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PPO2 Flashcards

1
Q

what is arcus?

A

form of degeneration around the limbus composed of CHOLESTEROL esters and LDL @ stroma. Usually @ inf. cornea and stroma. There are varying degrees.

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2
Q

what does a unilateral arcus possibly indicate? which side is “bad?”

A

vascular occlusion on the side WITHOUT the arcus.

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3
Q

what is limbal girdle of vogt? what does it mean?

A

Age-related sub-EPIthelium collagen degeneration @ cornea. There are white crystal appearances @ 3 & 9 o’clock.
**Type1– clear translucid zone due to Ca deposits at the Bowman’s layer, which is at a difference location on the sclera

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4
Q

hudson-Stahli line

A

iron deposit along Bowman’s layer that looks brown/yellow @ margins of inf. pupil. More common in dry eye people and frequency is the same with age (20y/o= 20% etc)

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5
Q

Descemet’s striae

A

striation in Descemet’s membrane @ cornea. If very very large–> maybe corneal edema.

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6
Q

What is Hassal-Henle bodies?when is it a guttata?

A
  • peripheral= hassal-Henle bodies=iron deposit @ bowman’s membrane
  • central cornea= guttata nodular thickening of Descemet’s membrane composed of collagen and byproduct of ENDO-thelial cells
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7
Q

what is grayson’s disease of cornea?

A

deterioration of layer–due to age mostly

  • peripheral cornea
  • vascularization may be present
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8
Q

what is the % of population that has arcus between 40-60 years old? past 70-90 years old?

A
  1. 60% have arcus

2. 90% have arcus

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9
Q

what eye disease is common in Hudson-stahli line?

A
  • dry eye or tear flow problems @ pupil margin
  • change increases with age
  • A NORMAL FINDING
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10
Q

what is Descemet’s striae?

A
  • Descemet’s membrane striation
  • normal finding that’s VERTICAL
    • bad if paried with stromal edma**
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11
Q

what is the aka of “crocodile shagreen”? what is characterized by this disease?

A
  • Mosaic Shagreen
  • gray/white opacity that has clear spaces–looks like crocodile!
  • mostly peripheral
  • due to Bowman’s Layer relaxation
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12
Q

what is a risk factor for pt. with guttata (which is normally age related)

A

Fuch’s endothelial dystrophy

  • look for corneal stromal edma
  • check pachymetry
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13
Q

what is corneal farinata?

A
  • tiny, dust like flecks @ STROMA–looks like sprinkled flour
  • retro illumination
  • bilateral w/ no VA change
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14
Q

what is band keratopathy?

A
  • Ca salts @ inter-palp zone (begins @ basement membrane)
  • corneal degeneration where corneal nerves penetrate Bowman’s
  • mostly central, but mild cases can be at 3&9 o’clock
    • if in KIDS= rheomoetoid arthritis is risk factor and get irididis
  • decreased VA
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15
Q

where does the Ca salts come from in band keratopathy?

A
  • tears that have Ca and Phosphate

- dry eye/evaporative tears increase solute concentration esp. @ INTRA-palp and the balance is affected

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16
Q

how do we get Band Keratopathy?

A
  • inflammation= uveitis, glauc, corneal edma

- systemic= hyper-parathyroid (immuno), juvenile rheumatoid arthritis, thiazides, vit. D toxicity, renal failure

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17
Q

what is treatment of band keratopathy?

A

ONLY IF VA AFFECTED—scraping with a knife + Ca binding agent EDTA
- surgical excimer laser keratectomy to polish cornea

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18
Q

what is Salzamann’s Nodular Degernation?

A
  • elongated basal epi cell lesions
  • plaques @ epi and Bowman’s= opaque color
  • has keratocytes, esp. at anterior
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19
Q

what is the dimensions of the normal cornea?

A
  1. 6mm x 10.6mm vertically

- central thickness 0.53 and 0.70

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20
Q

list layers of the cornea

A
  1. epi ( surface with microplicae+microvillie for absorption of mucin= rewetting, 5-7 layers of basal columnar cells attached via hemidesomosomes to BM + wing cells)
  2. BM
  3. bowman’s
  4. stroma (any break after here will scar)
  5. Descemet’s membrane
  6. endo
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21
Q

does the epithelium scar as a result of inflammation?

