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Infectious Disease and HEENT > HEENT Exam 1 Cards > Flashcards

HEENT Exam 1 Cards Flashcards

1
Q

Part of the eye that controls the lens shape

A

Ciliary body

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2
Q

Substance in the back of the eye

A

Vitreous humor

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3
Q

Substance in the front of the eye

A

Aqueous humor

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4
Q

Pigmented part of the retina located in the very center of the eye

A

Macula

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5
Q

Area of greatest visual acuity in the eye

A

Fovea

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6
Q

The lens in our eye is a _____________ lens

A

Convex

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7
Q

What does the lens do when we want to see something that is near?

A

The ciliary muscles contract, suspensory ligaments slacken, making the lens thicker and the focal length shorter

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8
Q

What does the lens do when we want to see something far away?

A

Ciliary muscles relax, suspensory ligaments tighten, making the lens thinner and the focal length longer

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9
Q

2 things that can cause myopia

A

Too curved cornea, too long eyeball

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10
Q

Correction for myopia

A

Use a concave lens to diverge light rays and make objects look smaller

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11
Q

2 things that can cause hyperopia

A

Not enough curvature of the cornea, Eye too short

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12
Q

Correction for hyperopia

A

Use a convex lens to converge light rays and make objects look larger

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13
Q

An irregular shape of the cornea or lens leading to multiple focal points

A

Astigmatism

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14
Q

Presbyopia

A

Age related farsightedness

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15
Q

Cornea becomes cone shaped causing blurred vision

A

Keratoconus

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16
Q

Purpose of aqueous humor

A

Maintains intraocular pressure

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17
Q

Where does aqueous humor come from and where does it go

A

Produced in ciliary body and absorbed by trabecular meshwork

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18
Q

Purpose of vitreous humor

A

Maintain shape of eyeball and hold retina in place

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19
Q

Result of a lesion before the optic chiasm

A

Blindness in one eye

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20
Q

Result of a lesion at the optic chiasm

A

Bitemporal hemianopsia

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21
Q

Result of lesion in the optic tract (after optic chiasm)

A

Homonymous hemianopsia (left or right visual field loss in both eyes) on the opposite side as the lesion

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22
Q

Parasympathetic pupillary effect

A

Constriction

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23
Q

Sympathetic pupillary effect

A

Dilation

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24
Q

One pupil being naturally larger that the other

A

Anisocoria

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25
Q

Cotton wool spots

A

Yellow-white lesions that look like clouds on the retinal surface - Caused by micro ischemia and nerve infarction

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26
Q

Physiologic anisocoria

A

The pupillary difference is the same in the light and dark

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27
Q

MCC of cotton wool spots (2)

A

Diabetic retinopathy, hypertensive retinopathy

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28
Q

Anisocoria that is more pronounced in the dark

A

The small pupil is abnormal

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29
Q

Anisocoria that is more pronounced in the light

A

Large pupil is abnormal

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30
Q

Marcus Gunn Pupil

A

Pupil only reacts to consensual light, not direct - indicates an optic nerve lesion

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31
Q

Horner syndrome triad

A

Ptosis, Anhydrosis, Miosis,

PAM Horner

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32
Q

Horner syndrome triad

A

Ptosis, Anhydrosis, Miosis,

PAM Horner

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33
Q

Cause of horner syndrome

A

Loss of sympathetic innervation to the eye

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34
Q

Adie’s pupil

A

Sluggish direct and consensual reaction to light couples with diminished DTRs

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35
Q

Accommodation reflex

A

The pupils get smaller looking at closer objects and larger looking at far away objects

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36
Q

Agyll Robertson pupil

A

Pupils have an accommodation reflex but NO pupillary reflex (to light)

ARP - Accommodation Reflex Present
Pupillary reflex Absent

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37
Q

Patient complains of a “curtain coming down over 1 eye”

A

Retinal detachment

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38
Q

Swelling of the optic nerve

A

Papilledema

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39
Q

4 signs of papilledema

A

Disc elevation
Venous distension and tortuosity
Obscured disk margin
Absent venous pulsations

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40
Q

Blood and thunder fundus

A

Widespread retinal hemorrhages with venous dilation and tortuosity

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41
Q

Cause of a cherry red spot on the fovea

A

Central retinal artery occlusion

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42
Q

Cause of blood and thunder fundus

A

Retinal vein occlusion

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43
Q

Cause of retinal boxcar segmentation

A

Retinal artery occlusion

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44
Q

A-V Nicking

A

A small artery crosses and small vein and compresses it - seen in hypertensive retinopathy and atherosclerosis

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45
Q

Silver and Copper wiring

A

Seen in hypertensive retinopathy and atherosclerosis - Silver is more serious

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46
Q

Hard exudates

A

Yellow/white spots with distinct borders - caused by a breakdown of blood retina border and due to diabetes

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47
Q

Flame hemmorhages

A

Caused by necrotic blood vessels bleeding into the retina caused by diabetes or hypertension

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48
Q

Dot-Blot hemmorhages

A

Caused by micro aneurism rupture in the deeper retinal layers

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49
Q

Optic cupping

A

Blood flow to the optic nerve is diminished because of damage to the nerve, the optic cup grows larger

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50
Q

2 conditions in which we might see fundoscopic neovascularization

A

DM retinopathy and macular degeneration

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51
Q

Retinal Drusen

A

Yellow deposits under the retina - dead retinal epithelial cells caused by age-related macular degeneration

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52
Q

What does a slit lamp look at?

