OCular Phys Flashcards

1
Q

• eyelid closure is the result of the orbicularis oculi muscles, NOT relaxation of the levator muscle

A

Blinking

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2
Q

Spontaneous blinking

A

◦ The most common type of blinking
◦ Resutls from the contraction of the palpebral portion of the orbicularis oculi in the absence of an external stimulus and occurs at an average rare of 12-15 blinks per minutes
◦ Spontaneous blinking helps to maintain the optics and comfort of the eye but stabilizing the tear film. During a spontaneous blink, new tears are secreted and spread across the ocular surface while old tears are pushed medically towards the nasolacrimal drainage system

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3
Q

Decreased rate in spontaneous blinking

A

resutls in decreased tear secretion and an increase in tear evaporation, resulting in dry eye sybdrome and secondary epiphora. A decreased blink rate commonly occurs when reading, watching TV, or after LASIK surgery due to a decrease in corneal sensitivity

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4
Q

Reflex blinking

A
◦ Caused by sensory stumiuli, including 
◦ auditory: loud noises sensed by CN VIII
◦ Touch or irritation: CN V
◦ dazzle: CN II
◦ Menace: CN II 

2,5,8

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5
Q

Cotton swab testing

A

evaluates the health of V1 by determining its ability to initiate reflex blinking in repsosne to an irritating stimulus

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6
Q

What type of reflex blinking does NOT involve the cortex

A

• The efferent loop of reflex blinking in repsosne to auditory, touch/irritation, and menacing stimuli begins in the frontal lobe. The dazzle reflex is the only reflex blink that does NOT involve the cortex. Remember that the efferent loop involves stimulation of the orbicularis oculi via CN VII

DAZZLE

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7
Q

Difference between reflex and spontaneous blinking

A

• Unlike reflex blinking, spontaneous blinking occurs in the absence of an external stimulus. The palpebral portion of the orbicularis is responsible for both spontaneous and reflex blinking

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8
Q

Voluntary blinking

A

◦ The amplitude and duration of voluntary blinking is varied and more prolonged compared to spontaneous and reflex blinking
◦ Winking: a form of voluntary blinking that requires simultaneous contraction of the orbital and palpebral portions of the orbicularis oculi

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9
Q

Eyelid spasm

A

• includes the condition benign essential blepharospasm
◦ Characterized by bilateral, involuntary, sustained twitching and/or closing of the eyelids
◦ Resutls from spasms of the orbicularis oculi, procerus, and corrugator musculature

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10
Q

Tight or forced eyelid closure rewuire

A

contraction of the orbital portion of the orbicularis oculi.

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11
Q

Bells phenomenon

A

normal defense reflex present in about 75% of the population, occurs after forced eyelid closure and is characterized by an upwards and outwards rotation of the globe

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12
Q

Orbital portion of the orbicularis

A

◦ Forced closure
◦ Bells phenomenon
◦ Voluntary blinking

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13
Q

Palpebral portion of the orbicularis oculi

A
◦ Forced closure 
◦ Reflex and spontaneous blinking 
      ◦ A. Horner
		‣ Shorten canaliculi 
		‣ Enlarge lacrimal sac 
	◦ B. Riolan 
		‣ Row, Tight, Divide ant/post (gray line
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14
Q

Meibomian glands

A

sebaceous glands located within the upper (25) and lower (20) tarsal plates of the eyelids that are responsible for secreting the anterior lipid layer of the tears. Blinking stimulates lips release via holocrine secretions

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15
Q

Accessory lacrimal glands

A

tubuloacinar exocrine glands that contribute to the aqueous layer of the tears
‣ Glands of Krause: more numerous and are located in the fornices
• Krause=crease
‣ Glands of Wolfring: less numerous and are found in the tarsal conjunctiva

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16
Q

Glands of Krause

A

Accessory lacrimal gland

In the crease

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17
Q

Glands of wolfring

A

Accessory lacrimal gland

Found in the tarsal conjunctiva, less numerous

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18
Q

Distribution of tears

A

◦ The upper eyelid closes lateral to medically during a blink, spreading the mucin layer of the tears evenly across the corneal epithelium and bulbar conjunctiva to aid in proper tear film formation

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19
Q

Drainage of tears

A

The lacrimal pump theory summarizes how eyelid closure affects tear drainage
‣ When the eye is OPEN, tears passively drain into the puncta via capillary attraction
‣ When the eyelids close during a blink, the muscle of Horner contracts, causing the canaliculi to shorten as they move medially towards the lacrimal sac. This action helps “pump” the tears into the lacrimal sac
‣ as the eyelids close, the orbicularis oculi also contracts, stretching the temporal wall of the lacrimal sac away from the nose. This action crease a negative pressure that helps to draw the tears into the lacrimal sac

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20
Q

Most common bacterial cause of canaliculitis

A

Actinomyces israeli

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21
Q

How does blinking occur

A

from the lateral to the medial canthus and helps to move tears towards the puncta. Blinking also lowers the pressure in the canaliculi, creating a pressure difference between the atmosphere and the lacrimal sac that promotes tear drainage

