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neurology > Otology and opthamology > Flashcards

Otology and opthamology Flashcards

1
Q

Where are low frequencies best heard?

A

apex (near helicotrema)

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2
Q

Where are high frequencies best heard?

A

base of cochlea

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3
Q

what is damaged in noise-induced hearing loss?

A

sterociliated cells in the organ of corti

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4
Q

what is damaged in presbycusis?

A

hair cells at cochlear base

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5
Q

what is cholesteatoma?

A

the overgrowth of desquamated keratin debris within the middle ear space - may erode ossicles, mastoid air cells, leading to conductive hearing loss

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6
Q

how does cholesteatoma present?

A

painless otorrhea

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7
Q

what is benign paroxysmal positional vertigo?

A

Benign cause of vertigo - caused by problem in inner ear

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8
Q

benign paroxysmal positional vertigo diagnosis ?

A

Dix-Hallpike Maneuver

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9
Q

How do you perform the dix-hallpike maneuver

A

extend and turn seated patients head then have them rapidly lay down - symptoms will appear after 5-10 seconds if it is benign paroxysmal positional vertigo

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10
Q

what is peripheral vertigo?

A

Caused by inner ear etiology

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11
Q

what type of vertigo is Meniere disease?

A

peripheral vertigo

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12
Q

what is the triad seen in meniere disease?

A

sensorineural hearing loss, vertigo, tinnitus

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13
Q

what causes menieres disease?

A

increased endolymph within the inner ear due to endolypmphatic hydrops

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14
Q

treatments for peripheral vertigo?

A

antihistamines anticholinergics, antiemetics

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15
Q

what additional treatments are used for menieres disease?

A

low salt diet and diuretics

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16
Q

how do you treat BPPV?

A

epley maneuver

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17
Q

what is central vertigo?

A

vertigo caused by a brain stem or cerebellar lesion

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18
Q

findings of central vertigo

A

directional or purely vertical nystagmus, skew deviation, diplopia, dysmetria

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19
Q

where in the eye do extraocular muscles insert?

A

sclera

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20
Q

what is scleritis?

A

inflammation of sclera that presents with a red eye and severe boring pain on movement
Associated with RA and can cause blindness

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21
Q

What is the treatment for episcleritis?

A

its self limitied

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22
Q

what is keratitis?

A

corneal inflammation more common in contact lens weareres that presents with pain and photophobia and can cause blindness

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23
Q

what is conjuctivitis?

A

inflammation of the conjunctiva

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24
Q

what are the different causes of conjunctivitis?

A

Allergic - will be bilateral
Bacterial - will have pus
Viral - will have swollen preauricular node

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25
Q

What is the most common cause of viral conjuctivitis?

A

adenovirus

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26
Q

Most common causes of bacterial conjunctivits in adults?

A

S. aureus, S. pneumo

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27
Q

Most common causes of bacterial conjunctivits in children?

A

H. influenza, S. pneumo

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28
Q

What bacteria are you worried about if you get a corneal abrasion?

A

pseudomonas

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29
Q

what antibiotic do you give for a corneal abrasion?

A

aprafloxacin

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30
Q

most refraction in the eye occurs where?

A

retina (but the lens adjusts)

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31
Q

what type of collagen is in the capsule that surrounds the lens?

A

type IV

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32
Q

what is hyperopia?

A

‘farsightedness’ - near objects are blurry

-eye too short for refractive power - light focuses behind retina

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33
Q

how do you correct hyperopia?

A

a convex (converging lens)

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34
Q

what is myopia?

A

‘nearsightedness’ - far objects are blurry - eye too long for refractive power - light focuses in front of retina

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35
Q

how do you correct myopia?

A

concave lens (divering) lens

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36
Q

what is astigmatism?

A

abnormal curvature of cornea - different refractive power at different axes

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37
Q

how to correct astigmatism?

A

cylindrical lens

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38
Q

what is presbyopia?

A

age-related impaired accomodation (focusing on near objects) caused by decrease in lens elasticity, changes in lens curvature and decreased strenght of the ciliary muscle

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39
Q

how to treat presbyopia?

A

reading glasses ‘magnifiers’

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40
Q

Risk factors for cataracts?