A

The anterior portion of the eye

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53
Q

Use of fluorescence staining

A

Helps us highlight corneal abrasions and foreign bodies

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54
Q

Presentation of bacterial conjunctivitis (3 things)

A

Purulent discharge, conjunctival injection, mild discomfort

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55
Q

3 MCCs of Bactierial conjunctivitis

A

S. aureus - Adults
Strep Pneumo - Children (followed by other OM causes)
Pseudomonas - Contact wearers

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56
Q

Treatment for mild bacterial conjunctivitis

A

Polymixin B/Trimethoprim (Polytrim)

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57
Q

3 treatments for severe bacterial conjunctivitis or pseudomonal conjunctivitis

A

Moxifloxacin (vigamox), Ofloxacin opthalmic (Ocuflox) Ciprofloxacin

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58
Q

Treatment for gonococcal conjunctivitis

A

Rocephin (ceftriaxone) with Erythromycin or bacitracin

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59
Q

Treatment for chlamydial conjunctivitis

A

1 dose azithromycin PO

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60
Q

Presentation of gonococcal conjunctivitis

A

Perfuse purulent exudate

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61
Q

Presentation of trachoma

A

Chlamydial conjunctivitis - Yellow follicle spots on inner eyelid

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62
Q

Clinical presentation of viral conjunctivitis

A

Usually bilateral, watery discharge, foreign body sensation, preauricular lymphadenopathy

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63
Q

MCC of viral conjunctivitis

A

Adenovirus from eye clinics or swimming pools

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64
Q

Treatment for viral conjunctivitis

A

Supportive care

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65
Q

Presentation of allergic conjunctivitis

A

May be seasonal. stringy discharge with cobblestone papillae on inner eyelid (big bumps), pruritis

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66
Q

Chemosis

A

Swelling of the conjunctiva - seen in allergic conjunctivitis

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67
Q

Treatment for allergic conjunctivitis
2 drugs

A

Topical antihistamines such as Ketotifen or Olopatadine

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68
Q

Uvea

A

Structures of the eye beneath the sclera
The iris
The ciliary body
The choroid

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69
Q

MC type of uveitis

A

Acute, nongranulomatous, anterior uveitis

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70
Q

Posterior Uvea

A

Choroid

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71
Q

Anterior Uvea

A

Iris and Ciliary body

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72
Q

1 thing NOT to do with opthalmic herpes

A

DONT give steroids

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73
Q

Non-granulomatous uveitis

A

Inflammation with predominantly polymorphonuclear cells rather than giant cells - usually presents acutely

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74
Q

Granulomatous uveitis

A

Inflammation where macrophages are the predominant cell - usually indolent with blurred vision

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75
Q

Causes of non-granulomatous anterior uveitis

A

Often linked to autoimmune condition such as UC or arthritis

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76
Q

Causes of anterior granulomatous uveitis

A

Syphillis, TB, Toxoplasmosis, Herpes

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77
Q

Fundus of ocular syphillis

A

Salt and pepper fundus

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78
Q

Diagnosis and clinical presentation of anterior uveitis

A

Use a slit lamp - Hypopyon or collection of pus in the cornea, Keratitic deposits seen - larger with granulomatous inflammation

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79
Q

General presentation of uveitic eyes

A

Red and painful with redness around the cornea

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80
Q

Old v New Posterior Uveitic lesions

A

New have less defined borders and are yellow, old have more definite margins

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81
Q

Clinical presentation of posterior uveitis

A

Gradual vision loss with floaters and often bilateral

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82
Q

Cause of posterior uveitis

A

Idiopathic, autoimmune, pars plantis, or agents that cause anterior granulomatous uveitis

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83
Q

Treatment for anterior uveitis

A

Topical corticosteroid with pupil dilation - treat agent if identified

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84
Q

Treatment for posterior uveitis

A

Corticosteroid therapy given more invasively - treat agent if identified

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85
Q

Keratitis

A

Inflammation of the cornea

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86
Q

Causes of bacterial keratitis

A

Most common in contact lenses worn overnight - most commonly pseudomonas, moraxella, staph or strep

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87
Q

Presentation of bacterial keratitis

A

Hazy cornea with ulcer, hypopyon, difficulty keeping eye open

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88
Q

Treatment for bacterial keratitis

A

Emergent referral and fluoroquinolone drops

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89
Q

Cause of viral keratitis

A

HSV

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90
Q

Key sign of herpes simplex keratitis

A

Dendritic (branching) lesion of the cornea

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91
Q

Treatment for viral keratitis

A

Urgent referral with topical or oral acyclovir or valacyclovir

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92
Q

Hutchinsons sign

A

Involvement of the tip of the nose or lid margins in HSV predicts eye involvement

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93
Q

Fungal kerititis

A

Candida, aspergillis, fusarium
Often from injury in an agricultural setting or with contacts and the immune compromised

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94
Q

Presentation of fungal keratitis

A

Feathery corneal infiltrate with satellite lesions and multiple stromal abscesses

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95
Q

Treatment for fungal keratitis

A

Natamycin, Amphotericin, Voriconazole

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96
Q

Acanthamoeba keratitis

A

Severe pain with ring shaped corneal infiltrate

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97
Q

Treatment for acanthamoeba keratitis

A

Needs long term treatment with topical biguamide (Polyhexamethylene or chlorahexadine)

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98
Q

Why does acanthamoeba keratitis need long term treatment

A

It can encyst with the corneal stroma

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99
Q

Subconjunctival hemmorhage

A

Well defined area of hemorrhage under the conjunctiva - usually self limiting and caused by HTN or trauma

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100
Q

How long does a subconjunctival hemorrhage usually last?

