Ocular Physiology Flashcards

What are the functions of the Eyelid?

1. Provides oxygen to tear film in closed eyes (sleeping)

2. Globe Protection

3. Spread Tears

4. Assists in Tear Drainage

5. Produce Tear Film Components

What are the muscles of the palpebrae?

• Orbicularis Oculi

  • Orbital Portion

  • Palpebral Portion

    • Horner’s

    • Riolan’s

• Levator

• Tarsal Muscles

  • Superior

  • Inferior

What Ligament is found in the palpebrae?

Whitnall’s Ligament

What nerve innervates the Orbicularis Oculi?

CN VII

What nerve innervates Horner’s Muscle?

CN VII

What nerve innervates Riolan’s Muscle?

CN VII

What nerve innervates the Levator Palpebrae Superioris

CN III

What nerve innervates the Tarsal Muscles (Muller’s)

Sympathetic Nervous System

What are the major structure of a sarcomere?

Actin and Myosin

What are the units that make up a myofibril?

Sarcomere

What do a bundle of myofibrils form?

A muscle fiber (a cell)

What do muscle fibers form?

Fasciculus

How does Sarcomere contract?

1. Myosin head associates with F-actin

2. The release of ADP/P induces myosin head to move/power stroke

3. Myosin head attaches to to ATP and releases F-actin (has ATPase to hydrolyze ATP)

4. ATP is hydrolyzed to ADP/P causing myosin head to bend backward, storing potential energy

How are skeletal muscle fibers categorized?

1. Speed of contraction

2. How ATP is generated

What types of skeletal muscles are there?

Type I, Type II a, Type II x
(Type II b is found in animals and is different)

What are the characteristics of Type I muscles?

• Slow twitch/slow oxidative

• Slow Myosin ATPase activity

• Higher capillary density

• More Mitochondria

• Utilize Aerobic Respiration > > > Anaerobic glycolysis

• Slow to fatigue

What are the characteristics of Type II a muscles?

• Fast twitch/fast oxidative

• Fast Myosin ATPase activity

• Lower capillary density than type I

• Fewer mitochondria

• Aerobic Respiration > anaerobic glycolysis

• Fatigues faster than type I

What are the characteristics of Type II x muscles?

• Fast twitch/fast glycotic

• Fast myosin ATPase activity

• Lowest capillary density

• Fewest mitochondria

• Anaerobic glycolysis > > > Aerobic Respiration

• Fatigue fastest

How does Anaerobic metabolism work?

Glucose is converted into pyruvic acid via glycolysis

How does Aerobic metabolism work?

Glucose is converted into pyruvic acid via glycolysis, which then undergoes the kreb cycle and ETC in the mitochondria.

What type of fibers does the Orbicularis Oculi have?

Type II > > > Type I

What type of fibers does the Levator (LPS) have?

Type II > > > Type I; is unique because it is resistant to fatigue

What is Type I fibers used for in Orbicularis Oculi?

It is for sustained closure

What is Type I fibers used for in the Levator m?

Sustained elevation of eyelids

What is Type II fibers used for in Orbicularis Oculi?

Rapid closure of palpebral

What is Type II fibers used for in Levator m?

Elevation during blinking

What is released between a neuromuscular junction?

Neurotransmitter; typically Acetylcholine/ACh, secreted from Synaptic Vesicles.

What does ACh do in the neuromuscular junction and muscle to cause contraction?

1. ACh binds to ACh receptors on the muscle cell, triggering the opening of ion channels.

2. Action potential is generated within the muscle cell within the T-tubules

3. The sarcoplasmic reticulum is triggered to release large amounts of calcium

4. Calcium binds to Troponin causing it to disassociate with F-actin

5. Troponin removal allows myosin to bind to actin and sarcomere contraction

What issues arise from faulty palpebral muscles?

Ptosis: drooping of superior eyelid
Diplopia: condition where a person sees two images of a single object
Peek sign: ocular surface uncovered following sustained closure

Issues with what muscle would cause Ptosis?

LPS, Muller muscle/tarsal muscle

Issues with what muscle would cause Diplopia?

EOM

Issues with what muscle would cause Peek sign?

Orbicularis Oculi

What is Ocular Myasthenia Gravis, and what are its symptoms?

An autoimmune neuromuscular junction (NMJ) disorder with unknown cause. Symptoms: weakness in eye muscles can lead to double vision, drooping eyelids, and difficulty focusing.

What causes Ocular Myasthenia Gravis?

Impaired NMJ commonly due to presence of antibodies binding to AChR of muscle cells in synaptic cleft, block ACh, and prevent receiving muscle cell from propagating signal

What type of muscles are more susceptible to Ocular Myasthenia Gravis

Type II Ocular Muscles

Why are fast twitch muscles more susceptible to Myasthenia Gravis?