A

no, epi has regenerative properties 7-14 days

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22
Q

does the BM lesion cause scar?

A

yes/no…takes 6-8weeks to regenerate and disruption can cause corneal erosions

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23
Q

does Bowman’s lesions cause scar?

A

YES, doe NOT regenerate—very STRONG though, so if finally break through, then will scar!

-aceulluar structure that will undergo hypertrrophy

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24
Q

what makes up your stroma?

A
  • collagen, fibroblasts with keratocytes etc.

* * DUA’S LAYER: acellular and pre-Descemet’s that separates the LAST row of keratocytes

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25
Q

where does the Descemet’s layer terminate at? Can descemet’s break?

A
  • ends at SWALBE’S line

- made of lattice collagen fibrils and can easily break from the stroma

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26
Q

what are the layers for gonio? What do we see in a closed angle like in glauc?

A
  1. swalbe’s = outer (attaches to Descemet’s)
  2. Trabecular Meshwork
  3. Sclera Spur
  4. Ciliary Body = inner most.

** will only see swalbe’s in a super close angle glaucoma!

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27
Q

what does corneal endo do? can it regenerate?

A
  • corneal endo: amitotic hexagonal cells used for PUMPS–maintain corneal aqueous flow!
  • decreased with age and DOES NOT REGENERATE–hypertrophy= pachymetry!
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28
Q

what is the cornea blood supply from?

A
  • avascular itself
  • conjunctival episcleral vessels around the limbus
  • O2 and nutrients supplied by atmosphere + tear film @ anterior
  • aqueous humor gives nutriens @ posterior

**closed eyes= no oxygen from conjunctival capillaries–wake up with dry eye

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29
Q

the limbus contains radial vessel “ridges” aka ___? that do what? what’s a disease that starts here?

A
  • AKA Palisades of Vogt’s
  • has lymphatics + blood for Oxygen–neovascularization starts here @ limbus!
  • needed for apithelial regeneration
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30
Q

what are the symptoms of corneal edema?

A
  • normally has 78% water, anything 5% and over is edema= light scatter=low VA
  • usually starts as stromal edema that leads to corneal edema
  • not a “disease” just response to disturbance of the balance in pump function wher ethere’s fluid accumulation that affects INTRAocular hydrostatic P
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31
Q

what is basis for epithelial healing? (summary)

A
  • adjacent cells cover damaged part
  • fibronectin secreted and acts like glue to hold together
  • mitotsis in 24hrs and Palisades of Vogt’s in chemical burns wher ewhole pithelium is damaged

**epi CANNOT adhere to Bowman’s without the BM, so if that’s damaged, it’ll take 6-8 weeks= need bandage to encourage healing!

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32
Q

what does it mean if the cornea is “performated?”

A
  • cornea is penetrated all the way through!

- use Seidel test to check for leaking aque. fluid= Fluoscein on wound and check for leaking dye (due to pH change

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33
Q

what’s the difference between abrasion and ulcer?

A
  1. ulcer= superficial loss of corneal tissue that led to necrosis from infection/inflammation
    - epi disurption w/ stroma problem–100% beyond Bowman’s!!
    - not immediately painful, more slow devleoping—red 360 degrees
    - cells and flare present
    - 2ndary to unattended epi. defect
    - **ultimate: enzymatic destruction of MACROMOLEC. that are part of cornea collagen
    - can lose sight!! (like CL over wear and pesudomonas growth)
  2. Abrasion–trauma and does NOT go beyond Bowman’s usually
    - small infiltrates and Flue stains do not “leak”–instead has small “halo” around it
    - no discharge, only red @ infected area
    - treat with antibiotics + cyclo to prevent iritis–NO ANESTHETICS!!
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34
Q

what are teh signs of neurotrophic ulcers

A
  • CN5 (trigeminal) paralysis= pt. can’t feel it

- can have hypopoyn with it: white leukocyte build up spot–inflammation @ ant. chamber (iritis, uveitis etc)

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35
Q

when do recurrent erosions happen? which type of staining is used to check? how’s it look?

