1What is the retina?
Thin, semi-transparent, multilayered neural tissue lining the inner wall of the posterior two-thirds of the eye.
2What is the embryologic origin of the retina?
Inner and outer layers of the embryonic optic cup
3How many layers does the retina have?
10 layers
4What is the most posterior part of the eye containing crucial visual structures?
Posterior pole
5What is the diameter of the posterior pole?
10 mm
6What structures are housed in the posterior pole?
Optic nerve and macula
7What is the function of the optic nerve?
Transmits visual information to the brain
8What is the macula also called?
Macula lutea, area centralis, or yellow spot
9What is the diameter of the macula?
5.5 mm
10What is the most anterior extension of the retina?
Ora serrata
11How far is the ora serrata from the equator?
5 mm
12Which ora serrata is more serrated?
Nasal ora serrata
13Which ora serrata is smoother?
Temporal ora serrata
14What are other landmarks of the retina?
Long ciliary nerve, short ciliary nerve, and ampulla for vortex veins
15What is the ampulla for vortex veins?
Area where vessels meet
16How far anterior to the equator is the far periphery?
15 mm
17What is another name for the mid-periphery?
Near periphery
18Where is the mid-periphery located?
10–15 mm anterior to the posterior pole and posterior to the equator
19What defines the posterior pole retinal zone?
Less than 10 mm
20What is the outermost limit of the macula?
Perifovea
21What is the width of the perifoveal ring?
1.5 mm
22What is the parafovea?
Region inside the perifovea encircling the fovea
23What is the width of the parafoveal ring?
0.5 mm
24Which retinal layers are thickest in the parafovea?
Ganglion cell, inner nuclear, and Henle layers
25What is the fovea also called?
Fovea centralis
26What is the diameter of the fovea?
1.5 mm
27What is the main photoreceptor in the fovea?
Cones
28What is the central depression within the macula?
Fovea
29What is the diameter of the foveola?
0.35 mm
30Which layers are absent in the foveola?
Inner nuclear layer and ganglion cell layer
31What is the foveola?
Central floor of the fovea and area of most acute vision
32Why is vision clearest in the foveola?
Absence of inner retinal layers and blood vessels minimizes light scattering
33What is the FAZ?
Foveal avascular zone, a capillary-free region within the fovea
34What is the approximate diameter of the FAZ?
0.35 mm
35What is the umbo?
Center of the foveola
36What does the umbo correspond to during fundoscopy?
Light reflex
37What is the function of optical coherence tomography (OCT)?
Produces cross-sectional images of retinal layers
38What are hyperreflective OCT bands?
Bright bands representing reflected light
39What are hyporeflective OCT bands?
Dark bands representing absorbed or less-reflected light
40What structures constitute the inner retina?
Internal limiting membrane through external limiting membrane
41What structures constitute the outer retina?
Photoreceptor layers through the choroid
42Which retinal layers receive choroidal blood supply?
Outer plexiform layer through retinal pigment epithelium
43Which retinal layers receive retinal blood supply?
Inner nuclear layer through nerve fiber layer
44What is the retinal pigment epithelium (RPE)?
Outermost pigmented retinal layer responsible for photoreceptor support and maintenance
45What is the role of RPE in the visual cycle?
Synthesizes and stores retinoids
46What vitamin does the RPE metabolize?
Vitamin A
47What does RPE generate for rhodopsin formation?
11-cis-retinaldehyde
48What gives the fundus its red-orange color?
Retinal pigment epithelium
49What is the basis of the red reflex?
Red-orange pigmentation of the RPE
50What is the RPE's role in photoreceptor maintenance?
Phagocytosis of photoreceptor outer segments and waste removal
51What does the RPE transport to photoreceptors?
Necessary nutrients and ions
52What junctions form the outer blood-retinal barrier?
Tight junctions or zonula occludens between RPE cells
53How does the RPE maintain the subretinal space?
Active fluid transport and pumping keep it dry
54What can excessive subretinal fluid cause?
Retinal detachment
55What pigment does the RPE synthesize for oxidative protection?
Melanin
56What is the function of melanin in the RPE?
