EENT Flashcards

1
Q

subconjunctival hemorrhage

A

red around the eye, benign

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2
Q

uveitis

A

inflammatory autoimmune - use steroids to treat

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3
Q

when to never use steroids in the eye

A

HSV infection- causes blindness

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4
Q

symptoms of glaucoma

A

orbital swelling, corneal clouding, decreased vision, fixed/dilated pupil

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5
Q

blepharitis

A

eyelid infection or inflammation

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6
Q

dacrocystitis

A

lacrimal sac inflammation

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7
Q

keratitis

A

cornea inflammation

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8
Q

cellulitis

A

inflammation of the skin to the subdermal tissues

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9
Q

symptoms of conjuctivitis

A

tearing, burning, erythema, discharge, crusting

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10
Q

what should be on the differential for possible conjunctivitis if blurry vision is present

A

uveitis, scleritis, glaucoma

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11
Q

most common cause of viral conjunctivitis

A

adenovirus (but consider HSV, HZV, and EBV)

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12
Q

is MORNING crusting more common with viral or bacterial conjunctivitis

A

viral

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13
Q

most common corneal infection in the US

A

HSV keratitis

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14
Q

what cranial nerve is affected with HSV keratitis

A

CN 5

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15
Q

what drugs treat HSV keratitis

A

acyclovir and valacyclovir

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16
Q

what indicates eye involvement in an HZV reactivation

A

lesion at the tip of the nose- Hutchinson sign

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17
Q

what cranial nerve is affected with chorioretinitis

A

CN 2

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18
Q

most common causes of chorioretinitis

A

CMV and toxoplasmosis

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19
Q

characteristic sign of chorioretinitis on exam

A

flame hemorrhages and patches

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20
Q

which STIs cause bacterial conjunctivitis- need referral

A

N. ghonorrhea, Chlamydia trachomatis

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21
Q

most common bacteria that cause bacterial conjunctivits

A

S. pneumo, S. aureus, M. catarrhalis, H. influ.

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22
Q

is bacterial conjunctivitis most commonly unilateral or bilateral

A

unilateral initially, spreads to second eye within 24-48 hours

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23
Q

when does bacterial conjunctivitis present with photophobia?

A

chlamydia

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24
Q

what is the treatment for bacterial conjunctivitis

A

topical antibiotics- TMP/polymixin B drops and erythromycin ointment

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25
Q

when is a stat opthamology referral required for bacterial conjunctivitis?

A

If suspected gonorrhea or chlamydia

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26
Q

what treatment should be given for chlamydia or gonorrhea resulting in bacterial conjuctivitis?

A

ceftriaxone AND azithromycin

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27
Q

common causes of orbital cellulitis

A

staph, strep, H. flu, anaerobes, and pseudomonas.In diabetics, often fungal- mucor or aspergillus

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28
Q

symptoms of orbital cellulitis

A

proptosis, opthalmoplegia, edema, erythema, headache, and fever

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29
Q

preseptal cellulitis

A

anterior to orbital septum, usually associated with trauma, no proptosis

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30
Q

Define Dacryoadenitis

A

Inflammation of the lacrimal gland.

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31
Q

Dacryoadenitis - DX

A

acute - unilateral,swollen lid and lacrimal system, severe pain and pressure in the supratemporal area of the orbit. no vision changes presents in hours to days
chronic - more common form. Can Presentbilaterally with painless enlargement of the lacrimal gland. no vision changes Note: infectious causes are rare, but when they occur, bacterial gram +ve

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32
Q

Dacryoadenitis - Treatment and Management

A

Viral (MC) - self-limiting, supportive measures (warm compress, NSAIDS)Bacterial - initiate with 1st gen cephalosporins (Keflex) until culturefungal or protozoan - treat accordinglyinflammatory - steroids and investigate for systemtic etiology

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33
Q

Dacryoadenitis - DDX

A
  • dacrocystitis
  • viral conjunctivitis
  • bacterial conjunctivitis
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34
Q

Dacrocystitis - Definition

A

lacrimal sac is inflammation of the lacrimal sac. Usually accompanied by blockage of the lacrimal duct

