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1241 Cards in this Set
- Front
- Back
what part of the retina do you tend to see cystoid degeneration in
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superior temporal quadrant. it starts at the ora, but can go all the way to the equator with age.
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is cystoid degeneration usually unilateral or bilateral
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usually bilateral and symmetrical
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describe the epidemiology of cystoid degeneration
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Common in children over age of 8 but progresses
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describe the pathophysiology of cystoid degeneration
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Cystoid spaces between retinal layers (outer
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is there an increased risk of retinal detachment with cystoid degeneration
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no
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is cystoid degeneration associated with any other ocular conditions
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retinoschisis
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what is the difference between a retinal detachment and retinoschisis
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RD is when all of the layers of the retina detach from the RPE. retinoschisis is when there is a cutting of the fibers at the inner nuclear layer or the outer plexiform layer.
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what is the difference between white with and without pressure in terms of management
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nothing. they are pretty much the same. the only difference is that one occurs with out pressure from scleral indentation and one does not.
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describe the orientation of lesions from white with and without pressure
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Usually parallel to ora
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can you see the retinal vessels over a white with or without pressure lesion
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yes, they stand out
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why is white with or without pressure commonly misdiagnosed as a retinal detachment
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because of the change of color, the lesion appears elevated. it is actually not elevated at all. -there would be no flap if you did scleral indentation though
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how common is white with or without pressure
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32% of total population Increases with age More common in more deeply pigmented races ((because it is easier to see)
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in what part of the retina do you tend to see white with and without pressure
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Between ora and equator Can extend to posterior pole inferior nasal least common
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is white with and without pressure preminant or transient
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white with and without pressure is transient. So don’t be supprised if you can’t see it on follow up, or if you see it in a different location than the previous visit.
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is white with or without pressure associated with any other conditions
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no
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describe the management of white with and without pressure
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No management unless vitreous degeneration,
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what does paving stone degeneration look like
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Appears as multiple round punched out lesions ((they have sharp discrete margins) Yellow white in appearance because seeing sclera ((so they are not holes because they are not red) Discrete margins often with pigment Can see large choroidal vessels at base Excavated not elevated - due to loss of outer retinal layers
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classic appearence of paving stone degeneration
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what part of the retina do you tend to see paving stone degeneration
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80% in inferotemporal quadrant Usually between ora and equator
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describe the incidence of paving stone degeneration
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22% of total population Increases with age
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describe the pathophysiology of paving stone degeneration
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Infarcts in choriocapillaris Inner retinal layers and vitreous are not affected
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describe the progression of paving stone degeneration
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Sometimes coalesce to yield scallops of pigment
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are there any other conditions associated with paving stone degeneration
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Sometimes coalesce to yield scallops of pigment
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describe the management of paving stone degeneration
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document. no tx necessary.
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what are the two main things you need to differentiate with when you think you see paving stone degeneration and how do you differentiate them
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DDX w/ histoplasmosis and toxoplasmosis Histo: usually in the posterior pole, not between the equator and the ora. histo spots tend to have less defined edges. less pigment associated with histo spots. Toxo: tends to have a lot of pigment. one lage lesion as opposed to many small lesions. toxo has less defined boarders
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describe the appearence of reticular senile pigmentary degeneration
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1. "net" like pigmented appearence 2. pigment aggregation around blood vessels
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is reticular senile pigmentary degeneration usually unilateral or bilateral
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bilateral in almost all cases
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in what part of the retina do you tend to see reticular senile pigmentary degeneration
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Can be anywhere but possibly more apparent nasal Can extend to equator (from the periphery)
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describe the epidemiology of retincular senile pigmentary degeneration
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Can be anywhere but possibly more apparent nasal Can extend to equator (from the periphery)
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describe the pathophysiology of reticular senile pigmentary degeneration
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Loss of pigment granules from some RPE cells with
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describe the management of reticular senile pigmentary degeneration
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none necessary
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is reticular senile pigmentary degeneration associated with any other conditions
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no
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what is the most important thing to differentiate reticular senile pigmentary degeneration with and how do you do this
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it is most important to differentiate between this and retinitis pigmentosa -there will be less bone spicule appearnce and their VISION WILL NOT BE AFFECTED as it would in RP -RSPD increases in prevelance with age
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what is another name for vitreoretinal tufts
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granular tags
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describe the appearence of vitreoretinal tufts
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Discrete white to gray irregular clumps on retinal surface Elevated Granular appearing
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what other finding to you tend to see with vitreoretinal tufts
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can be surrounded by cystoid degeneration
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vitreoretinal tuft with scleral indentation being performed
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describe the epidemiology of vitreoretinal tufts
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Noncystic tufts seen in up to 72% of population
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are vitreoretinal tufts unilateral or bilateral
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can be either (half the time)
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what part of the retina do you most commonly find vitreoretinal tufts
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Most common nasal Usually located just posterior to ora in vitreous base
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are vitreoretinal tufts associated with retinal break? why or why not?
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yes, because the vitreous is attached to the tuft. since there is force from the vitrous pulling on a small concentrated area there is a increased risk of retinal break.
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describe the pathophysiology of vitreoretinal tufts
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Small masses of cells of degenerated retina or
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describe the progression of vitreoretinal tufts
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Remain stationary in size and number
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what test do you need to do if you see a vitreoretinal tuft and why
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scleral indentation to see if there is a hole at the base of the tuft
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describe the management of vitreoretinal tufts
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if no holes, watch for holes. if there is a hole consider treatment with photocoagulation or cryoplexy.
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what subjective symptom would indicate that there is a hole from a vitreoretinal tuft
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Complaints of flashing lights ((particularly if there are always in one spot)
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what are meridonal folds a type of
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vitreoretinal tuft
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what are meridonal folds
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type of vitreoretinal tuft. they are elevated folds of the retina.
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describe the most common orientation of meridonal folds
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Most commonly aligned with processes (81%)
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can you see the vessels in the area of a meridonal fold
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vessels course over fold
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are meridonal folds more common in males or females
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males
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do meridonal fold occur singly or multiply
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singly 75% of the time
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are meridonal fold unilateral or bilateral
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either
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what quadrant of the retina are meridonal folds usually found
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superionasal
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what is a meridional complex
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Called “meridional complex” if meridional fold
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how are meridonal folds usually oriented with respect to the ora
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perpendicular
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describe the pathophysiology of meridonal folds
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Radially oriented folds of redundant retinal tissue
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describe the onset and progression of meridional folds
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Congenital Can increase in size with age
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are there any findings associated with meridional folds
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Vitreo-retinal tags at end of fold are common Holes at posterior end possible Can lead to retinal detachment
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what area of the retina is most suseptable to a retinal detachment if there is a meridional fold present and why
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temporal. there tends to be more thinning of retina in the inferior temporal area of the retina and more redundancy of retinal tissue in the superior nasal are
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describe the management of meridional folds
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Follow q 3 months for RD if hole and tag present If risks are present, cryopexy is preferred treatment due to accessibility
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what additional test do you need to do if you see a meridional fold and why
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scleral indentation to check for a retinal hole
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describe the classic appearence of lattice degeneration and how often does lattice appear in the classic form
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Well circumscribed oval or elliptical lesion Criss-cross pattern of white lines in "classic" Only present in 6 - 9% of cases -classic appearence is easy to diagnose, but it is not usually classic appearance
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is lattice degeneration unilateral or bilateral
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either; 50%. however tends towards bilaterality with age.
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what part of the retina is lattice degeneration located
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Between periphery and equator Vertical meridians between 5 - 7 and 11 - 1 o’clock
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describe the most common orientation of lesions from lattice degeneration
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parallel to the ora (circumferential)
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describe the epidemiology of lattice degeneration
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occurs in 6-10% of the population
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what percent of pts with lattice degeneration will have atrophic holes in the lesion
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18 to 30%
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what is circumfrential and radial
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refers to the orientation of a lesion (lattice degeneration) circumfrential: parallel to the ora radial: perpinducular to the ora
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what orientation of lattice degeneration is most common if the lesion is nearer to the equator
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If near equator tends to be radial and follow blood vessel
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of the two orinetations of lattice degeneration which is more concerning and why
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radial; more often associated with retinal detachment because lesion follows blood vessels and the blood vessels can act like the red strip that you use to open a pack of gum or a package of cigeretts
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describe the pathophysiology of lattice degeneration
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excavation of the retina due to atrophic retinal thinning. lines are functioning blood vessels with inflammed thickened walls (sclerosed). tent of vitreous with firm attachment to either side of the lesion. vitreous liquefaction common in area above the lesion.
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describe the pathophysiology of retinal detachment due to lattice degeneration
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if there is a hole from atrophic thinning the liquifed vitreous that is commonly found above the lesion could leak under the retina through the hole between the retina and the RPE causing a retinal detachment.
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what is the onset and progression of lattice degeneration
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becomes visable in teens. increases in obviousness and size with age.
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what are the fine white speks you can see in lattice degeneration
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fragmented pieces of inner retinal layers
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how can you tell where the borader of a lattice degeneration lesion is
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lesion extends beyond the pigmented area. the only way to tell the extent of the lesion is to do scleral indentation and look for increased whitening as you press on the retina (shows you where the vitreal attachments are). actual lesion is usually quite a bit broader than the pigmented are you see.
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describe the management associated with lattice degeneration
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follow regularly. consider laser treatment is holes present (depends on where the hole is) or risk factors of retinal detachment (flashes of light, pigment in vitreous, RD in other eye)
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what is important to remember before sending out a pt with lattice degeneration for cataract surgery
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if the have a hole there is an increased risk of developing a retinal detachment from the surgery. you need to tell the cataract surgen that lattice is present. when they pull on the lens capsule it pulls on the vitreous which pulls on the area of the lattice lesion. a lot of cataract surgens are doing prophylacitc treatment of holes assoicated with lattice degeneration before cataract surgery.
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name two events that increase the chance of developing a retinal detachment in the pt with lattice degeneration
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PVD or catarct surgery
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how do you tell if an atrophic hole associated with lattice degeneration is high risk for developing a retinal detachment or low risk
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remember that the vitreous makes a tent over the lattice lesion. and there is firm attachment of the vitrous on either side of the tent. you can see the edge of the lesion by doing scleral indentation and seeing where the retina no longer appears white. if the hole is close to, or goes past, the edge of the lesion there is a high risk of developing a retinal detachment because of the firm attachment. if the hole is entirely within the lesion and not close to the edge, then there is a low risk of RD.
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describe the appearance of atrophic retinal holes
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Look pinker or redder than surrounding tissue Round and discrete; "cut out"
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describe the pathophysiology of atrophic retinal holes
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hole in the retina due to atrophy. atrophic holes are like holes in your sock. It gets worn so thin that it wears all the way through creating a hole. There is nothiing pulling on it causing the hole as if you were to rip a hole in your socks.
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what quadrant of the retina do you tend to see atrophic retinal holes
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all quadrants
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is there a risk of RD with atrophic retinal holes
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seldom associated with RD
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describe the management associated with atrophic retinal holes
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Consider laser treatment if in periphery with traction or if any risks present (flashes of light, pigment in vitrous, RD in fellow eye) Must give patient symptoms of RD
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describe the subjective complaint that a pt will experience if they are having a retinal detachment
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"curtin" or shadow slowly comming across their vision. the curtin can come from any direction. there can be a red tint to their vision because broken blood vessels can release blood. recent onset or increase in number of floaters. -tell pt look of vision in any way in education. because you don't want them to start losing vision and think that it is not the same exact way that you described it and not come in when they are losing vision.
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what is a pseudo hole and how can you differentiate it with a real retinal hole
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where you have white without pressure throught the retina, but there is one area where you don't have it, it makes the area where you don't have it look like a retinal hole. you can tell because when you do scleral indentation there will be not flaps that lift off the retina.
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what is a horseshoe tear
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Elevated flap of light colored retinal tissue in “V” shape Horse "runs" to optic nerve (if you think of the direction that a horse wears it's shoes (tip of V towards head) the tear will be in a direction where the horse in facing the ONH)
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what is the difference between a retinal break a retinal hole and a retinal
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a break is a general term. it usually means that the surface of the retina facing the vitrous is not continuous. a hole is generally used where there is a more rounded appearance. a tear is where there is an elevated area of the retina that looks like it has been torn away.
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what part of the retina is a horseshoe tear most commonly seen and why
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much more common superior than inferior bc of the effect of gravity on the vitrous.
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horseshoe tear with retinal detachment. if there wasn't that area of detachment it would just be called a tear and not a detachment
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how can you tell the age of a tear
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if the flap is smaller than the tear (picture) this indicates that it is an older tear. when the flap is pulled away from the retina it looses its food source and starts to atrophy.
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describe the management of a horseshoe tear
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all horseshoe tears are sent out for treatment because there is a lose flap of retina that is still attached and could pull off more retina
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describe the pathophysiology of horseshoe tears
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often trauma induced tear.
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what is an operculated tear
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Retinal hole with flap of tissue completely torn off
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how can you tell the age of an operculated tear
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Operculum size compared to hole tells about age of hole Small operculum = longer duration
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what quadrant of the retina do operculated tears tend to occur
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any quadrant
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describe the pathophysiology of operculated tears
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often trauma induced
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if you seen an atrophic hole you always have to check in the vitrous for an operculum
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describe the management of an operculated tear
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less risk of retinal detachment than horseshoe tear, but management depends on surgeon and age of hole.
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new retinal detachments are much more obvious than old retinal detachments
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name four clinically observable signs of retinal detachment
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1. white folds of tissue that move when the pts eye moves 2. masks underlying choroidal details 3. shafer's sign 4. relative field loss
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name one clinically observable retinal sign of long standing retinal detachement
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Pigmented demarcation line if stable for at least 3 months
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how soon do you need to refer a pt w/ a retinal detachment
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if the macula is on withing 24 hours. if the macula is off you have longer.
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what is the difference between rhegmatogenous RD and nonrhegmatogenous RD
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Rhegmatogenous: secondary to retinal break Nonrhegmatogenous: secondary to traction, or fluid
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describe the pathophysiology of RD
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RD is when fluid accumulates between the RPE and the sensory retina
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what type of retinal detachment do you see shafer's sign with
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rhegmatogenous
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what is the mechanism for a RD from an optic pit
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non-rhegmatogenous: the vitreous gets under the retina through the pit
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what is a third type of retinal detachement besides rhegmatogenous and nonrhegmatogenous
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tractional. for example fibrosis from diabetes pulls retina off
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older retinal detachments can easily be confused with retinoschisis
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how does retinoschisis look different from a RD (6)
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it will look less like white floating tissue and more like a blister on the retina -fluid filled cyst -relatively immobile -blanches when depressed -white dots on inner surface (pieces of the cell bodies) -should be able to see choroidal details -absolute (not relative) scotoms (because you have cut the cell bodies from their axons)
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how can you differentiate between retinoschisis and retinal detachement base on field defect
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often it is to far out in the periphery to do a visual field. Retinoschisis is absolute scotoma. RD is relative scotoma. -you can tell by doing BIO. You shine your light over the area of detachment or schisis and place a pen or something in between your BIO and the condensing lens (this placement is important). That will cast a shadow over the affected area. Then you ask the pt if they can see a show that looks like a matchstick. If they can see it, it is a relative defect (RD), if they can’t see it, it is an absolute defect (retinoschisis) -this test works nearly 100% of the time (in a study with an N of 32 there was 100% specificity and selectivity)
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what is the most common quadrant to have a retinoschisis
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inferiotemporal
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describe the pathophysioloy of retinoschisis
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Retinal splitting between inner plexiform and outer
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do you tend to see a pigmented demarcation line with retinoschisis
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No demarcation line expected because there is no traction ont he retina ((if you see a pigmented demarcation line you should expect that it is an RD until proven otherwise)
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you may see two blood vessels in retinoschisis because the elevated vessel is casting a shadow on the retina (picture)
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describe the progression of retinoschisis
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progress very slowly
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are there any conditions associated with retinoschisis
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retinal holes in the inner or outer layers or both. very low potential for RD unless in both inner and outer layers because fluid can then get underneath the retina causing an RD
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describe the management of retinoschisis
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it is very important to differentially diagnose (DDX) between retinoschisis and retinal detachment (RD) because management is very different. retinoschisis: laser only if macular area in danger or it inner and outer holes present. if within 25 degrees of temporal arcades follow every 6 months and do fields, otherwise follow yearly.
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what is an avulsed vitreous base and what causes it
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where the bitreous base is pulled away from trauma. will appear as a floating white strip.
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what quadrant is an avulsed vitreous base usually
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superior nasal quadrant (gravity)
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describe the progression of avulsed vitreous base
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no changes
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are there any associated conditions with avulsed vitreous base
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vitreous hemorrhage, retinal tear (horseshoe or operculated)
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describe the management of avulsed vitreous base
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no treatment unless RD or tear. evaluate for other truama (no tears, angle recession etc)
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what are oral pearls and where are they located
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usually appear as white glistening round objects on dark background. on pars plana.
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describe the management of oral pearls
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Benign incidental finding No associated significant findings/risks No management needed
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what are pars plana cysts
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Look like blisters: raised clear lesion w/ smooth surface
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where are pars plana cysts located
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most likely temporal under the vitrous base
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are there any associated conditions with pars plana cysts
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more common in eyes with RD
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describe the management of pars plana cysts
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no management necessary
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New lecture: 15 OPT 633 - Tumors NeuralVascular 2010
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a
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what is a neoploasm
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A new and abnormal formation of tissue, as a tumor or growth.
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what is a melanoma
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tumor made up of malanin pigmented cells
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is melanoma a severe form of cancer
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yes, less common but more deadly
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what is an amelanotic melanoma
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a melanoma that lacks melanin
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what is a hamartoma? is it benign or maligmant?
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Composed of cells and tissues that normally occur in tissue (benign)
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what is a carcinoma
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A new growth or malignant tumor that occurs in epithelial tissue and may infiltrate local tissues or produce metastases.
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what is the most common conjunctival tumor
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conjunctival carcinoma
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what is another name for choroidal nevus
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benign choroidal melanoma
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what percent of pts have a choroidal nevus
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30% have to some degree
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describe the shape of a choroidal nevus
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typically flat or minimally elevated (less than 1mm). typically round or oval.
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describe the color of a choroidal nevus
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slate gray or brown
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are there any other retinal findings associated with choroidal nevus
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may see overlying drusen
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describe the onset and progression of a choridal nevus
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probably present at birth; maximal growth during prepuberal years; extremely rare to have growth after this time
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is it possible for a choroidal nevus to convert to malignancy
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it is possible. if the lesion is under 2 disc diameters (DD) 95% are benign and non-progressive when isolated with no other associated findings
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describe the management of choroidal nevus
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if under 2 DD Documentation and follow up on routine examinations if under 2 DD if 2 to 5 DD Suspect malignancy Need additional tests Ultrasound FA's Photodocument P32 Recall 6 months
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elevation, large size, feeder vessels and irregular shape or color on a lesion all indicate malignancy
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what does the green filter do
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it limits your view to neural retin because the green light is blocked by the RPE and doesn't go past it.
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what will happen to a choroidal nevus if you use the red-free filter
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it will disappear because it is outer to the RPE
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how common are choroidal malignant melanomas
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comprise the majority of all uveal tumors; 85%
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what is the most common primary intraocular tumor in adults
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choroidal molignant melanoma
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how big are choroidal malignant melanomas
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usually 10 DD or larger when first seen
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what population is choroidal malignant melanoma rare in
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extremely rare in african americans
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is malignant melanoma typically unilateral or bilateral
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typically unilateral. check the same quadrant in the fellow eye, if you see a similar pattern it might just be a physiological pigment variation.
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what color are choroidal malignant melanoma
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Pigmented, color varies from brown, mottled black, gray-green to white (amelanotic)
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choroidal malignant melanoma can look like a retinal detachment. a good retinal surgern will do ultrasonography before laser surgery to see if there is a mass behind the retina.
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choroidal malignant melanomas can grow to the point that they break through burch's membrane and extend in to the vitreous
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name three clinically observable retinal findings (other than the mass) that you see with choroidal malignant melanoma
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Serous detachments of the retina Choroidal folds Subretinal, vitreal and intraretinal hemorrhages hard exudates (neovascularization to feed the tumor leaks)
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name three other non-retinal clinically observable findings that you can see with choroidal malignant melanoma
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Secondary glaucoma (if the tumor impinges on the ciliary body or TM) Cataracts (if the tumor reaches the lens) Anterior and/or posterior uveitis (neovascular vessels leak a lot of inflammatory cytokines)
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what are the pts subjective complains comming in with a choroidal malignant melanoma
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none; can be asymptomatic; may have reduced VAs. may or may not have visual field defect.
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what two cancers should you ask about it you think you see a choroidal malignant melanoma
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lung cancer and breast cancer are the two big ones linked to choroidal malignant melanoma
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is choroidal malignant melanoma usually unilateral or bilateral
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Primary lesions are typically unilateral Secondary lesions from other cancers tend to be bilateral
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how can you DDX a choroidal malignant melanoma from a hemangioma with a transilluminator
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pigmented lesions do not transmit light. anesthetize the eye and place the transilluminator on the eye and look for any dark areas. dark areas indicate malignant melanoma; hemangioma will not have any dark areas.
