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Flashcards in Clinical- 7 Deck (56):
1

Review the eye anatomy

on yer own ya filthy animal

2

What is diplopia?

double vision

3

What causes diplopia?

misalignment of the eyes

4

What is opthalmoplegia?

When the extraocular muscle fxn is disrupted

5

How is the derp in opthalmoplegia?

You derp to the opposite direction because of unopposed action of the other muscles

6

What is ptosis?

droopy eyelid

7

What are the 2 causes for ptosis?

damage to either III (LPS) or symapathetics (sup tarsal)

8

Quick fire eye lesions/conditions/Sx: I will say a Sx and you tell me where the lesion is. Ready?

Total blindness of L eye

L optic n lesion

9

Bitemporal hemianopia

pituitary tumor/ optic chiasm lesion

10

L nasal hemianopia

calcified internal carotid

11

central scotoma

optic or retrobulbar neuritis

12

L homonymous hemianopia (2)

R optic tract lesion OR complete lesoion of the R optic radiation

13

L homonymous hemianopia + macular sparing

R PCA occlusion

14

L homonymous inferior quadrantanopia

R parietal lobe lesion

15

L homonymous supeiror quadrantanopia

R temporal lobe lesion

16

What is papilledema?

optic disk swelling due to increased intracranial pressure

17

What are the clinical features of papilledema?

almost always bilateral, typically doenst impair vision, no eye pain, assocaited w/just ↑ ICP Sx.

18

What happens in early papilledema?

retinal veins engorged; spontaneous venous pulsations absent; disk hyperemic (increased blood flow); linear hemorrhages at the disk borders; disk margins blurred

19

What happens in fully developed papilledema?

optic disk is elevated above the plane of the retina; blood vessels crossing the border of the disk are obscured

20

Papilledema- etiologies

• Intracranial mass (urgent evaluation!)
• Meningitis
• Venous sinus thrombosis, subarachnoid hemorrhage
• Polycythemia, endocrinopathy, hypervitaminosis A
• Pseudotumor cerebri (idiopathic intracranial hypertension)
• Congenital cyanotic heart disease
• Spinal cord tumor
• Guillan-Barre

21

What is the pathway for the pupillary light response?

light --> II --> optic tracts --> pretectal N. --> stimualtion of BOTH EWN --> PANS to ciliary gang --> ciliary m contraction

22

What are the 4 things to cause nonreactive pupils?

o local disease of the iris (trauma, iritis, glaucoma)
o oculomotor nerve compression (tumor, aneurysm)
o administration of a mydriatic agent
o optic nerve disorders (neuritis, M.S.)

23

What is light-near dissociation?

impaired reactivity to light but accomodation is fine.

24

What causes light-near dissociation?

neurosyphilis, diabetes, optic n disorders, tumors compressing the tectum

25

Argyll-Robertson- Sx

bilateral, small pupils and irregular and unequal

26

Argyll-Robertson- response

pupils will accomodate but wont react to light. no change with pilocarpine.

27

Argyll-Roberston- differential

neurosyphilis, diabetes, pineal region tumors, MS

28

Tonic/Adies- appearance

unilateral or bilateral, tonic pupil is larger

29

Adies- response

sluggish to react, reacts with pilocarpine, accommodation is less affected

30

Adies- differential

holmes-adies (benign, often familial disorder, women more affected), ocular trauma, ANS neuropathy, degeneration of the ciliary gang

31

Horners- Sx

unilateral small pupil, ptosis

32

Horners- response

normal reponse to lgiht

33

Relative Afferent/Marcus Gunn- reactivity

1 pupil constricts less in response to direct illumination (kinda like IL optic n dmg)

34

What are the common etiologies of III palsy?

vasculopathy > aneurysm > trauma > neoplasm

35

What are the common eitologies for IV palsy?

trauma > vasculopathy > neoplasm > aneurysm

36

What are common etiologies for VI palsy?

neoplasm > vasculopathy > trauma > aneurysm

37

Where is the lesion to cause internuclear opthalmoplegia (INO)?

a lesion of the MLF

38

What happens if you lesion the MLF?

Since it connects III and IV, a lesion causes the uncoupleig movements where IV tell cant tell III to contract the MR muscle to move both eyes to 1 side

39

True or false: INO can be oveercome by caloric stimulation

FALSE

40

What is the most common cause of INO in young adults, where its usually bilateral?

MS

41

What is the most common cause of INO in the elderly, where it's usually unilatereal involvement?

Brainstem strokes

42

Amaurosis fugax- clinical presentaiton

unilateral transient loss of vision over 1-5 mins

43

Amaurosis fugax- etiology

emboli from atherosclerotic lesion of the carotid bifurcation

44

Amaurosis fugax- complications

risk for subsequent hemispheric infarction

45

Amaurosis fugax- prognosis

endarterectomy+ ASA is the bestestest

46

Optic neuritis- Sx

unilateral impairment of visual acuity over hours-days. eye tenderness/pain. central scotoma. disk swelling. impaired constriction

47

Optic neuritis- etiology

demyelination. viral infection maybe. toxins maybe

48

Optic neuritis- associated problems

hyperintense lesions are seen in the brain in 50-70% of pts. many develop MS

49

Optic neuritis- prognosis

in acute demyelinating optic neuritis, visual acuity improves by 2-3 weeks with return to normal or near-normal vision

50

Anterior Ischemic Optic Neuropathy (AION)- Sx

sudden, painless, monocular vision loss. altitudinal visual defect common. disk swelling. have peripapillary hemorrhages.

51

AION- etiology

atherosclerotic in origin, will have a smaller than normal disk

52

AION- prognosis

in 25% of pts, the other eye is affected in 2-4 years. Tx is UNsuccessful after the swelling resolves. usually optic atrophy.

53

Giant cell arteritis (GCA)- sx

artritic infarction is the most devatating complication, sudden and total vision loss, disk is pale and swollen, increased ESR and CRP, accompanied by feer, malaise, night sweats, weight loss and headahce.

54

GCA- age group

70-80

55

GCA- Dx

bilateral temporal artery biopsy, icnrease in ESR

56

GCA- Tx

corticosteroids to preserve vision