Flashcards in Boards Prep: Ocular Physiology: Book Deck (100):
1. 3 Types of Blinking: name them
4. Which is the most common type of blinking?
1. What causes this blinking?
2. Avg rate of blinks per minute?
4. Decreased rate causes what?
1. Contraction of PALPEBRAL portion of Orbicularis Oculi
2. 12-15 blinks per minute
3. Maintain optics and comfort of the eye by STABILIZING the TEAR FILM
4. Decreased Tear secretion, increase tear evaporation --> DES and Secondary EPIPHORA.
1. Caused by what?
2. Auditory: Cause
3. Touch or irritation?
a. Cotton Swab Testing: What CN?
4. Dazzle: CN?
5. Menace: CN?
6. The Efferent Loop of Reflex Blinking for any of these begins where EXCEPT for DAZZLE?
7. What muscle is responsible for Reflex blinking?
1. Sensory Stimuli
4. CN 2
5. CN 2
6. Starts in the FRONTAL LOBE.
7. Orbicularis PALPEBRAL PORTION (for both Spontaneous and Reflex Blinking)
1. Winking: Type of Voluntary Blinking: uses what muscle?
1. Orbicularis Oculi: Uses both Palpebral and Orbital Portions
Spasm: Benign Essential Blepharospasm (BEB)
1. Characterized by what 3 things?
2. Results from SPASMS of what Muscles? (COP)
1. B/L, Involuntary, sustained twitching and/or closing of the eyelids.
2. Corrugator, Orbicularis Oculi, and Procerus (CN7: Zygomatic Branch)
*All are innervated by CN7
1. Tight or Forced Eyelid Closure: Requires contraction of what muscle?
2. Bell's Phenomenon: What is it?
1. Orbital Portion of Orbicularis Oculi
2. Normal defense reflex in about 75% of the population. Happens after forced lid closure and is characterized by UPWARDS and OUTWARDS ROTATION of the GLOBE
a. Protect the CORNEA!
Role of the Eyelids in Tear Processes: Production
1. Meibomian Glands
a. What are they?
d. How do they release substance?
2. Glands of Zeis and Moll
a. What are they?
3. Accessory Lacrimal Glands: Purpose
a. Glands of Krause: More/Less numerous? Location?
b. Glands of Wolfring: More/Less Numerous? Location?
1. a. Sebaceous Glands
b. Upper (30-40) and Lower (20-30) tarsal plates
c. Secrete ANTERIOR LIPID LAYER of tears
d. Blinking stimulates release via HOLOCRINE SECRETION
2. a. Modified Sebaceous and Modified Sweat Glands Respectively
b. Next to Hair Follicles
c. Minor contribution to Lipid layer of tears
3. Tubuloacinar Exocrine Glands...Contribute to AQ. LAYER of TEARS
a. More numerous; Fornices
b. Less numerous; Tarsal Cojunctiva
Role of the Eyelids in Tear Processes: Distribution
1. How do the upper eyelids close during a blink?
2. What does this do?
1. Laterally to Medially
2. Spreads MUCIN LAYER evenly across CORNEAL EPITHELIUM and Bulbar Conjunctiva. Aids in Proper tear film Formation
Role of the Eyelids in Tear Processes: Drainage
1. When the eye is OPEN, tears DRAIN PASSIVELY into the Puncta via what?
2. When eyelids close during a blink, what Muscle Contracts and what does it do?
a. This muscle is part of what portion of the Orbicularis Oculi?
b. As the Orbicularis Oculi Contracts, what does it do?
1. CAPILLARY ATTRACTION
2. Muscle of HORNER: Causes Canaliculi to SHORTEN as they move MEDIALLY towards the Lacrimal Sac. Helps "Pump" tears into the Lacrimal Sac.
a. Part of the Palpebral Portion
b. Stretches the TEMPORAL WALL of the Lacrimal Sac AWAY from the NOSE...Creates NEGATIVE PRESSURE...helps draw tears into the LACRIMAL SAC!
Protective Function of the Eyelids
1. Cilia (Eyelashes)
b. Number in upper lid vs. lower lid?
2. Glands of Eyelids
a. Help produce tear film, but also help do what?
1. a. Screening and Sensing the environment and inducing blink reflexes when needed.
b. Upper: 150; Lower: 75
2. a. Move debris away from the Cornea in concert w/Spontaneous Blinking.
Function of Tears
1. What are the 5 main functions of tears?
1. Optical: Main role.
2. Nutritional: Primary source of O2 for Corneal Epithelium
3. Mechanical: Collects debris and moves it away from cornea w/each blink.
4. Antibacterial: Aq. Layer: Has Lysozyme, Lactoferrin, IgA, and other proteins of immune System
5. Corneal Transparency: Tear film. Specific Osmolarity and pH that's maintained by secretory glands and the corneal Epithelial cells, thus helping to prevent corneal Edema
Production and Composition of Tears: Anterior Lipid Layer
1. Composed of what?
2. Secreted primarily by what?
3. Main purpose?
4. Although BLINKING is the primary method for releasing lipids from the glands, what else can help increase lipid secretion?
1. Free FAs, Cholesterol, and Waxy Esters
2. MEIBOMIAN GLANDS, and somewhat form Glands of Zeis and Moll
3. Slow Evaporation of the Aq. Layer of the Tears...helps maintain Optical Clarity
4. PSNS innvervation.
Production and Composition of Tears: Aq. Layer
1. 3 purposes?
2. Components (9 categories)
1. a. Protection via Antibacterial proteins
b. Nutrition via Glucose to Corneal Epithelium
c. Thickness to the tear film
2. a. Water (main component)
b. Electrolytes: Na, K, Cl
c. Antimicrobial Components: (IgA, Lactoferrin, Lysozyme, Beta-Lysin, Interferon)
d. Lipocalins: Decrease Surface Tension; increases spreadability; Acts as a carrier for All-Trans Retinol. Blocks Fe2+ binding receptors on the surface of bacteria
e. Vitamin A: in tears in form of All-Trans Retinol (needed to develop Goblet Cells)
f. Enzyme Cofactors (Fe, Mg, Cu, Ca): Maintain permeability of corneal epithelial cells
g. HCO3-: Buffer for tears
h. Solutes: GLUCOSE, urea, lactate, citrate, ascorbate, AAs
i. Other Proteins: Albumin, Growth Factors, Interleukins, and VEGF
Production and Composition of Tears: Aq. Layer (2)
1. Age: Does what to this layer?
2. CL Wear does what?
3. Closed Eye Conditions: What happens?
1. Decreased Lysozyme and Lactoferrin Proteins and overall decrease in Aq. Secretion
2. Increase in Electrolyte and Protein concentration d/t increased evaporation of the tears (purpose of replacement schedule)
3. Higher Concentration of IgA and serum albumin. Lysozyme and Lactoferrin levels are essentially the same.
Production and Composition of Tears: Aq. Layer (3)
1. Main Lacrimal Gland
2. Accessory Lacrimal Glands
3. Conventional Theory on each and their responsibility?
4. Sensory Nerves (V1) of cornea involved in Reflex arc that causes what?
1. inn via PSNS via CN7, Sympathetic Fibers, and Sensory Nerves of V1
2. Inn via PSNS; Neural control of secretions is not well understood.
3. Main LG: Reflex and Emotional Tearing
Accessory Lacrimal Glands: Maintenance (Basal Tearing)
*Newer theory states both are responsible for Basal Tearing.