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what will happen during the late phase of a fluorescein angiography
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the whole region will be bright because vessels have grown into the tumor to help it grow
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will a choroidal malignant melanoma show any changes on an ultrasound
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yes, it is changing the shape of the retina 3 dimensionally
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what is the name of the lab test you can use to DDX a choroidal malignant tumor and what is it
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P32 uptake. P32 is a chemical marker that is taken up more rapidly in malignant cells than it is in normal cells.
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CT and MRI are used to determine the extend of a choroidal malignant melanoma
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describe three tx for choroidal malignant melanoma
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1. enucleation (must be done carefully to prevent metastasis) 2. radioactive threapy (if caught early) 3. observation (for small tumors)
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you are very concerned of matastasis with choridal malignant melanoma; high incidence of death.
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name 6 ways you can tell if a lesion on the retina is benign or malignant
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when you take a picture of the retina you need to match the luminosity on the camera bc that will change the appearance of the lesion
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what percent of uveal tract melanomas are ciliary body malignant melanomas
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9%
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what part of the ciliary body is involved in a cilary body malignant melanoma
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May involve pigmented or non-pigmented epithelium or the stroma
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Because of the location of the ciliary body these tumors are hard to see unless the pupil is widely dilated. May grow to be very extensive size before they are actually seen. May be seen only after it grows large enough to extend into the pupil
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name 5 clinically observable signs that would indicate a ciliary body malignant melanoma
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1. irregular astigmatism 2. dislocation of the lens 3. focal opcity of the lens (pressure from the lesion) 4. focal dilation of eipscleral vessels 5. glaucoma
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what do you need to do if you see focal dilation of the episcleral vessels
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dilate really well and check the ciliary body for a tumor
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describe 5 methods you could use to detect a ciliary body malignant melanoma
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1. contact fundus lens to see ciliary body 2. transillumination of the sclera to check for dark spots 3. ultrasonography 4. P32 uptake 5. fluorescein angiography
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what is the tx for ciliary body malignant melanomas
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1. enucleation (usually) 2. sector resection (small tumors)
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Primary tumors of the eye are rare and usually benign (melanocytoma is an example)
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what is a melanocytoma
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dark black, elevated mass on the optic nerve
|
|
do melanocytomas tend to be unilateral or bilateral
|
almost always unilateral
|
|
what part of the ONH is involved with a melanocytoma
|
Usually involves the inferior part 10% may cover the majority of the optic disc
|
|
in VA affected in individuals with melanocytoma
|
no; if it is, there is only a slight reducetion 20/25 or so
|
|
what is the prognosis for melanocytoma
|
good. usually no progression and no loss of vision. rarely it will spread.
|
|
what does a melanocytoma look like on fluorescein angiography
|
hypofluorescence: blocks dye, no abnormal vascular findings
|
|
describe the management of melanocytoma
|
photodocument and routine follow up
|
|
why is the choroid a place where matastasis is likely to occur
|
because it is a spongy place that is very vascular
|
|
in what part of the retina do you tend to see a metastatic carcinoma of the choroid
|
posterior pole
|
|
describe the appearance of a metastatic carcinoma of the choroid
|
Flat, or slight elevation,
|
|
metastatic carcinoma of the choroid: can be multifocal or solitary. grow faster than malignant melanoma. less common than malignant melanoma.
|
|
|
a person with metastatic carcinoma of the choroid should have a Hx of cancer!
|
|
|
what ocular testing should be done on a pt with metastatic carcinoma of the choroid (3)
|
1. photodocumentation 2. ultrasound 3. P32 testing
|
|
what is the tx for metastatic carcinoma of the choroid
|
1. enucleation 2. irradiation threapy etc.
|
|
what signs indicate a pt has a metastatic carcinoma of the ONH (4)
|
Loss of VA. swollen ONH. venous tortuosity. central venous occlusion.
|
|
describe the prognosis associated with metastatic carcinoma of the ONH
|
poor. mean survival is 10 months.
|
|
leukemia: Infiltration of the leukemic cells in the optic nerve displace the normal neurons causing vision loss
|
|
|
what is the most common primary ocular tumor in chindren
|
retinoblastoma (1 in 20,000). second overall only to malignant melanoma.
|
|
is retinoblastoma unilateral or bilateral
|
Bilateral (1/3) or Unilateral (2/3)
|
|
what is the mortality rate associated with retinoblastoma
|
15-20%
|
|
does retinoblastoma have a heriditary component
|
yes, AD
|
|
name four conditions that can cause leukocoria
|
1. retinoblastoma (2/3 of cases) 2. cataract 3. coat's disease 4. retinopathy of prematurity
|
|
retinoblastom is reall tough to see on ophthalmoscopy (picture)
|
|
|
name four clues that indicate retinoblastoma
|
leukocoria, rubbing eyes (to stimulate phosphene), ophthalmoscopic findings, ultra sound (high calcium content to tumor)
|
|
what is the tx for retinoblastoma
|
1. enucleation 2. irradiation threapy etc. (if you detect it early you can save their vision; especially if bilateral)
|
|
what is medulloepithelioma
|
Ciliary Body equivalent to a retinoblastoma
|
|
most common age of onset for medulloepithelioma is in the first decade of life, but later than retinoblastoma
|
|
|
what is adult medulloepithelioma
|
A carcinoma Multiple white to gray fluffy mass of inner surface of the ciliary body Usually associated with trauma to the eye or post inflammation
|
|
what is (CHRPE)
|
congenital hypertrophy of the retinal pigment epithelium. enlargement or the RPE cells
|
|
how does CHRPE look
|
single or multiple black/dark gray sport of hypertrophyed RPE. if multiple in a bear track/animal track pattern
|
|
what part of the retina does CHRPE occur
|
anywhere
|
|
what is Halo Nevi
|
CHRPE may have an area of hypopigmentation surrounding the pigment. this is a diagnostic clue
|
|
are there any other conditions associated with CHRPE
|
if you have 6 or more CHRPE there is a risk of colon cancer FAP (in 40 yr old male)
|
|
what causes retinal pigment epithelial hyperplasia
|
Results from insult or trauma to retina Originates from many different conditions Chorioretinal inflammations Scars Choroidal neovascularization
|
|
|
|
|
describe the appearance of retinal pigment epithelial hyperplasia
|
Appears as a jet black irregular pigmentation, size and shape varies (picture left is RP right is RPE hyperplasia)
|
|
RPE hyperplasia is mechanism for pigment that develops with some lesions such as toxoplasmosis. RPE invastion into sensory retina.
|
|
|
what is a phakomatosis
|
Any genetic neurocutaneous disorders, in which anomalies are spread unevenly through the body. SEE: Hippel's disease; neurofibromatosis; sclerosis, tuberous; Sturge-Weber syndrome
|
|
what is the other name for von hipple-lindau disease
|
cerebroretinal angiomatosis
|
|
what is von hipple-lindau disease
|
Angiomatosis of Retina and Cerebellum Vascular tumors
|
|
what is a hemangioma
|
A benign tumor of dilated blood vessels.
|
|
is there a hereditary component to von hipple-lindau disease
|
yes
|
|
what is the age of onset for von hipple-lindau disease
|
30s
|
|
what percent of people with von hipple-lindau disease have ocular manifestations
|
25%
|
|
describe the retinal signs associated with von hipple-lindau disease
|
first microaneurysms, then small red nodules, then larger red-orange tumors. same process that is happening at the cerebellum. there will be hemorrhages and hard exudates from leaky vessels. you won't be able to tell the difference between the arteries and the veins.
|
|
|
|
|
describe the systemic involvement of von hipple-lindau disease
|
Involvement of cerebral, cerebellum, spinal cord tumors These cause neuropsychiatric symptoms, seizures, and mental retardation Other tumors have been found in the kidneys (66%), pancreas, liver and spleen
|
|
what is the other name for sturge-weber syndrome
|
encephalotrigeminal angiomatosis (less commonly used)
|
|
what is sturge-weber syndrome
|
Intracranial angioma, facial angioma, and choroidal angioma
|
|
are facial lesions associated with sturge-weber syndrome usually unilateral or bilateral
|
unilateral
|
|
what is the age of onset of sturge-weber syndrome
|
facial lesions are present at birth
|
|
name three systemic symptoms associated with sturge-weber syndrome
|
Can cause epileptic seizes Mental deficiency Hemiplegia
|
|
what is a nevus flammeus or port wine stain
|
cutaneous angioma present at birth in sturge-weber syndrome
|
|
describe the choroidal findings associated with sturge-weber syndrome
|
choroidal angioma. can be either localized or diffuse localized: yellowish to red orange lesion. elevated circular area. diffuse: entire fundus is deep red color. might miss unless compared to other eye
|
|
what percent of people with sturge-weber syndrome have a choroidal angioma
|
40%
|
|
what is your primary ocular concern with sturge-weber syndrome
|
congenital glaucoma
|
|
what percent of pts with sturge-weber syndrom develop glaucoma at some point
|
30%
|
|
at what age do people with sturge-weber syndrome develop glaucoma
|
Of those that develop glaucoma 60% by age 2 Buphthalmos, angle abnormalities 40% late childhood to early adulthood Angle is more normal Episcleral venous pressure increase from episcleral hemangioma
|
|
what non-retinal ocular findings are seen in sturge-weber syndrome (2)
|
heterochromia, dilated tortuous conjunctival vessels
|
|
what is arteriovenous malformation
|
Not a true phacomatoses Involves the retina and CNS with arteriovenous malformations These malformations are seen as markedly dilated and tortuous retinal arteries
|
|
what is another name for arteriovenous malformations
|
wyburn-mason syndrome
|
|
are arteriovenous malformatinos usually unilateral or bilateral
|
usually unilateral
|
|
what does the retinal of a person with arteriovenous malformations look like
|
enlarged tortuous vessels, more vessels, arteries and veins look the same
|
|
what systemic consequences are seen with arteriovenous malformatinos
|
hemorrhages in the brain cause stroke. epilepsy.
|
|
describe the progression of arteriovenous malformations
|
no progression. congenital.
|
|
what is another name for tuberous sclerosis
|
bourneville's disease
|
|
what are the cutaneous manifestatinos of tuberous sclerosis (3)
|
sebaceous adenoma: pale pink, usually around the nose and lip area of the face achromic nevi: congenital white patches or macules; hypopigented skin patches. shagreen patch: deffuse fibrous thickening of the skin usually located on the back
|
|
|
|
|
what are the ocular manifestations of tuberous sclerosis
|
May find small tumors on the conjunctiva May see hypopigmented iris spots May see retinal lesions (50%) astrocytoma
|
|
what is astrocytoma
|
abnormal growth of astrocytes (neural cells) in the retina. resembling a mulberry.
|
|
what part of the retina do you find an astrocytoma in
|
Usually located on the posterior pole near the optic nerve. Although, can be found anywhere
|
|
describe the prognosis for astrocytoma
|
pretty good. growth is very slow.
|
|
what is another name for neurofibromatosis
|
von recklinghausen's disease
|
|
what is neurofibromatosis
|
what the elephant man had
|
|
name 5 ocular manifestations of neurofibromatosis
|
1. ptosis of lid 2. orbital tumors 3. iris tumors (tan nodules) 4. retinal/choroidal tumors 5. glaucoma
|
|
New lecture: 16 AntSeg Traumaschool 09 NOTES
|
a
|
|
what does triage mean
|
The screening and classification of casualties to make optimal use of treatment resources and to maximize the survival and welfare of patients.
|
|
remember to ask what the pts vision was like prior to the accident with trauma
|
|
|
what is the diagnostic sequence for a trauma pt (8)
|
1. VAs 2. do fields on follow up 3. EOMs 4. pupils 5. color vision/red desaturation 6. gross observation 7. slit lamp -evert the lid (if superfical corneal abrasion) -conicle beam -anterior vitreous (have pt look all around, will help you see cells in the vitrous) 8. dilated BIO and NC or contact fundus lens (looking for RD. also helps if there is post-traumatic uveitis)
|
|
you may have to instil anesthetic on a trauma pt to get them to be able to take VAs
|
|
|
what is a closed globe and an open globe injury
|
closed: no full-thickness wound of the eye open: full-thickness wound of eye
|
|
what is a rupture
|
: Caused by blunt object increasing the IOP, wound is an inside-out mechanism and not necessarily at the impact site, tissue herniation is frequent and potentially substantial -choroidal herniation is common consequence of trauma
|
|
what is a laceration
|
Usually caused by a sharp object, wound is an outside-in mechanism at impact site
|
|
what is a penetrating injury
|
single entrance laceration
|
|
what is a intraocular foreign body injury
|
foriegn object retained in eye
|
|
what is a perforating injury
|
Two wounds (entrance and exit) caused by the same object
|
|
what is the most common type of trauma you will see
|
superficial corneal abrasion. pt scratched their cornea with finger nail or tree branch.
|
|
what should you do if a pt with a superifical corneal abrasion comes in complaining of foriegn body sensation
|
look for a foriegn body. if you don't see one, reassure them that it is normal for them to feel like there is something in there eye and that is just due to the inflammation. you can levage the eye just to make sure, but they will likely still feel a foreign body bc of the inflammation
|
|
|
|
|
what should you suspect if a trauma pt complains of photophobia
|
they will need a steroid because there is uveitis. it could just be that the abrasion is causing the glare though.
|
|
with trauma you may need to use proparocaine to look at the eye bc of blepharospasm
|
|
|
what can you tell about the injury when you put proparocaine in the eye
|
if the pain goes away, then the injury is limited to the cornea. if it is still there, there is deeper injury or uveitis
|
|
where does an abrasion due to CL overwear occur
|
centrally
|
|
if you see a vertical tracking pattern on the cornea where should you look for a foreign body
|
under the upper lid
|
|
the pattern of epithelial disruption on the cornea will tell you a lot about the cause of corneal trauma
|
|
|
how fast does the corneal epithelium heal
|
72 hours irregardless of the size of the defect if they are healthy. 6-12 hours for mild cases.
|
|
what are the three goals for treatment of ocular trauma
|
1. limit further trauma 2. reduce change of secondary infection 3. pt comfort
|
|
morgan lens: a system for ocular lavage (picture)
|
|
|
is pressure patching used to treat corneal abrasion
|
not currently considered standard of care. bandage CLs are a much better way to go. -pressure patches stabalize the lid which helps re-establish epithelium
|
|
how long can a pressure patch be worn
|
24 hour max! don't let the sun set twice on a pressure patch.
|
|
|
|
|
name two contraindications to pressure patch and why
|
if due to scratch from fingernail, due to risk of pseudomonas. if due to vegetative trauma due to risk of fungal infection.
|
|
what do you have to remember before removing a bandage CL
|
use artifical tears to help reduce the change of removing epithelium when you take off the lens. you can use a forcepts to remove the lens or you can just use your finger.
|
|
|
|
|
Dr. Yudcovitch fells that you should not use anesthetic before removing a bandage CL except in extreme cases where to pt won't let you get to the lens.
|
|
|
name three lenses approved for bandage soft CL use
|
ciba night and day, B&L purevision, acuvue oasys
|
|
how do you want to fit a bandage CL
|
steep to vault the cornea
|
|
how do you use an antibiotic on a pt w/ a bandage CL
|
add many of them directly over the lens
|
|
what are collagen shields
|
bandage CLs that disolve in the pts tear film with time. they come dehydrated and you can hydrate with saline or antibiotic. you can get ones that disolve in 12, 24 or 72 hours.
|
|
do you want to do warm or cold compresses with trauma?
|
heat may promote healing. cold may reduce swelling.
|
|
how can you treat corneal edema from trauma
|
hypertonics. they are not over the counter.
|
|
what do you do for treatment of a corneal abrasion
|
1. bandage CL for comfort 2. antibiotic to prevent infection 3. hot or cold compresses 4. hypertonics if swelling 5. cycloplegics if uveitis 6. topical or oral NSAIDS for pain
|
|
name one hypertonic drug
|
Muro-128
|
|
when should you follow up with a pt with a superifical corneal abrasion
|
18 to 24 hours for removal of patch. if small, non central abrasion, continue antibiotic 3-4 days and RTC. if large or central abrasion follow daily.
|
|
when can a Cl wearer resume CL wear after a superficial corneal abrasion.
|
2 to 3 days after complete resolution of abrasion.
|
|
lacerations are usually past bowman's layer into the stroma. that means that they will leave a scar. so you need to tell the pt that ahead of time, so they don't think that you messed up their treatment.
|
|
|
how can you tell clinically if a laceration has penetrated bowmans membrane
|
stain with fluorescein and if the stain leaks past the edge of the lesion (stromal glow) then you know that the laceration has penetrated bowman's membrane.
|
|
what do you do if there is a flap hanging off of a corneal abrasion
|
debride it off. you don't want to stick the flap back on and hope that it heals right.
|
|
what does it indicate if there is a shallow anterior chamber after trauma and why
|
that there has been some leakage of fluid. bc fluid that leaks from the anterior chamber will allow the contents of the posterior chamber to push the iris forward causing a shallow angle.
|
|
whta is the siedel sign
|
used to see if an injury to the globe is full-thickness. put fluorescein in the eye and have the pt blink firmly and watch for aqueous leakage. use a lot of fluroscein. IOP will be low if there is leakage.
|
|
how should you check pressures if there is trauma
|
use NCT so you don't have to touch a traumatized eye.
|
|
how could you reduce scaring if you have a corneal laceration that penetrates bowman's membrane
|
steroids will help reduce scarring.
|
|
what should you put on a deep corneal laceration as you are sending them out to the corneal specialist
|
don't use a pressure patch, use a shield patch
|
|
describe what you would do if a pt came in with a deep corneal laceration
|
1. consider culture if high risk of infection 2. rule out complications (traumatic uveitis, secondary ulcer) 3. lavage entire ocular surface 4. antibiotic ointment or drop 5. cycloplegics for AC response (if they are in pain or sensative to light, they will most likely develop a uveitis even if you don't see one) 6. NSAIDS 7. tells them ahead of time that there injury is going to scar
|
|
never pressure patch a full-thichness laceration!
|
|
|
theraputic CLs are the way to go over a pressure patch for deep corneal lacerations
|
|
|
how and why would you use a steroid on a deep corneal laceration
|
because steroids can reduce scarring. they also reduce healing. wait until laceration has begun to heal to start steroid therapy (there is controversy in this area). remember there is also an increased risk of infection with steroid use.
|
|
what is the RTC for a deep corneal laceration
|
24 hours
|
|
for a deep corneal laceration continue bandage CL therapy until the defect in about 1 mm in size.
|
|
|
if you are treating a deep corneal laceration, you should be following them daily. things should be constantly improving, if it ever starts to get worse, you need to reffer to a corneal specialist.
|
|
|
describe the follow up treatment associated with a deep corneal laceration
|
RTC 1 day. at innitial follow up: dc or continue cycloplegics, consider steroids for severe AC response. Pressure patch/theraputic SCL. continue antibiotics and NSAIDS. hypertonics if significant edema. RTC 1 day. -2nd follow up: if better dc cycloplegics. if worse add prednisolone q4h. continue antibiotics. RTC 24 to 48 hrs. -3rd follow up: findings should improve day to day. continue antibiotics.
|
|
what condition is a pt with a deep corneal laceration at risk for long term
|
recurrent corneal erosion.
|
|
what do you do if you get a pt full-thickness or perforating injury
|
STAT referral to the corneal specialist. transport with fox metal shield. DO NOT pressure patch.
|
|
why do they use systemic antibiotics for full-thickness corneal injuries
|
to prevent endophthalmitis
|
|
what is important to remember about the timeline of fungal infection
|
the infection occurs a long time after the innitial trauma, because it takes that long for the fungus to grow.
|
|
if you get glass in your eye it is very hard to see where it is to remove it. an anterior seg. OCT is helpful in determining where the glass is.
|
|
|
what is the white ring that surrounds a foriegn body on the corneal called
|
coat's ring
|
|
|
|
|
what is the rust ring that can surround a metalic foriegn body called
|
hemosiderosis
|
|
moderate to deep embedded foriegn bodies usually cause a __________
|
anteroir chamber reaction
|
|
what should you always check before you remove a foriegn body
|
depth, you don't want to remove a foreign body that it full thickness.
|
|
describe 7 methods of removing a foreign body
|
1. forced irrigation method: forcefully apply stream of liquid to the base of foreign body 2. sweeping swab method: wet a cotton q-tip and sweep over the FB 3. magnetic method: magnet used to remove metallic FB. not effective if embedded 4. needle method: come in tangential to the cornea with a needle. need to be careful. use a small needle. 5. bailey loop method: nylon loop at the end of a handle used to remove FB. 6 spud method: use spud to remove FB. get the smallest spud possible. 7. forceps method: use a forceps to remove FB
|
|
what types of foreign bodies (FB) does the sweeping swab method not work
|
it works for FBs on the conj. but does not work for FBs on the cornea bc you will remove large areas of epithelium.
|
|
why is it important to remove a rust ring from a pts cornea? what problem could be caused by its removal?
|
because bacteria like to live in the rust rings. -removal can cause chronic weakness that leads to erosions of the epithelium
|
|
descibe the nuance associated with removal of a rust ring.
|
you won't be able to get all of the rust out. however, over time, it will migrate anteriorly and slough it off over time.
|
|
what is the name of the instrument used to remove a rust ring from the cornea
|
alger brush
|
|
does your alger brush have a stop mechanism?