A

Older age, smoking, excessive alcohol, excessive sunlight, prolonged corticosteroid use, DM, trauma, infetion

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41
Q

what drugs decrease aqueous humour production?

A

B-blockers, A2-agonists, carbonic anyhdrase inhibitors

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42
Q

what is ectopia lentis?

A

Dislocation of lens - can be from trauma or associated with systemic disorder (Margrans, homocystinuria, etc)

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43
Q

What are the causes of secondary open-angle glaucoma?

A

A blocked trabecula meshwork from WBCs (uveitis), RBCs, retinal elements (such as retinal detachment)

44
Q

what causes primary open-angle glaucoma?

A

unknown

45
Q

closed angle glaucoma PRIMARY cause

A

enlargment or anterior movement of lens against central iris - > obstruction of normal aqueous flow through pupil - fluid builds up and pushes iris against cornea - obsturction of flow

46
Q

closed angle glaucoma SECONDARY cause

A

hypoxia from retinal disease (DM, vein occlusion) induces vasoproliferation in iris that contracts angle

47
Q

How does chronic closure closed angle glaucoma present?

A

often asymptomatic but causes damage to optic nerve and peripheral vision

48
Q

how does acute closed angle glaucoma present?

A

painful, red eye with sudden vision loss. Halos around lights, frontal headache, fixed and mid-dilated pupil, nausea and vomiting

49
Q

medical treatments of glaucoma?

A

acetazolamide, mannitol, timolol, pilocarpine

50
Q

treatment of acute closed angle glaucoma?

A

SURGERY - MEDICAL EMERGENCY

51
Q

what is uveitis?

A

inflammation of the uvea

52
Q

what is inflamed in anterior uveitis?

A

iris

53
Q

what is inflamed in posterior uveitis?

A

choroid and or retina

54
Q

what is a hypopyon?

A

accumulation of pus in antior chamber that may be seen in uveitis

55
Q

what disorders is uveitis associated with ?

A

sarcoidosis, RA, juvenile idiopathic arthritis, HLA-B27 associated conditions

56
Q

pathophys of age-related macular degeneration

A

Degeneration of macula that casues distortion and eventual loss of central vision

57
Q

what are the two types of age-related macular degeneration?

A

dry - nonexudative - deposition of yellow extracellular material between bruch membrane and retinl pigment epithelium with gradual vision loss

58
Q

how to prevent progression of dry age related macular degeneration?

A

multivitamins and antioxidants

59
Q

What is wet age-related macular degeneration?

A

rapid vision loss due to bleeding secondary to choroidal neovascularization

60
Q

how to treat wet age-related macular degeneration?

A

anti-VEGF injections (bevacizumab, ranibizumab)

61
Q

What are the two types of diabetic retinopathy?

A

nonproliferative and proliferative

62
Q

nonproliferative diabetic retinopathy pathophys

A

damaged capillaries leak blood leading to hemorrhages and macular edema

63
Q

proliferative diabetic retinopathy pathophys

A

chronic hypoxia results in new blood vessel formation causes traction on retina

64
Q

how to treat nonproliferative diabetic retinopathy

A

blood sugar control

65
Q

how to treat proliferative diabetic retinopathy

A

anti-VEGF injections, peripheral retinal photocaugulation surgery

66
Q

what causes hypertensive retinopathy?

A

retinal damage due to chronic uncontrolled HTN

67
Q

findings in hypertensive retinopathy

A

flame shaped retinal hemorrahges, arteriovenous nicking, microaneurysms, macular star, cotton-wol spoots

68
Q

pathophys of retinal vein occlusion

A

blockage of central or branch retinal vein, often due to compression of vein by atherosclerotic artery

69
Q

pathophys of retinal detachment

A

sepration of neurosensory layer of retina and pigmented epithelium -> degeneration of photoreceptios -> vision loss

70
Q

fundoscopy findings of retinal detachment

A

crinkling of retinal tissue and changes in vessel direction

71
Q

presentation of retinal detachment

A

‘curtain drawn down’ vision loss

72
Q

risk factors for retinal detachment

A

high myopia and history of head trauma

73
Q

presentation of central retinal artery occlusion

A

acute, painless monocular vision loss

74
Q

what causes central retinal artery occlusion?

