Eye

Question 1

90% of optic tract axons from the eye retina target the lateral geniculate nucleus (thalamus). What are 3 roles that the 10% remaining play?

Answer 1

1) to hypothalamus (suprachiastamtic): influence of light over neuroendocrine function and over sleep/wake cycle through pineal gland
2) to Pretectum - pupillary light and accommodation relfexes
3) to superior colliculus - coordinate vision with other sensory inputs, allows us to follow visual subjects clearly, visual motor reflexes

Question 2

What does it mean if a lesion somewhere along the visual system has abnormal pupillary reflex or normal pupillary reflex.

Answer 2

abnormal: before the LGN

Normal: after the LGN, optic radiation, visual cortex, because axons reaching pretectum will leave before synapsing

Question 3

what is a likely cause of a left contralateral homonymous superior quadrantanopia?

Answer 3

Right temporal lobe tumor, compressing the right Meyer loop

Question 4

Describe the autonomic control of the eye

Answer 4

Ciliary muscle: Contraction (M3)
for near vision or relaxation (β2) for distant vision

• Sphincter pupillae muscle: Contraction (M3) to decrease the diameter of the iris to reduce the amount of light
entering the eye.

• Dilator pupillae muscle: Contraction (alpha1) to increase the diameter of the pupil to allow more light to enter
the eye.

• Ciliary epithelium. ↑ production (β2) of aqueous humor- decrease (alpha2)

Question 5

How do beta blockers, and muscarinic agonists/cholinesterase inhibitors affect intraocular pressure

Answer 5

Beta blockers reduce production of aqueous humor to lower intraocular pressure. (beta receptors - ciliary body)

Muscarinic agonists or cholinesterase inhibitors facilitate outflow to reduce IOP.
(muscarinic receptors on ciliary body causes tension of trabecular meshwork to increase outflow of Canal of Schlemn)

Question 6

What are classes of drugs to treat glaucoma?

Answer 6

1. Prostaglandin analogs - increase outflow
2. Beta blocker - decrease aqueous humor production
3. Carbonic anhydrase inhibitors: decrease aqueous humor production
4. Alpha2-agonists - do both, decrease aqueous humor production, increase outflow
5. Cholinergic agonist/ cholinesterase inhibitors: contract muscle fibers in ciliary body, increase in AH outflow
6. Osmotic agents, increase the osmotic agents leading to fluid going into blood.

Question 7

What are some eye disorders that can be treated with pharmacology.

Answer 7

1. age related macular degeneration
2. dry eyes
3. allergic conjunctivitis
4. bacterial conjunctivitis

Question 8

The eye is relatively secluded from systemic access, so how come drugs applied topically to the eye can influence the systemic circulation?

Answer 8

lacrimal drainage goes to the nose, lined by highly vascular mucosal epithelium

Question 9

What are the three muscarinic receptor antagonists and how may they be used

Answer 9

1. tropicamide - duration of effect - 4 hours
   - this short duration is important for mydriasis on optic exam
   - (muscarinic activation cause contraction of pupillary constrictor muscle)
2. Scopolamine - 3-7 days
   - formulated as a patch for motion sickness,
3. Atropine - 7-10 days
   - target is the ciliary muscle because half life is too long, control accommodation.
   - effect is cycloplegia (blocking of accommodation important for the treatment of lazy eye amblyopia

Question 10

Antimuscarinic excess effect (too little acetylcholine effect, opposite of cholinergic excess.

Answer 10

Dry as a bone, blind as a bat, mad as a hatter, hot as hell, red as a beet, full as a flask.

• decrease secretion and salivation because exocrine glands feature M3 muscarinic receptors
• cycloplegia - ciliary muscle paralysis, can’t focus on close objects
• CNS excitation, restlessness, irritability
• decreased ability to sweat
• cutaneous vasodilation
• urinary retention

Question 11

What are the muscles of the eye under autonomic control

Answer 11

1. Sphincter pupillae - pupillary constrictor (parasympathetic, muscarinic)
2. Dilator pupillae: (sympathetic, alpha receptor)
3. Ciliary epithelium (sympathetic, beta)
4. Ciliary muscle (parasympathetic, muscarinic)

Question 12

What layer of V1 receives input.

M cells - gross stimulus features and movement

P cells - color, visual detail

Answer 12

M cells > magnocellular layers (first two) in LGN > layer 4Calpha > Layer 4B > V5

P cells > parvocellular > layer 4Cbeta > layer 2,3 blobs > V2,3,4

Question 13

Where are V2,3,4,5 located?