|
|
|
how do you treat after a foreign body is removed
|
after FB is removed tx is same as a corneal abrasion
|
|
what is this
|
iris prolapse
|
|
what is one cause of trauma where you would skip the case hx and go straight to treatment
|
chemical burn
|
|
curling iron burns to the eye are usually bad ones because heat supply doesn't reduce when it hits the wet surface of the eye like an ember would
|
|
|
how do you tx a radiation burn
|
like a superficial corneal abrasion
|
|
is an acid or alkali burn worse
|
alkali
|
|
what is the pH of the normal eye
|
around 7 (neutral)
|
|
describe the pathophysiology of an alkali burn
|
alkali saponifies (converts to soap) lipids in the epithelial cell membranes and it binds to the mucoproteins and collagen of the stroma. alkali continues to penetrate for hours to days after initial contact, even if rinsed off of the surface of the eye. can result in ulceration and melt.
|
|
you need to have the pt start washing out there eye immediately if they call in with a chemical burn. don't even have them come into the office first, just wash it out where ever they are at. then have them come into the office right away.
|
|
|
describe the progression of chemical burns
|
Alkali involvement may present moderately, then return as severe in 3 to 5 days (because tissue damage continues even after chemical is washed off the surface of the eye). Unlike other chemical burns, where the damage is usually maximal within hours.
|
|
describe the proceedure for lavage of a chemical burn
|
Need to pull the lids away for the eye and rinse the upper and lower cul-de-sac. Use sterile saline solution, or purfied water if they have it. if not use tap water.
|
|
for severe or moderate alkali burn refer directly to ___________
|
oculoplastic surgen
|
|
you need an emergency kit that has pH strips to determine the type of chemical burn that come into your office.
|
|
|
describe the treatement and follow up of a chemical burn
|
1. lavage immediately (before they leave for your office) for 20-30 min. 2. never put a bandage CL or a pressure patch on a chemical burn. the CL will act as a resivoir for the chemical causing damage to the eye. 3. rx antibiotic until there is no longer any staining 4. cycloplegics if AC reaction (steroid use is controversial) 5. RTC 24 hours until staining is gone
|
|
what do you need to remember if you are going to dilate a pt with a chemical burn
|
just use tropicamide, no phenlyephrine. because you don't want to constrict the blood vessels any more than they already are.
|
|
New lecture: 17 Blunt Trauma 09 NOTES
|
a
|
|
what will a pt experience visually from blunt trauma
|
The moment of impact is accompanied by intense pain and the sensation of a bright light
|
|
what is the hierchy of visual acuity results for people who can't see any letters on the chart (from best to worst vision)
|
1. counting fingers 2. hand motion 3. light projection 4. light perception
|
|
what is the difference between light projection and light perception
|
projection: they can localize the light source perception: they can only tell that there is, or is not light. they can't tell where it is comming from.
|
|
what type of IOP should you never do on a blunt trauma pt
|
digital
|
|
what tests do you need to do on a blunt trauma pt (7)
|
1. VA (do pinhole) 2. pupils 3. gross observation 4. IOP 5. EOMs 6. fields 7. dilated fundus exam
|
|
what do you need to educate a blunt trauma pt about
|
signs and symptoms of retinal detachment. they can occur a while after innitial trauma.
|
|
what other ocular condition besides retinal detachment can occur from blunt trauma
|
angle recession.
|
|
what is the mechanism for angle recession from blunt trauma
|
cornea, lens and iris displace posteriorly. cornea recovers, but lens still displaced. Angle tears.
|
|
what is the medical term for a bruise
|
ecchymosis
|
|
what is the tx and follow up for a black eye
|
cold compresses. typicall follow up in 5 days.
|
|
describe the progression of a black eye
|
it might actually look worse than innitial presentation after ecchymosis formation, but will eventually improve.
|
|
if there is hemorrhage on the outside of the eye, remember to look _______
|
on the inside of the eye
|
|
what tx is needed if an eye is so swollen that the pt can't close their eyelid
|
lubricating drops. you want to use a viscous gel (like refresh liquigel) because ointments need the lids to spread them across the eye. use copious amounts every 30 min to 1 hour.
|
|
what is the tx for subconjunctival hemorrhage
|
no tx, just education. -rest, no heavy lifting. sleep with head above heart for severe cases. avoid blood thinners. -may use cold or hot compresses
|
|
how long does it take for a subconjunctival hemorrhage to resolve
|
typically 1 week. severe cases can take 1 month.
|
|
you could drain a severe sub-conj. hemorrhage. you would need lots of antibiotics to prevent infection and to let the pt know that there will be blood running down the side of their face.
|
|
|
with a scleral laceration you may have low IOP. why?
|
because damage to the ciliary body causes temporary stopage of aqueous production
|
|
may see uveal prolapse with scleral laceration
|
|
|
what can you do if you don't have a metal shield for a pt with a severe laceration.
|
cut a styrofoam cup and make it shallow (metal shields are not expensive)
|
|
descemet's tears can occur from trauma or __________
|
forceps delivery (this is not done as much now)
|
|
what is iridoschisis
|
cleavage of the iris stroma
|
|
describe the management of iridoschisis
|
no tx. monitor for signs of angle closure
|
|
what is it called when the iris separates from the ciliary body
|
iridodialysis
|
|
what is it called when you have a tear in the iris that creates a second pupil
|
polycoria
|
|
why does iridodialysis increase the risk of glaucoma
|
because of scaring and fibrosis in the area of the trabecualar meshwork
|
|
what is angle recession
|
a tear between the longitudinal and circular muscles of the ciliary body. most often noted following blunt trauma.
|
|
angle recession can result in accommodative dysfunction
|
|
|
describe the management of angle recession
|
no tx, monitor for glaucoma
|
|
what is cyclodialysis
|
disinsertion of the ciliary body from the scleral spur which may produce a cyclodialysis cleft resulting in hypotony.
|
|
what is ocular hypotony
|
abnormally low IOP, usually less than 6 mmHg.
|
|
what is the mechanism for hyphema
|
rupture of the vascular supply to the iris and/or ciliary body
|
|
what ocular condition can you expect in almost all contusive injuries
|
uveitis
|
|
how is the IOP affected by trauma
|
IOPs typically low during the first week post-trauma. IOPs increase as the ciliary body recovers
|
|
is glaucoma associated with blunt ocular trauma? when is the onset?
|
Latent complication: Early: 2 months to 2 years: Related to amount of angle damage
|
|
what is the ring of pigment deposited on the lens after trauma called
|
vossius ring
|
|
what part of the orbit is broken in a blow out fracture
|
the orbital floor above the infraorbital canal
|
|
what is an avulsion of the optic nerve
|
most devistating consequence of severe ocular trauma that results in total blindness. A tearing away forcibly of the ONH.
|
|
New COURSE: Ocular Disease I
|
|
|
New lecture: Intro to Lid Disease 2009
|
|
|
what are the two parts of the orbicularis muscle
|
orbital portion and palpebral portion
|
|
what are the meibomian glands
|
sebaceous gland (oil) in the tarsal plate that provides the oily layer of the tear film. opening just behind the lashes
|
|
New lecture: Abnormal.Shape_posit. of lids.09.Victoria
|
|
|
Define ectropion
|
an abnormal eversion of the lower lid margin away from the globe.
|
|
what is the name of the surgery to repair ectropion
|
blepharoplasty
|
|
what are some subjective symptoms of ectropion?
|
tearing, eye or eyelid irritation, wiping eye, history of burns surgery or trauma around lids, bells palsy, asymptomatic.
|
|
Meaning of SOAP?
|
subjective objective assesment and plan.
|
|
Objective objective signs of ectropion
|
outward turning of the eyelid, exposure keratopathy, conjunctival injection, keratinization.
|
|
what is it called when you can't close your eyelids all the way
|
legophthalmos
|
|
some possible ways that ectropion can be acquired?
|
involutional (lid laxity from age), paralytic, cicatricial (scarring), mechanical (something is pushing or causing it), allergy (swelling).
|
|
the most common cause of acquired ectropion?
|
involutional. lid laxity with age.
|
|
its rare that ectropion be congenital but if its due to blepharophimosis syndrome what is this?
|
the abnormal narrowness of the palpebral fissure in the horizontal direction caused by the lateral displacement of the medial canthi
|
|
its rare that ectropion be congenital but if its due to microphthalmos what is this?
|
developmental anomaly where the globe is abnormally small.
|
|
congenital ectropion may be associated with buphthalmos which is?
|
An enlarged globe resulting from increased IOP. seen with pts that have congenital glaucoma.
|
|
Involutional Ectropion. Laxity-related ectropion typically begins laterally,centrally or medially
|
medially. with time central and lateral lid may evert.
|
|
four words that are used to describe ectropion based on their location
|
Punctal If you can see the puncta without manipulation, this is punctal ectropion Medial Can see an everted medial aspect of the lid Lateral Can see an everted lateral aspect of the lid Tarsal (complete) Can see the entire lower lid everted
|
|
name two ways that lower lid laxity can be tested
|
The lid distraction test how far the lid margin can be pulled away from the globe > 8mm = lid margin laxity The snap test How quickly the lid margin snaps back against the globe after it has been pulled away from it > 1-2 seconds indicates lid margin laxity
|
|
7th nerve palsy can be tested by asking the pt to do what?
|
show their teeth (rather than smile)
|
|
If the ectropion is due to a bells palsy when should you treat ectropion
|
wait for three months it usually will resovle on its own.
|
|
A cicatricial cause of ectropion could be due to?
|
chemical burn, surgery, eyelid laceration scar, or others
|
|
describe the management of ectropion
|
1. lubricating drops 2. taping possible 3. surgical treatment
|
|
what is it called when the lids are partially or completely sutured together
|
Tarsorrhaphy
|
|
external paste-on upper lid weights available for lagophthalmos/ectropion
|
|
|
subjective reports for entropion
|
ocular irritation, FB sensation, tearing, red eye, potopobia, decreased vision (possible)
|
|
objective signs for entropion.
|
turned in eyelid, SPK, FB tracking, conj injection, corneal ulcer, decreased cornela sensation, corneal scaring
|
|
causes of entropion
|
involutional, acute spastic, or congenital, cicatricial
|
|
entropion caused by acute spastic entropion is caused by what?
|
the orbicularis oculi muscle overwhelms the oppositional action of the lower eyelid retractors. (usually an involutional component as well)
|
|
you may have to ask the pt to ______in order to see acute spastic entropion.
|
blink
|
|
acute spastic entropion is usually the result of?
|
ocular irritation, may be due to an infectious, inflammatory or traumatic processes.
|
|
Congenital entropion is very rare but may arise due to underlying developmental abnormalities such as
|
dysgenesis, paucity of tissue vertically in the posterior lamella of eye lid, or tarsal kink syndrome
|
|
causes of cicatricial entropion could be?
|
scaring of the palpebral conj usually the result of trauma, infection, chemical burn or stevens-johnsons syndrome, ocular cicatricial pemphigoid
|
|
what is ocular cicatricial pemphigoid (OCP) (a cicatricial cause of entropion)
|
Rare inflammatory syndrome involving primarily the oral and ocular mucous membranes
|
|
entropion Must be distinguished from Epiblepharon which is?
|
A congenital condition in which the pretarsal orbicularis muscle and the skin covering the eyelid push the eyelashes vertically or inwards
|
|
Plan for entropion
|
Medical therapy- lubrication (may break cycle of spastic entropion due to dry eye). hygiene/ antibio and steroid to treat bleph. which coud be causing the spastic entropion. Botox-weakens pretarsal orbicularis.
|
|
Is it possible for blepharitis to cause the lashes to turn in?
|
Yes.
|
|
define trichiasis
|
The acquired misdirection of eyelashes toward the globe
|
|
describe some subjective complaint associated with trichiasis
|
FB sensation, red eye, pain, photophobia, tearing
|
|
what are some of the objective findings of trichiasis?
|
conjunctival scarring, FB tracking on cornea, Signs of entropion and horizontal lid laxity, Lashes growing from the meibomian gland orifices (distichiasis), symblepharon and fornix scars.
|
|
causes of trichiasis?
|
Infectious (blepharitis, zoster, trachoma), autoimmune (OCP), inflammatory (stevens-johnson, vernal keratoconjunctivitis), trauma.
|
|
describe the management of trichiasis
|
1. lubricants 2. tx causative disease 3. surgical proceedures
|
|
what are two procedures that can help with trichiasis?
|
lash/follicle destroying/repositioning, epilation
|
|
is epilation permanent or temporary
|
usually temporary it often leaves the lash follicle.
|
|
what is the most effective way of fixing trichiasis?
|
radiofrequency ablation
|
|
the treatment "normally done" for trichiasis?
|
epilation
|
|
where is the general location for an eyelid coloboma for the upper and lower lids? does it usually affect the upper or lower lid
|
upper- Usually between the inner and middle third of the lid lower- Usually between the middle and outer third of the lid -usually affects the upper lid
|
|
what is it called when there is failure of eyelid formation
|
cryptophthalmos: cryptophthalmos the eyelid skin grows continuously from the forhead to the cheeks
|
|
objective signs associated with eyelid coloboma
|
trichiasis, symblepharon, malformation of the caruncle, exposure keratopathy, obstruction of the lacrimal system, other colobomas
|
|
what type of tissue is defective during developement when a lid coloboma is formed?
|
mesodermal tissue, some research show that it may also be due to ischemia.
|
|
our primary goal with treatment of a lid coloboma?
|
corneal protection. Artificial tears and ointment Moist chamber optical bandages Bedtime patching
|
|
why would you want to wait until the infant is older if you have a small eyelid coloboma that is not causing too many problems
|
risks with anesthesia are greater with infants
|
|
are epicanthal folds usually unilateral or bilateral
|
almost always bilateral, however, may be asymmetric
|
|
should an infant with epicanthal folds be seen for the problem ever again?
|
yes in 6 months. if it is limiting the view then surgery could be done. also you want to check for a real esotropia, because it will be hard for the parents to tell.
|
|
are epicanthal folds associated with any ethnicity
|
asian
|
|
are epicanthal folds permanent
|
usually the child will grow out of it.
|
|
what is dermatochalasis?
|
Definition: Redundant and lax eyelid skin overhanging the margin
|
|
what age is the begining of dermatochalasis usually seen is?
|
40 and progresses with age. if it runs in the family it has been seen to start in the 20's
|
|
causes of dermatochalasis?
|
Loss of elastic tissue in the skin, and Weakening of the connective tissues of the eyelid -more common in the upper eyelid, but can be seen in the lower lid
|
|
subjective complaints with dermatochalasis?
|
cosmetic, ocular irritation, entropion of upper eyelid, ectropion of the lower lid, bleph, dermatitis.
|
|
objective findings of dermatochalasis
|
Presence of an upper eyelid crease should be noted and measured (look for lesions). Levator still functioning Normal upper eyelid margin position should fall ~1 mm below the superior limbus. orbital fat should be assessed
|
|
most common cause of dermatochalasis is? and others?
|
normal aging is most common. trauma, priorbital edema, chronic dermatitis, thyroid eye disease, blepharospasms, and flopp;y eyelid syndrome.
|
|
Plan for dermatochalasis?
|
generally surgery (blepharoplasty). patients with blepharitis may benefit from hygiene and topical antibiotics. dermatitis may use steroids.
|
|
New lecture: Lid Muscle Abnormalities.09.Victoria
|
|
|
define ptosis
|
An abnormally low position (drooping) of the upper eyelid
|
|
ptosis is also called
|
blepharoptosis
|
|
types of ptosis
|
Congenital Acquired
|
|
what percent of cases of ptosis are congenital
|
90% Congenital, and present at birth
|
|
what percent of congenital cases of ptosis are unilateral
|
70%
|
|
causes of congenital ptosis (2 types, remember the names)
|
irregularity of the levator muscle (mygenic) or abnormalities of the CN 3 superior division (neurogenic).
|
|
how can you DDX between congenital and acquired ptosis
|
look at old pictures. or look at lid position in downgaze: In congenital ptosis, the ptotic lid appears higher in downgaze In acquired ptosis, the ptotic lid is equal to the non-ptotic lid
|
|
what is marcus gunn syndrome?
|
anomalous innervation. lid elevation occurs with mastication or with movement of the jaw to the opposite side.
|
|
categories of aquired ptosis are?
|
neurogenic, myogenic, aponeurotic (where the levator aponeurosis has undergone structural changes which reduces its ability to lift the eyelid), and mechanical.
|
|
An example of acquired neurogenic ptosis?
|
Horners syndrome. ptosis miosis and anhidrosis. lack of sympathetic innervation. DM or aneurysms of the internal carotid artery.
|
|
why do you get heterochromia with Horner's syndrome
|
Because of the lack of sympathetic innervation to the iris melanocyte development, a difference in the iris color between the eyes may result (heterochromia)
|
|
what is an example of acquired myogenic ptosis? and what are the signs?
|
Myasthenia gravis. basically a muscle problem. bilateral but asymmetrical ptosis. the Pt may have a history of fluctuating ptosis and strabismus.
|
|
what is the most common type of aquired ptosis and is it unilateral or bi?
|
Aponeurotic ptosis and it is usually bilateral.
|
|
Acquired mechanical ptosis is caused by what?
|
excessive weight, like edema tumors or traumatic events such as lacerations effecting nerves or muscles.
|
|
what is one example of pseudoptosis?
|
dermatochalasis.
|
|
what are the values of mild, moderate and severe ptosis in mm.
|
-measure both palpebral fissures and find the difference Mild: 1-2mm Moderate: 2-3mm Severe: =4mm
|
|
Other than amblyopia what could a ptotic eye cause in regaurds to vision?
|
astigmatism from the compression.
|
|
what is the proper way to evaluate the levator function on a ptotic pt? and what are normal results
|
The patient looks downward as a ruler is positioned with a mark adjacent to the upper lid margin With the examiner's hand eliminating any brow (frontalis) action by the patient, the patient looks upward as far as possible without a change in head position Total lid elevation should be 8-14mm as patient looks from down gaze to up gaze
|
|
with a ptotic pt if you want to watch for amblyopia how often should you schedule a follow up?
|
3-4 months also look for signs of a head turn. -extrenal photographs can be helpful.
|
|
average number of blinks per minute?
|
15-20
|
|
what is blepharoclonus? and what causes it?
|
increased frequency of blinking, increased closure phase (time lid is actually closed), caused by irritation and inflammation.
|
|
what population is blepharoclonus usually seen in?
|
children
|
|
what is myokymia? what is it caused by?
|
twitching of a few bundles of the eyelid fibers. lid twitch, fasciculation of the orbicularis. stress, tension, fatigue, lack of sleep, caffeine...
|
|
treatment for myokymia?
|
remove the cause, inject botox, use antihistamines, or quinine (tonic water)
|
|
is blepharospasm usually unilateral or bilateral
|
blepharospams is bilateral
|
|
define blepharospasm
|
Any abnormal tic or twitch of the eyelid bilateral involuntary orbicularis contraction resulting in lid closure. spasmodic, idiopathic.
|
|
describe the pt demographic that most commonly experiences blepharospasm
|
>50, F>M,
|
|
describe the severity associated with blepharospasm
|
At one end - essential blepharospasm - manifested by simple increased blink rate and intermittent eyelid spasms On the other end of the spectrum - blepharospasm is a disabling condition with ocular pain and functional blindness
|
|
Blepharospasm commonly is associated with
|
dystonic movements of other facial muscles
|
|
objective: changes with long standing blepharospasms include?
|
eyelid and brow ptosis Dermatochalasis Entropion canthal tendon abnormalities
|
|
Early symptoms of blepharospasm include
|
increased blink rate, eyelid spasms, eye irritation, midfacial or lower facial spasm, brow spasm and eylid tic.
|
|
Conditions relieving blepharospasm included
|
sleep, relaxation, interior gaze, artificial tears, singing, humming.
|
|
therapy for blepharospasms
|
reassurance, botox and it would need to be re injected in 3-4 months. last choice would be surgical, it involves removal of the orbicularis.
|
|
what is a macule
|
a flat, discolored spot of varied size (<10 mm) and shape.
|
|
what is a patch
|
similar to a macule, but >10 mm
|
|
what is a papule
|
a solid, elevated lesion < 10 mm in diameter
|
|
what is a nodule
|
a solid lesion >10 mm in diameter that may or may not be elevated. projects above and below the surface.
|
|
what is the difference between a nodule and a tumor
|
tumors are larger nodules that are 20 mm or greater
|
|
what is a vessicle
|
a circumscribed, elevated lesion < 5 mm in diameter containing serous fluid. (a small blister)
|
|
what is a bulla (blister)
|
a vessicle > 5mm in diameter
|
|
what is a pustule
|
a superficial, elevated lesion containing pus
|
|
what is a telangiectasia
|
dilation of superficial blood vessels
|
|
New lecture: OPT 533 - Blepharitis 2009
|
|
|
what is another name for blepharitis
|
lid surface disease
|
|
what is blepharitis
|
inflammation of the eyelids and especially of their margins
|
|
what is the difference between anterior and posterior blepharitis
|
anterior: inflammation centered around eyelashes posterior: inflammation involving the meibomian glands and gland orifices
|
|
most common cause of anterior blepharitis? and two others
|
staphylococcal (aureous or epidermadis) and seborrheic, mixed
|
|
what is seborrhea
|
abnormally increased secretion and discharge of sebum producing an oily appearance of the skin and the formation of greasy scales
|
|
what is sebum
|
a fatty secretion of the sebaceous glands of the skin
|
|
what is another name for posterior blepharitis
|
meibomianitis.
