Special Senses Flashcards
1
Q
Function of outer ear
A
Transfer sound waves via ear drum
2
Q
Bones of middle ear
A
Ossicles: Malleus, Incus, Stapes
3
Q
Function of ossicles
A
Amplify sound from eardrum to inner ear
4
Q
Structure that contains basilar membrane
A
Cochlea
5
Q
Area of inner ear that best detects low frequency sounds
A
Apex of basilar membrane near helicotrema
6
Q
Area of inner ear that best detects high frequency sounds
A
Base of cochlea
7
Q
Location of tuning fork in Rinne test
A
Next to ear
8
Q
Purpose of Rinne test
A
Test for conductive hearing loss
9
Q
Abnormal Rinne test for conductive hearing loss
A
Bone conduction > Air conduction
10
Q
Location of tuning fork in Weber test
A
On top of head
11
Q
Purpose of Weber test
A
Localizes
12
Q
Abnormal Weber test for sensorineural hearing loss
A
Sound localizes to good ear
13
Q
Normal Rinne test
A
Air conduction > Bone conduction
14
Q
Abnormal Weber test for conductive hearing loss
A
Sound localizes to bad ear
15
Q
Abnormal Rinne test for sensorineural hearing loss
A
Air conduction > Bone conduction (can be normal)
16
Q
Normal Weber test
A
Sound heard equally in both ears
17
Q
Aging related sensorineural hearing loss
A
Presbycusis
18
Q
Mechanism of presbycusis
A
Destruction of hair cells at cochlear base
19
Q
Overgrowth of desquamated keratin debris within middle ear space leading to conductive hearing loss
A
Cholesteatoma
20
Q
Sensation of spinning while actually standing
A
Vertigo
21
Q
Types of vertigo
A
Peripheral and Central
22
Q
Etiology of peripheral vertigo
A
Inner ear defect
23
Q
Etiology of central vertigo
A
Brain stem or cerebellar lesion
24
Q
Which type of vertigo is more common
A
Peripheral
25
Causes of peripheral vertigo
Semicircular canal debris, vestibular nerve infection, Meniere disease, benign paroxysmal positional vertigo
26
Findings in central vertigo
Directional or vertical nystagmus, skew deviation, diplopia, dysmetria
27
Positional testing results in central vertigo
Immediate nystagmus in any direction, focal neurologic findings
28
Positional testing results in peripheral vertigo
delayed horizontal nystagmus
29
Outer layer of the eye
Sclera
30
Middle layer of the eye
Choroid
31
Inner layer of the eye
Retina
32
Structures within the optic canal
Optic nerve, central retinal vein and artery
33
Most common cause of conjunctivitis
Viral (adenovirus)
34
Presentation of viral conjunctivitis
Sparse mucus discharge and swollen preauricular lymph nodes
35
Treatment for bacterial conjunctivitis
Antibiotics
36
Presentation of allergic conjunctivitis
Bilateral itchy eyes
37
Presentation of bacterial conjunctivitis
Pus from infected eye
38
Where is light focused in relation to retina in hyperopia
Behind retina
39
Farsightedness
Hyperopia
40
Type corrective lens needed for hyperopia
Convex (converging) lens
41
Nearsightedness
Myopia
42
Type corrective lens needed for myopia
Concave (diverging) lens
43
Where is light focused in relation to retina in myopia
In front of retina
44
Abnormal curvature of cornea
Astigmatism
45
Type of corrective lens needed for astigmatism
Cylindrical lens
46
Where is light focused in relation to retina in astigmatism
Varies with axes
47
Aging-related impaired accommodation of lens
Presbyopia
48
Mechanism of presbyopia
Decreased elasticity of lens and strength of ciliary muscle and changes in lens curvature
49
Type of corrective lenses needed
Reading glasses
50
Painless, often bilateral opacification of lens resulting in decreased vision
Cataracts
51
Congenital risk factors for cataracts
Classic galactosemia, galactokinase deficiency, trisomies, ToRCHES infections, Marfan and Alport syndrome, myotonic dystrophy and NF2
52
Trabecular outflow for Aqueous humor
Drains through:
1. trabecular meshwork
2. canal of Schlemm
3. episcleral vasculature
53
Site of aqueous humor synthesis
Ciliary body
54
Drugs that decrease aqueous humor production
Beta blockers, alpha2-agonists and carbonic anhydrase inhibitors
55
Uveoscleral outflow for aqueous humor
Drains into uvea and sclera
56
Drugs that increase trabecular outflow of aqueous humor
M3 agonists
57
Drugs that increase uveoscleral outflow of aqueous humor
Prostaglandin agonists
58
Muscles that make up the iris
```
Dilator muscle (alpha-2)
Sphincter muscle (M3)
```
59
Receptors found on dilator muscle of the iris
Alpha-2 receptors
60
Receptors found on sphincter muscle of the iris
M-3 receptors
61
What effects lens shape for accommodation
Ciliary body muscle fibers
62
What suspends lens from ciliary body
Zonule fibers
63
Optic disc atrophy with cupping
Glaucoma
64
Cause of glaucoma
Increased intraocular pressure (IOP)
65
Consequence of untreated glaucoma
Progressive peripheral visual field loss
66
Treatment for glaucoma
Lowering IOP by drugs or surgery
67
Type of glaucoma more common in African-Americans secondary to blocked trabecular meshwork