A

Resorbs within 2 weeks

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101
Q

Dacryoadenitis

A

Inflammation or infection of the lacrimal gland

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102
Q

Dacryocystitis

A

Infection of the lacrimal sac/duct

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103
Q

Clinical Presentation of dacryoadenitis

A

Unilateral rapid onset swelling in the supratemporal region

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104
Q

Dacryocystitis clinical presentation

A

epiphora(overflow of tears), rapid unilateral onset, and inframedial swelling

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105
Q

2 potential causes of dacryoadenitis

A

Mumps, and autoimmune inflammatory

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106
Q

MC organisms for acute and chronic dacryocystitis

A

Acute - Staph aureus
Chronic - Staph epidermidis

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107
Q

Treatment for dacryoadenitis

A

Treat underlying cause and use systemic antibiotics if bacterial

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108
Q

Treatment for acute dacryocystitis

A

Lacrimal sac massage
Topical Tobramycin and Moxifloxacin if discharge only
Augmentin systemic if other s/s of infection are present

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109
Q

Treatment for chronic dacryocystitis

A

Can be kept latent with antibiotics - Surgery to relieve obstruction is definitive treatment

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110
Q

Anterior blepharitis

A

Involves the eyelids skin and eyelashes, may be associated with ulcers or seborrhea of the scalp, brows, and ears

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111
Q

Posterior blepharitis

A

Inflammation of meibomian glands at inner portion of the eyelid can be cause by infection, dysfunction, or skin conditions

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112
Q

Meibomian glands

A

Located in eyelids - secrete oily substance used to lubricate eyeball and prevent tear evaporation

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113
Q

Clinical presentation of anterior blepharitis

A

Red rimmed eyes with scales seen on eyelashes

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114
Q

Clinical presentation of posterior blepharitis

A

Greasy or frothy tears with rolled in lid margin with telangiectasia and hyperemesis - Waxy, congealed meibomian glands

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115
Q

Treatment for anterior blepharitis

A

Remove scales with a hot washcloth use bacitracin or erythromycin for an antistaph ointment

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116
Q

Treatment for mild poterior blepharitis

A

Meibomian gland expresseion and lid massage

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117
Q

Treatment for conjunctival and corneal inflammation

A

Tetracycline long term, Prednisolone short term

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118
Q

Hordeolum

A

Localized red, tender area of the eyelid caused by a staphylococcal abcess

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119
Q

External Hordeolum

A

Usually smaller and on the margin of the eyelid

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120
Q

Internal hordeolum

A

Often a Meibomian gland abscess pointing into the conjunctival surface of the lid, can cause lid cellulitis

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121
Q

Treatment for Hordeolum

A

May need to change any cosmetics, warm compress, and I&D if no progress
Antibiotics NOT indicated

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122
Q

I&D

A

Incision and Drainage

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123
Q

Chalazion

A

Hard, Non-tender swelling with redness of adjacent conjunctiva

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124
Q

Chalazion treatment

A

Often resolves on own with warm compress etc, may need to refer refractory for incision or steroids

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125
Q

Cause of Orbital cellulitis

A

Caused my OM pathogens and S. Aureus - often connected with a sinus infection (cause the sinuses are nearby)

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126
Q

Orbital cellulitis or Preseptal cellulitis - which one is an emergency

A

Orbital - think - it’s closer to the brain!!

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127
Q

Orbital cellulitis pathology

A

Infection of the fat and soft tissue that holds the eye in its socket

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128
Q

Clinical presentation of orbital cellulitis

A

Fever, Painful swelling, Proptosis, Ptosis, Limited movement

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129
Q

One thing you should do to assess for severity of preorbital cellulitis

A

Check pupillary reaction to light to assess ocular nerve involvement

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130
Q

Treatment for orbital cellulitis

A

Immediate IV Vanc and a later gen cephalosporin

May add metronidazole or Clinda for anaerobes

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131
Q

Orbital cellulitis treatment after symptoms are under control

A

Switch to oral Bactrim, Augmentin, or FQone for 2-3 weeks

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132
Q

Preseptal/Periorbital cellulitis

A

Bacterial infection superficial to the orbital septum - Usually secondary to another eyelid infection such as conjunctivitis

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133
Q

2 common agents of preseptal cellulitis

A

S. Aureus and S. Pneumo

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134
Q

Clinical presentation of preseptal/periorbital cellulitis

A

NO fever, NO proptosis, Eyelid swelling, Erythema, No vision impairment

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135
Q

Treatment for Preseptal/Periorbital cellulitis

A

PO - Augmentin or Omnicef with Bactrim or Clinda

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136
Q

Ciliary flush

A

Definitive for corneal pathology - red/violet streaks spreading out from the edges of the cornea

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137
Q

4 clinical presentations of a corneal ulcer

A

Ciliary flush, Irregular pupil, dendritic ulcer, mucopurulent discharge

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138
Q

Characteristics of Psudomonas Corneal ulcer

A

Gray/Yellow infiltrate at a break in the cornea, Contact lens wearing hx,

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139
Q

Treatment for corneal ulcer with pseudomonas

A

FQone or Tobra/Gentamycin

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140
Q

Characteristics of group A strep corneal ulcer

A

May include a hypopyon, Edematous corneal stroma, not as specific

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141
Q

Characteristic of a staph infected corneal ulcer

A

Ulcer bed feels firm when scraped

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142
Q

3 drugs to treat staph infected corneal ulcers

A

Cefazolin, Moxifloxacin, Gatifloxacin

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143
Q

Characteristics of Fungal corneal ulcers

A

Gray, irregular edged infiltrate with satellite lesions -slow growing

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144
Q

Treatment for fungal corneal ulcer

A

Amphotericin B, Voriconazole, Posaconazole

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145
Q

Characteristics of viral corneal ulcers

A

Hx of fever or blisters, Dendritic ulcer, photophobia

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146
Q

Treatment for viral corneal ulcer

A

Acyclovir PO or Idoxuridine/Gancyclovire Topical

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147
Q

Corneal ulcer placement and size

A

Can be a small dot at the EDGE of the cornea

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148
Q

Entropion

A

Inward turning of the eyelid - often in elderly patients

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149
Q

Treatment for entropion

A

Surgery if eyelashes rub against the cornea
Botulinum toxin injections may be used