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22
Q

Protective function of eyelids

A
  • cilia (eyelashes): screening and sensing the environment and induce blink reflexes. 150 UL, 75 LL
  • Glands of eyelid: produce the tear film and help move debris away from the cornea in concern with spontaneous blinking
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23
Q

Functions of tears

A
Optical
Nutritional 
Mechanical
Antibacterial
Corneal transparency
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24
Q

Optical function of tears

A

the primary role of the tear film is to create a smooth optical surface of clear vision. Remember, the largest change in RI occurs between the air/tear film interface

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25
Q

Nutritional role of tears

A

the primary source of O2 for the corneal epithelium is form diffusion of atmospheric O2 through the tear film

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26
Q

Mechanical role of tears

A

the tear film collects debris and moves it away from the cornea during blinking. It also helps to remove metabolic waste products from the corneal epithelial cells

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27
Q

Antibacterial role of tears

A

the aqueous layer of the tear film contains lysozyme, lacrtoferrin, IgA, and other proteins of the immune system

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28
Q

Corneal transparency role of tears

A

the tear film has a specific osmolarity (308) and pH (7.45) that is maintained by the secretory glands and the corneal epithelial cells, thus helping to prevent corneal edema

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29
Q

Total tear film thickness

A

3um

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30
Q

Anteiror lipid layer of tears

A

◦ Composed of free fatty acids, cholesterol and waxy esters. It is secreted by the meibomian glands. The main purpose of the anteiror lipid layer is to slow the evaporation of the aqueous layer of the tears. It also helps to maintain optical clarity
‣ Although blinking is the primary method for releasing lipids from the glands, parasympathetic innervation from nerves surrounding the glands may also increase lipid secretion
‣ Meibomian and zeiss=holocrine secretions and moll=apocrine
‣ Blinking=increased lipid layer

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31
Q

Awusous layer of tears function

A

‣ Provides protection through antibacterial proteins
‣ Provides nutrition by supplying glucose to the corneal epithelium
‣ Adds thickness to the tear film

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32
Q

Aqueous portion of tear film contains the following components

A

‣ Water (the main component of tears)
‣ Electrolytes: Na+, K+, and Cl-
‣ Antimicrobial components: IgA, lactoferrin, lysozyme, beta-lysin, and interferon
• Lysozyme cleaves peptidoglycan bonds in bacterial cell walls
• Lactoferrin chelates Fe2+, an essential nutrient for bacterial cell growth and metabolism
• Beta lysin destroys bacterial cytoplasmic membranes and acts in concert with lysozyme
• Lipocalins: decrease the surface tension to enhance spread abiltiy and act as a carrier for all-trans-retinol. Also blocks Fe2+ from binding to the surface of bacteria
• Vit A: present within the tears in the form of all-trans-retinol. Necessary for goblet cells
• Enzyme cofactors: help maintain membrane permeability of corneal epithelial cells
• HCO3-: buffer for tears
• Solutes: glucose, urea, lactate, citrate, ascorbate, and AA
• Additional protein including albumin, growth factors, interleukins, and VEGF

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33
Q

Composition of the aqueous layer of the tears and age

A

decreased levels of lysozyme and lactoferrin proteins within the tears, as well as an overall decrease in aqueous secretion

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34
Q

Aqueous layer of the tear film and CL wear

A

increase in electrolytes and protein concentration due to increase evaporation of the tears

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35
Q

Aqueous layer of the tear film under closed eye conditions

A

has a higher concentration of IgA and serum albumin compared to open eye conditions. Lysozyme and lactoferrin levels are essentially the same. Decreased pH

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36
Q

What secreted the aqueous layer of the tear film

A

◦ the main lacrimal gland and the accessory lacrimal glands of Krause and Wolfring secrete the aqueous layer of the tear film

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37
Q

Main lacrimal gland innervated by

A

parasympathetic fibers from CN VII (VIdian nerve), sympathetic fibers, and sensory nerves of V1

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38
Q

Accessory lacrimal gland innervated by

A

thought to be innervated by parasympathetic Nerves; however, neural control of the accessory lacrimal glands secretions is not well understood and conclusive researach is unavailable

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39
Q

What glands are responsible for reflex, emotional, and basal tearing

A

Main lacrimal gland

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40
Q

What glands are responsible for basal tearing only

A

Main lacrimal gland and accessory lacrimal gland

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41
Q

Blink reflex

A

‣ The sensory nerves (V1) of the cornea are involved in a reflex arc that causes lacrimation (through parasympathetic stimulation of the lacrimal gland via CN VII), miosis, and a protective blink. The dazzle blink reflex can also stimulate a lacrimal gland secretion

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42
Q

Mucous layer of the tears

A

◦ Consist of an outer mucin layer that interacts with the glycocalyx of the corneal epithelium and helps to spread the tears across the corneal surface, as well as trap debris, bacteria, and sloughed corneal epithelial cells

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43
Q

How are mucin molecules in the mucous layer of the tear film unique

A

they are capable of mixing with lipid AND water, this property allows the mucous layer of mix with the aqueous layer and spread it evenly over the hydrophobic corneal epithelial surface

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44
Q

How is the mucous layer of the tear film produced

A

by the goblet cells of the conjunctiva and the squamous cells of the cornea and conjunctiva
‣ Goblet cells are predominately found in the inferonasal fornix and the bulbar conjunctiva
‣ Goblet cells require vitamin A for development, which is found in the aqueous layer of the tears as all-trans-retinol. Vit A deficiency results in keratinization of the conjunctiva and cornea

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45
Q

Vit A deficiency

A

causes Bitot’s spots (foamy build up of keratin) on the conjunctiva

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46
Q

Nerves and goblet cells

A

◦ Sensory nerves in the corneal and conjunctival epithelium stimulate sympathetic and parasympathetic nerve endings surrounding goblet cells; parasympathetic stimulation causes an increase in mucous secretions.

