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Flashcards in ENT Deck (349):
1

what is involved in the ENT exam?

ear - external, otoscopy, tuning forks

nose- anterior rhinoscopy

throat- oral cavity/pharygeal exam

neck - palpation, thyroid exam

CN exam

respiratory

2

this is common in wrestlers, where blood collects between mucoperipchonidrium and cartilage.

auricular hematoma

tx: drainage and bolster dressing to avoid cauliflower ear

3

this is a benign condition, more common in AA. Difficult to treat because comes back, and is treated by surgical removal or steroids

keloid

4

this comes from an alkalotic environment/trauma by the pathogen pseudomonas or staph aureau

otitis externa (swimmers ear)

5

how is otitis externa treated?

oto-topical drops, oral abx (quinolones to tx pseudomonas)

6

what are complications of otitis externa and who are they more common in?

malignant otitis externa (skull base osteomyelitis)

more common in diabetics- usually admitted for IV abx

7

this is a fairly commonly seen benign body overgrowth of the ear canal. typically doesn't cause any problems or pain

osteomas

8

why does an ear drum become retracted?

eustachian tube dysfunction

9

common problem secondary to q-tips

ruptured tympanic membrane - wait 3 months for healing, keep dry, most heal on their own

10

what is the difference between otitis media and effusion?

otitis media is an inflammatory condition of the middle ear space - think eustachian tube dysfunction

effusion just means there is fluid in the middle ear space. middle ear liquid resulting from infection of inflammation (can be serous, mucoid, purulent)

11

different classifications of otitis media

acute ( 12 weeks)

12

what is acute otitis media?

fluid with infection
2nd most common disease in children (URI is #1)

13

what is the cause of acute otitis media?

eustachian tube dysfunction

sxs: fever, otalgia, bulging red TM

14

pathogens for otitis media

s pneumo, h flu, m cat

15

what is the first line treatment for otitis media?

amoxicillin (usually 45 mg/kg 2x a day)

beta-lactamase inhibitor is 2nd line

Tympanocentesis if not improving with abx

16

what is otitis media with effusion and how do you treat?

fluid without infection
cause: eustachian tube dysfunction
sxs: hearing loss, speech delay

treatment depends on chronicity, dont need antibiotics

17

these are used to help ventilate middle ear space and normalize pressures

ear tubes (surgery)

18

what are the indications for ear tubes?

recurrent acute otitis media - 3 infections in 6 months or 4 in 1 year with current effusion on exam

Chronic Otitis Media with Effusion – greater than 3 months of effusion with evidence of hearing loss

Think about the adenoids!!! – sits in posterior nasopharynx. If enlarged, can cause obstruction of orifices and can be cause

19

what will the tympanic membrane look like with otitis media with effusion and acute otitis media?

otitis media with effusion will have yellow or amber colored fluid behind tympanic membrane (indicated serous fluid)

acute otitis media with be Erythematous

20

what are some complications of otitis media/chronic ear disease?

they're uncommon now because of antibiotics but infection can spread to brain, sigmoid sinus, mastoid air cells (mastoiditis)

all need to be treated aggressively with IV antibiotics, ear tube drainage, possible mastoidectomy

21

#1 chronic complication of otitis media

cholesteatoma - skin debris gets trapped in middle ear space and continues to dequemate

22

inflammation of tympanic membrane as opposed to middle ear space in AOM. very painful, due to pathogen mycoplasma pneumonia

bullous myringitis

if associated with blisters in canal need to think about zoster infection

23

first test for hearing. you place the fork on the top of the head in midline. conduction losses latralize to side of lesion, sensorineural losses lateralize to opposite ear

WEBER

24

hearing test for bone vs air conduction

AC>BC in SNHL, BC>AC in CHL

25

t or f: almost all cases of conductive hearing loss are correctable with surgery

true - osteosclerosis

26

how should you treat a sudden sensorineural HL?

should be evaluated by an ENT within 24 hours and treated with steroids

27

asymmetric SNHL is what until proven otherwise?

acoustic neuroma- benign tumor on vestibulocochlear nerve. patient needs MRI

28

perception of motion in the absence of movement. usually described as the room spinning

vertigo - this is a symptom, not a diagnosis

29

what body parts are involved in balance system?

visual cues
propioception
brain input
vestibular system

30

this is caused by otoliths in the semicircular canal, lasts seconds to minutes, associated with head movement. patients usually say that they "“Lay in bed, turn to my right side and the room spins really badly for 2 min then goes away”

benign paroxysmal position vertigo (BPPV)

Dx: Dix-Hallpike test
Rotary nystagmus beating toward affected ear

Tx: Canolith repositioning – done in office. Lay back and hit mastoid bone repeatedly
Epley Maneuver

31

when someone has acute onset vertigo, what should be your first thought?

stroke

32

what is acute onset vertigo?

sudden onset that lasts hours to days, even weeks

diagnosis:
central: Central (neurologic cause) – NEEDS IMAGING!
Vestibular, unclear cause
Labrynthitis (associated with hearing loss) vs Vestibular Neuritis (just vertigo)
Hearing loss/tinnitus?

Tx
Supportive
Meclizine, valium, anti-emetics
Steroids

33

this is caused by an increase in endolymphatic pressure, and symptoms include episodic vertigo usually lasting several hours with fluctuating SNHL, aural fullness, and tinnitus.

meniere's disease

Tx
Initial main treatment goal is to reduce pressure in inner ear
Low salt diet
Diuretics

34

most common causes of epistaxis

mucosal drying and trauma (picking your nose)

35

Auto Dominant disorder with defect in contractile elements of blood vessels and formation of AV malformations

Osler-Weber-Rendu Syndrome (Hereditary Hemorrhagic Telangiectasia)

36

what is the difference between the classifications of sinusitis?

acute: 3 months

something going on thats causing poor drainage of the mucus at sinus ostia

37

most common pathogen of acute sinusitis

rhinovirus

then S. pneumo, H flu, M Cat
Fungus – Aspergillus/Mucor

Chronic
Staph Aureus, anaerobes

38

how do you treat sinusitis?

acute: abx 10-14 days
irrigations, decongestants

chronic: 3-6 weeks antibiotics, needs CT if not responding

39

benign, jelly filled sacks formed off the mucosa. can cause some secondary sinusitis because blocking drainage

polyps

40

septal perforations

think of intranasal drug use or trauma

41

benign oral presentations

mucoseal
geographical tongue
bony overgrowth of the palate
dark veins under tongue
Torus mandibularis

42

lymphoid tissue that sits in continuous circle in the oro and nasopharynx to accept Ag’s for the upper AD tract.

waldeyer's ring

43

if adenoids are enlarged (adenoid hypertrophy), what can they affect?

the eustachian tube (usually in kids)

44

what is the most frequent cause of otolaryngologic infection in children?

common cold

rhinovirus, influenza, parainfluenza, adenovirus, RSV

Viral pharyngitis usually more mild in presentation.

45

symptoms of common cold

sore throat, dysphagia, fever with tonsillar erythema

46

Small vesicles with erythematous base that become ulcers and spread

herpangia- Coxsackievirus


supportive care

47

high fever, malaise, large swollen dirty gray exudative tonsils. Hepatosplenomegaly
Large bilateral tender posterior LAD

EBV

Petechiae at junction of hard and soft palate not pathognomonic.

48

most specific test for EBV

monospot - latex agglutination assay

very specific but low sensitivity so high false negative rate- (False negative rates 25% in first week down to 5% by 3rd week.)

If clinical suspicion is high despite negative Monospot, can do EBV antibody testing.


49

treatment for EBV

usually supportive

50

what should be avoided in patients with EBV?

ampicillin because a rash can develop

51

when should you hospitalize a patient with EBV?

cases of severe hypertrophy with dehydration, upper airway obstruction – treat with steroids or emergent tonsillectomy if needed in rare cases.

52

most common pathogen for pharyngitis

group A streptococcus - Public health importance due to its frequency and serious sequelae.

53

treatment for Streptococcal Tonsillitis-Pharyngitis

PCN

54

symptoms of Streptococcal Tonsillitis-Pharyngitis

odyophagia (pain when swallowing food) , otalgia (ear pain), fever, headache, malaise, cervical adenopathy, enlarged red exudative tonsils

55

in which patients is thrush most common?

patients you use inhaled corticosteroids, diabetics

tx with nystatin, clotrimazole, diflucan

56

Classic complication of tonsillitis that brings patients to the ER for evaluation and treatment. patient presents with tonsillitis that is not responding appropriately to ABX and is now worsening after days of treatment. UNILATERAL symptoms, OTALGIA, drooling with severe odynophagia (poor PO intake), trismus (irritation of pterygoid musculature)

peritonsillar abscess (quinsy)

on exam, uvula pushed off midline

57

Can occur as a sequelae from an infection of the nose, sinuses, or pharynx since the lymph nodes of this space drain these areas. They usually occur in children less than 2 years old and present with some of the same symptoms in addition to having a stiff neck and sometimes some muffled speech.

retropharyngeal space abscess

58

indications for tonsillectomy

OSA
chronic tonsillitis (7 infections in one year, 5 for past two years, or 3/year for the past 3 years)--> just guidelines, everyone is diff

if one tonsil is bigger than other (unilateral), then most concerning so would probs do tonsillectomy

Note size of tonsils in children with loud snoring and breathing difficulties at night noted by parents.

