post midterm things

Question 1

what is the gray line/muscle of Riolan?

Answer 1

• superficial part of orbicularis muscle

- line roughly divides the eyelid in half, serves as an important surgical landmark

Question 2

what are some secretory cicatricial causes of secondary obstructive MGD?

Answer 2

trachoma, ocular pemphigoid, erythema multiforme, atopy

Question 3

what are some secretory non-cicatricial causes of secondary obstructive MGD?

Answer 3

seborrheic dermatisis, acne rosacea, atopy, psoriasis

Question 4

describe the role bacterial lipases and esterases play in MGD:

Answer 4

• bacterial lipases and esterases hydrolyzes sterol and wax esters in the MG secretions
• free fatty acids as a byproduct – these are irritating and promote the inflammatory cycle
• saponification: foamy tears, increased tear evaporation rate

Question 5

describe the Marx line grading system:

Answer 5

0 = Marx line (ML) totally posterior to meibomian orifices (MO)
1 = part of ML touches some MOs – most common, volcano presentation just starting to impinge into orifice
• this is when intervention is most useful
2 = all of ML runs through MO, level with orifices
3 = ML beyond MO to the anterior lid margin

Question 6

what is the tx for level 2 MGD?

Answer 6

maintain level 1 for everyone (hot compresses), add:
-fish oil, flax seed oil @ 1000mg BID-QID each
–fish oil decreases inflammation
–flax seed oil thins out the Meibomian secretions
treat non-specific inflammation if present

Question 7

what is the tx for level 3 MGD?

Answer 7

maintain levels 1 and 2:

• re-assess and treat concurrent disease
• add minocycline/doxycycline/azithromycin oral antibiotic for anti-inflammatory

Question 8

Describe some of the benefits of mino/doxy for MGD:

Answer 8

• inhibition of MMP, macrophages (reduce ability to produce cytokines such as IL-1 and TNF), and bacterial lipases (convert secretions into irritating free fatty acids which drive an inflammatory process)
• effect on circulating neutrophils
• reduce bacterial flora at lid margin

Question 9

describe some considerations for Rx’ing minocyc:

Answer 9

• bacteriostatic – don’t combine with bactericidal
• long half life – extended effectiveness; also low renal clearance
• long term effect (up to weeks) after Tx withdrawal – allows for use of pulsed therapy

Question 10

Tx for level 4 MGD:

Answer 10

maintain level 3; add Restasis, Tacrolimus, or other stronger anti-inflammatory med

Question 11

dosing levels for minocycline:

Answer 11

• begin 50mg BID x 2w, then 100mg BID x 10w

- use pulsed therapy, with 3mo on and 3mo off

Question 12

dosing levels for doxycycline:

what are periostat and oracea?

Answer 12

• 100mg BID x2w then 50mg BID x 6w, then 25mg BID x 4mo
• Periostat: 20mg formula for gingivitis can be used for maintenance therapy 1-2x/day – very expensive

*Oracea: 40mg made up of 30mg immediate release and 10mg delayed release, usually given once daily
• usually for rosacea

**both oracea and periostat take on empty stomach, 1h before or 2h after eating

Question 13

besides tetracyclines, what are some other antibiotic therapies for MGD? (also include dosing)

Answer 13

macrolide ABs:
-erythromycin: preg B
o	200mg BID x 30d
-azithromycin
o	250mg QD x14-21d
o	or 500mg/day x 3d in 3 cycles with 7d intervals

Question 14

describe the pop typically affected by seberrhea:

Answer 14

• ages 20-50y, slightly more males (sebaceous secretion influenced by androgens)
• 3-5% prevalence overall
• risk groups: immunocompromised/HIV infection, Parkinson’s disease (low skin mobility so offending organism is not eradicated), gender change (hormonal changes alter the glands)

Question 15

Describe the pathogenesis of seborrhea:

Answer 15

Malassezia yeast is an opportunistic pathogen, feeds on lipids

• enzymes break down lipids -> convert to free fatty aids which cause inflammation and irritation
• dandruff-like dermatitis that tends to be greasy (not always – depends on pts hygiene as well)
• increased neutrophils at sebaceous gland orificies -> glands plug, exfoliate a bit, turn over, etc.
• focal parakeratosis (superficial cells have nuclei signaling high cellular turnover), acanthosis, and spongiosis (cells break down and drift apart)

Question 16

what is Meibomian seborrhea?