A
  • usually in MORNING–eye is dry
  • usually due to organic abrasions-current
  • antibiotic ointment (ung) @ night, drops @ day for 1 week until healed

**use NEGATIVE staining!

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36
Q

how do anterior stormal punctures work? when are they used?

A
  • for recurrent erosions
  • needle punctures into Bowman’s into stroma (shallow depth)
  • promotes epi. binding to underlying tissue (Bowman’s )
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37
Q

what is Doxycycline (200mg, BID) used for?

A
  • recalcitrant recurrent corneal erosions
  • have increased MMA (matrix metalloproteinase enzym) that dissolve BM’s fibrils and hemidesomosomes and looses attachment= BAD

**doxycycline= tetracycline antibiotic + corticosteroid DECREASES MMP and prevent future erosions

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38
Q

how do we treat foreing body removal

A
  • Alger brush

- cotton swab “rolling around”

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39
Q

what are some diseases that give you Iron lines in the cornea? (ABNORMAL!)

A
  1. Ferry line= line around a bleb in post-op gluacoma
  2. stocker’s line= tip of ptyergium
  3. Fleischer’s ring= ring of keratokonus
  4. Coat’s ring= once you remove a ring, it’s what’s left
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40
Q

What are the 3 most common Grayson’s disease of cornea? what are hallmarks’ of Grayson’s?

A
  1. Kerotokonus 2. Fush’s dystrophy 3 Epi, BM disorder
  • bilateral, hereditary disease affecting central cornea
  • avascular and begins early
  • unrelated to other diseases
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41
Q

what are some hallmarks of keratoconus?

A
  • central and paracentral cornea
  • stromal thinning
  • apical protrusion
  • irregular mires
  • *NON inflammatory
  • 80% bilateral
  • hereditary= 8% relatives || associated with other CT disorders (Raynaud’s/syndactylyl/Down’s syndrome/Marfan’s/Ehlers-Danlos

**associated with Fleischer’s Ring & corneal thinning

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42
Q

what did the CLEK study find regarding kerotokonus?

A
  • collab longitudinal eval of keratoconus
  • 13.5% have blood rel. w/ disease
  • 50% eye rubbing
  • pt. have poor ability to process and eliminate oxy&nitrogen= oxidative damage
  • changes protein/DNA and lipid functions
  • more apoptosis @ ant. stromal keratocytes
43
Q

what are some hypothesis of how keratoconus happens?

A
  • collagen cross linking issues around puberty and stays that way for 10-20years= MAIN theory
  • proteoglycan abnormalities
  • fibrillation of Bowman’s layer that causes breaks + fibrous growth @ break points
44
Q

what is Munson’s sign? what disease is it in?

A
  • keratokonus late stage
  • shape of the cone shows convex of lower lid @ DOWN gaze
  • apex thinning + stria @ post. stroma
45
Q

what happens in later stage kerotoconus as cone developes?

A
  • reticular scaring @ bowman’s
  • can’t get 20/20 VA
  • Fleischer ring w/ Fe depositions @ epi (use colbalt blue)
  • stromal thinning + scarring= lamellae decrease
  • *may have Descemet’s membrane= stroma edema with decrease in VA + Pain!–resolves in a few months
  • treat w/ cyclo + hypertonic solution to lower Pressures
46
Q

what are the classifications of Keratoconus?

A
  1. mild= less than 48D
    - oblique astig + high myopia, but difficult to tell from externals
  2. moderate= 48-54D
    - 1+ corneal signs with corneal nerves present
    - 40%= Vogt’s striae
    - 50%Fleischer’s ring
    - 20% corneal scarring
  3. severe= greater than 54D
    - vogt’s striae 60%
    - 70% Fleischer’s ring + scaring
    - acute corneal hydrops (edema)–MMA is in stroma and “broke out”
47
Q

how is collagen cross linking surgery performed for kerotoconus?

