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Physical Diagnosis Midterm

OPTHALMOLOGY
Orbit
1. General Information
a. Quadralateral cavity (roof, floor, medial and lateral wall)
b. Pyramidal in shape also
2. Structures in each wall (always referring to right eye unless specified)
a. X-ray view required is the Caldwell View (head is erect, Central Beam is between FOREHEAD
and NOSE)
b. Will be able to see BOTH the right and left Apices
Caldwell View - Are all of the fissures and openings symmetrical?
a. If S.O.F. is enlarged
Dilation of Ophthalmic Veins (has widened the fissure)
This is due to a Carotid Jugular Fistula (the communication from a high to low pressure
system - rises the pressure in the veins)
b. Enlarged Optic Foramen
Optic Nerve Tumor
3. Roof of Orbit
a. Frontal Sinus located on medial side of Orbit
b. Superior Orbital NVB (Artery, Vein and Nerve) pass through notch of eye
c. Superior Orbital nerve branches into the Frontal Sinus
d. If pain is elicited on palpation here, an infection is possible
e.

The Floor of the Frontal Sinus is thin enough to transmit light through (Transiluminate)

4. Medial Wall
a. Right Nasal Fossa
b. Ethmoid Sinus / Air Cells
Wall is very thin
Called the Lamina Paparacia
c. Sphenoid Sinus
5. Lateral Wall
a. Temporal Fossa
b. Middle Cranial Fossa
6. Floor - via Mid Sagital section
a. Infraorbital groove
b. Infraorbital canal
c. Infraorbital foramen

Through theses, passes the Infraorbital NVB

d.

Alveolar canals

Part of the Infraorbital nerve extends through these canals into the Teeth

Primary disease of the teeth can climb up the canals and gain entrance into the orbit

e.

Antrum of Maxillary sinus

Infection could get through from this area as well

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Examination
1. With patient in PRIMARY GAZE (eyes aimed straight forward)
Cornea should line up with imaginary line from Superior Orbital Margin to the Inferior Orbital
Margin
(2 mm beyond line or 5 mm behind the line is the normal range)
a. Exopthalmos.
2 mm beyond line
Proptosis and Exopthalmos - both refer to forward displacement of the eye due to pathology

Pseudo-Exopthalmos

Eye looks "as if" it has been pushed forward and out of the orbit,
but nothing is wrong with the orbital contents (Periorbita)
None of the Periorbital is involved with condition NORMAL
Periorbita

POSSIBLE CAUSES:
1. Buphthalmos
Ox Eye deformity
2. High degree of Myopia
In cases where Myopia is due to elongated eye

Exopthalmos
(From pathology)

3. Paresis of Extraocular muscles

Does affect the Periorbita
The muscles are so weak, it doesn't hold the eye into the orbit
as it should
1. Thyroid Disease
Usually Hyperthyroidism (Graves - Thyrotoxicosis)
Orbit becomes very edematous (increase in ground substance,
which is hydrophilic
Also buildup of inflitrates (lymphocytes) BOTH leading to
edema
Hashimoto's Thyroiditis usually only occurs late in the disease
(Hypothyroidism) - but rare!!
1. Orbital Cellulitis
a. From Frontal Wall

From Frontal Sinusitis (infection through the wall of

Frontal Sinus)

From Lacrimal Gland infection

b.

From Lateral Wall

From Nasal Fossa or Ethmoid Sinus

c.

From Floor

Maxillary Sinus Infection

Dental Infection

Proptosis

2. Tumor
a. Tumors cause a forward displacement only when it is of a
significant size
b. Thus rely on visual abnormalities to identify this

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b. Enopthalmos
5 mm behind line (sunken back)
CAUSES:
1. Fat Atrophy
Causes eye to recede back into orbit
MOST COMMONLY SEEN!
2. Dehydration
3. Blow out fracture
See notes
Water's X-ray
Head is hyperextended
Central beam is directed between nose and the chin
Gives you a good view of the floor and the orbit
2 Findings with Water's View in a patient with BLOW OUT FRACTURE:
Wall appears to be thicker
a. Double Wall Osseous Density
b. Hanging Drop Density
4. Horner's Syndrome
a. Causes of Horners Syndrome (due to anything that affects the Superior Cervical Ganglion)
Pancost Tumor
C-spine fracture
Tabes Dorsalis
Syringomyelia
Apical TB
Cervical Cord tumor
b. Signs and Symptoms
Anhydrosis - Ipsilateral
Lid Ptosis
Myosis - pupillary constriction
5. Duane's Syndrome
Something wrong with innervation with Abducens nerve (CN VI)
OR
Adhesions have developed between the Periorbital tissue and the Lateral Rectus
a. Signs and Symptoms
When Medial Rectus aDducts, it pulls the orbit into the orbit because Lateral Rectus
is not opposing the motion
Ocular Adnexa
NORMAL
Eyelid
s

NORMAL
In position of primary gaze, there should be NO visible SCLERA between the
Superior or Inferior Limbus (Corneal / Scleral juntcion) also called LIMBAL
LINE
This means that eyes are in proper, normal position

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ABNORMALITIES - (with patient looking straight ahead / PRIMARY GAZE)
1. Dalrymple's Sign
Scleral strip seen at Superior Corneal/Scleral junction
CAUSES:
1) Exopthalmos or Proptosis MOST COMMON!
2) Spasm of Levator Palpebrae Superioris
2. Von Graefes Sign
1) Evaluation Method #1
If this patient goes into 2 gaze (without moving head, have patient look
up to the ceiling - Sursumduction)
Patient must pull back upper eyelid to do this (lid retraction)
Now have patient come back to position of 1 gaze
If eyelid stays "stuck" up there, coming back down in a few seconds
Von Graefes Sign
2) Evaluation Method #2
1 position to Deosursumduction (look down to floor without moving
head)
As eye comes down, lid should follow the eye (should stay with Superior
Limbus)
In this case, the lid doesn't follow and then "clunk" it drops down
Thus can see Sclera until it drops down

ABNORMAL
EYELIDS

CAUSES
1. Grave's Disease (Thyroid DZ)
2. Exophthalmic Goiter
3. Lid Ptosis
a. Paresis / Parlysis of Levator Palpebrae Superioris
b. Primary muscle diseases
c. Something in the eyelid that is heavy
Skin lesion
Skin tumor
Glandular infection
d. Epicanthus Tarsalis
Medial eyelid is drooping
Gives the impression that the patient is "cross eyed" (aDducted eye)
This is called a "Pseudo-Esotropia"
e. Epicanthus Inversis
Not as common as Tarsalis
Eyelid is "U-shaped" all the way around
f.

Blepharochalasis
When the whole upper lid droops down
Means redundant skin of the upper lid
Will see bags under the lower lid (due to herniation of fat there)
Congenital or acquired drooping of upper eyelid
1) Causes of acquired
a) Occulomotor Pathology
b) Horners Syndrome
c) Muscular Dystrophy
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Anatomy:
1. Levator Palpebrae Superioris
Innervated by Oculomotor nerve
Inserts on Tarsal Plate
2. Palpebral portion of Orbicularis Oculi
Innervated by Facial nerve
3. 1

Gaze Position = looking straight ahead

No visible sclera @ limbus junction of upper eyelid + lower eyelid
Upper eyelid = touches superior limbus
Lower eyelid = touches inferior limbus
Limbus = corneal sclera junction

4. Tarsal Plate
Dense CT
Excavations contain sebaceous glandular tissue (Glands of Mybomius)
There are glands in the Tarsal plate
Called Tarsal glands or Myobian glands (Sebaceous glands)
One in lower lid and upper lid
Helps to maintain position of lids
Levator
palpebrae

5. Intermarginal Sulcus

Fat

Orbital
septum

Orbicularis
oculi

6. Cilium of eyelid (eyelash)

Anterior part of eyelid
Has sebaceous glands of Zeiss
eyeball

LOWER EYELID
1. Inferior Limbus
2. Bulbar Conjunctiva
3. Palpebral Conjunctiva
4. Inferior Conjunctiva Fornix = sac (tear-filled)
5. Bulbar Conjunctiva
Next to eye

Intermarginal
sulcus
Tarsal plate
w/Glands of Mybomus

7. Orbital Septum
Helps keep eyeball in orbit
Runs length of orbital equator
Fat = behind septum

Inf. limbus
Bulbar C.

Inf. C. Fornix

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6. Palpebral Conjunctiva
Next to lid
7. Inferior Conjunctival Fornix
Sac formed by the two Conjunctiva
Filled with tear fluid
8. Follicle - All Follicles are equipped by glands which can become infected!!
a. External Hordeolum (Sty)
Infection of the Sebaceous Glands of Zeis
Readily seen area of localized redness + swelling
Possibility of purulent exudate (eyes stuck shut)
Possible Blephoritis infections:
1. Localized and Marginal Blephoritis
Blephoritis = inflammation of the lid
2. Diffuse Blephoritis
b.