Answer 13

V1,2,3 are medial and travel upwards (form/shape)

V4 is occipital, ventral medial (color)

V5 is temporal. (motion)

Question 14

• painless vision loss
• hemmorrhages in all 4 quadrants
• dilated tortuous veins
• optic nerve head swelling
• cotton wool spots
• macular edema
• optociliary shunt vessels

Answer 14

Central Retinal Branch Occlusion.

*if found in a young person - prompt inflammatory/hypercoaguability workup.

Question 15

Generalized breakdown of
blood-retinal barrier with
leakage
Treatment?

Answer 15

Diffuse macular edema

-laser, steroids, anti VEGF

Question 16

inflammation of:
iris  (iritis)
ciliary body (cyclitis)
choroid (choroiditis)
Encompasses a large group of  diverse diseases
This has many potential causes:
infectious
traumatic
neoplastic
*AUTOIMMUNE

Symptoms Treatments?

Answer 16

Uveitis:
Redness • Pain • Photophobia - it hurts when the iris moves back and forth so they get photophobia.

Treatments:
Medications
• Topical steroids - Durezol, prednisolone

Mydriatic and
Cycloplegic Agents
• Atropine Sulfate 1%
-the thought process is to keep the pupils dilated so as to keep the iris away from the lens capsule which inflammatory mediators can get the two stuck.

Oral prednisone • Quick onset of action. Less risk of
increase IOP and cataract.
Systemic side effects.

Immunomodulators • Humira, MTX, cyclosporin

Regional depot triamcinolone (4mg) • Periocular • Intraocular

Question 17

Optic nerve damage
• Ocular hypertension
• Visual field loss (peripheral>central)

Condition, diagnostics and treatment

Answer 17

Glaucoma.

Hypertension arises from the ciliary body and the Canal of Schlemn.

Most people with glaucoma are managed by topical
anti-hypertensive drops
• Beta blockers - decrease production of aqueous humor.

Put a valve connected to the anterior chamber which is equalized to a pressure. When pressure rises in the eye, the fluid will leave into the valve and take residence under the conjunctiva.

Question 18

The corneal blink reflex

Answer 18

Touch the side of the cornea > afferent (opthalmic division of trigeminal) > spinal trigeminal nucleus >efferent limb - orbital part squinting, palpebral part (blinking) - facial nerve.

Question 19

What is the role of the endothelium in the cornea?

Answer 19

deturgenscence - pumping ions out of the cornea to keep it transparent.

Question 20

Where do sty’s form?

Answer 20

sebaceous glands of eyelashes and apocrine glands of eyelids.

Question 21

Papilledema

Answer 21

Papilledema is swelling of the optic disk (papilla) due to
increased intracranial pressure (ICP) and is almost always
bilateral.

It may develop acutely (ruptured cerebral aneurysm)
or over the course of several weeks or months (tumor).
Patients may have symptoms of increased intracranial
pressure, such as headache or nausea and vomiting.
Papilledema requires an immediate search for the cause.
Diagnosis is by ophthalmoscopy with further tests, usually
brain imaging and sometimes subsequent lumbar puncture,
to determine cause. Treatment is directed at the underlying
condition.

Question 22

How would each of these look (VF)

occlusion of the right opthalmic artery

aneurysm of right internal carotid

left middle cerebral artery

left parietal lobe lesion

Answer 22

Monocular inferior scotoma

Right nasal hemianopia.

Contralateral homonymous superior quadrantanopsia.

Contralateral homonymous inferior quadrantanopsia

Question 23

How would optic tract lesion differ from a right PCA infarct?

Answer 23

They would both be contralateral homonymous hemianopia but the one in the primary visual cortex would have macular sparing.

Because macular representation is very large in primary visual cortex Also can receive blood supply from PCA and MCA

Question 24

Left homonymous superior quadrantanopia with macular sparing

Answer 24

Infarct of posterior cerebral artery branches supplying lingual gyri causing lesion to right occipital lobe and preserving the right occipital pole.

Question 25

Glaucoma vs macular degeneration loss of vision.

Answer 25

peripheral vision goes first in glaucoma.

In AMD (age related macular degeneration), it is characterized by progressive loss of central vision due to deposition of fatty tissue (drusen) behind the retina (dry) or neovascularization of retina (wet).
First to go is central visual field.