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47
Q

Mucous fishing syndrome

A

occurs as a result of patients fishing for and removing excess mucous in the conjunctiva. This results in damage to the conjunctival epithelium and a subsequent increase in mucous production, creating an unfortunate cycle that exacerbates symptoms. Dry eye syndrome is the msot common cause of mucous fishing sybdrome

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48
Q

Tear film distribution, structure, and stability

A

• recall that the eyelids play an important role in spreading the mucous layer evenly over the corneal epithelium. The mucin layer interacts with the glycocalyx of the corneal epithelium, allowing the tear film to be evenly spread across the corneal and conjunctival epithelium

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49
Q

How can the stability of the tears be examined

A

by analyzing the TBUT. NaFL is instilled in the eye and spreads evenly through the tears. Over time, the aqueous layer evaporates as a result of an insufficiency lipid layer, resulting in a break up of tears. Blinking promotes secretion of the anterior lipid layer and restores the tear film. A TBUT less than 10s is considered abnormal

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50
Q

Elimination of tears

A

• appx 25% of secreted tear volume is continually lost via evaporation. The remaining 75% of the tear volume drains through the nasolacrimal system or into the systemic circulation via absorption into the conjunctival and/or nasolacrimal vasculature

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51
Q

Total volume of the ocular surface

A

appx 7-9uL. The max amount of fluid the eye can hold within the tear film and the fornices is 20-30uL. Normal tear production is appx 1 uL/minute and the average eye drop contains 50uL. Drop instillation or tear production greater than 1uL/min results intear overflow onto the cheeks (epiphora)

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52
Q

Tear film osmolarity

A

308

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53
Q

What can tear film osmolarity depend on

A

Tear film osmolarity can vary depending on the blink rate, humidity, CL wear, and ocular pathology

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54
Q

What are the main contributors to tear film osmolarity

A

Na+ and Cl- ions within the aqueous portion of the tears are the main contributors to tear osmolarity.
-Ca2+ and K+ are also important components of the aqueous portion of the tears

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55
Q

Ca2+ in the tears

A

essential for hemidesmosome formation in the BM of the corneal epithelium,. Excess calcium can deposit on CL, forming “jelly bumps” that may decrease VA

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56
Q

K+ in the tears

A

helps to maintain the health of the corneal epithelium and has a 4X greater concentration in the tears compared to blood plasma

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57
Q

Dry eyes and osmolarity

A

Dry eye syndrome causes an increase in tear osmolarity. Hypotonic eye drops (osmolarity of 150 mOsm/L) are often utilized in treatment. There is an increase pH in dry eye so we use hypotonic drops to decrease it.

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58
Q

Ph, buffering and temperature of tear film

A

HCO3- within the aqueous layer of the tears are an excellent buffer and can tolerate ophthalmic solutions with a pH ranging from 3.5-10.5. The average pH of the tears is 7.45
‣ The pH of the tears during sleep decreases (becomes more acidic) due to the byproducts of anaerobic respiration
‣ Sleep=decreased O2-increased LA-decreased pH

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59
Q

Most ophthalmic drops are _____

A

Weak bases
Because the pH of the tears is 7.45, most ophthalmic drugs present in the non-ionized form within the tear film, promoting drug absorption across the hydrophobic corneal endothelium.

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60
Q

Middle ear

A

separated from the external ear by the tympanic membrane. Sound waves are amplified 10-20x by the tympanic membrane (eardrum) before being converted into mechanical vibrations and sent into the inner ear. The middle ear contains

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61
Q

Tympanic cavity

A

the space internal to the tympanic membrane (middle ear)

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62
Q

Auditory ossicles

A

the small ear bones, including the malleus, incus, and stapes. These bones are located in the series between the tympanic membrane and the oval window. The malleus is first in the series and is attached to the oval window. The auditory ossicles amplify and transmit vibrations received by the tympanic membrane

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63
Q

Stapedius and tensor tympani muscles

A

dampen the amount of vibrations placed on the auditory ossicles (STRAPEDIUS STOPS SOUNDS)
‣ The stapedius muscle is innervated by a branch of CN VII just before it exits the skull via the styalomastoid foramen
‣ The tensor tympani muscle is innervated by a branch from the mandibualr division (v3) if CN V.