Internal Hordeolum = infection of Mybomium Gland

If this is not treated, it will become an organized bump called a Chalazion
Must get surgically removed if it develops!!

9. Conjunctiva
Is a sheet of mucous membrane with a hole in it
Structures in the Conjunctiva:
a. Blood Vessels:
Not as many blood vessels around the opening
b. Glands
1. Glands of Krause (Serous glands)
2. Glands of Henle (Mucus glands)
c. The Hole
Cornea fits through the hole of the Conjunctiva
d. Bulbar Conjunctiva
The part of the Conjunctiva that is pushed up against the eye
e. Palpebral Conjunctiva
The leftover Conjunctiva
f.

Pinguecula
Lumps and bumps of Conjunctiva at the Medial Canthus
"Waxy" Hyaline appearance
Often mistaken for pathology, but has NO CLINICAL SIGNFICANCE!!

PATHOLOGIES
1. Palpebral Eversion or Ectropion
a. General Information

Eyelid has fallen forward

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Lower lid has lost its integrity (due to degeneration)

Since the dam has fallen down, the TEAR fluid is allowed to trickle out

Leads to an Epiphora (when tear fluid cannot be maintained within the Fornix)
b. Epiphora - Tear-level
Not good because you need tear fluid to keep the eye wet at all times
If it is significant enough, will cause Xerophthalmia
c.

Xerophthalmia

Dry eye

2. Palpebral Inversion or Entropion

Lower lid is too close to the eye
Eye lashes (Cilia) rub back and forth the Corneal surface
Leads to Trichasis
Trichasis

Acute Trichasis patient

In SEVERE Trichasis patient

Will get a Corneal Erosion (that does NOT go down below

Bowman's Membrane)
Epithelium will grow and fill in the hole

1. Corneal Ulcer can occur that erodes down to the Substantia

Propia
1. Collagen bundles are arranged in layers in a very Geometric
and Maticulous manner
2. Epithelial cells will fill in the hole in Epithelial layer
HOWEVER, the fibers in the Substantia Propia will fill in
a HAPHAZARD and random pattern
There will then be a spot in the Cornea where light
doesn't pass through properly!!!

3. Pterygium
An acquired pathology that continues to grow out over the corneal surface
Will eventually compromise the pupil
Triangular, vascular formation from the Medial Canthus
Usually develops from the Conjunctiva being bombarded by either:
CAUSES:
a. UV Light
b. Particulate matter
Salt in salt water that hits Surfer's eyes - Surfer's eye
Dust from ranching - Rancher's eye
Farmer's eye
4. Conjunctivitis
a. Signs and Symptoms:
Red, Hyperemic Conjunctiva
"Injected" Conjunctiva

Swollen Conjunctiva

"Chemosis"
NORMAL Conjunctiva should be clear and transparent!!

b. CAUSES of Conjunctivitis:
1. Chemical Exposure
Splashing something into the eye
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2. UV Light exposure
3. Bacterial Conjunctivitis
Most concerned with this!!!
A. Purulent exudate (yellow and icky)
Gonorrheal infection - (#1)
Tuberculosis infection
Vibrio Cholera infection
B. Mucopurulent - MOST are this type!!!
Staph. infection
Strep. infection
H. Influenza
E. Coli
Pneumococcus
4. Viral Conjunctivitis
Herpes Simplex Virus
Herpes Zoster Virus
5. Allergic Reaction
Lacrimal Systems
Upper Lacrimal System
1. Function:
Produces the tear fluid
Ducts drain Tear Fluid from Glands into the Superior Temporal Conjunctival Fornix
2. TEAR FILM:
a. Mucoid Layer
Made from Glands of Henle
b. Watery Layer
Lacrimal Gland
Glands of Kraus
Glands of Wolfring
c. Oily Layer
Meibomian Glands
Glands of Zeis
Need the TEAR FILM for:
Filling in the imperfections of the Corneal Layer
Nutrition of Cornea
Bactericidal properties
Tear fluid is almost isotonic to plasma
3. Lacrimal Gland
Can become infected
If the gland is infected, it is called a Dacryoadenitis

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Lower Lacrimal System

Drains the tear fluid
Lids close from TEMPORAL to NASAL (like a "zipper")
This makes the fluid flow towards the drainage area
If you flip the lid over, you will see:
1. Superior Lacrimal Puncta
2. Inferior Lacrimal Puncta
MECHANISM:
Fluid is drawn into the Superior and Inferior Lacrimal Canaliculis via Capillary attraction
The Nasolacrimal Sac will flow down the Nasolacrimal Duct
Exits into the Inferior Nasal Meatus
We will then either blow it out or swallow it
4 Tests for Tear blockage:
1. Taste Test
Take a solution of Sodium Saccharide, place a few drops in the Conjunctival sac
If person can taste it, you have established the patency of the Tear Drainage channels
2. Dye Test
Place some dye in the eye (Sterile Fluoricine)
Get out the Ophthalmoscope, using the Cobalt filter, it will fluoresce in the Nostril
Means things have gotten through
3. Schirmer I
Need filter paper (Wattman #41), 2 strips (one in each eye) for 5 minutes
Measure the length of the wetness
10 - 12 mm is NORMAL
4. Schirmer II
Tests for REFLEX TEARING
Do same as Shirmer I, but instead of letting them sit there, you take a dry applicator stick and
tickle the inside of the nose
This will stimulate tear production
Done subsequently to Shirmer I
Pathologies of the Lacrimal System
1. Fungus Infection - causing a Mycoelian Mat
Tears will not drain and have nowhere to go
Will run down the cheek (Epiphora)
Extraocular Muscles
4 Recti muscles form the "Muscle Cone"
These are the main muscles which hold eye so BOTH visual Axes are parallel to each other This is
so an image is formed (will only form if the 2 images are the same and overlap Fusion)
They should hold the "Visual Axis" of one eye to be parallel to the other eye
Fusion = similar retinal images in both eyes
Extraocular Muscle Examination
In Position of Primary Gaze (looking straight ahead), compare the:
1. Scleral Sector Examination
a. 2 Nasal Scleral Sectors
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b.

2 Temporal Scleral Sectors

Should be of the same volume (to assess if eyes are crossed)

2. Hirschberg's Test
Use Pen light
Shine in between the two eyes
If eyes are NOT Cross Eyed

If there is a DEVIANT EYE

Will get 2 Corneal light reflexes

In the CENTER of the Pupils

Corneal Reflex is not in the center of one eye

THAT is the Deviant eye!!

3. Cover Test
Cover eye and see where Non-occluded eye wanders
Uncover eye to see what happens in the Occluded eye
If you cover one eye, the brain is no longer operating in that area (no longer has to kick in it's
Fusional Mechanism)
Since Fusional Mechanism is not required, the "Covered Eye" can go wherever it really wants
to
4. Cover - Uncover Test
a. Cover then Uncover
Once Cover is taken away, it will be deviated!!
Eye will "snap" back into place once Fusional Mechanism kicks back in
May take SEVERAL attempts before you can catch the deviation
ORTHOPHORIC
If there is NOTHING abnormal

Patient appears to be Orthophoric!!

Means that there is NO obvious "Crosseyedness" (Strabismus)

HETEROTROPIA
If patient is Cross-Eyed
Patient has obvious Strabismus
Heterotropia (Obvious Strabismus, Cross
Eyedness)
If patient s Cross-eyed and is not corrected by
age 7, brain will adjust to not using it and vision
will be permanently affected!!!

Classification of Heterotropias:
1. Horizontal plane abnormalities (most common of deviations)
Esotropia

Eye is ADducted
More common than Exotropia (Esotropia OD,
OS or OU)

2. Vertical Plane Abnormailities - Not nearly as common!!

Hypertropia
Eye in Sirsumduction (looking up)

Exotropia
Eye is ABducted

Hypotropia
Eye in Desirsumduction (down)

3. Combinations of these:
a. Comittant Strabismus
b. Non-Comittant Strabismus
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Lots of complications can arise

Classifications of Heterophoria (Subtle Strabismus)

1. Horizontal Plane abnormalities
a. Esophoria

More common
b.