A
  • removing corneal epi (epi-off) and adding riboflavin (vit. B2)
  • UV-A the whole eye and produce rxn oxygen molecules that cause chemical bonds–> strengthn collagen fibrils

stops keroto progression

48
Q

what is Fush’s epi-endo dystrophy?

A
  • slow, progressive decline in endo. cell pumps/function= stromal epithelial edema
  • BILATERAL and has decreased vision + pain
  • females 50-60 y/o +
  • autosomal DOMINANT
  • cell density drops, pumps don’t work as well and cell density can be below 500 cells= dry eye + “subepi “bullae”= painful!

**use specular reflection

49
Q

what are early signs of Fuch’s? how does this disrupt eye?

A
  • endo acts as barrier to movement of salt& metabolites @ stroma
  • pumps bicarbonate ions OUT of stroma & into aque. humor
  • get GUTTATA 1st= endo layer impairment and decrease pump action
  • edema arises due to compromised stroma=get irregular epi. surface= bullous keratopathy+ corneal scarring

**use specular microscope to measure end. cell density–may need to strip Descemet’s membrane and put in a DONOR if below 500 cells

50
Q

what is the best way to view Fush’s dystrophy? what disease are Fuch’s pt. higher chance of?

A
  • sclerotic scatter–limbus light up

- more likely to get glaucoma because problems and the endothelium= problems at Trabec meshwork too

51
Q

what is Epi-basement dystrophy/disordered? what are the 5 signs to look for?

A
  • BM disruption causes (can see with (-) staining)–thicken and interferes with anchoring of epi to stroma
    1. dots (map-dot)–gray white intra-epi opacities= microcyst that have nuclear debri & lipids that can discharge randomly to corneal surface and produce erosion as it “disappears”
    2. maps= irregular geographic shaped and seen w/ dots usually.
  • related to laminar thickening of BM with aberrant membrane extending to epithelium
  • fibrillogranular material 2-6mm in thickness
    3. cysts
    4. fingerprints–BM projecting and trapping the ant. migrating cells (cluster of concentric lines)–view via retroillumination
    5. blebs–bubble like, fibrillogranular proteins @ api BM that inden basal epithelium
  • *prone to recurrent erosions
52
Q

are there any major symptoms wioth epi layer dystrophy. How do we look for signs?

A

nothing major, usually dry eye and recurrent erosions that have foreign body sensation and pain + photophobia
**usually dry eye worse in morning due to low pumping @ night

  • we use slit lamp + Fl staining or (-) staining and look for disruption
53
Q

what’s treatment for epi layer dystrophy?

A
  • lubrication for dry eye
  • ointnment + hyperosmotic for recurrent erosions
  • NO CL wear!
54
Q

what are some affects of drug deposition on the cornea?

A
  1. thiazides–antipsychotics
    - block Da= yellow brown deposits @ stroma @ ant. lens, UV triggers
    - retinapathy
  2. plaquenil–microdeposits
  3. amidarone (heart)–microdeposits (whorl kertopathy
  4. rheumatoid arthritis
    - yellow depotis @ post. stroma & descement’s
  5. retinoids-acutane–vit A related treatment for sporiasis—gives fine round sub epi opacitiy @ cornea
55
Q

what is the grey line on the adnexa?

A

-diving landmark on lid margin that separates lids into anterior/posterior

56
Q

what is the orbital septum? what’s it do?

A

-around the rim and creates barrier for th elids
-prevents pre-septal celluitis
-surgically important for IDing eye
fibrous sheath from the orbital rim

57
Q

what do 1. glands of Moll 2. gland of Zeiss 3. meibomian glands 4. Gland of Krause&wolfing do?