59

Questions/Critical exam features to look for in hoarse patient

progression over time
associated breathing problems
dysphagia
signs of infection
fever
stridor
drooling
poor secretion management
pain associated with voice changes

60

presents with drooling, hot potato voice, rapid progression, posturing forward, systemic toxicity/fever, inspiratory stridor

epiglottitis - now more common in adults (Group A strep, Staph aureus)

Thumbprint sign – inflamed/swollen epiglotis


treat with IV abx, rapidly secure airway if necessary

61

infection of the subglottic larynx causing biphasic stridor. commonly caused by parainfluenza virus but any upper repiratory infection in young child can cause it. steeple sign on xray

croup

62

how do you treat croup?

cool mist humidity, steroids in severe cases with hospital admit

63

usually presents slowly over few months and almost always in a chronic smoker/EtOH abuse but not always.

larynx cancer

64

common/benign disease of larynx

vocal cord nodules
vocal cord polyps
layngo-pharyngeal reflux

65

what are the symptoms of laryngopharyngeal (LPR) reflux?

hoareseness, globus, throat clearing, AM symptoms

diff from GERD which has heartburn, chest pain, regurgitation, and PM symptoms

66

how do you treat LPR (Laryngopharyngeal Reflux)?

more aggressive PPI (bid)

67

which salivary glands are most commonly affected in parotitis/sialoadenitis?

parotid and sublingual

68

common symptoms of Parotitis/Sialoadenitis?

painful swelling, often worse after eating. erythema over the area, purulent drainage from the duct

image looks like a swollen neck

69

common causes of parotitis/sialoadenitis?

sialolithiasis (a condition where a calcified mass or sialolith forms within a salivary gland, usually in the duct of the submandibular gland )
bacterial
viral
autoimmune

70

treatment of parotitis/sialoadenitits

conservative measures: massage, warm compresses, sialogogues

abx: augmentin, clindamycin

recurrent episodes may require excision of the gland

71

Most common non-cutaneous head and neck site for masses/cancer

oral cavity - vast majority is squamous cell carcinoma

risk factors: smoking/EtOH use

72

presentation of head and neck masses/cancer

unexplained throat pain, dysphagia, hoarseness especially in patient with above risk factors needs further workup

73

when evaluating a patient with a neck mass, what should be the first consideration?

age of the patient

Pediatric (0-15 years old)
Inflammatory>Congenital>Neoplasm

Young Adult (16-40 years old)
Inflammatory>Neoplasm>Congenital

Adult (40+ years old)
Neoplasm>Inflammatory>Congenital

74

second consideration of a patient with a neck mass?

location of the mass

If it is in the anterior compartment, think either thyroid neoplasm or lymphoma

75

when inflammation is suspected with a neck mass, what is the longest amount of time you can have an antibiotic trial?

2 weeks

76

what is the most cost effective and most productive single diagnostic evaluation available for a patient with a neck mass?

FNA (fine needle aspiration)

77

an undiagnosed neck mass in an adult is what until proven otherwise?

metastatic carcinoma

78

t or f: Excisional biopsy of a mass in an adult prior to a complete head and neck evaluation is recommended

FALSE. contraindicated and could lead to a worse treatment outcome

79

prefix for eyelids

blephar-

80

sebaceous glands of eye

Meibomian: inner eyelid
glands of zeis: outer eyelid

81

large sweat glands at the outer eyelid margin

glands of moll
eyelids are given shape and form by the tarsal plates within them

82

differences between chalazion and stye

chalazion is internal in the meibomian gland so treated from inside the eye

stye is outside so tx from outside

83

where are the lacrimal glands located?

upper outer eyelids. Tears are secreted from the glands secretory ducts --> collected at the nasal edge of the palpebral fissure and pass through the puncta into the sup &inf canaliculi --> lacrimal sac

From the lacrimal sac, they pass into the nasolacrimal duct and then into the nose in the inferior meatus (below the inferior turbinate)

84

blockage of tear duct/not fully matured in babies

dacrocystitis - tx with warm compress

85

function of tears

form smooth refractive surface on epithelium- inhibits bacterial growth

maintains moist environment for epithelium

carries oxygen to the eye

86

what is the term for inflammed conjuctivae?

chemosis

87

three coats of eye

inner layer - retina
-inner nerve layer (axons and ganglia)
- outer pigmented (photoreceptive layer with rods and cones)

middle vascular layer - uveal tract (iris, ciliary body, choroid)

outer fibrous layer (sclera)

88

white of the eye which surrounds the entire eye except for the cornea

sclera (superficial is episcler- and deep is scler-)

89

this composes the anterior 1/6 of the eye and is avascular

cornea - receives nourishment from aqueous humor

90

where does the greatest change in refractive index occur

at the air-corneal tear film interface

91

where does the bulbar conjuctiva meet the cornea?

limbus (limbic margin)

92

round sphincter muscle that controls pupil size

iris

Outer aspect of the iris forms an angle with the cornea (the “anterior chamber angle”) that is important in glaucoma

93

kayser-fleischer rings are associated with what?

wilsons disease - copper storage disease

94

term for pupillary dilation

midriasis - when the iris dilator muscle contracts (under SNS control), the pupil dilates

Pupils dilate under dark conditions and when focused on a distant object

95

term for pupillary constriction

miosis - When the iris constrictor muscle contracts (under PSNS control), the pupil constricts

Pupils constrict under light conditions and when focused on a near object
Both pupils should be equal

Pupils diameter should not vary by more than 1 mm between the eyes
Be sure to check in dim light if you see a difference in a bright room

96

term when there is a pupil size difference of > 1 mm

anisocoria

97

is the lens vascular or avascular?

avascular (65% water)

biconvex, colorless, transparent

98

when does the lens become thicker and thinner?

It is an elastic structure that becomes more spherical (thicker) when relaxed for near vision, and more flat (thinner) when stretched for far vision

99

what divides the eye into the aqueous cavity in front and a vitreous cavity behind?

the lens

100

what determines the shape of the lens?

ciliary muscle tension - lens is suspended from the suspensory ligaments that are attached to the ciliary muscle

Contraction of the ciliary muscles pulls on the choroid, thereby relaxing tension on the suspensory ligaments. This then allows the lens to assume a more spherical shape for near vision
Relaxation of the ciliary muscles results in more tension on choroid, thereby increasing tension on the suspensory ligaments. This then causes the lens to assume a more flattened shape for distance vision

101

the space between the cornea and iris, filled with aqueous humor

anterior chamber

102

what maintains IOP and nourishes the avascular lens and cornea?

aqueous humor

103

blood in the anterior chamber is called what?

hyphema

104

pus in the anterior chamber is called what?

hypopyon

105

the space between the iris and the lens, filled with aqueous humor

posterior chamber

106

large eye cavity located behind the lens

vitreous cavity

Filled with a jelly-like vitreous humor
*Acts as a “shock-absorber”

107

what are little dots, circles, lines, to clouds or cobwebs in the vitreous cavity?

floaters - if you have an increase, may be retinal detachment

108

The dark brown/black vascular coat of the eye, located between the sclera and retina

choroid

109

this is comprised of the iris, ciliary body and choroid

uveal tract
The anterior uveal tract consists of the iris & ciliary body
The posterior uveal tract consists of the choroid

110

yellow spot in the posterior central area of the retina, just lateral to the optic disk

macula lutea

111

this is an area in the macula lutea with densely packed cones, that is the area of most acute vision

fovea centralis - has deeper blood supply than the rest of the retina

The “fundus” refers to that part of the retina that is able to be visualized with an ophthalmoscope

Tasacks disease (sp?) – lipid disorder **cherry red spots - preserved in fovea

112

which area is responsible for the blind spot?

optic disk - point of transition from the retinal to the optic nerve

This area contains the optic nerve (containing over 1 million nerve axons), central retinal artery & vein

113

how many bones make up the walls of the orbit?