Exophoria

2. Vertical plane abnormalities

a. Hyperphoria
b. Hypophoria
3. Tests to detect this:
Hirschberg's Test
Cover Uncover test

6 Cardinal Positions of Gaze

2 Different muscles are responsible for each direction of movement (Conjugal Movement)

1. Right
Right Lateral Rectus
Left Medial Rectus
(2 different muscles, 2 different nerve supplies)
2. Oblique up
Superior Rectus
Inferior Oblique
Things we are looking for:
1. Conjugal movement
Be sure there is NO Saccadic eye movement
There should be complete ROM without restrictions
Should be NO End Positional Nystagmus
a. Saccadic Eye Movement
Ratchety, jerky eye movements
If present, it is PATHOLOGICAL
b. End Positional Nystagmus
True Nystagmus

End Positional Nystagmus

Always is QUICK and SLOW components

Will drift off slowly then click quickly back

Is more of an Oscillation at end range

No slow or quick component

EYEBALL
CORNEA
1. NORMAL:
Clear, transparent structure that fits in the Anterior Scleral Foramen
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2. Parts:
a. Anterior Scleral Foramen
b. Posterior Scleral Foramen
Optic nerve fibers exit here
3. Side view
a. Optical Zone
Want there to be EQUAL Radii of Curvature
If it is unequal, Cornea will have a "Torqued" Corneal Surface, creating Astigmatism
Keratoconus
When Optical Zone is "Cone" shaped
Usually seen in:
1) Down's Syndrome
2) Marfan's Syndrome
3) Retinitis Pigmentosa
4) Atopic Patient
Has some immunodeficiency (T Cells, AB)
Tend to have hay fever, Asthma, skin diseases
b.

Flattened zone

PATHOLOGIES OF THE CORNEA:

1. Rings and/or Streaks in Cornea
Pathology that cause RINGS in the Cornea

Pathology that cause STREAKS of the Cornea

1. Arcus Senilis
a. Presentation

Rings around the Cornea

Hazy, gray rings

b.

1. Band Keratopathy
a. Presentation

Calcium deposition within the

Substantia Propria of the Cornea

"Swiss cheese" look

Peri-Limbal sparing

Seen in:
1) Aging patient (not related to
Hyperlipidemia)
2) Patients under age 50
Suggestive of High
CHolesterol Levels
(Hyperlipidemia)

b.

2. Glaucoma
Intra-ocular pressure is markedly elevated

2. Kaiser Fleishcer Ring

a. Wilsen's Diseae
Abnormal Cu metabolism problems
with LIVER and become Cirrhotic
b.

Brownish ring

Seen in:

Chronic Inflammatory eye disease

3. Lines of Hudson-Staehli
Lines of iron
Seen in Geriatric patients with no clinical
significance
Orangish lines
4. Krukenberg's Spindle
Pigmentation in Cornea with NO clinical
significance

Ciliary Tract
Choroid
Ciliary Body

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Iris
When Choroid and Retina are inflamed:
(Impossible for one to be inflamed without the
other)

When Ciliary Body and Iris are inflamed

1. Anterior Uveitis
2. Iridocyclitis

1. Posterior Uveitis
2. Chroioretinitis

2. Keratitis - Inflammation of the Cornea

1. Tremendous infiltration of inflammatory cells with EDEMA
Edema produces a Lack-luster Cornea
STAGE I
Normal Cornea glistens, but this eye has NO more luster!!
2.

May also be a Ciliary Flush

1. Pannus Formation
Blood vessels actually start to grow into the Cornea itself (into
Bowman's Membrane)
Will produce a Keratoconjunctivitis, leading to an Entropion,
leading to a Trichiasis
STAGE II

Things that discolor the eye (not to be mistaken for discoloration)

1. Hyphema
Blood in the Anterior Chamber
2. Hypopyon
Purulent exudate in the Anterior Chamber (pus)

SCLERA
1. Drainage of Aqeuous Fluid - In order:
Aqueous Fluid is made at the Ciliary body (constantly) filling the POSTERIOR CHAMBER of the
eye
Trickles out across the surface of the lens and comes into and fills the ANTERIOR CHAMBER of
the EYE
Then goes to the Filtration angle (where Cornea meets the Iris
Trabecular Mesh (which has holes caled the Spaces of Fontana)
Inner Canals of Sonderman
Canal of Schlemm
Efferent Canals to Outer surface of Sclera
Epi-Scleral veins
Rate of production must EQUAL the rate of drainage!!!
To ensure this, there is a constant pressure gradient in the ANTERIOR CHAMBER called the
Intraocular pressure (IOP)
GLAUCOMA
Common etiology is that the IOP is too high!!
This directs flow into the Posterior Chamber of the Eye affects the Retina and the Optic Disc
Examination of Pressure of the Eyeball
1. Palpation (have patient close the eye and press two fingers on their eyelid)
a. Normal pressure

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Should feel like pushing on a hot water bottle with two fingers
Pressing on one should raise the other

PROCEDURE:
Ask patient to look down (Deosirsumduct the eye)
Upper eyelid always follows the Limbal line
With eye having a partially closed upper eyelid, palpate the SCLERA, NOT the Cornea.
2. Tonometry
Bring instrument up to the eye and apply the probe of the instrument onto the surface of the
Cornea
POSTERIOR SCLERAL FORAMEN
1. INNER PORTION of Sclera
Stretched across so that there are holes (like a screen)
This portion of "Fenestrated Scleral Wall" is called the Lamina Cribrosa
Once axons of 3rd order cell body passes through the Lamina Cribosa, it is surrounded by a
Myelin Sheath
A bundle of these axons makes up the Optic nerve
The outer surface of the Sclera blends in with the Outer sheath of the Optic nerve
2. Myelinated nerve head
When Myelin sheath has extended into the eye itself (through the Lamina Cribosa)
Color of Sclera
NORMAL

Blue Sclera

Porcelain white
Can have patient look left and right, pull their eye lids down and look up
and down, left and right, to see more of the Sclera.

Seen in:
1. Pseudo - Hypoparathyroidism
2. Long term use of Corticosteroids
3. Onchronosis
Inborn error of Tyrosine metabolism (can't breakdown
Homogenistic acid)
Missing the enzyme Homogentistic acid gets deposited in the
nailbeds, ear, Sclera of eye
4. Ectasia - Thinning of Sclera
From increase in I.O.P
Now the Choroid (Vascular Tunic) can be seen
The danger is that if the thinning continues, there will be a rupture
and the Choroid can herniate through (Staphyloma)
5. Osteogenesis Imperfecta

Yellow Sclera

2 types:
1. Age
Look carefully that the yellow does not go all the way up to the
LIMBAL LINE
Should be Peri-Limbal sparing
2. Icteric Sclera
a. Liver disease
b. Hemolytic disease
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Red Sclera

Appears to be the Sclera, but actually is the Conjunctiva

(Mucous Membrane)
In these patients, yellow discoloration is all the way to the
LIMBAL LINE
NO Peri-limbal sparing!

2 types:
1. Episcleritis
There is involvement of the vasculature and the Sclera (not involving
the Sclera Proper)
Unilateral, localized spot of inflammation of the Episclera
Thought to be a hypersensitivity reaction to some kind of disease
Episodic
2. Scleritis
Involves the WHOLE Sclera (the Sclera proper)
Bilateral (starts off unilateral)
Much darker color (more Violet)

1. Scleral Nevus (mole on the Sclera)

Nevus = mole
Brown discoloration
Chromatophores are cells which contain pigment
Melanosis Oculi = lots of brown spots all over the Cornea (Precancerous condition)
END OF OUTSIDE OF EYEBALL
INSIDE THE EYEBALL
1. Iris
a. General Information
Ordinarily, is RARE to have pathology
All we do is note the color
b.

Possible complications
1) Peripheral Iridotomy
Via Glaucoma therapy
A Hole in the Iris that helps drain Aqueous fluid from Posterior chamber

2. Pupil
a. Pupillary diameter

Should be equal Bilaterally (+/- 4 mm)

b.
c.

Round and regular

Margins are round and all the same curvature (regular)

Direct and Consentual Light Reflex

Direct Light Reflex

1. Place hand on Centrum of nose, to prevent light to each side of eye
2. Swing light from POSTERO-LATERAL
DO NOT create a "Menace reflex!"
Any object that approaches the visual field will be interpreted as a menace to the eye and will
constrict in response to that!

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THERFORE, to do it properly, only go from Posterolateral (hold it there), then flood it from the
front (and hold it) only once!!

