Study Questions for Physical Diagnosis Exam #3 Dr.

Mannello
Page references are in the 8
th
Edition of Bates

Ear Examination

1. List reasons for performing an ear examination.
a. Part of a complete physical exam
b. Patient complains of hearing loss
c. Patient experiencing vertigo and dizziness
d. Tinnitus (ringing of the ear)
e. Otorrhea (discharge from the ear)
f. Otalgia (ear pain)
g. Pruritis (itching)

2. What are the two types of hearing loss? What differentiates them? Page 196-
197
a. Sensorineural deafness hearing impairment due to lesions or dysfunction
of the inner ear, the cochlea or the retrocochlear nerve tracts or along the
auditory pathway to the brainstem, as opposed to conductive deafness.
b. Conductive deafness hearing impairment caused by interference with
sound or vibratory energy in the external canal, middle ear, or ossicles
which impairs the conduction of sound to the inner ear
The Weber and Rinne tests are used to differentiate the two types of
hearing loss.
Weber (placing a vibrating tuning fork on the skull midline) will be positive
for CONDUCTIVE hearing loss if lateralization is to the affected side.
SENSORINEURAL hearing loss is present if lateralization occurs to the
good ear.

3. Provide causes for hearing loss in children and adults.
Conductive Deafness Sensorineural Deafness
Children:
Congenital Congenital
Acute Otitis Media Mumps Labyrinthitis
Chronic Otitis Media Maternal Rubella during
Cerum en Buildup 1
st
Trimester
Trauma Birth Trauma
Congenital Syphilis
Adults:
Serous Otitis Media Delayed Onset Congenital
Chronic Otitis Media Menieres Disease
Otosclerosis Ototoxic Drugs
External Otitis Viral Labyrinthitis
Cerumen Buildup Acoustic Neuroma
Cholesteatoma Presbycussis (age-related
Blocked Eustachian Tube deafness)
Viral Myringitis

4. Provide causes for vertigo.
Vertigo refers to the false perception that either the patient or the
environment is spinning or rotating. These sensations primarily point to a
problem in the inner ear, the cochlear nerve, or its central connections to
the brain. (Table 5-2, page 174)
Info from Assessment of Cervicogenic Vertigo 3 theories on the
etiology of cervical vertigo
1. Cervical sympathetic irritation
2. Abnormal neck reflex
3. Mechanical compression or stenosis of the vertebral artery
If it comes from: Type of Vertigo:
Vestibular Nerve Central Vertigo
Cervical Spine Cervical Vertigo
Inflammatory Process Transient Vertigo
Tumor Chronic Vertigo

5. What is tinnitus? What might cause tinnitus?
a. It is noise in the ear (ringing, whistling, booming, etc.) has no
external stimulus; can involve one or both ears; can accompany
hearing loss; increases in frequency with age.
b. Causes can include:
1. Menieres Disease
2. Drug toxicity as from aminoglycosides or alcohol
3. Tumor, pressing on CN VIII
c. Handout Common Causes of Tinnitus
Location Pulsatile/Clicking Nonpulsatile
External Ear External Otitis Cerumen
Bullous Myringitis Tympanic Membrane
Perforation
Foreign Body Foreign Body

Middle Ear Otitis Media Otosclerosis
Vascular Anomalies Serous Otitis
Neoplasm
Eustachian Tube Dysfunction

Inner Ear Vascular Anomalies Cochlear Otosclerosis
Menieres Disease
Labyrinthitis
Noise Trauma
Drug Toxicity
Presbycusis
CNS Vascular Anomalies Syphilis
Hypertension Degenerative Disease
Cerebral Atherosclerosis

6. What is the clinical triad for Menieres syndrome?
It is characterized clinically by vertigo, nausea, vomiting, tinnitus and
progressive deafness (aka auditory vertigo; endolymphatic hydrops;
labyrinthine vertigo; Menieres syndrome)
Page 139 says tinnitus, hearing loss and vertigo = Menieres disease.
Handout on Menieres Syndrome triad is episodic vertigo, fluctuating
sensorineural hearing loss and tinnitus (often severe; usually unilateral)

7. List causes for otalgia.
Otalgia refers to ear pain. The pain can be referred from teeth, pharynx
or cervical spine. It can be due to inflammation, trauma, or neoplasia
anywhere along the course of CN V, VII, VIII, IX, X or cervical nerves C2
or C3. Lastly, external otitis or otitis media can be causes of pain.