A
  1. Moll= secretes fatty material + sweat into hair follicles
  2. Zeiss= lipid material into hair follicles
  3. meibomian glands= sebaceous glands
  4. Krause and Wilfing= accessory lamcrimal
58
Q

Lid Colomboma

A
  • gaps & notes @ lids= incomplate lid formation–incompletely development (NOT hereditary)
  • get dry eye and eye disccation
59
Q

epicanthal folds

A
  • lid formation mainly in ASIANS
  • autosomal dominant + bilateral
  • redundant folds of skin from upper lid to inner canthus
  • can get pseudostrabismus (ESOTROPE fake)

**can be w/ down syndrome

60
Q

Distichiasis

A
  • rare + auto. DOMINANT
  • meibomian glands replaced by abnormal row of lashes (cilia!)
  • results: 2ndary dry eye + hyperemia (red eye) due to increased injection
  • Fl stain: damages the epi cells will stain more
  • create SPK: due to inflammation

**to treat: bandage CL +epilation (tweezer to pull out) + electrolysis (destroy actual hair follicles so it falls out) +cryotherapy (liquid nitrogen to destroy lashes)

61
Q

Blepharimosis

A
  • auto. dominant due to FETAL ALCOHOL SYNDROME!
  • flatter bridge and nose area with BILATERAL ptosis of upper lids and picanthal folds
  • leator muscle can be affect
62
Q

ectropian

A

lids NOT appositional, actually flipped out

  • excessive tearing and hyperemia due to exposure and SPK
  • treat w/ art. tears 4-6x/day or use gel lubrication (supportive treatment)

-cause: congenital (rate), involution due to age (common!)= loose muscles, Bell’s CN7–ectropian on SAME side as paralysis

63
Q

entropian

A
  • inward turning life/lashes and irritates cornea
  • excessive tearing,
  • conj irritate
  • foreign body sensation
  • Trochoma= bacterial conjunctivitis @ upper life w/ red eye
64
Q

dermatochalasis

A
  • older, middle aged pt. common
  • loosen/redundant skin on eyelid
  • pseudoptosis
  • bilateral + asymmetric appearance
  • decreased VA, VF (frontalis affected)
  • trichiasis
65
Q

what are the 2 types of papilloma?

A
  1. pedunculated: sticking out at you, still benign

2. sessile: FLAT, nothing is coming out

66
Q

what is the difference between pseudoriferous cyst and sebaceous cyst?

A
  • pseudoriferous cyst= clear fluid due to plugged gland of MOLL–like a blister
  • sebaceous scyst= yellowy fluid due to plugged sebacous gland (“lance”/cut it off)
67
Q

what are the ABC’s to check for malignant lid tumors?

A 
A= asymmetry
-non uniform or fast growing changes
B= bleeding
-bleeding or sloughing of skin or hair growth change
C= Color
-change from original color
68
Q

what is the difference between Nodular form and ulcerative form and sclerosing form of malignant tumors

A
  1. Nodular: common + raised + 5-10mm with pearl/translucent edges + teangietatic vessles
  2. ulcerative= raised w/ LESS fine edges + umbilication+ eorsions for an ulcerative center
    - causes mechanical ectropion
  3. Sclerosing= rare + pale yellow + indistinct borders
69
Q

what are clinical signs of ACUTE staph. Blepharitis vs. CHRONIC?

A
  1. ACUTE: sudden onset
    - unilateral that becomes bilateral within 24/48hrs
    - inflammed lid margins + colarettes @ lash base + conj. hyperemia
    - tylosis
  • CHRONIC: NEED ANTIBIOTICS!!
  • long period of time + other lid problems developing like..
  • madarosis + trichiasis +2ndary dary eye

**Both will have NORMAL EOM/VA/Pupils!

70
Q

what are some signs of Staph Belpharitis?

A
  • rossettes= dilated vessels
  • colarettes= stuff at base of lashes
  • hordeolum= acute focal infections @ gland of ZEISS
  • Chalazion=granulomous, non-inflammatory infection of the oil gland (Meibomian)–a bump
71
Q

what is the difference between staph. blepharitis and SEBORRHEIC bleph?

A
  • seborrheic= involves scalp + face+ brow
  • infection/stress/nutrion play a role
  • foreign body sensation/ burning/BILATERAL
  • NO ulcers, tyolysis or other abnormality
72
Q

what is the underly part of angular blepharitis?