3. See if pupils constrict Pupillary Meiosis

Indirect / Consentual Light Reflex

1. When pupil of opposite eye constricts in reaction to the directly stimulated eye
2. If there is a problem, the effect will be different:
More sluggish response (delayed response)
It will not constrict to the same degree
Pupillary Conditions:
1. Fixed Mydriasis (Over 6 mm in Dilation FIXED means that it will NOT respond to light)
a. Increase in Intracranial Pressure
NEED TO BE CONCERNED ABOUT THIS!!
b. Acute Glaucoma
If there was pain in the eye
c. Drugs
Anything that has Atropine (used clinically in Opthamology in patients with Strabismus to stop mechanism of Accomodation)
Atropine also used in GI Pathology - to decrease GI motility, decrease secretions (AntiMuscarinic)
2. Fixed Meiosis (less than 2mm in diameter that does NOT react to Darkness)
a. Patient is under treatment for Glaucoma (b/c keeping pupil constricted is good for the condition)
b. Anterior Segment Irritation
c. Horner's Syndrome
d. Drugs
e. Morphine
REVIEW: - Pupil should be:
1. Equal
2. Round
3. Reaction
Light
Accomodation
To list this:
P.E.R.L.A (Pupils equal, round, regular that react to Light and Accommodation)
Accommodation
1. Mechanism of Accommodation
a. Eyes converge
b. Pupils constrict

This is the ONLY thing Pupils do with Accommodation!!!

c.

Ciliary muscle contracts

Ciliary muscle contracts causing A - P diameter of lens to increase INCREASES

REFRACTORY Power of lens

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CRYSTALLINE LENS
NORMAL

ABNORMAL

Clear and transparent

If opaque
Need to use a +12 Lens

CATARACTS
1. Types of Cataracts
a. Nuclear Cataract

The nucleus of the Lens is becoming opaque

b.

Posterior Subcapsular Cataract

Hard to see because it develops in the posterior lens

c.

Cuneiform Cataract

Starting in periphery to center of Lens

2. Signs and Symptoms of patient developing Cataracts:

a. Glare

Water filled structure refracts more light when light hits it

b.
c.
d.
e.

Visual Discolorations

Blue or yellow casts to objects in room

Halos seen around lights
"Fog" or "Haze" seen
Reduction in visual acuity

TREATMENT:
Needs to ripen or mature before surgery is performed (will become totally opaque!!
Surgery cannot be done on patients with Aphakia
1. Aphakia
a. General Information

Patient does not have a Crystalline lens

In these patients, the corrective lens will placed ON the eye --> use contact lenses
b.

Iridodenesis

Pupils will dance back and forth

c.

TREATMENT

Transplant a lens

Aphakic contact lenses

Aphakic glasses (magnifies view of eye - can see Iridodenesis)

VITREAL BODY
1. Consistency
Sol-gel
More Sol than Gel
2. Patellar Fossa
For the reception of the Lens
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It fits into this space

3. Hyaloid Canal
Hyaloid Artery runs through this to supply the developing Lens
When Lens is fully developed, it no longer needs this artery -->artery will atrophy
Canal will fill in with Lens substance (sol-gel substance)
Sometimes, remnants of the atrophied Hyaloid Artery remain and can be seen with an
Opthalmoscope - Mittendorff's Dot
RETINA
Cup-like structure
1. Retinal Fundus
Base of the cup (Posterior concavity of cup)
2. Optic Disc
a. Location

On nasal side of the Retina

b.

Shape

Shape is Oval - Round

Is more oval than round (vertical length is greater than horizontal length)

c.

Margins

Superior, Temporal and Inferior margins are clearly demarcated!! (well - defined!)

Nasal margin is fuzzy

d.

Color of the Disc

NORMAL

Salmon colored (orange-pink)

e.

ABNORMAL
Red Disc
White Disc

Physiological Cup
A depression in the Disc
This is where vascular emergence and convergence occurs (vessels come out and in to it)
There must be APPRECIABLE disc material between borders of disc and physiolgical cup
If borders are not seen, this is bad!!
NORMAL

Cup Disc Ratio

Should be 1:2

Blood Vessels of Retina

1. Superior Papillary Artery
Bifurcates superior to the Edge of the Disc
2. Inferior Papillay Artery
Bifurcates ON the confines of the disc
3. Temporal Branches System
4. Nasal Branch System
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ABNORMAL
If borders between Physiological cup and
Optic Disc are not seen
Yellowish cast color

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How to differentiate between Arteries and Veins

1. Color
Artery = red
Veins = darker
2. Diameter
Veins are larger
3. Light reflex
When light hits it, you will 2 tracts of red (you will see a strip of light on the artery)
This does not occur with Veins
4. Pulsations
Veins often pulsate near or on the disc
5. AV Cross
Artery lies on top of vein on periphery of Retina
NORMAL AV CROSS
1. Long Axis Angle is always less than 90
(Acute angle)
2. Artery is always on top of the vein
(superficial)
3. Blood of vein always comes up to the margin
of the artery

PATHOLOGICAL AV CROSS
1. Atherosclerosis of the Lumen
Causes vessel to get heavy and sink into
the underlying vein
Looks as if there is NO blood circulating
around the artery
Looks like blood is falling just short of the
artery AV Nicking or Concealment
2. AV Long Axis angle widens past 90

The Undifferentiated Retina

The outer wall of the Retina

Diffusely red
Mixture of Rods and Cones

Differentiated Retina (Macula)

Will look darker!!
Fovea Centralis = may be seen as a tiny white
dot (this is the end of the visual axis)
Only contains cones

Pathologies of the Eye

1. Diabetic Retinopathy
Proliferative Stage
(Later stage of Diabetic retinopathy)

Non-proliferative Stage
(Background Retinopathy)

Only 5% progress to this stage!!

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Series of things that develop:

1. Micro-aneurysms (small red dots)
Micro-aneurysms develop around the
margin of the Optic Disc

Neurovascular proliferation occurs (new vessels) to

supply areas of ISCHEMIA / INFARCTION!!
These NEW vessels are:
a) VERY Friable!
Rupture easy
Retinal tears - from friable vessels
leading to Retinal Detachment

2. Hemorrhages develop (3 types)

a. Dot = small dot
b. Blot = ill-defined dot (larger)
c. Flame = jagged-looking large blot
3. Exudates form: (2 types)
a. Soft Exudates (Cotton-wool exudates)
Areas of RETINAL Ischemia /
Infarction

b) Grow into the ANTERIOR CHAMBER of the

eye
Can end up blocking venous flow out of the
eye leading to 2 GLAUCOMA!

d. Hard Exudates
Lipid deposition

2. Macular Degeneration
1. Central visual field is Blurred or Foggy

Signs and Symptoms

2. Drusen
Herniation of Brups Membrane (yellow dots)
3. Raised area of macula
4. Neo-vascularization

Types of Macular
Degeneration

1. Dry (Drusen) - 80%

Presence of Drusen (pieces of material within the macula)
3 12 pieces (the fewer the pieces, the larger they are)
2. Wet (Neovascular / Swollen) -20%
1. Dry (Drusen)
Microlenses (Sub normal visual aids)

TREATMENT
2. Wet (Neovascular / Swollen) -20%
Surgery Laser Photo-coagulation

Diagnosis

Amsler Grid (5mm graph paper)

Patient looks at paper 12 from eye
ALL horizontal lines should be parallel!
ALL vertical lines should be parallel!
If there are ANY Wavy lines Metamorphopsia!!

3. Hypertensive Retinopathy

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Lots of pressure against WEAKER walled vessels

1. Increase in Arterial Tortuosity
Width of light reflex INCREASES due to Atherosclerotic
changes
As it widens, the color of the arteries changes to a Copper
Color!
Early

2. AV Ratio
Normal AV Ratio: 2 : 3
Hypertension AV Ratio: 1 : 3 (widens due to light reflex)
3. AV Nicking / Concealment
Gunns Sign: Venous blood flow does not come up to
Arterial wall
Salus Sign: There is a 90 between the artery and vein
1. Flame type hemorrhages

Intermediate

2. Silver wire artery

Arterial wall changes color
Lighter and more Silver!
3. Cotton Wool exudates
Indicates areas of infarction

Severe

Papilledema

4. Papilledema (aka Blurred Disc or Choked Disc)

1. Very Red optic disc
Disc is red and swollen because it is Choked
Blood cannot get out!
Signs and Symptoms of
the Optic Disc

2. Swollen physiological cup obliterated

Margins are very raised and blurred!
3. No distinct margination
4. Dilated veins returning peripheral blood
Because blood cannot get back in
1. ed Intra-cranial pressure
MC at Posterior Cranial Fossa

Caused by

2. SEVERE Hypertensive Retinopathy

3. Central retinal vein occlusion
4. Cranial Arteritis
Optic nerve arteritis from MULTIPLE SCLEROSIS

5. Glaucoma
a. Physiological cup becomes ECCENTRIC to the Temporal side
Nasal Displacement of Vessels = Vessels appear to be on the Nasal side of the cup
In reality, it is the cup that has moved TEMPORALLY!

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b. Margin with Disc margin becomes ONE margin
c. Increased pressure on Physiological cup causes:
Cup Diameter to increase
Cup Depth to increase
Cup gets WIDENED and DEEPER!!
Normal pressure = 10 22 mmHg / Glaucoma = 30 40 mmHg
d. Can SEE portions of the Lamina Cribosa!!!