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150
Q

Ectropion

A

Outward turning of the lower eyelid - associated with tear leakage

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151
Q

Blepharospasm and treatment

A

Abnormal eyelid muscle contraction (eye twitching) - treated by alleviating stress and possibly botox

152
Q

3 Neurological diseases that can cause Ptosis

A

Horner’s syndrome
3rd nerve palsy
Myasthenia gravis

153
Q

Mild, Moderate, and Severe Ptosis

A

2, 3, and 4 mm drop

154
Q

Treatment for Ptosis

A

Oxymetazoline eye drops (alpha adrenergic stimulators)
Surgery usually reserved for those with an obscured visual field

155
Q

Pterygium

A

Encroachment of the conjunctiva onto the nasal side of the cornea - often due to prolonged exposure to wind, sand, dust, etc.

156
Q

Treatment for pterygium

A

Artificial tears, NSAIDS and steroid can be used, surgery in extreme cases

157
Q

Pinguecula

A

Yellow/orange raised conjunctival lesion that DOES NOT cross into the cornea - exposure or dust caused

158
Q

Clinical findings of dry eye

A

Itching, Absence of tear meniscus on lower lid, Excess mucous production, blurred vision

159
Q

Tests to detect dry eye

A

Fluorescence staining to find dry spots
Rose Bengal and Lissamine Green for epithelial defects
Schirmer’s tear production test
Tear breakup time

160
Q

3 complications of dry eye

A

Corneal scarring and vascularization, Corneal ulceration, Impaired vision

161
Q

First line treatment for dry eye

A

Artificial tears 3-4 times a day and ointment, Plugs, Cyclosporine for immune inhibition

162
Q

Cataract

A

Lens opacity usually resulting from age, can also be related to smoking and alcohol use

163
Q

Clinical presentation of cataracts

A

Progressive blurring of vision, monocular double vision, cloudy lens, Glare with bright lights

164
Q

Cataract treatment

A

Refer to ophthalmology for surgery

165
Q

Part of the eye effected by cataracts

A

Lens not the cornea

166
Q

Clinical presentation of macular degenerations

A

Loss of central vision first that is usually bilateral

167
Q

Atrophic macular degeneration (dry)

A

Atrophy and degeneration of the retina and retinal pigment with retinal drusen

168
Q

Retinal drusen

A

Hard, discrete, yellow retinal deposits

169
Q

Neovascular (wet) macular degeneration

A

Excess growth of vasculature under the retina leads to fluid accumulateion, hemorrhage, and fibrosis - more rapid vision loss

170
Q

Narrow angle glaucoma

A

Acute glaucoma - a medical emergency

171
Q

Open angle glaucoma

A

Chronic glaucoma - less emergent

172
Q

Glaucoma

A

Neuropathy of the optic nerve with or without intraocular pressure, also with cupping of the optic disk

173
Q

Creation and drainage of aqueous humor

A

Made by ciliary body, drained by trabecular meshwork

174
Q

Etiology of acute angle closure glaucoma

A

Lens is pushed forward leading to closure of the angle between the cornea and the iris and impaired drainage of aqueous humor

175
Q

3 risk factors for narrow angle glaucoma

A

Asian descent
Female, 40-50 years old
Farsightedness

176
Q

Primary angle closure glaucoma

A

Lens located too far forward anatomically, leading to closed angle

177
Q

Secondary angle closure glaucoma

A

Conditions that push the ciliary body forward or pull on the iris creating a closed angle

178
Q

Clinical presentation of acute angle closure glaucoma

A

Halo’s around lights, with onset more common when it is dark, Red steamy cornea with sluggish dilated pupils and IOP over 50mmg

179
Q

Gold standard diagnostic for narrow angle glaucoma

A

Gonioscopy is the gold standard for diagnosis - views the irideocorneal angle

180
Q

Initial treatment for angle closure glaucoma

A

Place the patient supine and refer to opthalmology urgently

181
Q

Pharmacology for Narrow angle glaucoma

A

First line: Acetazolamide (CAI) PO or IV
Pilocarpine drops administered later
Recheck IOP every 30-60 minutes

182
Q

3 Non-first line topicals for acute angle closure glaucoma

A

Latanoprost, Timolol, Apraclonidine

183
Q

Definitive treatment for angle closure glaucoma

A

Laser peripheral iridotomy, creates a hole in the peripheral iris to releive the pupillary block

184
Q

5 things to give someone with Angle closure glaucoma while waiting for the ambulance

A

Lie on back
Acetazolamide
Pilocarpine
Anagesia
Antiemetic

185
Q

Clinical presentation of open angle glaucoma

A

Gradual peripheral vision loss with high IOP (over 40mmHg)

186
Q

Screening recommendations for glaucoma

A

every 5-10 years for under 40
to ever 1-2 years over 65
Refer any pt with cupping!

187
Q

IOP at which to refer

A

30-40 is Urgent, anything higher is emergent

188
Q

3 types of therapy for open angle glaucoma

A

Pharm - acetazolamide
Laser therapy
Surgery

189
Q

4 drugs for open angle glaucoma

A

Topical prostaglandins - Lataprost
Topical beta blockers - Timolol
Topical Alpha 2 agonists - Apraclonidine
(reduces aqueous humor production by dilating eyes)
Cholinergic agonists - Pilocarpine

190
Q

Surgical therapy for any glaucoma

A

Laser periperal iridotomy - put a hole in the peripheral iris for drainage

191
Q

Cause of a corneal abrasion

A

Often from trauma - fingernail, contact lens, paper, etc.