4. Lacrimation (via PSNS stimulation of LG via CN7), MIOSIS, and PROTECTIVE BLINK.
Dazzle Blink reflex can also stimulate Lacrimal Gland Secretion
Production and Composition of Tears: Mucous Layer
2. Why are they so unique?
3. Made by what cells?
a. Found mainly where?
1. Interacts w/Glycocalyx of Corneal Epithelium; helps spread tears, trap debris, Bacteria, and sloughed corneal epithelial cells.
2. Can Mix w/Lipid AND Water.
3. GOBLET CELLS
a. INFERONASAL FORNIX and the BULBAR CONJUNCTIVA (most concentrated temporally): NOT NEAR LIMBUS!
*VIT A: DEVELOPMENT of Goblet cells. Deficiency --> Keratinization of Conjunctiva and Cornea.
Deficiency of Vit A can result in BITOT's SPOTS (Foamy build-up of keratin) on the Conjunctiva.
Production and Composition of Tears: Mucous Layer
1. Mucous Fishing Syndrome: What is it?
2. What cells secrete Glycocalyx on the Cornea?
1. Pts "fish" for and remove excess mucous in the Conjunctiva. Causes DAMAGE to the Conjunctiva Epithelium and a subsequent increase in Mucous Production, causing an unfortunate cycle that exacerbates symptoms. **DES = MOST COMMON cause of this.
2. Surface Cells
Elimination of Tears
1. What % of tear volume is continuously lost via evaporation?
2. Tear Volume on ocular surface?
3. Max amt of fluid the eye can hold w/in the tear film and fornices?
4. Normal Tear production is ~ what?
5. Avg Eye drop has how much?
1. ~25%; The rest drains thru nasolacrimal system.
2. 7-9 uL
3. 20-30 uL
4. 1 uL/min
5. ~50 uL.
*Epiphora: when tear production is more than 1 uL/min or drop instillation is more than this rate.
Physico-Chemical Properties of Tears
1. Normal Tear Film Osmolarity?
a. Main Ions that contribute to Osmolarity?
b. Calcium is essential for what?
c. What does Potassium do?
2. What causes an INCREASE in Tear Osmolarity?
3. What is used in DES Tx?
4. Avg pH of tears?
5. pH tears during Sleep?
6. pH in DES?
1. 308 mOsm/L; Isotonic; Healthy Corneal Surface
a. Na and Cl ions (aq. Layer)
b. Hemidesmosome Formation in BM of Corneal Epithelium. (Excess calcium can deposit on CL --> decreased VA)
c. Maintain health of Corneal epithelium; 4x GREATER CONCENTRATION in the TEARS compared to Blood Plasma.
3. HYPOTONIC EYE DROPS (150 mOsm/L)
5. Decreases (MORE ACIDIC) d/t ANAEROBIC RESPIRATION
6. INCREASES (More basic) d/t Increase in Tear Osmolarity
EOMs: Vestibular Control Mechanisms
1. Middle Ear
a. Sound waves are amplified 10-20x's by what?
2. Tympanic Cavity: What is it?
3. Auditory Ossicles: What r they, and order?
4. Stapedius and Tensor Tympani Muscles: What do they do?
5. Chorda Tympani nerve of CN 7 does what?
1. Tympanic Membrane
2. Middle Ear...after Tympanic Membrane
3. Malleus, Incus, Stapes (B/w Tympanic Membrane and Oval Window)
4. Dampen amt of vibrations placed on Auditory Ossicles.
a. Stapedius Muscle: Inn by CN 7 before it exits the skull via the Stylomastoid Foramen
b. Tensor Tympani Muscle Inn by branch from Mandibular Division (V3) of CN 5.
5. Taste sensations from Ant 2/3 of tongue; and Tympanic nerve Plexus (from CN 9) travel w/in, but DO NOT INNERVATE, the middle ear cavity.
EOMs: Vestibular Control Mechanisms
1. Inner Ear
a. What does it do?
2. Bony Labryrinth: 3 Parts that are innervated by CN 8
a. Cochlea: What does it do?
b. Vestibule: What does it do?
c. Semi-Circular Canals: What does it do?
1. a. Converts mechanical vibrations to neural signals
b. Vestibulocochlear organs help maintain balance, receive sound, and contribute to ocular reflex actions
2. a. Shell shaped; Has Organ of Corti which has Hair Cells that CONTROL HEARING
b. Has Utricle (Detects Horizontal Linear movement), and Saccule (Detects Vertical Linear Movement), that help maintain balance. Causes reflex eye movements (LINEAR VOR!) equal and opposite to motion of the head!
Vestibule AREA = Continuous w/Cochlear duct for Hearing
c. Communicate w/Vestibule and has Ampullae (Detects Angular ACCELERATION...rotational movements of body or head) and cause reflex eye movements (ANGULAR VOR)
EOMs: Supranuclear Control of Eye Movements
c. Horizontal saccades controlled by what?
b Controlled by what?
a. Controlled by what?
b. Divergence and Convergence driven by what?
1. a. FAST eye movements.
b. Maintain fixation (Foveation) on object
c. C/L FRONTAL EYE FIELD in Frontal Lobe and Superior Colliculus
2. a. Smooth tracking to maintain foveation on SLOW-MOVING OBJECTS
b. IPSILATERAL PARIETAL LOBE
3. a. Brainstem level
b. RETINAL DISPARITY. Help maintain sensory fusion and stereopsis.
Cornea: Permeability Characteristics of Corneal Layers
1. Corneal Epithelium
a. Type of Junctions?
b. Epithelium: Highly Lipophilic/phobic?
2. Corneal Stroma
a. Highly Hydrophilic/phobic?
a. What kind of Junctions?
b. Highly Lipophilic/Phobic?
1. a. Zonula Occluden Junctions
b. Highly Lipophilic (limits absorption of hydrophilic, ionized molecules)
2. a. Highly Hydrophilic (d/t GAGs)
b. Allow these types of substances to pass thru corneal stroma (water loving ionized stuff)
3. a. Macula Occludens Junctions
b. Highly Lipophilic.
Theories of Corneal Transparency
2. Corneal Epithelium and Bowman's Layer: Purpose?
3. Cornea TRANSMITS light w/wavelength of what?
4. Visible wavelengths (400-700 nm) are transmitted thru cornea w/high precision. More than what % of light above wavelength of 400nm is transmitted thru the cornea?
5. Corneal Epithelium is MOST SENSITIVE to RADIATION of what range?
a. Can cause what?
1. a. 200-290 nm. MOST DANGEROUS
b. 290-320 nm
c. 320-400 nm
2. Protect inner layers. Absorb shorter wavelengths of UV light (UV-C and UV-B below 300 nm)
3. of 300 nm (UV) to 2500 nm (Infrared)
5. UV-C Range (260-280 nm)
b. UV-Keratitis: Snow-blindness, welder's keratitis, tanning sun lamps.
Theories of Corneal Transparency (2)
1. Corneal Crystallins: Purpose and location?
2. Ascorbate (Vit C) and Glutathione: Purpose/location?
1. Cytoplasm of Epithelial and endothelial cells. Help maintain transparency: Limit LIGHT SCATTER.
2. w/in Epithelial cells. Protect cornea from UV rays and free radical scavengers
Theories of Corneal Transparency (3)
1. Corneal Stroma
a. 200-250 layers of what?
b. Collagen Fibrils: UNIFORM SIZE w/what?
