HEENT 01: Eye/Head Anatomy Flashcards
What is the sclera?
white outer protective layer
What is the choroid?
vascular layer that provides oxygen and nutrients to eye
What is the retina?
neural tissue containing photoreceptors
What is the bulbar conjunctiva?
clear mucous membrane that covers sclera up to cornea
What is the palpebral conjunctiva?
lines inside of eyelids
What is the cornea?
modified transparent sclera that allows light to enter eye
- not covered by conjunctiva
What is the optic disk?
where optic nerve leaves eye
- does not respond to light (known as blind spot)
What is the macula?
yellowish pigmented spot at back of eye that contains fovea
What is the fovea?
thinned-out, cone-only portion of retina where visual acuity is greatest
- rods predominate outside fovea
- eyes are normally moved so that light rays coming from object fall on fovea
What are the layers of the retinal epithelium? (6)
- pigmented epithelium: absorbs light
- outer nuclear layer: contains photoreceptors, rods, and cones
- outer plexiform layer
- inner nuclear layer: contains cell bodies of various types of excitatory and inhibitory interneurons including bipolar cells, horizontal cells, and amacrine cells
- inner plexiform layer
- inner limiting membrane: boundary between retina and vitreous chamber
What is age-related macular degeneration?
progressive, chronic disease of central retina that results in rapid vision loss if untreated
What are the 2 processes of age-related macular degeneration?
- dry: geographic atrophy
- wet: exudative
What is dry age-related macular degeneration?
(geographic atrophy)
- yellow lipid deposits (drusen) form under retinal epithelium
- loss of retinal epithelium, capillaries, and photoreceptors
What is wet age-related macular degeneration?
(exudative)
- neovascularization of choroidal blood vessels into retina, leaking fluid, lipids and blood, leads to fibrous scarring
- treatable at certain stage, but permanent atrophic damage to fovea with loss of central vision (scotoma) can occur
What are the risk factors for age-related macular degeneration? (4)
- cigarette smoking
- obesity
- low intake vitamin A, C, E, and zinc, lutein, omega-3 fatty acids
- cardiovasular risk factors – hypertension, hyperlipidemia, hypercholesterolemia
What are some non-pharmacological/lifestyle measures for age-related macular degeneration? (4)
- stop smoking
- weight loss
- antihypertensive and lipid/cholesterol lowering therapies (if indicated)
- dietary supplements containing vitamins C and E, β-carotene, and zinc may delay progression
What is the treatment for wet age-related macular degeneration?
MOA
suppress action of vascular endothelial growth factor (VEGF) – key regulator of neovascularization pathogenesis (angiogenesis and vascular permeability)
What is the treatment for wet age-related macular degeneration?
Drugs (3)
- ranibizumab – antibody fragment that binds VEGF isoforms
- bevacizumab – antibody against VEGF (off-label)
- aflibercept – acts like VEGF receptor
What is the pathogenesis of hydroxychloroquine-induced retinal toxicity?
- bilateral, ‘bulls eye’ pattern of retinal damage
- central, concentric, parafoveal
- progresses centrally towards fovea
What are the risk factors for hydroxychloroquine-induced retinal toxicity? (4)
- duration of use (> 5 years, high cumulative dose > 1 kg)
- concomitant treatment with tamoxifen
- significant renal disease (> 50% decline in GFR)
- pre-existing retinal and macular disease
How does hydroxychloroquine induce retinal toxicity?
- hydroxychloroquine inhibits uptake of all-trans-retinol (vitamin A) by retinal pigment epithelium cells (RPECs)
- photoreceptors contain rhodopsin (rods) or photopsin (cones) – GPCR that contains retinal
- vitamin A is precursor of retinal, therefore this depletes retinal in RPECs
What is the management strategy for hydroxychloroquine-induced retinal toxicity?
screen for retinal toxicity initially during first year of treatment, and annually after 5 years of therapy
- no relationship between blood levels and retinal toxicity established, but hydroxychloroquine tends to accumulate in tissues
- hydroxychloroquine has very long half life (40-50 days) – after stopping therapy, negative effects on retina can continue for months
- dose should be < 5 mg/kg to maximum daily dose of 400 mg to limit retinal toxicity
What is the lacrimal gland?
secretes tears spread over eyeball by blinking, and remove dust and foreign particles
- parasympathetic innervation – VII nerve via pterygopalatine ganglion
- drains via nasolacrimal duct
What is dacryostenosis?
obstruction of nasolacrimal duct
What is dacryocystitis?
infection of lacrimal sac
- S. aureus
- S. pneumonia
- H. influenzae
- S. marcessans
- P. aeruginosa
What are the symptoms of dry eyes (xerophthalmia)?
- discomfort – redness, burning, stinging, foreign body sensation, pruritus
- visual disturbances – photophobia
What is the pathological changes contributing to dry eyes (xerophthalmia)? (40
- dry eye with reduced tear production (aqueous deficient)
- dry eye with ↑ evaporation of tear film (hyperevaporative) due to dysfunction of meibomiam glands
- combination of the above
- late stage associated with conjunctival scarring and corneal complications (kerastitis)
Describe the muscarinic receptors of lacrimal glands.
parasympathetic nerve activate M3 receptor on secretory globular acinar cell to stimulate tear secretion
Describe the muscarinic receptors of conjunctiva.
parasympathetic nerves acting on M3 receptors cause goblet cells in conjunctival epithelium to release mucin and other protein secretion into tear for eye lubrication
What drugs can cause dry eyes and how?
anticholinergics (muscarinic receptor antagonists)
- block activation of M3 receptor
- ie. antihistamines
What is Sjogren’s syndrome?
incurable autoimmune disorder of mucous membranes that leads to dryness of eyes, mouth, skin, nasal, and vaginal passages
- mostly in women
- can have antibodies to M3 receptor – thought to disrupt lacrimal and salivary gland function, leading to dry mouth (xerostomia) and dry eyes (xerophthalmia)
- symptoms may be treated with muscarinic receptor agonists (along with artificial tears, saliva)
What is conjunctivitis (pink eye)?
inflammation of transparent lubricating mucous membrane that covers globe of eye and under surface of eyelid
What are the symptoms of conjunctiva? (3)
- discharge – purulent, mucopurulent, or watery
- erythema
- pruritis
What causes conjunctivitis? (3)
- allergic conjunctivitis: seasonal allergies (most frequent)
- viral: adenovirus
- bacterial: H. influenzae in infants and toddlers, S. aureus in older children and adults
What is external hordeolum (stye)?
staphylococcal infection of hair follicle of (upper) eyelid
- produces pimple-like abscess that can swell and reddening eyelid that can be painful
What causes external hordeolum (stye)?
blocking of zeis gland (secrete sebum) and moll gland (produce IgA, mucin, lysosomes) due to thickening, drying, or stasis of their secretions promotes infection
What is internal hordeolum?
infection of meibomiam gland (sebaceous gland that produce oily layer to help with lubrication) in conjunctiva
- more painful
What is chalazion?
cyst-like nodules that remain after hordeolum heals
- normally red, but not painful
What is blepharitis?
inflammation of eyelids, often at base of eyelashes
- erythematous, pruritic eyelids, conjunctival injection, crusting or matting of eyelids, and occasionally flaking of eyelid skin