8. Discuss causes for nodules in and around the ear.
Table 5-17, Page 192-193. Eight Different Types or Causes:
1. Chondrodermatitis Helicis starts as a painful, tender papule
that is usually on the helix, but may be on the antihelix.
Usually seen as a single lesion, but can be more. Reddening
may occur. Older men usually affected. Biopsy needed to
distinguish from carcinoma.
2. Cutaneous Cyst a sebaceous cyst usually behind the ear. It is
a benign, closed, firm sac which forms a dome shape. A dark
dot may be visible on its surface. Histologically, one of two
diagnoses is likely:
a. Epidermoid Cyst common on face and neck
b. Pilar (Trichilemmal) Cyst common on scalp
3. Squamous Cell Carcinoma most common in light-skinned
people who are frequently exposed to the sun. Commonly
seen on helix with a raised, crusted border. Spreads locally. It
can metastasize to lymph nodes. Biopsy will confirm diagnosis.
4. Basal Cell Carcinoma raised nodule shows a lustrous surface
and telangiectatic vessels. Ulceration may occur in the absence
of treatment. Also, often seen in people with light skin.
5. Tophi deposit of uric acid crystals typical of gout. Appear as
hard nodules in helix or antihelix. May discharge chalky white
crystals through skin.
6. Rheumatoid Nodules found on patients with chronic arthritis.
DO NOT mistake these for tophi. These nodules will usually be
present elsewhere (i.e. hands, knees)
7. Keliod a firm, nodular, hypertrophic mass of scar tissue that
extends beyond the area of injury. Most common on the
shoulders and upper chest. Dark skinned people most likely to
develop these.
8. Lepromatour Leprosy the ear is one site for this manifestation
of Hansens Disease (result of infection from mycobacterium
leprae). Seen as multiple papules and nodules on auricles.
Often, lesions are typically found on other parts of the body.

9. How would the examination procedure differ when evaluating the inner ear of
a child vs. an adult?
The inner ear is quite sensitive. It may be necessary to restrain the child
carefully. Place the patient supine, arms extended and close to the side
of the head. Carefully insert the otoscope and manipulate the auricle with
the opposite hand. Buffer the arm holding the otoscope to avoid contact
if the child makes any sudden quick movements.
My notes say for an adult pull up and posterior and for a child pull down
and posterior (until about age 4 or 5 when the ear canal starts to
change). The Welch-Allyn booklet says to retract the pinna horizontally
backwards.

10. What are the features of the normal tympanic membrane? (Page 194)
1. Should appear intact
2. Smooth contour
3. Translucent and pearly gray
4. No perforations
5. Look for hand of malleolus
6. Cone of light should be visible

11. How is patency of the eustachian tube determined?
Normal tympanic membrane moves in and out with changes in pressure
within the external canal. Have patient hold their nose and swallow.

12. Discuss the Weber and Rinne hearing test. What can be determined by
lateralization and air vs. bone conduction?
Weber Test stimulates inner ear directly
Purpose tests lateralization
Uses 512 Hz tuning fork
Places vibrating tuning fork on top, center of head
Ask patient Can you hear this equally in both ears?
Conductive hearing loss lateralizes to impaired ear
Sensorineural hearing loss lateralizes to good ear
Rinne Test
Purpose compares air conduction to bone conduction
Uses 512 Hz tuing fork
Places vibrating tuing fork on one mastoid process (stimulates inner
ear directly)
Ask patient to tell doctor when they cant hear it anymore
Then place tuning fork by patients ear (same side as mastoid
process tested)
Pathway external ear ! middle ear ! inner ear
Then ask patient Can you hear it now?
Repeat on other side
Conduction loss BC > AC or BC = AC (negative Rinne test)
Sensorineural loss AC > BC (positive Rinne test)

13. List the signs/symptoms for otitis externa, bacterial and secretory otitis media
- Handout
Otitis Externa
Initial Symptoms Itching in ear canal
Pain Intense with movement of pinna, chewing
Discharge Watery, then purulent and tick, mixed with pus and
epithelial cells; musty, foul-smelling
Hearing Conductive loss caused by exudate and swelling of ear
canal
Inspection Canal is red, edematous; tympanic membrane
obscured
Bacterial Otitis Media
Initial Symptoms Fever, feeling of blockage
Pain Deep-seated earache
Discharge Only if tympanic membrane ruptures; foul-smelling
Hearing Conductive loss as middle ear fills with pus
Inspection Tympanic membrane is red, thickened, bulging
Secretory Otitis Media
Initial Symptoms Sticking or cracking sound on yawning or
swallowing
Pain Uncommon feeling of fullness
Discharge Uncommon
Hearing Conductive loss as middle ear fills with fluid
Inspection Tympanic membrane is retracted, yellowish; air
bubbles may be present

14. How would a perforation look with an otoscopic exam? Welch Allyn Booklet,
Page 23
Central perforation of the tympanic membrane perforation of the pars
tensa of the tympanic membrane can result from infection or trauma. In
this case the large central perforation resulted from repeated middle ear
infections. When a large perforation heals, the middle fibrous layer of the
tympanic membrane remains deficient so that a thin semi-transparent
pseudomembrane resembling an open perforation may be seen. Gentle
use of the pneumatic otoscope will, however, demonstrate that the drum
is intact. This thinned segment of a healed tympanic membrane lacks the
strength of a normal drum and forceful syringing may result in
reperforation.