2. Proteoglycans: Found where? Purpose?
3. Precise spacing of collagen fibrils does what?
4. What 2 other things help w/transparency?
5. Major Proteoglycan in the Corneal Stroma is what?
1. a. of 30nm Lamellae made of Collagen Fibrils w/in a network of GAGs
b. and PRECISELY SPACED less than one half the wavelength of visible light from one another.
2. Found in Ground Substance that fills space b/w corneal cells and collagen fibrils and lamellae; Their side chains help maintain the right collagen spacing by forming negatively charged bonds w/water molecules
3. Increase Destructive interference, minimizing light scattering and increasing corneal transparency.
4. Cornea is Avascular and has HIGH WATER CONTENT.
5. KERATIN SULFATE!
Factors Influencing Corneal Thickness/Hydration
1. Corneal Deturgescence
a. What is it?
b. Relies on what?
1. a. state of relative dehydration maintained by normal cornea (75-80% stromal water content is optimal)
b. Endothelial cells (main contributor) and Epithelial transport mechanisms
Factors Influencing Corneal Thickness/Hydration: Epithelial Pump Mechanisms
1. Basal Membrane of Epithelial cells: 2 transport mechanisms
2. how does Na get into an epithelial cell?
3. Movement of K+ into the Aq. Humor will stimulate what Ion to MOVE INTO TEARS?
4. How does the K+ channel respond to a Hypoxic cornea?
a. What happens in a Hypoxic Cornea?
1. Na/K/ATPase pump and Na/K/Cl cotransporter
2. PASSIVELY from Tear Film
4. Moves more K+ into the Aq., causing more Cl- and H2O to enter the tear film, restoring normal Corneal Thickness
a. Higher acidity and Increased Thickness d/t corneal swelling.
Factors Influencing Corneal Thickness/Hydration: Endothelial Pump mechanisms
1. Na/K/ATPase Pump
b. What does it do?
2. Na+/H+ Pump
a. Uses the Na+ Concentration gradient to do what?
b. What does this do?
c. CO2 will combine with what?
3. What are the Major factors for water transport across corneal epithelium and endothelium?
1. a. Basolateral membrane
b. Pumps Na+ into Aq Humor --> higher concentration of Na+ in Aq. Humor vs. Corneal Endothelium
2. a. to move H+ out of endothelial cells to Aq. Humor, and puts Na+ back into endothelial cells.
b. Decreases Extracellular pH --> CO2 diffusing into the Endothelial cell.
c. H2O --> Makes H2CO3 --> dissociates to H+ and HCO3- (Bicarbonate) then HCO3- and Cl- Move out of Endothelial cell into the Aq. Humor.
4. Cl- EXCRETION and Na+ ABSORPTION!!!
1. Total Atmosphere pressure?
a. Partial Pressure (PP) of O2?
2. Open Eye Conditions
a. PP O2 w/in tears?
b. Major contributor to O2?
c. Minor contributors?
3. Closed Eye Conditions
a. PPO2 w/in tears?
b. Supply to Cornea from Epithelium to Anterior Stroma?
c. O2 supply to Posterior Stroma and Endothelium?
4. Critical PPO2 for the cornea?
a. Why is this a concern?
1. 760 mmHg
a. 155 mmHg
2. a. 155 mmHg
b. Air...Entire cornea
c. Aq. Humor, Limbal capillaries
3. a. 55 mmHg
b. Sup Palpebral Conjunctiva (main contributor) and limbal vasculature
c. Aq. Humor
4. 10-20 mmHg
a. CL wear over night. Minus lenses are thinner in the center and thus more likely to transport O2 than Plus lenses, so big concern for Plus lenses. CLs have to maintain PPO2 above 10-20 mmHg.
O2 Diffusion: CL Wear
2. What is essential for maintaining corneal transparency?
3. Decreased corneal pH does what?
1. J/A = Dk/t(P1-P2)
J/A = O2 flow
Dk = O2 permeability.
Dk/T = Transmissibility = how well O2 can diffuse thru the thickness.
2. Control of pH in cornea. Decreased O2 levels --> accumulation of H+ ions made in Glycolysis --> increased acidity of the corneal cells.
3. change in K+ channels --> massive efflux of K+ from the keratocytes w/subsequent collagen damage and scar formation.
Nutrients for Cornea
1. Glucose is made thru what 3 ways?
a. Which is the major player?
2. Concentration of Glucose in tears?
a. In Aq. Humor?
3. Aq. Humor is primary source for what nutrients for all layers of the cornea?
4. What can CORNEAL EPITHELIAL CELLS do?
1. Anaerobic Glycolysis, Aerobic Glycolysis, and HMP Shunt
a. Anaerobic (85%)
a. HIGH...main contributor
3. Glucose, AAs, Vitamins
4. Store lots of GLYCOGEN for basal cell mitosis and epithelial wound healing.
*Endothelium stores a lot of energy to maintain Na/K/ATPase to maintain corneal transparency.
a. The entire epithelium is replaced in how many days?
b. Only Mitotic Cells?
c. Basal cells do what?
a. First Step?
b. Second Step?
c. Third Step?
d. How fast does healing occur?
e. When does it take 8 weeks?
3. What can degrade Hemidesmosome Function?
a. What can decrease the activity of these?
1. a. 7-14 DAYS
b. BASAL CELLS (made from differentiating limbal stem cells from PALISADES of VOGT)
c. Differentiate into WING CELLS --> Squamous cells --> Corneal surface
2. a. Inhibit BASAL CELL MITOSIS
b. Fibronectin released (scaffolding) --> Epithelial cells migrate --> New Hemidesmosomes are made (adhesion to these migrated epithelial cells and Basement Membrane)
c. Basal cell mitosis resumes at a REALLY FAST PACE.
d. REALLY FAST.
e. if Basement Membrane is also damaged (complete healing can take up to 8 weeks)
3. Inflammation (Matrix Metalloproteinases)...can cause the Hemidesmosomes to attach.
a. Corticosteroids and Tetracyclines...so put a Pt on them if they have RCEs!!! (so...like a course of DOXYCYCLINE!)
1. What 2 layers of the Cornea can REGENERATE?
2. What 2 layers CANNOT?
3. What can replace itself if damaged, but has a different textured tissue? Why does this occur?
What does this refer to: "Bows Out" and "D-3?"
1. Epithelium and Descemet's
2. Bowman's Layer and Endothelium
3. Stroma; New collagen is LARGER and less organized --> SCAR.
4. Bows = Bowmans will NOT Regenerate!
D-3: Descemet's will! and it TRIPLES in it's lifetime (from ~5 um to 15 um)
1. Main function of Corneal Nerves?
a. What can reduce corneal sensitivity?
2. Neurotrophic Keratitis: describe it.
1. TROPHIC...i.e., need this sensory innervation to have EPITHELIAL CELL MAINTENANCE and REGENERATION
a. LASIK and AGE
2. D/t CN 5 DAMAGE! and decreased corneal sensitivity. Dx'd via COTTON SWAB TEST!
a. HERPES SIMPLEX and ZOSTER, stroke, DM and common causes.