7

Many Friendly Zebras Enjoy Lazy Summer Picnics

Maxillary
Frontal
Zygomatic
Ethmoid
Lacrimal
Sphenoid
Palatine

114

a lesion here will result in bi-temporal vision loss?

optic chiasm

Galactoria and bitemporal visual field loss – PITUITARY ADENOMA

115

a lesion here will result in homonymous (same side) defects

optic tracts and radiations

116

a lesion here will result in loss of vision of only this one eye

optic nerve

117

90% of eye's blood supply is through what?

choroid layer blood supply - Supplied by 10-20 short posterior ciliary arteries that enter near the optic nerve

118

normal cup: disk ratio

119

hemorrhages with central clearing

roth spots - endocarditis

Blot hemorrhages occur deep in the retina

Flame hemorrhages are superficial hemorrhages that follow the nerve layer pattern

120

these represent focal retinal ischemia

soft (cotton wool) exudates

Must be distinguished from myelination of the optic nerve

121

Represent leakage of proteins and lipids from blood vessels

hard exudates

122

represent small white hyaline (a substance from cell degeneration) deposits that develop beneath the retinal pigment epithelium. Occur most frequently in persons older than 60 y/o (a consequence of aging)
May be a precursor of age-related macular degeneration
Must be distinguished from hard exudates

drusen

123

difference in vision loss between glaucoma and macula

macula is central vision loss
glaucoma is peripheral vision loss

124

Psudopapilledema

drusen is deposited right over where you would see optic nerve

125

patients describe this as a curtain being drawn over vision

retinal detachment

Sometimes gravity will help so just have them lay supine

126

cherry red spots are pathomneumonic for what?

Tay-Sachs

127

no refractive error

emmetropia

128

farsightedness

hyperopia (shorter than normal eye)

Require a bi-convex lens to converge the light rays more

129

nearsightedness

myopia (longer than normal eye)

Light rays focus in front of the eye

Require a bi-concave lens to diverge the light rays more

130

A distortion of vision caused by a difference in refractive power along different meridians of any of the main refractive surfaces (cornea, anterior lens, or posterior lens surfaces)

astigmatism

a pinhole corrector will overcome most refraction errors and is helpful in determining in refraction is the cause of visual loss or not

131

outward displacement of the eyeball with a widening of the palpebral fissure

Exophthalmos

May be bilateral or unilateral

More serious (pathological) causes:
Thyroid orbitopathy (e.g., Graves Disease)
Intraorbital inflammation and edema (cellulitis)
Intraorbital tumor
Intraorbital trauma (to bones or EOMs resulting in hemorrhage)
Endocrine disorders

132

lack of parallelism (misalignment) of the visual axes of the eyes such that the optic axes cannot be directed to the same object (eyes don't focus and move together properly)

strabismus

May be convergent strabismus (“Esotropia”) resulting in crossed-eyes,

or divergent strabismus (“Exotropia”)

May be unilateral, bilateral, alternating

May be permanent or intermittent

133

at what age should you be concerned about strabisumus?

after age 6, when binocular vision should be well established

Leads to vision loss if not corrected early-on (by age 5 or 6 at the latest)
Eye patching in kids may cause an iatrogenic strabismus!

134

this refers to poor or complete loss of vision in one eye that cannot be corrected with a lens. It usually is the end result of when the images of the two eyes cannot be properly fused into one, leading the occipital cortex of the brain to ignore one of the images. Complication or sequela of strabismus

Amblyopia

can be caused by :
Strabismus (misalignment of the eyes)

Anisometropia (a large diffference in refraction between the eyes)

Opacity anywhere along the visual axis (corneal opacity, congential cataract, etc.)

135

how do you treat amblyopia

Correct the underlying cause as soon as possible
Congenital cataracts should be corrected in the first few months of life
If underlying cause of the amblyopia is not corrected by age 5 or 6, the brain will permanently ignore the bad eye’s image
Patch the good eye to force the brain to use the image from the bad eye

136

double vision

diplopia. usually from an imbalance in EOMs.
May result from many different causes, such as orbital blowout fracture, myasthenia gravis, head injury, intracranial tumors, et al.

You must distinguish between binocular diplopia and monocular diplopia. You must distinguish between horizontal diplopia and vertical diplopia

137

painful aversion to light

photophobia

Potential causes:
Corneal inflammation (abrasions, ulcerations, etc.)
Inflammation of the iris
Inflammation of the sclera
During acute glaucoma

138

what are potential causes of eye pain?

Inflammation of the EOMs
Inflammation of the uveal tract (iris, ciliary body, choroid)
Corneal abrasion or ulceration
Acute closed angle glaucoma (markedly elevated IOP)
Referred pain from extra-orbital problems (e.g., sinusitis)

139

spots that are occasionally seen floating across the visual field
and are usually due to vitreous opacities and are of no consequence

floaters

140

sudden onset of floaters or a marked increase in the number of floaters, especially if associated with other signs or symptoms of eye disease, may be associated with what?

Posterior uveitis (inflammatory cells in the vitreous humor cause floaters)
Retinal tears or detachments (floaters + photopsia ( flashes of light))


141

how are most ophthalmic meds administered?

topically. ointments have greater therapeutic effectiveness than solutions but drops are preferred to ointments because they do not retain discharge or interfere with vision

Should be administered systemically for intraocular infections, orbital cellulitis, GC keratitis, severe conjunctivitis

142

most common ophthalmic antibiotic

Sulfacetamide sodium (Sulamyd) 10% opthalmic soln. or ointment TID X 2-3 days
(unless sulfa allergy)

143

topical antiviral

Idoxuridine (Stoxil), an antimetabolite is used for Herpes simplex keratitis

Several antiviral agents are now available (Viroptic), et al.

Want to treat herpetic infections, so treat systemically(gancyclovirs) and antiviral drops

144

what should you always remember with topical anesthetics

Never send a patient home with topical ophthalmic anesthetics!
Don’t want to send some with number because won’t realize that its hurting and will touch it and cause more harm (think if dog cones)

145

Adrenergic (SNS) Agent for pupil dilation

Phenylephrine Hydrochloride (Neo-Synephrine)
Exhibit little cycloplegic effect
Effects last 2-3 hours

146

Anti-Cholinergic (anti-PSNS) Agents

Both mydriatic & cycloplegic agents

Atropine sulfate

Scopolamine Hydrobromide

147

Paralyze the ciliary muscles AND dilate the pupil. By paralyzing the ciliary muscles, there is less pull on the choroid leading to more tension on the suspensory ligaments. This causes the lens to flatten more, helps increase the distance between the lens and adjacent iris
May help prevent synechiae formation in anterior uveitis
Reduce the pain associated with ciliary muscle spasm in certain conditions

cycloplegic-mydriatics

Tropicanamide (Mydriacyl)
Shorter acting, lasting only 15-20 min.
Cyclopentolate Hydrochloride (Cyclogyl)
Lasts

148

Decongestants/Anti-histamines

Visine
Patanol
Ophcon-A or Naphcon-A

149

Systemic Medications That Affect The Eye

Anticholinergics (e.g. atropine, scopolamine): dilate the pupil
Steroids: may cause cataracts, increase IOP, reactivate Herpes simplex, increase risk of infection
Morphine: causes pupillary constriction
Streptomycin: may cause optic neuritis
Tetracycline: pseudotumor cerebri
Quinine (chloroquine): may lead to acute blindness
Ethambutal: may cause optic neuritis & loss of color vision
Plaquenil (Hydroxychloroquine)
Retinopathy
Cordarone (Amiodarone)
Optic Neuropathy/neuritis

150

technique for examining the circulation of the retina using the dye tracing method.Sensitive way of demonstrating changes of diabetic retinopathy, Retinal vein thrombosis, macular degeneration

fluorescein angiography

151

when should you refer to an audiologist in an adult?

Reports change in hearing
Hearing Loss – Sudden, Gradual, or fluctuating.
Reports of being able to hear but not being able to understand conversations
Tinnitus
Dizziness or Vertigo
Aural Fullness/Pressure
Ear Infections/Otitis Media
TV/Radio volume loud.
Tympanic membrane perforation
History of ear surgery
Head Trauma

152

when should you refer to an audiologist in pediatric patients?

DNP newborn hearing screening.
Recurrent/Chronic Otitis media.
Ear drainage
Speech development slower than peers.
Child decreases amount of talking.
Child less responsive to name and other familiar sounds.
Says “huh” or “what” frequently.
Has learning difficulties.
Hyperactive or overly inattentive.
Family history of childhood hearing loss.
Syndrome associated with hearing loss.
Trauma to head/ear
Ear anomalies – microtia or atresia, ear pits/tags

153

pulsatile (rhythm with heart beat) tinnitus suggests what

vascular etiology

154

what is in the middle ear?