Nose and Paranasal Sinuses Examination

15. What are the reasons for performing this exam and differentials for these?
a. Complete physical exam
b. Obstruction or blockage
c. Discharge
d. Bleeding
e. Facial pain in sinus area

16. Discuss causes for obstruction and differentials for various types of discharge.
a. Rhinitis stuffy nose, congestion of nasal mucous; symptoms include
obstruction, sneezing, and clear, watery discharge.
b. Thin and watery viral or allergic condition
c. Thick and purulent bacterial infection
d. Bloody neoplasm, trauma or fungal infection
e. Foul-smelling foreign bodies, chronic sinusitis, malignant tumor
f. Epitaxis bloody nose (nose picking, chronic sinusitis, malignancy in
the sinuses, cocaine abuse)
g. CSF clear and watery that increases with bending of head

17. What is noted during the examination of the vestibule? The nasal septum?
Tenderness of the nasal tip suggests local infection (folliculitis)
Color of the nasal mucosa is deep pink or dull red and moist
Deeper diffuse redness and swelling indicates inflammatory conditions
(non-allergic reaction)
Localized deeper redness furuncle
Pale or bluish allergy-associated exudate
Deviation of septum trauma
Polyps allergies of asthma
Turbinates (inferior and middle) same color as the area
HANDOUT
Furuncle of the nose Furuncles are quite common in the nasal vestibule.
The area is tender and may be red and swollen; then a typical pustule
forms. Gentle examination is mandatory. Avoid manipulation since this
may spread the infection.
Acute rhinitis the common cold The nasal mucosa is red and swollen.
Nasal discharge, which is at first watery and copious, becomes thick and
mucopurulent.
Allergic rhinitis The nasal mucosa is swollen, pale, boggy, and usually
gray. A dull red or bluish color may also be seen. Similar findings are
seen in some patients with non-allergic vasomotor rhinitis.
Nasal polyps Nasal polyps may develop in patients with allergic rhinitis.
They are usually found in the middle meatus, where they appear as
gelatinous or soft, pale gray structures. Unlike the turbinates, for which
they are sometimes mistaken, they are mobile.
Septal deviation some degree of septal deviation is common in most
adults. Illustrated on the handout is one of the most frequent types
displacement of the nose. Septal deviation may produce nasal obstruction
but the turbinates often accommodate to the asymmetry.

18. How are the turbinates clinically differentiated from a polyp?
Both are the same color but polyps move easily, whereas turbinates are
fixed.

19. How does acute rhinitis differ from allergic rhinitis?
a. Acute rhinitis nasal mucosa is red and swollen; nasal discharge is
first watery and copious, becomes thick and mucopurulent
b. Allergic rhinitis mucosa swollen; pale, baggy, gray; a dull red or
bluish color is seen; similar to nonallergic vasomotor rhinitis.

20. What are the four cranial/facial sinuses and how are they evaluated? Which
of the four paranasal sinuses can be examined clinically?
a. Maxillary light lateral to nose, illuminate the light down into the mouth
(open)
b. Frontal light on meial aspect of the supraorbital rim and look for a dim
red glow above the eyebrow
c. Ethmoid evaluated by x-ray
d. Sphenoid evaluated by x-ray

21. List the location of pain and clinical signs/symptoms of sinus disease.
HANDOUT
a. Maxillary
Local pain behind eye, cheek, nose, upper teeth, upper lip
Referred pain teeth, retrobulbar
b. Ethmoid
Local pain periorbital, retronasal, retrobulbar
Referred pain occipital, upper cervicals
c. Frontal
Local pain supraorbital, frontal
Referred pain bitemporal, occipital headache
Diseases
1. Maxillary diplopia, proptosis, epiphora, obstruction, rhinorrhea,
epitaxis, loosening of teeth
2. Ethmoid orbit swelling, obstruction, rhinorrhea, proptosis, diplopia
3. Frontal obstruction, rhinorrhea, tenderness, pus (middle meatus),
meningitis

Oral Cavitiy and Throat Examination

22. What are some of the reasons for performing an exam of the oral cavity or
throat? What are some differentials for these symptoms?
Part of a complete physical exam
Pain location, OPPQRST
Ulceration, bleeding, mass
Halitosis bad breath

23. What structures are evaluated in this exam? What are the normal findings?
(Page 160-162)
Lips observe color and moisture, note any lumps, ulcers, cracking or
scaliness
Teeth and gums color of gums is normally pink; patchy brownness may be
present, especially but not exclusively in black people; inspect the gum
margins and the interdental papillae for swelling or ulceration; inspect the
teeth for missing, discoloration, misshapen, abnormal positioning and/or
looseness.
Buccal mucosa inspect for color, ulcers, white patches and nodules
Tongue observe color and texture of the dorsum; inspect for symmetry
(tests CN XII); inspect the underside of the tongue and floor of the mouth,
palpate and look for any white or red areas, nodules or ulcerations
Hard palate observe color and architecture
Soft palate, uvula, tonsils, pharynx, parotid duct note color and symmetry;
look for exudate, swelling, ulcerations or tonsilar enlargements; palpate for
tenderness.