192
Q

Clinical presentation of a corneal abraision

A

Tearing, Foreign body sensation, may have ciliary flush or change in visual acuity, photophobia

193
Q

Complications for a corneal abrasion

A

Bacterial keratitis leading to ulcers and hypopyon

194
Q

Diagnostics for a corneal abraision

A

Evert eyelid to rule out foreign body, check visual acuity, stain to find abrasion

195
Q

3 treatments for corneal abrasions

A

Antibiotics - bactrim-polymixin
NSAID eye drop
Cycloplegic to stop ciliary spasms and pain

196
Q

Are alkali or acidic burns worse?

A

Alkali

197
Q

4 factors effecting the severity of a chemical eye injury

A

Toxicity
Length of exposure
Depth of penetration
Area of involvement

198
Q

Treatment for chemical eye injury

A

Irrigate with pH monitoring
May use a cycloplegic

199
Q

Presentation of welder’s flash photophobia

A

6-12 hours after exposure to UV radiation, Staining reveals corneal speckles

200
Q

Treatment for welder’s flash potophobia

A

Binocular patching with Cyclopentolate (cycloplegic drug)

201
Q

What MUST you do when you suspect a foreign body?

A

Always evert the eyelid

202
Q

Rust ring

A

formed by an iron containing foreign body - remove if not resolved in 2-3 days

203
Q

Hyphema

A

Injury causing a hemorrhage into the anterior chamber of the eye causing pain, photophobia and blurred vision

204
Q

Non-pharm management for a hyphema

A

Prevent further bleeding, keep patient supine with head elevated 45 degrees and a hard eye shield

205
Q

Pharm management of hyphema

A

NO NSAIDs or Aspirin
Pain meds and antiemetics

206
Q

Bone at the top of the orbit

A

Frontal bone

207
Q

2 Bones on the outside edge of the orbit

A

Zygomatic bone and sphenoid bone

208
Q

2 Bones on the bottom of the orbit

A

Maxilla and zygomatic bone

209
Q

2 Bones on the inside edge of the orbit

A

Maxilla and ethmoid bone

210
Q

Bones in back of the orbit (4)

A

Sphenoid, Palatine, Ethmoid, Maxilla

211
Q

Action of the inferior oblique

A

Moves the eye upwards and inwards

212
Q

Action of superior oblique

A

Moves the eye downwards and inwards

213
Q

Most common bone injured in an orbital blowout fracture

A

Maxilla

214
Q

Clinical presetation of an orbital blowout fracture

A

Pain and ecchymosis around the eye
Decreased movement - especially looking upwards due to trapped inferior rectus
Localized facial anesthesia (trigeminal nerve)
Enopthalmos (sunken in eyes - indicates inferior displacement of orbital contents through the orbital floor)

215
Q

3 Evaluation steps for an orbital blowout

A

Obtain mechanism of injury
Examine eye contents and check visual acuity
CT of the orbit

216
Q

4 things to look for on an orbital CT from an orbital blowout fracture

A

Emphysema (air in the orbit) with crepitus
Fracture of floor or medial wall of orbit
Soft tissue extending into maxillary sinus (could become ischemic)
Opacification of maxillary sinus from blood or edema

217
Q

3 things we do not want someone with an orbital blowout fracture doing

A

Throwing up
Sneezing
Blowing nose
(or anything like unto it)

218
Q

2 pharm treatments for orbital blowout

A

Systemic antibiotics and steroids for swelling

219
Q

3 symptoms that are indicative of a ruptured globe in penetrating trauma

A

Teardrop shaped pupil, eyeball appears deflated, afferent pupillary defect

220
Q

Afferent pupillary defect

A

Response to light is more sluggish in one eye

221
Q

3 treatment points for penetrating trauma or ruptured globe

A

Protective eye shield
Elevate head 45 degrees
Vancomycin and Ceftazidime or FQone

222
Q

Amaurosis fujax

A

Transient monocular blindness, symptom not a diagnosis

223
Q

3 things that might cause amaurosis fujax

A

Migraine, Retinal emboli, giant cell arteritis

224
Q

Clinical presentation of amaurosis fujax

A

Described as a curtain coming down over the visual field with a few minutes of complete vision loss

225
Q

Monocular ischemia pattern and mechanism

A

Monocular rapid onset due to a retinal embolism

226
Q

Giant cell arteritis vision loss pattern and mechanism

A

Usually monocular w/ headache, due to optic nerve ischemia

227
Q

Papilledema vision loss pattern and mechanism

A

Monocular graying or blurring with diplopia from elevated intercranial pressure

228
Q

Idiopathic retinal vasospasm

A

Accompanied by a headache and monocular vision loss

229
Q

Migraine vision loss

A

Binocular due to cortical depression and possible retinal vasospasm

230
Q

Vision loss of vertebrobasilar ischemia

A

Homonymous hemianopia caused by an embolism

231
Q

Vision loss of an ictal seizure

A

Binocular and lateralized due to epileptic discharge

232
Q

Postictal vision loss

A

lasts 20+ minutes, binocular visual field loss due to cortical inhibition

233
Q

Clinical presentation of central retinal artery occlusion

A

Sudden profound painless monocular loss of vision with a cherry red spot and afferent pupillary defect and boxcar segmentation

234
Q

Management for central retinal artery occlusion

A

Lay patient flat, give acetazolamide and vasodilators and ocular massage with O2. Thrombolysis given CAREFULLY

