things

A

substance

  • Anti Tb meds: ethambutol, isoniazid
  • cancer chemotherapy agents

-lead, methanol, tobacco

38
Q

______optic neuropathy is usually seen after treatment for ocular, sinus, intracranial and infraorbital malignancies. It is due to cumulative damage to _____cells and vascular _____ cells. It can occur after 3 years of radiation. No proven treatment, but steroids may help. HISTORY here becomes critical

A

Radiation; glial; endothelial

39
Q

Hereditary optic neuropathy can be autosomal dominant, autosomal recessive, ____ linked or mitochondrial

A

X

40
Q

_____ hereditary optic neuropathy is a _____ disorder which is contributed maternally. Begins at age ___-35

A

Lebers’ mitochondrial; 25

41
Q

Leber’s is acute severe vision loss in ____ eye. Fellow eye is involved in 2-4 weeks. It may be triggered by alcohol/tobacco abuse. VF loss will be central or ceco central scotoma. Optic nerve will initially be _____ then pale. There will be dilation of peripapillary retinal vessels and optic nerve does not leak on _____

A

one; hyperemic; FA

42
Q

Diff between Lebers and AION is that:

A

AION is within 24 hours/days, Lebers is within a couple of weeks. AION is pallid and its in older females. AION will leak on FA

43
Q

How do you manage Lebers

A
  1. Rule out other causes by neuroimaging, lab tests
  2. Genetic counseling once genetic mutation has been identified.
  3. Electrocardiogram: may have associated cardiac conduction deficits.
  4. Advised to limit tobacco and alcohol intake.
  5. No FDA approved treatment.
  6. Oral administration of idebenone. Enters brain to stimulate ATP formation in mitochondria.
  7. Gene therapy
44
Q

Autosomal dominant Optic ATrophy is more common than Lebers, it is the most common inherited optic neuropathy and is also called Kjers Dominant Optic atrophy. It is ____ , symmetric, slowly progressive central VF loss. Vision abnormalities begin in childhood (4-10). VA ranges from 20/30 - ______. They will have a ____ color vision defect. They will present with NFL defect in _______ bundle

A

bilateral; 20/200; tritan; papillomacular

45
Q

The gene that encodes for mitochondrial gene, not the actual mitochondria is mutated in autosomal dominant optic atrophy. There is an equal prevalence in M and F. Treat with ____ ____ aids and prognosis is usually stable after adulthood

A

low vision

Ocular Disease III (16 decks)

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