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35
Q

Dacrocystitis - Dx

A

Diagnosis is based on clinical presentation

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36
Q

Dacrocystitis - Treatment

A
  • Distended and erythematous with discharge and tenderness: I&D Non-tender without discharge:
  • massage in infants
  • irrigation in adults
  • midly tender with discharge: warm compresses and antibiotics (depends on culture), but first line is Augmentin
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37
Q

Dacrocystitis - Clinical Presentation

A
  • lacrimal sac is frequently blocked, with tears draining out of eye
  • palpable and visible mass over lacrimal sac, which is located just inferior to the medial canthus
  • in acute, sometimes with erythema, tenderness and discharge (indicative of infection as complication)
  • can be chronic, then manage surgically by opening blocked duct
  • can also be congenital
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38
Q

Thyroid Eye Disease (TED)Definition

A
  • Autoimmune disorder often, but not always in hyperthyroid patients
  • e.g., Hashimotos thyroiditis
  • leads to characteristic changes in the eye
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39
Q

TED - Epidemiology

A
  • Women more likely than men
    But, men more likely to develop SEVERE TED
  • Smoking linked to TED and progression (dose-response dependent based on cigarette #)
  • RAI (treatment for thyroid) may worsen TED
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40
Q

TED - Management and Prevention(Get Euthyroid first)

A
  • Mild -
  • Most cases and mild and will improve spontaneously
  • 74% in study needed no Rx or supportive therapy only
  • artificial tears
  • establish euthyroid status
  • selenium - slowed progression
    2. Moderate/Severe -
  • IV methylprednisolone pulse, PO steriods later with taper (effective, but hard to do outside Europe)
  • orbital radiation
  • Rituximab (Mab) - Note that this treatment is still experimental. can have bad side effects like serum sickness and infusion reaction. Also $$ Surgical -
  • Emergent - immediate decompression when CON unresponsive to IV steriods or severe proptosis with exposure Elective - delay until pt. is euthyroid and stable for 6-9 months Sequenced approach:
  • decompression
  • extraocular muscle surgery
  • lid retraction surgery
  • dermatochalasis (fat protrusion)
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41
Q

What is the common name for Keratoconjunctivities Sicca?

A

Dry Eye

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42
Q

Dry Eye (KS) - Epidemiology

A
  • very common (5-30%)
  • Elderly
  • Female
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43
Q

Dry Eye (KS) - Treatment/Management

A

Non-pharmacologic

  • blink more often
  • avoid ac/heating
  • use humidifier (esp. at night)
  • moisture chamber glasses/goggles
  • Artificial Tears - Mainstay (OTC)
  • Restasis (topical cyclosporine) - prescription with immunosuppressive char. Must fail OTC artificial tears. Doesn’t work for everyone and really expensive (donut hole)
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44
Q

Dry Eye - Diagnosis and Tests

A
  • tear break-up time (E)
  • Schirmer’s tear test - (LP)
  • corneal sensation (LP) - low sensitivity
  • tear hyperosmolarity (non-specific)
  • ocular surface inflammatio (non-specific) Questionnaires (non-specific)
  • ocular surface disease index (OSDI)
  • impact of dry eye on everyday life (IDEEL)
  • Salisbury eye evaluation questionnaire (SEE)
    (E) = evaporative(LP) = low production
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45
Q

Dry Eye - Clinical PresentationSymptomsSigns

A

Symptoms:

  • irritation
  • feeling of grittiness or sand
  • redness
  • photophobia
  • burning
  • blurry vision
  • Signs:
  • conjunctival injection
  • loss of luster
  • mebomian gland dysfunction
  • punctate epithelial lesions
  • neovascularization
  • corneal scarring
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46
Q

Dry Eye - Decreased Tear ProductionPathophysiology

A
  • Sjogren Syndrome - autoimmune disease that cuases decreased fluid secretion
  • Age-related duct obstruction
  • infiltrative disease (attacks lacrimal gland) - sarcoidosis, lymphoma, graft-vs-host
  • contact lens use (reflexive decrease in tears)
  • DM
    Decreased tear production–>hyperosmolar tear film–>inflammation of ocular surface cells on cornea
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47
Q