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64
Q

Chords tympani

A

‣ the chorda tympani nerve of CN V and the tympanic nerve plexus (CN IX) travel within but do not innervate the middle ear cavity

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65
Q

Inner ear

A

converts mechanical vibrations into neural signals

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66
Q

Vestibulocochlear organ of inner ear

A

help to maintain balance, receive sound, and contribute to ocular reflex actions

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67
Q

Bony labyrinth of inner ear

A

consists of three parts that are innervated by CN VII:
‣ Cochlea
-vestibulae
-semi circular canals

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68
Q

Cochlea

A

Inner ear

shell shaped portion of the inner ear. Contains the organ of corti that contains hair cells that control hearing

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69
Q

Vestibulae

A

Inner ear
consists of the utricle and saccule that help maintain balance. These organs detect static linear acceleration and cause reflex eye movements (linear VOR) that are equal and opposite to the motion of the head
• The utricle detects horizontal linear movements
• The saccule detects vertical linear movements

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70
Q

Semi circular canals

A

Inner ear
communicate with the vestibule and contain the ampullae that detect angular acceleration (rotational) and cause the reflex eye movement known as the angular VOR

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71
Q

Tympanic membrane the oval window

A

• The tympanic membrane separates the external and middle ear. The oval winded separates the middle and inner ear. The TM is much larger, allowing amplification of sound. The malleus, incus, and stapes bones lie between the TM and OW.

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72
Q

Supranuclear control of saccades

A

◦ Rapid eye movements that maintain fixation (aka foveation) on the object of regard
◦ Horizontal saccades are controlled by the contralateral FEF in the frontal lobe and the superior colliculus. For example, the right frontal lobes controls saccades towards the left

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73
Q

Supranuclear control of pursuits

A

◦ Smooth tracking movements that maintain foveation on slow moving objects
◦ Controlled by the ipsilateral parietal lobe. For example, the right pursuit is controlled by the right parietal lobe, and the left pursuit is driven by the left parietal lobe

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74
Q

Supranuclear control of vergences

A

◦ Control of vergences is presumably located at the level of the brainstem
◦ Divergence and convergence eye movements are likely driven by retinal disparity and help to maintain sensory fusion and stereopsis

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75
Q

If spinning the OKN drum clockwise, what parts of the brain are being used

A

‣ Left FEF and superior colliculus for right saccades

‣ Left parietal lobe for left pursuits

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76
Q

The order of the ear structure

A
External ear 
Tympanic membrane 
Middle ear (malleus, incus, stapes)
Oval window 
Inner ear (VOR)
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77
Q

Corneal epithelium permeability characteristics

A

contains zonula occludens junctions (tight junctions) that force molecules to travel THROUGH the cells rather than passing between them. The epithelium is highlight lipophilic (hydrophobic), limiting the absorption of hydrophilic, ionized molecules

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78
Q

Permeability of the corneal stroma

A

highly hydrophilic. Hydrophilic, ionized substances can easily pass through the corneal structures

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79
Q

Permeability of the corneal endothelium

A

contains macula occludens junctions. The endothelium is highly lipophilic (similar to epi) and allows only lipophilic, non-ionized substances to pass through

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80
Q

UV-C

A

100-280

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81
Q

UV-B

A

280-315

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82
Q

UV-A

A

315-400

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83
Q

What layers protect against UV C

A

Corneal epithelium and bowmans

Anything below 300 so some UV-B too

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84
Q

What structures protect against UV B

A

Lens and vitreous

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85
Q

The cornea transmits light with a wavelgnth of

A

300-2500 (infrared)

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86
Q

The visible wavelengths of light and the cornea

A

tranmistted through the cornea with a high degree of precision. More than 99% of light above a wavelength of 400nm is transmitted through the cornea

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87
Q

What range of UV light is the cornea most sensitive to

A

most sensitive to radiation in the UV-C range (particularly 260-280nm); snow blindness, welder’s keratitis, and tanning sun lamps can cause UV keratitis

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88
Q

What contributes to minimal light scattering, allowing for optical transparency of the cornea

A
Corneal crystallines
Ascorbate (vit C)
Glutathione 
Precise spacing of collagen fibrils in stroma
Avascular 
High water content
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89
Q

Corneal crystllines

A

located in the cytoplasm of epithelial and endothelial cells and help to maintain corneal transparency by limiting light scattering, similar to crystallins in the lens

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90
Q

Ascorbate (vit C) in the cornea

A

and glutathione are located within the epithelial cells and help to protect the cornea from UV rays and free radical scavengers

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91
Q

Precise arrangement of collagen fibrils in the corneal stroma

A

The corneal stroma contains appx 200-250 layers of 30nm lamellae composed of collagen fibrils (n-1.55) that lie within a network of GAGs (n=1.345). Collagen fibrils have a uniform size and are precisely spaced less than one half the wavelgnth of visible light from one another
‣ Proteoglycans (PGs) are present within the ground substance that fills the space between the corneal cells and collagen fibrils and lemellae. The glycosaminoglycan side chains of PGs help to maintain appropriate collagen spacing by forming negatively charged bonds with water molecules
‣ Precise spacing of the collagen fibrils increases destructive interference, thereby minimizing light scattering and increasing transparency