TM
ossicles
ET

155

what are behavioral hearing tests?

gold standard

Behavioral Observation Audiometry
Visual Reinforcement Audiometry
Conditioned Play Audiometry
Conventional Audiometry

156

this auditory test records acoustic energy created by active mechanism of outer hair cells (cochlea)

otoacoustic emisisons (OAE)

not a test of hearing, this is pre-neural

157

when is otoacoustic emissions (OAE) usually done?

newborn hearing screening
differential diagnosis of site of lesion (sensory vs. neural)
monitoring effects of ototoxicity or noise exposure

158

this auditory test measures electrical activity of the nerve up to brainstem

auditory brainstem response (ABR)

The other screening tool used for infants at high-risk for hearing loss is auditory brainstem response. Electrodes are placed on the babies head, and sound presented to the ear. A brainwave is recorded in response to the sound.

measures beyond cochlea

159

when is ABR test used?

newborn hearing screening

Diagnostic ABR
assesses the auditory pathway;
look at latencies of the waveform;
generally used in the adult population
Identify presence or absence auditory neuropathy
Hearing threshold estimation
Intensity is reduced and Wave V threshold is tracked to estimate hearing.
Can be done in natural sleep or performed under sedation.
Not a test of hearing – makes estimate

160

this test measures admittance of sound energy into middle ear. used in diagnosis of OME and eustachian tube dysfunction

tympanometry - Not a measure of hearing, but rather a measure of middle ear status.

161

gold standard of diagnostic hearing test

pure-tone audiometry

This is a subjective measure that tells us the quietest level at which the patient is responding to sound. The patient can “tell” us they hear the sound in any number of ways. (Button press
Raising hand, Clapping, Toy in bucket, Head turn)

VRA (visual reinforcement)– testing method used in children 6 months to 3 years old and children with developmental delays. Speech and tonal sounds are presented through speakers or headphones and the child’s head turn response is reinforced with lights and/or animated toys.


162

this is a visual depiction of hearing loss

audiogram
x-axis is frequency (pitch)
y-axis is intensity (loudness)

Test through air conduction (AC) and through bone conduction (BC).

163

Occurs when there is damage or obstruction in the outer and/or middle ear, but the inner ear is intact.

conductive hearing loss

164

causes of conductive hearing loss

otitis externa or otitis media - acute or chronic
-otitis media is the number one cause of conductive hearing loss in children. Fortunately, it is usually transient.


impacted cerumen

foreign object in ear canal

Rupture or perforation of the tympanic membrane

Otosclerosis – calcification of the middle ear bones, particularly the stapes.

Cholesteatoma – skin cyst, can erode ossicles causing hearing loss

165

hearing loss caused by damage to the cochlea or auditory nerve

sensorineural hearing loss - can be congenital or acquired

166

causes of sensorineural hearing loss

meningitis
Ototoxicity (gentamicin, cisplatin, carboplatin…)
Noise Induced
Viral infections
Labyrinthitis – inflammation of the labyrinth
Head trauma
Meniere’s disease
Auto immune inner ear disease
Acoustic neuroma/Vestibular Schwannoma
Presbyacusis

167

what is mixed hearing loss?

Air conduction thresholds and bone conduction thresholds are outside the normal range and there must be a significant air bone gap.
Example: Combination of presbyacusis and tympanic membrane perforation.

168

what gene is strongly associated with congenital non-syndromic hearing loss?

GJB2 or connexin-26 gene.

169

treatments for conductive hearing loss

Effusive otitis media
Antibiotics
PE tubes
Adenoidectomy

Cholesteatoma
Surgery

170

treatment for sensorineural and permanent conductive hearing loss

Hearing aids

Baha/Cochlear implants

Nonsurgical alternatives
Visual communication
Deaf community

171

how do cochlear implants work?

Stimulate cochlear bundle of auditory nerve
Appropriate for severe to profound sensory hearing loss
Not appropriate for retrocochlear loss (e.g., neurofibromatosis)

172

what are the CDC guidelines for managing hearing loss?

1-3-6 guideline

tested by one month of age
confirmed diagnosis by 3 months of age
intervention by 6 months of age

173

difference between dizziness and vertigo

Dizziness – Sensation of lightheadedness, faintness, or unsteadiness. Does not involve a rotational component.
Vertigo – Perception of movement or spinning, either of self or surrounding.

174

Intense short duration of vertigo that occurs with changes in head/body position.
Caused by displaced otoconia that move from saccule into one of the semi-circular canals

benign paroxysmal positional vertigo

175

inflammation caused by viral infection that affects hearing and balance. pt experiences a sudden onset of hearing loss, tinnitus, and aural fullness. Vertigo lasts for several days until central compensation occurs.
May have residual lightheadedness after compensation.

labyrinthitis

Vestibular Neuritis is also caused by viral infection. Damage to vestibular function only.
No auditory component.
Vertigo/dizziness symptoms last for several days.

176

Benign slow growing tumor on the 8th nerve
Occurs in area of IAC / CPA
Can affect hearing, balance, and/or facial nerve function
Always concerned when asymmetric hearing is noted on audiogram

acoustic neuroma/vestibular schwannoma

177

Cause is unknown but thought to be a result of excessive endolymph fluid in inner ear.
Can affect both ears, but usually is unilateral.
Results in fluctuating hearing, tinnitus, aural fullness, vertigo.
Vertigo generally lasts for several hours and is often accompanied by nausea and vomiting.

Meniere's disease - no cure

Manage symptoms with medications and diet – reducing sodium/diuretic.

178

Occurs when the defense capabilities of a mal-functioning immune system harm the cells of the body that affect the ear.
Some examples are Cogan’s syndrome, Wegener’s granulomatosis, systemic lupus, Sjogren’s syndrome.

autoimmune inner ear disease

179

tests for assessing vestibular/balance function

Electronystagmography/Videonystagmography (ENG/VNG) – most common; assessing peripheral vestibular function and central control of eye movements

Rotary chair testing – if ENG is normal and pt is still dizzy; peds; not ear specific

Vestibular Evoked Myogenic Potential (VEMP) – concern for SSCD and/or vestibular migraine.

Dynamic Posturography – functional balance measurement; predominantly used by physical therapists

180

Usually described as ringing or buzzing in the ears.
Is a symptom that reflects some region of unhealthiness in the auditory system.
Results from spontaneous nerve activity that the brain interprets as sound.

tinnitus

181

what are some tinnitus aggravators?

Loud noise exposure w/o use of adequate hearing protection.
Medications
Cerumen
High blood pressure
Dental problems
Stress/Fatigue
Caffeine, Alcohol, Nicotine

182

is there a cure for tinnitus?

no, but various treatment options available.
Use sound to take attention away from tinnitus.
Use sound to improve sleep, concentration, and relaxation.
Use Background Noise to make tinnitus less noticeable. Ex: fan noise, white noise, nature sounds, water sounds, etc
Use attention-getting sounds to distract you from tinnitus. Ex: Lectures, book on tape, talk shows, etc

183

Opening/Dehiscence in the bone overlying the uppermost semicircular canal within the inner ear.
Patients present with:
Autophony (increased resonance of own voice)
vertigo and oscipllopsia with loud noise or changes in middle ear or intra cranial pressure (coughing, sneezing, or straining)
Hypersensitivity to bone conducted sounds
Conductive hearing loss in low frequencies on audiometry with no other findings to support conductive hearing loss.

Superior Semicircular Canal Dehiscence

184

what is the most common eye disease?

conjunctivitis

most cases are infectious (non-STD)

Allergic Conjunctivitis (would have sneezing, etc)
Infectious (STD-Associated Conjunctivitis):

185

viral conjunctivitis presentation

Erythematous palpebral & bulbar conjunctivae
Copious watery discharge
Scanty exudate
Hallmark: lymph follicles are prominent in the lower conjunctival fornix
Look for palpable pre-auricular adenopathy

186

treatment for viral conjunctivitis

warm compress, usually clears in 2 weeks

Local topical ophthalmic antimicrobial agents to prevent secondary bacterial infection

187

presentation of bacterial conjunctivitis

Purulent discharge
More of a tendency to be unilateral (unlike viral conjunctivitis)
No blurring of vision after blinking (unlike allergic conjunctivitis)
Mild discomfort
Contagious, but less contagious than viral conjunctivitis
Self-limiting in 10-14 days (if untreated), but it should be treated

188

treatment for bacterial conjunctivitis

Polymyxin B/Bacitracin (Polysporin) ophthalmic drops or ointment
Sulfacetamide sodium (Sulamyd) 10% opthalmic solution or ointment
Gentamycin sulfate (Garamycin) ophthalmic drops or ointment
Erythromycin (Ilotycin) ophthalmic drops or ointment

Vigamox is most expensive and unecessary

189

Itching, tearing, redness
Stringy discharge that causing blurriness when blinking
Often follows a seasonal occurrence (esp. in Spring, Summer, or Fall), but may be perennial

allergic conjunctivitis -

tx : Topical ophthalmic mast cell stabilizers (cromolyn sodium), or topical antihistamines
Topical vasoconstrictors or vasoconstrictor-antihistamine combinations
Avoid allergens, if possible

190

Copious purulent eye discharge
A markedly inflamed eye with swollen lids

Gonococcal Conjunctivitis - Opthalmologic Emergency!
Rapidly leads to ulcerations and perforation of the cornea, and destruction of the eye if not treated within 1-2 days

diagnosed by gram stain and C&S

191

what are seen in conjunctival scrapings with Chlamydial Conjunctivitis or trachoma?

intracellular "inclusion bodies"

192

Acute erythema of conjunctivae

Eye discharge & irritation

Suspect this condition especially if conjunctivitis is associated with urethritis & urethral discharge

Conjunctivitis of the eyelids often lead to entropion and trichiasis with secondary central corneal scarring.