Acts as a free-radical scavenger
57What accumulates in the RPE in age-related macular degeneration?
Lipofuscin
58What happens when the RPE deteriorates or is lost?
Atrophy of overlying photoreceptors and underlying choriocapillaris
59What are the inner and outer segments of the retina composed of?
Light-sensitive photoreceptor elements: rods and cones
60What structures are found in photoreceptor segments?
Mitochondria, cilia, and discs
61What does the IS-OS junction indicate on OCT?
Photoreceptor integrity
62Why are photoreceptors susceptible to ciliopathies?
They are modified sensory cilia
63What is the external limiting membrane?
Junctional site between photoreceptors and Müller cells
64What does the outer nuclear layer contain?
Nuclei and cell bodies of rods and cones
65What occurs in the outer plexiform layer?
Synapses between photoreceptors and bipolar and horizontal cells
66What does the inner nuclear layer contain?
Bipolar, horizontal, and amacrine cell bodies and nuclei
67What occurs in the inner plexiform layer?
Synapses between bipolar cell axons and ganglion cell dendrites
68What does the ganglion cell layer contain?
Ganglion cell nuclei
69Where is the ganglion cell layer absent?
Foveola
70Where is the ganglion cell layer thickest?
Parafovea
71What does the nerve fiber layer contain?
Ganglion cell axons
72Where do ganglion cell axons converge?
Optic nerve
73Where is the nerve fiber layer thicker?
Nasal perifovea
74What forms the internal limiting membrane?
Fused Müller cell foot processes
75What are the main supporting cells of the retina?
Müller cells
76What are the functions of Müller cells?
Structural support and sensory retinal metabolism
77Where are integrator neurons found?
Inner nuclear layer
78What is the role of bipolar cells?
First-order neurons in the visual pathway
79What is the function of horizontal cells?
Provide horizontal interconnections between photoreceptors and bipolar cells in the OPL
80What is the function of amacrine cells?
Connect with ganglion cell axons
81Which are the primary photoreceptors?
Rods and cones
82Approximately how many rods are present in the retina?
120–130 million
83Approximately how many cones are present in the retina?
6 million
84What is the approximate ratio of rods to cones?
$20:1$
85Where are cones most concentrated?
Fovea
86Where is rod density greatest?
Approximately 20 degrees from fixation
87What happens to rod density toward the periphery?
It decreases
88What is the shape of rod outer segments?
Cylindrical
89What is the shape of cone outer segments?
Conical
90What visual pigment is found in rods?
Rhodopsin
91What visual pigments are found in cones?
Photopsin and iodopsin
92What type of vision is mediated by rods?
Scotopic and peripheral vision
93What type of vision is mediated by cones?
Photopic, color, and high-resolution vision
94Which photoreceptors function predominantly at night?
Rods
95Which photoreceptors are responsible for color perception?
Cones
96What is the primary blood supply of the eye derived from?
Internal carotid artery
97Which artery branches from the internal carotid artery to supply the eye?
Ophthalmic artery
98What supplies the outer retina?
Choriocapillaris
99Which arteries give rise to the choriocapillaris?
Short posterior ciliary arteries
100What supplies the inner retina?
Central retinal artery
101How many major branches supply the retinal quadrants?
Four
102What are the four branches of the central retinal artery?
Superonasal, inferonasal, inferotemporal, and superotemporal
103What artery supplies the papillomacular bundle?
Cilioretinal artery
104What is the papillomacular bundle?
Area between the optic nerve and center of the macula
105What happens to the FAZ in diabetic retinopathy with capillary non-perfusion?
It may enlarge, causing decreased visual acuity
106What can macular edema do to the FAZ?
Make it disappear due to fluid extravasation
107What structures maintain the blood-ocular barriers?
Tight junctions between barrier cells
108What are the four blood-ocular barriers described in the lecture?
Ciliary body epithelium, iris capillary endothelium, retinal capillary endothelium, and RPE
109What forms the inner blood-retinal barrier?
Non-fenestrated retinal capillary endothelial cells
110What forms the outer blood-retinal barrier?