END FOR MIDTERM 1

OTORINOLARYNGOLOGY
External Ear
1. Pinna
Anatomy of the External Ear:
1. Helix (1)
See PAS diagrams page 23
The outer rim of the ear
2.
3.
4.
5.
6.
7.

Scapha (2)
Darwins Tubercle (3)
Tragus (4)
Anti-tragus (5)
Cavum/concha (6) depression
Fossa (7)

8. Franks Crease (8)

An indentation in the lobule
Suggested that 60% of these patients may develop Coronary Artery Disease
9. Lobule
a. Properties
Made of Fibro-fatty tissue
NO Cartilage
A stiff lobule may suggest Addisons

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b. Must look for presence of KELOID
In Keloid Formers, when their Lobule is damaged (usually from ear piercing), the
scar formation will remain hypertrophied!! (big ugly bump)

2. EAM
Middle Ear or Tympanic Cleft
Is NOT a Cavity!!
Inner Ear
1. Cochlea
Includes the Organ of Corti
For hearing
2. Vestibular Apparatus
For balance
Pathologies of the External Ear:
1. Darwins Tubercle normal finding
a. Chondro-dermatitis Helicus Chronicus
Benign lesion of Darwins Tubercle
If Darwins Tubercle is red or inflamed, you must biopsy the bump because it may be this
disease (a form of skin cancer)
2. Sodium Urate Deposits = When patients reach 3 Stage of Gouty Arthritis
Tophi may be seen in the HELIX or ANTI-HELIX
If you squeezed them (which you would never do), a "toothpaste" looking stuff would ooze out
(Sodium Urate)
3. Cauliflower Deformity, causes:
a. Hematoma can form between perichondrium & cartilage proper
The hematoma is NOT reabsorbed very well!
Will organize and become a MASS of scar tissue instead!!
1. Found at region b/t HELIX and ANTI-HELIX
a. Usually in the Fossa Triangularis or the Scapha
2. Direct trauma to the cartilage of the ear
3. Treatment (post trauma)
Pack the Fossa Triangularis or Scapha with GAUZE and COMPRESS!
This is to prevent a Hematoma from forming
4. Onchronosis
Blue spots
5. Basal Cell Tumor
Very invasive (around EAM, cavum, near temporal bone)
hemorrhage
Infection possible
MC of all skin cancers
6. Seborrheic Dermatitis (Pitirospora vulgaris yeast)
a. Migratory
Eyebrows
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Eyelids
Malar aspect of face
Midline of chest
Post-auricular sulcus
Cavum to EAM
Pinnae

b. Eczema
Juicy papules
Red
Scaly
Ill-defined
7. Psoriasis Vulgaris
a) Found in many places (Same locations similar to Seborrheic Dermatitis)
In @ around ear
Pre-auricular area
Post-auricular area
8. Herpetic Infection
Tracks Trigeminal nerve
Can infect Geniculate ganglion of CN VII
Herpes Zoster Oticus (Ramsey-Hunt Syndrom)
9. Sebaceous Cyst
Can form over cavum (posterior side of ear)

EAR CANAL (24 mm in length)

1. Cartilaginous portion (outer 1/3 of canal = 8 mm)
See PAS diagrams page 25
a. General Information
8 mm
Made up of little bits of cartilage, just like the Pinna
This portion of the Canal has FLEXIBILITY!!!
Thus, ideally when you insert Speculum into ear, you must keep it in this section (because
you need to move it around for the examination)
b. Clefts of Santarini = spaces between the cartilage
1) ANTERIOR to this portion of the canal are:
Parotid gland
TMJ
These Clefts were a pathway of disease and could get to the TMJ or Parotid Gland
2) POSTERIOR to this part of the canal:

Mastoid Air Cells - Disease that got through would lead to Mastoiditis
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c.

This does not occur anymore due to Antibiotics!!

Skin = thicker in canal (vs. osseus portion)

1. Hair follicles - Need to rule these out!
Folliculitis
Furunculosis
2. Sebaceous glands produces Cerumen
a. Scant amount of Cerumen in the lumen
Possible skin disease in the Canal
May produce a dry canal Pruritic (Itchy)
Leads to itchy canal we will scratch it a lot!
b. Excessive Cerumen in Lumen
If we see it, you don't do anything
Do not advance Speculum or try to clean it out
In absence of symptoms = do nothing
If there are symptoms = must clean out wax and inspect ear canal

2. Bony portion (inner 2/3 of canal = 16 mm)

A) Otoscopic examination
Keep tip of speculum in outer 1/3 of canal, OUT of this Bony portion!!!
Skin is tightly adhered to the Canal
There are NO hair follicles and NO Sebaceous glands
Thus easily damaged if Otoscope Speculum is advanced into this area
B) Pathologies/problems
1) Itchy lumen due to dryness. Scratching can cause:
Introduction of bacteria
Breaking of the skin (because the skin is TIGHTLY adhered to this portion of the canal)
May be due to underlying Dermatitis
2) Cerumen Impaction = Most common finding!
3) Folliculitis
4) Furunculosis
5) Otitis Externa
The EAM has normal skin flora (Staph. epidermis mainly)
Cerumen keeps the Endogenous Flora from multiplying via a LOW pH (bacteriostatic)
IF no wax, bacteria multiply and invade the skin
This inflames the skin allowing the invasion of EXOGENOUS BACTERIA
FINDINGS:
1. Pre or Post Auricular Adenopathy
2. Pain
Look for this by pulling on Pinna
3. Look at Osteum (EAM) for signs of Otorrhea (drainage of debris)
If this is present, you must refer out!!

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4. Wall will be red and edematous (swollen)
5. ed diameter of the Lumen ( caliber)
6. Exudation in the lumen
Pus
Serous fluid
Keratin debris (from exfoliation)

See PAS diagrams page 26

6) Aural Polyp (3) - Pedunculated red mass (bulb like)can also be sessile (flat like)
MOTILE if you push on it with a stick
DOES NOT PULSATE!
Causes: aspirin, asthama, allergies, mycoplasma pneumonia, cystic fribrosis
7) Glomus Jugulare (4)
Benign Tumor that arises from the Tunica Adventitia of the Jugular bulb
Erodes through floor of canal, invading the middle-ear cleft
Pulsates
Can arise on either side of tympanic membrane
TO D/DX FROM AN AURAL POLYP:
If you touch a stick to it IT WILL NOT MOVE!!
Pulsates
8) Cholesteatoma (5)
Can be found on either side of tympanic membrane
Mass of B9 skin cells
9) Exostoses (6)
Bone proliferation due to lots of Cold Water swimming
Thus is MC in Cold water swimmers!
Can project to either side of tympanic membrane
10) Chondroma
Benign tumor of epithelium
Mass of skin cells
Found in outer Cartilaginous portion
11) Foreign body in the Ear Canal (lice)
12) Sagging Scutum
Basal part of cochlea gives Isthmus of Canal
2 to Mastoiditis
Scutum = Superior & Posterior part of wall thin
Begins to sag due to Mastoiditis
13) Otalgia ear pain
Can refer to CN III, V3, VII , X (occulomotor, mandibular of trigeminal, facial, vagus)
TYMPANIC MEMBRANE
General Information
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The lateral wall of the Middle ear cleft
NOT part of the External ear
Sits in a position where it is reflected SUPERIORLY (tilted)

3 - Layered Membrane
1. Outer Epithelium layer (skin)
2. Core
Made of collagen fibers (thicker fibers at middle)
3. Inner Mucus Membrane (cuboidal epithelium)

See PAS diagrams page 26

Parts
1) Annulus (1) = outer ring
2) Malleolar Folds thick (look thicker than other folds because they have more collagen)
a) Posterior Fold (2)
b) Anterior Fold (3)
3) Pars Flaccida or Sharpnells Membrane (4)
Thin triangular membrane
4) Pars Tensa (5)
Bony Landmarks of Drum
1. Malleus - Responsible for position of Tympanic Membrane
a. Manubrium Long process (a)
b. Short Process (7)
c.

2.