Chlamydial Conjunctivitis

tx: Oral tetracycline, doxycycline, or erthromycin

Doxy is usually the drug of choice – 100 BID x 7 days -photosensitivity and yellow teeth **standard tx for clymidia

193

is a subconjunctival hemorrhage benign?

yes - 21st bday, vomiting, childbirth

A large area of the conjunctiva appears “blood-red”

No treatment is necessary

Reassurance +/- artificial tears

Usually resolves without sequella in about 2 weeks (like a bruise does)

194

A triangular fold of abnormal conjunctival tissue that may grow and extends from the inner canthus (nasal side only) over the cornea, towards the pupil

The apex of the triangle points TOWARD the pupil.

Occurs most frequently in persons exposed to dust or wind (farmers, etc.)

pterygium

195

A yellowish, triangular thickening or nodule of the bulbar conjunctiva, nasal or temporal to the cornea
The apex of the triangle points AWAY from the pupil.
No treatment is needed since these do not grow over the cornea and obstruct vision.

pinguecula

196

inflammation of the cornea

keratitis-

exposure: Due to desiccation of the cornea from eyelid closure abnormalities or problems with tear secretions

Keratitis secondary to corneal abrasions

Keratitis secondary to ulcerating viral or bacterial infections

197

diagnostic test for hypofunctional tear glands

schirmer test

198

management for corneal abrasion

Record visual acuity PRIOR TO manipulation or treatment of the eye
Exception: when eye must be flushed immediately due to alkali or acid injury
Instill a topical ophthalmic anesthetic (after visual acuity is recorded!)
Perform a thorough eye exam (including lid eversion with a cotton-tipped applicator)
Remove the offending foreign body, if possible, with a moistened cotton-tipped applicator or needle

Apply fluorescein dye to check for corneal abrasion or ulceration
Damaged corneal epithelium stains a deeper green than the surrounding area
Apply a preventive ophthalmic antibiotic ointment (usually polymyxin-bacitracin)
When the corneal epithelium is disrupted, the cornea is very vulnerable to infection
Eye patching is no longer recommended

199

who has the highest risk of bacterial corneal ulcers?

extended-wear soft contact lens users
Patient will have eye pain, photophobia, tearing, and decreased vision

200

common etiologies of corneal ulcerations

Infectious: bacterial, viral (usually Herpes simplex or zoster), fungal, amoebic

Non-Infectious: Exposure keratitis, severe dry eyes, et al.

201

clinical findings of Viral (Herpetic) Keratitis/Ulceration

Characteristic “dendritic” (branching) ulcer is best seen after flourescein staining

202

tx for Viral (Herpetic) Keratitis/Ulceration

Immediate Ophthalmologic referral
The treatment regimen depends on whether the infection is limited to the corneal epithelium or if it is deeper into the stroma. Treatment may involve:
Topical antiviral agents
Oral antiviral agents
Topical corticosteroids, only under strict ophthalmologic supervision
Corneal grafting, if severe scarring results

203

which types of burns cause more damage, acid or alkali?

alkali - Alkali burn penetrate tissues, are not easily removed, and act for an hour or more


Acid burns are non-progressive
Penetration of acid is limited by the buffering action of the tissues
Damage is immediately visible

Must perform copious eye irrigation IMMEDIATELY with normal saline or plain water
Irrigate the eye away from the uninvolved eye

alkali: Continuous irrigation for at least 30 min. for alkali burns (use IV setup). A red eye is good because a white eye means that all blood vessels are dead!

204

inward turning of the eyelids

trichiasis

205

Eyelid margins turn inward
Surgery is indicated if the lashes rub against the eye and irritate the cornea and conjunctiva (“trichiasis”)

entropion

ectropion: eyelid margins turn outward. Potential causes:
May be age related (“senile ectroption”). This is commonly seen!

206

what are potential causes of ptosis?

Paresis of a branch of CN III
Weakness of the levator muscle
Horner’s Syndrome
Myasthenia Gravis
Tumors or infections of the eyelids

207

an external hordeolum is also known as what?

stye- Infection of glands of Moll or Zeis
Smaller abscesses located on external lid margin, points away from the conjunctival surface

Treat with warm compress (15 min, 3-4 times a day) + Antibiotic ophthalmic ointment (usually polymyxin-bacitracin or erythromycin)

May need I&D if no resolution within 48 hours

208

A hard, nontender swelling of upper or lower lid
May have some associated localized conjunctival inflammation. A common granulomatous inflammation (granuloma) of a Meibomian gland that may follow an internal hordeolum

chalazion

209

A common, chronic (usually bilateral) inflammation of the lid margins

blepharitis
Classifed as Anterior, Posterior, or Mixed blepharitis

Lid hygiene (baby shampoo applied with a damp cotton applicator)
Warm compresses

210

Refers to an acute or chronic (usually unilateral) inflammation of the lacrimal sac that is caused by a partial obstruction of the nasolacrimal duct. Characterized by a red, painful swelling near the inner canthus of the eye

dacrocystitis

Treated with immediate, vigorous, systemic antibiotics to prevent fistula formation to the skin or extension into the orbit or other intracranial structures
Dacrocystitis most commonly occurs in infants (Due to delayed opening in the lower portion of the nasolacrimal duct or at the orifice to the inferior meatus) and in adults over age 40 y/o

tx infant with massages with warm compress to ty to open up the duct

211

Red Eye due to Inflammation Of The Uveal Tract

uveitis

212

Inflammation of the “uveal tract” involves what?

the iris, ciliary body, choroid

Iritis refers to inflammation of the iris

Cyclitis refers to inflammation of the ciliary body

Choroiditis refers to inflammation of the choroid

213

anterior vs posterior uveitis

“Anterior” uveal tract inflammation involves the iris and ciliary body, producing iritis or iridocyclitis

“Posterior” uveal tract inflammation involves the choroid (and often also involves the retina), producing choroiditis or chorioretinitis

214

clinical findings of uveitis

Unilateral “ciliary flush” or “ciliary injection” (a ring of injection at junction of cornea & sclera)
Eye pain (due to ciliary spasm)
Photophobia (due to an inflamed iris)
Decreased visual acuity (blurred vision from ciliary inflammation & problems with accommodation)
Pupil small, irregular, & poorly reactive

May present acutely, with unilateral pain, redness, photophobia, or visual loss

May present less acutely, with blurred vision and mildly inflamed eye

215

diagnosis for uveitis is confirmed with what?

by presence of free lymphocyte & plasma cells (“inflammatory cells”) in the aqueous humor noted by slit lamp exam

tx: Antimicrobial therapy if infectious

Refer to Ophthalmology (EMERGENCY):

Topical corticosteroids +/- systemic steroids

Topical mydriatics to dilate the pupil and prevent posterior synechias

216

Clinical Presentation & Findings of posterior uveitis

Gradual visual loss, may be bilateral

Inflammatory cells in the vitreous humor are seen on slit lamp exam

Fundoscopic findings: pigmented scars, patchy yellow or white areas, hemorrhages along eye vessels, opacities on retina

Always refer to ophthalmologist (EMERGENCY)

217

what is CMV retinitis in AIDS patients?

posterior uveitis (“tomato sauce on a white tablecloth,” or “pizza pie” fundus, or “crumpled cheese and catsup”)

CMV retinitis is the most common ocular opportunistic infection in AIDS patients

Syphilis produces a characteristic “salt and pepper” fundus

Mydriatics & cycloplegics are NOT needed in posterior uveitis because the iris and ciliary body are not involved

218

inflammation of both the anterior and posterior uveal tract

panuveitis (uveitis universalis)

219

superficial inflammation of the sclera. Redness, pain, photophobia, tearing. Characterized by a unilateral and localized inflammation of the sclera

episcleritis **benign

Resembles conjunctivitis, but: Episcleritis is a more localized and deeper inflammation

Dilated vessels do blanch with topical vasoconstrictor (phenylephrine) as they do in conjunctivitis. Scleritis will NOT.