A
  • usually related to alcoholics
  • red/itchy path of skin @ temporal lid by fornix (corner of eye
  • treat with antibiotics + zinc if due to moraxella for 7-10 days
73
Q

what is the difference between internal hordeolum (stye) vs. chalazion?

A
  1. hordeolum is just infection of lid margin area, @ oil gland (ZEISS gland)
    - will be RED, tender to touch, warm
  2. chalazion= deep within meibomian gland is clogged with high lipid deposits–NOT an infection
    - will not have same redness/not painful
74
Q

what is demodex? where does it appear on eye? (life cycle approx 14 days)

A
  • 8 legged mites in all age groups @ the bilateral hair follicles (like lashes)
    1. dem Folliculorum– @ hair follicle
  • larger, abdomen is rounder
  • eggs are 0.1mm (big) and arrow shaped)
  1. Dem Brevis @ sebaceous gland and smaller
    -has oval eggs that’s 0.06mm (smaller)
    -
75
Q

what disease is phthiriasis palpebrarum due to? what to check if it’s in kids?

A
  • pediculus parasite which is same as 8 legged thing that cause sexual crabs
  • mus tonctact child services if see in young children–due o sex. abuse or poverty
76
Q

what is molluscum contagiosum? what are findings?

A
  • transmitted via contact and around 2-10mm
  • cheesy center + multiple lesions
  • causes collicular conjunctivitis
77
Q

what causes varruca?

A
  • HPV virus

- looks like a small caulliflower on the lid region

78
Q

what are some normal findings of how the lacrimal system should look/work?

A
  • want patency betewen puncta and lacrimal sac
  • appositional of puncta to the globe (puncta adhering to globe)
  • Jone’s Test: put dye in eye and blow it out to see lacrimal duct drainage (one uses anesthetics+ keretometer)
79
Q

what are the layers of the tear film and what do each do?

A
  1. meibomian + Zeiss= lipid layer for stabilizing tear film–most outter layer
    - damage due to Cl wear or Bell’s palsy or other lid closure problems= dry eye, or osmolarity changes
  2. aqueous layer (largest!)= lacrimal gland _ accessory lacrimal (Krause _ Wolfring)
    - salts, proteins, glucose, lactate
  3. Mucin= inner most and has goblet cells + crypts of Henle, Gland of Manz
    - vit A deficient, LASIK, trachoma can all affect here
    - trochoma= destroy goblet cells
    - glycocalyx normally binds mucin to cornea surface here
80
Q

what is Sjogren’s syndrome and how do it affect the eye?

A
  • autoimmune disease w/ TRIAD

1. dry eye 2. dry mouth 3. rheumatoid arthritis!

81
Q

where is the Line of Marks?

A

-lid margin, near interpalp zone

82
Q

what can “filaments” along the cornea mean? what are filaments? What stain do we use?

A
  • in SEVERE dry eye
  • loss of epi cells where the dead cells cling” onto the corneal surface and looks like “String” vertically
  • use Rose Bengal to check
83
Q

which layer will the punctal plugs help maintain? (out of superficial lipid, aque, mucin layer)

A

–aqueous layer!!

**meibomian gland deficiency will not use this as that’s a mucin/goblet cell disorder

84
Q

what is the measurement of the nasolacrimalgland?

A
  • veritcal= 2mm
  • horizontal= 8mm

**the actual nasolacrimal duct is about 17mm vertically long to the nose

85
Q

how long to collagen plugs stay for? how are they used?

A
  • lasts 4-6weeks and will dissolve on its own?
  • diagnostic+prognostic indicator–like using a trial before doing it for real
  • those with Sjogren’s can try this out to see if there’s improvement before using permanent ones

**watch for epiphora= excessive tearing due to lack of drainage

-blocks 80% (@ lower puncta, 60% @ upper puncta) of tears from draining!

86
Q

what are teh 3 signs of “dry eye” defintion?

A
  1. inflammation of the ocular surface
  2. VA drop
  3. ocular surface damage

**can cause discomfot, low VA, tear film instability, increased osmolarity of eye

87
Q

what are signs of dry eye and what are the associated symptoms?