Tight junctions between RPE cells
111What substances are normally prevented from crossing the inner blood-retinal barrier?
Tracer substances such as fluorescein dye
112What can disruption of blood-ocular barriers cause?
Edema, exudation, and neurosensory detachment
113Which retinal layer absorbs light first?
RPE
114What is the only pigmented portion of the retina?
RPE
115What is the correct pathway of incoming light through the eye?
Cornea → lens → vitreous body → retina
116What is retinal transduction?
Conversion of light energy into electrochemical energy
117What is the sequence of visual signal transmission?
Photoreceptors → integrator neurons → ganglion cells → optic nerve → visual cortex
118What happens after light reaches the RPE?
It is reflected back toward the nerve fiber layer and optic nerve
119What is metamorphopsia?
Distortion of visual images
120What is micropsia?
Objects appear smaller than their actual size
121What is macropsia?
Objects appear larger than their actual size
122What is dyschromatopsia?
Abnormal color vision
123What is scotoma?
Visual field defect or blind spot
124What is nyctalopia?
Night blindness
125What are muscae volitantes?
Floaters
126What are photopsias?
Flashes of light
127What is the importance of asking whether visual changes are sudden or gradual?
Helps characterize the onset and progression of retinal disease
128Why should the location of visual disturbance be established?
To determine whether central or peripheral vision is affected
129What symptom is rarely present in retinal problems?
Pain
130Pain is more commonly associated with what ocular condition?
Glaucoma
131What historical details should be obtained in recurrent visual complaints?
Timing, sequence, duration, and interval
132What should be established in bilateral visual complaints?
Which eye was affected first and the temporal relationship between eyes
133What previous ocular treatments should be documented?
Medications, surgery, laser, and injections
134What systemic conditions should be included in retinal patient history?
Hypertension, diabetes, kidney disease, cardiopulmonary problems, cancer, and blood dyscrasias
135What should be assessed in family history?
Hereditary eye and systemic diseases
136What should be included in social history?
Occupation, travel, chemical exposure, sports, pets, diet, drugs, smoking, and alcohol
137What additional history should be obtained?
Sexual history
138What is the most basic component of the comprehensive eye examination?
Visual acuity
139What does the pinhole test help differentiate?
Refractive error from retinal disease
140What does improvement with pinhole suggest?
Refractive error
141What does failure to improve with pinhole suggest?
Retinal problem
142What anterior eye conditions may improve with pinhole?
Corneal astigmatism and cataract
143Are ocular adnexa usually affected in retinal diseases?
No
144What pupillary reactions should be examined?
Direct and consensual
145What does ROR stand for?
Red-orange reflex
146What may cause an absent or faint red-orange reflex?
Cataract, vitreous hemorrhage, or corneal opacity
147What is leukocoria?
White pupillary reflex
148What serious condition should leukocoria raise suspicion for in a child?
Retinoblastoma
149What is the normal extraocular muscle movement in most retinal diseases?
Normal
150What deviation may occur in severe longstanding retinal disease?
Exotropia
151Why can longstanding retinal disease cause ocular deviation?
Poor fixation due to impaired vision
152What is the normal intraocular pressure palpation comparison?
Similar firmness to tapping the nose
153What does hypotonic intraocular pressure feel like?
Softer than the nose
154What conditions may cause hypotonic pressure?
Retinal detachment, choroidal detachment, and ciliary body inflammation
155What does elevated intraocular pressure feel like?
Harder than the nose
156What condition can cause neovascular glaucoma?
End-stage proliferative diabetic retinopathy
157What does direct ophthalmoscopy produce?
Erect, highly magnified image
158What is the magnification of direct ophthalmoscopy?
15x
159What is the field of view of direct ophthalmoscopy?
5 degrees
160What is the working distance of direct ophthalmoscopy?
1–2 inches
161Does direct ophthalmoscopy provide stereopsis?
No
162What does indirect ophthalmoscopy produce?
Inverted and laterally reversed image
163What is the magnification of indirect ophthalmoscopy?
3.5x
164What is the field of view of indirect ophthalmoscopy?