235
Q

Treatment for giant cell arteritis

A

High dose corticosteroids

236
Q

~Pexy

A

Root for fixation of something

237
Q

Clinical presentation of Central retinal vein occlusion

A

Painless monocular vision loss often first noticed upon awakening with a blood and thunder fundus - starts out blurry

238
Q

Treatment for retinal vein occlusion

A

Anti VEGF first line
Intravitreal corticosteroids second line
Laser photocoagulation

239
Q

Laser photocoagulation

A

Uses lasers to seal leaky vessels and prevent VEGF formation

240
Q

2 common risk factors for retinal detachment

A

Nearsighted (longer eyeball)
Cataract extraction

241
Q

Clinical findings of a retinal detachment

A

Monocular decreased vision, Eye pain, Central vision is last to go
Flashing lights and floaters

242
Q

Treatment of retinal detachment

A

Can often be cured surgically, prognosis depends upon length of time and extent of detachment

243
Q

Optic neuritis

A

Strongly associated with MS - inflammation of the optic nerve can also be HSV or autoimmune

244
Q

Clinical presentation of optic neuritis

A

Pain behind the eye with loss of color vision/perception andcentral field loss
Unilateral w/ pupillary defect

245
Q

Fundoscopic findings for optic neuritis

A

Swollen disc with diffuse borders and a few homrrhages

246
Q

Treatment for Optic neuritis

A

IV methylprednisone for 3 days and then oral prednisone
May need more prolonged therapy for chronic/non-acute cases

247
Q

Optic disk swelling due to intercranial pressure

A

Papilledema

248
Q

Clinical presentation of papilledema

A

Bilateral with blurred margins and flame hemorrhages - may have NO visual symptoms

249
Q

Treatment for Papilledema

A

DONT perform a lumbar puncture!!
MRI for diagnostics and treat underlying cause

250
Q

Why no lumbar puncture for papilledema

A

Risk of herniation

251
Q

Ischemic optic neuropathy

A

Inadequate perfusion of ciliary arteries leading to infarction of the optic disk

252
Q

Clinical presentation of Ischemic optic neuropathy

A

PAINLESS monocular vision loss usually affecting the superior and inferior visual field
Treated with HIGH dose corticosteroids and referral

253
Q

Fundoscopic exam for ischemic optic neuropathy

A

Optic disk swelling, central cotton with flame shaped hemorrhage (nonarteric) Large central palor/cotton wool spot (Arteric)

254
Q

6 eye complaints that can be treated in primary care w/o urgent follow up

A

Hordeolum
Chalazion
Blepharitis
Subconjuntival Hemorrhage
Conjunctivitis
Dry eye syndrome

255
Q

3 eye complaints that can be treated in primary care BUT need urgent follow up

A

Corneal Abrasion
Corneal foreign body
Contact lens over wear

256
Q

3 ophthalmic signs of hypertension

A

Cotton wool spots, Open angle glaucoma, Copper and silver wiring

257
Q

3 signs of diabetic retinopathy

A

Hard exudates, Neovascularization, Ischemic optic neuropathy

258
Q

3 ophthalmic signs of thyroid disease

A

Protruding eyes, Color dullness, difficulty moving eyes

259
Q

2 ophthalmic signs of hyperlipidemia

A

Macular degeneration, Blood and thunder fundus from venous occlusion

260
Q

2 ophthalmic signs of sarcoidosis

A

Granulomatous anterior uveitis
Optic neuritis

261
Q

Ophthalmic signs of myasthenia gravis

A

Diplopia and ptosis due to muscle weakness

262
Q

Ocular signs of HIV/AIDS (4)

A

Patchy salmon appearance from conjunctival lymphoma
Opportunistic fungal infections
Cytomegalovirus with yellow around vascular distribution

Something w/ blue sclera in newborns

263
Q

4 things that need to be determined in a hearing loss evaluation

A

Nature of impairment
Severity of impairment
Anatomy of impairment
Etiology of impairment

264
Q

3 times that we screen hearing

A

Within 1 month of birth
Kindergarten
Pre-employment/Military service

265
Q

2 screening tests for infants

A

Otoacoustic emissions (bounces sound waves off of the tympanic membrane)
Auditory brainstem responses

266
Q

Otoacoustic emissions

A

Tests the ears response to sound - can tell if sound is responded to or not - should be an echo if hearing is intact

267
Q

Auditory brainstem response

A

Uses electrodes to detect whether or not the brain is receiving sound information in a clear manner

268
Q

What do you do is a baby does not pass initial hearing screenings?

A

Obtain a full hearing evaluation before 3 months of age

269
Q

Full infant hearing eval

A

Repeat ABR
See how baby reacts to sounds
See how ears respond to sound

270
Q

5 signs of hearing loss in a baby

A

Not being startled by loud sounds
Not turning towards a sound after 6 months of age
Not saying single words at 1 year
Turns head it they see you but not if you call out their name
Seems to hear some sounds but not others

271
Q

When should children at risk for hearing loss be retested

A

By 2.5 years

272
Q

Visual reinforcement audiometry

A

6 months to 2 years - Child is trained to look towards the source of a sound

273
Q

Conditioned play audiometry

A

2-5 years old - child is trained to perform and activity when a sound is heard

274
Q

3 hearing tests for children and adults

A

Tuning fork, Whisper testing, Audiometric screening (with headphones)

275
Q

Pure tone audiogram

A

Determines the faintest a tones a person can hear at pitches from low to high

276
Q

X axis of audiogram

A

Frequency in Hertz

277
Q

Y axis of audiogram

A

Hearing threshold level in decibels

278
Q

6 hearing loss categories with dB number

A

Slight, Mild, Moderate, Moderately severe, Severe, Profound - start at 10 dB for slight and add 15 each time

