The Eye B&B Flashcards
describe the parasympathetic control of miosis (pupillary constriction) - name the specific nuclei involved (2)
2 neuron pathway:
1. begins at Edinger-Westphal nucleus in midbrain, near CN III nucleus
2. nerve fibers enter orbit with CN III
3. synapse at ciliary ganglion, which signals to sphincter pupillae and activates muscarinic receptors (ACh)
contrast the clinical significance of the following:
a. eye down and out + pupillary dilation
b. eye down and out + absence of pupillary dilation
[eye down/out = CN III lesion]
parasympathetic fibers control pupillary constriction and run on the outside of CN III
CN III lesion + dilation = parasympathetic nerves impacted, such as by compression by mass (Pcomm aneurysm)
CN III lesion alone = ischemia, such as by diabetes (neuropathy damages interior of the nerve, sparing PNS fibers on the outside)
“Rule of the Pupil”
Adie’s Tonic Pupil
unilateral dilated pupil due to blocked parasympathetic innervation
mostly idiopathic, can be caused by disorders of ciliary ganglion (tumor, inflammation, trauma, surgery, infection)
which adrenergic receptors control mydriasis (pupillary dilation)?
norepinephrine binding alpha1 receptors —> activate dilator pupillae
what are the steps of the pathway controlling mydriasis (pupillary dilation)? (3)
- post hypothalamus to spinal cord, ending at ciliospinal centre of Budge (C8-T2)
- spinal cord to superior cervical ganglion - exits at T1 and crosses apical pleura of lung, then travels with cervical sympathetic chain near subclavian
- superior cervical ganglion to dilator pupillae, courses with internal carotid artery and passes through cavernous sinus
how can cocaine be used as a diagnostic test for Horner’s Syndrome?
cocaine blocks NE reuptake, but for this to work it still requires NE to be released
Horner’s Syndrome = impaired sympathetic innervation to face
test: topically apply cocaine to the eye - normal eye will dilate, Horner Syndrome eye will be unable to dilate
anisocoria
difference in pupil sizes
what nuclei are involved in the pupillary light reflex? (3)
- light signals to pretectal nucleus in the midbrain
- pretectal nucleus signals to bilateral Edinger Westphal nuclei
- EWN travel with CN III and signal to ciliary ganglion on each side to activate sphincter pupillae
does not involve cortex
Marcus Gunn Pupil
relative afferent pupillary defect (RAPD) - shining light in one eye produces less constriction than shining light in the other eye, caused by a lesion in the afferent component of light reflex (not sensing light appropriately)
diagnosed with the swinging flashlight test
what is Marcus Gunn Pupil classically caused by?
optic neuritis: inflammatory, demyelinating disease commonly occurring in multiple sclerosis
Marcus Gunn pupil = relative afferent pupillary defect (RAPD) - shining light in one eye produces less constriction than shining light in the other eye
Argyll Robertson Pupil
bilateral constricted pupils - no constriction to light, but WILL constrict for accommodation (“light-near dissociation”)
strongly associated with tertiary neurosyphilis - causes damage to pretectal nucleus, which is part of light reflex but not accommodation
PERRLA
pupils equal, round, reactive to light and accommodation
most refraction of the eye is performed by the ____
cornea (fixed)
[some refraction is performed by adjustable lens as well]
what type of collagen is found in the lens of the eye
type IV collagen
avascular structure, uses anaerobic metabolism (glucose —> lactic acid)
effect of ciliary muscle relaxation vs contraction
ciliary muscles relaxed = flat lens = far sight
ciliary muscles contract = round lens = near sight
what is the cause of myopia? how is it corrected?
aka nearsightedness: focal point is in front of the retina because the eye is too long or the cornea is too curved
corrected with a negative lens (concave, spreads light out more as it hits the cornea)
what is the cause of hyperopia? how is it corrected?
aka farsightedness: focal point is behind retina because the eye is too short or the cornea is too flat
corrected with a positive lens (convex, causes light beams to converge more as it hits cornea)
which 2 systemic disorders are associated with ectopia lentis (lens dislocation)?
- Marfan’s (most commonly): AD mutation in fibrillin —> upward/outward lens dislocation
- homocystinuria: deficiency of cystathionine beta synthase —> high homocysteine levels, Marfanoid body habitus, intellectual disability, downward/inward lens dislocation
how can diabetes lead to cataracts?
via polyol pathway: high glucose or galactose is converted to sorbitol or galactitol, respectively, by aldose reductase
sorbitol and galactitol are osmotically active, accumulation can cause lens damage leading to cataracts
which 2 inherited metabolic disorders can present with cataracts and why?
classic galactosemia (liver failure + cataracts) and galactokinase deficiency (milder, cataracts)
via polyol pathway: high galactose is converted to galactitol via aldose reductase —> osmotically active, accumulation can cause lens damage leading to cataracts
which TORCH infection classically causes infantile cataracts?
congenital rubella syndrome: cataracts + sensineural deafness + cardiac malformations + blueberry muffin rash (extramedullary hematopoiesis)
what is contained in the macula
oval-shaped area near center of retina, contains fovea (high cone density for high-resolution color vision)
retinitis pigmentosa - describe this disorder and how it appears on fundoscopy
inherited retinal disorder characterized by visual loss beginning in childhood due to loss of photoreceptors (rods/cones)
night/peripheral vision lost progressively, constricted visual field
fundoscopy shows bone-spicule pattern with lots of dark pigmented spots where photoreceptors are missing (around periphery)
what is the classic cause of retinitis? in which patients does this occur? how does it appear on fundoscopy?
retinal edema/necrosis (can cause floaters) classically caused by cytomegalovirus (CMV) in patients with HIV/AIDS (low CD4 count, <50! Usually first sign of CMV infection in these patients)
also occurs in transplant patients on immunosuppression (also at risk for CMV!)
fundoscopy shows whitish appearance of retina (“pizza”)