|
|
what is angular blepharitis and name two organisms that cuase it
|
blepharitis localized to the canthus. caused by staphylococcus and moraxella
|
|
what is staphylococcal blepharitis
|
infection of the lash follicles and lid margins with staphylococcus aureus and/or an overgrowth of staphylococcus epidermidis (epidermidis is part of the normal flora of most individuals; aureus is normally present in only a small number of individuals)
|
|
what type of bacteria are staphylococcal?
|
gram + cocci
|
|
what are the three types of blepharitis?
|
anterior, posterior, and angular
|
|
how does staphylococcal blepharitis affect the tear film
|
the bacteria produce lipase which breaks down lipids in the tear film creating free fatty acids. this triggers inflammatory and irritative response.
|
|
what makes up pus
|
dead PMNs and protein clots. -presence of pus indicates bacterial infection
|
|
what are PMN's?
|
polymorphonuclear leukocytes (WBC's) that move into the tissues during an inflammation response
|
|
staph bleph subjective complaints
|
may be asymptomatic, depends on severity. chronic irritation and burning, FB sen,tender lids (could have recurrent hordeola or chalazia), crusts on lashes, stuck lids, pt may complain of red irritated lids.
|
|
name 11 clinically observable objective signs associated with staphylococcal blepharitis
|
1. Crusts along the lash line at the base of the lashes 2. collarettes 3. madarosis 4. infected folicles 5. ulcers at the base of the lashes 6. trichiasis 7. lid erythema 8. secondary conjunctivitis 9. PEE 10. phlyctenule 11. marginal infiltrate
|
|
Crust can encircle lash are called what?
|
collarette
|
|
will the crusts always be crusty?
|
no they could have an oily appearance but there is still the presentation of yellow goodness.
|
|
loss of lashes or eyebrows is called:
|
Madarosis
|
|
staph bleph can also cause a misdirection of the lashes called? the tx for this is?
|
trichiasis, epilation
|
|
what is the conjunctivitis secondary to staphylococcus blepharitis sometimes called.
|
staphylococcal blepharoconjunctivitis
|
|
what is the mechanism for PEE caused by staphylococcal blepharitis
|
The baceria produce exotoxins that damage the cornea.
|
|
what is the difference b/t PEE and an ulcer of the cornea?
|
PEE is only missing epi. an ulcer is a hole that has missing epi and dermis (or stroma). (damage that is limited to the epithelium is considered an erosion)
|
|
tx of staph bleph includes (5)
|
1. lid hygiene: remove crusts, remove bacteria 2. increase blood flow by performing a warm compress 3. lid scrubs 4. antibiotic (ointment and oral when severe) 5. lubricants
|
|
what do you need to remember to tell the pt when you are rxing warm compresses for blepharitis
|
the compresses are going to make their eyes red bc you are opening up the blood vessels, but that is good because it lets the blood cells get in there and fight the infection.
|
|
instructions for warm compresses
|
soak lids with warm, wet compress with the eyelids closed for 10-15 min, bid-qid.
|
|
instructions for lid scrubs
|
1. Wash your hands thoroughly. 2. Mix warm water and a small amount of non-irritating (baby) shampoo (1-1 to 10-1) or use a commercially prepared lid scrub solution recommended by your optometrist. 3. Using a clean cloth (a different one for each eye) rub the solution back and forth across the eyelashes and edge of the closed eyelid. 4. Rinse THOROUGHLY with clear water. 5. Repeat with the other eye.
|
|
name four antibiotic ointments used for staphylococcus blepharitis and their class
|
Bacitracin Cell wall inhibitor Erythromycin Macrolide Gentamicin Aminoglycoside Tobramycin Aminoglycoside
|
|
how many times should a pt apply the antibiotic ointment for moderate and severe staph bleph?
|
Moderate: qhs or bid Severe: tid or qid
|
|
If the staph bleph is extremely severe what drug may you need to use? what is the regimen
|
oral antibiotics such as doxycycline 100 mg PO bid for 7-10 days
|
|
how can antibiotics like tetracycline or doxycycline be helpful for staphylococcal blepharitis even if the bacteria is resistant to it? (staph bleph)
|
tetracyclines inhibit the lipase synthesis by the bacteria and doxycycline inhibits exotoxin induced cytokines and chemokines. they also have an antiinflammatory response.-good for rosacea.
|
|
important points for patient education when talking about staph bleph?
|
Chronic condition - Usually exacerbations and remissions Goal: to control not cure Importance of daily lid hygiene Medication for acute flare-ups
|
|
a pt with staph bleph may have WBC's infiltrate their cornea. where are they located? can they do damage?
|
in the periphery btwn the epi and the stroma. they can damage the cornea when they die b/c they release enzymes.
|
|
do corneal infiltrates stain with fluorescein
|
may or may not stain. may stain in a sporadic punctate pattern
|
|
what causes marginal infiltrates due to staphylococcus blepharitis
|
hypersensitivity to staph. toxins. white spot is accumulation of WBCs (infiltrate means WBCs)
|
|
tx for marginal infiltrate associated with staph bleph?
|
treat the staph bleph and also add a topical steroid q2h to qid such prednisolone acetate, dexamethasone or loteprednol. or use a combo antibiotic/steroid like tobradex or zylet q2h to qid.
|
|
what is a phlyctenule
|
a small vesicle or pustule ; especially : one on the conjunctiva or cornea of the eye. it is a collection of WBCs. it is due to a hypersensativity reaction to different pathogens.
|
|
what is the name of a raised white lesion due to hypersensitivity to staph toxins and where is it located?
|
phlyctenule. may be on the conj limbus or cornea and may move across the cornea pulling vessles with it and creating a scar.
|
|
How do you treat a phlyctenule associated with staph bleph?
|
treat the staph bleph and also add a topical steroid q2h to qid such prednisolone acetate, dexamethasone or loteprednol. or use a combo antibiotic/steroid like tobradex or zylet.
|
|
what was the most common cause of phlyctenule several years ago? what is it now? why?
|
was TB, now it is staphylococcus. b/c we are better at controling TB.
|
|
seborrheic blepharitis is often associated with what? and what is that?
|
seborrheic dermatitis a disorder of the skin in areas with abundant sebaceous glands. dandruff is excessive shedding of the dead skin cells of the scalp; it is a symptom of seborrheic dermatitis
|
|
what is another name for dandruff
|
scurf
|
|
subjective symptoms for seborrheic blepharitis?
|
Frequently asymptomatic Possible morning “mattering” Dry eye complaints (poor tear film), Symptoms may depend on other concurrent processes
|
|
objective signs for seborrheic blepharitis (3)
|
greasy, waxy scales at the base of the lashes that flake off easily (scurf). skin of the lids a little greasy. PEE
|
|
where and what kind of damage to the cornea occurs from seborrheic blepharitis
|
Interpalpebral PEE that is located more centrally.
|
|
Tx for seborrheic bleph?
|
lid hygiene, lubricants, patient ed on chronicity of condition.
|
|
Mixed bleph is a combo of what?
|
staph bleph and seborrheic bleph.
|
|
Tx for mixed bleph?
|
same as just staph bleph. use an antibiotic such as tobramycin.
|
|
describe the pathophysiology of meibonian seborrheic blepharitis?
|
excessive oil production from the meibomian glands, and quality of oil is abnormal.
|
|
what are the subjective symptoms associated with meibomian seborrheic blepharitis
|
dry eye complaints
|
|
objective findings for meibomian seborrheic blepharitis (3)?
|
1. frothing of tears (oil slick in tear film) 2. reduced TBUT 3. conjunctival injection -lid tissue appears normal
|
|
Tx for meibomian seborrheic bleph?
|
keep lid margins clean and lubricants.
|
|
angular blepharitis what is it?
|
Localized eczematoid inflammation of the lid at the outer canthus and sometimes medial canthal region. may also involve the conj.
|
|
there are two causes of angular bleph. what are they and how do the lids differ in their appearance between the two causes.
|
1 staphylococcal form, dry and scaly 2 moraxella form, wet, macerated lid with whitish frothy discharge.
|
|
Tx for Angular blepharitis?
|
treat with an antibiotic ointment. (may need to try different antibiotics based on bacteria type)
|
|
New lecture: Surgical Procedures Of Eyelid Lesions And Anomalies
|
|
|
if you need to anesthatize the eye or a lid proceedure, where are the nerves located
|
|
|
questions to ask the pt before any kind of surgical proceedure to the eye
|
Are you allergic to any anesthetics? When you cut yourself do you stop bleeding quickly? Are you taking any anti-coagulant medications? - aspirin - coumadin (warfarin) - heparin
|
|
New lecture: OPT 533 - Meibomianitis Skin 2009
|
|
|
describe the pathophysiology associated with meibomian gland dysfunction?
|
its not considered infectious entity, the gland metabolism is altered, secretions become thick and the block the opening, stagnant material grows bac. lipase is released triggering inflammation.
|
|
meibomian gland dysfunction is often associated with what skin disorder?
|
rasacea (acne),
|
|
what is (acne) rosacea
|
chronic inflammatory disorder involving skin and eye. the sebaceous glands are involved.
|
|
describe the epidemiology associated with (acne) rosacea
|
"celtic" northern ancestry (genetic component). adults 30-60 years old
|
|
what percent of people with rosacea have ocular problems
|
30%
|
|
there are some bumps that are associated with rosacea they can come in two forms what are they called and which comes first.
|
pustules and papule. papules usually proceed to pustules.
|
|
where is the cellular debris in a papule?
|
in the dermis
|
|
what is a pustule associated with rosacea
|
a typical pimple. red and inflammed with a white head. papules often progress to pustules
|
|
what is this
|
telangiectasias associated with rosacea
|
|
Telangiectasias associated with rosacea what are they
|
sisible dilated small blood vessels on the nose or cheeks. you can also get them on the eye lids. even on the bulbar conj.
|
|
rhinophyma what is it?
|
red, bullous nose (sebaceous gland hypertrophy); associated with rosacea
|
|
Tx and regimen for rosacea?
|
usually oral doxycycline 100mg bid X 4-6 weeks. you could also use a topical cream (metrodiazole gel) bid X 5-8 weeks.
|
|
what are some things that may trigger rosacea
|
hot spices, alcohol, heated beverages, chocolate, tomatoes, citrus fruits, Sun exposure, winds, stress, fear, anxiety, hellobacter pylori, ace inhibitors b/c they are vaso dilators.
|
|
what type of ocular manifestations can rosacea have on lids (5)?
|
Meibomian gland dysfunction Blepharitis, Hordeolum, Chalazion, Inflammation and infection of the lids
|
|
what type of ocular manifestations can rosacea have on eye itself (5)?
|
Poor tear film, Conjunctival injection, PEE (SPK), Corneal vascularization, Corneal thinning
|
|
what could you do to tx a pt with rosacea if it is not affecting the eyes.
|
nothing dont Tx them; if it's not affecting the eyes refer it out.
|
|
what should you educate the pt about if they have ocular rasacea?
|
lid hygiene, dietary restrictions and environmental triggers.
|
|
how can you check for meibomian gland dysfunction clinically
|
transillumination of meibomian glands
|
|
normal transilluminated meibomian gland
|
abnormal transilluminated meibomian gland
|
|
what is this
|
plugged meibomian glands (caps)
|
|
objective signs of meibomian dysfunction (4)
|
1. pouting of meibomian glands 2. inflammation of lids surrounding glands 3. serrated lid margin 4. conjunctival injection
|
|
if you perfom a toothpast test and squeez a meibomian gland what color should the excretions be normally?
|
clear
|
|
when evaluating meibomian gland dysfuction what other conditions must you look for
|
staph bleph, seborrheic bleph, and rosacea.
|
|
Tx for meibomian gland dysfunction?
|
1. warm compresses 2. in-office/at home expression of meibomian glands 3. manage dry eye. 4. consider doxycycline 100mg bid for 6 -10 weeks if severe or not responding to therapy. taper to lowest dose if possible. this works by inhibiting lipase production.
|
|
Pt education for meibomian gland dysfunction?
|
its a chronic condition, there is no cure all we can do is manage it.
|
|
agents causing angular blepharitis?
|
Moraxella lacunata Staphylococcus epidermidis Staphylococcus aureus
|
|
drugs used for moraxella? drugs used for staphylococcus?
|
M - zinc sulfate .25% solution S - bacitracin or erythromycin
|
|
what condition is this
|
impetigo
|
|
what is impetigo
|
Skin infection with Staphylococcus aureus or Streptococcus pyogenes
|
|
true or false impetigo is not contagious?
|
false it is contagious
|
|
describe the epidmiology associated with impetigo
|
most common in children under 6, sometimes in the elderly. also people exposed to poor hygienic conditions (common in homeless population)
|
|
what are the objective signs associated with impetigo (1)
|
a rash with crusts ("honey crusts") on the face and distal extremities
|
|
describe the tx associated with impetigo
|
dermatologist will tx this condition. oral antibiotics, wash involved areas, topical antibiotic after washing.
|
|
what condition is this
|
erysipelas
|
|
what is erysipelas
|
A skin infection involving the superficial dermal lymphatics swell up. that affects the legs and face most frequently.
|
|
what bug causes erysipelas?
|
streptococcus pyogenes
|
|
how do you tell the difference b/t Erysipelas and Rosacea?
|
Erysipelas will have started recently and Erysipelas will cause fever, chills, and pain.
|
|
Is erysipelas contagous or not?
|
yes but not as much as impetigo because erysipelas it is in a deeper layer of the skin
|
|
Tx for erysipelas?
|
refer to PCP or dermatologist. you would use penicillin
|
|
New lecture: Thyroid Eye Disease.2009.FCH.Victoria
|
|
|
how does the thyroid gland work
|
Take iodine, found in many foods, and convert it into thyroid hormones: Thyroxine (T4) Triiodothyronine (T3) T3 and T4 are then released into the blood stream and are transported throughout the body where they control metabolism
|
|
true or false Every cell in the body depends upon thyroid hormones for regulation of their metabolism?
|
true
|
|
what percentage of each of T4 and T3 does the thyroid gland produce?
|
80% T4 and 20% T3
|
|
which is more powerful T4 or T3?
|
T3 4X more powerful
|
|
what gland controls the thyroid and how does it do that
|
When the level of thyroid hormones (T3 & T4) drops too low, the pituitary gland produces Thyroid Stimulating Hormone (TSH) Under the influence of TSH, the thyroid will manufacture and secrete T3 and T4 thereby raising their blood levels The pituitary senses this and responds by decreasing its TSH production
|
|
the hypothalamus produces____and the pituitary produces____ which stimulates the thyroid gland.
|
TSH releasing hormone and thyroid stimulating hormone.
|
|
what percent of women have some degree of hypothyroid
|
as many as 10%
|
|
What are the two major causes of hypothyroid
|
1. inflammation 2. The broad category of “medical treatments”
|
|
what is the most common inflammatory cause of hyopthyroid disease
|
autoimmune thyroiditis (hashimotos disease).
|
|
what is hashimoto's thyroiditis
|
an aoutimmunie illness in which there is infmallation, and then destruction and fibrosis of the thyroid gland, ultimately resulting in hypothyroidism.
|
|
what is a goiter
|
thyroid gland enlargement
|
|
true or false and explain. a goiter only occurs in hyothyroidism.
|
false it can be seen in hyperthyroidism also
|
|
how would a medical treatment cause hypothyroid
|
The treatment of many thyroid conditions warrants surgical removal of a portion or all of the thyroid gland If the total mass of thyroid producing cells left within the body are not enough to meet the needs of the body, the patient will develop hypothyroidism
|
|
Most common underlying cause of hyperthyroidism is
|
Graves' disease
|
|
how does graves disease cause hyperthyroid disease
|
Antibodies, that the patient's immune system makes, attach to specific activating sites on a thyroid gland which causes the thyroid to make more hormone
|
|
is it more common for a goiter to produce too much or too little thyroid hormone
|
onlty a small percent of goiters produce too much thyroid hormone
|
|
what are the three major clinical signs of graves disease
|
[1] over activity of the thyroid gland (hyperthyroidism), [2] thickening of the skin over the lower legs (pretibial myxedema), and [3] inflammation of the tissues around the eyes causing swelling
|
|
what percent of people with graves disease will have serious eye problems
|
About 1 out of 20 people with Graves' dz will suffer more severe eye problems If these serious problems are not recognized and treated, they can permanently damage the eyes and even cause blindness
|
|
how do thyroid problems and eye problems due to graves disease link up chronologically
|
Thyroid and eye involvement in Graves' dz generally run a parallel course Eye problems resolving slowly after hyperthyroidism is controlled
|
|
Ophthalmic Graves disease (euthyroid condition) is when?
|
When the eye signs of Graves' disease occur in a patient who is not clinically hyperthyroid
|
|
In ______ of cases, thyroid ophthalmopathy occurs in the absence of both clinical and biochemical evidence of thyroid dysfunction
|
10-25%
|
|
Thyroid eye disease affects women or men more? how much?
|
women 8:1 to men
|
|
what is the typical age of onset of thyroid eye disease? is there a genetic component?
|
20-45 yo, familial pattern
|
|
what is another name for hyperthyroidism
|
thyrotoxicosis
|
|
Risk Factors for thyroid eye disease
|
smoking (giving up smoking will reduce their risk), radioiodine (treatment for hyperthyroidism), and gender.
|
|
Three classifications systems for graves dz are?
|
NOSPECS (pneumonic) Clinical Activity Score (CAS) By structure
|
|
NOSPECS' (graves disease classification system) usage is limited b/c?
|
it lacks a means of measuring the rate of progression or treatment induced regression.
|
|
|
picture
|
|
what is the von graefe's sign
|
immobility or lagging of the upper eyelid when looking downward. this is a sign of graves' disease.
|
|
what is dalrymple's sign
|
retraction of the eyelids causing an abnormally widened palpebral fissure, in primary gaze. this is a sign of graves' disease.
|
|
describe a class 0 (N) rating on the NOSPECS classification system
|
No signs or symptoms. routine physical and eye exams.
|
|
Class 1 – O. in NOSPECS means what?
|
Only signs, no symptoms (non-infiltrative stage) upper eyelid retraction (dalrymeple's sign) Upper lid "lag" on down gaze (von Graefe sign)
|
|
Management of NOSPECS Class one signs.
|
Lubrication Medication-Topical alpha adrenergic blockers – relaxes muscles(Dapiprazole) Topical beta adrenergic blockers-provides releif of hyperadrenergic symptoms (Propranolol) lastly surgery (levator surgery, muller's muscle recession)
|
|
what is the first stage of infiltrative ophthalmopathy of the NOSPECS classification system of graves disease
|
class 2 NOSPECS
|
|
Class 2 -S in NOSPECS what is it?
|
Soft tissue involvement (1st stage of infiltrative ophthalmopathy)
|
|
subjective symptoms of class 2 S- of NOSPECS
|
Lacrimation Photophobia FB sensation Retrobulbar discomfort
|
|
objective signs of class 2 S- of NOSPECS
|
Lid and conjunctival edema Lid and conjunctival hyperemia (redness) Conjunctival chemosis (edema of the conj) Extrusion of orbital fat Lacrimal gland swelling Inflammation near EOM insertion
|
|
Management of class 2- S of NOSPECS
|
Lubrication Elevate head during sleep Tinted cosmetic lenses Steroids (systemic and periocular)
|
|
class 3 P In NOSPECS what is it
|
Proptosis (exophthalmos)
|
|
what is the most common cause of unilateral proptosis
|
Hyperthyroidism is most common cause of unilateral proptosis
|
|
whatpercent of all patients with bilateral exophthalmos will have graves' disease
|
80%
|
|
Management of class 3- P in NOSPECS
|
Management - may be permanent and require no TX Lubrication Lid taping Steroids Tarsorrhaphy (stitching)
|
|
average and upper limit of normal exophthalmometry values for healthy white and african american individuals
|
|
|
Class 4 - E in NOSPECS what is it
|
EOM involvement. (palsy leading to diplopia)
|
|
what are the two most commonly affected EOMs by graves disease
|
IR (60-70%) followed by MR
|
|
which two muscles are most commonly affected by graves dz
|
IR 60-70% of the time followed by MR.
|
|
management of class 4 problems?
|
Lubrication Eye patching or prisms Meds Steroids botulinum toxin Surgery - wait 6 months to 1 year
|
|
Class 5 - C in NOSPECS is what?
|
Corneal involvement Exposure keratopathy (can pose serious threat to vision)
|
|
Management fo class 5 C in nospecs.
|
Lubrication Meds-Antibiotics,Steroids Orbital radiation Orbital decompression
|
|
class 6 S in NOSPECS is what?
|
Sight loss (ON involvement)
|
|
signs associated with class 6 S in NOSPECS
|
Optic disc edema Painless, gradual loss of vision
|
|
management of class 6 S of NOSPECS.
|
Correction of thyroid imbalance Meds-Steroids,Cytotoxic or immunosuppressive agents Orbital radiation Orbital decompression -70% improve without tx
|
|
b/c of criticism regarding the NOSPECS pneumonic a new system was proposed called the?
|
CAS clinical activity score.
|
|
how does the CAS system work?
|
one point is given for each condition found on the pt from a given list. when all of the scores are added up to get a predictive value for therapeutic outcome.
