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Step 1 Neurology-First Aid 2017 > Special Senses > Flashcards

Special Senses Flashcards

1
Q

Function of outer ear

A

Transfer sound waves via ear drum

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2
Q

Bones of middle ear

A

Ossicles: Malleus, Incus, Stapes

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3
Q

Function of ossicles

A

Amplify sound from eardrum to inner ear

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4
Q

Structure that contains basilar membrane

A

Cochlea

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5
Q

Area of inner ear that best detects low frequency sounds

A

Apex of basilar membrane near helicotrema

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6
Q

Area of inner ear that best detects high frequency sounds

A

Base of cochlea

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7
Q

Location of tuning fork in Rinne test

A

Next to ear

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8
Q

Purpose of Rinne test

A

Test for conductive hearing loss

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9
Q

Abnormal Rinne test for conductive hearing loss

A

Bone conduction > Air conduction

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10
Q

Location of tuning fork in Weber test

A

On top of head

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11
Q

Purpose of Weber test

A

Localizes

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12
Q

Abnormal Weber test for sensorineural hearing loss

A

Sound localizes to good ear

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13
Q

Normal Rinne test

A

Air conduction > Bone conduction

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14
Q

Abnormal Weber test for conductive hearing loss

A

Sound localizes to bad ear

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15
Q

Normal Weber test

A

Sound heard equally in both ears

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16
Q

Aging related sensorineural hearing loss

A

Presbycusis

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17
Q

Mechanism of presbycusis

A

Destruction of hair cells at cochlear base

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18
Q

Overgrowth of desquamated keratin debris within middle ear space leading to conductive hearing loss

A

Cholesteatoma

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19
Q

Sensation of spinning while actually standing

A

Vertigo

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20
Q

Types of vertigo

A

Peripheral and Central

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21
Q

Etiology of peripheral vertigo

A

Inner ear defect

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22
Q

Etiology of central vertigo

A

Brain stem or cerebellar lesion

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23
Q

Which type of vertigo is more common

A

Peripheral

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24
Q

Causes of peripheral vertigo

A

Semicircular canal debris, vestibular nerve infection, Meniere disease, benign paroxysmal positional vertigo

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25
Q

Findings in central vertigo

A

Directional or vertical nystagmus, skew deviation, diplopia, dysmetria

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26
Q

Positional testing results in central vertigo

A

Immediate nystagmus in any direction, focal neurologic findings

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27
Q

Positional testing results in peripheral vertigo

A

delayed horizontal nystagmus

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28
Q

Outer layer of the eye

A

Sclera

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29
Q

Middle layer of the eye

A

Choroid

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30
Q

Inner layer of the eye

A

Retina

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31
Q

Structures within the optic canal

A

Optic nerve, central retinal vein and artery

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32
Q

Most common cause of conjunctivitis

A

Viral (adenovirus)

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33
Q

Presentation of viral conjunctivitis

A

Sparse mucus discharge and swollen preauricular lymph nodes

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34
Q

Treatment for bacterial conjunctivitis

A

Antibiotics

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35
Q

Presentation of allergic conjunctivitis

A

Bilateral itchy eyes

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36
Q

Presentation of bacterial conjunctivitis

A

Pus from infected eye

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37
Q

Where is light focused in relation to retina in hyperopia

A

Behind retina

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38
Q

Farsightedness

A

Hyperopia

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39
Q

Type corrective lens needed for hyperopia

A

Convex (converging) lens

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40
Q

Nearsightedness

A

Myopia

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41
Q

Type corrective lens needed for myopia

A

Concave (diverging) lens

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42
Q

Where is light focused in relation to retina in myopia

A

In front of retina

43
Q

Abnormal curvature of cornea

A

Astigmatism

44
Q

Type of corrective lens needed for astigmatism

A

Cylindrical lens

45
Q

Aging-related impaired accommodation of lens

A

Presbyopia

46
Q

Mechanism of presbyopia

A

Decreased elasticity of lens and strength of ciliary muscle and changes in lens curvature

47
Q

Painless, often bilateral opacification of lens resulting in decreased vision

A

Cataracts

48
Q

Trabecular outflow for Aqueous humor

A

Drains through:

  1. trabecular meshwork
  2. canal of Schlemm
  3. episcleral vasculature
49
Q

Site of aqueous humor synthesis

A

Ciliary body

50
Q

Drugs that decrease aqueous humor production

A

Beta blockers, alpha2-agonists and carbonic anhydrase inhibitors

51
Q

Drugs that increase trabecular outflow of aqueous humor

A

M3 agonists

52
Q

Drugs that increase uveoscleral outflow of aqueous humor

A

Prostaglandin agonists

53
Q

Muscles that make up the iris

A 
Dilator muscle (alpha-2)
Sphincter muscle (M3)
54
Q

Receptors found on dilator muscle of the iris

A

Alpha-2 receptors

55
Q

Receptors found on sphincter muscle of the iris

A

M-3 receptors

56
Q

What effects lens shape for accommodation

A

Ciliary body muscle fibers

57
Q

What suspends lens from ciliary body

A

Zonule fibers

58
Q

Optic disc atrophy with cupping

A

Glaucoma

59
Q

Cause of glaucoma

A

Increased intraocular pressure (IOP)

60
Q

Consequence of untreated glaucoma

A

Progressive peripheral visual field loss

61
Q

Type of glaucoma more common in African-Americans secondary to blocked trabecular meshwork