Umbo (6) = tip of Manubrium

In approximate center of Pars Tensa
Point where processes touch the Tympanic membrane

Incus
a. Lenticular Process (b)
Articulates w/stapes
b. Long Crus (8) (+/)
May be hidden parallel behind Long Process (or may not be)

3. Chordae Tympani (9) (+/)

D/DX between fluid line (from effusion) bring patient from supine to seated
Fluid line = fluctuates with movement
Chordae Tympani = vertical while supine
Break the Drum into 4 Quadrants
Criteria of Normal Tympanic Membrane
Color

Should be pearl gray opulescent structure

Bony Landmarks

Should be able to identify the Manubrium

Drum

Avascular

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Cone of Light (10)

Major criterion of healthy membrane (can be seen in normal ear)

When light of the Otoscope strikes the drum, there is a reflection of
light back to us
Called a "Cone of Light"
Must reflect off the Lower portion of the Anterior/Inferior Quadrant

Tympanic Membrane

Mobile (ear drum should move)

(Examine using Pneumatic Insufflation insufflation)

Pathologies of the Tympanic Membrane

Most are from reflections/results of pathologies of middle-ear cleft
1) Barotrauma
Not commonly seen because of airplane pressurized cabins
Bleeding into drum from subservient vessels
2) Vesicular Myringitis
Tiny eruptions of Ramsey-Hunt Syndrome via herpetic infection
3) Puncture Wounds (could be from a myringotomy to release exudates in tympanosclerosis from a
lymphadenopathy)
a) External to internal = rare
b) Internal to external = MOST COMMON!
c) Healing of puncture wounds
1. Collagen does not regenerate
2. epithelium regenerates
3. healed are is thinner (a top view would look like an hour glass)
d) Findings of healing from hole in drum
1. thin areas look greyed - with otoscopic light examination (like a shadow)
2. tympano-sclerosis deposition of Ca (white spots on drum)
e) pain is from stretching of drum
MIDDLE EAR
Pathologies
1) Otosclerosis - Redundant visualized bone incorporates the foot plate
Severe conduction hearing loss
Medial wall of cleft ONLY!
EXAM FINDINGS:
Schwartz Sign: Bluish pink color of drum occurs (Sclerotic bone)
All other suspected findings are NORMAL
2) Otitis Media infections that respond to Antibiotic therapy
a) Serous probably VIRAL induced
Other causes:
Bacterial
Allergic Reaction
Signs and Symptoms:
1) Amber discoloration of drum
Serous-sanguinous type of exudate
2) Fluid line
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3) Bubbles
4) Cone of light will be distorted (abnormal)
5) Mobility
No response to insufflation
b) Purulent - BACTERIA induced
Bulging of Tympanic Membrane into the Canal (may rupture)
Buildup of exudate causes vascularization Red and swollen drum!

3) Tympanosclerosis via lymphadenopathy (originating from nasopharyngeal area)

a) Organs of Rosenmuller
Involved (oral cavity tonsils: adenoid aka pharyngeal, lingual, and palantines) part of
Waldyers Ring
b) Eustacean Tube = occluded from infection
Air trapped in tube
Air from middle ear cleft pulled into tube

See PAS diagrams page 29

c) Retraction of tympanic membrane (concavity) occurs

Cone of Light = abnormally replaced
Tympanic Membrane = mobility upon insufflation
Short process = very prominent via drum retraction
SIGNS and SYMPTOMS:
1. Hearing deficit
Middle-Ear Cleft = devoid of ear
Fullness of ear felt
2. Build-up of exudate
Causes vascularization Red and swollen drum!
TREATMENT
1. Usually ANTIBIOTICS
BUT lymph does NOT respond to Antibiotic therapy (purulence = treated)
2. Myringotomy
Poke hole in drum (releasing exudate)
HEALING:
Collagen does not regenerate
Epithelium does regenerate, but the healed area is THINNER!
Findings of a hole in the drum healing:
Thin areas look greyed w/otoscopic light examination
Tympano-sclerosis = deposition of Ca2+ (white spots on drum)
Pain = from stretching of drum
3. Tympanostomy Tube
Allowing constant drainage
4. a spontaneous rupture can also result, which is most common at the annulus

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INNER EAR

Cochlear Division Hearing Evaluation

Test
Whispered Voice Test
(Depends on intensity of whisper)
Spoken Voice Test

Notes

Silly to do because these tests are NOT Standardized!

Watch Tick Test

Pure-Tone Audiometry

Tuning Fork Evaluation

Hartman Set of tuning forks

2048 cps = not currently manufactured
1024 cps
512 cps = for screening purposes
256 cps
128 cps = not in human speech range

Hearing Evaluation

Fingers rubbing together

Evaluation Steps
1. Evaluate canal
2. Evaluate drum choose the largest speculum to fit the
canal
3. Hold OTOSCOPE like pencil (battery handle pointing
anterior or superior)
Must rest hand against face prevents pain/trauma
from movement of patient
4. Tip head to opposite side if necessary

Otoscopic Evaluation

5. Look at opening to RULE OUT these: (STOP if these are

seen disallows view of drum thus dont advance!)
Otorrhea draining
Impaction of Cerumen - Wall of wax
6. Put on correct size speculum
Choose largest speculum to fit canal
7. Flexibility of Cartilaginous canal (normal direction =
anterior & inferior)
8. Need to straighten out cartilaginous canal grasp Pinnae
Adult
Pull superior & posterior
Infant

Pull superior

9. Look through OTOSCOPE as you insert speculum

10. Insufflator keep bulb in palm of hand

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General Hearing Evaluation

Rules
1) Patient must know signal prior to testing (strike fork @ heel of hand)
2) Inform patient what to do (instructed to say when can hear signal)
3) Patient must close eyes
4) Non-test ear must be masked from distracting noises
Not absence of sound
Push Tragus back & forth
5) DOCTOR STANCE - in front of patient
6) Strike tuning fork at heel of hand
Holding at arms length until can no longer hear signal

DC is the standard

Hold fork so sound waves = parallel to patients ear

Estimate distance from ear (e.g. in line w/shoulder)

Note DL and DR

DL DR
If DL DR

Normal
ABNORMAL: requires 4 tests to D/DX deafness:
1. Conduction deafness
a. Canal damage from:
1. Atresia of canal via congenitally missing Pinnae
2. Impaction (MC = cerumen)
3. Pathologies
Aural polyp(s)
Chondroma
b. Drum damage from:
Perforation
Barotrauma not common
c. Ossicular Chain damage from:
Otosclerosis
Dislocation
Fracture rare
2. Sensory Loss
a. In a normal individual, 90 dB:
Can produce permanent hearing deficit
Destroys inner & outer hair cells (in cochlea)
b. Cochlea damage from:
1. Sound at high dB
2. Presbycusis
Old hearing degeneration
Organ of Corti (cochlea)
Spiral ganglion degeneration (pericaria)

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3. Acoustic Neuroma rare

Rare
Neurofibromatosis II (bilateral)
Cerebello-pontine Angle Tumor = more common
Neurofibromatosis I = Von Recklinghausens DZ
Caf au Lait spots
Development of neuromas on skin
4. Menieres Disease (Endolymphatic Hydrops)
5. Hypothyroidism (Cretin) = irreversible
6. Hypothyroidism (acquired) = reversible
D/DX Tests for Hearing Deficits

Normal: Air Conduction = 2 x Bone Conduction

HEARING TESTING
TEST

Conduction

Sensory

Louder in BAD ear

Louder in GOOD ear

BC (time) > AC (time)

AC = 2 x BC

NEGATIVE Rinnes

POSITIVE Test
(Normal pattern)

Patients time = longer

DCs time = longer

Webers

Place vibrating fork on vertex

NORMAL = equal loudness in BOTH ears

Rinnes

Eyes closed
Mask non-test ear
DC in front of patient
Strike & hold fork @ arms length until silent
Place fork on mastoid
Record time
When pt. cannot hear bring fork in front of ear
(Fork on mastoid = 30 sec, fork front of ear = 60 sec)

POSITIVE Rinne = normal findings

Schwabachs

Compare patients hearing to DCs

Mask other ear
Strike & hold fork at arms length until silent
Put fork on mastoid (record time)

Bings

Hold vibrating fork on mastoid

Occlude Canal by pushing against patients Tragus

No change
OR

Normal

Sound is LOUDER with occlusion

Sound softens with NO occlusion!