|
|
objective signs associated with grave's disease (13)
|
1. puffy lids (enroth's sign) 2. lid retraction (dalrymple's sign) 3. lid lag -delay of upper lid in following globe movement in downward gaze (graefe's sign) -jerky downward movement of the eyelid (boston's sign) -delay of lower lid in following globe movement in upward gaze (grifith's sign) 4. tremor of closed eyelids (rosenbach's sign) 5. reduced blinking (stellwag's sign) 6. conjunctival injection 7. chemosis 8. exposure keratopathy 9. exophthalmos 10. ocular bruit 11. EOM gaze restictions 12. swollen nerve head 13. disc pallor
|
|
enlarged ocular muscles due to graves dz is due to what?
|
accumulations of glycoproteins, lymphocytes and fibrosis.
|
|
what can the enlargement of EOMs cause?
|
pressure on the optic nerve, and reduced eye movements.
|
|
New lecture: Atypical Lid Bumps 2009
|
|
|
name four types of cell growth?
|
hyperplasia, metaplasia, dysplasia, neoplasia
|
|
what is hyperplasia?
|
increase in the number of cells
|
|
what is metaplasia?
|
a change in type of adult cells which is abnormal for that tissue.
|
|
what is dysplasia?
|
alteration in size, shape, organization of adult cells.
|
|
what is neoplasia
|
uncontrolled cell growth. mass of new cells which proliferate without control and serve no useful function
|
|
what is anaplasia
|
reversion of cells to a more primitive or undifferentiated form
|
|
which one a benign or malignant tumor is surrounded by a capsule?
|
benign, it doesnt infiltrate the surrounding tissue like a malignant tumor.
|
|
true or false both malignant and benign tumors could recur is excised?
|
mostly false a malignant could definitly come back if excised a benign usually will not.
|
|
can a malignant tumor kill you? what about a benign tumor?
|
A malignant tumor, if untreated, may kill the patient wherever it
|
|
what grow more rapidly a malignant tumor or benign?
|
malignant tumors grow faster.
|
|
how are cancer cells named?
|
by parenchymal cell of orgin
|
|
what is the name given to tumors from epithelial tissue?
|
carcinoma
|
|
what is the name given to a tumor derived from CT, bone, cartilage, fat, or muscle?
|
sarcoma
|
|
what are the three general options for Tx of cancer.
|
chemotherapy (attack cells that divide the quickest), radiotherapy (rays are lethal to all cells), and surgery (surgery being the first line of tx).
|
|
objective signs that indicate a lesion is neoplastic
|
1. quality of tissue is irregular 2. irregular changes in appearance 3. neovascular pattern within or around lesion 4. infection or inflammation at the site 5. bleeding 6. ulceration 7. uncharacteristically large in size 8. erosion of the margins or surface
|
|
A,B,C,D's - rule of thumb for cancers?
|
asymmetry, borders, color, and diameter.
|
|
another name for a freckle?
|
ephilis (ephilides is plural)
|
|
management for suspicious lump/bump
|
1. with serious doubt or suspicion regarding any lump or bump of the lid, recommend excision and biopsy 2. photodocument 3. diagram and acurately measure 4. RTC q 3 months
|
|
how do freckels compare with normal skin
|
larger sized melanocytes (normal in number)
|
|
freckels are intensified by sun exposure
|
|
|
what is this
|
solar lentigines
|
|
what is another name for solar lentigines
|
(liver spots, age spots)
|
|
what are solar lentigines
|
expanding macules that occur in response to sunlight
|
|
another name for a mole?
|
Nevus
|
|
can a nevus change shape/size?
|
yes they may rise up, grow, hairs, disapear, or change color.
|
|
name the four types of Nevus?
|
dermal, junctional, compound, and dysplastic.
|
|
out of the four types of nevus which one is most common, and what layer of the skin is it located in
|
dermal. it is located in the dermis
|
|
what is a junctional nevus and can it convert to melanoma
|
located at the dermoepidermal junction. superficial and usually flat. may convert to melanoma.
|
|
out of the four types of nevus which one is located in teh dermoepidermal junction and dermis, and is transitional to malignancy?
|
compound. may convert to malignancy
|
|
out of the four types of nevus which one appears like a fried egg (darker in the middle), and has an increased risk for melanoma if there is multiple ones and a FHx.
|
dysplastic
|
|
when is it common for a nevus to increase in size?
|
with aging especially with kids when they hit puberty.
|
|
what is a common place to find a nevus on the anterior segment
|
lid margins. usually less than 10 mm in diameter
|
|
is it a good or a bad sign to have hairs growing from a nevus
|
good
|
|
what is the RTC for a lid nevus
|
1 year if normal appearance. 3-6 months if suspicious. refer for biopsy if changes occur.
|
|
what is a malignant melanoma
|
a malignant tumor that is derived from melanocytes?
|
|
describe the virulence and commonality of malignant melanoma
|
comprise 3% of primary skin cancers but account for 79% of skin cancer related deaths
|
|
what are the objective findings for malignant melanoma
|
asymmetric, pigmented, irrregular borders, variable coloration and the diameter is usually greater than 5mm
|
|
name and describe the types of malignant melanoma
|
superfical spreading melanoma: rapid increase in size, lower incidence of metastases nodular melanoma - vertical growth with more penetration into tissue, metastasize very early
|
|
what is the most common malignant lid tumor
|
basal cell carcinoma
|
|
what is the most common skin cancer
|
basal cell carcinoma
|
|
what is the general ocular location for basal cell carcinoma
|
more common on the lower lid
|
|
name and describe the two types of basal cell carcinoma
|
sclerosing: sooks like a worm noduloulcerative: looks like a nodule
|
|
what is the general appearance of basal cell carcinoma
|
PEARLY BORDERS, varying degrees of central umbilicated centers, rolled boarders, early forms may look like vascularized nodules.
|
|
what location of basal cell carcinoma requires more rapid attention and why?
|
the inner canthal region b/c it is more locally invasive and could eat bone and flesh
|
|
is metastasis common in basal cell carcinoma
|
no
|
|
what is the plan of attack for basal cell carcinoma
|
derm consult with in 3 months. antibiotic steroid combo is secondarily infected or inflammed.
|
|
what is the etiology and the appearance of squamous cell carcinoma
|
etiology is keratinizing epidermal cells Dx is scab that doesnt heal, reddish, scaly plaque,
|
|
describe the epidemiology associated with meibomian gland carcinoma
|
rare in north america, but common india and asia
|
|
what does meibomian gland carcinoma resemble?
|
it is like a persistent recurrent meibomian gland chalazion. get a biopsy if the pt says that they have had a chalazion for 6 months to a year. persistant bleph is also common. it metastisizes early
|
|
what is the most common precurser of cancer
|
actinic keratosis
|
|
what is another name for actinic keratosis
|
sun spots (solar keratosis)
|
|
what is actinic keratosis
|
squamous cell dysplasia
|
|
actinic keratosis, what is the objective finding
|
dry, scaly lesions 2-5 mm. minimally elevated.
|
|
what is a common drug used for many skin cancers and is a cream
|
imiquimod - for 6 weeks
|
|
what is a keratocanthoma
|
papular lesion. benign proliferation of squamous epidermal cells.
|
|
can a keratocanthoma convert to a malignancy
|
yes, can convert to squamous cell carcinoma. it is a percusor to cancer.
|
|
is a keratocanthoma related to sun exposure
|
no
|
|
can a keratocanthoma spontaneously regress
|
yes
|
|
describe the objective appearance of keratocanthoma
|
starts as a erythematous papule. grows into a firm, raised indurated nodule up to 2 cm. keratin filled center.
|
|
what is another name for lentigo meligna
|
hutchinson's freckle
|
|
can lentigo maligna conver to malignancy
|
precursor to melanoma. could have the lesion 20 years before it converts to malignancy.
|
|
what is lentigo maligna
|
dysplastic nevus
|
|
what age group is lentigo maligna (hutchinsons freckle) usually seen in
|
older pts
|
|
what is the appearance of lentigo maligna (hutchinsons freckle)?
|
dark macular lesion with irregular serpiginous pigment and margins.
|
|
what is an acrochordon
|
this is a skin tag/soft wart, benign, and usually pedunculated usually found on the obese
|
|
manegment for acrochordon
|
snip it freeze it or zap it.
|
|
what is a papilloma
|
a benign epithelial tumor that is lobulated, and may be right on the lid margin
|
|
describe the management for papilloma
|
((oculoplastics are lid surgery specialists; you want to send here not to a general opthamolagist) ((there is a risk of permanent damage to the ability to produce tear film and they are usually not malignant; pt education is necessary)
|
|
what is seborrheic keratosis
|
hyperkeratinized plaques. benign epidermal tumor.
|
|
describe the etiology of seborrheic keratosis
|
basal cell hyperplasia
|
|
is seborrheic keratosis related to the sun or not?
|
NO
|
|
what is lichen planus
|
common, pruritic eruption; chronic mucocutaneous disease that affects the skin and the oral mucosa, and presents itself in the form of papules, lesions or rashes.
|
|
what is the etiology of lichen planus
|
it is possibly immune response, may be viral
|
|
what is the name of a benign skin tumor that is caused by HPV
|
verrucae
|
|
what is the difference b/t verrucae and papilloma?
|
verrucae is considered an active papilloma that is typically seen in kids and is contagious papilloma is usually found on the lid margins
|
|
what benign skin tumor is asociated with STD and HIV and is mildly contagous
|
molluscum contagiosum (viral warts)
|
|
what is the key objetive observation with molluscum contagiosum
|
that it is umbilicated nodule with a central core, this central hole differentiates it from papilloma and verrucae
|
|
what is the plan for molluscum contagiosum?
|
if it is quiet leave it alone, if there is central discharge express it excision cryo or topical salicylic acid pt ed. because it is contagious
|
|
New lecture: Opt 533 - Hordeolum Chalazion Cyst 2009
|
|
|
an external hordeolu is an infection of what?
|
the zeis gland
|
|
what is an internal hordeolum an infection of
|
the meibomian gland
|
|
what is the infectious agent in 90-95% of hordeolum
|
staph aureus
|
|
what is the subjective symptoms of a hordeolum
|
painful, swelling on one eyelid, erythema, tender. history of similar problems is common.
|
|
hordeolums are found more frequently in people who have ?
|
diabetes (reduced kidney, eye and immunological functions), chronic bleph, seborrhea.
|
|
what is an external hordeolum
|
a localized, raised, red bump near the lid margin that points to the skin side of the lid
|
|
what is an internal hordeolum
|
a locatized, red, raised bump that points to the conjunctival side of the lid.
|
|
what is an important thing that you need to educate pts with a hordeolum about
|
dont squeez it it could spread into pre ceptal cellulitis
|
|
describe the management associated with external hordeolum
|
1. not treatment, usually are self-limiting (most eventually drain by themselves) 2. warm soaks are the main treatment (qid for 15 min) 3. or topical antibiotics may be used for recurrent lesions and for those that are actively draining 4. epilation of eyelash associated with infected follicle may enhance drainage of pus
|
|
large internal hordeolum can discharge anteriorly through the skin
|
|
|
what type of infection can an internal hordeolum turn into
|
preseptal cellulitis
|
|
what is the Tx/plan for an internal hordeolum
|
1. usually are self limited but you can do warm soaks 2. for recurent lesions and those actively draining you can use a topical antibiotic 3. for a pointed lesion you could do surgical drainage to speed up the process. 4. systemic antibiotics are indicated only when inflammation has spread beyond the immediate are of the hordeolum
|
|
how should drainage of an internal hordeolum be done
|
Stab incision at the site of pointing using an 18-gauge needle or a #11 blade External incisions lead to scarring, so making external eyelid incisions or punctures is inadvisable, unless the hordeolum already is pointing externally A large abscess may have multiple pockets and require multiple stabs. Internal incisions should be made vertically to minimize the area of cornea swept by a scar during blinking Leave the incision open with a clean margin
|
|
what is another name for chalazion
|
meibomian cyst
|
|
what is a chalazion
|
lipogranulomatous infiltration of the meibomian gland. may follow an internal hordeolum.
|
|
objective signs associated with chalazion
|
firm nodule within tarsal plate. non-tender, non-inflammed
|
|
describe the tx for chalazion
|
1. warm compresses 10-15 min. qid to q2h 2. you could do a steroid injection into the lesion 3. incision and curettage if the steroids dont work.
|
|
what is a cyst that arises from a blocked sweat secreting gland.
|
cyst of moll
|
|
what is another name for a cyst of moll
|
suderiferous cyst
|
|
describe the appearance of a cyst of moll
|
dome shaped, non tender, no inflammation, translucent, fluid filled, anterior margin.
|
|
what is the Tx for cyst of moll
|
thisis primarily a cosmetic concern, it can be aspirated with a fine needle but rcurrence is common. you can also excise it by removing the whole sac to reduce the reccurence.
|
|
what cyst is not translucent and arises from blocked oil secreting glands associated with cilia
|
cyst of Zeis
|
|
describe the appearance of a cyst of zeis
|
contains oily secretions and is less translucent than a cyst of moll
|
|
what cyst can be found on any part of the body and it arises in a blocked oil gland, has a central punctum and if squeezed it will exude stringy, cheesy white material
|
sebaceous cyst
|
|
plan for a sebaceous cyst
|
if you are going to remove it you need to remove the whole sac. you cant just excise out the cheesy material it will come back. if infected, an oral antibiotic shoudl be rxed
|
|
New lecture: OPT 533 - Lacrimal Disease 2009
|
|
|
|
picture
|
|
what is a collection of amniotic fluid within an obstructed lacrimal sac called? It appears as a firm bluish mass on the side of the nose and inferior to the medial canthus.
|
Congenital dacryocele
|
|
how do you treat a congenital dacryocele?
|
Hot compresses and massage, most infants will require probing.
|
|
what is the result of a failure of the nasolacrimal duct to completely canalize during gestation? And what could it cause as a secondary problem?
|
Congenital nasolacrimal duct obstruction, and it could cause bacterial dacryocystitis and or conjuctivitis, because the tears are held in the canals allowing bacteria to grow.
|
|
how common is congenital nasolacrimal duct obstruction
|
very common. 2-4% of full-term infants.
|
|
in congenital nasolacrimal duct obstruction, which end of the duct is normally obstructed
|
nasal end (valve of hasner)
|
|
is congenital nasolacrimal duct obstruction usually unilateral or bilateral
|
can be either.
|
|
describe the objective signs associated with congenital nasolacrimal duct obstruction
|
1. tearing 2. crusting 3. mucus reflux from the punctum with compression over the lacrimal sac
|
|
How do you manage a congenital nasolactimal duct obstruction?
|
warm compresses bid to qid, also use a topical antibiotic such as erythromycin bid for one week if there is a mucopurulent discharge. also have parents massage downward to open valve of hasner. If it doesn't resolve spontaneously by the age of 6 to 13 months probe it. (if probing is not successful, treatment is surgical)
|
|
what percent of the time will congenital nasolacrimal duct obstruction resolve spontaneously
|
90% with the assistance of massage
|
|
discribe three signs and symptoms associated with congenital glaucoma
|
tearing, photophobia, large cornea
|
|
name three conditions that can cause acquired nasolacrimal duct obstruction
|
1. chronic sinus disease 2. age-related stenosis 3. naso/orbital trauma
|
|
how could you test for Acquired nasolacrimal duct obstruction?
|
Jones test
|
|
Acquired nasolacrimal duct obstruction could often lead to?
|
Acute dacryocystitis. (inflammation of lacrimal sac).
|
|
How do you treat Acquired nasolacrimal duct obstruction?
|
first try warm compresses, a topical antibiotic- steroid if there is partial obstruction. then try dilation/irrigation and or probing. If this is not successful then turn to surgery. Dacryocystorhinostomy (DCR). the insertion of a silicone tube (Jones tube).
|
|
describe the pathophysiology associated with acut dacryocystitis
|
nasolacrimal duct becomes obstructed. tears stagnate in lacrimal sac. lacrimal sac becomes infected.
|
|
what type of bacteria cause the infection acute dacryocystitis?
|
staphylococci, streptococci, E. coli, pseudomonas, and other gram negatives.
|
|
what would show as a tender red bump in the area inferior to the medial canthus? could extend about 2 cm below canthus.
|
Acute dacryocystitis
|
|
signs and symptoms associated with acute dacryocystitis (8)
|
tenderness, erythema and swelling over the nasal portion of the lower lid. epiphora, purulent punctal discharge (particularly when pressure is applied to the lacrimal sac), fever and malaise, preseptal cellulitis, conjunctivitis
|
|
what is the treatment for Acute dacryocystitis?
|
-consider referal to specialist -Warm compress tid, -systemic antibiotic such as oral augmentin -also a topical antibiotic such as erythromycin if conjunctivitis exists -aspirate the lacrimal sac contents with 19 gauge needle for culture testing. -could consider incision and drainage. -if pointing abscess, consider incision and drainage -after infection resolved, irrigation and/or probing to relieve obstruction - Consider dacryocystorhinostomy DCR.
|
|
If the infection in the lacrimal region has no sign of being acute reactions it should be considered
|
chronic daryocystitis
|
|
Which lobe of the lacrimal gland is affected more frequently in dacryoadenitis?
|
the palpebral more than the orbital.
|
|
Most often Acute dacryoadenitis is caused by?
|
Acute dacryoadeitis is usually associated with systemic infections such as mumps, epsein barr virus and herpes zoster.
|
|
name 8 objective ocular and systemic signs that indicate acute dacrysoadenitis
|
temporal upper eyelid inflammation (S-shaped deformity), upper eyelid tenderness, warmth, tearing, discharge, fever, and possible proptosis (if the orbital lobe is involved) -Swollen palpebral lobe of the lacrimal gland can be easily visualized in the supratemporal fornix by elevating the upper lid while having the patient looking down
|
|
management acute dacryoadenitis?
|
treat the underlying infection or inflammation.
|
|
what is more common chronic or acute dacryoadenitis?
|
chronic
|
|
underlying etiology of chronic dacryoadenitis
|
seen primarily in young black females, and could be associated with sarcoidosis, thyroid ophthalmopathy, sjogrens syndrome, or a tumor?
|
|
what is the triad of sjogrens syndrome?
|
dry eye, dry mouth and arthritis.
|
|
how can sjogrens syndrome affect the lacrimal gland
|
Lacrimal gland infiltrated with lymphocytes à may be enlarged. -sjogren's is an autoimmune disease
|
|
what is canaliculitis
|
infection of the canaliculus (duct between the punctum and the lacrimal sac)
|
|
what is the most common and the second most common causative agent in canaliculitis?
|
1. actinomyces Israelii (filamentous grom + rod) 2. Candida albicans (yeast)
|
|
name 5 objective signs associated with canaliculitis
|
erythema and swelling of punctum and adjacent tissues, also conjunctivitis around the medial canthus. expression of the canaliculus causes discharge from the punctum, canalicular concretion
|
|
describe the management of canaliculitis
|
1. warm compresses 2. culture 3. remove concretion form canalicula 4. appropriate systemic and topical antibiotics
|
|
New lecture: Preseptal and Orbital Cellulitis 09 Victoria
|
|
|
what is preseptal cellulitis
|
a relatively common eyelid infection that involves the periorbital tissue anterior to the orbital septum?
|
|
what are some possible causes of preseptal cellulitis?
|
URI, spread of an eyelid infection (hordeolum), trauma to the lids, insect bite.
|
|
how do you differentiate between inflammation from insect bite and orbital cellulitis from insect bite
|
If edema responds to antihistimine, it is probably just inflammation.
|
|
what tissue is invaded during preseptal cellulitis?
|
subcutaneous.
|
|
if there is no sign of trauma or local lid infection what is the usual cause of preseptal cellulitis
|
URI
|
|
what is the most common offending pathogens for preseptal cellulitis? what about in children?
|
staph aureus, staph epidermidis, streptococcus species, possibly H flu but it is not common now that we have the vaccine. Now a days streptococcus pneumoniae is the most common offender in children.
|
|
true or false preseptal cellulitis could be secondary to things such as TB, Clamydia, juvenile idiopathic arthritis, or MRSA.
|
true
|
|
what must you rule out if you see preseptal cellulitis
|
orbital cellulitis
|
|
5 signs and symptoms of preseptal cellulitis (and 4 things they don't have)
|
Red swollen eyelid, pain, epiphora, red eye, with a possible fever -no proptosis, no pain on EOMs, no EOM restriction, VAs usually normal
|
|
is preseptal cellulitis primarily a pediatric disease or adult?
|
pediatric disease. about 80% younger than 10. -want to co-manage with a pediatrician
|
|
If you cannot rule out orbital cellulitis what do you need to do? -would be the case if the eye was swollen shut
|
order a CT.
|
|
what is the treatment for preseptal cellulitis in an adult or older child? what is the follow up?
|
Amoxicillin/clavulanate (augentin) 500 mg p.o. tid for 10 days. also you must follow up in 24 hours.
|
|
what is the treatment for younger children (older than 5) that have preseptal cellulitis? What is the follow up?
|
amoxicillin/clavulanate (augmentin) 20 - 40 mg/kg/day by mouth divided into three doses X 10 days -again must follow up in 24 hours
|
|
what do you need to use for preseptal cellulitis if a person is allergic to PCN?
|
trimethoprim/sulfamethoxazole. an example is Bactrim.
|
|
describe the management for anyone with moderate to severe preseptal cellulitis, children under 5 years old, or anyone not responding to therapy
|
Hospitalize for iv antibiotics.
|
|
what is orbital cellulitis
|
an infection of orbital soft tissue posterior to the orbital septum
|
|
is orbital cellulitis more common in adults or children?