24. Discuss some abnormalities found on or around:
Lips Page 198-199 Herpes Simplex (Cold Sore, Fever Blister); Angular
Cheilitis; Actinic Cheilitis; Carcinoma of the Lip; Angioedema; Chancre of
Syphilis; Hereditary Hemorrhagic Telangiectasia; Peutz-Jeghers Syndrome

The buccal mucosa and hard palate Page 200-201 Pharyngitis; Large
Normal Tonsils; Exudative Tonsilitis; Diphtheria; Torus Palatinus; Thrush
on the Palate (Candidiasis); Kaposis Sarcoma in AIDS; Aphthous ulcer
(Canker Sore), Fordyce Spots

Tongue Page 206-207 Fissured; Hairy; Geographic; Smooth (Atrophic
Glossitis); Hairy Leukoplakia; Candidiasis; Varicose Veins; Aphthous Ulcer
(Canker Sore), Leukoplakia; Mucous Patches of Syphilis; Tori
Mandibulares; Carcinoma Floor of the Mouth

Gums and teeth Page 203-205 Marginal Gingivitis; Chronic Gingivitus;
Periodontitis; Acute Necrotizinng Ulcerative Gingivitis; Gingival
Enlargement (Gingival Hyperplasia); Head or Bismuth Line; Melanin
Pigmentation; Dental Caries; Hutchinsons Teeth; Abrasion of Teeth with
Notching; Pregnancy Tumor (Epulis, Pyogenic Granuloma); Kaposis
Sarcoma in AIDS; Lead Line; Attrition of Teeth; Recession of Gums;
Erosion of Teeth

Pharynx Page 200-202 Acute Pharyngitis; Viral Pharyngitis;
Streptococcal Pharyngitis; Acute Follicular Tonsillitis; Submandibular
Cellulitis; Acute Membranous Pharyngitis; Peritonsilar Abscess; Acute
Rheumatic Fever; Large Normal Tonsils; Exudative Tonsillitis; Diphtheria;
Torus Palatinus; Thrush on the Palate (Candidiasis); Kaposis Sarcoma in
AIDS; Kopliks Spots; Fordyce Spots (Fordyce Granules); Petechiae;
Leukoplakia

25. List etiologies of acute pharyngitis. HANDOUT
a. Viral infection
b. Bacterial infection
c. Fungal infection
d. Trauma
e. Allergy
f. Foreign body
g. Neoplasm (benign or malignant)

26. What are some likely findings associated with acute follicular tonsillitis,
streptococcal pharyngitis and pharyngitis in mononucleosis? HANDOUTS
a. Acute Follicular Tonsillitis The most common offending organisms are
beta-hemollytic stretococci, pneumococci, Haemophilus influenza and
any of a myriad of respiraoty viruses. The most common findings are:
1. Enlarged, inflamed palatine tonsils
2. White, yellow or grayish exudates obstructing tnsillar crypts
3. Erythema and edema of the uvula
4. Coated tongue
b. Streptococcal paryngitis Group A beta-hemolytic streptococci prompt
the greatest concern because of their non-suppurative complications.
The most common findings are:
1. Reddened throat without exudate
2. Redness and vascularity of the pillars and uvula are mild to
moderate
3. Patient would usually complain of a sore throat
c. Pharyngitis in infectious mononucleosis Posterior cervical
lymphadenitis in a patient under age 25 with acute pharyngitis
suggests infectious mononucleosis. Other possible signs include:
1. Eyelid edema
2. Mild icterus (jaundice)
3. Fever
4. Splenomegaly
5. Generalized lymphadenopathy
6. Exudative tonsillitis
7. Palatine petechiae (minute hemorrhagic spots, of pinpoint to
pinhead size, in the skin, which are not blanched by discopy)

27. What are some of the complications of streptococcal pharyngitis? HANDOUT
a. Non-suppurative (non-pus forming) complications include:
1. Acute rheumatic fever
2. Acute glomerulonephritis
b. Suppurative (forms pus) complications include:
1. Meningitis
2. Sinusitis
3. Mastoiditis
4. Retroparyngeal Abscess
5. Peritonsillar Abscess
6. Ludwigs Angina
7. Arthritis
8. Suppurative Cervical Lymphadenitis
9. Pneumonitis
10. Mediastinitis
11. Lung Abscess
12. Otitis Media
13. Acute Bacterial Endocarditis