1. Which meridian flattens? causes increase in what?
2. Light scattering?
3. Corneal sensitivity?
4. Basement membrane?
5. Corneal arcus in perpipheral stroma?
7. Endothelial cell density?
1. VERTICAL; Increased ATR astigmatism
6. Thickens --> increase Hassall-Henle Bodies in CORNEAL PERIPHERY
1. What happens to the lens during accommodation?
1. PSNS --> Contraction Ciliary muscle --> Decrease in Tension in lens zonules
2. Ant Pole of lens moves FORWARD --> Ant Curvature INCREASES
3. Post Pole of lens moves back slightly and post curvature INCREASES
4. Lens thickness (Ant-Post Dimension) INCREASES, decreases AC depth
5. Lens Diameter Decreases
6. Lens Power Increases
*These can cause Pupillary block, causing Elevated IOP...important adverse effects of MIOTIC DRUGS (Pilocarpine)
1. Can it cause a temporary increase/decrease in IOP?
1. DECREASE. Ciliary Muscle contraction pulls SS posteriorly, and Opes up pores of TM.
1. What's in it?
2. Production of new what?
3. Maintenance of what?
4. 70% of glucose for lens comes from what?
5. What 2 metabolisms are limited to the lens epithelium?
6. How is Sorbitol made?
a. What can it do to the lens?
1. Largest Concentration of Proteins of any structure in the body.
2. NEW LENS FIBERS and Protein Synthesis.
3. Na/K/ATPase Pump...helps establish a balance b/w H20 and ions w/in the lens to maintain lens transparency. *H20 follows Na+ into Aq. Humor --> Lens dehydration and transparency
4. Anaerobic Glycolysis
5. Kreb's Cycle; ETC
6. Glucose converted to it via Aldose Reductase...when Hexokinase isn't around.
a. Accumulates in the lens. --> creates osmotic gradient that favors movement of H20 into the lens --> swelling, lens fiber damage, and cataract formation.
Regulation of Lens Proteins
1. Glutathione: What is it and what does it do?
2. What happens w/Glutathione diffusion into the lens with age?
3. Ascorbic Acid: Purpose?
1. Protects against oxidative damage to lens; REDUCING AGENT (H2O2); comes from Aq. Humor to Lens. Some lens epithelial cells can make it tho.
2. it DECREASES --> increases formation of Cataracts
3. Protects lens from Oxidative Damage. Ascorbic Acid is found in a much higher concentration in the lens compared to Aq. Humor.
Theories of Lens Transparency
1. 6 things that may help maintain lens transparency:
1. Na/K/ATPase pumps ---> Na to Aq humor; K to lens
2. Avascular lens
3. Lens fiber cells: No membrane bound organelles (decrease light scattering)
4. Lens fiber Cells: Closely packed, uniformly space
5. Cytoplasm in lens fibers: tons of crystallins...minimize light scatter d/t destructive interference
6. Tons of Transport mechanisms...limit Ca2+ concentration in the lens...prevent cataracts.
Mitotic Activity of Lens Epithelium
1. Primary lens fibers made by what?
2. Anterior lens epithelium makes what?
3. Where does fiber cell mitosis occur?
1. Posterior lens epithelium during embryological development!
2. 2ndary lens fibers!
3. in GERMINATIVE ZONE of the ANTERIOR LENS EPITHELIUM.
Aging Changes in Composition of the Lens
3. Anterior Lens Capsule
4. Where is lens capsule thickest?
b. It's the thickest what?
c. Made of what kind of Collagen?
6. Center of lens?
7. AA concentration?
8. Glutathione activity?
9. Nuclear fibers start to do what?
1. Decrease in Crystallins; Increase in Insoluble Lens Proteins (d/t increased cross-linking b/w lens fiber cells --> alters amt of H2O in the lens)
a. Alpha Crystallins: decrease like crazy w/age. Age 45: NO ALPHA CRYSTALLINS in the lens nucleus.
b. Alpha Crystallins: MOLECULAR CHAPERONES prevent the degradation of other crystallins.
2. 0.02 mm per year increase. Lens diameter is relatively stable after teenage years
3. Increases w/ age
4. Anterior Midperipheral part of lens (Pre-equatorial region)
a. Posterior Pole
b. Thickest BM in the entire body.
c. Type 4 Collagen
5. Ant and Post lens decreases w/age
6. Moves anteriorly....causes decrease in AC depth w/age
7. DECREASES w/Age.
8. Decreases. Na, Ca, and H20 concentrations in the lens increase
9. Start to lose their nucleus and organelles. Start accumulating a yellow brown pigment that contributes to the formation of a nuclear sclerotic cataract. NS starts in Embryonic nucleus then expands to fetal and adult nuclei. Most common cataract d/t aging.
Choroid: Main function?
High protein content. Makes a Protein gradient. Promotes the absorption of excess H2O from the retina into the choroid.
Aging Changes of the Choroid
1. Choroidal thickness?
3. Bruch's Membrane?
1. Decreases with age overall
2. Decreases in thickness w/age
3. Increases in thickness with age. Drusen accumulates on Bruch's membrane with age.
1. UV that it filters?
2. Storage area for what stuff?
3. What GAG is there and purpose?
4. Vit C concentration compared to blood plasma?
5. AAs concentration compared to blood plasma?
1. light in the 300-350 nm range.
2. O2, H2O, Na, K, Cl, Phosphate, Glucose, Proteins
3. HYALURONIC ACID...non-sulfated....support to collagen fibers...helps maintain proper collagen fibril spacing and maintains viscosity of the vitreous
4. higher (like 40x's higher)
UV Radiation: Wavelength absorption
1. Below 300 nm
2. 300-400 nm
3. above 400 nm
4. Lens does what?
4. Absorbs most of UV-A and UV-B light...protecting the retina from UV damage.
Age Change in Vitreous
1. Hyaluronic Acid: Stable until when.
a. Concentration increases when? Causes what?
1. 20-50 yrs
a. after age 50. H2O Increases.
1. Blood Flow: F (Flow) = ?
2. Mean Arterial Pressure
a. Entering Eye?
b. Episcleral veins leaving eye?
3. Perfusion Pressure
a. In Eye?
b. What is it?
4. Ocular Perfusion Pressure (OPP): What is it?
a. Glaucoma Pts w/this are 1.5 x's are more likely to develop what?
b. If IOP DECREASES, OPP does what?
c. If Diastolic BP DECREASES, OPP does what?
5. Pericytes are most likely responsible for autoregulation within the blood supply of what 2 things?
6. Transmural Pressure: What is it?
7. Critical Closing Pressure: What is it?
1. (Parteries (entering a tissue) - Pveins (leaving Tissue))/ R(Resistance)..Autoregulation
2. a. 65 mmHg
b. 15 mmHg
3. a. 50 mmHg
b. how easy blood passes thru a tissue: difference b/w pressure of BF entering eye, and leaving the eye.
4. Diastolic BP - IOP
a. progressive Optic Neuropathy secondary to ischemia.
5. RETINA and OPTIC NERVE.
6. Pressure over a BV wall. Subtract pressure outside the vessel from pressure inside the vessel.
7. Pressure where the BV collapses and BF stops.
Circulation: Elevated IOP in ACUTE ANGLE-CLOSURE
1. What does it do the the CRA?
2. What's the immediate threat to vision in ACUTE ANGLE CLOSURE?
1. Decreases BF in CR --> Decrease in PERFUSION PRESSURE --> change in transmural pressure --> causes Retinal vessels to increase diameter via autoregulation to improve perfusion --> CRAO if IOP is elevated acutely for long enough.
ANS control of BVs: Sympathetic Innervation
1. Symp Fibers are prevalent through the UVEAL TRACT, but DO NOT INNERVATE what?
2. What does symp. inn. cause Uveal BVs to do?
3. A sudden increase in BP, increases what?
a. What does the Symp NS do?