Louder with Tragus CLOSED

Softer with Tragus OPEN

NEGATIVE Test

POSITIVE Bing = normal findings

DDX Tests for Hearing Deficits (VESTIBULAR APPARATUS)

LABYRINTHITIS
-endolymphatichydrox: endolymph has water in it
-old Tx: aluminum hydroxide (draws fluid out of places it doesnt belong)
1. Rhomberg Test
a. Patient Position
Tight adduction of lower extremities
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POSITIVE BING
(Normal pattern)

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Arms at side
Close eyes
Caution patient may sway

2. Kobrak Test (cold/warm water stimulation) Nystagmus

Nystagmus is the finding that is expected. It should occur within 10-12 seconds, with the effects
lasting 2-3 minutes. The direction of the nystagmus is named for the quick component. If it is
less than 10 seconds = hyperactive. If it is greater than 12 seconds = hypoactive. If no reaction
= dead
Cold-water opposite side
Warm water same side
NOSE & PARANASAL SINUSES
EVALUATION (patients head in hyperextension so Dr. can see the Base of the Nose)
1. Check for Rhinorrhea (exudate from external nares)
See PAS diagrams page 33
If present stop examination and REFER OUT IMMEDIATELY!!
Triangle of Danger
If infection present in nose possibility of pushing it back into Cavernous Sinus
2. Look for symmetry of both EXTERNAL NARES
Symmetrical

Normal

pic
Asymmetrical
1. The SMALLER one is the NORMAL one
2. DILATED one is due to:
Obstruction of Nasal Passages to getting
air through!
So it is compensating by enlarging

3. Palpation
Palpate nasal ala to center
Assess patency of Fossa
Push RIGHT ala to septum
Ask patient to breathe w/mouth closed
Evaluate other side
ANATOMY
1. Nasal Vestibule
Has hair follicles
2. Mucocutaneous Junction
Location where crusts form (boogers)
3. Superior Turbinate
Superior cannot view

See PAS diagrams page 33

4. Middle Turbinate
Can see the Anterior tip of this
5. Inferior Turbinate!
Can see the Anterior tip of this
6. Nasal Septum
Rarely is the Septum PERPENDICULAR to the floor (except in newborns)

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7. Middle Nasal Meatus

Can see this
8. Hiatus Semi-lunaris
Depression deep into bone UNDER the Middle Nasal Meatus
Has Fronto-Nasal Duct which enters Frontal Sinus (drainage from high)
Opening into Maxillary Sinus (drainage from low)
The osteomeatal unit = the maxillary sinus and the openings to the ethmoid sinus
Normal = NO exudate should be seen!

INSTRUMENTATION
1. Protocol
Extend head push on tip of nose
Check for rhinnorhea
2. Look at the VESTIBULE for:
a. Folliculitis
Red, swollen with exudation
From nose picking
b. Furunculosis / Abscess
Multi-abscesses = furuncle
c. Crusts
Often in curved morphology
3. Look at Middle Meatus:
Should have NO evidence of Exudation
4. Advance speculum to view Medial & Lateral Wall
a. Mucous membrane (medial wall & other structures)
Should be shiny
b. Septum
1. NO abscesses or lesions

Normal

2. NO perforations (usually via CHRONIC low grade infections)

Tuberculin infections
Syphilis Chancres
Cocaine use
3. NO deviation
As long as the Septum does NOT encroach onto the Turbinates,
it is NOT DEVIATED!!
Even if it is not straight

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Deviated Septum

Kisselbaches Plexus

Septum encroaches onto the Turbinates

Site for nose bleed
It is where vessels ANASTAMOSE (at Littles Area)
Littles Area = blood supply to the septum
Superior branch: greater palatine artery.
Posterior branch: sphenopalantine artery
Inferior branch: anterior ethmoidal artery
Anterior branch: septal branch of superior labial artery
2 Types of Epistaxis
1. 90% of nose bleeds: Anterior bleed At Kisselbaches Plexus
2. Posterior bleed
3. causes: dryness, picking, aspirin abuse, TB, cocaine, syphyillis, gun
shot wound, HCl, fire, masturbation

Hematoma
c. Turbinates
Should be pink & moist (glistening)
1 2 mm space between the SEPTUM & TURBINATES
Middle nasal meatus should have no evidence of exudation!!

5. Remove speculum for sterilization

6. COLOR of MUCOSA
Red Mucus membrane

Infection

Blanched White

Allergies

Blue / Cyanotic

Vasomotor Disturbance (rhinitis)

7. Paranasal Sinuses
a. Frontal Sinus
Palpate and Percuss
NORMAL

No pain

Congested Sinus

No pain

Frontal Sinus Infection

Tenderness and Pain at Supra-orbital Notch

Trans-illuminate

Palpate Supra-orbital Notch (or Foramen) for PAIN!

1) Supra-orbital nerve branches into frontal sinus
2) Frontal Sinus infections = tender/pain at SON
3) Palpate SON & sinuses
THE SECOND PART OF THE SINUS EXAMINATION:

Trans-Illumination

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1. Use OTOSCOPE with the largest caliber speculum

2. Frontal Sinus
Push under bony ridge of supra-orbital margin
Light should illuminate sinus
NORMAL

Should see orange glow (do bilateral)

Abnormal (infection)

No glow

3. Maxillary Sinus
Palpate and percuss (between the SUPERIOR GINGIVA and INFERIOR ORBIT)
Push against the TEETH with a Tongue blade
Hyperextend head and open the mouth
Flash light onto MAXILLARY SINUS (from the outside of the sinus)
Orange illumination should come down from maxillary sinus
Look at hard palate for this glow
NORMAL

Should see orange glow (do bilateral)

Abnormal (infection)

No glow

Complications of sinus infections:

Osteomyelitis
Facial cellulitis
Meningitis abscess
Mucosal causing ocular displacement
Cacosmia: odor that really is not there. Imaginary.

Oropharyngeal Exam (2-part)

Oral examination
1. Upper & Lower Lip
May have scar
(Connecting upper lip to nose)

Angio-neurotic edema

Hare-lip or Cleft-lip deformity

MC associated w/cleft-palate
Corrected at birth

Allergic base
Episodic recurrences of swollen lips (marked deformity)

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Vesicles

Subgingiva Stomatitis at Corners of Mouth

Via HSV-I infection (probably at childhood)
90% of infections go clinically unrecognized!
When they heal, the viruses hide and come out later in times of
stress!
Causes of REACTIVATION:
Stress
Sunlight
Menses

Cracks/fissures & beginning

ulcerations

Found at the Corners of mouth

CAUSES:
1. Cheilosis
From marked riboflavin (B2) deficiency
2. Loose-fitting dentures in elderly
3. Yeast infection at the corners of the mouth
MOST COMMON!!

2. Vermillion Border of lip

Mucocele

Leukoplakia (benign)

Steel - blue Nodule (Benign lesion)

Signs and Symptoms:
1. MC on lower lip via chronic resting of pipe-stem
2. White patch on lips
3. Slightly raised
4. Always PRE-CANCEROUS
Develops into Squamous Cell carcinoma
Caused by: Pipe smoking for a long time

3. GINGIVA
Normal

Epelis

Gum Recession

Trench Mouth
Gingivitis

Moist & pink

Indicates osteomyelitis
Arises from alveolar periosteum
Seen between teeth emanating out of gum
Benign small fibrous tumor (Fibroma)
MC seen in pregnancy

Roots of teeth seen

Gum recession
Most commonly seen in dental immunes (probably due to high
acidity of saliva)
Aka Vincents Angina
Inflammation of gum tissue (as well as mouth)
MC in WWI

Inflammation of gum tissue due to INFECTION

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Pyorrhea

Gingivitis via pyogenic bacteria

Exudate seen

Gingival hyperplasia

Dentures
Dilantin therapy (older patients)
Leukemia

1. Solid blue wavy line

Lead intoxication

2. Pb sources
Designer mugs
Pb pipes
1. Stippled blue wavy line

Bismuth intoxication

2. Bismuth sources
Pepto-bismol
Peptic medications

4. BUCCAL MUCOSA / Oral Cavity

Need Tongue Depressor (good idea to keep wet)
Need pen light
Disposable glove
PROTOCOL:
1. Take tongue depressor & push cheek out
2. Look at buccal mucosa
Should be moist & pink
3. Identify opening of Stensons Duct
Drains parotid gland
Opens opposite 2nd molar
4. RULE OUT:
i) Edema
ii) Inflammation
iii) Infection and Drainage
iv) White lesions (Leukoplakia, Thrush, Reticulated lesions (Lichens planus)
FINDINGS IN BUCCAL MUCOSA
Fordyce Spots
(Geriatric patients)

Found in Older patients

Due to Mucus membrane atrophy
Creamy-yellow sebaceous glands (holocrine)
Normal finding

Kopliks Spots

Rubeola in young children

White spots

Leukoplakia

Signs and Symptoms:

1. White patch on lips
2. Slightly raised
3. Always PRE-CANCEROUS
Develops into Squamous Cell carcinoma
Caused by: Pipe smoking for a long time

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Reticulated White Spot

Lace-like (non-homogenous)
Seen in Lichen-planis patients

Thrush

Via C. albicans
Cottage-cheese appearance

White excavation with Red base (Canchre sore)

seen on gum, tongue, buccal mucosa
very painful
caused by: stress, new toothbrush, acidity

Aphthous Ulcer

5. TEETH
1) Remove dentures
2) Observe # of teeth (check into marked loss)
32 teeth total
Are teeth intact or loose run tongue blade over surface of teeth
Teeth are in good repair NOT a lot of plaque present
3) Observe # of fillings
a. Composition of fillings (important if strange sensations perceived)
Metal taste
Radio messages to teeth
Hutchinsons Triad

Syphilis
Upper notched incisors
8th nerve deafness
Interstitial keratitis
See PAS diagrams page 38

6. TONGUE
The Lingual tonsils are in the far back and lateral portions, and are not seen. There is a Foramen Cecum
(in the middle) that leads to the Thyroglossal Duct, to the Thyroid Gland. Longitudinal fissures of the
tongue indicate dehydration.
Normal Findings
Normal
(Gross movements)
No clinical significance!