279
Q

Symbol for left ear

A

X

280
Q

Symbol for right ear

A

O

281
Q

2 symbols used for bone conduction on the right

A

[ or <

282
Q

2 symbols used for bone conduction on the left

A

] or >

283
Q

Tympanogram

A

Measures the motility of the tympanic membrane
Types A B and C

284
Q

5 things that can be diagnosed with a tympanogram

A

Otitis Media, Fluid in middle ear space, Eustachian tube dysfunction, Indirectly diagnose hearing loss, Tympanic membrane perforation

285
Q

How does a tympanogram work

A

It introduces pressure into the ear canal while emitting sound waves to see how the TM is responding - measures pressure and flexibility

286
Q

Type A tympanogram

A

Normal finding - central peak

287
Q

Type B tympanogram

A

Gentle decline - No compliance

288
Q

Type C tympanogram

A

Early peak with rapid decline - Eustachian tube dysfunction (negative pressure in the ear space)

289
Q

3 Rinne test results and what they mean

A

Air>Bone - No loss or sensoneurial
Bone>Air - Conductive hearing loss

290
Q

3 Weber test results and what they mean

A

Hearing in both ears -Normal
Hearing in good ear - Sensorineural
Hearing in Affected ear - Conductive

291
Q

Conductive hearing loss

A

Sound is not conducted efficiently through the outer or middle ear leading to better bone conductivity than air conductivity

292
Q

Sensorineural hearing loss

A

Occurs because of damage to the inner ear or auditory nerve - may hear unclear or only low pitched sound

293
Q

Correction of sensorineural hearing loss

A

Permanent loss usually

294
Q

Infectious causes of hearing loss

A

TORCH
Toxoplasmosis
Other agents (Syphillis, Parvovirus, Listeria)
Rubella
Cytomegalovirus
Herpes Simplex Virus

295
Q

Ototoxic drugs - what do they cause?

A

Cause BILATERAL tinnitus or hearing loss

296
Q

List of ototoxic drugs (7)

A

Medications neglected can loss auditory vestibular system
M - Malaria and Macrolide
N - Nsaid
C - Cisplatin
L - Loop diuretic
A - Aminoglycoside
V - Vancomycin and Vincristine
S - Salcilic acid (ASA)

297
Q

Otosclerosis

A

Stapes affixes to the oval window causing conductive hearing loss - autosomal dominant

298
Q

Clinical presentation of otosclerosis

A

Slow uni or bilateral hearing loss with possible improved hearing of background noise

299
Q

Treatment for otosclerosis

A

surgical with stapedectomy

300
Q

Otoscopy findings of otosclerosis

A

Flamingo flush over the tympanic membrane or normal tympanic membrane

301
Q

Otoscopy finding for tympanosclerosis

A

White chalky patches on tympanic membrane

302
Q

Presbyacusis

A

Sensorineural - Bilateral age related hearing loss that is most remarkable at high frequencies - most severe in males

303
Q

Age-related change to the cochlea

A

Degeneration of outer and inner hair cells

304
Q

Ossicular change related to age

A

Joint between bones calcify and become thinner

305
Q

Treatment for presbyacusis

A

Hearing aids, cochlear implants if severe, OTC CoQ may help

306
Q

2 clinical signs of presebyacusis

A

Increased wax production with decreased TM compliance

307
Q

Acoustic neuroma

A

Benign tumor of schwann cells on nerve VIII causing UNILATERAL sensorineural hearing loss (rarely affects CN VII)

308
Q

Clinical presentation of acoustic neuroma

A

Progressive unilateral hearing loss with tinnitus, dizziness, and balance problems

309
Q

Diagnostic and treatment for acoustic neuroma

A

MRI to diagnose
Depending on severity, monitoring, radiation, or surgery

310
Q

Noise induced hearing loss

A

Permanent hearing impairment cause by hair cell death that results from prolonged exposure to high levels of noise

311
Q

Decibel level that causes noise induced hearing loss and frequencies usually lost

A

85+ decibels
2000-4000 hertz

312
Q

Decibels of a vacuum cleaner

A

70

313
Q

2 causes of hearing loss that may not need a referral

A

Cerumen impaction and OM

314
Q

What patient needs an urgent referral for hearing problems

A

Idiopathic, sudden sensorineural hearing loss - can use corticosteroids

315
Q

People who should have routine audiologic screenings

A

Prior exposure to injurious noise and over 65

316
Q

Gold standard for auditory rehabilitation

A

Cochlear implant

317
Q

Dizziness

A

Imprecise symptom that can describe many conditions

318
Q

Vertigo

A

Sensation of movement when there is none - can be caused by spinning or by vestibular dysfunction

319
Q

Lightheadedness

A

Feeling like one is about to loose consciousness

320
Q

Disequlilibrium

A

Feeling off balance may be CNS lesion or vestibular

321
Q

Peripheral vertigo

A

Vertigo that originates OUTSIDE of the CNS

322
Q

Central Vertigo

A

Vertigo that originates INSIDE the CNS - can be mixed (ie. migraines)

323
Q

General presentation of peripheral vertigo

A

Often sudden with hearing symptoms

324
Q

General presentation of central vertigo

A

Often gradual with no hearing symptoms or bilateral ones

325
Q

Nystagmus

A

Involuntary back and forth movement of the eyes - can be suppressed by

326
Q

Eye movement indication of cerebellar pathology

A

Abnormal pursuit/saccades

327
Q

Head impulse test

A

Patient looks forward and their head is turned to the side

328
Q

Positive head impulse test

A

Patient’s eyes move WITH the head - they can’t keep their gaze on the examiner or take time returning their gaze to the examiner after returning of head to its position - PATHOLOGICAL

329
Q

Dix-Hallpike test

A

Patient sits upright with head turned 45 degrees, patient is layed down so that their head is 30 degrees below horizontal

330
Q

Positive Dix-Hallpike test

A

Nystagmus upon performance

331
Q

What does the Dix-Hallpike test test for

A

Benign Paroxysmal Positional Vertigo

332
Q

What does the head impulse test test for?