1. the CRA past the Lamina Cribrosa...so they DO NOT INFLUENCE RETINAL BF!
3. Increases FORCE of BF thru the small vessels of the UVEA.
a. In response, they cause CONSTRICTION of BVs --> Compensatory Reduction in BF.
ANS control of BVs: Parasymp Inn
1. PSNS Fibers from Oculomotor and Facial Nerves are also prevalent where?
a. What do they do?
b. PSNS Inn causes what?
2. Unlike the Choroid, what Vasculature is NOT UNDER AUTONOMIC CONTROL?
1. thru the Uveal Tract.
a. Most prominent in Anterior UVEA and has MINIMAL Influence on CHoroidal and Retinal BF.
b. Causes VASODILATION of the Uveal BVs in response to sudden DECREASES in BP!
2. RETINAL Vasculature.
Eye Environment. Unique things to KNOW!
1. IOP has to be Greater/lesser than Episcleral Venous Pressure? Why?
2. IOP has to be Greater/Lesser than ICP? Why?
3. What causes PAPILLEDEMA? (Patho..)
4. IOP has to be Higher/Lower than pressure in retinal and uveal arteries. Why?
5. Protein Content has to be Higher/Lower in the Choroidal Vasculature? Why?
1. GREATER; so Aq. Humor can DRAIN from the AC! thru the CORNEOSCLERAL MESHWORK and into the Venous System.
2. GREATER; to maintain AXOPLASMIC Gradient that flows from ON towards the Brain.
3. Reversal of Axoplasmic Gradient b/w eye and brain d/t INCREASE in ICP. Basically, CSF will spill into Subarachnoid space onto the Optic Disc Margins, and surrounding RNFL (Eye Pressure TOO LOW or ICP too HIGH)
4. LOWER; so nutrients can go from Choriocapillaris to RPE Cells.
5. LOWER; so excess water is pulled from the retina, across the RPE, and into the Choroid, promoting adherence b/w RPE and the Neurosensory Retina.
1. Choroid: Majority of BF occurs where?
a. What's found w/in Choroidal Vessels and why?
b. What's the Primary Responsibility of the Choroid?
a. Has what? Made by what?
3. What 2 things have FENESTRATED CAPILLARIES?
a. Has what?
5. What 2 areas of the eye have NON-FENESTRATED CAPILLARIES?
1. Choriocapillaris (~60%)
a. HUGE FENESTRATIONS w/in choroidal vessels. let nutrients diffuse out of vessels and into the RPE and outer 5 layers of the retina.
b. Give outer retina nutrients (Oxygen, Glucose, and Vitamin A, etc)
2. a. MACI; ACAs and LPCAs
3. CB and CHOROIDAL CAPILLARIES
4. a. MACI...made by anastomoses of IRIS RADIAL VESSELS.
b. Major circle --> Minor Circle --> Pupillary Margin, then back again.
5. IRIS and RETINAL CAPILLARIES. Contribute to Blood Aq and Blood-Retinal Barriers respectively.
1. Blood Supply?
2. What part of the retina is supplied by BOTH the CRA and CHOROID?
3. 2 Capillaries are formed w/in the Inner retinal layers.
a. Location of Superficial Capillary Network?
b. Location of the Deep Capillary Network?
c. Where do the Capillary Networks become VERY DENSE? Why?
d. What part of the retina gets its blood supply from the Choriocapillaris?
4. Where else is the Retina Avascular?
1. DUAL BLOOD SUPPLY
a. Inner 2/3rds: CRA; Outer 1/3rd: Choroid
3. a. RNFL
c. Around the FOVEA; Cuz the Fovea is AVASCULAR!
d. the Central Fovea
4. Extreme Anterior edges of the Peripheral Retina (~0.5 mm from the ORA SERRATA)
Retinal BF: Blood Retinal Barrier
1. Formed by TIGHT JUNCTIONS in what 2 places?
1. B/w Endothelial cells lining Retinal Vessels, and B/w the RPE Cells.
1. Composition of Outer Disc Segments?
2. Formation of Disc Outer Segments?
3. Composition of Visual Pigments?
a. Opsin = ?
b. Chromophore = ?
4. Formation of Visual Pigments?
1. Stacks of discs w/photopigments: Rhodopsin (w/in plasma membrane) = Rods; Iodopsins = Cones (stored in invaginations of Plasma membrane)
2. Photopigments made in Photoreceptor inner segment, travel thru CILIUM to Outer Segment. Discs and Plasma membranes made in Outer Segment.
3. 3 cone photopigments (Cyanolabe, Erythrolabe, and Chlorolabe): PHOTOPIC VISION and COLOR VISION. Rhodopsin = SCOTOPIC VISION.
a. Membrane Apoprotein
b. 11-cis retinal (Vit A Derivative)
4. Light absorption damages photoreceptors; Rod outer segments shed in the MORNING (Phagocytosis via RPE) and Cone Outer segments are shed and renewed in the EVENING!
Retina (2): Stages of Visual Cycle
1. How does it work?
1. Light absorbed (Photoreceptor) --> converts 11-cis retinal to ALL-Trans Retinal --> All-Trans Retinal moves from disc lumen to Cytoplasm --> Converted to All-Trans Retinol --> transported to RPE cells --> Converted to 11-Cis Retinol --> Oxidized to 11-cis Retinal --> Shuttled back to Photoreceptors to go back into Photopigments in the disc OUTER SEGMENTS.
Retina (3): Photoreceptor Electrophysiology
a. Photoreceptors: charge in the dark?
b. Purpose of Na/K/ATPase pumps on inner segment plasma membrane?
c. How does Na get in?
d. What is this flow of cations called?
2. Membrane Potential of a Photoreceptor?
3. What triggers PHOTOTRANSDUCTION?
1. a. -50 mV
b. Use ATP. Pump Na OUT of inner segment and move K into the inner segment.
c. via Na Channels found in the Outer Segment
d. DARK CURRENT.
2. -50 mV...constantly DEPOLARIZED and thus constantly release GLUTAMATE to BIPOLAR CELLS (cGMP keeps Na Channels open to promote depolarization)
3. Absorption of Light by RHODOPSIN. Rhodopsin dissociates, causing G protein to turn on (TRANSDUCIN) --> cascade --> DECREASE in cGMP --> CLOSURE of NA CHANNELS! --> Increase in (-) charge of cell membrane (-65 mV...HYPERPOLARIZES). --> DECREASE in RELEASE of GLUTAMATE to BIPOLAR CELLS **WHEN LIGHTS TURN ON!!
Retina (4): Retinal NTs
1. Glutamate: What is it?
2. GABA and GLYCINE: What are they?
1. Excitatory; Released by RODS, CONES, Bipolar cells, most ganglion cells.
2. Inhibitory NTs. Released by Horizontal Cells, and most Amacrine Cells
Retina (5): Function of Retinal Cells
1. Bipolar Cells
a. Type of Receptive Fields?
b. On-Center Bipolar Cells
c. Off-Center Bipolar Cells
2. Rod Bipolar Cells?
3. Horizontal Cells
a. Input from what?
b. Hyperpolarize or Depolarize to Light?
c. Horizontal cells impact what?
d. Provide what? Purpose?
4. Amacrine Cells
a. Type of Receptive fields?
b. Respond with what?
c. Do what in light?
