Eyelids and Adnexa Flashcards
macule
colour change without infiltration or elevation (ex. freckle, cafe au lait spots)
papule
small solid elevation of skin (<1cm)
ex. cherry angioma, common warts
nodule
small solid elevation of ski (>1cm)
ulcer
circumscribed area of tissue loss, extends through epidermis into dermis (ex. in basal cell carcinoma)
cyst
nodule with an epithelial lined cavity, filled with fluid or semi-solid material
Which is translucent and which is not: cyst of Zeis and cyst of Moll?
Cyst of Zeis is non-translucent, cyst of Moll is translucent (also called apocrine hidrocystoma)
pustule vs. vesicle
pustule is a small pus-filled lesion, vesicle is a small serous fluid-filled lesion (ex. in Herpes)
Herpes zoster ophthalmicus skin changes:
-viral release from the sensory nerve endings results in a macular rash, which becomes papular, then vesicular which develop (~4 days) to become pustular and eventually rupture. When acute phase subsides, the rash crusts over and dissipates.
Contact Dermatitis
common inflammatory disorder that often involves the thin skin of the eyelid, associated with hypersensitivity response or direct irritation
can caused periocular skin to be red, edematous, scaly or fissured
treating Contact Dermatitis
topical corticosteroids and removal of offending agents
rosacea dermatitis
common, chronic inflammatory eruption of the face (forehead, nose, cheeks) can involve malar flushing, telangiectasia, papules, pustules, sebaceous gland hypertrophy, rhinophyma, etc.
ocular rosacea
in about 50% rosacea cases
symptoms: burning, photophobia, FBS
blepharitis and MGD are most common findings
treating Ocular Rosacea
avoiding foods and environments that worsen flushing
oral antibiotics (tetracycline, doxy, azithromycin) topical metronidazole cream/gel on skin
topical corticosteroids
collarettes (on eyelashes)
ring-like formation around lash-shaft, mucous debris and dead epithelium
can be caused by phthirus pubis or demodex mites
trichiasis
posteriorly misdirected lashes rubbing against globe, chronic rubbing can lead to corneal problems
may be secondary to scarring - from trauma, mucous membrane pemphigoid, Stevens-Johnson syndrome
treating Trichiasis
- epilation!
- electrolysis
- cryotherapy
- argon laser ablation
- surgery
distichiasis
partial or complete second row of lashes - emerge at or behind a meibomian gland orifice (cells differentiate into a pilosebaceous unit instead of MG cell)
trichomegaly
excessive eyelash growth, may be congenital or acquired, can be induced by drugs (prostaglandins), malnutrition, AIDs, hypothyroidism
madarosis
decrease in the number of lashes, can be caused by: chronic lid margin disease, lid tumour, burns, alopecia, psoriasis, SLE, syphilis, leprosy, trichotillomania,etc.
poliosis
premature whitening of hair which can involve lashes and brows
ocular causes - chronic blepharitis, idiopathic uveitis
systemic causes - vitiligo, Vogt Koyanagi Harada syndrome, Marfans, TB
potentially malignant characteristics of anterior eyelid:
- nodular pearly consistency
- ulceration
- induration/hardening
- irregular borders
- suspicious telangiectasias
- madarosis
- loss of lid architecture
meibomian gland dysfunction
-increased lipid viscosity and opacity, needs heat (warm compresses)
congenital ptosis
unilateral or bilateral, superior VF defect
aponeurotic ptosis
most common form of ptosis, usually bilateral, associated with age (involutional), eye sx, trauma, pregnant, chronic swelling, etc. Levator aponeurosis stretching (functions fine), symptoms worse at the end of the day as Muller’s muscle fatigues after trying to compensate
treating involutional ptosis
Upneeq (oxymetazoline) a direct-acting alpha-adrenergic receptor agonist, targets Muller’s muscle to elevate the upper eyelid
mechanical ptosis
decreased elevation of the eyelid secondary to eyelid mass or scarring
myogenic ptosis
ptosis secondary to inherent levator or Muller muscle dysfunction, weakness of the actual muscle - from chronic progressive external ophthalmoplegia, myotonic dystrophy, myasthenia gravis, etc
neurogenic ptosis
caused by Horner’s syndrome or CN3 palsy -innervation defect
ICA aneurysm ocular signs
ptosis, pupil mid-dilated minimally reactive to light
pseudoptosis
false ptosis due to decreased orbital volume, contralateral lid retraction, ipsilateral hypotropia, or dermatochalasis
eyelash ptosis
downward sag of upper eyelid lashes (no turning in of the lid margin)
brow ptosis
excessive skin on the brow and forehead leading to a pseudoptosis, may be due to CNVII palsy, often accompanies dermatochalasis
Bell’s palsy
acute facial nerve palsy of unknown etiology, sudden, temporary weakness in facial muscles, typical recovery in ~6 months
involutional ectropion
outward rolling of lower lid due to horizontal lid laxity, medial/lateral canthal tendon laxity, may present gradually with tearing, redness, irritation, tear film abnormalities, dry eye, or conjunctival keratinization
cicatricial ectropion
due to scarring and contracture, trauma, burns, chronic inflammation, pulls lid away from eye
paralytic ectropion
due to ipsilateral CNVII palsy, can be temporary, may cause exposure keratopathy and epiphora
mechanical ectropion
lesion on or near lid margin, the weight causes lid eversion
involutional entropion
horizontal lower eyelid laxity, contraction of pretarsal orbicularis oculi fibres forces the lower lid margin inward
presents with more acute pain, FBS, photophobia, etc.
treating involutional entropion
temporary - lubricants, lid taping, BCL, botox
Surgical techniques - everting sutures and canthal slings
congenital entropion
mechanical effects of microphthalmos (if involving the upper lid), can involve lower lid due to improper development of inferior retractor aponeurosis