Common

Benign & self-limited, with no permanent eye damage
tx: topical corticosteroids

220

deep inflammation of the sclera

scleritis- More likely to accompany systemic disease (rheumatoid arthritis, lupus, gout, psoriasis, sarcoidosis, TB, syphilis)

more severe pain than with episcleritis and more risk of permanent eye damage.

tx is difficult, refer to opthalmologist. Systemic steroids or systemic anti-rheumatic drugs to treat underlying cause. NSAIDS

221

what is glaucoma?

family of diseases with normal or increased IOP ultimately leading to interruption of the vascular blood supply to the nerve bundles --> death of ganglion cells --> visual field deficits, cupping of disc and other abnormalities of vision

Lens gets stiffer (less pliable) as you age and gets deposits. Doesn’t move with the angle as much

Asians and eskimos have much higher risk for complete glaucoma (closed angle)

222

where does aquous humor go in the eye?

90% reabsorbed by trabecular meshwork, 10% goes into bloodstream through schlemms canal

223

what is the most common type of glaucoma?

open angle- leading cause of blindness in the US

Primary Open-Angle glaucoma (low tension glaucoma)

Secondary Open-Angle glaucoma
Trabecular meshwork is clogged with debris from uveitis, or other ocular or systemic abnormality

224

what type of glaucoma is an emergency?

acute closure glaucoma

225

what causes Secondary Angle-Closure glaucoma

The angle is closed from a lens-iris adhesion (anterior uveitis), subluxed lens, neovascularization of the iris or anterior chamber angle from diabetes or CRVO, tumor, or other ocular abnormality

226

when is congenital glaucoma seen?

within first 3- months

other developmental glaucoma:

Juvenile Open Angle Glaucoma
Marfan’s Syndrome
Others (traumatic)

227

what are risk factors for glaucoma?

-ocular hypertension
-increased cup:disk ratio of >0.5, or an asymmetry of >0.2 between the two eyes
(Stereoscopic, magnified instrumentation is a better way of measuring cup:disc ratio than direct ophthalmoscopy)

-Refractive error
Hyperopes and those with smaller eyes are at greater risk for angle-closure glaucoma
Myopes are at greater risk for open-angle glaucoma

-increasing age
-race (AA females have higher incidence of open angle glaucoma, whites & Asians have a higher incidence of angle-closure glaucoma)

-family history (The stronger the family history, the earlier the glaucoma is seen (familial effect)


228

what is normal IOP?

16+/- 5 mm. Hg (11-21 mm. Hg), representing 2.5 standard deviations on population distribution curve)

Up to 10% of all persons with ocular hypertension will go on to develop glaucoma

Glaucoma can occur in the absence of ocular hypertension (normotensive glaucoma)
30-50% of glaucoma is normotensive glaucoma!

229

is IOP symmetrical and when is it highest?

yes (within 2 mm Hg), highest in AM but IOP tends to be lowest in the EARLY morning.

Increases with age
Higher in women (probably due to smaller eye)
Reduced by exercise, alcohol, marijuana (transient)
Increased by steroids, fever

230

how is IOP measured?

tonometry - goldman applanation tonometry is the "gold standard"

231

should you have pain associated with glaucoma?

NO, no eye pain of VA changes (asymptomatic)

Eye pain if the problem develops acutely (acute angle-closure glaucoma)

232

how do you evaluate the depth of the anterior chamber?

corneal light reflux

The chamber will be nml in open-angle glaucoma and narrow in angle closure glaucoma

233

what will be seen on the fundoscopic exam for glaucoma?

Asymmetry of the Cup:Disc Ratio between the two eyes >0.2


A deterioration in the width (area) or health of the neural retinal rim (look at the disc donut, not the hole) occurs as the cup enlarges

234

signs and symptoms of open angle glaucoma?

Elevation of IOP is bilateral, chronic, and relatively slight. It may occur over years before it is detected. This is why primary open-angle glaucoma is known as “low-tension glaucoma.”

Visual fields gradually constrict (producing “tunnel vision”), but central vision remains good until late in the disease

235

how often should people be screened for glaucoma?

every 2-5 years if over age 40, more frequently if there is a family history of glaucoma

Over months or years, this condition, if untreated, leads to optic atrophy (and potential blindness)

236

medical treatments to lower IOP

prostaglandin agonist - Work to lower IOP (by 35-37%) by increasing uveal-scleral outflow

Topical Ophthalmic Beta Blockers (Timolol maleate (Timoptic, Betimol)
Betaxolol (Betoptic)
Levobunolol (Betagan)
Metipranolol (Optipranolol)
Carteolol (Ocupress)

Topical Cholinergic (Parasympathomimetic) Agents (Miotics)
-These constrict the pupil and affect ciliary muscle tone with the end result of putting traction on the trabecular meshwork to open it up and improve drainage
-pilocarpine

Carbonic Anhydrase Inhibitors- decrease aqueous production and lower IOP

Topical Ophthalmic Adrenergic Agonist (Sympathomimetic, Epinephrine-like agents):

Although these agents cause pupillary dilation, they predominately increase outflow of aqueous humor

Neuroprotective Agents- treatment directed more at level of optic nerve head and preservation of ganglion cell axons

Exercise Therapy- Recent studies have shown that exercise may be as good or better than beta blockers

237

what are surgical options to create new outflow channel to lower IOP?

trabeculoplasty
trabeculectomy
iridotomy (narrow angle or closed angle)

238

what is the prognosis for glaucoma?

1/2 to 3/4 of cases of open-angle glaucoma progress despite appropriate treatment (the bad news!)
Untreated chronic glaucoma will cause blindness within about 20 years

239

this occurs from closure of a pre-existing narrow anterior chamber

acute angle closure glaucoma
-precipitated by pupil dilation or lens enlargement with age

240

this presents with extreme eye pain, photophobia, red and stony hard eye, hazy "steamy" cornea, nausea, vomiting, prostration

acute closed angle glaucoma

241

emergency management of acute closed angle glaucoma

Administration of IV carbonic anhydrase inhibitor diuretics, such as acetazolamide (Diamox)

Administration of hypertonic solutions (oral glycerol, or IV mannitol or urea) to lower IOP

Administration of vasoconstricting eye drops, such as Pilocarpine, to pull the peripheral iris away from the trabecular meshwork

242

what is the definitive surgical treatment for acute closed angle glaucoma

peripheral iridotomy- A pie-shaped hole is made in the iris to create an opening between the posterior and anterior chambers so that fluid from the posterior chamber can drain into the anterior chamber

243

prognosis of acute angle-closure glaucoma

Untreated acute angle-closure glaucoma results in severe and permanent visual loss within 2 to 5 days after the onset of symptoms


Screening
Under 40 yrs old: Every 2 years (w/risk factors)
Every 4 years (no risk factors)

4o years and older: Every year (w/risk factors)
Every 2 years (no risk factors)

244

hereditary disorder, disease of the rods, may be mild or total blindness. Findings: bone spicules, waxy pallor, retinal vessel attenuation

retinitis pigmentosa

tx: vita A for night blindness
genetic counseling

245

this presents with blurred vision in one eye, becoming progressively worse. “A curtain (or shadow) came down over my eye”Sensation of light flashes or “floaters”

retinal detachment
Central vision remains intact until the macula becomes detached

tx: Maintain patient in a position that allows the detached portion of retina to fall back in place with the assistance of gravity

246

presents with sudden visual loss (minor to near complete). sudden onset of "floaters) . Examiner is unable to see the fundus clearly, despite a clear lens, due to a “Red-out”

vitreous hemorrhage

occurs due to : Retinal tears, with or without detachment. Diabetic proliferative retinopathy. Central retinal vein occlusions. Trauma, Other Causes

247

most common malignant tumor of the orbit in the 1st 10 years of life. presents with ptosis, proptosis, rapid progression with mets to brain and lung

rhabdomyosarcoma

248

most common intraocular malignancies in adults

metastatic intraocular tumors

249

highly malignant primary tumor of the retina. present from birth and the most common intraocular tumor of childhood

retinoblastoma

-Someone notices a white pupil (“Leucocoria”), or the absence of red reflex on photographs, etc.
It is a rare, but life-threatening tumor with a 20% mortality rate

tx: Enucleation

250

The most common primary intraocular tumor of adulthood

malignant melanoma- Arises from the pigmented cells of the choroid

251

tumor of the optic nerve itself

glioma- Dx in children with decreased VA, proptosis, papilledema, optic atrophy and strabismus

252

what is the leading cause of worldwide blindness?

cataracts, followed by macular degeneration , then glaucoma

F>M

253

what is a cataract?

an opacity of the lens cortex, lens nucleus, or lens capsule


Normally the lens is clear
“Opalescence” refers to lens opacification
“Brunescence” refers to a yellowing or browning of the lens
“Sclerosis” refers to lens hardening

254

whats happens to the lens with age?

larger and less elastic

As the cataract matures, the fundus becomes less and less visible

255

what accelerates occurance of cataracts and macular degeneration

smoking

256

what are signs and symptoms of cataracts?

glaring and scanting of bright lights, especially at night

diminished acuity

red reflex decreased or absent

May develop “phakomorphic” angle-closure glaucoma

257

3 types of cataracts

cortical
nuclear
secondary

258

stages of cataracts

immature: : Not all of the lens has opacified
mature: All of the lens is opaque
hypermature: The cataract is so advanced that some of the cortical proteins have begun to liquefy

259

what is the most common cause of cataracts?

age --> "senile" cataract

52-64 y/o: 5%
65-74 y/o: 18%
75-85 y/o: 46% (approx. 50% of persons over age 75)

260

how do you get a congenital cataract?

intrauterine infection such as rubella
Rubella cataracts need to be removed by 6 weeks of age, otherwise amblyopia abnosia develops (visual cortex of brain won’t develop properly)

261

what is drug induced cataract result from?

secondary to systemic corticosteroid treatment (prednisone)

Phenothiazine antipsychotics, Amiodarone, certain poisons, certain lab chemicals, et al.