Undulations

Geographic Tongue

Areas of tongue are:

Red & slick
Devoid of papillae
Week by week = random appearance of new areas

PATHOLOGIES:

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Fasiculations
Tic
Smooth Tongue
(Regular areas)
Hairy Tongue

Hairy Leukoplakia

Tongue Deviation

Whartons Duct
(at Ventrum of Tongue)

Abnormal finding
Portion of muscle spasms
Abnormal finding
Whole muscle spasm
ALL of tongue is RED, SLICK and DEVOID of Papillae!!
B12 deficiency
Fe deficiency

Via dirty deposits (tongue is NOT kept clean)

(Smoking, bad oral hygiene)

White horn-like projections (On sides of tongue)

AIDS related (marker), precursor for CA
Particularly see at the glossalpalantine arch aka Coffins area (far
back and lateral sides of tongue) where most cancers develop

CN XII
Tongue points to side of lesion

There is an ed chance of SALIVARY STASIS here because:

1. Horizontal plane of ducts
2. Tortuosity of the ducts
Prone to calcifications Salivary Calculus
Lingual nerve crosses 2x

Caviar Lesions
(at Ventrum of Tongue)

Plexus of veins caviar lesions

Strawberry tongue

Kawasaki Syndrome, Scarlet fever

Black tongue

from antibiotic use for fungal infection (Aspergillos niger)

Strength & ROM of Tongue

a. Strength
Push tongue to sides of cheek
Best: Use Tongue blade for resisted ROM
Muscle test = dart tongue in & out rapidly
b. ROM
Use tongue blade for resisted ROM
c. ROM / muscle test
Ask pt. to touch nose w/tongue

7. HARD PALATE
Exostoses

Torus Mandibularis

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Midline at:
LINGUAL side of mandible

(Redundant bone)

Midline of hard palate

Pharyngeal examination
1. Soft Palate
a. Phonation
Aahh
Palantine arches rise symmetrically

Normal

Uvula Deviation
(Asymmetric rising)

Not too loud or too soft or else it will yield FALSE POSITIVES!

Vagus nerve Innervation

Side of uvula deviation is CONTRALATERAL to lesion
Quinces Disease = infected uvula. Presents swollen

b. Tonsils determine presence or absence of the Tonsils

Absence

Tonsilar tissue

Tonsillectomy
Tends to regenerate
Partial = Tonsilar Tags
Full Regeneration
Quincys = tonsillitis. A peritonsilar abscess

Abnormalities in Tonsilar Location

Normal Tonsil

Draw a line down from the Posterior Tonsilar Pillar and Anterior
Tonsilar Pillar
Tonsils should not extend passed that IMAGINARY LINE!!

Palatine Tonsil +1

Partially extends outside pillar boundaries

Palatine Tonsil +2

way between boundary & uvula

Palatine Tonsil +3

Abuts LATERAL aspect of uvula

Palatine Tonsil +4

Bilateral approximation in midline

Tonsils = considered NOT enlarged unless found w/pathology

Pathologies
1) Tonsilitis
Injected (red)
Enlarged b/c swollen
Enlarged Crypts
White exudates
Quincys
2) Syphilitic Chancre (ulceration)
Can be anywhere in Oral Pharyngeal area, but Tonsils are a favorable spot for Spirochetes!
3) Cancer = an open lesion on the tonsil may be tonsil cancer
POSTERIOR PHARYNGEAL WALL
Tongue Blade
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To minimize Gag Reflex = use wet tongue blade
To keep tongue out of way = push down & pull forward

1. 2 types of Pharyngitis
1. Posterior wall pain = mildly injected
2. No evidence of edema
3. Studded w/bumps (Lymphatic hyperplasia)
In response to Viral infection!

Granular Pharyngitis (viral)

Follicular Pharyngitis (bacterial)

Greatly injected (VERY red!!)

Studded w/yellow creamy exudate
Marked Erythema VERY PAINFUL!!

2. Post-Nasal Drip
a. Soft palantine arches rise symmetrically
b. Palantine arches are present
c. Posterior pharyngeal wall without evidence of pharyngitis or post-nasal drip present
d. Signs and Symptoms
Will see a RED track where Nasal Exudate is dripping!
e. Causes:
Chronic Sinus Infection
Chronic Nasal Infection
2nd PART OF ORAL EXAMINATION: Use a RUBBER GLOVE!
1. Palpate floor of mouth via a Pincer move
2. Palpate sides of Tongue in same manner
Looking for Lumps and/or Bumps
Indicative of Cancer!
ANTERIOR NECK EXAMINATION
1) Thyroid Cartilage / Larynx
Should be symmetrical
Should NOT be prominent (displaced in a forward position)
2) Thyroid Gland
a) Normal = non-palpable
b) Palpable
In thin necks
If palpable, should feel like the Strap muscles
c) Bi-lobed lobes wrap around trachea
Isthmus crosses 2nd Tracheal Ring
d) Pyramidal Lobe (anatomical variant) a miniature lobe stemming superior from the isthmus
e) Right Lobe - Slightly larger than the Left Lobe
1) Superior pole = found as high as mid-lower 1/3 of thyroid cartilage
2) Inferior pole
Reaches as far as 5th or 6th tracheal ring
Hidden beneath SCM
3) a high lying thyroid is seen subtly on hyperextension of the neck. A low lying thyroid is inferiorly
displaced over the superior end of the manubrium which can be palpated.
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Technique of Thyroid Exam

1. Patient holds mouthful of H2O (dont swallow yet)
2. DC stands behind patient palpate in area of gland
3. Ask patient to flex forward & lateral flex toward side of examination
Fingers down on medial SCM pushing against trachea
Ask patient to swallow H2O
Inferior poles should move superior
Do bilaterally
Normal = non-palpable
Looking for bumps (isolated thyroid nodule)
4. Isolated Thyroid Nodule
Most are BENIGN!
Malignant = possible
Berrys sign = palpable tumor over the carotid. If the pulse is felt, it is benign. If not, then
it is malignant.
5. Enlarged Thyroid Gland Bosillated (multiple bumps)
Indicates metabolic change
Bruit = can be heard on auscultation (can hear at angle of jaw)
Thyromegaly not all necessarily anterior (can have substernal goiter)
Pempertons sign is possible. Results from a retrosternal goiter. Raise hands, and the
face flushes and patient may get giddy because of the lack of oxygen to the head.
Possibly faint.
f)

Trachea
Thyroid cartilage is symmetrical & not unduly prominent
Thyroid gland is non-palpable
Trachea is palpable in the midline

Check for midline position make sure it is CENTERED!

Fingers should fit between equal spaces between SCM and trachea (bilaterally)
Palpate through the Supra-manubrial notch
~ 80% Tracheal tugs are due to NORMAL VARIANTS
~ 20% are due to Pathology!
LATERAL NECK Vascular Evaluation

1. Carotid Evaluation
Palpate LOW in neck (but listen HIGH), medial to SCM
Stay away from bifurcation Carotid receptors (at angle of jaw)
1) Rate
2) Rhythm
3) Symmetry
Rate & rhythm are symmetrical
Carotid arteries are compressible
2. Check for bruits (finding of atherosclerosis) 3 possibilities
Auscultate posterior to angle of jaw, using bell and taking a deep breath and hold it
Bruit proximal to bifurcation
a. Carotid Occlusive Arterial Disease
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b. Thyromegaly
Can cause bruit at angle of jaw
If no bruit at thyroid then bruit at jaw is from Atherosclerosis so check the friggin thyroid
c. Aortic Stenosis
RIGHT Peri-sternal border, 2nd Intercostal space will hear bruits! murmurs
d. Distended Neck Veins from Congestive Heart Failure
3. Lymphadenopathy
1) Sub-mental
Area of chin
2) Sub-mandibular
Middle of mandible
3) Tonsilar
Posterior to Ramus of jaw
4) Jugular chain
Anterior to SCM
5) Anterior cervical chain
Posterior Cervical Triangle
Posterior border of SCM
6) Deep cervical chain = deep to SCM
7) Posterior cervical chain / Pre-Trapezius Chain
Anterior to Trapezius
8) Sub-occipital
ABNORMALITIES:
Soft painful nodule

Infection

Hard, NON-painful

Metastatic Disease

Hard nodule

Calcified Lymph node from an old infection

4. C-spine evaluation
Palpate over SPs looking for tenderness
Check for ROM of neck in all positions

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