Optho path Flashcards

1
Q

Flame hemorrhages

A

Located in Nerve fiber layer (most superficial hemorrhage)

- Erythrocytes track along axons

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2
Q

Blot and dot hemorrhages

A

Located deeper in retina where axons perpendicular to RPE/Bruch’s membrane

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3
Q

Scaphoid (boat-shaped) hemorrhages

A

Hemorrhagic detachment of Inner Limiting membrane

Subhyaloid hemorrhage

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4
Q

Blood-retinal barrier

A

Inner retina: endothelial tight junctions

RPE apical tight junctions between layers

Outer retina= leaky fenestrated choriocapillaries

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5
Q

Hard exudates

A

Pools of proteinaceous fluid in outer plexiform layer (btwn inner and outer layer= watershed area)

Macular star figure= hard exudates in radial perifoveal Henle fibers

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6
Q

Cotton wool spots

A

“soft exudates”, really focal infarctions of NFL (neurofiber layer)

  • Marker for ischemia, systemic disease
  • Blockage of axoplasmic flow

Focally ballooned axon–> cytoid body (resembles nucleus)
- Formed when ischemic

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7
Q

Central retinal artery occlusion

A

“Mini-stroke” of retina

  • Normally transparent to allow light to reach rods and cones
  • Infarction of retinal cells–> opacification

Window of transparent retina shows underlying choroid= “cherry red spot”

Causes:

  • Atherosclerosis of CRA at/posterior to lamina cribosa
  • Emboli: cholesterol, platelet fibrin (carotids), Calficific, tumor (atrial myxoma in young patients
  • Vasculitis (GCA, collagen vascular disease)
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8
Q

Central retinal vein occlusion

A

Massive intraocular hemorrhage= “squashed tomato sign”

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9
Q

Chronic HTN on retinal arterioles

A

Retinal arteriosclerosis
- Fibrosis due to HTN

Normal: Healthy retinal vessels are transparent
- Can only see BLOOD in vessels

Fibrosis–> opacifies vessel wall–> obscured blood column
- “copper wire” arteriolarsclerosis

In Malignant HTN–> Spasm of vessel walls

  • Leads to necrosis
  • Vascular incompetence
  • Optic disc edema
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10
Q

Background diabetic retinopathy

A

Hard, soft exudates
Hemorrhages
Cotton wool spots= ischemia–> progresses to proliferative diabetic retinopathy

Early stages: capillary changes

  • Pericytes are lost preferentially in early stages of diabetic retinopathy
  • Pericytes have inhibitory effect on proliferation of endothelial cells

Later stages–> capillary nonperfusion

  • Retinal ischemia–> VEGF upregulation
  • Stimulates proliferation of new vessels
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11
Q

Proliferative diabetic retinopathy

A

Vitreoretinal neovascularization

  • Leads to retinal detachment
  • New vessels cannot invade vitreous gel
  • Grow on back surface of vitreous when it detaches

Vessels–> fibrosis–> pulls retina anteriorly (with vitreous)–> detachment (traction)

Can see adhesions blocking aqueous drainage (VEGF–> neovascularization–> adhesions–> neovascular glaucoma)

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12
Q

Mucormycosis

A

Mold infection beginning in paranasal sinuses

  • Invades eye
  • ocular proptosis
  • Eye no longer moves, must be removed
  • See vascular infiltration by fungus
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13
Q

Retinal detachment

A

Outer 1/3 separated from choriocapilaris (loses nutrients)

  • Leads to death of rods and cones if not promptly treated
  • Can’t regenerate
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14
Q

Rhegmatogenous Retinal Detachment

A

Horseshoe tear–> vitroretinal traction–> detachment

  • See flashes of light + floaters (BAD sign)
  • Can develop retinal hole
  • Increased risk in myopes (eye outgrows vitreous)

Exudative retinal detachment : seen in malignant melanoma

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15
Q

Coats disease

A

Abnormal retinal vessels–> leak

  • Secondary retina detachment
  • See cholesterol crystals and protein in sub-retinal space
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16
Q