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92
Q

Proteoglycans in the corneal stroma

A

present within the ground substance that fills the space between the corneal cells and collagen fibrils and lemellae. The glycosaminoglycan side chains of PGs help to maintain appropriate collagen spacing by forming negatively charged bonds with water molecules

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93
Q

Precise spacing of the collagen fibrils does what (cornea)

A

increases destructive interference, thereby minimizing light scattering and increasing transparency

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94
Q

High water content of the cornea

A

helps maintain a regular spacing of collagen
‣ Sclera has lower concentration of GAGs compared to cornea, and is thus dehydrated and less transparent compared to the corneal stroma

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95
Q

Proteoglycan composition

A

proteoglycans are composed of a core protein with one or more covalently linked GAG side chains. Sulfonation of the GAG side chains in the corneal stroma allows PGs to bind to water, creating a hydrophilic environment that’s helps maintain the precise spacing of collagen. The major PGs is keratin sulfate

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96
Q

Major proteoglycan in the cornea

A

Keratin sulfate

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97
Q

The most important factors that influence corneal thickness (hydration) and maintain corneal deturgesnce

A

epithelial pump mechanisms, endothelial pump mechanisms, and aquaporins

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98
Q

Corneal deturgescenc

A

state of relative dehydration maintained by the normal cornea that is necessary for transparency; 75-80% stromal water content is optimal. Deturgescence relies on the endothelial (main contributor) and epithelial transports mechanisms

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99
Q

What kind of pumps are on the epithelium

A

NAK

NA/K/Cl cotransporter

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100
Q

Corneal epithelial pump mechanisms

A

NAK ATPase, Na/K/Cl co
-Na+ passively enters the epithelial cell from the tear film covering the anterior surface of the cell. The Na+/K+ ATPase pump actively moves Na+ from the epithelial cell into the corneal stroma, creating a higher Na+ concentration in the stroma compared to the epithelium
-The Na+/K+/Cl- cotransporter utilizes the Na+ concentration gradient to passively move Na+, K+, and 2Cl- from the stroma into the epithelial cells. Cl- and K+ each have their own channels that allow for passive diffusion back into the tears and towards the aqueous humor, respectively
-Movement of K+ into the aqueous humor will stimulate Cl- to move into the tears. Water will follow Cl-, contributing to the dehydration of the cornea.
• The K+ channel has been shown to respond to pH changes within the cornea. A hypoxia cornea will have high acidity and increased thickness due to corneal swelling
• The K+ channel responds by moving more K+ into the aqueous causing more Cl- and H20 to move into the tear film to restore normal corneal thickness

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101
Q

Corneal endothelial pump mechanisms

A

NAK ATPase
‣ Na+ enters the endothelial cell from the corneal stroma via ion exchangers. The Na+/K+ ATPase pump, located on the basolateral membrane of the endothelial cell, pumps Na+ out of the endothelial cell into the aqueous humor, establishing a higher Na+ concentration in the aqueous humor compared to the endothelium
‣ The Na+/H+ pump utilizes the Na+ concentration gradient to move H+ ions out of the endothelial cells into the aqueous in exchange for the transfer of Na+ ions back into the endothelial cells. Movement of H+ ions into the aqueous humor results in a decrease in extracellular pH, causing CO2 to diffuse into the endothelial cell
‣ CO2 is combined with H20 for form H2CO3, which then dissociated into H+ and HCO3- (bicarbonate ions)
‣ Bicarbonate and Cl- move out of the endothelial cell and into the aqueous humor. H20 will then follow, contributing to the dehydration of the cornea

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102
Q

Major factors for water transport across the corneal epithelium and endothelium

A

Cl- excretion and Na+ absorption

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103
Q

Aquaporins

A

◦ Proteins embedded within the apical and basal membranes of corneal epithelial and endothelial cells that regulate bi-directional waters transport

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104
Q

Where does cornea get O2 from

A

• The entire cornea receives oxygen primarily from the atmosphere. The aqueous humor, limbal vasculature, and palpebral conjunctiva caps provide a minor contribution of O2 to the cornea under open eye conditions

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105
Q

ppO2 of the atmosphere

A

155

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106
Q

PpO2 within the tears

A

155

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107
Q

During closed eye conditions, ppO2 of tears

A

55
‣ The superior palpebral conjunctiva (primary contributor) and the limbal vasculature supply the epithelium and the anteiror stroma
‣ The aqueous humor supplies the posterior stroma and endothelium

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108
Q

Corneal edema in the AM

A

• Mild cornea edema occurs after awakening in all healthy individuals; in fact the cornea is always thickest in the AM. Mile corneal edema is due to a build up of lactate from anaerobic respiration and the limited supply of O2 when the eye is closed

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109
Q

Critical ppO2 for the cornea

A

10-20mmHg. A CL that is worn while sleeping must maintain a PP)2 above the critical value. Remember that minus lenses are thinner in the center and thus are likely more capable of transporting O2 compared to plus lenses

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110
Q

Oxygen to the cornea open eye

A

Tears for all layers

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111
Q

Nutrients to the cornea, open eye

A

AA, glucose, Vit C from tears

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112
Q

O2 for cornea during closed eye

A

Lids for the outer layers

aqueous for endothelium

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113
Q

Nutrients for cornea under closed eye

A

AA, glucose, Vit C from aqueous

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114
Q

Formula used for O2 flow to cornea and CL wear

A

J/A=DK/t (P1-P2)