28. What are Ludwigs Angina, Quinsys Abscess, and Vincents Angina?
HANDOUTS
a. Ludwigs Angina cellulitis, usually of odontogenic origin, bilaterally
involving the submandibular, sublingual and submental spaces,
resulting in painful swelling of the floor of the mouth, elecation of the
tongue, dysphasia, dysphonia and (at times) compromise of the
airway.
b. Quinsys Abscess (aka peritonsillar abscess) extension of tonsillar
infection beyond the capsule with abscess formation usually above and
behind the tonsil.
c. Vincents Angina an ulcerative infection of the oral soft tissues
including the tonsils and pharynx caused by fusiform and spirochetal
organisms; it is usually associated with necrotizing ulcerative gingivitis
and may progress to noma. Death from suffocation or sepsis may
occur.

Eye Examination

29. List reasons for performing an eye exam and differentials for these reasons.
To check for
1. Visual acuity
2. Visual fields by confrontation
3. Position and alignment of the eyes
4. Quantity and distribution of the eyebrows
5. Eyelids
6. Lacrimal apparatus
7. Conjunctiva and sclera
8. Cornea, lens, iris and pupils
9. Extraocular muscles and function of CN III, IV and VI
10. Opthalmoscopic findings

30. What are some of the common visual eye symptoms and the causes?
HANDOUT
1. Loss of vision optic neuritis, detached retina, retinal hemorrhage,
central retinal vascular occlusion, central nervous system disease
2. Spots no pathological significance (may precede a retinal
detachment or may be associated with fertility drugs)
3. Flashes migraine, retinal detachment, posterior vitreous detachment
4. Loss of visual field or presence of shadows or curtains retinal
detachment, retinal hemorrhage
5. Glare, photophobia iritis (inflammation of the iris), meningitis
6. Distortion of vision retinal detachment, macular edema
7. Difficulty seeing in dim light myopia, Vitamin A deficiency, retinal
degeneration
8. Colored haloes around lights acute narrow angle glaucoma, opacities
in lens or cornea
9. Colored vision changes cataracts, drugs (digitalis increases yellow
vision)
10. Double vision extraocular muscle paresis or paralysis
31. Discuss some of the common nonvisual painful and painless symptoms with
associated disease states. HANDOUT (Symptom/cause)
a. Painful
1. Foreign body sensation foreign body, corneal abrasion
2. Burning uncorrected refractive error, conjunctivitis, Sjogrens
syndrome
3. Throbbing, aching acute iritis, sinusitis
4. Tenderness lid inflammation, conjunctivitis, iritis
5. Headache refractive errors, migraine, sinusitis
6. Drawing sensation unorrected refractive errors
b. Painless
1. Itching dry eyes, eye fatigue, allergies
2. Tearing - emotional states, hypersecretion of tears, blockage of
drainage
3. Dryness Sjogrens syndrome, decreased secretion as a result of
aging
4. Sandiness, grittiness conjunctivitis
5. Fullness of eyes proptosis (bulging of the eyeball), aging changes
in the lids
6. Twitching fibrillation of orbicularis oculi
7. Eyelid heaviness fatigue, lid edema
8. Dizziness refractive error, cerebellar disease, vestibular disease
8. Blinking local irritation, facial tic
9. Lids sticking together inflammatory disease of lids or conjunctivae

32. Provide a differential diagnosis and distinguishing features for red eye.
Table 5-7, Page 179

33. Discuss some of the abnormal inspection findings around and in the eye, the
cornea and lens, iris, and the pupils. Pages 177-181
1. Eyelids ptosis, retracted lid, exophthalmos, epicanthus, ectropion,
entropion, periorbital edema, herniated fat, pinguecula, sty (acute
hordeolum), chalazion, episcleritis, inflammation of the lacrimal sac
(dacryocystitis), xanthelasma
2. Red eyes (above table)
3. Cornea and Lens corneal arcus, corneal scar, pterygium, cataracts
(nuclear and peripheral)
4. Pupils unequal pupils (anisocoria), tonic pupil (Adies pupil),
Oculomotor Nerve (CN III) paralysis, Horners syndrome, equal pupils
and one blind eye, small irregular pupils (miosis = constriction of
pupils; mydriasis = dilation)
5. Iris if the iris bows abnormally far forward, it forms a very narrow
angle with the cornea, casts a crescent-shaped shadow on
examination, increases the risk of acute narrow-angle glaucoma.