262

what are some metabolic causes of cataracts?

diabetes, thyroid disease, parathyroid disease or tumor, Wilson'd disease


Low anti-oxidant status (especially of lutein, glutathione, and ascorbic acid)

263

other causes of cataracts

exposure to UV light (solar radiation) --2-3X risk of cataracts @ southern latitudes- preventative to wear sunglasses/ decrease exposure to solar radiation

Poor Nutrition

Smoking- Smoking decreases antioxidants and accelerates atherosclerosis

ETOHism

264

what is the treatment for cataracts?

extracapsular cataract extraction (ECCE) surgery - 99% effective and only takes 15-45 minutes- no longer done in the US

265

dietary changes that can prevent cataracts

increase anti-oxidants - neutralize free radicals that contribute to cell degeneration in aging and disease

vitamin C (ascorbic acid) - oranges, cartenoids (spinach, kale, carrots)
Spinach is the #1 best foot to prevent cataract & macular degeneration

5 portions of fruits and veggies

vitamin E

266

what is more common macular degeneration or glaucoma?

Macular degeneration - in next 10 years, the # of persons with it will double

**central vision loss

267

what is the most common form of macular degeneration?

dry ('atrophic') form -Formation of small, discrete “hard” drusen
and rarely causes blindness

268

what is the most severe form of macular degeneration?

wet ('exudative') form-Less common for (10% of cases), but more severe with a more rapid onset!
Formation of larger, less distinct, confluent “soft” drusen
Caused by abnormal growth of leaky blood vessels behind the retina

269

signs/symptoms of macular degeneration

-painless and can develop so slowly that it is hardly noticed
-may progress quickly, leading to impaired vision in one or both eyes
-Atrophy of the foveal (center) vision, with peripheral vision remaining intact
-blurred vision
-seeing straight lines as crooked ones

270

what are detection tests used for macular degeneration?

amsler grid
low light resolution testing
recovery after glare testing

**standard eye charts are NOT satisfactory for screening for macular degeneration

271

how can you prevent macular degeneration?

exercise
proper nutrition (lutein and vitamin E are most important)
increase antioxidants

272

what is the treatment for macular degeneration?

nutritional therapy --> high lutein diet

273

what is the treatment for the dry form of macular degeneration?

none, only prevention

274

what is the treatment for the wet form of macular degeneration?

laser photocoagulation
Photo Dynamic Therapy involves destruction of blood vessels using a low power (non-heat producing) infrared laser, along with a photosensitive dye ($8-10,000 per treatment x 3-4 treatments required)

275

unequal pupil size >1.0 mm

anisocoria

276

is the sympathetic afferent or efferent?

efferent only -midriasis

277

is the parasympathetic pathway afferent or efferent?

both - miosis

278

what occurs with the afferent path in the parasympathetic pathway?

light stimulates the retina, Travels optic nerve, chiasm, lateral geniculate nucleus to superior colliculus where fibers synapse
Fibers travel to Edinger-Westphal nucleus

279

what occurs with the efferent path in the parasympathetic pathway?

Fibers travel w/oculomotor nerve (III) through Cavernous Sinus
Follows inferior split of CN III
Synapses at ciliary ganglion
Short Post. Ciliary Nerve innervates the sphincter of the iris and ciliary body muscle
Outcome is miosis and accomodation

280

what is the sympathetic effect on the pupil?

dilation

281

what is the parasympathetic effect on the pupil?

constriction and accommodation

282

when should you check for accommodation?

only when direct and/or consensual response is abnormal

Have patient look at distant target and then near target at 40 cm

Response-convergence stimulates miosis

283

what does PERRLA stand for?

pupils equal round reaction light

284

difference between afferent and efferent pupillary defects

Afferent- Failure of response d/t blockage of transmission from eye to brainstem

Efferent- Failure of response d/t blockage of circuit from brainstem to eye

285

what is a unilateral afferent pupillary defect due to damage to optic nerve or retina. Consensual response induced by good eye is GREATER than the direct response produced by diseased eye
Diseased pupil appears to dilate with direct light stimulus

marcus gunn pupil / APD

286

what is the most common etiology of afferent pupilary defect?

optic nerve damage (Atrophy/Neuritis/neuropathy, Tumor, Glaucoma)

287

this is a pupil which constantly contracts and dilates. normal occurrence

HIPPUS

288

what is the different between physiologic and pathalogical anisocoria?

physiologic - same size difference in light and dark, less noticeable in light

pathological - Pupil size asymmetry changes under different illuminations
Size asymmetry increase in dim illumination=abnormality of dilation
Size asymmetry increase in bright light=abnormality of constriction

289

No anisocoria evident in normal light
No direct light response, therefore the eyes appear to dilate
Intact consensual light response depending on the condition. (exception—CN III palsy)
Can only be a unilateral finding
Blockage of the Afferent pathway (PSNS)

afferent pupillary defect

290

a dilated pupil usually represents a deficit in which pathway?

PS (A/E)

Differential Diagnosis
CN III Palsy
Trauma
Adie’s tonic pupil
Acute glaucoma attack
Drug-induced (Iatrogenic)
Fixed dilated pupil “Blown”
Amaurotic Pupil
Dorsal Midbrain Syndrome

291

this presents with ptosis, motility disturbances (eye deviated out and down), no VA changes.

oculomotor (III) palsy- neurosurgical emergency and intracranial mass should be ruled out

292

what is the triad for cranial nerve III palsy?

mid-dilated pupil
total lid ptosis
eye positioned down and out

reduced direct response to light

-etiology is based on age

293

if someone is having a painful CN III palsy, what should you suspect?

aneurysm
-incomplete palsy (partial limitation of ocular movements) is a sign of intracranial aneurysm

294

what is the workup for CN III palsy?

MRI/MRA, although arteriogram is gold standard

*Myasthenia Gravis may mimic CN III palsy

295

Pt. c/o Horizontal diplopia (Abduction deficit)
May turn head toward palsied muscle
Sudden onset=ischemia (especially in those w/known vascular dz)

CN VI palsy (LR)

296

Depression, abducting and intorsion
Vertical diplopia
Head tilt in opposite direction
Etiologies-Trauma and as above

CN IV palsy (SO)

297

this is an anatomic defect with enlarged pupil w/no direct light response, no consensual response, and no near object response

fixed dilated pupil "blown"

298

unilateral phenomenon that may occur when a rapidly expanding intracranial mass, including blood from a hemorrhage, is compressing cranial nerve III.

blown pupil

299

this occurs in females more than males, 20-40 year olds. large pupils which react slowly to light. in 70% of patients there is also absence of tendon reflexes

adie's tonic pupil

May follow infection (HSV, Trauma)

Pharmacological Testing
.8% or 1.0% Pilocarpine will induce miosis in Adie’s pupil **Even lesser amount due to hypersensitivity

300

what is the management for adie's tonic pupil?

chronic cholinergic therapy, reading glasses due to unequal accommodation and reassurance that this is usually BENIGN

301

What causes iatrogenic dilation of the pupils?

dilating drops (tx for Iritis)
cycloplegics!

302

this is a functional problem of an enlarged pupil causing total blindness and no direct response/"no light perception" +consensual response intact. therefore known as "blind eye" due to retina or optic nerve problem

amaurotic pupil (afferent problem)

303

this is due to a compression in midbrain and causes bilateral mydriasis, Lid retraction
, and inability to look upward. no reaction to light, but (+) accomodation

dorsal midbrain syndrome --most common cause is a mass in pineal region

304

horners syndrome involved damage to which system?

sympathetic

305

what is part of the horners triad?

Miosis
lid ptosis
facial anhydrosis (absence of sweat)

Increase in accommodation of affected eye

306

if a patient presents with horner's triad + pain ipsilateral face/neck, recent injury or accident, or pulsatile noise ipsilateral (tinnitus), what should you think of?

carotid artery dissection- EMERGENCY

307

Pharmacological Testing for Horner’s

Cocaine 4-10% ophthalmic solution
Hydroxyamphetamine 1% ophthalmic soln.