◦ J/A=how much oxygen flows over a certain time
◦ Dk=oxygen permeability of the lens
◦ DK/t=transmissibility, measure of how much oxygen will diffuse thougha contact lens with a given thickness

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115
Q

Proper control of pH within the cornea

A

pH-7-7.3) is essential for maintaining corneal transparency. Decreased levels of O2 (hypoxia) can lead to accumulation of H+ ions produced in glycolysis, resulting in increased acidity of the corneal cells

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116
Q

Decreased corneal pH

A

causes a change in K+ channels, resulting in a massive reflux from the keratocytes with subsequent collagen damage and scar formation

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117
Q

Glucose for the cornea

A

produced for the cornea via anaerobic glycolysis, aerobic glycolysis, and the HMP manophosphate shunt

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118
Q

Glucose cxn in tears

A

low in the tears, but is high inthe aqueous humor. As a result, the aqueous humor is the primary contributor of glucose to all corneal layers.

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119
Q

What is the primary contributor of glucose to all layers of the cornea

A

AQUEOUS

Also serves as the primary source for AA and vitamins for all layers of the cornea

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120
Q

Why are corneal epithelial cells unique

A

because they can store large amounts of glycogen for basal cell mitosis and epithelial wound healing. The endothelium also requires large stores of energy in order to maintain the function of the Na+/K+ ATPase pumps that contribute to corneal transparency

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121
Q

Maintenance epithelial regeneration

A

The entire corneal epithelium replaces itself every 7-14 days
‣ Basal cells are the only mitotic cells in the epithelium. They are derived from differentiating limbal stem cells from the palisades of Vogt
‣ Basal cells differentiate into wing cells and then squamous cells before reaching the corneal surface. Old superficial corneal cells are shed as this process occurs

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122
Q

Traumatic epithelial regeneration

A
  1. Basal mitosis is stopped
  2. Scaffold
  3. Rapid basal cell mitosis

If the BM remains intact, corneal regenerate occurs quickly. If the BM is damaged, corneal regeneration occurs more slowly
‣ Complete healing of the BM (with creation of intact hemidesmosomes) takes appx 8 weeks

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123
Q

Complete healing of the BM (intact hemidesmosomes) takes

A

8 weeks

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124
Q

MMPs and hemidesmosomes

A

‣ Matrix metalloproteinases can degrade hemidesmosome formation. Because corticosteroids and tetracylclines have been shown to decrease th activity of metalloproteinases, the yare often included in the treatment regimen of RCEs
‣ Corneal abrasions result from trauma. RCEs occur in eyes with poor adhesions between the corneal epithelium and BM from previous abrasions or corneal dystrophies

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125
Q

Which corneal layers can regenerated

A

Epithelium

Descemets

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126
Q

Which corneal layers cannot regerenate

A

Bowmans

Endothelium

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127
Q

Stroma regeneration

A

will replace itself if damaged, but with a very different textured tissue. The new collagen is larger and less organized, resulting in a scar.

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128
Q

Which layer of the cornea is always growing throughout life

A

Descemets

Can triple in thickness

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129
Q

Corneal nerves

A

there are NO NERVEs in Descemets membrane or the endothelium. Corneal nerves enter at the level of the mid stroma and travel through Bowmans layer to the corneal epithelium

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130
Q

Tropic function of corneal nerves

A

sensory innervation is essential for epithelial cell maintenance and regeneration
◦ Reduced corneal sensitivity is typical after LASIK and with aging

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131
Q

Neurotrophic keratitis

A

characterized by CN V damage and decreased corneal sensitivity and can be diagnosed with the cotton swab test. HSV and HZV, stroke, and DM are common causes of neurotrophic keratitis

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132
Q

Aging changes of the cornea

A
  • the vertical meridian flattens, resulting in an increase in ATR astigmatism
  • light scattering increases
  • Corneal sensitivity decreases
  • The BM thickens
  • The degree of corneal arcus in the peripheral stroma increases
  • Descemets membrane thickens, causing an increase in the number of Hassal-Henle bodies in the corneal periphery
  • The endothelium cell density decreases as the endothelium becomes thinner with age
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133
Q

Function of the lens

A

• provides 1/3 of the total dioptric power of the eye and allows for accommodation to near objects.

