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Clin med 1 > HEENT 1-5 only > Flashcards

HEENT 1-5 only Flashcards

1
Q

What are some causes of orbital fractures?

A

Motor vehicle accidents, industrial accidents, sports related facial trauma, assaults (domestic violence)

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2
Q

What are the 7 bones of the orbit?

A
  1. Sphenoid
  2. Zygoma
  3. Maxilla
  4. Ethmoid
  5. Palantine
  6. Lacrimal
  7. Frontal
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3
Q

What is another name for the zygoma bone?

A

Lamina papyrcea

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4
Q

What makes up the superior wall of the orbit?

A

Frontal and sphenoid bone (lesser wing)

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5
Q

What makes up the inferior wall of the orbit?

A

Maxilla, zygomatic and palantine bones

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6
Q

What makes up the medial wall of the orbit? (thinnest)

A

Ethmoid, maxilla, lacrimal, sphenoid

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7
Q

What makes up the lateral wall of the orbit? (thickest)

A

Zygomatic and sphenoid bone

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8
Q

Some additional orbital structures include

A

Eye, extraocular muscles, sinuses, medial/lateral canthal ligaments, nerves, fat

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9
Q

Lateral rectus muscle action

A

abduction

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10
Q

Medial rectus muscle action

A

adduction

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11
Q

Superior rectus muscle action

A

upward and inward

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12
Q

Inferior rectus muscle action

A

downward and inward

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13
Q

Superior oblique muscle acion

A

rotate inferior and lateral

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14
Q

Inferior oblique muscle action

A

rotate superior and lateral

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15
Q

What muscle attaches to the eyelids and allows for eyelid raise?

A

Levator palpebrae

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16
Q

The three sinuses involved in the orbit?

A

Maxilla, frontal, ethmoid

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17
Q

What is the medial canthal ligament?

A

Attaches to the corner of the tarsal plate to the orbital wall

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18
Q

What is the lateral canthal ligament?

A

Attaches to the lateral aspect of orbital wall

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19
Q

What can disruption of the two canthal ligaments cause?

A

Malpositioning of the eyelids (entropion/ectropion)

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20
Q

What makes up the lacrimal duct system?

A

Lacrimal gland, sac, and the nasolacrimal duct

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21
Q

The infraorbital nerve innervates what?

A

The lower eyelid, nose and upper lip

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22
Q

The supraorbital nerve innervates what?

A

Upper eyelid, forehead and scalp

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23
Q

What structures are associated with the superior orbital wall? (2)

A

Frontal sinus, supraorbital nerve

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24
Q

What structures are associated with the inferior orbital wall? (4)

A

Inferior oblique muscles, inferior rectus muscle, maxillary sinus, infraorbital nerve

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25
Q

What structures are associated with the lateral wall? (1)

A

Lateral canthal ligament

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26
Q

What structures are associated with the medial wall? (5)

A

Medial rectus muscle, ethmoid sinus, medial canthal ligament, lacrimal duct system

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27
Q

What are the types of orbital fractures?

A

Orbital zygomatic fracture, Nasoethmoid fracture (NOE), orbital roof fracture (rare), orbital floor fracture

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28
Q

What is the most common type of orbital fracture?

A

Orbital floor fracture

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29
Q

Blowout fracture

A

Orbital floor fracture without fracture of the orbital rim with herniation of contents

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30
Q

What can happen in a blowout fracture?

A

Bone defect is filled w/soft tissue and fat from orbit, alters support mechanism for EOM, nerve damage can result

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31
Q

Impure blowout fracture

A

fracture line extends to orbital rim

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32
Q

Trapdoor blowout fracture

A

bone fragments involving the central area of bone

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33
Q

Most common type of blowout fracture?

A

Inferior floor

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34
Q

Blow-out fracture complications include what

A

Entrapment of inferior rectus, damage to infraorbital nerve

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35
Q

How can we assess orbital fractures?

A

History-mechanism of injury, inspecting face and eye, palpating crepitus and for sensation deficit

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36
Q

Orbital fracture symptoms

A

Facial pain, ocular pain on movement, neuropraxia, diplopia, color changes, floaters hazy vision clouds fog, flashers veil or curtain, foreign body sensation

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37
Q

What will be inspected for an orbital fracture exam?

A

Periorbital edema and ecchymosis, a depression/defect of the orbit, epistaxis or CSF leakage

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38
Q

What will be palpated during an orbital fracture exam?

A

Nerve neuropraxia (loss of sensation), emphysema, pain, step-off deformity

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39
Q

What test can be done for an orbital fracture involving the visual acuity?

A

Snellen chart-progressive loss may mean increased IOP or optic nerve injury

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40
Q

Physical exam findings for an orbital eye fracture

A

Lid lacerations, periocular ecchymosis, exophthalmos/proptosis (bulging eye), hypoglobus (blood in ant chamber), traumatic mydriasis, canthal ligament disruptions

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41
Q

Other physical exam findings of an orbital eye fracture

A

Epipora (tearing of eye w/no drainage), corneal abrasion, ruptured globe, vitreous hemorrhage, retinal detachment/tears, EOM entrapment

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42
Q

What is the gold standard to diagnose an orbital fracture?

A

CT scan of the orbit

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43
Q

What view is best for an orbital fracture (CT)

A

Axial view: for frontal fractures, NOE fractures, zygomatic arch, vertical orbital walls
Coronal view: orbital roofs, orbital floors, ptyergyoid plates

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44
Q

Some other additional diagnostic exams for an orbital fracture

A

Forced ductions test (specialist needs to preform), fluorescein stain, hertel exophtalmometer

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45
Q

Major complications of an orbital fracture associated with blindness

A

Ruptured globe, hyphema, retinal injury (detachment), optic nerve sheath hematoma, glaucoma

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46
Q

Major complications of an orbital fracture associated with EOM entrapment?

A

Orbital floor: inferior rectus

Lateral wall: medial rectus

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47
Q

Major complications of an orbital fracture associated with orbital dystopia/cosmetic issues?

A

Enopthalmos (eye pushed back), hypoglobus

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48
Q

Other complications that can arise from an orbital fracture

A

Long term diplopia, infection, neuropraxia, intracranial bleed (superior orbit)

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49
Q

Treatment options for an orbital fracture

A

Nonsurgical, surgical (controversial for indications, emergent vs. non emergent)

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50
Q

Non surgical initial management for orbital fracture

A

Ice for 48 hours, elevation of HOB, nasal decongestants (increase drainage), broad antibiotics, AVOID aspirin and nose blowing, +/- steroids for orbital edema w/diplopia. Follow up w/ophthalmologist in 7 days

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51
Q

Anterior chamber of the eye

A

Fluid-filled space of Aqueous humor. bordered by cornea, iris, angle and lens

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52
Q

What can interrupted aqeuous flow by blood cause?

