Optho Part 4

Question 1

Optic nerve disease: Optic disc elevation: Ischemic optic neuropathy

Answer 1

arteritic – Giant cell arteritis, temporally artery biopsy

non-arteritic – hypertension, aspirin therapy

Question 2

Scotoma

Answer 2

an area in the overall visual field where vision is either absent or diminished.

Question 3

Hemianopia

Answer 3

Homonymous hemianopia

Bitemporal hemianopia

Question 4

Anatomy of vitreous and retina: Vitreous

Answer 4

the gel like collagen matrix that fills the portion of the eye between the retina and the lens

Question 5

Anatomy of vitreous and retina: Arterioles

Answer 5

generally more narrow, lie slightly anterior to venules when they cross.

Question 6

Anatomy of vitreous and retina: Venules

Answer 6

generally larger than arterioles, generally lie deep to arterioles when they cross.

Question 7

Location of rods and cones relative to vitreous and choroid

Answer 7

Bottom of the thing

Question 8

Retinal pigment epithelium

Answer 8

the pigmented cell layer just outside the neurosensory retina that nourishes retinal visual cells, and is firmly attached to the underlying choroid and overlying retinal photoreceptor cells.

Question 9

Macula

Answer 9

• is an oval-shaped highly pigmented yellow spot near the center of the retina of the human eye. It has a diameter of around 5 mm and is often histologically defined as having two or more layers of ganglion cells. Near its center is the fovea, a small pit that contains the largest concentration of cone cells in the eye and is responsible for central, high resolution vision

Question 10

Choroid

Answer 10

the vascular layer of the eye, containing connective tissue, and lying between the retina and the sclera. The human choroid is thickest at the far extreme rear of the eye (at 0.2 mm), while in the outlying areas it narrows to 0.1 mm.[1] The choroid provides oxygen and nourishment to the outer layers of the retina. Along with the ciliary body and iris, the choroid forms the uveal tract.

Question 11

Symptoms suggestive of vitreoretinal disorders

Answer 11

1. Flashes – the sensation of light the appears abruptly in one eye, most often casues by tugging on the retina by the vitreous. Flashes may be the first sign of a retinal detachment
2. Floaters - deposits of various size, shape, consistency, refractive index, and motility within the eye’s vitreous. They may appear as spots, threads, or fragments of cobwebs, which float slowly before the observer’s eyes. They are most often the result of benign vitreous degeneration, but may also be associated with intraocular bleeding

Question 12

Abnormalities of central visual acuity

Answer 12

blurring – due to subretinal fluids, poor photoreceptor function

distortion – subretinal fluid

. minimalization – edema “stretching out “ the photorecptors so that fewer are affected by stimulation of a given size.

scotoma – loss, or relative loss of an area in the field of vision.

Question 13

Abrupt or progressive dimming of vision in one eye

Answer 13

vitreous hemorrhage, retinal detachment.

Question 14

Abrupt or progressive loss of peripheral visual field in one eye

Answer 14

peripheral retinal detachment.

Question 15

Abnormal fundus features: General

Answer 15

a. Loss of normal red reflex – cataract, retinoblastoma, retinal detachment
b. Dark spots in red reflex – cataract, hemmorhage

Question 16

Fundus features of important systemic diseases: Diabetes Mellitus

Answer 16

the incidence of diabetic retinopathy is higher in type 1 than type 2.

Question 17

Non-proliferative (background) diabetic retinopathy

Answer 17

caused by microvascular occlusion and leakage. Capilaary changes include thickening of the basement membrane, endothelial cell damage, deformation of the red blood cells and changes in platelets that lead to increased aggregation. Loss of pericytes allow liquids to leak from the capillaries and leads to edema, dot and blot hemorrhages and hard exudates (lipid accumulation within the retina). All of these factors combine to lead to retinal ischemia. Central macular edema can be treated with focal laser therapy.

Question 18

Proliferative diabetic retinopathy

Answer 18

proliferation of abnormal blood vessels as a response to chronic ischemia. Can lead to profound and irreversible vision loss. If found early, can be treated with pan-retinal photocoagulation.

Question 19

Systemic hypertension

Answer 19

i. Vasospastic (accelerated) retinopathy
ii. Sclerotic (chronic) retinopathy – narrowing of the arterioles, copper and silver wiring.
iii. Central retinal vein occlusion – increased pressure in the central retinal artery compresses the central retinal vein and leads to diffuse retinal hemorrhaging and vision loss.
iv. Branch retinal vein occlusion – caused by the compression of a branch retinal vein by a branch retinal artery at an area of crossing.
v. Ocular ischemia (carotid disease) – appears as unilateral diabetic retinopathy. Even in a patient with DM, assymetrical disease is indication for carotid studies.

Question 20

Embolic cardiovascular disease

Answer 20

i. Central retinal artery occlusion – thromboembolic occlusion of the central retinal artery, accompanied by severe rapid vision loss, ischemic changes
ii. Branch retinal artery occlusion – embolic event that causes the occlusion of a branch retinal artery and may result in local ischemic changes.

Question 21

HIV/ AIDS

Answer 21

cytomegalovirus can cause severe retinopathy in patients with low CD4 sounts.