The fast twitch muscles require repeated nervous stimulation, therefore they are more susceptible

Patients with Ocular Myasthenia Gravis will develop what issue later?

Systemic muscle weakness within 2 years, becoming Generalized Myasthenia Gravis.

What Muscles can Generalized Myasthenia Gravis affect?

Any skeletal muscles; seen as limb weakness, dysphagia, slurred speech, respiratory muscles.

How many patients with Ocular Myasthenia Gravis get Generalized Myasthenia Gravis

2/3 patients

What ages do males get more susceptible for OMG?

60-80 yrs

What ages do females get more susceptible for OMG?

23-30 and 60-80 yrs

What type of muscles are Muller’s Muscles/Tarsal Muscles

Smooth Muscle

What innervates Muller’s Muscle/Tarsal muscles

Sympathetic Innervation

Features/characteristics of skeletal muscles

• Striated

• Multinuclear

• Voluntary Movement

Features/characteristics of Smooth Muscles

• Not striated

• Single nucleus

• Involuntary

• Net-like structure

Steps for Smooth Muscle Contraction

1. Influx of calcium triggers more calcium release from SR

2. Calcium binds to Calmodulin

3. Ca-CaM activates myosin light chain kinase (MLCK)

4. MLCK activates myosin

5. Myosin contracts and pulls on actin

What is Horner’s Syndrome

A neurological condition caused by disruption of the sympathetic nerves supplying the eye and surrounding structures

Symptoms of Horner’s Syndrome

1. Ptosis: Muller muscle is inhibited, causing dropping of the upper eyelid

2. Miosis: constricted pupil d/t unopposed action of the parasympathetic system

3. Facial Anhidrosis: decreased or absent sweating depending on nerve damage

4. Enophthalmos: eye may appear sunken

Orders of Horner’s Syndrome

First Order: lesion before the hypothalamus and Superior Cervical Ganglion (SCG)

Second Order: lesion after the hypothalamus, but before the SCG

Third Order: lesion after the hypothalamus and SCG

What are the types of palpebral motions?

• voluntary blink/closure

• spontaneous blink to protect

• reflexive blink from drying tear film sensed by a decrease in temperature

• coordination with EOM

How do the parts of the eyelids move during a blink?

• Nasal angle remains immobile

• Temporal angle moves nasally and downward

• Upper lid moves down and medially

• Lower lid moves mostly medially

What does the LPS do during the down-phase of a blink?

It relaxes to allow the closing of the eyelids

What does the LPS do during the up-phase of a blink?

It contracts

Why do blinks close faster than they open?

Whitnall’s Ligament/Canthal Tendons lower superior palpebral AND population of fiber cell types differ between muscles

List the order of events that occur duing a blink

1. Baseline levator motorneuron firing ceases

2. LPS muslces relax

3. Passive downward force of canthal tendons lowers superior palpebrae

4. Orbicularis motoneuron firing begins causing further palpebral closure

5. Orbicularis motorneuron firing and muscle activity ceases

6. LPS motorneuron resume firing at baseline tonal rate, reopnening the palpebral aperature and re-stretching canthal tendons

Characteristics of spontaneous blink

• multiple times per minute

• duration is ¼ second

• synchronous

• amplitude varies

What increase blink rate?

• decreased humidity

• contact lens use

• older age

• speaking

• emotional states

• birth control medication

What decreases blink rate ?

• increased humidity

• younger age

• during sustained visual tracking

• reading

• daydreaming

• downward gaze

Dopamine’s affects on spontaneous blink rate

dopamine is a neurotransmitter, drugs that stimulate dopaminergic nerves increases SBR; drugs that inhibit dopaminergic nerves reduce SBR

How does Parkinson’s disease affects on SBR?

It decreases dopamine release, thus is associated with decreased SBR

How does Schizophrenia affect SBR?

It increases dopamine release; associated with increase in SBR

Which way does the eye move during a reflexive/spontaneous blink?

In primary gaze, it rotates downward and nasalward

In large saccade movements, what typically happens?

a blink

What controls the saccade (rapid simultaneous movement of both eyes in the same direction from one point of fixation to another)

Saccade is controled by the Frontal Eye Fields (FEF) and superior colliculus

What is Bell’s Phenomenon

Upward and outward (abducting) rotation of the eyes on prolonged bilateral closure or attempted closure

What is visual suppression?

The brain’s ability to temporarily ignore visual input during saccades or blinks

Where does a patient’s eye look when they have ptosis?