A

Increased IOP -> blindness

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53
Q

Hyphema

A

Grossly visible blood in the anterior chamber. Bleeding from tears on the vessels of the ciliary body or iris

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54
Q

How can hyphema occur?

A

Trauma and spontaneous (pts with underlying conditions)

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55
Q

What are some differential diagnoses for hyphema?

A

Corneal abrasion, retinal detachment, globe rupture, glaucoma

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56
Q

Symptoms of hyphema

A

Decreased visual acuity, photophobia, pain

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57
Q

Physical exam findings of hyphema

A

Layer of blood in ant. chamber, decreased visual acuity, photophobia, anisocoria, elevated intraocular pressure

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58
Q

Anisocoria

A

Mydriasis, uneven pupils

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59
Q

What tools are used to diagnose hyphema?

A

Ophthalmoscope, slit lamp, tonopen* (very difficult to use)

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60
Q

Treatment of hyphema

A

Eye shield, elevate HOB 30 degrees at bed rest, cycloplegia (paralyze the eye), bed rest, pain control PO, control N/V with antiemetics, 5% require surgery

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61
Q

What would 5% of pts with hyphema need surgery for?

A

To evacuate the clot

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62
Q

What is used to paralyze the eye for treatment of hyphema?

A

Cyclopentolate or homatropine

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63
Q

Follow-up for hyphema

A

Referral to Ophthalmologist ALWAYS

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64
Q

What is hyphema emergent?

A

If: open globe, orbital compartment syndrome, large hymphemas (grade 3 or 4), hyphemas associated with bleeding dyscrasia

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65
Q

What are some complications of hyphema?

A

Intractable glaucoma: permanent vision loss and blindness, 2ndary hemorrhage (worse prognosis), posterior or peripheral synechiae, optic atrophy

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66
Q

Posterior synechiae

A

Complication of hyphema, when the iris adheres to the lens

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67
Q

Peripheral synechiae

A

Complication of hyphema, when the iris adheres to the cornea

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68
Q

What is the most frequent cause of visits for ophthalmic emergencies?

A

Corneal foreign body

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69
Q

Corneal foreign body symptoms

A

Pain, foreign body sensation, photophobia, tear, red eye, blurred vision

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70
Q

Corneal foreign body physical exam

A

Visual acuity, inspection of eye and eyelid (evert), slit lamp exam, fluorescein stain uptake (woods lamp or slit lamp)

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71
Q

Corneal foreign body physical exam findings

A

Normal/decreased acuity, conjunctival infection, ciliary injection, VISIBLE FOREIGN BODY, rust ring, epithelial defects w/stain w/fluorescein, anterior chamber cell/flare, excessive tear production, corneal edema

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72
Q

What is the Seidel test?

A

Tests for corneal perforation, can be in an exam finding for a corneal foreign body

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73
Q

Differential of corneal foreign body

A

Keratitis, intraocular foreign body, corneal abrasion

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74
Q

Corneal foreign body removal treatment

A

Apply topical anesthetic first, irrigation (morgans lens or direction irrigation), cotton Qtip, sterile needle tip or automatic burr

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75
Q

How do you remove a rust ring?

A

Experienced clinicians do this using a slit lamp, best to refer to opthalmologist in this case

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76
Q

Corneal foreign body medical management

A

Topical antibiotic; erythromycin or ciprofloxacin, topical cycloplegic, avoid contact lens, eye patch, tetanus

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77
Q

What is a corneal abrasion?

A

Any defect in the corneal surface

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78
Q

How many layers does the cornea have?

A

6, endothelium mostly involved w/abrasions

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79
Q

What is the cornea innervated by?

A

Deeply innervated by sensory fibers of the trigeminal nerve

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80
Q

Corneal abrasion symptoms

A

Pain foreign body sensation, photophobia, tear, red eye, burred vision

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81
Q

Corneal abrasion differential diagnosis

A

Acute globe rupture, retained foreign body, infectious keratitis, corneal ulcer, acute angle glaucoma

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82
Q

Corneal abrasion physical exam

A

Visual acuity, inspect eye and evert the lids, slip lamp eye exam, fluorescein stain (woods lamp, slit lamp)

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83
Q

Corneal abrasion physical exam findings

A

Normal/decreased visual acuity, conjunctival injections, visible foreign body, rust ring, epithelial defects w/stain w/fluorescein, ant. chamber cell/flare, excessive tear production, corneal edema

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84
Q

Corneal abrasion treatments-antibiotics

A

Topical: Mainstay of treatment*

ointment preferred, Erythromycin. For contact lens: Ciprofloxacin drops

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85
Q

Corneal abrasion pain control treatment

A

Mild to mod: NSAIDs PO or topical (diclofenac/ketorolac)
Severe: Oral opioids for 48 hours
Cycloplegics: Prevents pupillary constriction

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86
Q

Corneal abrasion follow-up

A

No follow-up needed, heal 24-48 hours

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87
Q

When would you have a corneal abrasion pt follow-up with an opthalmologist?

A

Large abrasions, contact lens wearers, rust ring, abrasion in young children, abrasions with vision changes

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88
Q

What are the infectious causes of corneal ulcers?

A

VIRAL, bacterial, fungal, amoebas

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89
Q

What are the non-infectious causes of corneal ulcers?

A

Exposure keratitis: Exophthalmos, Bells palsy with lid lag, allergic disease, severe dry eye, inflammatory/autoimmune, VitA deficiency

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90
Q

Bacterial causes for corneal ulcers

A

Pseudomonas, moraxella liquefaciens, strep, MRSA
Contacts: Pseudomonas
DM, alcoholics, immunosuppressed: Moraxella

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91
Q

Viral causes for corneal ulcers

A

HSV/Zoster

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92
Q

Amoebic causes for corneal ulcers

A

Acanthamoeba, contaminated water, contact lens with poor hygeine

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93
Q

Corneal ulcer risk factors

A

Contact lens, previous eye surgery, eye injury, Hx of HSV, immunocompromised, topical or systemic steroid use

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94
Q

Corneal ulcer symptoms

A

Pain, photophobia, tearing, reduced vision, lid and ocular swelling, injected conjunctiva, injected eyelid, foreign body sensation, miotic pupil, clear or mucopurulent discharge

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95
Q

Corneal ulcer physical exam

A

Visual acuity, slit lamp, fluorescein stain

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96
Q

Corneal ulcer physical exam findings

A

Punctate or diffuse branching dendritic lesions (HSV/Zoster), Corneal ulceration (varying patterns), Hypopyon (pus in ant. chamber), anterior cell/flare

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97
Q

Corneal ulcer diagnosis

A

Slit lamp and fluorescein stain, culture and gram stain or PCR (done by ophthalmologist)

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98
Q

Corneal ulcer treatment

A

Aggressive! Always place on Abx unless dendritic pattern-acyclovir, PROMT referral to opthalmologist 24 hours

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99
Q

Bacterial Abxs used for corneal ulcers

A

Fluoroquinolone*** Fluconazole for fungal, topical acyclovir for viral

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100
Q

Pain management for corneal ulcer

A

Cycloplegics topical or oral NSAID

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101
Q

Corneal ulcer complications

A

Corneal scarring, corneal perforation, anterior/posterior synechiae, glaucoma, cataracts, blindness

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102
Q

What are the two kinds of Otitis media?