5. Ganglion Cells
a. Type of Receptive Fields?
b. On-Center/Off-Surround do what?
c. Off-Center/Off Surround Ganglion cells do what?
d. MIDGET GANGLION CELLS: do what?
1. a. Center-Surround (spatial antagonism)
b. INHIBITED by GLUTAMATE (Hyperpolarized in DARK); LIGHT --> Less glutamate release --> DEPOLARIZATION
c. EXCITED by GLUTAMATE (Depolarized in DARK); LIGHT --> Less glutamate released --> HYPERPOLARIZATION
2. ALWAYS DEPOLARIZE in response to LIGHT.
3. a. Large number of photoreceptors. (Do Not have center/surround receptive fields)
b. Graded potentials; HYPERPOLARIZE to light
c. Impact SURROUND RESPONSES of Bipolar Cells...via Inhibitory feedback to photoreceptor cells or via DIRECT SYNAPSE w/Bipolar Cell (FEED FORWARD RESPONSE)
d. LATERAL INHIBITION; fine-tune neural signal from neighboring photoreceptors
4. a. Center/Surround
d. Fine-tune signal b/w bipolar and ganglion cells
5. a. Center/surround. APs
b. Synapse w/ON-CENTER BIPOLAR CELLS; DEPOLARIZE to LIGHT
c. Synapse w/OFF-Center Bipolar Cells; HYPERPOLARIZE to LIGHT
d. Small ganglion cells. Single Dendrite. Synapse w/1 MIDGET BIPOLAR CELL which synapses w/a SINGLE cone in the FOVEA...RESOLUTION of VERY FINE DETAIL.
Aging Retinal Changes
1. Retinal Nerve Fibers?
2. ILM does what?
3. Rod Density?
4. Total number of RPE Cells?
a. What increases w/in RPE cells with age?
5. What happens around the Optic Disc? what else?
1. w/in ON decrease --> Increase diameter of VERTICAL CUP.
2. Thickens; --> DIMMER FLR.
3. DECREASES; Scotopic function does not change.
4. Decrease SIGNIFICANTLY.
a. Lipofuscin and Drusen.
5. Atrophy (PPA); Also in Posterior Pole (Decrease in Pigmentation in RPE/Choroid); Peripheral Atrophy (PAVINGSTONE DEGENERATION)
1. Pyramidal Motor Pathway
a. Starts where?
c. Form what in the FOREBRAIN?
d. Fibers innervating CNs break from the path in parts of the Middle Pons and Middle Medula...what's the TRACT CALLED?
e. DECUSSATES where? Becomes what TRACT?
f. Remaining fibers?
2. A Lesion ABOVE the MEDULLA will cause motor problems where?
1. a. Motor Cortex
b. Role in Complicated Voluntary Movements
c. Pyramidal Motor cell axons --> Form INTERNAL CAPSULE
d. CORTICOBULBAR TRACT
e. CAUDAL MEDULLA (85-90%) cross...LATERAL CORTICOSPINAL TRACT
f. ANTERIOR CORTICOSPINAL TRACT...decussate at SPINAL CORD.
1. Reticulospinal Pathway
b. Fibers: Origin?
c. How do they travel?
1. a. Help Control Complex Voluntary Movements; Integrate SENSORY INFO to Direct Motor Control.
b. Reticular Formation w/in Pons and Medulla
c. Travel IPSILATERALLY then synapse w/neurons at every level of the SPINAL CORD.
Neurophysiology (3): Tectospinal Pathway
2. Origin of Fibers?
3. Cross where?
4. Descend to what?
5. Synapse where?
1. Reflex head movements in response to Visual Stimuli
2. SUPERIOR COLLICULUS
4. Descend thru PONS and MEDULLA, traveling ANTERIOR to the MLF.
5. Cervical level of SPINAL CORD
Neurophysiology (4): Auditory Pathways
1. What 2 Nerves form CN8?
2. Cochlear Nerve
a. Origin of Fibers?
b. Travel thru what?
c. 2nd order neurons? First location of what?
d. 3rd Order neurons?
1. COCHLEAR and VESTIBULAR NERVES
a. Info to PRIMARY AUDITORY CORTEX, Cerebellum, Spinal Cord...Hearing and Balance.
2. a. SPIRAL GANGLION of the Cochlea.
b. Organ of Corti; Exit thru INTERNAL MEATUS and end at cells bodies in Cochlear Nuclei of the Medulla.
c. Descend on both sides of the Trapezoid Body to the SUPERIOR OLIVARY COMPLEX in Brainstem; of BILATERAL AUDITORY INPUT.
d. From Superior Olivary Complex (3rd order neurons) form LEMNISCUS PATHWAY and synapse in INFERIOR COLLICULUS of Midbrain and MGN in Thalamus (4th order neurons) then travel to PRIMARY AUDITORY CORTEX.
Neurophysiology (5): Vestibular Pathways
1. Vestibular Nerve
a. Made of what?
b. Join Cochlear nerve of CN8 and carry what?
c. Fibers project to what?
d. Primary ascending fibers: from Superior and Lateral Vestibular Nuclei do what?
e. Ascending Fibers from Superior and Medial Vestibular Nuclei travel thru what?
f. Ascending Fibers: Inf and Medial Vestibular Nuclei?
g. Descending Fibers: Lateral Vestibular Nuclei?
h. Descending Fibers: Medial Vestibular Nuclei?
1. a. Axons from Vestibular Ganglia at DISTAL END of INTERNAL AUDITORY MEATUS.
b. Sensory info from SEMICIRCULAR CANALS and OTOLITH ORGANS of the ear.
c. 4 Vestibular Nuclei; Cerebellum (via Inf. Cerebellar Peduncle...movements for balance)
d. Sensory info to THALAMUS --> Fibers to PRIMARY VESTIBULAR CORTEX
e. Travel thru MLF to CN 3,4, 6 --> Help coordinate head and eye movements.
f. travel to CEREBELLUM...coordinate balance.
g. form LATERAL VESTIBULOSPINAL PATHWAY ...control movements that let us walk upright.
h. MEDIAL Vestibulospinal Pathway. Integrate Head Movements w/Eye Movements.
Neurophysiology (6): Spinothalamic Pathway
a. Nerve endings in Periphery synapse where? Fibers then leave this, cross the MIDLINE and become what?
b. Fibers remain CONTRALATERAL until they terminate where?
1. PAIN and TEMPERATURE info from the BODY.
a. At SUBSTANTIA GELATINOSA --> Cross midline --> LATERAL SPINOTHALAMIC PATHWAY.
b. in VENTRAL POSTERIOR THALAMUS (VPL)
Neurophysiology (7): Trigeminothalamic Pathway
3. Axons travel where?
4. Axons from neurons w/in Trigeminal complex cross what?
5. LESION in TRIGEMINOTHALAMIC PATHWAY above crossover point will do what?
1. Pain and Temperature info from the Face.
2. Trigeminal Ganglion Cells.
3. Descend into Medulla...synapse onto 2nd order neurons (SPINAL TRACT of CRANIAL NERVE V)
4. Cross spinal column in medulla and ascend Contralaterally until they terminate in the thalamus.
5. Cause loss of pain or temperature info from the Contralateral side of the face
Neurophysiology (8): Medial Lemniscus Pathway
1. TOUCH, PRESSURE, VIBRATION
2. Peripheral info (Upper Body: CUNEATE TRACT); Lower Body: GRACILIS TRACT ---> Cuneatus and Gracilis Nuclei in Caudal Medulla. ---> CROSS Midline and become INTERNAL ARCUATE FIBERS --> Terminate in the VPL.