|
children. mean age of hospitilization is 7-12 years old.
|
|
describe the prognosis associated with orbital cellulitis
|
11% can have vision loss if not diagnosed right away. can lead to death if not treated (meningitis).
|
|
what kind of surgery must you ask about if a pt has orbital cellulitis.
|
dental work
|
|
possible causes of orbital cellulitis?
|
most common cause is ethmoid sinusitis (90%). dental work is another common cause (you need to ask about recent dental work if you have a pt you suspect orbital cellulitis). extension of an infection from the periorbital structures and sinuses, infection of the orbit following trauma, or surgery, or hematogenous spread of bacteremia.
|
|
what are the most common bacterial pathogens that cause orbital cellulitis?
|
stph aureus, strept species, and H flu
|
|
fungal infections can also cause orbital cellulitis. they are rare, but have a high mortality rate
|
|
|
signs and symptoms of orbital cellulitis (14)
|
1. lid erythema 2. lid edema 3. fever/malaise 4. hx of URI infection or sinusitis 5. red eye 6. pain 7. pain on eye movement 8. decreased vision 9. restricted EOMs 10. proptosis 11. chemosis 12. elevated IOP 13. ONH edema 14. APD -red indicators help differentiate with prespetal cellulitis
|
|
what four things does orbital cellulitis have that preseptal cellulitis does not have
|
pain on eye movement decreased vision restricted EOMs proptosis
|
|
objective: decreased vision, lid edema and erythema, proptosis, conjunctival chemosis, restriction on EOM's, pain on eye movement, and may have elevated IOP, optic disc edema. what is it?
|
orbital cellulitis.
|
|
the key findings for orbital cellulitis are?
|
ophthalmoplegia and proptosis.
|
|
treatment for orbital cellulitis?
|
HOSPITALIZATION!!!! IV whith broad spectrum antibiotics such as ampicillin-sulbactam. may also require surgical drainage.
|
|
New lecture: Parasitic Lid Disease 2009
|
|
|
what is the common name for a mite infection
|
demodex infestation/demodicosis
|
|
what part of the face do mites infect
|
eyelid, facial hair, and eyebrow
|
|
describe the prevalence of demodex/mite infestation
|
Prevalence
|
|
what are the two common spicies of mites
|
demodex folliculorum, demodex brevis
|
|
demodex that is cigar shaped, likes to be in a colony of 3 or more per follicle, and usually reside on the collarettes/cuffs of the hair follicles what are they?
|
demodex folliculorum. -collarettes/cuffs are the best clinical diagnostic sign
|
|
the demodex brevis is smaller and solitary where do they reside?
|
in the sebaceous glands which can cause blockage that can lead to dry eye, or the formation of a chalazion. (must be small to get into the gland.)
|
|
what would be the subjective symptoms of a person that has a demodex infection.
|
itching, burning, crusting, swelling of lid margins, and lash loss.
|
|
what are the objective findings on a person that has a demodex infection?
|
lid margin erythema, conj infection, blepharitis, cuffing around lashes, plugging of meibomian glands and madarosis.
|
|
what is the treatment for a demodex infection?
|
almost imposible to completely eradicate. the treatment is the same as treating bleph. lid hygiene, ung hs X 10 - 14 days (ointment use at night.) for anti-microbial treatment erythromycin is a good choice.
|
|
what is the technical name for lid infection with lice (2 types)
|
phthiriasis palpebrarum/pediculosis palpebrarum
|
|
name three species of lice
|
phthirus pubis (carb louse) pediculus corporis (body louse) pediculus capitus (head louse)
|
|
what is the most common lice found on the lids?
|
the crab louse, (phthirus pubis) because of the spacing of follicles matches up with their legs. usually spread by sexual contact. (pubic lice much more common than head lice)
|
|
what serious disease can be caused by lice?
|
typhus: One of several rickettsial infections transmitted to people by lice, fleas, or mites.
|
|
if you find louse on a person what other questions should you ask?
|
have you noticed any itching anywhere else on your body? (looking for concurent genital infection)
|
|
what is the difference between the pediculus and the phthirus spicies of lices
|
pediculus are free-moving; phthirus is stationary (ped means foot). -also note that these lice like the dark, so if they are able, they will move away from the beam of your slit lamp.
|
|
what are some subjective findings for a person with a lice infection?
|
itching, red eye infection, insomnia due to irritability, occasional preauricular lymphadenopathy.
|
|
what are the objective findings of patient with a lice infection?
|
nit cases at base, crusty lid margins, madarosis, conj injection, lid edema, erythema, you may also see brown fecal matter or red blood from the host.
|
|
what is the treatment for a lice infection.
|
remove and drowned in alcohol. then prescribe erythromycin or bacitracin ung tid for 10 to 14 days. also physostigmine .25 % ung 2 applications 1 week apart. refer if other areas of the body infected.
|
|
is it possible for a person to get a crab louse infection in the eyelids without direct sexual contact
|
it is possible for crab louse to be transmitted without direct sexual contact but it is unlikely.
|
|
New lecture: Auto Imm Dz 09 Victoria
|
|
|
what is a disease that involves loss of pigmentation where there is hair?
|
Poliosis
|
|
what is the cause of poliosis?
|
It is an immune response to melanin. cauases loss of pigmentation of eyelashes.
|
|
name three causes of poliosis
|
staph bleph, albinism, or vogt-Koyanagi-Harada syndrome.
|
|
what is the treatment for poliosis for an OD?
|
If the the underlying cause is bleph then treat it, if it is albinism or VKH then refer.
|
|
what condition is this
|
vitiligo
|
|
what is vitiligo
|
characterized by the loclized loss of melanocytes, with patchy loss of skin pigment.
|
|
is there a heriditary component to vitiligo
|
frequent positive family Hx
|
|
what is the age of onset of vitiligo
|
usually presents before age 20
|
|
is vitiligo a progressive or stable condition
|
progressive
|
|
what is vogt-koyanagi-harada syndrome
|
a rare multisystem disorder. possible autoimmune disease against pigmented tissues.
|
|
what is the age of onset and ethnicity typically associated with vogt-koyanagi-harada syndrome
|
common in ages 20-50. affects darker pigmented individuals, asian, hispanic, native american, middle eastern
|
|
3 out of 4 of the following need to be present to diagnose vogt-koyanagi-harada syndrome
|
diagnosis of at least 3 of the four following - bilateral chronic anterior uveitis - posterior uveitis - neurological features such as deafness and menengitis - cutaneous lesions
|
|
name and describe the phases of vogt-koyanagi-harada syndrome
|
phase 1: prodromal phase (lasts a few days). meningitis, encephalopathy, auditory disturbances. phase. 2: acute uveitic phase (soon after phase 1). anterior uveitis, posterior uveitis, retinal detachment phase 3: convalescent phase (follows several weeks later). alopecia 60%, poliosis, vitiligo, fundus lesions, depigmented limbal lesions (sugiura sign) phase 4: chonic-recurrent phase. smoldering anterior uveitis with exacerbations.
|
|
what is the hallmark eye sign of vogt-koyanagi-harada syndrome
|
acute serous retinal detachment. note that serous refers to serous fluid.
|
|
what is the treatment for VKH?
|
oral steroids the dose depends on the severity. you can also give steroid drops for the uveitis. if steroids are not enough then immunosurpressants like cyclosporine may be needed. periocular injection of steroids are also a posibility.
|
|
what condition is this
|
ocular cicatricial pemphigoid (OCP)
|
|
what is another name for ocular cicatricial pemphigoid
|
benign mucous membrane pemphigoid (BMMP)
|
|
what is ocular cicatricial pemphigoid
|
an autoimmune disease characterized by recurrent subepithelial blisters or bullae of the skin and mucous membrnes with a tendency to scar.
|
|
name two distinct forms of OCP
|
idiopathic and drug induced pseudo OCP
|
|
what percent of people with OCP have ocular involvement
|
70%
|
|
OCP is typically diagnosed in what decades of life?
|
6th or 7th
|
|
early detection of OCP is critical to preserve their sight. we are responsible for early detection. we can be the first to diagnose.
|
|
|
7 signs and symptoms associated with ocular cicatricial pemphagoid
|
1. oral mucosa lesions 2. dermatological involvement 3. shrinkage of the conjunctiva (every time a blister pops the conj. shrinks) 4. chronic red eye 5. irritation 6. burning 7. tearing
|
|
what are the four stages of OCP?
|
1 - conjuctivitis 2 - conjunctival scarring and shrinkage 3 - symblepheron formation 4 - end stage with corneal scarring and ankyloblepheron.
|
|
what is symblepheron
|
|
|
what is ankyloblepheron?
|
|
|
stage one OCP is what?
|
conjunctivitis, red eye, tearing, burning, irritation, and mucous discharge.
|
|
stage 2 OCP is what?
|
conj scarring and shrinkage, worsens within 3 to 4 years
|
|
stage 3 OCP is what?
|
involves progression to symblepheron this is the attachment of the palpebral conj to the bulbar conj.
|
|
stage 4 OCP involves what?
|
severe dry eye, ankyloblepheron, and corneal scarring. ankyloblepheron is when the corners of the lids begin to shut.
|
|
what is the most common initial objective sign of OCP?
|
conjunctivitis associated with subepithelial fibrosis.
|
|
what type problems can chronic contraction of conjunctival tissue lead to?
|
shortening of the fornicies, entropion, and trichiasis. (ocular cicatricial pemphagoid)
|
|
what causes vision loss in ocular cicatricial pemphagoid
|
keratinization of the cornea
|
|
what testing can help diagnose ocular cicatricial pemphagoid
|
conjunctival biopsy. 83% are diagnosed with biopsy. 17% continue with disease progression in spite of negative biopsy.
|
|
what is the therapy for OCP?
|
topical steroids but they are not usually adequate alone. oral steroids are needed. start heavy with 40 to 60 mg of prednisone QD and then taper to a lower maintanence dose after significant remission of symptoms. -ocular tx: dry eye therapy, eyelash epilation, soft CLs (careful of infection), corneal transplant not very sucessful because stem cells are destroyed
|
|
what causes the dry eye in ocular cicatricial pemphagoid
|
destruction of the goblet cells and meibomian glands
|
|
what is erythema multiforme
|
an acute but generally self-limiting disorder of the skin and mucous membranes.
|
|
erythema multiforme is divided into two types what are they?
|
minor and major.
|
|
what form of erythema multiforme consists of tergetoid skin lesions with well defined borders? and may or may not involve one mucosal membrane.
|
EM minor
|
|
which form of erythema multiform involves 2 or more mucosal membranes. and is more severe.
|
EM major -seteven's-johnson syndrome was characterized as EM major for more than 30 years but now has its own category
|
|
Is erythema multiforme the same as steven johnson syndrome? if not what is the difference?
|
no they were for a long time but now they are different. EM is when it is only on the limbs. It is SJS when the trunk is effected also. -unsure about this slide, I didn't make it
|
|
why is SJS important to OD's?
|
in 50% of the cases their is an ocular involvement.
|
|
what is steven's-johnson syndrome
|
acute inflammatory skin and mucous membrane disorder. rare. bullous lesions involving 10-20% of the body surface. erosive involvement of two or more mucous membranes (often the conj.). morality rate 1-5%.
|
|
are there any systemic symptoms associated with steven's-johnson syndrome
|
malaise, fever, sore throat, HA
|
|
what is a more severe case of steven's-johnson syndrome?
|
TEN - toxic epidermal necrolysis.
|
|
what is toxic epidermal necrolysis
|
massive denudation of the epidermis involving >20% of the total body surface. a more severe variant of steven's-johnson syndrome. -sometimes these pts will go blind because the physicians are more worried about them dying.
|
|
are there any systemic symptoms associated with toxic epidermal necrolysis
|
same as SJS. malaise, fever, sore throat, HA
|
|
what is the mortality rate and the rate of ocular involvement in toxic epidermal necrolysis
|
25-35% mortality rate. ocular involvement in 50%.
|
|
SJS and TEN can be caused by drug reactions what are some of the common ones? They can also be caused by infections by what pathogens?
|
sulfonamides, tetracycline, penicillin, NSAIDS. mycoplasma pneumoniae and HSV
|
|
what type of skin lesions are involved with SJS and TEN
|
target or bull's eye lesion which have an reythematous center surround by a pale zone, usually on extremities. vessicles and bullae and epidermal necrosis develop, predominantly on the trunk of the body (double check that).
|
|
describe SJS and TEN ocular involvement
|
lids are swollen, crusted, and ulcerated. conjunctivitis with possible pseudomembrane or membrane formation. bullae formation followed by rapid rupture and scarring in the area of the epithelial erosion. entropion, trichiasis, symblepharon, corneal opacification, lacrimal dysfunction.
|
|
what is the management of SJS and TEN?
|
no specific treatment exists for systemic, manage pain and remove causative agent is possible. -For ocular involvement use steroids, cold compresses may help, soft CLs, epilation, dry eye therapy
|
|
ocular complications of SJS and TEN are easily overlooked by physicians due to the seriousness of the condition.
|
|
|
New lecture: Allergic Lid Disease 2009
|
|
|
describe the difference b/t type one and type 4 allergic reactions.
|
type one is immediate and is due to the release of substances such histamine. this will take place in minutes to hours. type four is a delayed reaction caused by sensitized lymphocytes (t cells). this takes place hours to days later.
|
|
what is contact dermatitis
|
what is the term used for the inflammation due to the skin coming into contact with an allergic agent.
|
|
what are the types of contact dermatitis
|
irritant and allergic contact dermatitis
|
|
which is the more common type of contact dermatitis?
|
irritant contact dermatitis.
|
|
what is dermatitis
|
any inflammation of the epidermis
|
|
describe irritant contact dermatitis
|
Nonspecific response of skin to chemical damage that releases mediators of inflammation from epidermal cells
|
|
describe allergic contact dermatitis
|
Here there is itching and involves a cell mediated immunity response. examples is poison ivy, latex, drugs, could also be chemical like irritant dermatitis but here it is not directly damaging the skin.
|
|
how soon after contact with an allergen does irritant and allergic contact dermatitis occur? what accounts for this difference?
|
irritant: 1-24 hours, can occur within minuets allergic: usually in 48 hours -allergic takes longer because there is a cell mediated immunity response, this requires a latency period.
|
|
subjective symptoms associated with irritant contact dermatitis
|
1. Hx 2. red rash 3. pain 4. burning/stinging -maybe no itching
|
|
occupations that commonly experience irritant contact dermatitis
|
cleaning, hospital care, food prep, hairdressing (often affects hands)
|
|
irritant contact dermatitis: common irritants
|
soap and water, solvent, microtrauma, dry air, cleaners
|
|
objectice signs of irritant contact dermatitis
|
1. erythema 2. edema 3. glazed, parched, scalded appearance 4. dry, scaly skin
|
|
treatment for irritant contact dermatitis
|
1. avoid irritant 2. non-sensatizing moisturizers (patroleum jelly) 3. soaps with low irritant effect (dove) -no topical steroids
|
|
objective signs for allergic contact dermatitis
|
1. PRURITIS 2. erythema 3. edema 4. vessicles 5. weeping rash 6. chemosis 7. keratitis may develop
|
|
treatment for allergic contact dermatitis?
|
remove allergen, cold compresses 4-6 days, topical steroids 5 - 10 days (something like hydrocortisone), consider oral antihisamine, and ocular lubricants
|
|
what is atopic dermatitis
|
a type of eczema. an inflammatory, chronically relapsing, non-contagous, pruritic skin disorder.
|
|
what is eczema
|
A general term for an itchy red rash that initially weeps or oozes serum and may become crusted, thickened, or scaly.
|
|
what is the age of onset for atopic dermatitis
|
infancy. -most common skin disease in children
|
|
is there a heriditary component to atopic dermatitis
|
yes
|
|
signs and symptoms of atopic dermatitis
|
1. rash that is exudative 2. vesicular to maculopapular 3. itching later stages 4. dry lichenified skin 5. excoriated areas -most common location is face (cheeks), scalp and knees
|
|
atopic dermatitis: pt is more prone to dexondary infection with staph or streptococcus. usual susceptibility to herpes simplex and molluscum contagiosum
|
|
|
describe the progression associated with atopic dermatitis
|
unpredictable, but usually subsides by age 3 or 4 with exacerbations and remissions frequently recurring throughout childhood, adolescence and adulthood.
|
|
what is urticaria and what is a common name(s) for it
|
Multiple swollen raised areas on the skin that are intensely itchy and last up to 24 hr; they may appear primarily on the chest, back, extremities, face, or scalp. -AKA hives or welts
|
|
what are the clinical features of urticaria?
|
intense pruritus, raised welts surrounded by erythematous flare.
|
|
what is angioedema
|
when skin appears normal but deeper layers of the skin are edematous,
|
|
treatment for urticaria and angioedema
|
cold compresses, antihistamine, systemic steroids
|
|
is there itching with angioedema? what areas of the body are most commonly involved
|
a little pruritus. most often involves face, lips, eyelid, toungue, throat, hands, feet
|
|
Causes of urticaria and angioedema
|
1.
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|
tx for urticaria and angioedema
|
1. avoid cause 2. cold compresses 3. antihistamine 4. systemic steroids 5. epinephrine for acute pharyngeal or laryngeal angioedema
|
|
New lecture: DryEye Seminar2009
|
|
|
what is dry eye
|
Tear film disorder due to tear deficiency or excessive tear evaporation causing damage to the interpalpebral ocular surface and associated with symptoms of ocular discomfort resulting from localized immune-mediated inflammation affecting both the lacrimal gland and the ocular surface -aka ocular surface disease
|
|
describe the cycle that triggers dry eye symptoms
|
|
|
how does inflammation of the lacirmal gland and ocular surface lead to tear deficiency/instability
|
tear instability due to altered composition
|
|
what are the three components of normal tear film
|
superficial lipid layer, aqueous layer, mucin layer
|
|
name three functions of the normal tear film
|
maintain health of the epithelium, fight infection, lubricate
|
|
what could cause a disruption of the lipid layer of the tear film
|
deficiency is rare. meibomian gland dysfunction can cause excessive output and disrupt stability of tear film.
|
|
how can we assess the aqueous layer of the tear film clinically
|
look at the tear meniscus, which sits at the junction between the lower lid and the globe.
|
|
what is the term for dry eye due to a deficiency in the aqueous layer
|
keratoconjunctivitis sicca
|
|
systemic and ocular causes of deficiency of the aqueous layer of the tear film
|
Systemic Rheumatoid arthritis (25%) Sjögren’s Systemic lupus Ocular Decreased lacrimal and accessory lacrimal gland output Age, inflammation, scaring, etc
|
|
what layer of the tear film is least commonly the cause of tear film instability and dry eye
|
mucin layer
|
|
describe the pathophysiology behind tear film instability due to deficiency in the mucin layer of the tear film
|
decreased goblet cells
|
|
common causes of decreased goblet cells leading to tear film instability
|
Hypovitamin A Ocular pemphigoid Steven Johnson Syndrome Trachoma Alkali burns LASIK
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why does menopause lead to dry eye
|
decreased androgens
|
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what are some environmental stresses that cause dry eye
|
contact lens wear, wind, air pollution, low humidity (heating/air conditioning), lack of sleep, use of computers
|
|
name two ocular surgeries that tend to be associated with dry eye
|
LASIK, corneal transplant
|
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many medications are associated with dry eye. preservatives in topical medications can cause irritation leading to dry eye.
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|
|
why would a contact lens wearer be uncomfortable in airplanes and in the mall
|
Planes and the mall have very low humidity so that the people crammed in there will be less sweaty. Low humidity will dry out your lenses.
|
|
why do autoimmune diseases like rheumatoid arthritis and lupus tend to cause dry eye
|
All can result in immune-mediated inflammation in the eye Inflammatory mediators secreted into tears Promote inflammation of ocular surface
|
|
subjective symptoms associated with dry eye
|
1. foriegn body sensation 2. excessive tearing 3. dryness 4. burning, stinging 5. blurry vision 6. photophobia (caused by damage to the corneal epithelium) 7. itching 8. redness 9. contact lens discomfort
|
|
dry eye assessment: in the slit lamp watch them blink. notice the rate and look for complete closure.