A
  1. corneal/conj staining–sandy/gritty/foregin body sensation
  2. MGD–burning
  3. reduced TBUT (les than 10sec) + reduced Schirmir’s (less than 1010mm/5mins)–tearing
88
Q

there are 2 types of dry eye, what are they and which one is the popular one? what % has this?

A
  • evaporative= MGD deficient= lipid deficient–when tears evaporate too fast
  • *POPULAR=86% have evap!**

-aque. deficient= decrease in lac. gland production= eyes does not stay moist

89
Q

wher eis the lid wiper vs. the line of marx? Is it same as the gray line?

A
  1. Lid wiper= more on the inner part of kessing’s space
    - part of the parakeratinized cells located near surface of muoco junction of eyelid and cornea, TOUCHES the ocular surface and can have that “scratchy” feeling
  2. line of Marx= never touches ocular surfaces, more on the “flat” part of the lid margin
    - where the epi of the palp conjunctiva abuts against the epi of the eyelid.

NOT THE GRAY LINE!!

90
Q

if the patient says they feel every blink and it hurts to blink, what is linkely prblem?

A

lid wiper epitheliopathy

-touches ocular surfaces and stains with FL due to lack of lipid lubrication

91
Q

what is the Korb-blackie light test? what does it check?

A
  • use transilluminator and shine on closed lids
  • check for leaks of light @ the lid margins to see if pt. completely closes their eyes
  • checks dry eyes
92
Q

what is the chemical compounds BAK? what drops is it in and what does i t do to eye?

A

-BAK is in Visine for dry eyes–benzo chloride
-damages corneal epi
reduces nerve fiber density + reduce aqu. tear production
-nerve degeneration
-increased inflammatory cell infiltration

93
Q

what 2 classes of drugs help with antiinflammatory?

A
  • NSAIDS + corticosteroids
    1. corticosteroids= inhibits phosolipids conversion to arachdonic acid
    2. NSAID (non-steroids responding drugs)= inhibits COX2 to convert for clotting TxA2

-anti inflammatory properties and can increase tear production and decrease immune response

94
Q

what 2 muscles govern blink and oil production during blink?

A
  1. muscle obicularis
  2. muscle of Riolan–encircle terminal ends of the meibomian glands–the gray line

-exert pressure on meibomian glands

95
Q

is FCC an objective or subjective test?

A
  • assessing lead/lag
  • SUBJECTIVE test

watch out for accommodators and can change their CLC–not good for young pt

96
Q

what are the age group for presbyope ADDs?

A
  • 45= +1.00D
  • 55= +2.00D
  • everything else is between this
97
Q

if you decrease the cyl power of an Rx by -1.00, how does that change the over all Rx? how do you fix it?

A

**must keep SE, so decrease in -1.00 is a drop in -0.50 in SE sphere power so much increase the (-) power by -0.50D to compensate for the drop in cyl

98
Q

patients with anisometropia can experience anisoPHORIA when reading…what can this create and how to fix it?

A
  • can experience vertical imbalance due to the difference prism affects when they look through peripheral vision (not @ optical center)

**switch to CL, get 2 pairs of glasses or raising the seg height/dropping optical centers, slab off glasses

99
Q

what pupil related disease comes with anisocoria?

A
  1. physiological
  2. parasymp= dilated
    - Adie’s, pharmacologic, CN3 palsy/Bell’s
  3. symp= constricted
    - horner’s–ptosis, miosis, anhydrosis
  4. L-N dissociation
    - argyll- Robertson
    - dorsal midbrain syndrome
100
Q

what is virulence mean?

A

exhibit pathogenity when present in small numbers

101
Q

what will a smear show in primarily bacterial conjunctivitis? what about viral conj?

A
  1. BACTERIAL–neutrophils

2. VIRAL–lymphocytes

102
Q

what are signs of basic conjunctivitis?

A
  • hyperemial= redness
  • chemosis- swelling of lid/eye
  • discharge–mucous? watery?
  • papillae
  • follicles
103
Q

vernal allergy conjunctivitis=?

A

seasonal+ giant papillary conj + men> women + children

PPO (3 decks)

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