A
  1. AOM: acute otitis media

2. OME: otitis media with effusion (chronic)

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103
Q

What is the gold stand for the diagnosis of OM?

A

Pneumatic otoscopy

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104
Q

Acute or new OM is what?

A

When the symptoms have been going on for LESS THAN or equal to 48 hours

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105
Q

Severe OM is what?

A

Toxic/sick appearing child, persistent otalgia longer than 48 hours, temp higher than 102.2 in past 48 hours

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106
Q

MEE

A

Middle ear effusion: fluid behind tympanic membrane

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107
Q

What are the diagnostic features of AOM?

A

mod-severe bulging of the TM or otorrhea (discharge from ear), mild bulging TM and recent ear pain OR intense redness

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108
Q

What are the diagnostic features of OME?

A

MEE without signs or symptoms of acute ear infection, tympanocentesis and pneumatic otoscopy (fluid sitting behind ear)

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109
Q

AOM possible pathogens

A

Strep pneumoniae and H.influenza most common** M.catarrhalis, viruses and ostiomeatal complex dysfunction

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110
Q

OME pathophys

A

Ostiomeatal complex/eustachian tube dysfunction, sequelae of AOM, viral, bacterial antigens, biofilm

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111
Q

OME management

A

Watchful waiting: for children that are not at increased risk for speech language or learning problems
Tubes, surgery, prednisone oral or topical, antihistamines/decongestants

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112
Q

What is the surgery like for OME?

A

Myringotomy with tympanostomy tube insertion, tympanocentesis (stick needle in to drain out fluid), adenoidectomy

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113
Q

Out of the OME management, which are not recommended to do, but are still given?

A

Prednisone oral or topical, and the antihistamines/decongestants

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114
Q

Severe AOM

A

Abx if the child is greater than 6 mos, with mod-severe signs OR symptoms OR a temp higher than 102.2

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115
Q

Nonsevere AOM

A

Abx or observe in 6-23 mos if unilateral if and only if you have good follow up
Abx greater than 24 mos if bilateral
Abx or observe if greater than 24 mos

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116
Q

AOM treatment

A

1st line: Amoxicillin. Alternate: Quinolone drops
2nd choice: Augmentin, Bactrim, 2nd or 3rd gen ceph
Ceftriaxone: if patient has severe vomiting

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117
Q

Other AOM treatments

A

Azithromycin, Clindamycin

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118
Q

AOM Management

A

Pain relief: Acetaminophen, ibuprofen, Auralgan
Topical decongestant: not recommended
Cold meds: not for under 2yo, probably not under 4yo, older then 4 maybe

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119
Q

AOM Follow-up

A

Improvement expected in 24-48 hours, Re-evaluate in 2 weeks

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120
Q

AOM prophylaxis

A

Penumococcal vaccine, breast feeding, smoke-free environment, no bottles in bed
Abx prophylaxis: Amox or Sulfasoxazole (not recommended)

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121
Q

How does a TM perforation occur?

A

Blows to the ear, severe atmospheric overpressure, exposure to excessive water pressure, improper attempts at wax removal or ear cleaning

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122
Q

TM Perforation things to avoid

A

Avoid: eardorps containing gentamycin, neomycin, sulfate, or tobramycin

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123
Q

TM Perf treatment

A

Systemic antibiotics if otorrhea, paper-patch method in office, Gelfoam plug, fibrin glue, surgery

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124
Q

What is the most common treatment for a TM perf?

A

Most heal spontaneously- can refer pt if not better in 2 mos, have significant hearing loss or have ossicular trauma

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125
Q

Auricular hematoma

A

Results from direct trauma, shearing forces cause the separation of the anterior auricular perichondrium from the cartilage, hematoma forms

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126
Q

Treatment for an auricular hematoma

A

Early identification: drainage with a needle, I&D, splints, compression

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127
Q

Mastoiditis treatment

A

Consult, medical, surgical

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128
Q

How do tongue and lip cancers present?

A

As exophytic (outward growth) or ulcerative lesions

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129
Q

What types of oral lesions should be biopsied?

A

Persistent papules, plaques, erosions or ulcers

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130
Q

What accounts for up to 80% of squamous cell carcinoma of the head and neck?

A

Tobacco and ETOH

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131
Q

Cancer of oral cavity

A

Associated with ulcers or masses that do not heal

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132
Q

What is aphthous stomatitis

A

Canker sore, painful oral lesions, sometimes genital with repeated development

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133
Q

What is the most common acute oral lesion?

A

Aphthous stomatitis

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134
Q

What are the classifications of aphthous stomatitis>

A
  1. Simple aphthous (Mikulicz)

2. Complex aphthous

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135
Q

Simple aphthous

A

Several episodes a years, lasting up to 14 days, limited to oral mucosa, most common form of disease

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136
Q

Complex aphthous

A

Oral and genital, more numerous lesions, larger than 1cm, 4-6 weeks to resolve, patients almost always have them

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137
Q

Ulcer morphology (aphthous stomatitis)

A

Minor ulcers <1cm major >1cm

Herpetiform 1 to 2 cm typically in clusters

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138
Q

Pathogenesis behing aphthous stomatitis

A

Unknown, likely multifactorial involving immune dysregulation, weak anti-inflammatory response, possible genetic predisposition

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139
Q

What diseases can aphthous stomatitis be seen in?

A

Celiac disease, IBD, Crohns. Diseases that cause decrease in mucosal thickening

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140
Q

Risk factors for aphthous stomatitis

A

Smoking cessation, familial tenency, trauma-dental cleaning, hormonal factors-progestin levels fall in luteal phase of menstrual cycle, emotional stress, HIV

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141
Q

Clinical presentation of aphthous stomatitis

A

1-5, round to oval, clearly defined ulcers, erythematous rim, yellowish central, small 1-3 cm, painful

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142
Q

How to diagnose aphthous stomatitis

A

Hx and PE, history of recurrent self-limited oral ulcers, Bx not needed

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143
Q

Management of aphthous stomatitis

A

Oral hygeine: non alcoholmouth wash and soft toothbursh
Pain control: viscous lidocaine applied or swish and spit, Diphenhydramine liquid swish and spit, dyclonine losenges
Topical steroids: Dexamethasone elixir swish and spit, Clobetasol gel, Triamcinolone paste

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144
Q

Management of complex aphthous stomatitis

A

Intralesional or glucocorticoids for recalcitrant lesions or sever disease, Colchicine, Dapsone, Pentoxifylline (bronchodilator), Thalidomide in HIV pts

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145
Q

Oral leukoplakia is what?