35–45 degrees
165What is the working distance of indirect ophthalmoscopy?
Arm's length
166Does indirect ophthalmoscopy provide stereopsis?
Yes
167Which ophthalmoscope provides a wider field of view?
Indirect ophthalmoscope
168Which ophthalmoscope provides greater magnification?
Direct ophthalmoscope
169What structures can slit-lamp biomicroscopy with special lenses examine?
Vitreous, retina, and optic disc
170What does ocular ultrasound evaluate?
Anatomic relationships of the vitreous, retina, and choroid
171When is ocular ultrasound particularly useful?
When media opacity prevents adequate fundoscopy
172What is the normal ultrasound appearance of the eye?
Hypoechoic
173How does clear vitreous appear on ultrasound?
Hypoechoic
174How does the retina appear on ultrasound?
Hyperechoic
175What ultrasound finding suggests endophthalmitis?
Choroidal thickening and hyperechoic or moderate-echoic vitreous densities
176What distinguishes vitreous hemorrhage from endophthalmitis on ultrasound?
Absence of choroidal thickening
177What ultrasound finding suggests retinal detachment?
V-shaped membrane continuous with the optic nerve
178What is fluorescein angiography?
Imaging of retinal and choroidal circulation using sodium fluorescein dye
179Where is fluorescein dye injected?
Antecubital vein
180What does fundus photography document?
Appearance of the retina and fundus
181What does OCT provide?
Cross-sectional imaging of retinal structures
182What does electroretinography assess?
Electrical activity and function of retinal layers
183What is electrooculography used to assess?
Retinal function through electrical activity measurements
184What is the most common group of retinal diseases in the lecture?
Diabetic retinopathy, hypertensive retinopathy, CRVO, CRAO, AMD, retinal detachment, vitreous hemorrhage, retinitis pigmentosa, ROP, and retinoblastoma
185What is diabetic retinopathy?
Retinal vascular changes caused by diabetes mellitus
186What percentage of patients with type 1 diabetes develop retinopathy after approximately 20 years?
90%
187What percentage of patients with type 2 diabetes develop retinopathy according to the lecture?
60%
188What is the key modifiable risk factor for diabetic retinopathy?
Strict glucose control
189What is the DCCT?
Diabetes Control and Complications Trial
190What is the UKPDS?
United Kingdom Prospective Diabetes Study
191How much can strict glucose control reduce diabetic retinopathy risk in type 1 diabetes?
76%
192How much can strict glucose control slow progression of existing diabetic retinopathy in type 1 diabetes?
54%
193How much can strict glucose control reduce nephropathy occurrence?
50%
194How much can strict glucose control reduce neuropathy occurrence?
60%
195What reduction in advanced retinopathy risk was associated with strict glucose control in type 2 diabetes in UKPDS?
31%
196What additional systemic factor helps delay diabetic retinopathy progression?
Blood pressure control
197What is the most common symptom of diabetic retinopathy?
Blurring of vision
198What causes floaters in advanced diabetic retinopathy?
Vitreous hemorrhage from abnormal new vessels
199What may cause diplopia in diabetic retinopathy?
Transient exophoria
200What characterizes non-proliferative diabetic retinopathy?
Microvascular changes within the neurosensory retina
201What causes non-proliferative diabetic retinopathy?
Chronic elevation of blood sugar
202What are the retinal findings in non-proliferative diabetic retinopathy?
Microaneurysms, intraretinal hemorrhages, exudates, macular edema, and macular ischemia
203What is the cause of macular ischemia in diabetic retinopathy?
Enlargement of the foveal avascular zone
204Which barrier is disrupted in non-proliferative diabetic retinopathy?
Inner blood-retinal barrier
205What characterizes proliferative diabetic retinopathy?
Extraretinal vascular proliferation
206What is neovascularization?
New blood vessel growth outside the retina
207What tissue may proliferate around the optic nerve in proliferative diabetic retinopathy?
Fibrous tissue
208What causes traction retinal detachment in proliferative diabetic retinopathy?