Their eye looks downward and lateral. CN III is damaged, so the IR, SR, MR, and IO don’t work, but CN VI does, so the LR and SO still work.

Marcus Gunn Jaw Winking Phenomenon

Chewing/sucking motions occur with eyelid motions because pterygoid muscle CN V linked to levator CN III; ptosis at rest

Pathway taken for tactile reflex blinking

Starts at CN5 at cornea, goes to trigeminal ganglion of opthalmic branch, goes to trigeminal brain stem nuclear complex or TBNC, goes to inter-neuron to facial nucleus and ocular motor nucleus before taking CN 7&3 to cause blink

Pathway taken for menance or dazzle

Starts at CN2 going to lateral geniculate nucleus, then visual cortex

Pathway taken for auditory reflex

Starts at cochlea, takes CN8 to go to auditory nucleus, inter-neurons to go to facial nucleus and oculomotor nucleus, takes CN7 and 3 to go to O.O. muscle

Blepharospasm

Involuntary, forceful and repetitive bilateral spasms of lid closure. Begins with elevated blink rate that progressively increases

Causes of Blepharospasm

Idiopathic, but is associated with Trigeminal reflex blink hyperexcitability contractioning of orbicularis oculi. (not associated with other neurological abnormalities; more common in women vs men. associated with parkinsons)

What is Myokymia

Involuntary focal hyper-excitability of peripheral nerve motor axons of the orbicularis oculi (eye twitch)

What is used to treat blepharospasm?

Botulism toxin, it works by cleaving specific SNARE proteins (used to anchor the synaptic vesicles against the cell membrane to release neurotransmitters)

Lid-Opening Apraxis (LOA) is what?

The inability to initiate and sustain eyelid opening after voluntary or involuntary eye closure

What causes LOA?

Abnormal involuntary inhibition of of LPS basal tonic activity or contraction of the pretarsal portion of O.O. muscle

Are blepharospasms observed with Lid-opening apraxia?

Yes, typically together.

Lagophtalmos is what

A condition that prevents the patient from closing their eyelids. Also seen with widening of palpebral aperture and laxity of lower lid

What causes Lagophthalmos

Infranuclear lesion of CN VII

Bell’s Palsy is defined as what?

acute unilateral facial weakness

Thyroid eye disease is caused by what?

An autoimmune disorder where the thyroid stimulating hormone receptor is stimulated

Risk factors for Thyroid Eye Disease

Women 5-6x more likely vs Men & smoking

What are potential ocular issues from TED

• Retraction of the upper lid/ Dalrymple’s Sign: activation of levator and Muller muscles and exophthalamos from orbital tissue swelling

• Von Graefe’s Sign: upper lid lag on downward gase d/t overstimulation of levator muscle

• Vision threat: Exposure keratopathy & compressive Optic neuropathy

What is Pseudo-Graefe Phenomenon?

Misdirection of fibers intented for the medial rectus to the levator, causing lid rectraction in downward inward gaze

What causes Pseudo-Graefe Phenomenon?

Typically, recovery from CN III paralysis

What are the function of tear

• Maintain smooth optical surface

• Primary source of atmospheric oxygen for cornea

• Source of glucose/nutrients for cornea

• Traps exogenous debris, helps remove sloughed cells, and flushes out metabolic/cellular waste products

• Pathogen defense: physical barrier and contains antibacterial substances

• Aids corneal hydration

• aids wound repair

• lubricates globe/eyelid apposition during palpebral closure

What layers compose the tear film structure?

top: lipid layer → mucin-aqueous glycocalyx gel→ thicker mucin layers → corneal epithelium

What is the thickness of the tear film?

Central thickness: ~3 micromemters
Meniscus: ~270 micrometers

How thick is the lipid layer?

50-100 nm lipid layer thickness

What is the tear volume in the eye?

~6.5 microliters

How much tear is drained/evaporated per minute?

~1.2 microliters per minutes

What are the types of tears?

• basal tears

• reflective tears

• psycho-emotional tears

What are basal tears?

continuous basal rate of lacrimal secretion; decreases with age

What are reflexive tears?

• response to external stimuli

  • Temperature

  • Chemical irritation

  • Pressure (oculo-lacrimal)

  • Nasal

  • Photo-lacrimal

• Not found in infants

What are Psycho-emotional tears?

Tears made from emotional responses, unique to humans

What are the most common ions in tears?

Na, Cl, K, and HCO3

How are ions transported into the tears?

The are transported across plasma membranes of lacrimal and ocular surface cells for the purposes of transporting water via paracellular and transcellular pathways.

What is unique about glucose in tears?

The concentration in tears correlates with blood glucose

What is the typical glucose concentration in tears?

7.4 mg/dl