A

A benign reactive process, significance depends on degree of and presence of dysplasia.

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146
Q

What is there an association with?

A

Oral leukoplakia and HPV

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147
Q

Epidemiology of Oral leukoplakia

A

1-20% progress to carcinoma in 10 yrs, similar to squamous cell carcinoma, common in smokeless tobacco users

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148
Q

Clinical manifestations of Oral leukoplakia

A

Lekoplatic lesions that show up in trauma prone regions (cheek, dorsum of tongue)
Thin areas of mucosa, not painful, whitish grey lesions, flat, not well defined, cant scrape off easily*

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149
Q

Diagnosis of Oral leukoplakia

A

Hx and PE, whitish area cant be scarped off that should tip you off, all indurated areas should be biopsied

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150
Q

Management of Oral leukoplakia

A

Most dont need treatment, surgical removal, cryoprobe, recenter interest in chemoprevention, oral retinoids showing promise

151
Q

Oral hairy leukoplakia

A

Separate from oral leukoplakia, not premalignant, EBV associated, occurs almost entirely in HIV affected patients

152
Q

HSV-1 Herpes

A

Herpes labialis, effects multiple sites in the body, perioral and oral cavity, HSV 1 causes 80% of oral lesions, 20% of genital lesions

153
Q

Epidemiology of HSV-1

A

Associated with increasing cases of genital herpes, more common in women, majority are transmitted by people who dont know they have it

154
Q

Pathophys of HSV-1

A

HSV enters, undergoes latency and can survive in neural ganglia. Prevents elimination by immune response, recurrent infection is common-usually local symptoms only

155
Q

What are the types of infections? (HSV1)

A

Primary and Secondary

156
Q

What is primary HSV1

A

Highly variable usually severe, systemic

157
Q

What is secondary HSV1

A

Common typically less severe, local

158
Q

Clinical manifestation of HSV1

A

Primary infection: systemic symptoms, usually affects the gingiva. Herpetic gingivastomatitis most common*

159
Q

What do the lesions look like in herpes simplex infection?

A

Multiple oral vesicular lesions and erosions surrounded by erythematous base, painful

160
Q

Young children with herpes simplex can also have

A

Fever, LAD, drooling, decreased oral intake

161
Q

Other clinical manifestations of herpes

A

Prodromal signs of burning, tingling pain 24 hours prior to outbreak, recurrent outbreaks usualyl on lip borders, recurrence may be first indication of infection

162
Q

Risk factors for herpes

A

Sunlight exposure, stress, trauma

163
Q

How can you diagnose HSV1?

A

Tzanck smear, immunofluoresence smear or viral cx, unroof th evesicle, serology for HSV by PCR

164
Q

Management of HSV1

A

Systemic antivirals: Acyclovir, Valacyclovir, Famciclovir
Swish and spit miracle mouthwash
Supportive, popsicles

165
Q

What involves the mucous membranes- oropharyngeal and esophageal

A

Oral candida (thrush)

166
Q

Epidemiology of thrush

A

Young infants, older adults who wear dentures, Abx, chemotherapy, radiation head and neck, immunodeficiency, inhalers, xerostomia

167
Q

Pathogens most commonly causing thrush

A

Candida albicans, Candida glabrata, Candida krusei, Candida tropicalis

168
Q

Classification of thrush

A

Pseudomembranous and atrophic

169
Q

PSeudomembranous thrush

A

Most common form. white plaques on buccalmucosa, palate, tongue and orophyarnx

170
Q

Atrophic thrush

A

(Denture stomatitis), most common form in older adults. Found under the upper dentures, erythema without plaques

171
Q

Clinical manifestations of thrush

A

Asymptomatic: dry mouth, loss of taste, pain with swallowing or eating
White plaques on buccal mucosa, palate, or tongue, erythema without plaques in denture wearers, painful, beefy red tongue angular chelitis and painful fissuring

172
Q

Diagnosis of thrush

A

White plaques usually removable, fungal Cx, KOH prep, refractory thrush should warrant HIV testing

173
Q

Management of thrush

A

Local therapy, Nystatin suspension swish and swallow, Clotrimazole troches (lozenges), Miconazole buccal tabs, Diflucan PO

174
Q

What is known as the Red eye

A

Conjunctivitis

175
Q

Conjunctivitis

A

Usually benign and self-limited, inflammation of the conjunctiva- injection
Thin tissue that lines the insides of lid and top of the globe, generally transparent

176
Q

Classifications fo conjuncitivitis

A

Bacterial, viral, allergic, traumatic, toxic

177
Q

Bacterial conjunctivitis

A

More common in children, spread by direct contact, highly contagious

178
Q

Pathogens that cause bacterial conjunctivitis

A

S. aureus, S. pneumoniae, H. influenzae

179
Q

Clinical manifestations of bacterial conjunctivitis

A

Red eye usually unilateral, discharge-green, yellow, white. Often complain of eyes stuck shut, itchy, feels gritty like sand

180
Q

More clinical manifestations of bacterial conjunctivitis

A

Dry crusty stuff at lid margins and corner of eye, purulent discharge

181
Q

What should be done for each eye complaint of bacterial conjunctivitis?

A

Fluorescein every eye complaint* do Fundoscopy on every eye complaint

182
Q

Management of bacterial conjunctivitis

A

Erythromycin ophthalmic ointment, Trimetoprim-Polymyxin drops

183
Q

Alternative treatments for bacterial conjunctivitis

A

Bacitracin ointment, Sulfacetamide ointment, Fluoroquinolone drops good in contact lens wearers

184
Q

Viral conjunctivitis

A

Usually part of a viral prodrome, patients have sore throat, fever, LAD, pharyngitis, highly contagious, spread by direct contact

185
Q

Which virus commonly causes viral conjunctivitis?

A

Typical pathogen in adenovirus

186
Q

Clinical manifestations of viral conjunctivitis

A

Red eye, mucoserous or watery discharge, burning, sandy or gritty feeling, both eyes usually involved in 24-48 hours. New rapid (10 min) test for adenovirus is now available

187
Q

Management of viral conjunctivitis

A

Self-limited, warm or cool compresses, gets wrorse in first 3-5 days, gradual resolution

188
Q

Allergic conjunctivitis

A

Caused by airborne allergens that come in contact with the eye, specific IgE cause mast ell degranulation and histamine release
Pts have hx of allergies, itchy eyes look for corneal abrasions!