1. Scan of choice for what?
2. Uses what?
3. Used for Dx and Management of what eye issue?
4. Cells--> Apoptosis ---> What enters?
1. BONE and CALCIFICATION and EMERGENT SITUATIONS
2. Ionizing radiation --> 3 mm thick cross-sectional images and compares calcium density
3. ORBITAL FRACTURES
4. Calcium. Increases Density of the Tissue.
1. METABOLIC ACTIVITY OF TISSUES is analyzed....CANCER METASTASIS monitoring.
1. Generally: Diseased tissue has what?
1. Higher water Content than healthy...so more free protons.
2. Severe Claustrophobia, Magnetically implanted devices.
1. LGN Location
1. Dorsolateral part of Thalamus
2. Retinal Ganglion cells (Drivers for LGN Output); Superior Colliculus; Feedback from V1.
3. Magno: 1, 2 (Ventral); Parvo (3-6) (Dorsal); Koniocellular Layers (b/w each of layers 1-6)
Visual Pathway: LGN Travel
1. Medial --> Lateral = ?
2. Anterior --> Posterior = ?
3. Dorsal --> Ventral = ?
1. Fovea --> Peripheral VF
2. Inferior --> Superior VF
3. SAME SPOT in VF
Visual Pathway: Receptive Field of LGN
1. Types of Receptive fields?
2. Parvo Cells?
3. Magno Cells?
4. Konio Cells?
2. most sensitive to Red-Green, Fine detail (High spatial frequencies), slow motion (low temporal frequencies) and slower speed of transmission of visual signals
3. Monochromatic, Fast movements (High temporal frequencies), large details (low spatial frequencies)
4. Respond to Blue-Yellow Contrast
Visual Pathway: V1
1. First location of what kind of processing?
2. First location to evaluating what?
3. Discriminates what?
4. Layer 4: receives PRIMARY INPUT from what?
a. Cells are organized into what?
b. Purpose of these cells?
5. Layer 3?
6. Layers 5 and 6?
7. Which layer provides DIRECT FEEDBACK to the LGN?
1. BINOCULAR PROCESSING
2. Size, Orientation, Direction of Movement of stimulus
3. Shape and Texture of Objects
a. OCULAR DOMINANCE COLUMNS
b. respond to visual input from one eye. Organized into HYPERCOLUMNS (ocular dominance column from one eye combined with an Orientation column (cells that respond to a specific orientation))
5. Sends axons to other cortical layers
6. Sends axons to SUBCORTICAL AREAS (Superior Colliculus, thalamus, midbrain, pons)
7. Layer 6.
Visual Pathway: V2-V5
3. Inferotemporal (IT) CORTEX: Purpose?
4. Middle Temporal (MT) Cortex: Purpose?
5. Superior Colliculus?
6. Frontal Eye Fields?
1. Lateral part of Occipital Cortex
2. Complex processing of visual info.
3. Identifies OBJECT (WHAT)
4. Identifies Spatial relationship of object to its surroundings (WHERE)
5. Gets info from V1 and fibers from Posterior Optic Tract going to LGN. SACCADES, VISUAL ORIENTATION, FOVEATION! (Does not analyze visual input for perception)
6. Gets info only from V1. Found in FRONTAL LOBE: Pupillary response to NEAR OBJECTS; Activates during INITIATION of Voluntary and Reflex Eye Movements
Visual Pathway: Receptive Field Properties (Visual Cortex Cells)
1. Simple Cells
2. Complex Cells
3. Hypercomplex Cells
1. Elongated Center-surround Receptive Fields
a. Orientation of Stimuli; Detect Complex structures (BARS and EDGES) (Probably made up of input from multiple circular center-surround RFs of LGN Cells)
2. Higher level details; Motion and Orientation of Visual Stimuli. NO CENTER-SURROUND ORIENTATION. Made up of input of MANY SIMPLE CORTICAL CELLS
3. Combined input from many Complex cells. Stimuli of a SPECIFIC LENGTH and ORIENTATION.
1. What does it do?
2. Electrical Potential: Lowest after how many minutes of Dark Adaptation?
3. Arden Ratio?
a. Greater than what is NORMAL?
b. What is Subnormal?
4. Can be helpful for what diseases?
1. Measure difference in electrical charge b/w front and back of the EYE. (HEALTH OF RPE)
2. 8 minutes
a. 10 minutes
3. Light Rise/Dark Trough (Indicates Health of RPE)
c. less than 1.65
4. BESTS DISEASE; Stargardt's Disease, Advanced Drusen, and Patterned RPE Anomalies.
2. Activity of what?
3. Pt has to do what?
4. Pt tested under what conditions?
5. ERG Wave
a. A Wave
b. B Wave
c. C Wave
d. Electronegative ERG is characterized by loss of what?
6. Rod:Cone Proportion?
a. % of Rod contribution to b wave?
b. % of Cone contribution to b wave?
1. Records graded potentials.
2. OUTER RETINAL LAYERS activity. (Photoreceptors and Bipolar cells). NOT GANGLION CELL LAYER
3. Maximally dilated. Dark Adapted for 45 minutes
4. Dark-adapted and Light-adapted conditions (isolates rod and cone function)
5. a. Negative wave. Photoreceptor activity
b. Positive wave. Bipolar and Muller cells
c. Positive wave. RPE CElls. (rarely evaluated). EOG = Best choice for RPE Function
d. Loss of B-Wave
1. Pattern ERG?
2. Multifocal ERG?
3. Serial ERG?
4. RP: Characterized by what?
a. When will ERG look abnormal?
1. Targets Ganglion cells...uses a COMPLEX STIMULUS instead of a simple flash of light.
2. records responses in multiple locations w/in the retina. Lets us LOCALIZE a RETINAL DISEASE
3. Track Intraocular foreign bodies that can't be removed
4. Vessel attenuation, bone-spicule pigmentation, waxy optic disc pallor.
a. Early RP. Only Scotopic (Rod) ERG is abnormal.
Late Stage: ERG completely extinguished d/t poor function of rods and cones.
1. Does what?
2. What does a Pt do?
3. Normal VEP?
4. Can detect an anomaly b/w what?
5. VEPs: Can be helpful in diagnosis and evaluation of conditions including what?
1. Analyzes Electrical response (latency) of brain activity to a visual stimulus
2. Wires put on scalp that overlies V1. Pt sits and stares at an alternating checkerboard pattern
3. Large Positive wave that peaks at 90-110 msec after initial stimulus presentation. Waves peak after 110 msec = ABNORMAL
4. b/w fovea and V1 but CANT localize defect
5. Optic Neuritis, Optic Nerve Tumors, Retinal Disorders, Demyelinating Diseases
1. What is the Tectotegmental tract?
a. What happens if this tract is damaged?
b. What is this Dz associated with? (3)
2. After synapsing on EW, what pathway is taken?
3. The Near Triad Reflex is mediated by what input?
1. Pupillary Fibers --> Superior Colliculus --> Pretectal Nucleus --> I/L and C/L EW Nuclei.
a. Can cause ARGYLL-ROBERTSON PUPIL (Light-near response dissociation)
b. Neurosyphilis, Diabetes, Alcoholism
2. Pre-Ganglionic PSNS Fiber --> Ciliary Ganglion --> Post-Ganglionic PSNS Fibers to Iris Sphincter and Ciliary Muscles.
3. Via Supranuclear Input from the FRONTAL EYE FIELDS which activates EW nucleus to cause pupil constriction.
Relationships b/w Pupillary Pathways and CNS
1. What inhibits actively the EW nucleus?
a. When uninhibited, EW neurons constantly fire APs to Sphincter muscle, causing what?
b. Sympathetic Stimulation during waking hours does what?
c. During SLEEP, or Anesthesia, what happens?