Dry Eye - Increased Evaporative LossEtiology/Pathophys

A
  • meibomian gland dysfunction (aka posterior blepharitis) - decreased lipid in tears, so they evaporate faster
  • decreased blinking - staring at a computer screen
  • decreased eyelid integrity (TED, entropian)
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48
Q

Allergic Eye Disease - Definition and subtypes

A

Allergic conjunctivitisacute allergic conjunctivitis
* exposure to allergen
* rapid (less than one hour) onset
seasonal allergic conjunctivitis (Hay Fever)Outdoor environmental allergen
* spring = tree pollens
* summer = grass pollens
* late summer/early fall = weed pollens
* slow onset, constant through season
perennial allergic conjunctivitis - year-round symptoms to ubiquitous allergens (mold, dust mites, etc.)

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49
Q

Allergic Eye Disease - Epi

A
  • 20% of the population
  • more common in young
  • decreasing prevalence with age commonly co-occurs with other allergic disorders
  • allergic rhinitis
  • atopic dermatitis
  • asthma
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50
Q

Allergic Eye Disease - Pathophys.

A

IgE mediated hypersensitivity reactionMast cells cause histamine release which in turn, causes vasodilation, vasopermeability, itchingattracts, eosinophils, basophils and neutrophilsthen monocytes and lymphocytes

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51
Q

Allergic Eye Disease - Clinical Presentation

A
  • itchy
  • burning
  • red
    bilateral
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52
Q

Allergic Eye Disease - DDX

A
  • dry eye
  • viral conjunctivitis
  • keratitis (esp. if unilateral)
  • blepharitis
  • toxic exposure
  • acute angle closure glaucoma
  • episcleritis - layer on top of sclera inflammed(if eye pain)
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53
Q

Allergic Eye Disease - Management and Treatment

A
  • don’t rub eyes
  • cool compresses
  • artificial tears
  • discontinue contact lens use
  • allergen avoidance antihistamines/mast cell stabilizers (goal is vasoconstriction)
  • visine-A (antihistamine/vasoconstric)
  • alaway - (antihistamine/mast cell stab.)
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54
Q

Age-Related Macular Degeneration (AMD)Definition

A
  • degeneration of the macula resulting in central vision loss
  • normal part of aging
  • can be accelerated by certain risk factors
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55
Q

AMD - Epi

A
  • Age - 40% of 75+ have some form
  • white>Asian>Hispanic>Black
  • F>M
  • Genetics - Ask about FH Disease-related factors
  • High BMI
  • CV Disease
  • inflammatory conditions
  • Smoking (2x more likely) - progress from dry to wet faster
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56
Q

AMD - Clinical Presentation

A

Symptoms - gradual onset of blurred central vision in one or both eyesSigns - Drusen body accumulation around the macula (dist. from hard exudates). Amsler grid distortion

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57
Q

AMD - Pathophysiology

A

Vascular Endothelial Growth Factor (VGEF) - produced in excess in eye promotes neovascularization but the vessels do not reach maturity. They are friable and bleed and leak. Leaking vessels is more prominent in wet, which is advanced form. Most are dry (80%) and stay dry.

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58
Q

AMD - Treatment and Management

A
  • quit smoking
  • vitamin and mineral supplements (lutein in particular)
  • Advanced disease - injectable VEGF inhibitors (4-8 weeks)
  • photodynamic therapy
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59
Q

Primary Open-Angle Glaucoma (POAG)Definition

A

Progressive degeneration of the optic nerve with cupping of the optic disc and visual field defects. NB: CAN OCCUR WITH NORMAL IOP

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60
Q

POAG - Pathophysiology

A
  • poor drainage of aqueous humor at trabecular mesh network
  • increases anterior chamber pressure
  • translation of pressure to rest of globe
  • nerve damage due to IOP increase
    but, there’s issues with this model (because IOP can be normal)
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61
Q

POAG - Epi

A
  • 1/2 of people aware they have disease
  • cited as second leading cause of irreversible blindness
  • 2.25 over 40 in U.S. have POAG
62
Q

POAG - Clinical Presentation

A

hx of eye pain or redness halos around lights (rainbows) diminshed peripheral vision headache (elevated IOP) previous ocular disease