189
Q

Clinical manifestations of allergic conjunctivitis

A

Bilateral eye redness, itching, grittiness, burning, irritation, watery dc, morning crusting, marked chemosis, infraorbital edema: allergic shiners

190
Q

Management of allergic conjunctivitis

A

Remove offending agent, wear sunglasses, change filters

191
Q

Managemtn of allergic conjunctivitis (drugs)

A

Antihistamine/Vasoconstrictor combo: Naphazoline/pheneramine (Naphcon-A)
Antihistamines with mast cell stabilizer properties: Olopatadine (Patanol)
Mast cell stabilizers: Cromolyn sodium (Optocrom)

192
Q

Glucocorticoids used in allergic conjunctivitis

A

Loteprednol (lotemax), use carefully, can rise IOP, up to 2 weeks only*

193
Q

Traumatic conjunctivitis

A

Due to foreign body, treatment is removal

194
Q

Toxic conjunctivitis

A

Smoke, liquid, fumes, chemicals, akalai and acidic
Use litmus paper for pH testing- 7.0 normal
20% of chemical injuries result in significant visual and cosmetic disability

195
Q

Pathophys of toxic conjunctivitis

A

Acid burns: dissociate into hydrogen ions in cornea, hydrogen damages ocular surface by altering pH, produces protein coagulation, preventing deeper penetration of acids into the eye. Hydrofluoric acid acts as an alkali

196
Q

Common acids in toxic conjunctivitis

A 
Battery acids: Sulfuric acid
Bleach: sulfurous acid
Glass polish: hydrofluoric acid
Vinegar: Acetic acid
Hydrochloric acid
197
Q

Which type of burns are the worst?

A

Alkali, dissociated into a hydroxyl ion, liquifies the fatty acid of a cell membrane and penetrates cell membrane

198
Q

Common alkalis found in toxic conjunctivitis

A 
Ammonia: Cleaning products, fertilizer
Lye: drain cleaners
Lime: plaster, mortar
Airbag rupture: sodium hydroxide
Fireworks: magnesium hydroxide
199
Q

Management of toxic conjunctivitis

A

Tetracaine drops, immediate flushing of the eye until pH is normal, use morgans lens for irrigation

200
Q

Conjunctivitis key points

A

Diagnosis based on hx and exam, hx is important. Fluoroscein and do a fundoscope for every eye patient, ophthalmology referral

201
Q

What is an infection of the anterior portion of the eyelid?

A

Preseptal/periorbital cellulitis

202
Q

Preseptal/periorbital cellulitis

A

Doesnt involve the orbit or other ocular structures. Mild condition-rarely leads to complications, can advance to orbital cellulitis

203
Q

Etiology of preseptal/periorbital cellulitis

A

insect bites, animal bites, foreign body, Dacryocystitis (tear sac inflammation), Conjunctivitis, Hordeolum (stye)

204
Q

What are the common pathogens causing preseptal/periorbital cellulitis

A

S. aureus, s. pneumoniae, MRSA

205
Q

Clinical manifestations of preseptal/periorbital cellulitis

A

Ocular pain, eyelid swelling, erythema, warmth

206
Q

Diagnosis of preseptal/periorbital cellulitis

A

History and PE, CT or MRI, need to distinguish between preseptal or orbital cellulitis

207
Q

Management of preseptal/periorbital cellulitis

A

Doxycyline: not approved for kids under 8

Clindamycin PO, Bactrim plus Amox or Augmenting or Cefpodoxime or Cefdinir PO

208
Q

Orbital Cellulitis

A

Infection involving contents of the orbit: fat, muscles, no globe involvement, more common in children

209
Q

Causes of Orbital Cellulitis

A

Rhinosinusitis most common, orbital trauma, dacryocystitis, tooth infection, ophtlamic surgery

210
Q

Most common pathogens causing Orbital Cellulitis

A

S. aureus and streptococci

211
Q

Clinical manifestations of Orbital Cellulitis

A

Swelling, erythema, warmth, ophthalmoplegia, proptosis, pain with eye movement, diplopia

212
Q

Complications of Orbital Cellulitis

A

Orbital abscess, subperiosteal abscess, brain abscess, cavernous sinus thrombophlebitis

213
Q

What tools can be used to diagnose Orbital Cellulitis?

A

Confirmed with a CT or MRI

214
Q

Management of Orbital Cellulitis

A

Vancomycin plus Ceftriazone or Cefotaxime or Bactrim or Zosyn

215
Q

When should we start to see symptoms improvement for Orbital Cellulitis?

A

24-48 hours, if no improvement surgery sholdl be considered

216
Q

Herpes Keratitis

A

Corneal infection and inflammatoin

217
Q

What is a major cause of blindness from corneal scarring?

A

Herpes keratitis

218
Q

How is herpes keratitis spread?

A

Direct contact with mucous membrane

219
Q

Classification of herpes keratitis

A
  1. Infectious epithelial keratitis
  2. Stromal keratitis
  3. Endotheliitis
  4. Neurotrophic keratopathy
220
Q

Stromal keratitis

A

Viral infection of the stroma

221
Q

Endotheliitis

A

Immune reaction

222
Q

Neurotrophic keratopathy

A

Cornea hypesthesia from damage to the optic nerve

223
Q

Epidemiology of herpes keratitis

A

Endemic in humans, incubation is 1-5 days. Majority of cases are unilateral*

224
Q

What three processes are involved in herpes keratitis?

A
  1. Active infection
  2. Inflammation caused by infection
  3. Immune reaction
225
Q

What is the result in herpes keratitis?

A

Structural changes in the cornea

226
Q

Clinical manifestations of Herpes keratitis

A

Pain, visual burning, tearing

227
Q

How can we diagnose herpes keratitis?

A

Conjunctival infection, dendritic lesions on fluorescein*

228
Q

Management of herpes keratitis

A

Topical antiviral agents: Trifluridine, Ganciclovir, Acyclovir
Oral agents: Valacyclovir, Famcyclovir, Ganciclovir

229
Q

What are meibomian glands?

A

Inside rim of eyelids, 50 on upper lid and 25 on lower lid.

230
Q

What is the function of the meibomian glands?

A

Sebaceous glands that secrete oily substances to keep the eye lubricated. Prevents the evaporation of tears and dysfxn leads to dry eyes

231
Q

What is blepharitis?

A

Chronic eye condition characterized by inflammation of the eyelids with intermittent exacerbations

232
Q

What are the two types of blepharitis>?

A

Anterior and posterior blepharitis

233
Q

Which type of blepharitis is more common?

A

Posterior

234
Q

Anterior blepharitis

A

Inflammation at the base of the eyelids, more likely in young and female

235
Q

What are the two variants of anterior blepharitis?

A

Staphylococcal and Seborrheic

236
Q

Pathophys of anterior blepharitis?