308

horners triad + heterochromia (different colored eyes)

congenital horner's-Always refer if not previously documented
Neuroblastoma workup

309

inflammation of the iris

iritis (iridocycltis)

310

Signature of neurosyphilis/ Tertiary Syphilis
small, irregular pupils
bilateral and asymmetric
react briskly to near but not to light stimulus

argyll robertson pupil (parasympathetic problem)

311

J. Lawton Smith’s 9 Commandments for argyll robertson

Decreased light response
Preserved near response
Miosis
Irregular borders
Bilateral/ Asymmetric
Poor Dilation
Iris atrophy
Must have SOME vision
Other signs of syphilis

312

management of argyll robertson

IV penicillin
Repeat Serology
Suspect Recurrence

313

is vision preserved with acute papilledema?

yes

314

General BILATERAL Optic Disc Swelling

papilledema

315

what can you automatically diagnose with papilledema?

HTN (grade IV)

due to ICP, infection, vascular problems

316

what is cushings triad?

HA, papilledema, vomiting

317

what is the treatment for papilledema?

reduce ICP
Elevate head of bed (HOB)
Hyperventilation
Diuretics
Osmotherapy (Mannitol/Hypertonic saline)
Corticosteroids—only in inflammatory causes
Surgical

318

Young-middle age, fertile, obese women presents with papilledema

psuedotumor cerebri

Often idiopathic (as its name states) but a cause is sometimes identified:

319

inflammation or demyelinating disease of the optic nerve

optic neuritis

320

what is the most common ocular manifestation of MS?

optic neuritis
*20-25% initial presenting sign
50% will develop MS within 15 yrs

321

cardinal symptoms of optic neuritis

UNILATERAL loss of vision
Pain in eye, especially with EOMs (it’s an inflammatory disorder) *This is a hallmark sign

tx: systemic steroids

322

An older person with a sudden painless loss of vision (usually IRREVERSIBLE), often only the superior or inferior visual fields affected

HA, jaw claudication w/chewing, malaise, fever and scalp tenderness

*Elevated ESR in arteritic form

temporal arteritis


Significant risk to other eye within 1-3 months (upwards of 75%)—specifically, 40% in arteriosclerotic type and 70% of arteritic cases

323

etiology of psudopapilledema

Marked hyperopia
Drusen Bodies (deposits of hyaline material) in optic nerve create the illusion that the disc is swollen, especially in young people. Often confused with true papilledema because it mimics it

324

Autosomal dominant condition causes accumulation of calcium in the substance of the optic nerve. Appear as multiple glistening mounds and the optic discs appear "swollen"

drusen

325

Death of nerve fibers (ganglion cell) in retina and optic nerve, following injury anywhere along its course produces a very pale or white optic disc

optic atrophy

326

Mean age = 60 yo
Sudden, nearly complete, painless, unilateral (permanent) visual loss (may only be able to count fingers or worse)
Symptoms can occur 15min-hours after occlusion
"Cherry-red” macula

central retinal artery occlusion (CRAO)
Results from loss of blood supply to the inner layer of the ophthalmic artery

"cherry red macular" -> temporal arteritis

327

how do you treat central retinal artery occlusion?

This condition is an ophthalmologic emergency (permanent vision loss within 1-2 hrs.)

Urgent ESR (giant cell arteritis)
CBC (anemia,polycythemia,platelets)
Fibrinogen, antiphospholipid ab, pt/ptt (coagulopathies)
Glucose (DM, atherosclerosis)
Lipids
ANA, anti-DNA
Carotid duplex
EKG (a-fib)
Echo (valvular dz)
Blood cultures (bacterial endocarditis)

328

Branch Retinal Artery Occlusion (BRAO)

Only a branch of a retinal artery is occluded by an emboli
Same etiologies as with CRAO
Less severe VF loss

329

a transient, but complete blindness in one eye

amaurosis fugax

330

Predominantly >50 yo
Visual impairment from mild to severe
*Key finding is retinal hemorrhages in ALL four quandrants

central Retinal Vein Occlusion (CRVO)

2 forms (fluorescein can differentiate)
Non-ischemic
70% will have a partial occlusion
Moderate reduction in VA
No relative afferent pupil defect (RAPD)
Mild disc swelling, mild cotton wool spots

Ischemic
30% of cases
VA severely reduced
(+) RAPD
Many cotton wool spots, retinal heme

331

when will you see "blood and thunder" fundus?

central Retinal Vein Occlusion (CRVO)

Dilated, tortuous veins (venous engorgement)
Retinal edema
Diffuse retinal flame & blot hemorrhages, esp. along the course of the veins
Cotton wool spots may occur (secondary to occlusion of small arterioles from the retinal edema)

332

Second most common retinal vasc dz after diabetic retinopathy
Clinical Presentation
Chief complaint is blurred vision (or sudden segmental loss of vision if the macula is involved)
May be an incidental finding on funduscopic exam and present asymptomatically
Commonly in the supertemporal quadrant

branch retinal vein occlusion

333

Fundoscopic findings for branch retinal vein occlusion

Hemorrhages & cotton wool spots in wedge-shaped area (area drained by the occluded vein)
Occlusion may be seen at the site of the AV crossing

334

when are retinal changes usually seen with HTN?

Retinal changes usually not visible until diastolic >110mm Hg

The effects of BP on the retinal & choroidal vessels depends upon the degree of BP elevation, the rapidity of its rise, and its duration

335

what should normal retinal vessels look like?

Should be normally transparent but are visualized because of the blood contained within them
In long standing HTN, a compensatory thickening and hyalinization occurs. They develop a “copper-wire reflex” and then a “silver-wire reflex”.

At the jxns, the arteries and veins share a common sheath, therefore thickening of the arteriole may cause indentation of the venule (aka “AV nicking”). This can lead to retinal vein occlusion

336

normal A:V ratio

3:4

337

what keith-wagener classifications are considered medical emergencies and referred to as malignant hypertension

III and IV

338

Generalized severe arteriolar narrowing with A:V ratio about 1:4
Focal arteriolar spasm (1:3 ratio of spasmotic area to proximal arteriole)
Hemorrhages
Dot hemorrhages are deeper in the retina and probably represent microaneurysms
Blot hemorrhages are deeper
Flame hemorrhages are more superficial
Linear hemorrhages may also be seen
Exudates
Soft exudates (cotton wool spots) represent focal retinal ischemia
Hard exudates represent leaking blood vessels (mainly proteins & lipids)

grade III retinopathy

339

Arteriolar narrowing resembles fine fibrous cords

Focal arteriolar spasm with total obliteration of distal flow

Hemorrhages

Exudates

Papilledema (“malignant” HTN)

grade IV retinopathy

340

what is the most common type of vascular retinopathy?

diabetic retinopathy

341

what are the two types of retinopathy and which is most common?

proliferative and non-proliferative

non-proliferative

342

what is non-proliferative/background
retinopathy?

This is a clinical reflection of the hyperpermeability and incompetence of involved vessels.
The capillaries develop tiny dot-like outpouchings called microaneurysms and the retinal veins become dilated and tortuous. Multiple hemorrhages may appear.
Macular edema is the cause of visual loss in these patients. This is caused by a breakdown of the inner blood-retinal barrier at the level of the retinal capillary endothelium allowing leakage of fluid and plasma products into the surrounding retina.

343

what is background retinopathy characterized by?

by microaneurysms, venous dilation, hemorrhages, exudates, and retinal edema

344

what is the key finding for Pre-Proliferative Background Retinopathy?

Multiple cotton wool spots (ischemia)

345

this presents with Chronic and progressive retinal ischemia stimulates the formation of delicate new vessels that leak serum and proteins in large amounts. Neovascularization (the growth of new vessels) freq grow on the surface of the disk and become elevated and can pull on the vitreous resulting in massive heme or detachment.

proliferative retinopathy

-Poor visual prognosis
Vitreous hemorrhages (“red-out”) are a common sequela
-retinal detachments

346

this type of retinopathy leads to more new cases of blindness, and is common in Type-2 diabetics

proliferative retinopathy

347

Diagnosis of Retinopathy:

Type I diabetics should be referred for ophthalmologic exam within 3 years after diagnosis and then re-examined annually
Type II diabetics should be referred at the time of diagnosis and then re-examined annually
Pregnancy: Retinopathy can be particularly aggressive so they should be screened in the first trimester and every 3 months thereafter.
IV flourescein angiography (by an ophthalmologist)—new vessels leak the dye at a fast rate

348

basic physiology of diabetic retinopathy

Atherosclerosis and progressive degeneration of capillary walls leads to:
Blockage of small arterioles
Leakage (hemorrhages & exudates)
Vessel wall damage with diffuse & focal expansion (microaneurysms)
Macular edema (main cause of blurry va)
Ischemia of the retina which stimulates neovascularization & fibrous growth
a

349

an abnormal white reflection from the retina of the eye. resembles eye shine

leukocoria