A

Vestibulo-occular reflex

333
Q

Normal caloric testing result

A

Warm beats ipsilateral
Cold beats contralateral

334
Q

Abnormal caloric testing result

A

Lack of any nystagmus

335
Q

Medications that can interfere with the caloric reflex

A

Antihistamines, anxiolytics, antidepressants

336
Q

ENG or VNG testing

A

Uses electrodes to trace eye movements and record the presence of nystagmus

337
Q

VEMP testing

A

Vestibular evoked myogenic potential
looks at the reaction time between a sound and muscle response

338
Q

Cervical VEMP

A

Assesses Saccule

339
Q

Ocular VEMP

A

Assess Utricle

340
Q

Etiology of BPPV

A

Canalithiasis - calcium deposits in SCC can also be from a free floating otoconia

341
Q

Presentation of BPPV

A

Vertigo appears upon changes in head position and presents with no other neurological deficits

342
Q

BBPV of posterior canal

A

Upward rotary nystagmus

343
Q

BBPV of anterior canal

A

Downward rotary nystagmus

344
Q

Horizonal canal BBPV

A

Beating towards the floor

345
Q

Otolith repositioning for BPPV

A

Epley maneuver

346
Q

2 deconditioning exercises for BPPV

A

Brandt-Daroff and Sermont

347
Q

Vestibular neuronitis

A

Viral or post viral inflammatory response only affecting that vestibular division of CN VIII

348
Q

Vestibular labyrinthitis

A

Viral or post viral inflammatory response that effects the vestibular AND cochlear division of CN VIII

349
Q

Clinical presentation of Vestibular neuronitis or labrynthitis

A

Sudden onset vertigo
Nystagmus AWAY from the affected side
Normal head impulse test for central lesion

350
Q

Treatment for vestibular neuronitis/labrynthitis

A

Corticosteroids - prednisone or methyl prednisone for 10 days to 3 weeks
May try antivirals or antimicrobials if suspected

351
Q

2 drugs for vertigo suppression and 2 for nasuea

A

Antihistamines and Benzodiazepines
Promethazine and Ondansetron

352
Q

Meniere’s disease (endolymphatic hydrops)

A

Thought to be related to excessive fluid in the inner ear may be due to syphillis and blocked endolymphatic ducts

353
Q

Classic meniere’s disease triad

A

Episodic vertigo, Unilateral hearing impairment, Tinnitus w/ low tone blowing

Aural fullness is also a symptom

354
Q

Testing for meniere’s disease

A

2 spontaneous episodes lasting at least 20 minutes
Abnormal caloric testing
Hearing normal between attacks

355
Q

Treatment for meniere’s disease

A

Restrict salt, alcohol, and caffeine

356
Q

Medication for acute Meniere’s disease

A

Meclizine, diazepam, promethazine

357
Q

Medication for chronic meniere’s disease

A

Acetazolamide - Diuretic to remove salt water

358
Q

Perilymphatic fistula

A

Leakage of fluid from the inner to the middle ear

359
Q

Perilymphatic dehiscence

A

Abnormal thinning or asence of bone above the superior semicircular canal

360
Q

Clinical presentation of peri lymphatic fistula or semicircular canal dehiscence

A

Sensorineural hearing loss
Brief recurrent episodes of vertigo with specific triggers
Physical exam usually unremarkable

361
Q

Treatment for peri lymphatic fistula or semicircular canal dehiscence

A

Referral, Bed rest with head elevation, meds for symptoms, may need a surgical patch if refractory

362
Q

Barotrauma

A

Buildup of pressure between the middle and inner ear due to eustachian tube dysfunction, flight, SCUBA, etc.

363
Q

Type of pressure usually present in barotrauma

A

Negative pressure in the middle ear

364
Q

Presentation of Barotrauma

A

Pain, Pressure, Tinnitus, Hearing loss
Hemorrhage behind TM or perforation may be seen

365
Q

Treatment for barotrauma

A

Most heal over time, refractory may need myringoplasty or tympanoplasty

366
Q

Prevention of barotrauma

A

Decongestants, slow depth/altitude changes, Chewing gum or pacifier, frequent swallowing

367
Q

Tinnitus

A

Sounds in the absence of an exogenous source - pulsatile or non-pulsatile. Continuous or intermittent

368
Q

Pulsatile tinnitus

A

Can result from carotid bruits, Muscle spasms or open Eustachian tube (loud breath sounds)

369
Q

Non-pulsatile tinnitus

A

Due to sensorineural hearing loss, otosclerosis, meniere’s disease, etc.

TL/DR - More directly ear related

370
Q

Paragnaglioma

A

Tumor of the middle ear - causes pulsatile tinnitus and can be removed surgically
Look for high vascularity
Treat sugically

371
Q

Patulous eustachian tube

A

Tube stays open leading to roaring from breath sounds and unusually loud hearing of one’s own voice

372
Q

Treatment for patulous eustachian tube

A

Premarin (mucosal irritant)
Surgery

373
Q

Exacerbating factors of tinnitus

A

Depression and insomnia
21% suicide rate

374
Q

Therapy for tinnitus

A

Noise reducing generators with retraining therapy, Stress reducing CBT

375
Q

Other interventions for tinnitus

A

BZD, Intra TM steroids, Misoprostol, Transcranial magnetic stimulation

Infectious Disease and HEENT (4 decks)

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