A

Staph colonization of eyelids, possibly due to direct infection, reaction to staph exotoxin, allergic response to staph antigens

237
Q

Clinical manifestations of anterior blepharitis

A

Eyelid edges pink irritated swollen with crust, malposition of eyelids in chronic cases. eyelashes may be misdirected, thinning. Diffuse conjunctival injection

238
Q

Posterior blepharitis

A

More common, associated with skin conditions like rosacea and seborrheic dermatitis

239
Q

Pathophys of posterior blepharitis

A

Inflammation of meibomian glands, causes dysfxn and altered secretions. Increase in: free fatty acids, unsaturated fatty acids and an impaired lipid layer of tear film

240
Q

Clinical manifestations of posterior blepharitis

A

Red eyes, gritty sensation, burning, excessive tearing, itchy eyelids, red swollen eyes, crusting, flaking eyelid skin, photophobia, blurred vision

241
Q

Diagnosis of blepharitis

A

No confirmatory diagnostics or lab tests. Want to distinguish between ant and post

242
Q

What are the differences when diagnosing anterior vs posterior blepharitis?

A

Anterior has the base of eyelash swelling, redness, crust and posterior has the meibomian gland enlargement, plugging with waxy secretions

243
Q

Management of blepharitis

A

Counseling, alleviate acute sx, warm compresses, lid massage, lid washing, artifical tears

244
Q

What topical ointments or drops can be used for blepharitis?

A

Azithromycin, Erythromycin, Bacitracin (more effective with anterior)
Oral tetracycline or Doxycyline 2-4 weeks for severe or chronic cases

245
Q

What is a hordeolum?

A

Stye. Acute, purulent inflammation of the eyelid. May be sterile or show bacteria

246
Q

What is the most common pathogen that causes hordeolum?

A

Staph

247
Q

Internal hordeolum

A

Infection of meibomian glands at the conjunctival side

248
Q

External hordeolum

A

Infection of eyelash follicle at the lid margin

249
Q

What is the management of a hordeolum

A

Warm compresses, topical abx, may harden to a chalazion

250
Q

Chalazion

A

Chronic inflammatory lesions due to blockage and swelling of meibomina glands of eyelid

251
Q

When is chalazion commonly seen?

A

In patients with eyelid margin blepharitis and rosacea

252
Q

Epidemiology of chalazion

A

More common in adults 30-50. Can start out red, tender, swollen then becomes a painless and larger, rubbery nodular lesion

253
Q

Is a chalazion due to an infection?

A

No

254
Q

Treatment of chalazion

A

Minimal, usually self-limiting. Can take a few weeks to a month. Use warm compresses, eyelid massage

255
Q

What can you do if the chalazion is non-resolving?

A

Refer them to an ophthalmologist for I&D or give a glucocorticoid injection

256
Q

Ectropion

A

Lower eyelid is rolled out, sagging of the eyelid leaves the eye dry, exposed, and irritated

257
Q

Etiology of ectropion

A

Aging: connective tissue sagging, facial nerve paralysis: Bells palsy, stroke, trauma or scarring, certain dog breeds

258
Q

Clinical manifestations of ectropion

A

Wet inner conjunctiva is exposed and visible, excessive tearing, chronic inflammation, redness, gritty feeling, dry eye, crusting, multiple infections

259
Q

Management of ectropion

A

Temporary: Artifical tears, ointments to lubricate the eye
Permanent: Surgery, incision of skin of outside corner to shorten and tighten the lower lid

260
Q

Entropion

A

Eyelid rolls inward toward the eye, eyelashes rub against the conjunctiva, chronic irritation

261
Q

Etiology of entropion

A

Aging and weakening of certain muscles, trauma, scarring, surgery

262
Q

Clinical manifestations of entropion

A

Red eyes, irritated, gritty sensation, tearing, mucous discharge, photophobia. Lower eyelid rolled in, absent eyelashes, corneal abrasion

263
Q

Management of entroption

A

Temporary: Artificial tears
Permanent: Tightening of the eyelid and its attachments to restore eyelid position

264
Q

Dacryadenitis

A

Inflammation of the lacrimal glands, most commonly caused by bacterial or virus

265
Q

What can cause dacryadenitis?

A

Viral, bacterial, fungal, inflammatory

266
Q

What are the bacterial pathogens that can cause dacryadenitis?

A

Staph aureus, strep, n. gonorrhea, treponema, m. tuberculosis, chlamydia, borrelia burgdorferi

267
Q

What are the viral pathogens that can cause dacryadenitis?

A

Mumps, EBV, coxackie, herpes zoster, mono

268
Q

What are the fungal pathogens that can cause dacryadenitis?

A

Histoplasmosis, Blastomycosis, Pasaties, Protozoa

269
Q

What inflammatory conditions can cause dacryadenitis?

A

Sarcoidosis, Graves, Sjogrens

270
Q

Clinical manifestations of acute dacryadenitis

A

Unilateral, severe pain, redness, swelling, supraorbital pressure, rapid onset. Conjunctival swelling and redness, discharge, erythema of entire eyelid, submandibular LAD, exopthalmos, ocular motility restriction

271
Q

Clinical manifestations of systemic dacryadenitis

A

Fever, parotid gland enlargement, URI, malaise

272
Q

Clinical manifestations of chronic dacryadenitis

A

Usually bilateral, painless enlargement, present more than a month, more common than acute

273
Q

To diagnose dacryadenitis

A

Lacriam gland often enlarged and easily seen with eversion of upper eyelid. Can do a CT of the orbits with contrast

274
Q

Management of dacryadenitis

A

Viral: self-limiting, supportive
Bacterial: Keflex (1st gen ceph)
Protozoal or fungal: Antifunal or antiamoebic
Inflammatory: Investigate for systemic causes and treat accordingly

275
Q

Dacryostenosis

A

Nasolacrimal duct obstruction, most common cause of persistent tearing in infants

276
Q

Dacryostenosis treatment

A

Massage, lacrimal duct probing. Spontaneous resolution by 6-12 months of age

277
Q

Keratoconjunctivitis Sicca

A

Dry eyes, multifactorial disease of the tears and ocular surface. Results in ocular discomfort and vision impairment

278
Q

Epidemiology of Keratoconjunctivitis Sicca

A

Difficulty defining disease, lack of confirmatory diagnostic test, more prevalent in women

279
Q

What do the tear films consist of in Keratoconjunctivitis Sicca

A

Aqeous mucous an dlipid components

280
Q

Any dysfxn of what can lead to dry eyes?

A

Lacrimal functional unit: eyelids, lacrimal glands, eye surface

281
Q

What are the two classifications of Keratoconjunctivitis Sicca

A

Decreased tear production

Increased evaporative loss

282
Q

Decreased tear production (Keratoconjunctivitis Sicca)

A

Lacrimal gland dysfxn or destruction
Sjogren syndrome: systemic autoimmune inflammatory infiltration of the lacrimal glands. Leads to cell death and hyposecretion

283
Q

Lacrimal dysfunction without systemic findings can be classified as what?

