ENT Flashcards
1
Q
what is involved in the ENT exam?
A
ear - external, otoscopy, tuning forks
nose- anterior rhinoscopy
throat- oral cavity/pharygeal exam
neck - palpation, thyroid exam
CN exam
respiratory
2
Q
this is common in wrestlers, where blood collects between mucoperipchonidrium and cartilage.
A
auricular hematoma
tx: drainage and bolster dressing to avoid cauliflower ear
3
Q
this is a benign condition, more common in AA. Difficult to treat because comes back, and is treated by surgical removal or steroids
A
keloid
4
Q
this comes from an alkalotic environment/trauma by the pathogen pseudomonas or staph aureau
A
otitis externa (swimmers ear)
5
Q
how is otitis externa treated?
A
oto-topical drops, oral abx (quinolones to tx pseudomonas)
6
Q
what are complications of otitis externa and who are they more common in?
A
malignant otitis externa (skull base osteomyelitis)
more common in diabetics- usually admitted for IV abx
7
Q
this is a fairly commonly seen benign body overgrowth of the ear canal. typically doesn’t cause any problems or pain
A
osteomas
8
Q
why does an ear drum become retracted?
A
eustachian tube dysfunction
9
Q
common problem secondary to q-tips
A
ruptured tympanic membrane - wait 3 months for healing, keep dry, most heal on their own
10
Q
what is the difference between otitis media and effusion?
A
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
Q
different classifications of otitis media
A
acute ( 12 weeks)
12
Q
what is acute otitis media?
A
fluid with infection
2nd most common disease in children (URI is #1)
13
Q
what is the cause of acute otitis media?
A
eustachian tube dysfunction
sxs: fever, otalgia, bulging red TM
14
Q
pathogens for otitis media
A
s pneumo, h flu, m cat
15
Q
what is the first line treatment for otitis media?
A
amoxicillin (usually 45 mg/kg 2x a day)
beta-lactamase inhibitor is 2nd line
Tympanocentesis if not improving with abx
16
Q
what is otitis media with effusion and how do you treat?
A
fluid without infection
cause: eustachian tube dysfunction
sxs: hearing loss, speech delay
treatment depends on chronicity, dont need antibiotics
17
Q
these are used to help ventilate middle ear space and normalize pressures
A
ear tubes (surgery)
18
Q
what are the indications for ear tubes?
A
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
Q
what will the tympanic membrane look like with otitis media with effusion and acute otitis media?
A
otitis media with effusion will have yellow or amber colored fluid behind tympanic membrane (indicated serous fluid)
acute otitis media with be Erythematous
20
Q
what are some complications of otitis media/chronic ear disease?
A
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
Q
1 chronic complication of otitis media
A
cholesteatoma - skin debris gets trapped in middle ear space and continues to dequemate
22
Q
inflammation of tympanic membrane as opposed to middle ear space in AOM. very painful, due to pathogen mycoplasma pneumonia
A
bullous myringitis
if associated with blisters in canal need to think about zoster infection
23
Q
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
A
WEBER
24
Q
hearing test for bone vs air conduction
A
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
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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
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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
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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
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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
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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)
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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
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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?
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dilating drops (tx for Iritis)
cycloplegics!
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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
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Decreased light response
Preserved near response
Miosis
Irregular borders
Bilateral/ Asymmetric
Poor Dilation
Iris atrophy
Must have SOME vision
Other signs of syphilis
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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?
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reduce ICP
Elevate head of bed (HOB)
Hyperventilation
Diuretics
Osmotherapy (Mannitol/Hypertonic saline)
Corticosteroids—only in inflammatory causes
Surgical
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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
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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
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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.)
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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)
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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)
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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
```
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Ischemic
30% of cases
VA severely reduced
(+) RAPD
Many cotton wool spots, retinal heme
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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