Answer 16

increased meibomian secretion/lipids -> easy for bacteria to chew on, forming free fatty acids and stimulating an inflammatory process

Question 17

describe some of the changes you will see with the lids in seborrhea

Answer 17

-hyperemia and oily skin along the seborrheic zones
-scurf (flaky, dandruff) forms in later states
• pityriasis sicca: fine, brittle, dry scale
• pityriasis steatoides: oily, greasy looking scale
-scurfs on cilia – oily sleeves (or partial sleeves) that are pretty sticky and can glue the lashes together
-tylosis, lid corrugation
-MGD/posterior blepharitis: hyposectory or hypersecetory

Question 18

Describe the pt profile for rosacea:

Answer 18

10% of adults, females 2-3x more than males but males usually more severe,

• onset 20-50y
• 50% of facial rosacea has ocular involvement, presenting sign in 20%

Question 19

describe pathogen of

Answer 19

• intermittent vasodilation of skin capillaries – become permanent telangiectasias
• facial flushing when eat vasoactive amines (chocolate, cheese, red wine, nuts), with hormonal changes, environmental changes (sunlight), certain meds, emotional stress -> because the vessels are damaged and have weak walls they dilate easily
• sebaceous glands hypertrophy with papule and pustule formation
• unknown underlying cause, technically, but strong indication not infection

*damage vessels via wind, UV, toxins – become permanently dilated – leak immune complexes that lodge in skin to drive non-specific inflammatory response -> more dilation and leakage with vasoactive amines

Question 20

Describe the stages and symptoms of rosacea:

Answer 20

stage 1 (early onset) – cheeks, nose, forehead flushing
2 – persistent erythema and beginning telangiectasias
3 – skin papules and pustules – firm changes in skin, sebaceous gland involvement – skin is not flat, but rather has a ruddy texture
4 – rhinophyma, most often in males
•nose looks bulbous, lumpy with sebacoues hyperplasia and telangiectasia
•medical Tx: debulking (dig out the glands) with surgical scalpel, dermabrasion, or resurfacing with CO2 laser

Question 21

what are some signs/symptoms of facial rosacea?

Answer 21

• burning, irritation, itching
• signs/symptoms correlate weakly with ocular disease -> pts may have mild facial findings but severe ocular disease
• facial flush may be exacerbated by drinking alcohol, hot fluids, or eating foods with high vasoactive amines

Question 22

Describe the signs and symptoms you find with ocular rosacea:

Answer 22

Sx: burning, irritation, dryness, photophobia, blurred vision
lids: tylosis, telangiectasias, hyperemia, obstructive MGD, cicatrical MGD (more with rosacea than with seborrhea), hordeola, chalazia (rosacea&raquo_space; seborrhea), secondary blepharitis with greasy scurfs at lash bases

• conj – tarsal papillae (non-specific inflammation), hyperemia, variscosity, chemosis
• nodular and diffuse episcleritis – in females, episcleritis is usually idiopathic but there is a real association with rosacea if pt has rosacea
• limbus: inflammatory pannus / phlyctenules – chronic and long term so epi breakdown, ulceration, secondary superinfection may occur, scarring
• cornea: PEE, SPK, erosion

o fungal or sterile ulcers can occur – chronic steroid use may predispose fungal infection

Question 23

how can you tx some of the facial telangiectasias in rosacea?

Answer 23

CO2 laser for telangiectasias – send earlier rather than later for Tx

Question 24

what is Metronizadole gel and what is it used for?

Answer 24

imidazole derivative - antibacterial, antiparasitic, anti-inflammatory
• mode of action: oral/IV reduces DNA synthesis in anaerobic bacteria, topical acts as anti-inflammatory

Question 25

describe pathogen of demodex:

Answer 25

mites have a 14d life cycle

• burrow into cilia/sebaceous gland, migrating to surface at night to mate and lay eggs, then crawl back in during the day
• mites eat dead epithelial cells and keratin, promote follicular distension, keratinization, epi hyperplasia -> ultimately plug the glands because enter gland/shaft orifice of the cilia
• fairly high association with ocular rosacea – rosacea creates favorable environment for demodex

Question 26

describe all the ways demodex affects the eye:

Answer 26

• pathognomonic cylindrical dandruff/sleeve like coating
• non-specific scurf, red lid margins
• AM burning/itching
• lashes are easily broken and removed because the lids are destroyed -> madarosis and trichiasis
• Meibomitis: they enter into and block the glands
• injection, PEE, PEK, pannus, scarring, phlyctenule, Salzmann’s nodular

•can have the mites (and the associated inflammation) for 20-30y, resulting in long-term complications

Question 27

describe traditional vs newer demodex tx:

Answer 27

traditional: smother the mites using heavy ointment on the lid margins at night
- pilocarpine gel: reduce bronchiole constriction – but side effects
- yellow mercuric oxide 1% - OTC, smears over the margins, suffocates the mites and mercury is also toxic
- erythromycin – no specific killing, just smothering

5-10% Tea Tree Oil (OTC) – effective

• 0.5% proparicaine -> apply TTO to lash margin
• -repeat weekly for 3-6w
• -cut with mineral or macadamia nut oil to give 5% dilution, or use Cliradex device/towelettes
• throw out make-up
• wash and heat dry bedding weekly
• tea tree oil decreases overall surface inflammation on face -> less inflammation means less activity of the mites