A

Non-Sjogrens

284
Q

Increased evaporative loss (Keratoconjunctivitis Sicca)

A

Excessive water loss form ocular surface, meibomian gland dysfxn, decreased blind function, structural abnormalities of the eyelid, eye drops, chronic contact wearing, ocular allergy syndrome

285
Q

Clinial manifestations of Keratoconjunctivitis Sicca

A

Dryness, redness, irritaiton, gritty sensation, excessive tearing, photophobia, blurred vision

286
Q

Diagnosis of Keratoconjunctivitis Sicca

A

Fluorescein stain, Tear break-up time, Schirmers test (# tears produced by each eye), Corneal sensation, tear hyperosmolarity

287
Q

Management of Keratoconjunctivitis Sicca

A

1st line: Artificial tears** they contain cellulose to maintain viscosity

288
Q

What else can be used to treat Keratoconjunctivitis Sicca

A

Topical Cyclosporine (restasis), Xiidra-integrin antagonist, Sodum Hyaluronate, Topical glucocorticoids, autologous serum tears, tear stimulation, vitamin A, punctal occlusion, scleral contact lenses

289
Q

What are the organs for body movement?

A

Semicircular canals

290
Q

Organ for hearing

A

Cochlear

291
Q

The information from the vestibular labyrinth is relayed via CNVIII to

A
  1. Cerebellum
  2. Ocular nuclei
  3. Spinal cord
292
Q

What part of the semicircular canal detects when the head tilts down towards the shoulder?

A

Posterior

293
Q

What part of the semicircular canal detects when the head shakes side to side in “no” motion?

A

Lateral

294
Q

What part of the semicircular canal detects when the head nods up and down in “yes” motion?

A

Superior

295
Q

The otolith organs sense what?

A

Gravity and linear acceleration

296
Q

Utricle registers accelerations in the what plane?

A

Horizontal, its horizontal in the head

297
Q

Saccule resgisters accelerations in the what plane?

A

Vertical, vertical in the head

298
Q

CN VIII

A

Vestibulocochlear Nerve (AKA auditory nerve)

299
Q

Which nerve is responsible for balance and orientation in space and auditory function?

A

CN VIII Vestibulocochlear

300
Q

What is the length of the eustachian tube?

A

36-38 mm in adults, children are shorter

301
Q

What is the function of the eustachian tube?

A

Provides ventilation and drainage for the middle ear cleft

302
Q

Is the eustachian tube usually open or closed?

A

Normally closed, open only during swallow/yawning

303
Q

What happens when the eustachian tube gets compromised?

A

Air trapped in the middle gets absorbed creating negative pressure TM retraction

304
Q

Some other normal functions of the eustachian tube include

A

Equalizing pressure across TM, protecting middle ear from infection and reflux of nasopharyngeal contents, clearance of middle ear secretions

305
Q

What are the two most common ways the ET (eustachian tube) can be blocked?

A

Allergic response, URI

others: sinusitis, chronic otitis media, congenital or acquired stenosis, neoplasms

306
Q

The failure of ET opening is generally due to what?

A

Functional or anatomic obstruction

307
Q

Eustachian Tube Dysfunction

A

Impaired protective function, Impaired clearance, Pressure dysregulation

308
Q

What happens when the ET has impaired protective function?

A

Reflux of nasopharyngeal pathogens into the ET

309
Q

What happens when the ET has imapried clearance?

A

Loss of mucociliary function contributing to the inability to clear pathogens

310
Q

What happens when the ET has pressure dysregulation?

A

Fails to open to allow ventilation

311
Q

What is dilatory dysfunction of the ET?

A

The tube does not dilate due to: inflammation, pressure dysregulation, acquired anatomic abnormalities

312
Q

What is patulous dysfunction of the ET?

A

Valve incompetency leads to chronic patency (stuck open)

313
Q

Clinical presentation of ET dysfunction

A

“Fullness” in the ear, mild-mod decrease in hearing, “popping” sound can be heard from swallowing or yawning, ear pain

314
Q

Physical exam findings of ET dysfunction

A

Retracted TM on affected side, decreased TM mobility

315
Q

What is the hallmark presentation of dilatory ET dysfunction?

A

Accompanying symptoms of hearing loss and abnormalities of the tympanic membrane like: retraction and middle ear effusion

316
Q

What will be seen on the otoscopic exam when looking at dilatory ET dysfunction?

A

Effusion, scarring, thickening of TM
TM may also have: retractions, effusions, cholesteatomas, perforations, tympanosclerotic plaques, Weber test can show conductive hearing loss

317
Q

What is the hallmark presentation of patulous ET dysfunction?

A

“Autophony” patient hears own voice amplified, the symptoms fluctuate, worsened by exercise and prolonged speaking, ear fullness

318
Q

Physical exam findings of patulous ET dysfunction

A

Breathing induced excursions )movements) of the TM, sensorineural hearing loss

319
Q

What is the treatment for dilatory ET dysfunction?

A

Treat underlying etiology with: antihistamines, decongestants, nasal steroids, valsalva

320
Q

What is the treatment for patulous ET dysfunction?

A

Treat if severe symptoms >6weeks, ventilation tubes in severe cases

321
Q

What else can you do for someone with an ET dysfunction?

A

Refer to ENT! Nasal endoscopy, audiology studies, CT or MRI w/contrast if >3mos of symptoms or with middle ear effusion, surgery (tubes), balloon dilatation

322
Q

What is vertigo?

A

Symptom of illusory movement, described as sensation of motion when there is no motion, or an exaggerated sense of motion in response to movement

323
Q

What is the key to diagnosis of vertigo?

A

Duration of episodes and association with hearing loss

324
Q

Peripheral and central vertigo symptoms are caused by what?

A

Vestibular damage/dysfunction

325
Q

Peripheral vertigo involves which organs?

A

Semicircular canals, otolith organs

326
Q

Onset of peripheral vertigo?

A

Sudden, often associated with tinnitus and hearing loss, horizontal nystagmus may be present

327
Q

Central vertigo involves what organs?

A

Cerebellum, CN VIII, brainstem

328
Q

Onset of central vertigo?

A

Gradual, no associated auditory symptoms

329
Q

Etiology of peripheral vertigo

A

Benign Paroxysmal Positional Vertigo (BPPV), Vestibular neuritis (Labrythititis), Meniere’s Disease, Herpes zoster oticus (Ramsey Hunt), Acoustic neuroma, Aminoglycoside toxicity, Superior Semicircular Dehiscence Syndrome

330
Q

Etiology of central vertigo

A

Migraines, Cerebral tumor on CN VIII, Chiari malformation, brain ischemia (cerebllar infarct and hemorrhage), TIA, MS

331
Q

What drugs are ototoxic?