A

Embolus (may occur with a PDA, carotid artery atherosclerosis, etc.)

75
Q

Findings in central retinal artery occlusion

A

Cherry red spot and cloudy retina

76
Q

what causes the cherry red spot in tay sachs disease

A

accumulation of sphinolipids

77
Q

What is retinitis pigmentosa?

A

inherited retinal degeneration

78
Q

presentation of retinitis pigmentosa

A

begins with night blindness (rods in peripheral vision affected first)

79
Q

fundoscopy findings in retinitis pigmentosa

A

bone spicule-shaped deposits around macula

80
Q

pathophys of papillodeama

A

optic disc swelling due to increased ICP

81
Q

presentation of papillodema

A

enlarged blind spot and elevated optic disc with blurred margins

82
Q

what is leukocoria

A

loss (whitening) of the red reflex

83
Q

which patients commonly have retinitis

A

AIDs patients with CD4 less than 50

84
Q

Miosis neuro pathway

A

VIA parasympathetic
1st neuron goes from idenger-westphal nucleus to ciliary ganglion via CNIII and synapses
2nd neuron sends short ciliary nerves to sphinctor pupillae muscles and constrcts pupil

85
Q

How does the pupillary light reflex work?

A

light in either retina send signal via CNII to pretectal nuclei which signals to bilateral edinger-westphal nuclei to contstrict both pupils

86
Q

Neuron pathway for mydriasis

A

1st neuron: hypothalamus to ciliospinal center of budge
2nd neuron: exits at T1 to superior cervical ganglion
3rd neuron: travels along internal carotid through cavernous sinus and enters orbit as long ciliary nerve to pupillary dilater muscles and inervates SM of eyelids, sweat glands of forehead and face as well

87
Q

what spinal level is the ciliospinal center of budge found?

A

C8-T2

88
Q

Marcus Gunn Pupil

A

Normal eye causes constriction of both pupils upon light, but damaged eye (optic nerve damage) results in dilation of both pupils due to light (or they constrict less than they should)

89
Q

what causes horner syndrome?

A

sympathetic denervation of face

90
Q

Common presentation of CN III palsy

A

down and out eye, ‘blown’ pupil

91
Q

which direction does the superior oblique move the eye?

A

down and medial

92
Q

findings with CN IV damage

A

eye is higher in affected side

patient tilts head towards unaffected side to compensate

93
Q

how does CN VI damage present

A

cannot abduct eye, it will be medially displaced

94
Q

what is estropia?

A

misalignment of the eyes

95
Q

is meyner loop responsible for upper or lower quadrant vision?

A

upper

96
Q

is the dorsal optic radiation responsible for upper or low quadrant vision?

A

lower

97
Q

where is meyer loop?

A

temporal lobe

98
Q

where is the dorsal optic radiation?

A

parietal lobe

99
Q

what is contained in the cavernous sinus?

A

internal carotid artery

CN III, IV, Va, Vb and VI and sympathetic fibers (CN III)

100
Q

what is medial in the cavernous sinus?

A

internal carotid artery and CN VI

101
Q

what is just below the sella tursica?

A

sphenoid sinus

102
Q

what is amacrosis fugax?

A

painless transient vision loss commonly presents as symptom of TIA (due to ischemia)

103
Q

which two nerves does the medial longitudinal fasciculus coordinate?

A

CN III, CN VI

104
Q

what is internuclear opthalmoplegia?

A

lesion in MLF that results in a conjugate gaze palsy

105
Q

how does internuclear opthalmoplegia present?

A

CNVI activates ipsilateral lateral rectus, which moves eye laterally. BUT CNIII nucleus does not stimulate redial rectus in contralateral eye and thus it does not adduct. This causes nystagmus in the ipsilateral eye.

106
Q

how would right INO present?

A

right refers to the eye that cannot ADDuct - right eye cannot adduct and left eye will have nystagmus

107
Q

what is the PPRF?

A

the part that initiates lateral gaze from the brainstem. (whereas the medial LF will mediate the opposite eye). If you get a lesion here you cannot look towards the side of the lesion (ipsilateral gaze palsy)

neurology (9 decks)

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