Thick fibrous membranes pulling on the retina
209What is an end-stage complication of proliferative diabetic retinopathy?
Neovascular glaucoma
210How does neovascular glaucoma develop in proliferative diabetic retinopathy?
New vessels obstruct the trabecular meshwork, increasing intraocular pressure
211What is the most basic management of diabetic retinopathy?
Laser photocoagulation
212What is the purpose of laser photocoagulation in diabetic retinopathy?
Regression of neovascularization by treating ischemic retinal areas
213Why does retinal ischemia cause neovascularization?
Ischemic retina produces chemicals that stimulate abnormal vessel growth
214When is intravitreal anti-VEGF used in diabetic retinopathy?
For neovascularization and macular edema
215Is anti-VEGF treatment permanent?
No, repeated injections may be necessary
216When is pars plana vitrectomy indicated in diabetic retinopathy?
Advanced disease with retinal detachment or persistent vitreous hemorrhage
217What duration of uncleared vitreous hemorrhage may indicate vitrectomy?
More than 3 months
218What is the most important preventive measure for diabetic retinopathy?
Good blood glucose control
219What is the key to preventing visual loss from diabetic retinopathy?
Early detection
220When should retinal evaluation occur in adults newly diagnosed with diabetes?
At the time of diagnosis
221How frequently should diabetic patients generally undergo retinal follow-up?
Yearly
222When should retinal examination begin for diabetes onset before age 30?
Five years after onset
223What is the recommended follow-up for diabetes onset at age 30 or older?
Yearly from diagnosis
224What is the recommended retinal evaluation before pregnancy?
Before conception or early in the first trimester
225What is the recommended follow-up for no to moderate diabetic retinopathy during pregnancy?
Every 3–12 months
226What is the recommended follow-up for more severe diabetic retinopathy during pregnancy?
Every 1–3 months
227What percentage of patients may be saved from visual loss with timely consultation?
95%
228What is hypertensive retinopathy?
Retinal, choroidal, and optic nerve changes due to chronic elevation of blood pressure
229Is hypertensive retinopathy usually symptomatic?
No, usually asymptomatic
230Which retinal vessels are affected in hypertensive retinopathy?
Precapillary arterioles and capillaries
231What is the normal arteriovenous ratio of retinal vessels?
$2:3$
232What is arteriolar narrowing in hypertensive retinopathy?
Reduction in the caliber of retinal arterioles
233What are cotton wool spots?
Ischemic areas of retinal nerve fibers
234What are blot hemorrhages?
Retinal hemorrhages also seen in diabetic retinopathy
235What is AV nicking?
Arteriovenous crossing abnormality or disconnection of vessels
236What do retinal exudates represent?
Lipids in the retina
237What is disc edema?
Swelling and elevation of the optic nerve head
238What is copper wiring?
Widening and brightening of the central arteriolar light reflex, producing a copper appearance
239What characterizes stage 0 hypertensive retinopathy?
No retinal changes
240What characterizes stage I hypertensive retinopathy?
Mild to moderate arteriolar narrowing
241What characterizes stage II hypertensive retinopathy?
Marked arteriolar narrowing, increased central light reflex, intermittent constrictions, and AV crossing defects
242What characterizes stage III hypertensive retinopathy?
Stage I and II changes plus cotton wool spots, hard exudates, hemorrhages, and macular star
243What characterizes stage IV hypertensive retinopathy?
All previous changes plus disc edema
244What vascular complications may occur in hypertensive retinopathy?
Branch retinal artery occlusion and central retinal artery occlusion
245What happens when hypertension and diabetes coexist?
Combined capillary and precapillary injury may produce more severe complications
246How is hypertensive retinopathy diagnosed?
Mainly clinically
247What is the main treatment for hypertensive retinopathy?
Systemic blood pressure management
248What is CRVO?
Central retinal vein occlusion, also called venous stasis retinopathy
249What happens in CRVO?
Partial or complete blockage of the central retinal vein
250What is the pathophysiologic basis of CRVO?
Thrombosis and compression of the central retinal vein
251What are the three components of Virchow's triad?