34. How and why do we evaluate the anterior chamber of the eye?
The anterior chamber is evaluated by visual inspection of the cornea with
attention focused on opacities of the cornea. Further evaluation is
performed via opthalmoscopy. The anterior chamber, along with the
posterior chamber, contain aqueous humor which drains via the canal of
Schlemm. This circulatory system helps control the pressure inside the
eye.

35. What should happen with the light reflex (direct and consensual response)
and discuss abnormalities of the afferent vs. efferent fibers.
Direct/Consensual Response
Light in the eye should cause the pupil to constrict (direct) and the other
eye will also constrict (consensual)
Lesion of afferent part of the reflex (in eye that light is shone in) = a (-)
direct and a (-) indirect response (neither eye will constrict)
Lesion of efferent part of the reflex (in eye that light is shone in) = a (-)
direct and a (+) indirect response (eye that light is shone is wont
constrict, the other eye will constrict)
This will not work if there are problems other than afferent and efferent
lesions (such as blindness, iriditis, glaucoma, etc.) and the test should be
done in normal room light.

36. What is the accommodation response? Near reaction: Ask the patient to look
at a distant object then put an object about 10 cm from the bridge of the nose
Eyes should converge
Pupils should constrict light waves to thickest part of the lens
Lens should accommodates
Afferent impulses relative to pupillary response are in affect also
Involves:
a. pupillary constriction
b. eye convergence
c. lens accomodation

37. Discuss visual acuity testing. Page 144-145
Distant - Snellen eye chart patient 20 feet from chart, with glasses if
they wear them. Cover one eye with a card, read the smallest line
possible. It is recorded as a fraction: 20/30 the first number indicates
the distance the patient is from the chart; the second indicates the
distance the normal eye can read that line of letters. The larger the
second number, the worse the vision.
Near - Rosenbaum Chart held 14 from center of the nose also has a
distance equivalents on it. Has numbers, Es or Xs and Os.
Recording: 2 methods
1. The last line with 50% correct
2. The entire line must be correct, or the vast majority correct with
notation (20/24 1 (missed one) 20/20 +1 correct from 20/15
vision)

38. How are the visual fields tested? List some visual field defects and findings.
(Page 145, 176, HANDOUT)
They are checked by confrontation and if further testing is indicated, the
Dr. and the patient each cover one eye at a time and the Dr. moves their
fingers into the visual field.
Lesions/Defects from table 5-4
1. Horizontal Defect occlusion of a branch of the central retinal artery
may cause a horizontal (altitudinal) defect. Occlusion of the superior
branch of this artery results in a lower field defect (see diagrams in
book).
2. Blind Right Eye (Right Optic Nerve) a lesion of the optic nerve, and
of course of the eye itself, produces unilateral blindness.
3. Bitemporal Hemianopsia (Optic Chiasm) a lesions at the optic chiasm
may involve only the fibers that are crossing over to the oposite side.
Since these fibers originate in the nasal half of each retina, visual loss
involves the temporal half of each field.
4. Left Homonymous Hemianopsia (Right Optic Tract) a lesion of the
optic tract interrupts fibers originating on the same side of both eyes.
Visual loss in the eyes is therefore similar (homonymous) and involves
half of each field (hemianopsia).
5. Homonymous Left Superior Quadrantic Defect (Right Optic Radiation,
Partial) a partial lesion of the optic radiation may involve only a
portion of the nerve fibers, producing, for example, a homonymous
quadrantic defect.
6. Left Homonymous Hemianopsia (Right Optic Radiation) a complete
interruption of fibers in the optic radiation produces a visual defect
similar to that produced by a lesions of the optic tract.

39. How are the extraocular muscles tested and what cranial nerves are
involved? HANDOUT
They are tested by performing the cardinal gaze test moving an object
in an H pattern slowly in front of the patient.
Medial rectus adduction (eye moves nasally) CN III (Oculomotor)
Lateral rectus abduction (eye moves temporally away from the nose)
CN VI (Abducens)
Inferior rectus depression (eye moves down); extorsion (the 12 oclock
position on the cornea rotates nasally median axis); adduction CN III
Superior rectus elevation (eye moves up); intorsion (the 12 oclock
position on the cornea rotates nasally median axis); adduction CN III
Superior oblique depression, intorsion, abduction CN IV (Troclear)
Inferior oblique elecation, extorsion, abduction CN III
Paretic Muscle (weak) Direction Eye Wont Move
Medial rectus Nasal
Inferior Oblique Up and nasal
Superior Oblique Down and nasal
Lateral Rectus Temporal
Superior Rectus Up and temporal
Inferior Rectus Down and temporal