63
Q

POAG - Diagnosis (Testing)

A

usually found on routine eye exam (most are covered every 2 years)

  • normal IOP is 12-22 mmHg
  • ocular hypertension >22 mmHg with no evidence of glaucoma
  • Increasing cup:disk ratio (greater than 0.5)
  • Photograph retina to tell extent of nerve damage
  • Perimetry - available in ophtho.
64
Q

POAG - Rx and Prevention

A
  • Regular screening of IOP and peripheral vision
  • medications (topical protaglandins increase uveoscleral outflow) - the “prosts” (Bimatoprost/Lumigan; Travoprost/Travatan; Latanoprost/Xalatan)
  • topical Beta Blockers (decrease aqueous humor production) - Timolol (Timoptic)
  • Laser trabeculoplasty surgical trabulectomy
  • last two focus on improving drainage
65
Q

Cataracts - Definition

A
  • opacification of the lens
66
Q

Cataracts - Clinical Presentation

A
  • People complain of decline in vision, but it is really color vision and sharpnessthat goes
  • glare - daytime glare/night driving
  • second sight (aka myopic shift) - presbyopia disappears because of “tired” lens changing shape
  • cloudiness on the lens during exam
67
Q

Cataract - Treatment

A
  • sunglasses for glare
  • avoid night driving
  • surgical replacement with artificial lens
68
Q

Diabetic Retinopathy - Definition

A

Disease of the retina from persistent hyperglycemia. Leads to destruction of the retina and blindness.

69
Q

Diabetic Retinopathy - Epidemiology

A

Type I - 3-5 years after onset of systemic disease

Type II - DR usually present at the time of diagnosis of DM

Can occur with GD Risk factors: chronic hyperglycemia hypertension hypercholesterolemia smoking

70
Q

Diabetic Retinopathy - Clinical Presntation

A
Fundoscopic Exam:Non-Proliferative	
* Dot and Blot hemmorrhages	
* hard exudates (lipid deposition)	
* microaneurysms	
* cotton wool spots	
* flame hemorrhages - within superficial nerve fiber layer
Proliferative	
* neovascularization	
* vitreous hemorrhage (due to new blood vessels that are friable permeating into humor)
71
Q

Diabetic Retinopathy - Rx

A
  • Treat DM Then, for non-proliferative DR:
  • Anti-VEGFs
  • intravitreal corticosteriod implants
  • focal photocoagulation therapy
  • vitrectomy For proliferative
  • panretinal laser photocoagulation
72
Q

Papilledema - Definition

A

swelling of the optic nerve and disc

73
Q

Papilldema - Causes

A
  • tumors
  • space-occupying lesions of the CNS
  • subarachnoid hemorrhage
74
Q

Papilledema (Clinical Presentation)

A
Early			
* blurred disc margins		
* disc hyperemia		
* small peripapillary hemorrhages		
* loss of venous pulsation			
Late			
* very blurry disc margins		
* elevation of disc		
* venous congestion with small hemorrhages, exudates, cotton wool spots
75
Q

Hypertensive Retinopathy - Clinical Pres.

A
  • arterial narrowing
  • AV nicking
  • copper or silver wiring
  • flame shaped hemorrhages
  • cotton wool spots
  • hard exudates
76
Q

Hypertensive Retinopathy - RX

A
  • Treat the underlying HTN Then:
  • laser therapy
  • intravitreal corticosteriod injection
  • anti-VEGF
77
Q

define serous otitis media

A

transudation of fluid due to prolonged eustachian tube dysfunction with resultant negative middle ear pressure

78
Q

when does serous otitis media occur in adults

A

after a URI, barotrauma, or chronic allergic rhinitis

79
Q

must not miss dx for persistent unilateral serous otitis media

A

nasopharyngeal carcinoma

80
Q

appearance of tympanic membrane in serous otitis media

A

dull, hypomobile, retraction, and sometimes air bubbles

81
Q

does serous otitis media cause sensorineuro or conductive hearing loss?

A

conductive

82
Q

treatment of serous otitis media

A

oral steroids vs oral abxif failed response- ventilation tubes

83
Q

define tympanosclerosis

A

calcification of the TM and middle ear structures from inflammation

84
Q

define myringosclerosis

A

calcification of the TM only

85
Q

does tympanosclerosis or myringosclerosis cause hearing loss?