Vessel damage, stasis, and hypercoagulability
252Where do the central retinal artery and vein share an adventitial sheath?
Arteriovenous crossing
253Where is the thrombus usually located in CRVO?
At or just proximal to the lamina cribrosa
254How many retinal quadrants are involved in CRVO?
Four quadrants
255How many quadrants are usually involved in BRVO?
One or two quadrants
256What is the typical visual presentation of CRVO?
Acute unilateral blurring or loss of vision
257What are the risk factors for CRVO?
Older age, hypertension, hyperlipidemia, diabetes, high IOP, smoking, oral contraceptives, and hypercoagulability
258What are the two classifications of CRVO?
Ischemic and non-ischemic
259What characterizes non-ischemic CRVO?
Perfused retina with generally better visual acuity and prognosis
260What characterizes ischemic CRVO?
Non-perfused retina with severe visual impairment and poorer prognosis
261What is the visual acuity typically seen in non-ischemic CRVO?
Better than 20/200
262What is the visual acuity typically seen in ischemic CRVO?
Worse than 20/200
263Is RAPD usually present in ischemic CRVO?
Yes
264Is RAPD usually present in non-ischemic CRVO?
Mild or absent
265What is a common visual field finding in ischemic CRVO?
Visual field defect
266What does fluorescein angiography assess in CRVO?
Extent of retinal capillary non-perfusion
267What degree of non-perfusion suggests ischemic CRVO in the lecture?
More than 10 disc areas
268What ERG finding is associated with ischemic CRVO?
Reduced B-wave amplitude
269What is the prognosis of non-ischemic CRVO?
Generally good
270What is the prognosis of ischemic CRVO?
Poor, with increased risk of neovascular glaucoma
271What is a common complication occurring within 90 days of CRVO?
Neovascular glaucoma
272What causes blurred and distorted vision in CRVO?
Macular edema
273What are common symptoms of CRVO?
Transient visual obscurations, blurry vision, and distorted vision
274How is CRVO primarily diagnosed?
Clinical examination
275Which test differentiates ischemic from non-ischemic CRVO?
Fluorescein angiography
276Which test confirms macular edema in CRVO?
Optical coherence tomography
277What is the role of laser photocoagulation in CRVO?
Treatment of extensive capillary non-perfusion
278When are intravitreal anti-VEGF or corticosteroids used in CRVO?
When macular edema is present
279When is pars plana vitrectomy used in CRVO?
When vitreous hemorrhage occurs
280What is CRAO?
Central retinal artery occlusion
281What is the classic presentation of CRAO?
Sudden, painless, severe monocular vision loss
282What is amaurosis fugax?
Transient loss of vision lasting seconds to minutes
283How does vision appear during amaurosis fugax?
White or gray
284What age group is more commonly associated with cardiac calcific emboli in CRAO?
Younger than 40 years
285What is the common embolic source in patients older than 40 with CRAO?
Carotid artery cholesterol emboli
286What other emboli may cause CRAO?
Platelet-fibrin emboli
287What are other causes of CRAO?
Vasculitis and intravenous particulate medications
288Why is CRAO a true ophthalmologic emergency?
It can cause irreversible retinal damage
289Within what time should CRAO be diagnosed and managed?
Within 90 minutes
290What may happen after 90 minutes of CRAO?
Permanent retinal damage
291What is the characteristic funduscopic finding in CRAO?
Cherry-red spot
292Why does a cherry-red spot occur in CRAO?
Surrounding retinal edema and whitening make the central foveal reflex prominent
293What is the primary diagnosis of CRAO based on?
Clinical examination
294What does fluorescein angiography show in CRAO?
Delayed or sluggish retinal arterial blood flow
295What does OCT show in CRAO?
Hyperreflective, thickened, edematous inner retinal layers
296What does ERG show in CRAO?
Diminished B-wave amplitude
297Is there a proven treatment that restores vision in CRAO?
No
298What percentage of CRAO cases may resolve spontaneously?
22%
299What percentage may achieve meaningful visual acuity after CRAO?
10%
300What is the purpose of ocular massage in CRAO?
Attempt to dislodge emboli