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134
Q

The following occur during accommodation (lens)

A

◦ 1. Parasympathetic stimulation causes contraction of the ciliary muscle, resulting in a decrease in the tension on the lens zonules
◦ 2. The anterior pole of the lens moves forward and the anterior curvature increases
◦ 3. The posterior pole of th lens moves back slightly and the posterior curvature increases
◦ 4. The lens thickness (anterior-posterior dimension) increases and the anterior chamber depth decreases
◦ 5. The lens diameter decreases
◦ 6. The lens power increases

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135
Q

IOP and accommodation

A

accommodation causes a temporary decrease in IOP because the ciliary muscle contraction pulls the scleral spur posteriorly and opens up the pores of the TM. Accommodation may also result in a temporary IOP increase due to a decrease in the depth of the AC because the anterior pole of the lens moves forward, the anterior lens curvature increases and the lens thickness increases. In patients with narrow angles, these changes may induce pupillary block and result in significantly elevated IPO, which are important adverse effects of miotic drugs such as pilocarpine

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136
Q

How does pilocarpine work

A

increases uveoscleral output
◦ Long muscle of CB pulls SS down, open up TM
◦ IOP decreases

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137
Q

Lens and nutrients

A

although the lens is avascular, it has the largest concentration of proteins of any structure in the body and this requires glucose and oxygen from the aqueous in order to maintain the following functions
◦ 1. Production of new lens fibers and protein synthesis
◦ 2. Maintenance of the Na+/K+ ATPase pump that helps to establish a balance between H20 and ions within the lens to maintain lens transparency
‣ The Na+/K+ ATPase pump on the epithelial cells constantly move Na+ into the aqueous humor (and K+ into the lens). H20 ultimately follows Na+ into the aqueous, contributing to lens dehydration and transparency

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138
Q

What do the NAK pumps on the lens do

A

On the epithelium
constantly move Na+ into the aqueous humor (and K+ into the lens). H20 ultimately follows Na+ into the aqueous, contributing to lens dehydration and transparency

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139
Q

How does the lens get glucose

A

70% of the glucose required by the lens is produced through anaerobic glycolysis. Aerobic metabolism is limited to the lens epithelium

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140
Q

Hexokinase and the lens

A

The first step in both aerobic and anaerobic respiration involves the conversion of glucose to glucose-6-phosphate via th enzyme hexokinase. If hexokinase is not available, glucose is converted to sorbitol via the enzyme aldose reductase

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141
Q

Excess sorbitol in the lens

A

can accumulate in the lens, creating an osmotic gradient that favors the movement of H20 into the lens, ultimately causing lens swelling, lens fiber damage, and cataract formation

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142
Q

Diabetes and the lens

A

‣ Excessive levels of glucose in diabetes leads to the accumulation of sorbitol within the lens, ultimately leading to early cataract development and an acute shift in refractive error secondary to lens swelling

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143
Q

What is a lot of needed for lens metabolism

A

A lot of ATP

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144
Q

Effects of glutathione on lens clarity

A

the primary protector against oxidative damage in the lens
‣ Acts as a reducing agent and detoxifies hydrogen peroxide
‣ Transported into the lens from the aqueous but can also be synthesized from lens epithelial cells and superficial fiber cells
‣ Deep fiber cells ad nuclear cells produce minimally glutathione and thus rely on diffusion of glutathione from the superficial fibers and lens epithelial cells

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145
Q

What is the primary protector against oxidative damage in the lens

A

Glutathione

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146
Q

Glutathione and age

A

diffusion diminishes with age and is a factor in the formation of cataracts

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147
Q

Ascorbic acid and lens clarity

A

helps to protect the lens from oxidative damage. Ascorbic acid is found in a much higher concentration in the lens compared to the aqueous humor

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148
Q

What do we want in the lens to have lens clarity

A

Increased crystalline
Increased glutathione
Increased vit C
Decreased Ca2+ (but balanced)

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149
Q

What helps maintain lens transparency

A
  • NAK pumps on the epithelium (NA in, K out)
  • avascular
  • cells lack membrane bound organelles
  • lens fibers packed very close
  • cytoplasm have tons of crystllines
  • very well balanced Ca2+ in lens
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150
Q

Growth of the embryonic nucleus

A

formed from primary lens fibers of the posterior lens epithelium during embryological development. All remaining growth of the lens is due to the production of secondary lens fibers by the anterior lens epithelium

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151
Q

Mitosis of lens fiber cells

A

occurs in the germinative zone of the anterior lens epithelium. After mitosis, lens fiber cells gradually migrate through the transition zone and into the equator, where fiber elongation occurs. During this process, lens fibers lose their membrane bound organelles and acquire crystallins
◦ The anterior lens epithelium has the greatest metabolism demand of all lens components and thus contains a significant amount of mitochondria to produce energy for mitosis. Remember that aerobic respiration is limited to the anteiror lens epithelium!

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152
Q

What has the greates metabolic demand of lens components

A

anterior lens epithelium has the greatest metabolism demand of all lens components and thus contains a significant amount of mitochondria to produce energy for mitosis. Remember that aerobic respiration is limited to the anteiror lens epithelium!

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153
Q

Where is the ONLY place in the lens that aerobic respiration occurs

A

Anterior lens epithelium

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154
Q

Crystlines in the lens and age

A

Alpha cryslines in the lens decrease with age. There are NONE by age 45 in the lens nucleus

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155
Q

What do alpha crystallines do

A

function as molecular chaperones by preventing the degradation of other crystallins. A reduction in alpha crystallins results in an increase in degradation of lens fiber cells and ultimately contributes to cataract formation

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156
Q

Lens thickness and age

A

Increases 0.02mm per year

Diamter relatively stable after teen years

157
Q

Anterior lens capsule and age

A

thickness (produced by the anterior lens epithelium) increases with age. The posterior lens capsule thickness is relatively stable with age

158
Q

Where is the lens capsule the thickest

A

anteiror midperipheral portion of the lens (pre-equatorial region) and is thinnest at the posterior pole. It is the thickest BM in the entire body and is comprised of type IV collagen

159
Q

What is the thickest BM in the entire body

A

Anterior midperiehral portion of the lens capsule.