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should you use anesthetic for the phenol red thread test, or the schirmer test to assess dry eye
|
((if you put anesthetic in and measure right away you will measure the amount of drop not the amount of team film; you need to consider your procedure and base it against your own judgement, not the standards) ((anesthetic will stop reflux tearing and measure base tear volume)
|
|
how do you tell if a pt has dry eye after doing the schirmer test
|
Dry eye is indicated if less than 10 mm of the strip becomes wet with tears after 5 minutes of exposure
|
|
5 tests that assess dry eye
|
1. biomicroscopy 2. schirmer test 3. phenol red thread test 4. tear break up time 5. rose bangal/lissamine gree staining other: nanolite osmometer (measures osmolarity), tearscope (keeler; evaluates the lipid layer of the tear film), fluorophotometer (estimates drainage)
|
|
tricks for tear break-up time: ((with fluorescence you want as small an amount as possible to be able to notice staining) ((you need to notice how often the pt normally blinks, and compare the break up time to blink rate; just examine the cornea and notice if the tear film breaks before the pt blinks)
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|
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how does tear osmolarity change with aqueous evaporation
|
osmolarity increases. tear film becomes hyperosmotic because the tears are evaporating; this will cause the tears film to draw fluid out of the cells of the eye
|
|
what is the best way to evaluate ocular surface disease
|
rose bengal staining
|
|
why is a pt with dry eye at an increased risk of infection
|
with dry eye the natural defenses of the eye are compromised (lactoferrin, etc.) and they are at increased risk for secondary infection
|
|
Lubrication types of Artificial tears May require frequent dosing Low viscosity to high viscosity Hypo-osmotic, iso-osmotic, hyper-osmotic Preservative verse preservative free Vitamin A supplementation Omego-3 fatty acids (Thera-tears) Systane emulsion of castor oil
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|
|
how often should you use artificial tears for dry eye
|
drops don’t work as well if you use them when your eyes are already bothering you; you need to use them as prophylaxis when you know you are in a condition that will cause irritation. start with frequent instillation and once symptoms are under control, back off frequency until you start to have symptoms again, then you will know how often you need to use the drops
|
|
what are gel artificial tears and name one
|
Between ointments and solutions Last longer with less blur Refresh Liquigel
|
|
8 treatments for dry eye
|
1. artificial tears (gels, ointments) 2. ocular inserts 3. punctal plug 4. glasses with large wrap reduce evaporation 5. lid hygeine 6. topical testosterone (increases lacrimal production) 7. omega-3 fatty acids 8. steroids
|
|
punctal plugs may make things worse for the first couple days
|
|
|
describe the neuronal feedback loop that regulated normal tearing
|
In the normal eye, the ocular surface, lacrimal glands, and the neuronal feedback loop that links them effectively constitute a single functional unit for the maintenance of ocular surface homeostasis The main and accessory lacrimal glands Produce aqueous tears, growth factors, and other proteins that promote ocular surface health Supported by constant neural input, maintained in a noninflammatory state by circulating androgens The ocular surface is richly innervated with sensory nerve endings Contributes vital components to the tear film: eg, mucin that helps wet the ocular surface Homeostasis of the healthy functional unit (neuronal feedback loop): Lacrimal glands secrete tears that lubricate and support the ocular surface Sensory (afferent) traffic travels from the ocular surface via the ophthalmic branch of the trigeminal nerve (V) to the brain stem and midbrain where it is integrated Ocular surface irritation or inflammation will impact afferent signaling Efferent traffic travels via the facial nerve (VII) and synapses to lacrimal glands, controlling secretion and tear production. Control of the accessory lacrimal glands and goblet cell secretion is under active investigation Dysfunction in any elements can eventually lead to dysfunction of all, with subsequent inflammation and dry eye disease
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|
how does dry eye impact the neuronal feedback loop that regulates normal tearing
|
Dry eye disease Results from localized immune-mediated inflammation that ultimately affects the entire ocular surface/lacrimal gland/neural feedback functional unit The main and accessory lacrimal glands Susceptible to inflammation due to decreased neural or androgen support Activation of lymphocytes leads to T-cell-mediated inflammation, cytokine production, the presence of cytokines in tears, and acinar cell apoptosis The ocular surface Cytokines in tears trigger inflammation (T-cell and epithelial cell activation, leukocyte recruitment) on the ocular surface, disrupt epithelial cell function, interfere with mucin production Irritation can also trigger chemically mediated inflammation leading to activation of trafficking lymphocytes (T cells) The neural feedback loop Sensory activity on the ocular surface is disrupted by pro-inflammatory cytokines and compromised epithelial cells, impacting afferent signaling Sensory input to the lacrimal glands is decreased by disruption of the neuronal loop and by the direct inhibitory effect of inflammatory cytokines in the glands on secretomotor nerve endings Dysfunction in any one element can lead to dysfunction in all elements, with subsequent development of chronic inflammation and dry eye disease Inadequate tear production, altered tear composition, or secretion of inflammatory substances into tears can result in ocular surface inflammation
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|
what drug and what type of drug is restasis? what is it used for?
|
cyclosporin, immunomodulator (anti-inflammatory). used for severe forms of dry eye.
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|
New lecture: OPT 533 - Conj Disease Intro 2009
|
|
|
what is the technical name for red eye (or conjunctival injection)
|
conjunctival hyperemia
|
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what causes conjunctival hyperemia
|
anything that makes the conj. "unhappy" (irritation, inflammation etc.)
|
|
between what layers does a subconjunctival hemorrhage occur
|
between the conjunctiva and the episclera
|
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when would a subconjunctival hemorrhage be concerning
|
if it was recurrent.
|
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what should you do if you have a pt with conjunctival hyperemia, but no other findings
|
you know the conjunctiva is “unhappy” but you don’t know why Rx lubricants and have the patient come back if the problem doesn’t get better or gets worse
|
|
what is the leading cause of chemosis
|
allergy
|
|
what are papillae
|
Elevations of the conjunctiva Vascular core surrounded by edema and mixed inflammatory cells under the epithelium
|
|
where are papillae most prominent
|
Most prominent on the palpebral conjunctiva of the upper lid
|
|
note increasing diffusion of the light reflex with increasing severity of papillae
|
picture
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picture
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what are the types of papillae (3)
|
normal papillae, giant papillae, cobblestone papillae
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how could you tell is papillae are caused by allergy or bacteria
|
-eosinophils are related to allergic reation. PMNs are related to bacterial infection. You can culture to determine which is involved.
|
|
what are follicles
|
Yellowish to grayish white Discrete Round elevations of the conjunctiva Avascular but dilated blood vessels may surround the base and sweep up over the elevations Usually 0.2 mm to 2 mm in size but larger follicles can be seen Consist of plasma cells and lymphocytes
|
|
name 4 types of conditions you can see follicles in
|
1. viral disease 2. chlamydial disease 3. parinaud's oculoglandular syndrome 4. toxid drug reactions
|
|
how do you differentiate between papillae and follicles
|
In general, if conjunctival bumps are on the upper lid, think papillae first If conjunctival bumps are on the lower lid, think follicles first A few diseases have both on both lids; eg chlamydial disease also, papillae have a vascular core and follicles do not (but they may be surrounded by vessels)
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|
what does mucopurulent discharge indicate
|
pus indicates PMNs which indicates bacterial infection
|
|
what does hyperpurulence indicate
|
gonococcal infection
|
|
what is a true membrane
|
Fibrinous exudate firmly adherent to conjunctiva Bleeds and scars when removed . It is a fibrin exudative material that sticks to the conjunctiva
|
|
name three conditions in which you would see a true membrane
|
Some bacterial conjunctivitis Stevens-Johnson syndrome Burns
|
|
what is a pseudomembrane
|
Fibrinous exudate that is loosely attached to conjunctiva Avascular
|
|
name three conditions in which you could see pseudomembrane formation
|
Mild allergic conjunctivitis Mild bacterial conjunctivitis Epidemic keratoconjunctivitis
|
|
what is hyphema
|
red blood cells in the anteroir chamber
|
|
New lecture: OPT 533 - Conj Pigment Anomalies 2009
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|
|
what is this
|
racial pigmentation
|
|
what is another name for racial pigmentation
|
epithelial melanosis
|
|
describe the epidemiology for epithelial melanosis
|
frequently occurs in african american and others with dark complexions
|
|
describe the age of onset and the progression associated with epithelial melanosis
|
Seen in the first few years of life and static by early adulthood
|
|
is epithelial melanosis fixed or free moving
|
Pigmentation is within epithelium and moves freely over globe
|
|
describe the pathophysiology of epithelial melanosis
|
Pigmented cells come from melanocytic cells that normally exist in the basal layer of the conjunctival epithelium. everyone has these melanocytes, but the pigment is usually not noticable
|
|
what is this
|
conjunctival nevus
|
|
what is a conjuctival nevus
|
Discrete, flat or slightly elevated, variably pigmented lesion Presentation is usually during the first two decades of life May enlarge or become more pigmented during puberty Cystic spaces within the lesion are frequently seen Amount of pigmentation is variable and almost non-pigmented nevi can be seen
|
|
what is the most common location for a conjunctival nevus
|
Most common location is the juxtalimbal area
|
|
why is this picture suspicious
|
blood vessels surrounding the nevus are called sentinel vessels. they are suspicous and my indicate a more serious condition
|
|
what is a conjunctival melanoma
|
Solitary, black or grey nodules that is fixed to episclera or Non-pigmented lesion with a smooth surface Often contains blood vessels
|
|
how common is conjunctival melanoma
|
Rare tumor - 2% of eye malignancies
|
|
is a conjunctival melanoma typically fixed, or movable
|
typically do not move over the globe like a nevus does
|
|
describe the epidemiology and age of onset associated with conjunctival melanoma
|
Predominantly in whites, rarely in blacks Presentation is usually in the sixth decade
|
|
what is the mortality rate associated with conjunctival melanoma
|
Overall mortality rate is 25% Rate increases to 40% - 44% if tumor arose from PAM ((primary acquired melanosis)
|
|
-the eyes and the lung are connected in terms of metastasis occurring from one structure to the other.
|
|
|
describe some changes that would make you suspicious that a nevus is turning into a conjunctival melanoma
|
Increased vascularity Increased size Increased solidity Become fixed to the underlying sclera (except at limbus) Elevation
|
|
what condition is this
|
primary acquired melanosis
|
|
what is primary acquired melanosis (PAM)
|
Mobile, patchy, diffuse, flat, brown lesions Indistinct margins
|
|
is primary acquired melanosis a stable or progressive condition
|
may grow
|
|
describe the epidemiology associated with primary acquired melanosis
|
occurs in white, middle-aged or older adults
|
|
how do you differentiate between a nevus and primary acquired melanosis
|
PAM will have indistince margins, and will grow into adulthood (nevus can grown in childhood). Normally the benign pigmentation will occur in “dark skinned” population, not in white population.
|
|
what changes would indicated that primary acquired melanosis is converting into melanoma
|
Sudden appearance of one or more nodules in otherwise flat lesions A melanoma becomes fixed to the underlying tissue, which is not a feature of PAM
|
|
does primary acquired melanosis increase the risk of melanoma
|
yes
|
|
what condition is this
|
ocular melanocytosis
|
|
what is ocular melanocytosis
|
Multiple blue-gray or slate-gray patches of pigmentation in the episclera Things become bluer as they get deeper. Browner as they go towards surface.
|
|
is ocular melanocytosis fixed or movable
|
Pigmentation cannot be moved over the surface of the globe
|
|
what condition is this
|
oculodermal melanocytosis
|
|
what is another name for oculodermal melanocytosis
|
nevus of ota
|
|
are there any conditions associated with ocular melanocytosis
|
Ipsilateral iris hyperchromia Melanomas of the uveal tract (you should probably dilated these pts) Ipsilateral glaucoma
|
|
what is a pinguecula
|
Conjunctival degeneration Yellow-white subepithelial deposits of abnormal collagen
|
|
what direction does a pterygium point
|
Triangular base on the conjunctiva or limbus Triangular apex toward the center of the cornea
|
|
can a pinguecula turn into a pterygium
|
yes
|
|
what is the deposit at the leading edge of a pterygium called and what type of material is deposited there.
|
stocker's line. iron deposit.
|
|
what type of light picks an iron deposit best
|
cobalt blue
|
|
what layers of the corne are damaged by a pterygium
|
destroys bowman's membrane
|
|
how does a pterygium affect vision
|
induces astigmatism, may decrease vision if crosses the visual axis
|
|
describe the management of pterygium and pinguecula
|
1. lubricants 2. sunglasses for protection 3. vasoconstrictors 4. steroids if inflammed 5. possible surgery for pterygium that is affection vision
|
|
what percentof pterygium will return after surgery? what can be done to reduce recurrence
|
1/3. mitomycin C (antimetabolite).
|
|
what is a concretion
|
Minute hard yellow spots in the palpebral conjunctiva Caused when debris from cellular degeneration remains trapped in the conjunctiva and becomes calcified
|
|
can concretions be revomed
|
If necessary can be removed using a needle under topical anesthesia
|
|
what is this
|
conjunctival cyst
|
|
what is a conjunctival cyst
|
Thin-walled cysts filled with clear watery fluid
|
|
are conjunctival cysts usually problematic
|
Usually do not cause any symptoms If large, they may be ruptured or excised
|
|
what cells does lissamine green stain
|
only stains dead cells. can be seen in severe dry eye.
|
|
what is this
|
bitot's spot
|
|
what is a bitot's spot and what causes it
|
Drying and wrinkling of the conjunctiva May have a foamy appearance and do not wet easily Manifestation of severe vitamin A deficiency Rarely seen in the USA
|
|
New lecture: Allergic Conjunctivitis 2009
|
|
|
just rubbing your eyes will cause degranulation of mast cells and make your eyes itch. So could be that their eyes are simply irritated and they are rubbing them.
|
|
|
what should you educated your pts on in regards to the tx of allergic conjunctivitis
|
-remember to tell your pts that therapy is only going to relieve symptoms, not cure the allergy. So they can not stop taking medications
|
|
what can happen if you use too much of a vasoconstricter
|
-if you use too much of visine (etc.; vasoconstricter) you can have a rebound hyperemia. Your eyes will become red. -vasoconstricters such as visine are just for looks
|
|
8 types of treatment for allergic conjunctivitis
|
1. remove allergen 2. cold compresses 3. artifical tears 4. vasoconstrictors 5. antihistamines 6. mast cell stabilizers 7. topical steroids 8. topical NSAIDs
|
|
what is the mechanism of action for topical vasoconstrictors
|
Mechanism of action - binds to alpha receptors on blood vessels and
|
|
topical vasoconstrictors specific agents
|
Phenylephrine
|
|
what ocular side effect can be caused by oral anithistamines
|
dry eye; caused by anticholinergic effect
|
|
what is histamine and what are its effects on the body
|
Chemotactic factor for eosinophils
|
|
how do antihistamines work
|
bind to histamine receptors
|
|
what is the generic name for benedryl
|
diphenhydramine
|
|
name five oral antihistamines and whether they are over the counter or prescription
|
1. zyrtec (OTC) 2. allegra (RX) 3. clarinex (RX) 4. claritin (OTC) 5. benadryl (OTC)
|
|
are mast cell stabilizers safe drugs
|
very safe drugs
|
|
name five topical antihistamines
|
zaditor alaway patanol pataday claratin eyes
|
|
name 4 optical mast cell stabilizers. which one acts the fastest?
|
a.
|
|
what are steroids used to tx allergic conjunctivitis
|
inhibits inflammation of all kinds, but has ocular side effects.
|
|
name the only topical steroid FDA approved for treating allergic conjunctivitis
|
Alrex (loteprednol etabonate 0.2%) qid = ONLY TOPICAL STEROID FDA APPROVED FOR OCULAR ALLERGY TX
|
|
generic and trad names of three topical NSAIDS
|
Acular, Acular PF, Acular LS (ketorolac tromethamine 0.5% and 0.4% soln) qid
|
|
what is the common name for seasonal allergic conjunctivitis (SAC)
|
hay fever conjunctivitis
|
|
what is seasonal allergic conjunctivitis
|
the ocular component of hay fever. triggered by airborne antigens.
|
|
describe the pathophysiology associated with seasonal allergic conjunctivitis
|
Conversion of arachidonic acid to prostaglandins and leukotrienes results in inflammation
|
|
what type of allergic reaction causes seasonal allergic conjunctivitis
|
type 1
|
|
8 signs and symptoms associated with seasonal allergic conjunctivitis
|
1. mild to moderate itching 2. tearing 3. conjunctival hyperemia 4. lid edema 5. white stringy discharge 6. chemosis 7. papillary reaction 8. possible rhinitis
|
|
what is perennial allergic conjunctivitis
|
Clinically similar to SAC but persists throughout the year B.
|
|
what is acute allergic conjunctivitis
|
Urticarial rxn caused by large amount of allergen reaching the conj Subjective similar to SAC EX. Young children after playing in grass or with pets
|
|
objective appearance of acut allergic conjunctivitis
|
Sudden onset of severe chemosis and swelling of lids
|
|
describe the management associated with acute allergic conjunctivitis
|
TX/Management No specific TX needed – resolve spontaneously within a few hours
|
|
is giant papillary conjunctivitis an allergic reaction
|
not an allergic reaction per se; actual etiology is controversial)
|
|
what is giant papillary conjunctivitis
|
Specific conj inflammatory rxn characterized by papillary hypertrophy in the superior tarsal conj
|
|
what causes giant papillary conjunctivitis
|
Response to chronic, physical trauma Causes a.
|
|
it is good practice to evert the lids on all contact lens pts to check the upper lid
|
|
|
is giant papillary conjunctivitis unilateral or bilateral
|
almost always bilateral
|
|
what is another name for vernal keratoconjunctivitis
|
spring catarrh
|
|
what is vernal keratoconjunctivitis
|
a rare form of allergic disease that is seasonal/climate related
|
|
is vernal keratoconjunctivitis usually unilateral or bilateral
|
bilateral
|
|
8 objective signs associated with vernal keratoconjunctivitis
|
1. cobblestone papillae on superior tarsal plate (pretty specific to vernal) 2. lid edema 3. thick white stringy discharge 4. conjunctival hyperemia 5. superior SPK 6. superior limbal infiltreates 7. tranta's dots 8. sterile corneal ulcer
|
|
describe the epidemiology associated with vernal kertoconjunctivitis
|
young males with a hx of atopy
|
|
subjective symptoms associated with vernal keratoconjunctivitis
|
1. extreme itch 2. blepharospasm 3. blurriness 4. photophobia
|
|
what is atopic keratoconjunctivitis
|
Relatively RARE but potentially serious condition which affects young men with atopic dermatitis
|
|
9 objective signs of atopic keratoconjunctivitis
|
1. thick white stringy discharge 2. lid edema 3. papillae (inferior palpebral conj) 4. conjuncitival hyperemia 5. chemosis 6. mod-severe SPK (near 100%) 7. limbal infiltrates 8. tranta's dots 9. cicatrizing conjunctivitis with symblepharon formation
|
|
how does the onset of atopic ocular symptoms relate to the onset of other atopic symptoms
|
Ocular SXs usually develop years after onset of other atopic features
|
|
do the symptoms associated with atopic keratoconjunctivitis occur year round or do they come and go
|
SXs persist year round ((seasonal or vernal are not year round)
|
|
New lecture: Bacterial conjunctivitis 09 Print
|
|
|
what is bacterial conjunctivitis
|
Infectious inflammation of the conjunctiva with bacteria as the causative agent
|
|
what is the difference between acute and chronic bacterial conjunctivitis
|
It can be classified as acute (less than 4 weeks duration) or Chronic (greater than 4 weeks duration)
|
|
bacterial conjunctivitis can occur in otherwise health individuals
|
|
|
what is the most common causative agent for bacterial conjunctivitis for all ages
|
s. aureus
|
|
list four common causative agents for acute bacterial conjuncitvitis
|
1. s. aureus 2. s. epidermidis 3. s. pneumoniae 4. h. influenzae
|
|
is acute bacterial conjunctivitis usually unilateral or bilateral
|
Unilateral initially Becomes bilateral by auto inoculation
|
|
how do you differentiate between bacterial and viral conjunctivitis
|
with bacterial the lids will be stuck shut in the morning. eyes to not stick shut with viral infection or allergic reaction
|
|
how does the color variation of the blood vessels differ between bacterial and viral infection
|
if vessels are beefy red think bacterial; if they are pink think viral.
|
|
what things do you want to ask about in the history if you think you might have bacterial conjunctivitis
|
Exposure to people with an infection Age Recurrence Systemic illness/treatment Drops used ((side effects) Contact Lens wear Think of STDs Recent travels
|
|
8 objective signs associated with acute bacterial conjunctivitis
|
1. conjunctival injection 2. purulent discharge 3. chemosis 4. subconjunctival hemorrhage (with s. pneumoniae, h. flu) 5. papillae 6. marginal infiltrates 7. SPK (exotoxins) 8. pseudomembrane or membrane (in severe cases, esp if s. aureus or c. diptheriae are the cause) -VA usually normal, usually no AC reaction, normal pupils, usually no-preauricular adenopathy
|
|
when do you typically do a culture on an acute bacterial infection
|
Cultures can be beneficial in non-responsive or hyper-acute cases Not usually done for routine cases.
|
|
what is the minimum dosing schedule for topical antibiotic
|
you don't want to give an antibiotic less than qid becuase bacteria will develop resistance
|
|
how do you treat an acute bacterial conjunctivitis (name 9)
|
empiric treatment with broad spectrum antibiotic Trimethoprim and Polymyxin B (Polytrim) ophth. sol. Gentamicin, Tobramycin ophth. sols. Bacitracin and Polymyxin B (polysporin) ophth. ung. Ofloxacin (Ocuflox), Ciprofloxacin (Ciloxan), Levofloxacin (Quixin) ophth. sols. Ciprofloxacin (Ciloxan) ophth. ung. Gatifloxacin(Zymar) Moxifloxacin (Vigamox) Tid X 7 days
|
|
name 2 fourth generation fluoroquinolones
|
4th generation fluoroquinolones Gatifloxacin(Zymar) Q2h for the first 2 days, then qid for 5 more days. Moxifloxacin (Vigamox) Tid X 7 days
|
|
how long do you need to have a pt on antibiotics for acute bacterial conjunctivitis
|
7-14 days. until resolved!