A

Open-angle glaucoma

62
Q

What is contraindicated in patient presenting with very painful, red eye, sudden vision loss, halos around lights, frontal headache with fixed and mid-dilated pupils

A

Epinephrine (has acute closed angle glaucoma)

63
Q

Presentation of chronic closed angle glaucoma

A

Often asymptomatic with damage to optic nerve and peripheral vision

64
Q

Mechanism of primary closed angle glaucoma

A

Enlargement or forward movement of lens against central iris

65
Q

Treatment for Dry age-related macular degeneration

A

Multivitamin and antioxidant supplements

66
Q

Treatment for Wet age-related macular degeneration

A

Ranibizumab injections (anti-VEGF)

67
Q

Most common type of age-related macular degeneration

A

Dry (non-exudative)

68
Q

Mechanism of Dry age-related macular degeneration

A

Deposition of yellowish extracellular material between Bruch membrane and retinal pigment epithelium

69
Q

Mechanism for Wet age-related macular degeneration

A

Rapid loss of vision due to bleeding secondary to choroidal neovascularization

70
Q

Retinal damage due to chronic hyperglycemia

A

Diabetic retinopathy

71
Q

Types of diabetic retinopathy

A

Non-proliferative and proliferative

72
Q

Mechanism for proliferative diabetic retinopathy

A

Chronic hypoxia causes angiogenesis resulting in traction on retina

73
Q

Mechanism for non-proliferative diabetic retinopathy

A

Leaky capillaries cause lipids and fluid to seep into retina resulting in hemorrhages and macular edema

74
Q

Treatment for proliferative diabetic retinopathy

A

Peripheral retinal photocoagulation, surgery, anti-VEGF

75
Q

Treatment for non-proliferative diabetic retinopathy

A

Blood sugar control

76
Q

Mechanism of retinal vein occlusion

A

Blocked central or branch retinal vein from nearby arterial atherosclerosis

77
Q

Separation of neurosensory layer of retina from outermost pigmented epithelium

A

Retinal detachment

78
Q

Consequence of retinal detachment

A

Degeneration of photoreceptors leading to vision loss

79
Q

Retinal detachment findings on fundoscopy

A

Crinkling of retinal tissue and changes in vessel direction

80
Q

Eye condition presenting with acute painless mononuclear vision loss and cloudy retina with attenuated vessels and cherry-red spot on fovea

A

Central retinal artery occlusion

81
Q

What is needs to be done next once diagnosis of central retinal artery occlusion is made?

A

Evaluate for embolic source

82
Q

Inherited retinal degeneration presenting with painless, progressive vison loss beginning with night blindness and bony spicule pattern around macula

A

Retinitis pigmentosa

83
Q

Retinal edema and necrosis leading to scar; often viral but bacterial also; associated with immunosuppression

A

Retinitis

84
Q

Bilateral optic disc swelling from increased ICP with enlarged blind spot and elevated optic disc with blurred vision

A

Papilledema

85
Q

Parasympathetic constriction of eyes

A

Miosis

86
Q

Control of miosis

A

1st neuron: Edinger-Westphal nucleus to ciliary ganglion via CN III
2nd neuron: short ciliary nerves to sphincter muscles

87
Q

Pupillary light reflex

A

Light enter retina, enters CN III to Pretectal nuclei in midbrain, activating both Edinger-Westphal nuclei causing consensual constriction

88
Q

Sympathetic dilation of eyes

A

Mydriasis

89
Q

Mydriasis pathway

A

1st neuron: hypothalamus to ciliospinal center of Budge (C8-T2)
2nd neuron: exits at T1 to superior ganglion
3rd neuron: plexus along internal carotid to cavernous sinus entering orbit as ciliary nerve to pupillary dilators

90
Q

Afferent pupillary defect from optic nerve damage decreasing pupillary constriction when light is shone in bad eye relative to good eye

A

Marcus Gunn pupil

91
Q

Sympathetic denervation of face causing ptosis, miosis, anhydrosis associated with lesions above T1 or Pancoast tumors

A

Horner syndrome

92
Q

Action of superior oblique

A

Abducts, intorts and depresses adducted eye

93
Q

Position of superior and inferior obliques when tested

A

Adducted

94
Q

Motor signs with CN III damage

A

Ptosis and “down-and-out” gaze

95
Q

Parasympathetic signs with CN III damage

A

Diminished or absent pupillary light reflex, “blown pupil” often with “down-and-out” gaze

96
Q

Motor signs with CN IV damage

A

Eye moves upward with contralateral gaze

97
Q

Motor signs with CN VI damage

A

Medially directed eye that cannot abduct

98
Q

Visual field deficit with damage to optic nerve

A

Ipsilateral whole field (right anopia)

99
Q

Visual field deficit with damage to optic chiasm

A

Temporal both eyes (bitemporal hemianopia)

100
Q

Visual field deficit with damage to optic tract

A

Temporal contralateral eye/Nasal ipsilateral eye (homonymous hemianopia)

101
Q

Visual field deficit with damage to temporal lobe (Meyer loop)

A

Upper: temporal contralateral/nasal ipsilateral (upper quadrantanopsia)

102
Q

Visual field deficit with damage to parietal lobe

A

Lower: temporal contralateral/nasal ipsilateral (lower quadrantanopsia)

103
Q

Lesion in MLF leads to what disorder

A

Internuclear ophthalmoplegia

104
Q

MLF function

A

Connects CN III to CN VI to coordinate horizontal eye movements

Step 1 Neurology-First Aid 2017 (5 decks)

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