40. What is strabismus (paralytic vs. nonparalytic)? Discuss testing and findings.
Page 182
Strabismus crossed eyes; heterotropia; heterotropy; squint; a manifest
lack of parallelism of the visual axes of the eyes.
a. Paralytic strabismus (incomitant strabismus); strabismus due to
weakness or adhesion of ocular muscles deviation varies
depending on the direction of gaze.
b. Nonparalytic strabismus; caused by imbalance in ocular muscle tone;
it has many causes, may be hereditary, and usually appears early in
childhood deviation is constant in all directions of gaze.
Causes:
a. Paralytic - usually weakness or paralysis of one or more extraocular
muscles.
b. Nonparalytic an imbalance in ocular muscle tone, may be hereditary,
usually appears in early childhood. Classified according to direction
Convergent Strabismus (esotropia) and Divergent Strabismus
(exotropia)
SEE TABLE FOR TEST PROCEDURES/RESULTS

41. What is nystagmus?
Nystagmus ocular ataxis; rhythmical oscillation of the eyeballs, either
pendular or jerky.

42. What structures are visualized in an ophthalmoscopic exam?
1. Optic disc
2. Blood vessels
3. Macula and fovea centralis
4. Background of retina
5. Physiological cup

43. How should these structures appear normally?
Optic discs 1.5 2.0 mm in diameter, round and pale pink with sharp
margins.
Blood vessels arterioles are light red, smaller and brighter; veins are
dark red, larger and pale
Macula avascular, yellowish, 1 disc diameter in size
Fovea centralis red, pinpoint reflective center
Physiological cup yellowish white, less than ! diameter of optic disc

44. How does the doctor accommodate for myopia and hyperopia regarding
diopters?
a. Myopia near-sightedness prescribe negative diopters
b. Hyperopia far-sightedness prescribe positive diopters

45. How does the normal optic disc and physiologic cup appear? Discuss
abnormal findings or causes of blurring of margins. Page 183-184
Normal optic disc is 1.5 2.0 mm in diameter, round and pale pink with
sharp margins, vessels are tiny. The physiological cup is located centrally
(or a little temporally). It be obvious or not. Size is usually less than half
of the disc.
Optic Atrophy death of optic nerve fibers leads to loss of the tiny disc
vessels. It appears white and the disc vessels are absent.
Papilledema venous stasis leads to engorgement and swelling. It is pink
and hyperemic. The disc vessels are more visible, more numerous and
curve of the borders of the disc. The disc is swollen with blurred margins
and the cup isnt visible.
Glaucomatous Cupping increased pressure within the eye leads to
increased cupping (backward depression of the disc) and atrophy. The
base of the enlarged cup is pale and it occupies more than half of the
discs diameter. The vessels sink in and under it, and may be displaced
nasally.

46. Discuss features that would differentiate arterioles and veins. Page 154
Arteries are light red, smaller (2/3 to 4/5 the diameter of veins) and the
light reflection is bright.
Veins are dark red, larger, and the light reflection is inconspicuous or
absent.

47. Discuss abnormal findings: Changes in size, color, or light reflexes.
HANDOUT and Page 185
Arteriolosclerosis (arteriolosclerotic retinopathy)
Arteriolar light reflex
Normal fine yellow line, red blood column
Grade I Broadened yellow line, red blood column
Grade II Broad yellow line, copper wire, blood column
not visible
Grade III Broad white line, silver wire, blood column not
visible
Grade IV Fibrous cords, blood column not visible
AV crossing defects (arteriolar length and tortuosity increase with
severity)
Normal None
Grade I Mild depression of vein
Grade II Depression or humping of vein
Grade III Right-angle deviation, taperiong, and
disappearance of vein under arteriole, distal dilatation of
vein
Grade IV Same as Grade III
Hypertension
General Narrowing AV Ratio (this is the ratio of arteriolar to venous
diameters)
Normal 3:4
Grade I 1:2
Grade II 1:3
Grade III 1:4
Grade IV Fine, fibrous cords
Focal spasm (the ratio of diameters of region of spasm to proximal
arteriole)
Normal and Grade I 1:1
Grade II 2:3
Grade III 1:3
Grade IV Obliteration of distal flow
Hemorrhages
Normal, Grade I and Grade II not present
Grade III and IV present
Exudates
Normal, Grade I, and Grade II not present
Grade III and IV present
Papilledema
Normal, Grade I, Grade II, Grade III not present
Grade IV present

48. Note the features of the Keith, Wagner, Barker (KWB) classification for HTN.
HANDOUT on Classification of hypertensive and arteriolosclerotic
retinopathy (all the info in #47)

