Download - Retina.pptx
Retina Zarieh Dawn L. Novela
Medicine 2
Retina
Layers of Retina1. Pigment epithelium• Derived from outer layer
of optic cup• Composed of single layer
of polygonal cells • Source of metabolic
enzymes, as well as vit.A• Phagocytosis of
degenerated fragments of outer segment
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Layers of Retina1. Pigment epithelium• It prevents light reflection
throughout the eyeball• w/o it, light rays would be
reflected in all directions within the eyeball and would diffuse lighting of retina
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Layers of Retina2. Rods and Cones
(photoreceptors)• Outer segment
– Contains light sensitive photochemicals converting light energy into chemical energy nerve impulse
• Inner segment– Connected to outer
segment by constriction containing cilia (w/c transmits impulses)
– Mitochondria: amplifies weak impulses
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Layers of Retina3. External limiting
membrane• Fenestrated membrane
composed of terminal bars
• Formed by junctional attachment bw membrane of Muller’s cells and inner segment of photoreceptors
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Layers of Retina4. Outer nuclear layer• Composed of nuclei of
photoreceptors
5. Outer plexiform layer• Composed of axons of
photoreceptors and dendrites of bipolar cells
6. Inner nuclear layer• Composed of nuclei of
several cells (bipolar, Muller, horizontal and amacrine cells)
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Layers of Retina7. Inner plexiform layer• Composed of axons of
bipolar cells and dendrites of ganglion cells
8. Ganglion cell layer• Composed of ganglion
cells
9. Nerve fiber layer• Composed of axons of
ganglion cells wc converge toward posterior pole of eye forming optic nerve
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Layers of Retina10. Inner plexiform layer• The cuticular derivative of
Muller’s cells • Serves to delineate the
retina from overlying vitreous
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• Blood supply– Central retinal artery and vein (wc enters the
eye thru optic disk)• As retinal arteries enter the eye, it loses it
internal elastic lamina and the medial muscular coat becomes incomplete.
• The neurosensory retina has no sensory supply – Thus disorders of retina are painless
• 2 capillary networks in retina– In nerve fiber layer and inner nuclear layer
Physiology and Biochemistry of retina• Rods
– func at low level illumination or night vision (scotopic vision)
– peripheral vision– 500x more photosensitive than cones
• Cones– func at high level illumination or daytime vision
(photopic vision) – Central vision– 3 typers: Blue, Green, and Red cones
Physiology and Biochemistry of retina• Fovea centralis
– Center of acute vision (point at which visual perception is sharpest)
– Contains only cones (each with its own neural supply)– Light stimuli in this region can directly act on the sensory
cells because bipolar cells and ganglion cells are displaced peripherally.
• Retina is dependent on constant supply of glucose for its metabolism
• Muller cells– Storehouse of glucose in the form of glycogen
Symptomatology• Principal symptom: visual disturbance Visual blurring
If macula is involved (central serous retinopathy, macular degeneration) – central vision is affected
If extramacular (pigmentary degeneration) – peripheral vision
Photopsia Seeing flashes of light Caused by the fact that any stimulus on eye results in
only one retinal response, that is seeing light May be experienced in retinal and vitreous detachment
Symptomatology Sector visual field defect
Actual loss of part of field of vision or Sensation of curtain or fog covering the involved portion
of field vision Condi: partial retinal defect, branch occlusion on retinal
vessels, and large retinal hemorrhage Disturbance of image size or shape
Metamophopsia: distorted image Micropsia: small image Macropsia: large image Main cause – disturbance in alignment and position of
visual cells
Central retinal artery occlusion (CRAO)• Definition: Retinal infarction due to occlusion of an
artery in the lamina cribrosa or a branch retinal artery occlusion.
• Epidemiology. CRAO occur less often than vein occlusions.
• Common symptom– Blurring or complete loss of vision– Impairment of central vision
Vascular Disturbance
CRAO
• in ophthalmoscope constricted retinal arteries pale optic disk rest of the eye ground is white (due to
coagulation necrosis) cherry red spot“box car” appearance - uninterrupted blood
stream
CRAO
Central retinal artery occlusion (CRAO)• Tx:• Ocular massage, medications that reduce intraocular
pressure, or paracentesis are applied in an attempt to drain the embolus in a peripheral retinal vessel.
• Calcium antagonists or hemodilution are applied in an attempt to improve vascular supply.
• Work-up to identify the source of the embolus is important in order to treat the underlying disease and prevent another embolization (such as stroke).
Vascular Disturbance
Central retinal vein occlusion (CRVO)• Definition: Vein occlusion occurs as a result of
circulatory dysfunction in the central vein or one of its branches.
• Epidemiology. CRVO is the second most frequent vascular retinal disorder after diabetic retinopathy.
• Etiology. Frequently due to local thrombosis at sites where sclerotic arteries compress the veins.
• Common symptom: rapid loss of vision (but not as instant nor complete as CRAO)
Vascular Disturbance
CRVO
• in ophthalmoscope retinal engorgement retinal hemorrhage“hotdog and catsup” appearanceDisk is hyperemic with blurring of the margin
Central retinal vein occlusion (CRVO)• Common complication: Glaucoma
– Occurs 3 mos after onset– Shows neurovascularization of iris surface (rubeosis
iridis) w/ occasional vitreous hemorrhage
• Treatment– In acute stage, hematocrit should be reduced to 35–38%
by hemodilution. – The underlying disorders have to be treated. – Laser treatment is performed in ischemic occlusion that
progresses to neovascularization or rubeosis iridis.
Vascular Disturbance
Hypertensive retinopathy• Definition: Arterial changes in hpn are primarily
caused by vasospasm• Pathogenesis.
– High bp can cause breakdown of the blood–retina barrier or obliteration of capillaries.