1. SNS via Supranuclear Control.
b. Sympathetic Stimulation Causes SUPRANUCLEAR INHIBITION --> Decrease in EW activity --> Normal Pupil Size
c. Supranuclear input is reduced --> Increase in EW activity --> MIOTIC Pupils
1. Goldmann Applanation Tonometry
a. Size of probe?
b. Based on what Law?
c. Assumes all cornea's are what thickness?
2. Noncontact Tonometry
3. PASCAL Tonometry
1. a. Diameter: 3.06 mm
b. Imbert-Fick Law (Pressure inside an infinitely thin, dry sphere, covered by a thin membrane is EQUAL to force needed to just flatten that sphere). So, Force of TF surface tension cancels opposing elasticity of the cornea.
c. 520 um. (Overestimate IOP in thicker corneas).
2. Air Puffer. Flattens a circular area of the cornea. IOP measured b/w Time to start airstream and Peak response of Photocell. IOP is variable.
3. Dynamic Contour Tonometry. Tono Tip looks like the shape of the cornea when pressure on both sides of the probe is equal. Idea is to minimize corneal thickness on IOP measurement.
1. Avg IOP?
2. 2 Standard Deviations?
3. 3 Standard Deviations?
4. When is IOP highest?
5. Normal IOP Variation in normal people?
6. IOP Variation possible in Glaucoma patients?
1. 15.5 mmHg
2. 21 mmHg
3. 22 mmHg
4. At night (12-6 AM)...Diurnal variation.
5. 2-5 mmHg
6. 10 mmHg or more.
Factors Controlling Aq. Production
1. What 7 things can DECREASE Aq. PRODUCTION?
1. A-2 Agonists
4. Cardiac Glycosides
5. Hyperosmotic Agents
6. Significant Decline in BP (minimal effect)
7. Uveitis (Inflamed, sick CB produces LESS AQUEOUS)
1. Corneoscleral Outflow
a. Drains how much?
c. Rate of Drainage depends on what?
2. Uveoscleral Outflow
a. Drains how much?
c. Rate of drainage depends on what?
1. a. 2.25 uL/min (80% of Aq. Outflow)
b. AC --> TM --> Schlemm's Canal --> Episcleral veins drain Aq from Schlemm's Canal
c. PRESSURE. So...as IOP increases, Aq. Drainage increases...but if Acutely elevated, Schlemm's Canal may collapse on itself, preventing entry of Aq. Humor into the Venous System.
2. a. 0.25 uL/min (20%)
b. Aq. --> Ciliary Stroma --> Surrounding vessels of Venous system.
c. INDEPENDENT of IOP!
Aq. Outflow (2)
2. About how long does it take to drain the total volume of Aq. Humor? (How long for it to be completely replaced)
3. What are 2 Conditions that can increase EVP?
1. F out = Corneoscleral (IOP-EVP) + Uveoscleral
a. F out = Aq. Outflow
b. EVP: Episcleral Venous Pressure
2. ~100 minutes. (Total volume is 250 uL)
3. Sturge-Weber Syndrome and Arteriovenous Fistulas.
Factors Influencing IOP
1. 6 of them. Name them and how they affect IOP.
1. Body position: IOP Highest in Supine position
2. Blinking/squeezing eyes/straining: Increase IOP
3. BP: No consistent effect on IOP
4. Caffeine: transient rise in IOP
5. Corneal Thickness: Thicker = Artificially high readings
6. Prolonged Exercise: Can DECREASE IOP
1. What are the 3 main roles?
1. Maintain pressure and shape of the eye
2. Nutrition to Cornea, Lens, Ant Vitreous, and TM.
3. Collects Waste products and clears out inflammatory products from blood and globe.
1. 250 uL...replaced every 2 hours. (~100 minutes)
2. Slightly hyperosmotic to Plasma d/t Na+ and Bicarbonate
3. 1.025-1.040 relative to Water.
1. how is it formed?
1. Made and secreted by NPCE of ciliary processes. (Involved Diffusion, Ultrafiltration, and ACTIVE SECRETION (Produces the most)).
1. Diffusion: How and where.
2. Ultrafiltration: How and where
3. Active Secretion
a. NA/K/ATPase Pumps
b. Carbonic Anhydrase: What disrupts this enzyme?
1. passive movement of ions across a membrane. Small lipid soluble stuff diffuse out of FENESTRATED CAPILLARIES of CB and into the CILIARY STROMA. (Minimal Role)
2. Passive flow of Blood Plasma from Capillaries to Ciliary Stroma. D/T increase in Hydrostatic Pressure (pressure from the heart) compared to pressure w/in surrounding tissue.
3. Large, Water-Soluble, Charged stuff. Across NPCE against Electrochemical Gradient; Requires ATP. 80-90% of TOTAL Aq. HUMOR FORMATION.
a. w/in NPCE cell. Uses ATP to pump Na+ out of NPCE to Posterior Chamber w/WATER FOLLOWING. Helps maintain Gradient to constantly move Na from Ciliary Stroma into the NPCE.
b. Catalyzes formation of Bicarbonate in the PE Cells. Increases Aq. Production by Increasing Cl- and Na+ flux into the Posterior Chamber.
**CAIs and Oral Cardiac Glycosides.
Factors that Influence Rate of Flow: TM
1. Diabetes: how?
1. PDR --> Neo in Angle --> Obstructs TM and Acute angle closure 2ndary to PAS Formation.
a. Also, CRVO, OIS, and RDs --> Neo of the Angle as well
2. Inflammatory cells Clog TM. PS and PAS can form --> Angle Closure
3. Blunt Trauma --> Bleeding of Iris and/or CB --> Blood in AC --> Impedes Aq. Outflow thru the angle.
Factors that Influence Rate of Flow: Injury to TM
1. Fuch's heterochomic Iritis
2. Glaucomatocyclitic Iritis
3. Angle Recession Glaucoma
1. Chronic inflammation --> Permanent damage to TM
2. Acute inflammation of TM --> Acute and big rise in IOP (Trabeculitis)
3. Trauma to Iris --> Separation of Iris from IRIS ROOT --> Angle recession --> Damage to TM. Angle recession = Very wide Ciliary Band on Gonioscopy.
Factors that Influence Rate of Flow: Occlusions of TM
1. Pseudoexfoliative Glaucoma
2. Pigment Dispersion Glaucoma
1. Old Epithelial Cells of Iris BM and Lens Capsule release pigment and pseudoexfoliative material respectively --> Accumulates w/in Angle and Damages TM
2. Pigment released from Posterior LAYER of the IRIS (usually d/t posterior bowing of the iris against lens zonules) and accumulates w/in the angle. Causes damage to TM.
Composition of Aq. Humor
1. What is it made of?
1. Less protein (less than 1%), more AAs than Plasma.
2. High amts of Vit C. (20x's that of plasma)
3. More lactate than Plasma (d/t Anaerobic Glycolysis in lens and Cornea)
4. Less Bicarbonate Ions than Plasma...slightly more acidic (pH = 7.2)