Cataract

A

Opacification or optical dysfunction of crystalline lens

Four types:

  1. Normal development= nuclear sclerosis
    - Lens adds new layers in periphery
    - Cells in center eventually dehydrate–> accumulate yellow-brown pigment

Surgical correction: patients complain of “blue vision”

17
Q

Ectopia lentis

A

Spontaneous dislocation of lens
Occurs in heritable connective tissue disease
Ex: Marfan’s= fibrillin-1 defect

18
Q

Glaucoma

A

Risk factor:

  • Elevation of IOP (intra-ocular pressure)
  • Damages nerve as it enters globe through lamina cribosa

Excess aqueous humor produced by ciliary body
Blockage of drainage through trabecular meshwork–> Schlemm’s canal (most common type

Aqueous veins of asher= dilated veins on surface of eyeball draining excess aqueous humor

Can cause death of retinal ganglion cells

  • Axonal atrophy
  • Ganglion cells DON’T regenerate
  • Surgery to protect/preserve what’s there

Mueller’s cells= span thickness of retina, only thing left once ganglion cells die

See cupping of optic nerve=
- Glaucomatous optic atrophy (bean pot)

Macula lutea (yellow spot/pigment on retina)
- Protects against damaging blue light wave
19
Q

Uveal Malignant Melanoma

A

Most common ocular tumor in Caucasians (US/European)

  • 1,800 new cases yearly
  • May be pigmented

Almond shape–> rupture through Bruch’s membrane–> mushroom shaped tumor

  • *50% mortality
  • Liver mets seen in 90%

Prognosis:

  • Epithelioid cells present: 63% mortality in 15 years
  • No epithelioid cells: 28% in 15 years
20
Q

Retinoblastoma

A

Leukocoria= white pupil

  • Classical manifestation
  • Can also have physiological leukocoria (white pupil due to looking 15 degree angle in photo–> see nerve)

US mortality= almost 0%
Worldwide= 50% (poor/no access to care)

Resembles mini brain tumor

  • Arises from inner retinal layer (endophytic)
  • Arises from outer retinal layer (exophytic)–> detachment (can be confused with Coate’s disease

See enhanced mitotic activity

  • Basophilic cells
  • Cells outgrow blood supply–> die–> eosinophilic
  • Apoptotic cells, scanty cytoplasm
  • may see seondary calcification
Tumor= Blue
Calcium= Purple
Necrosis= pink

Photoreceptor Differentiation= Rosettes, Fleurettes

  • Flexner-Wintersteiner rosettes
  • Neoplastic rods and cones
  • Tumor entirely composed of fleurettes= precursor to retinoblastoma

If tumor gets behind lamina cribosa= CHEMO

  • Resect as much of nerve as possible
  • Germline cases= bilateral retinoblastoma (occurs earlier)
21
Q

Orbital lesions

A

Space occupying
- Cause ocular proptosis/exopthalmos

Direction of displacement= indicates location of orbital lesions

Ex. Mucocele (ethmoid)- eye lateral
Maxillary sinus- eye up

22
Q

Enopthalmos

A

Due to blow-out fracture

  • Eye sinks into space below
  • Can also be caused by metastatic scirrhous breast carcinoma
23
Q

Exopthalmos

A

Most common cause= Grave’s disease

  • Patchy chronic inflammation sparing tendon, fat
  • Enlarged EOMs–> proptosis
24
Q

Cavernous Hemangioma

A

Benign tumor

Can cause proptosis

25
Rhabdomyosarcoma
Child with proptosis (esp. upper orbit) - Malignant tumor of orbit - Can be confused with infection/inflammation because it grows so quickly - Stain for diagnosis Botryoid= associated with conjunctiva
26
Teratoma of orbit
Congenital tumor
27
Cryptophthalmos
Eyes underneath skin | - Associated with Fraser Syndrome
28
Synophthalmos
Cyclopia - Nose ABOVE eye (nasal probosis) - 2 small eyes fused together - Related to sonic hedgehog abnormality Also see holoprosencephaly - Brain does not divide into 2 hemispheres