A

Aminoglycosides, Antidepressants, anxiolytics, furosemide, amiodarone, ASA

332
Q

Clinical presentation of vertigo KEYS

A

Duration and Hearing loss

333
Q

Nystagmus

A

Uncontrolled movement of the eyes, reflex to adjust for slight movement of head and help stabilize and sharpen an image

334
Q

Tinnitus

A

Perception of sound int he absence of an external source, usually buzzing, ringing, or hissing in 1 or both ears

335
Q

Benign paroxysmal position vertigo (BPPV)

A

Provoked by specific head movements: turning in bed, tilting head backward to look up

336
Q

What is BPPV caused by?

A

Calcium debris in semicircular canals (posterior canal most common)

337
Q

BPPV Symptoms

A

Vertigo sensation: short in duration (seconds to minutes), ear pain hearing loss and tinnitus are all ABSENT

338
Q

BPPV Clinical presentation

A

Rapid onset of dizziness or spinning, nystagmus (clockwise, rotary nystagmus)

339
Q

Nystagmus in BPPV

A

Fatigable, with Dix-Hallpike testing. Typically the sensation of motion precipitated by sudden head movements of moving the head in certain way, N/V also common

340
Q

BPPV Diagnostics/Testing

A

Dix-Hallpike positional testing: 5-15 sec between supine positioning and onset of nystagmus. Induces vertigo/spinning nystagmus

341
Q

Further testing for BPPV if needed

A

Electronystagmography: records eye movements. MRI/CT to rule out other causes

342
Q

BPPV Treatment with pharmacotherapy

A

Symptomatic tx, self-revolving within months. Can use antihistamines, antiemetics, BZDs, Scopolamine patch

343
Q

BPPV vestibular rehab

A

Gaze stimulation exercises, repositioning maneuvers (Epley Maneuver), surgery (only after 6 mos, very rare)

344
Q

Labrynthitis (Vestibular Neuritis)

A

Viral or postviral inflammatory disorder, affecting the vestibular portion of CN VIII
Vesitublar neuritis -> vertigo w/o hearing loss
Labrynthitis -> vertigo w/unilateral hearing loss

345
Q

Clinical presentation of vestibular neuritis

A

Rapid onset of sever, persistent vertigo, N/V, gait instability, decreased hearing in 1 ear in Labrynthitis, horizontal nystagmus, +head thrust, if patient falls -> toward the affected side

346
Q

Imaging for vestibular neuritis

A

MRI/MRA for infarct, CT if MRI/A not available

347
Q

Treatment for vestibular neuritis

A

Corticosteroid therapy, symptomatic treatment: antihistamines, antiemetics, vestibular rehab

348
Q

Meniere’s Disease

A

Peripheral vestibular disorder attributed to excess endolymphatic fluid pressure

349
Q

What does Meniere’s disease cause

A

Episodic inner ear dysfunction “labyrinthine hydrops”

350
Q

What parts of the ear are affected in Meniere’s?

A

Cochlea, semicircular canals, otolithic organs

351
Q

What are some risks associated with Meniere’s?

A

Allergy, stress, viral

352
Q

Clinical presentation of Meniere’s

A

Vertigo, sensorineural hearing loss, tinnitus. Episodes are unpredictable, can last hours, be recurring, and are followed by fatigue

353
Q

How long can the symptoms last for in Meniere’s?

A

Spontaneous- 20 min-24 hours, 6-11 attacks per year

354
Q

Symptoms of Meniere’s

A

Unilateral sensorineural hearing loss, tinnitus, fullness/pressure in the ear, N/V, disabling imbalance, horizontal-torsional nystagmus seen during acute attack

355
Q

Imaging for Meniere’s diease

A

Audiometry: low frequency sensorineural hearing loss
Electronystagmography: Unlitearly reduced vestibular response
Caloric testing: often shows loss/impairment of thermally induced nystagmus on affected side. MRI, lab and RPR to rule out others

356
Q

Vestibular testing for Meniere’s (results)

A

ENG abnormal on affected side, rotatory chair test, computerized dynamic posturography

357
Q

Audiometry testing for Meniere’s

A

If low frequency sensorineural hearing loss -> helps confirm

358
Q

Caloric testing for Meniere’s

A

This is an otoneurolgic evaluation of the status of the vestibular-ocular reflex. Put cold then warm water into ear, nystagmus will appear

359
Q

COWS

A

Cold opposite, warm same (test for meiniere’s)

360
Q

Meniere’s treatment

A

Reduce frequency and severity of vertigo attacks, eliminate hearing loss and tinnitus, minimize disability, prevent disease progression

361
Q

Acute symptom treatment for Meniere’s

A

Antihistamines, antiemetics, BZDs, anticholingerigcs

362
Q

Long-term symptom treatment for Meniere’s

A

Lifestyle adjustment, salt restriction, limit caffeine and nicotine, limit alcohol, if tinnitus avoid excessive noise

363
Q

Procedural treatments for Meniere’s

A

Surgical: succulotomy, intratympanic glucocorticoids, positive pressure pulse generator, intratympanic gentamicin injection, surgical labyrinthectomy, vestibular nerve resection

364
Q

Minors Syndrome

A

Also called Semicircular Canal Dehiscence Syndrome

365
Q

Semicircular Canal Dehiscence Syndrome

A

Thinning of bone that separates the superior semicircular canal from middle cranial fossa, allowing pressure to be transmitted to inner ear

366
Q

Symptoms of Semicircular Canal Dehiscence Syndrome

A

Vertigo provoked by coughing, sneezing, Valsalva, nausea, hearing loss in some pts

367
Q

Semicircular Canal Dehiscence Syndrome can be tested how>

A

cVEMP: cervical vestibular evoked myogenic potential

368
Q

Pulsatile tinnitus etiology

A

Listening to won heartbeat, vascular disorders, arteriovenous shunts, venous hums, ET dysfunciton, arterial bruits

369
Q

Non-pulsatile tinnitus etiology

A

Clicking tinnitis, secondary to middle ear spasm, unilateral

370
Q

Tinnitus etiology other

A

Ototoxic meds, presbycusiss (sensorineural loss with aging),

371
Q

What is a Chiarai malformation?

A

low lying cerebellar tonsils cause tension on auditory nerve

372
Q

What is otosclerosis?

A

abnormal bone repair of stapes footplate bone

373
Q

Diagnosis/Imaging for tinnitus

A

Audiometry to R/O associated hearing loss, MRI if unilateral especially with hearing loss to R/O retrocochlear lesions (Vestibular schwannoma)

374
Q

Tinnitus treatment

A

Avoid excessive noise, treat underlying depression and insomnia, cochlear implants, retraining therapy

Clin med 1 (9 decks)

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