A

tympanosclerosis

86
Q

what is a retraction pocket?

A

chronic inflammation and negative pressure causes invagination of the pars tensa or pars flaccida.produces atrophy and atelectasis

87
Q

what does chronic retraction and inflammation result in?

A

adhesive otitis- predisposes to formation of cholesteatoma or fixation and erosion of the ossicles

88
Q

define cholesteatoma

A

greasy or pearly white mass in a retraction pocket or perforation- causes destruction of temporal boneHallmark is painless otorrhea

89
Q

symptoms of cholesteatoma

A

persistent, recurrent, foul smelling otorrhea

90
Q

treatment of TM perforation due to AOM

A

ototopical abx for 10-14 days. refer for hearing evaluation. if it doesn’t heal on it’s own, surgery can correct.

91
Q

etiology of chronic suppurative otitis media

A

persistent otorrhea with tympanostomy tubes or TM perforation. has ongoing purulent ear drainage. may be associated with cholesteatomachronic infection with mucosal edema, ulceration, granulation tissue, and polyp formation

92
Q

bacteria associated with chronic suppurative otitis media

A

P aeruginosa, S aureus, Proteus, Klebsiella pneumoniae, and diphtheroids

93
Q

if chronic suppurative otitis media fails culture directed treatment, what is the ddx?

A

foreign body, neoplasm, langerhan’s cell histiocytosis, tuberculosis, granulomatosis, fungal infection, or petrositis

94
Q

treatment of chronic suppurative otitis media

A

culture drainage and treat with appropriate abx

95
Q

pathogenesis of mastoiditis

A

infection from middle ear spreads to the mastoid portion of temporal bone into air-filled spaces

96
Q

most common affected age group for mastoiditis

A

60% younger than 2

97
Q

symptoms of mastoiditis

A

postauricular pain, fever, outwardly displaced pinnamastoid is indurated and red, swollen, and fluctuantmastoid is tenderAOM almost always present

98
Q

imaging for mastoiditis

A

CT- initially looks like AOM

progression of disease shows coalescence of mastoid air cells

99
Q

pathogens of mastoiditis

A

S pneumo, H influenzae, and S pyogenes

100
Q

ddx of mastoiditis

A

lymphadenitis, parotitis, trauma, tumor, histiocytosis, OE, furuncle

101
Q

major complication of mastoiditis

A

meningitis or brain abscess

102
Q

treatment of mastoiditis

A

IV abx- depends on culture, must cross blood-brain barrierif no improvement in 24-48 hours requires sugery- tympanostomy tube and culture vs I and D vs cortical mastoidectomy

103
Q

prognosis for mastoiditis

A

good. typically full recovery

104
Q

symptoms of AOM

A

otalgia, aural pressure, decreased hearing, and fever

105
Q

treatment of AOM

A

abx- amoxicillin and nasal decongestants can use cefaclor or augmentin for resistant cases

106
Q

chronic otitis media essentials of dx

A

chronic otorrhea, TM perforation with conductive hearing loss

107
Q

most common bacteria causing chronic otitis media

A

P aeruginosa, Proteus, S aureus, and mixed anaerobes

108
Q

define cholesteatoma

A

variety of chronic otitis media, most commonly due to eustachian tube dysfunctioninward migration of tympanic membrane creating a squamous epithelium-lined sac- fills with desquamated keratin and becomes infected. Can erode bone, destroy ossicular chain, erode inner ear, effect the facial nerve and spread intercranially

109
Q

define otosclerosis

A

lesions of footplate of the stapes impede passage of sound, causing conductive hearing losslesions can impede on the cochlea causing sensory hearing loss

110
Q

middle ear neoplasia

A

rarepresents with pulsatile tinnitus and hearing loss

111
Q

nerves involved with middle ear neoplasia

A

VII, IX, X, XI, and XII

112
Q

treatment of middle ear neoplasia

A

surgery, radiotherapy or both

113
Q

ototoxic medication

A

aminoglycosides, loop diuretics, antineoplastic agents

114
Q

Describe pinna hematoma- location, etiology, major complication

A

Between perichondrium and cartilageCauliflower appearance if untreatedCaused by trauma