|
|
what do you need to tell pts with acute bacterial conjunctivitis to prevent the spread of infection
|
Avoid sharing towels and linens. Wash hands often. Avoid touching non-infected eye. Avoid contaminating public swimming pools
|
|
when should the initial follow up be for acute bacterial conjunctivitis
|
2-3 days
|
|
what does petechial hemorrhages in acute bacterial conjunctivitis indicate
|
H.flu or strep
|
|
|
Rx writing example
|
|
name two of the most common organisms causing chronic bacterial conjunctivitis
|
S. aureus S. epidermidis
|
|
describe the progression of symptoms associated with chronic bacterial conjunctivitis
|
Symptoms “wax and wane” ((better and worse)
|
|
6 signs of chronic lid tissue distruction
|
1. induration 2. superficial neovascularization 3. red lid margin 4. poliosis 5. madarosis 6. trichiasis
|
|
5 signs of meibomian gland dysfunction (MGD)
|
1. blockage of secretion 2. focal swelling of meibomian gland orifices (serration) 3. lid erythema 4. lid edema 5. signs of composition changes
|
|
2 signs of hypersensativity to exotoxins
|
1. marginal corneal infiltrates 2. phlyctenule
|
|
tx of chronic bacterial conjunctivitis
|
1. eliminate cause 2. tx conjunctivitis 3. ab-steroid combo if combined with an inflammatory component
|
|
what is the most common cause of hyper-acute bacterial conjunctivitis
|
gonahrea
|
|
is ocular involvement common in gonorrhea
|
not common
|
|
symptoms of genital gonorrhea infection
|
men: none, pain on urination, white yellow or green penile discharge, swollen or painful testicles women: none, (non-specific, can be mistaken for bladder infection), pain on urination, increased vaginal discharge, vaginal bleeding between peroids
|
|
gonorrhea can cause serious complications regardless of presence or severity of Sxs. Pelvic Inflammatory Disease (PID) Infertility Risk for ectopic pregnancies
|
|
|
organism that causes gonococcal conjunctivitis
|
Neisseria gonorrhoeae
|
|
other (than gonococcal) less common causes of hyper-acute bacterial conjunctivitis: Neisseria meningitidis, Staph aureus. Strep. H flu. Moraxella E.coli Pseudomonas
|
|
|
describe the progression of hyper-acute bacterial conjunctivitis
|
Urgent/Emergent Condition Neisseria can penetrate an intact cornea in 48 hours Ulceration, perforation endophthalmitis
|
|
Bacteria that can penetrate an intact cornea: Neisseria gonorrhea Corynebacterium diptheria Listeria H. Egypticus Acanthamoeba
|
|
|
12 signs and symptoms of hyper-acute bacterial conjunctivitis
|
1. extreme discharge 2. severe hyperemia 3. chemosis 4. lid edema 5. pain and tenderness 6. blurred vision 7. preauricular lymphadenopathy 8. cells and flare 9. hypopion 10. PEE 11. marginal infiltrates 12. ulceration/perforation
|
|
complications if hyper-acute bacterial conjunctivitis is not treated promptly (4)
|
Preseptal cellulitis with fever Corneal ulceration and perforation Dacryoadenitis Potential septicemia
|
|
what test do you need to do with hyper-acute bacterial infection
|
culture
|
|
what class of antibiotics is no longer recommended for the treatment of gonorrhea by the CDC
|
fluoroquinolones Ongoing data from CDC 's Gonococcal Isolate Surveillance Project (GISP), including preliminary findings from 2006, demonstrate that fluoroquinolone-resistant gonorrhea is continuing to spread and is now widespread in the United States. As a consequence, and as reported in the MMWR, April 13, 2007, this class of antibiotics is no longer recommended for the treatment of gonorrhea in the United States.
|
|
what is the only current CDC approved class of antibiotics to treat gonorrhea
|
cephalosporins
|
|
describe the treatment of gonococcal conjunctivitis
|
Non-septicemic adults & children over 20 kg. Ceftriaxone 1g IM in a single dose No topical tx is necessary! Irrigation with saline to dilute local virulence factor -usually treated for concurrent chlymidial infection if not ruled out
|
|
what is the systemic treatment for chlamydia
|
Azithromycin 1g p.o., single dose OR Doxycycline 100 mg p.o., bid X 1 week
|
|
what are the contraindications for doxycycline
|
doxycycline is a contraindication for children under 8 or pregnant/lactating women.
|
|
what is the follow up schedule for hyper-acute bacterial conjunctivitis
|
every day until consistant improvement
|
|
how long after starting treatment until the purulence calms
|
Purulence calms in 48+ with proper treatment Conjunctivitis may last 1-2 weeks
|
|
New lecture: Viral Conjunctivitis 2009
|
|
|
what is the common name for viral conjunctivitis
|
pink eye
|
|
viral conjunctivitis is very contageous. it is standard of care to rx antibiotic for viral conjunctivitis
|
no, that will only increase resistance. only if there was a break in the epithelium and antibiotic was used for prophylaxis would this be appropriate.
|
|
virus: Can not grow independently, requires protein synthesis from other source
|
|
|
Reduction of immune system and physical barriers enhance viral susceptibility, spread and duration EXAMPLES diabetes, nutrition, Virus can live in ganglion or host cells, remain dormant and then reactivate due to aggravating factors, such as stress, sunlight, intense cold or heat.
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|
|
describe the treatment for viral conjunctivitis
|
No treatment. lubricants. Warm compresses? ((helps fight the infection, but make the eye more red and increase discomfort) Cold compresses? ((vasoconstrict; may be more pleasant for the pt) Remove pseudomembranous fibrin deposits ((can use topical anesthetic)
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|
what do you need to remember to do after a pt with viral conjunctivitis comes through the office
|
disinfect the office. there are some adenoviruses that can survive 30 days on a surface.
|
|
what is pharyngoconunctival fever
|
viral conjunctivitis with pharyngitis and fever
|
|
describe the demographic associated with pharyngoconjunctival fever
|
usually in children age 5-15
|
|
9 objective signs associated with pharyngoconjunctival fever
|
1. pharyngitis 2. conjunctivitis 3. fever 4. keratitis (30%) 5. lid edema 6. preauricular lymphadenopathy (not tender) 7. serous watery discharge 8. possible pseudomembrane 9. possible conj. hemorrhages
|
|
describe the progression of pharyngoconjunctival fever
|
self-limiting, lasting 1-3 weeks.
|
|
what is epidemic keratoconjunctivitis
|
Acute
|
|
what age range normally get epidemic keratoconjunctivitis (EKC)
|
Age - 15+ years
|
|
what is the rule of 8 associated with epidemic keratoconjunctivitis
|
First 8 days: mild to moderate burning, irritation, and photophobia. 2)
|
|
is epidemic keratoconjunctivitis usually unilateral or bilateral
|
usually starts in one eye and spreads to the other
|
|
what percent of cases of epidemic keratoconjunctivitis have corneal involvement
|
80%
|
|
describe the corneal involvement associated with epidemic keratoconjunctivitis (EKC)
|
1)
|
|
will there be preauricular adenopathy with epidemic keratoconjunctivitis
|
ipsilateral preauricular lymphadenopathy. will be tender.
|
|
|
|
|
name two viral medications
|
Viroptic (triflouridene) ((effects all cells; toxic) ((SPK) Acyclovir (oral) ((good at targeting viral infected cells; relatively safe)
|
|
what is the most common cause of acute conjunctivitis
|
adenovirus
|
|
you can transmitt and contract both viral and bacterial conjunctivitis from the pool
|
|
|
7 objective signs associated with viral conjunctivitis
|
1. pink bulbar hyperemia 2. follicles (synonymous with viral conjunctivitis) 3. chemosis 4. periorbital edema 5. serous watery discharge 6. possible ipsilateral preauricular lymphadenopathy 7. pseudomembranes or true membranes
|
|
use of steroids for subepithelial infiltrates in epidemic keratoconjunctivitis is controversial
|
|
|
Infection of skin by Molluscum contagiosum virus
|
2.
|
|
tx for molluscum contageosum
|
When inactive leave it alone
|
|
what is acute hemorrhagic conjunctivitis
|
rare in the US. it is a hyper-acute viral conjunctivitis. conjunctival hemorrhaging common.
|
|
what is another name for cat scratch fever
|
Parinauds oculoglandular fever
|
|
what is parinauds oculoglandular fever
|
virus from cats. systemic involvlement: fever, malaise, HA. ocular involvement:
|
|
three objective signs associated with parinaud's oculoglandular fever
|
1. large follicular development 2. extensive preauricular involvement 3. neuroretinitis (edema of the ONH and macula)
|
|
what is newcastle's disease
|
virus transmitted by infected birds (likely candidates are poultry workers)
|
|
New lecture: Corneal Disease Victoria 09
|
|
|
what is another name for phlyctenular keratoconjunctivitis
|
phlyctenulosis
|
|
what is phlyctenular keratoconjunctivitis
|
A nodular inflammation of the perilimbal tissue characterized by the formation of a small, circumscribed lesion affecting the conjunctiva, limbus or cornea
|
|
what are the two types of phlyctenular keratoconjunctivitis
|
Two types: based on location of lesion: Conjunctival Corneal
|
|
describe the pathophysiology behind phlyctenular keratoconjunctivitis
|
A non-specific allergic hypersensitivity response to diverse antigens:
|
|
in what age range is phlyctenular keratoconjunctivitis most common
|
more common in children and yound adults
|
|
what do you need to remember to ask about
|
you need to be concerned about TB. ask if they have had recent travels or are an immigrant. -you also need to keep up on recent TB outbreaks in the US
|
|
9 signs and symptoms of phlyctenular keratoconjunctivitis
|
1. FB sensation 2. injectino 3. itching 4. tearing 5. discharge 6. pain (moderate to severe) 7. photobia (moderate to severe) 8. blepharospasm 9. blurry vision
|
|
does conjunctival phlyctenular keratoconjunctivitis or corneal PKC have more symptoms
|
conjunctival: less symptomatic corneal: more symptomatic
|
|
describe teh appearance of a conjunctival phlyctenule
|
small, raised nodular lesion. pinkish white in color. surrounded by dilated blood vessels
|
|
what is the most common place to find conjunctival phlyctenule
|
Usually close to limbus but can occur anywhere on bulbar conj. Most common at 8, and 4 o’clock.
|
|
ciliary spasm at least contributes to the pain associated with corneal phlyctenular keratoconjunctivitis (if not causes it)
|
|
|
describe the appearance of a corneal phlyctenule
|
Wedge shaped, white mound at limbus with radial pattern of vascularization Migrate towards center of cornea as a gray-white superficial ulcer Leave a triangular leash of vasculerized pannus
|
|
where do junctional (corneal) phlyctenular lesions occur
|
limbal lesions occur in the inferior aspect of the eye near the lid margin
|
|
Severe Corneal phlyctenular lesions: May result in:
|
Ulcers Scarring Vasculerization Perforation
|
|
phlyctenular keratoconjunctivitis has a pretty typical diagnostic appearance
|
|
|
does loteprednot or pred forte seem to raise IOP more
|
pred forte
|
|
what is the generic name for pred forte
|
prednisolone acetate
|
|
describe the management of phlyctenular keratoconjunctivitis
|
1. TB needs to be ruled out 2. 1% pred forte q2h for 4 days, qid for 3 days , then tapered -or 0.5% loteprednol 3. cycloplegic for comfort if necessary 4. necessary tx may be less for conj. lesions. they are typically self limiting 5. treat the underlying cause
|
|
if there is severe pain associated with phlyctenular keratoconjunctivitis, what should you expect is the cause
|
chlamydia or herpes simplex virus (tx systemically)
|
|
describe the prognosis associated with phlyctenular keratoconjunctivitis
|
Good, if conjunctival or limbal and is treated adequately. Potentially blinding if corneal and not treated adequately
|
|
6 causes of exposure keratopathy
|
Incomplete blink Lagophthalmos Nocturnal Lagophthalmos Ectropion Bell’s Palsy Graves’ disease
|
|
objective signs of exposure keratopathy
|
1. PEE (inferior or interpalpebral cornea) 2. conjunctival injection 3. micropannus, scarring and corneal thinning in severe cases
|
|
describe the management of exposure keratopathy
|
1. lubricating therapies (drops, gels, ointments) 2. mechanical (eyelid taping at night, eyelid weights, bandage CL) 3. tarsorrhaphy in severe cases
|
|
what is this
|
filamentary keratitis
|
|
what is filamentary keratitis
|
Strands of epithelial cells and mucus attached to the cornea ((can’t blink it off)
|
|
what stain works well with filamentary keratitis
|
stains well with rose bengal. does not stain well with fluorescein.
|
|
what causes the pain associated with filamentary keratitis
|
one end attached to the cornea, the other end is free floating. So when the pt blinks they move and pull on the cornea
|
|
what is the most common cause of filamentary keratitis
|
condition is always secondary to another disease. Most common etiology is dry eye. -other causes: Sjogren’s Syndrome Superior Limbic Keratoconjunctivitis Recurrent corneal erosions Neurotrophic keratopathy Chronic bullous keratopathy Patching Adjacent to surgical wound
|
|
what is the tx for filamentary keratitis
|
Treat underlying condition if present Debridement of the filaments. Apply topical anesthetic Remove filaments from their base -bandage contact lens
|
|
what is thygeson's superficial punctate keratitis (TSPK)
|
A chronic, bilateral, recurrent corneal epithelial keratitis
|
|
describe the appearence of thygeson's superficial punctate keratitis
|
Round conglomerates of distinct, granular, punctate epithelial lesions
|
|
what is thygeson's superifical punctate keratitis likely to be confused with
|
many people confuse it with a subepithelial infiltrate, but if you look closely the stroma is not involved.
|
|
|
|
|
describe the progression of thygeson's superificial punctate keratitis
|
Chronic course with exacerbations and remissions Lasts few to several years
|
|
what is the typical age of onset of thygeson's superificial punctate keratitis
|
onset in teens to twenties
|
|
why is it important to look at indirect illumination of the cornea on slit lamp
|
-it is very important to look at the cornea with an indirect illumination because you will miss a lot the stuff that your light will wash out.
|
|
how does thygeson's superficial punctate keratitis affect vision
|
slight decrease in VA
|
|
8 signs and symptoms of thygeson's superficial keratitis
|
1. FB sensation 2. tearing 3. photophobia 4. slight decrease in VA 5. burning 6. itching 7. multiple epithelial lesions (gray-white, course, granular, raised, can move) 8. subepithelial opacities (caused by edema, or inactive lesion) -no red eye, no anterior chamber reaction,
|
|
management of thygeson's superficial punctate keratitis
|
1. artificial tears (and ointment qhs) 2. mild topical steroid 3. bandage CL
|
|
describe the prognosis associated with thygeson's superificial punctate keratopathy
|
good visual prognosis
|
|
what do you need to be concerned about with using a bandage CL to tx exposure keratopathy
|
the cornea is already exposed because of PEEs. They are more susceptible to infection if they aren’t responsible with the CLs.
|
|
New lecture: Herpes Zoster and Other Viral Lid DZs 2009
|
|
|
what is the name of the disease that causes shingles
|
herpes zoster
|
|
what primary infection can result in shingles
|
. The initial infection with varicella zoster virus (VZV) causes the acute (short-lived) illness chickenpox which generally occurs in children and young people. Once an episode of chickenpox has resolved, the virus is not eliminated from the body but can go on to cause shingles—an illness with very different symptoms—often many years after the initial infection
|
|
describe the objective signs associated with chickenpox
|
Fever
|
|
what is the name of the disease that causes chickenpox
|
varicella zoster virus (VZV).
|
|
are there any ocular complications associated with chickenpox? are they common
|
Ocular complications - rare
|
|
describe the tx associated with chicken pox
|
Analgesic
|
|
what structure does the chicken pox virus lie dorment in
|
1. Within the dorsal root ganglion ((also trigeminal ganglion) 2. Within the sensory ganglia of the spinal cord - thoracic nerves
|
|
what percent of people who had chickenpox will develop shingles
|
20%
|
|
objective systemic signs associated with singles
|
1. vesicular eruptions along the nerve lines 2. vesicles become ulcerated and crusty
|
|
how long does the pain associated with singles last
|
weeks, months, even years.
|
|
what is herpes zoster opthalmicus
|
infects tissues innervated by the ophthalmic division of the
|
|
what percent of all zoster cases have herpes zoster ophthalmicus
|
7-15%
|
|
what part of the trigeminal nerve is most commonly involved in herpes zoster ophthalmicus
|
Usually affects first division of trigemial CN
|
|
what percent of people with herpes zoster ophthlmicus develop ocular lesions
|
50-75%
|
|
how soon do you need to start treatment for herpes zoster ophthalmicus
|
((it is very important not to misdiagnose herpes zoster ophthalmicus, because it can be extremely devastating if they are not place on acyclovir within 72 hours) ((lesions often respect the midline) ((needs to be treated with acyclovir within 72 hours) ((need to ask if they have a rash anywhere else, or if they have tingling or any pain)
|
|
objective signs associated with herpes zoster ophthalmicus
|
CAN MIMIC OR CAUSE ALMOST ANY OCULAR DISEASE!
|
|
what is the treatment for herpes zoster ophthalmicus (specific regimine)
|
1. Oral acyclovir (Zovirax) 600 to 800 mg 5x/day for 7 - 10 days -alternative drugs: famciclovir, valacyclovir 2. non-narcotic/narcotic analgesics -capsaicin cream 3. tx each specific ocular complecation
|
|
vaccination: Zostavax for shingles
|
1.
|
|
what is variola
|
smallpox: systemic viral disease characterized by skin lesions (up to 40% fatality rate depending on type). eradicated from the world (last known case in 1977).
|
|
what is monkeypox
|
an exotic viral illness spread by contact will ill animals or direct/respiratory contact with infected persons
|
|
what is cowpox
|
Virus used for smallpox vaccination 2.
|
|
what is another name for measles
|
rubeola
|
|
what is rubeola
|
acute, highly contagious virus marked by maculopapular rash, inflammation of the respiratory tract. vaccination: MMR
|
|
what is another name for german measles
|
rubella
|
|
what is rubella
|
mild, febrile childhood disease with maculopapular rash. prevention: MMR vaccine
|
|
what is the mumps
|
acute viral disease characterized by fever, swelling and tenderness of the salivary glands. prevention: MMR vaccine
|
|
New lecture: Herpes Simplex 2009
|
|
|
humans are the only host for herpes simplex virus (HSV)
|
|
|
name and discribe the two types of herpes simplex
|
Herpes simplex is divided into two types HSV type 1 and HSV type 2.[1] HSV1 primarily causes mouth, throat, face, eye, and central nervous system infections well HSV2 primarily causes anogenital infections.[1] However each may cause infections in all areas.[1]
|
|
describe the transmission associated with herpes simplex
|
Infection results from direct contact with infected individuals
|
|
which of the two types of herpes simplex is more likely to have ocualr complications
|
HSV 1 - above the waist, leading ocular type
|
|
describe the prevelance of hepres simplex
|
Systemic HSV infection
|
|
systemic and ocular signs associated with herpes simplex
|
1. cutaneous eruptions/vessicles 2. acute unilateral follicular conjunctivitis 3. preauricular adenopathy 4. PEE 5. dendritic epithelial keraitis
|
|
corneal involvement is rare in primary infection with herpes simplex. more common in secondary infection.
|
|
|
|
Tx optional 1. no steroids
|
|
areas affected in secondary (recurrent) herpes simplex
|
Reactivation --> sensory nerve to target tissue
|
|
how does recurring herpes simplex keratitis affect corneal sensativity
|
((with each recurrence you get damage to the nerve and corneal sensitivity will decrease; corneal sensitivity test)
|
|
with each recurrence of herpes simplex keratitis, then chances of another recurrence go up.
|
|
|
what is epithelail keratitis (herpes simplex)
|
Symptoms are variable - absent to severe; eye may be painful during
|
|
what is dendritis keratitis (herpes simplex)
|
Dendritic keratitis starts as PEEs that coalesce
|
|
tx for herpes simplex keratitis
|
1. debridement 2. viroptic: : 1 gt q2h (not to exceed
|
|
antivirals not to exceed ___ days!
|
21
|
|
what is metaherpetic/trophic keratitis
|
chronic (indolent) ulcer secondary to epithelial dendriform keraitis
|
|
what is the etiology of metaherpetic/trophic keratitis
|
lack of healing due to damage to the basement membrane
|
|
tx for metaherpetic/trophic keratitis
|
Promotion of epithelial healing
|
|
stromal keratitis can occur secondary to herpes simplex keratitis: Patients usually have experienced a number of previous attacks of
|
|
|
what is interstitial keratitis
|
stromal keratitis with neovascularization
|
|
steroids are okay to use for stomal keratitis secondary to herpes simplex
|
|
|
what is another name for disciform keratitis
|
endotheliitis
|
|
what is disciform keratitis
|
area of stromal edema (disc-shaped) with associated uveitis; can arise without epithelial defect deing present
|
|
pathophysiology behind disciform keratitis
|
May be a Type IV hypersensitivity reaction or a viral reactivation of
|
|
objective signs of disciform keratitis
|
1. central zone of epithelial edema overlying an area of stromal thickening 2. folds in descemet's membrane
|
|
types of keratitis associated with herpes simplex
|
1. epithelial keratitis 2. dendritic keratitis (may be the same as epithelial) 3. metaherpetic/trophic keratitis 4. stromal keratitis/interstitial keratitis 5. disciform keratitis
|
|
what is the most common site of recurrent herpes simplex infection
|
mucocutaneous borders of
|