Question 22

Disseminated metastatic cancer

Answer 22

the choroid is highly vascular, and is sometimes the target of metastases.

Question 23

Retinoblastoma

Answer 23

Initial signs are a white reflex (“cat’s eye reflex”) rather than the usually seen red reflex.

Leukocoria, which is a white pupil in place of a red reflex

Non-paralytic strabismus may also be found.

Thermotherapy, Chemotherapy, Cryotherapy, laser and radiation therapy. In severe cases, removal of the eye may be necessary (enucleation)

Question 24

Retinoblastoma 2

Answer 24

– Most common primary intraocular malignancy of childhood (1 in 15,000 to 16,000 live births)
– 95% diagnosed before age 5
– Sporadic and hereditary forms (germline mutation)
– 13q14, encodes a nuclear protein that acts as a tumor suppressor
– 25% cases are bilateral
– Presents most commonly with leukocoria (54%) and strabismus (19%)
– If untreated, retinoblastoma grows to fill the eye and destroys the internal architecture of the globe.
– Metastatic spread usually begins after six months, and death occurs within a matter of years.
– Spontaneous regression may occur in a small number of cases, but is a rare occurrence.

Question 25

Retinoblastoma 3

Answer 25

Retinoblastoma is an embryonal malignant tumor arising from the retina, often during the first 2 years of life. Normally occurs in children between 1-6 years of age. Transmitted either by an autosomal dominant trait (80% penetrance) or chromosomal mutation. Many retinoblastomas have been associated with a deletion of chromosome 13q14.2. The gene encodes a phosphoprotein that regulates the cell cycle as it progresses through the G1 phase. 20% of patients with a chromosome 13 abnormality (13q- syndrome) develop Rb . If both Rb genes are deleted, then patient will have biocular retinoblastomas, and the damaged DNA will be transmitted to offspring. If only one gene is deleted, then DNA damage (UV, etc.) must inactivate the functional Rb gene to form a uniocular retinoblastoma. Non-inherited retinoblastoma is rare, because it would need two somatic mutations before a tumor would develop.

Question 26

Retinoblastoma 4

Answer 26

The RB1 gene is located on human chromosome 13. In familial retinoblastoma, the fertilized egg carries one defective copy of the RB1 gene, and all retinal cells in this offspring carry only a single functional RB1 gene copy. If this surviving copy is eliminated in a retinal cell by a somatic mutation (the second hit of the Knudson two-hit hypothesis), the cell will lack RB1 gene function and will proliferate into a tumor. In sporadic retinoblastoma, the fertilized egg is genetically wild type at the RB1 locus. In the retina of this offspring, retinoblastoma development requires two successive somatic mutations striking both copies of the RB1 gene in the retinal precursor cells. Because only a single somatic mutation is needed to eliminate RB1 function in familial cases, multiple cells in both eyes are affected. In contrast, the two somatic mutations required in sporadic disease are unlikely to affect a single cell lineage, yielding at most one tumor.

Question 27

Retinoblastoma 5

Answer 27

Non-paralytic strabismus is where the eyes cannot focus on the same point simultaneously, but the cause of this is not muscle paralysis. In this case, when the dominant eye is covered, the non-dominant eye will focus on the point. The characteristic finding is a chalky, white-gray retinal mass with a soft, friable consistency

Question 28

Retinal detachment

Answer 28

Retinal detachments are time sensitive, requiring an immediate referral to an ophthalmologist to maximize chances of saving vision. Retinal detachments must be treated surgically. Prior to surgery, patients should have bed rest to avoid worsening the condition. If there is a break (rhegmatogenous RD), then it must be sealed and fluid must be drained from the sub-retinal space. Gas may be injected into the vitreous cavity to alleviate vitreous traction (see traction in Discussion section), or strips of silicon may be applied to the sclera of the eye to short its diameter, also reducing vitreous traction.

Question 29

Retinal detachment: | Vitrectomy

Answer 29

Removal of vitreous material Three sclerotomies are made on the outside of the eye, one that allows fluid to infuse into the eye, and two others that are used to introduce instruments into the back part of the eye. Using a light pipe and a vitreous cutter all of the central and peripheral vitreous is removed and all of the vitreoretinal traction on any of the breaks excised.

Question 30

Retinal detachment: | Vitrectomy 2

Answer 30

Patients with more complicated retinal detachments may require an additional vitrectomy. With this procedure, three sclerotomies are made on the outside of the eye, one that allows fluid to infuse into the eye, and two others that are used to introduce instruments into the back part of the eye. Using a light pipe and a vitreous cutter all of the central and peripheral vitreous is removed and all of the vitreoretinal traction on any of the breaks excised. The patient's retina can be flattened intraoperatively using an air bubble or heavier than water perfluorocarbon liquid. These patients are usually left with intravitreal air, a long acting gas bubble (SF6 or C3F8), or silicone oil. Vitrectomy leads to successful retinal reattachment approximately 80 to 90 percent of the time after one surgery. In cases of failures, patients often require more extensive vitreoretinal procedures such as combined cataract extraction and intraocular lens placement, lensectomy, extensive epiretinal membrane peeling, subretinal fibrous band removal, relaxing retinotomies, and silicone oil tamponade. Virtually all patients over age 50 treated with vitrectomy will develop progressive cataract.