Open-angle glaucoma
68
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
Epinephrine (has acute closed angle glaucoma)
69
Presentation of chronic closed angle glaucoma
Often asymptomatic with damage to optic nerve and peripheral vision
70
Mechanism of primary closed angle glaucoma
Enlargement or forward movement of lens against central iris
71
Mechanism of secondary closed angle glaucoma
Hypoxia from retinal disease inducing vasoproliferation in iris that contracts angle
72
Uveitis associations
Systemic inflammatory disorders
73
Treatment for Dry age-related macular degeneration
Multivitamin and antioxidant supplements
74
Treatment for Wet age-related macular degeneration
Ranibizumab injections (anti-VEGF)
75
Most common type of age-related macular degeneration
Dry (non-exudative)
76
Mechanism of Dry age-related macular degeneration
Deposition of yellowish extracellular material between Bruch membrane and retinal pigment epithelium
77
Mechanism for Wet age-related macular degeneration
Rapid loss of vision due to bleeding secondary to choroidal neovascularization
78
Retinal damage due to chronic hyperglycemia
Diabetic retinopathy
79
Types of diabetic retinopathy
Non-proliferative and proliferative
80
Mechanism for proliferative diabetic retinopathy
Chronic hypoxia causes angiogenesis resulting in traction on retina
81
Mechanism for non-proliferative diabetic retinopathy
Leaky capillaries cause lipids and fluid to seep into retina resulting in hemorrhages and macular edema
82
Treatment for proliferative diabetic retinopathy
Peripheral retinal photocoagulation, surgery, anti-VEGF
83
Treatment for non-proliferative diabetic retinopathy
Blood sugar control
84
Mechanism of retinal vein occlusion
Blocked central or branch retinal vein from nearby arterial atherosclerosis
85
Separation of neurosensory layer of retina from outermost pigmented epithelium
Retinal detachment
86
Consequence of retinal detachment
Degeneration of photoreceptors leading to vision loss
87
Retinal detachment findings on fundoscopy
Crinkling of retinal tissue and changes in vessel direction
88
Eye condition presenting with acute painless mononuclear vision loss and cloudy retina with attenuated vessels and cherry-red spot on fovea
Central retinal artery occlusion
89
What is needs to be done next once diagnosis of central retinal artery occlusion is made?
Evaluate for embolic source
90
Inherited retinal degeneration presenting with painless, progressive vison loss beginning with night blindness and bony spicule pattern around macula
Retinitis pigmentosa
91
Retinal edema and necrosis leading to scar; often viral but bacterial also; associated with immunosuppression
Retinitis
92
Bilateral optic disc swelling from increased ICP with enlarged blind spot and elevated optic disc with blurred vision
Papilledema
93
Parasympathetic constriction of eyes
Miosis
94
Control of miosis
1st neuron: Edinger-Westphal nucleus to ciliary ganglion via CN III
2nd neuron: short ciliary nerves to sphincter muscles
95
Pupillary light reflex
Light enter retina, enters CN III to Pretectal nuclei in midbrain, activating both Edinger-Westphal nuclei causing consensual constriction
96
Sympathetic dilation of eyes
Mydriasis
97
Mydriasis pathway
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
98
Afferent pupillary defect from optic nerve damage decreasing pupillary constriction when light is shone in bad eye relative to good eye
Marcus Gunn pupil
99
Sympathetic denervation of face causing ptosis, miosis, anhydrosis associated with lesions above T1 or Pancoast tumors
Horner syndrome
100
Action of superior oblique
Abducts, intorts and depresses adducted eye
101
Position of superior and inferior obliques when tested
Adducted
102
Motor signs with CN III damage
Ptosis and "down-and-out" gaze
103
Parasympathetic signs with CN III damage
Diminished or absent pupillary light reflex, "blown pupil" often with "down-and-out" gaze
104
Motor signs with CN IV damage
Eye moves upward with contralateral gaze
105
Motor signs with CN VI damage
Medially directed eye that cannot abduct
106
Visual field deficit with damage to optic nerve
Ipsilateral whole field (right anopia)
107
Visual field deficit with damage to optic chiasm
Temporal both eyes (bitemporal hemianopia)
108
Visual field deficit with damage to optic tract
Temporal contralateral eye/Nasal ipsilateral eye (homonymous hemianopia)
109
Visual field deficit with damage to temporal lobe (Meyer loop)
Upper: temporal contralateral/nasal ipsilateral (upper quadrantanopsia)
110
Visual field deficit with damage to parietal lobe
Lower: temporal contralateral/nasal ipsilateral (lower quadrantanopsia)
111
Lesion in MLF leads to what disorder
Internuclear ophthalmoplegia
112
MLF function
Connects CN III to CN VI to coordinate horizontal eye movements