– This results in intraretinal bleeding, cotton- wool spots, retinal edema, or swelling of the optic disc.
• Symptoms. – headache or eye pain dt high bp– Impaired vision or loss of visual acuity only occurs in
stage III or IV hypertensive vascular changes.
Retinopathy
Hypertensive retinopathy
Retinopathy
High degree of narrowing
Reduced flow to retina
Anorexia
Incd capillary permeability
Serum or whole blood leaks out into tissue
Retinal edema, exudates or
hemorrhage results
• Severe edema may involve the optic disk → papilledema/chocked disk
• Absorption of edema fluid may leave protein residues → form yellow spots “hard exudate”
• At region of macula, residues are arranged in the form of fan → “macular star”
• Hemorrhage located in nerve fiber layer → “striate or flame-shaped appearance”
• Marked constriction of terminal arterioles may produce zone of infarcts → “cotton wool” patches
Hypertensive retinopathy
Retinopathy
Hypertensive retinopathy
Hypertensive retinopathy
Arteriosclerotic retinopathy• Definition: Arterial changes in hpn as a result of
thickening of the wall of the arteriole.• Commonly seen in atherosclerosis and arteriole
sclerosis• Atherosclerosis.
– Whitish plaques of lipid deposits seen in wall of retinal a.– Lipoidal infiltration as white streak at side of blood
column (“pipestem sheathing”)
Retinopathy
Arteriosclerotic retinopathy• Arteriole sclerosis. 1. Change in median arterioles light streak
Median streak is produced by light reflexed from cylindrical blood column of artery
In thickening and hyalinization of medial coat, MS widens
“copper-wire artery” – when MS completely covers entire blood column
“silver-wire artery” – when sclerosis reaches the advance stage (wc reflects back all the light falling on its surface
Retinopathy
Arteriosclerotic retinopathy• Arteriole sclerosis. 1. Atrio-venous crossing changes
Concealment of vein (Gunn’s sign) Tapering of veins – dt extension of arteriosclerotic
changes Depression of vein – dt pressure by hardened arterial
wall Humping of vein (Salus arch) Venous banking – dt dilatation of vein prox to AV
crossing Deflection of vein as S or Z-shaped bent Turtousity of vessels – dt inc length of arterioles Attenuation of arteries – dt thickening of arterial wall
Retinopathy
Arteriosclerotic retinopathy
Retinopathy
Central serous retinopathy• Edema of macular region• More common in male• Occurs >20 y/o• Either defect in retinal pigment epith allowing
choroidal transudate to seep into retina, some form choroiditis or vascular spasm
• Principal symptoms– Blurring of central vision– Metamorphopsia, micropsia and macropsia – dt
disruption of arrangement of visual cells by edema
Retinopathy
Pigment degeneration of Retina• Charac initially by premature death of
photoreceptor cells w/ subsequent changes in pigment epith
• Transmitted as dominant, recessive or sex-linked trait
• Mc initial symptom is night blindness – dt early involvement of rods
• Field studies show ring of scotoma wc extends peripherally → loss of peripheral vision
• End stage: central vision eventually fades away
Retinopathy
Retinal detachment
• Definition: Retinal detachment refers to the separation of the neurosensory retina from the underlying retinal pigment epithelium, to which normally it is loosely attached.
Primary retinal detachment Always asso w/ breaks (usually in periphery) in retina Vitreous fluid seeps in thru retinal break and initiate separation
Retinal detachment
• Secondary retinal detachment– Dt dse process of retina, vitreous or choroid– Caused by exudates (choroiditis, Harada’s
dse); tumor cells or traction on retina
• MC symptom: photopsia• Ophthalmoscopic findigs– Elevated retina– Grayish retina– Retinal vessels appear constricted and darker
Retinoblastoma
• Definition: Retinoblastoma is a malignant tumor of early childhood that develops from immature retinal cells.
• MC intraocular tumor• Pathogenesis.
– A somatic mutation is detected in about 95% of patients. – In other patients, it is inherited as an autosomal-dominant
trait. – Changes on chromosome 13q have been observed in germ-
cell mutations• Symptoms.
– manifests itself before the age of 2 in 70% of affected children.
– Parents observe leukocoria, a whitish-yellow pupil; in 60% of these children, strabismus in 20%, and a reddened eye in 10%.
Leucocoria “cat’s eye reflex”
Retinoblastoma
• Intraocular stage: – soapy white mass in retina
• Glaucomatous stage– IOP increased– Ocular congestion and corneal edema– Vitreous filled with tumor cells
• Extraocular stage– Tumor extends out of eye into orbit via occular emissaria or thru
optic nerve• Metastasis
– Hematogenous spread to long bones– Manifests as painfull swelling of prox/distal ends
• Treatment. – Tumors <4 pupil diameters can be managed with radiation therapy
delivered by plaques of radioactive ruthenium or iodine (brachytherapy) and cryotherapy.
– Larger tumors require enucleation of the eye.
“Now, Eye’m gonna ask questions coz Eye saw you listening”
Short Quiz!
No. 110 layers of retina
(from outside to inside)
No. 2In visual blurring, if macula is involved, what
vision is affected? (Central/Peripheral)
No. 3
What retinal disease is this?
No. 4
What retinal disease is this?
No. 5What stage of hypertensive retinopathy shows areas of
hemorrhage, cotton wool spots and papilledema?
No. 6It refers to the separation of the neurosensory retina from the underlying retinal pigment epithelium, to which normally it is
loosely attached.
No. 7What do you call this condition? What disease
manifests it?
No. 8True or False:
Pulsation in retinal vein is normal.
No. 9True or False:
Disorders of the retina are painful.
No. 10What is the function of Vitamin A in the retina?
Thank you!