115
Q

How to treat pinna hematoma

A

Pressure dressing after lancing within 2 days (use abx prophylaxis)- cannot for chronic injury due to coagulation

116
Q

When should you never irrigate the ear

A

TM perforation, if there is a foreign body which absorbs water, or if foreign body is a battery

117
Q

Symptoms of cerumen impaction

A

pain, pressure, vertigo, hearing loss

118
Q

Most common age group for foreign body

A

less than 8

119
Q

most common tools used for foreign body removal

A

alligator forceps, suction, cerumen loop, balloon catheter, right angle hook

120
Q

3 causes of otitis externa

A

trauma, bacteria, fungi

121
Q

most common etiology of otitis externa

A

recent swimming

122
Q

common symptoms of otitis externa

A

tragus and pinna tenderness, erythema, epithelial edema, TM can be mildly inflammed

123
Q

most common causes of chronic otitis externa

A

hearing aids and foreign bodieslasts longer than 6 weeks

124
Q

When to order a CT for otitis externa

A

mastoiditis

125
Q

mortality rate of mastoiditis or malignant otitis externa

A

50%

126
Q

major sign of physical abuse in ears

A

bilateral atraumatic tympanic membrane perforation

127
Q

etiology of TM perforations

A

foreign body, iatrogenic, forceful irrigation, otitis media, or barotrauma

128
Q

for TM perforation does sound lateralize toward or away from affected ear during the weber test

A

toward

129
Q

TM perforation treatment if infectious

A

keep dry, surgery usually not necessary abx drops + oral abx controversial need audiology referral, then ENT

130
Q

treatment for middle ear hematoma

A

watchful waiting hearing returns 6-8 weeks, can refer to ENT for audiometry

131
Q

What is the most common cause of bacterial AOM in infants less than three months?

A

E. coli

S. aureus

132
Q

What is the most common cause of bacterial AOM in kids 3 months-14 years?

A

S. pneumo
H. influenza
M. catarrhalis

133
Q

What’s the most common cause of bacterial AOM in those older than 14?

A

S pneumo
GAS
S aureus

134
Q

Weber test

A

Lateralizes to affected ear in conductive

Lateralizes to the normal ear in sensorineural

135
Q

Rinne Test

A

AC>BC in sensorineural and normal

BC>AC in conductive

136
Q

Which frequencies are lost first in SNL hearing loss?

A

high frequencies (front of cochlea and less protected)

137
Q

What’s a characteristic finding of noise induced hearing loss?

A

a notch at 4k on audiogram

138
Q

What test should you always do with unilateral sensorineural hearing loss?

A

MRI of the cerebellopontine angle (CPA) with gadolinium. (looking for neuroma)

139
Q

Which type of vertigo has horizontal nystagmus that suppresses with fixation?

A

peripheral

140
Q

Which type of vertigo has vertical nystagmus that does not suppress with fixation?

A

central

141
Q

cold water calorics causes the fast phase of the nystagmus to beat where?

A

to the opposite side of the stimulus (COWS)

142
Q

What disease is marked by tinnitus, vertigo and hearing loss?

A

Meniere’s Disease

143
Q

What is an indication in a neuro PE of acoustic neuroma?

A

Romberg +ve for drift towards affected side

144
Q

What is first-line and 2nd line pharmacotherapy in POAG?

A
  1. Latanoprost drops

2. Timolol drops

145
Q

Orbital Cellulitis treatment

A

IV Vancomycin and Cephalosporins or Amp/Sub and Piper/Tazo or fluroquinolones if PenCeph allergy

146
Q

What is the RX for viral Conjunctivitis

A

Topical antihistamines/decongestants (Naphcon-A or Ocuhist)

147
Q

What is the Rx for bacterial conjunctivitis

A

Cipro drops

148
Q

What is the Rx for HSV keratitis?

A

trifluridine eye drops

149
Q

what is the rx for dacrocystitis that is mild tenderness with discharge?

A

Amoxicillin-clavunate (PO)

150
Q

What is an Rx to bridge to surgery for Entropion?

A

Botox