49. What are the changes with macular degeneration?
***********?????????????**************

50. Discuss some abnormal findings of the fundus (hemorrhages and light
colored spots) and the significance of these. Page 186-187 and HANDOUT
Light colored lesions
1. Cotton-wool spots
a. Etiology hypertension, diabetic retinopathy, AIDS, lupus
erythematosis, dermatomyositis, papilledema
b. Border fuzzy
c. Shape irregular
d. Patterns variable
e. Comments caused by an ischemic infract of the nerve
fiber later of the reina. Obscures retinal blood vessels.
Usually several in number
2. Fatty exudates
a. Etiology diabetes mellitus, retinal venous occlusion,
hypertensive retinopathy
b. Border well definded
c. Shape small, irregular
d. Patterns often clustered I circles or stars
e. Comments in deep retinal layer
3. Drusen
a. Etiology normal with aging
b. Border well defined, nonpigmented
c. Shape round, well circumscribed
d. Patterns variable, symmetrical in both eyes
e. Comments often confused with fatty exudates, deep to
retinal blood vessels
4. Chorioretinitis
a. Etiology toxoplsmosis, sarcoidosis
b. Border often large with ragged edge, heavily pigmented
c. Shape very variable
d. Patterns variable
e. Comments acute with white exudate, healed lesion with
pigmented scar

Hemorrhages
1. Superficial Retinal Hemorrhages - small linear, flame-shaped, red
streaks in the fundi; shaped by the superficial bundles of nerve
fibers that radiate from the optic disc (see page 186); sometimes
occur in clusters and simulate a larger hemorrhage but the linear
streaking at the edges shows the true nature; seen in severe
hypertension, papilledema and occlusion of the retinal vein, and
other conditions.
2. Deep Retinal Hemorrhages small, rounded, slightly irregular red
spots that are sometimes called dot or blot hemorrhages; they
occur in a deeper layer of the retina than flame-shaped
hemorrhages; common cause is diabetes mellitis.
3. Preretinal Hemorrhage aka subhyaloid hemorrhage develops
when blood escapes into the potential space between retina and
vitreous; larger than retinal hemorrhages. Because it is anterior to
the retina, it obscures any underlying retinal vessels. When
standing, RBCs settle and create a horizontal line of demarcation
between the plasma above and cells below. Causes include a
sudden increase in intracranial pressure.
4. Microaneurysms tiny, round, red spots seen commonly but not
exclusively in and around the macular area. Minute dilatations of
very small retinal vessels, but the vascular connections are too
small to be seen ophthalmoscopically. Characteristic of diabetic
retiopathy but not specific to it.
5. Neovascularization formation of new blood vessels; more
numerous, more tortuous and narrower than other blood vessels in
the area and form disorderly looking red arcades; common cause if
the late proliferative stage of diabetic retinopathy. Vessels can
grow into the vitreous, where retinal detachment or hemorrhage
may cause loss of vision.


51. Describe retinal characteristics of diabetes, hypertension and papilledema.
HANDOUT
Diabetes
1. Primary findings microaneurysms, neovascularization, retinitis
proliferans (A growth of a light-colored sheet of opaque
connective tissue over the inner surface of the retina.
Neovascularization of this tissue with tortuous vessels is seen.
These vessels bleed easily.)
2. Distribution posterior pole
3. Secondary findings hard exudates (small intraretinal lesions
caused by retinal disturbances in a variety of disorders), deep
hemorrhages, retinal venous occlusions, vitreous hemorrhages
Hypertension
1. Primary findings anteriolar narrowing, Copper wiring, flame
hemorrhages, arteriovenous nicking
2. Distribution throughout retina
3. Secondary findings hard and soft exudates, retinal venous
occlusions, macular stars
Papilledema
1. Primary findings hyperemia of the dis, venous engorgement,
retinal hemorrhages, disc elevation, loss of spontaneous venous
pulsations, cotton-wool spots.
2. Distribution on or near disc
3. Secondary findings hard exudates, optic atrophy (late)

52. Discuss characteristics of narrow angle vs. simple glaucoma. HANDOUT
Narrow Angle Chronic Simple

Occurrence 15% of all glaucoma cases 85% of all glaucoma cases

Cause Closed angle prevents Unclear thought to be
Aqueous drainage a defect in the trabecular
network ultrastructure

Age of Onset 50-60 Variable

Type of Patient Type A personality Not specific

Anterior Chamber Shallow Usually normal

Chamber angle Narrow Normal

Symptoms Headache, haloes around Generally none;
lights, sudden onset of Decreased vision, late
severe eye pain, vomiting
during attack.

Cupping of disc After untreated attack(s) Progressive if not treated

Visual fields Involvement is a late sign Peripheral fields involved
early; central involvement
a very late sign.

Ocular pressure Early with provocative Progressively higher if
tests only. Late high not medically controlled

Other signs Fixed, mid-dilated pupil, conjunctival
Injection; Steamy cornea (like
looking through a steamy window)

Treatment Surgical Medical, laser surgery

Prognosis Good Good, if recognized early
Very dependent upon
patient compliance