160
Q

What type of collagen is the lens capsule

A

Type IV

161
Q

ROC of the anteiror and posterior lens with age

A

Decreased (becomes more convex)

162
Q

Center of the lens moves ____ with age

A

Anteirorly

Decreased AC depth

163
Q

AA concentration in the lens with age

A

Decreases

Remember that the lens usually contains higher concentration of AA for protein synthesis compared to the aqueous humor

164
Q

Glutathione and age in the lens

A

activity decreases. Na+, ca2+, and H20 concentrations in the lens increase

165
Q

What increases in the lens with age

A

Na
Ca
H20

166
Q

What contributes to cataract formation in the lens with age

A

Increased Ca
Decreased glutathione
Decreased alpha crystalline

167
Q

Nuclear fibers of the lens with ag

A

begin to lose their nucleus and organelles. They also accumulate a yellow brown pigment that contributes to the formation of a NSC

168
Q

Where does NS cataracts begin

A

begins in the embryonic nucleus and expands to include the fetal nucleus and adult nuclei. It is the most common cataract due to aging

169
Q

RI of the lens

A

• Remember that the embryonic nucleus (center of the lens) has the highest RI (1.41) because it has the highest concentration of crystallins in the lens. Also recall that the Y sutures seen during slit lamp biomicroscopy demarcate the boundaries of the fetal nucleus

170
Q

Function of the iris

A

• regulates pupil size to control the amount of light entering the eye and to reduce spherical, coma, and chromatic aberrations
◦ Pupil size helps to optimize retinal image quality by regulating the amount of light that reaches the retina. For example, the pupil size is larger under dim conditions to increase the amount of light reaching the retina
◦ Smaller pupils reduce SA and chromatic aberrations and incrrease the depth of field

171
Q

Aging changes of the iris

A
  • increase in pigment deposition on the anterior structures of the eye from the posterior pigmented iris epithelium
  • The pupil becomes more resistance to dialtion due to aging changes in the iris sphincter and dilator muscles
172
Q

Functions of the CB

A
  • contains the ciliary muscle for accommodation
  • Produces and secretes aqueous humor
  • Contains the ciliary stroma that contributes to aqueous humor drainage via the uveoscleral meshwork
173
Q

Aging changes of the CB

A
  • aqueous humor formation decreases with age
  • Ciliary muscle contraction DOES NOT decrease with age. Loss of accommodation with age is secondary to changes in the lens

IOP increases in older patietns becauwe of outflow problem

174
Q

Functions of the choroid

A

• provides nutrients to the outer layers of the retina and contains pigment that absorbs excess light that passes through the RPE
• Contains the suprachordal space that serves as a passage way for nerves and artery from their posterior insertion sites to the anterior segment of the eye
• Contains a high protein content relative to the retina, establishing a protein gradient that promotes the absorption of excess H20 from the retina into the choroid
◦ Allows RPE to pump water across

175
Q

Aging changes in the choroid

A

• Bruch’s membrane increase in thickness with age; drusen accumulates on Bruch’s membrane with age (inner colalgenous zone)
• The choriocapillaris decreases in thickness with age
◦ The overall choroidal thickness DECREASES with age

176
Q

Drusen-bruchs becomes ______

A

Hydrophobic

177
Q

Functions of the vitreous

A
  • provides a transparent, unhindered medium for the passage of light. Also acts a UV filter by decreasing the transmission of light at 300-350nm in order to protect the retina
  • Provides structure to the eye and likely cushions the glove (especially the retina and the lens) by absorbing vibrations and other external forces during eye movements and trauma
  • Serves as a storage area for ions and nutrients for the retina and lens, including O2, H20, Na+, K+, Cl-, phosphate, glucose, and proteins
178
Q

Where is there lots of glucose stored in the eye

A

Vitreous

Corneal epi

179
Q

Drugs and the vitreous

A

◦ The gel like consistency of the vitreous decreases the bioavailability of topical drugs entering the posterior segment

180
Q

What kind of collage is the vitreous

A

II

181
Q

Volume of vitreous

A

4mL

182
Q

How much of the total volume of the eye does the vitreous take

A

80%

183
Q

Composition of the lens

A

weighs appx 4 grams and is composed of appx 99% H20 combined with type II collagen fibrils and hyaluronic acid (GAG) molecules that create a gel like consistency

184
Q

HA

A

non-sulfates GAG in the vitreous that provides support to collagen fibers, helps maintain proper collagen fibril spacing, and maintains the viscosity of the vitreous

185
Q

Vit C in the vitreous

A

higher in the vitreous compared to the blood plasma. AA are found in lower concentration in the vitreous than in the blood

• Vitamin C (ascorbate) concentration in the vitreous is as high as 40x greater than in the blood plasma. Vitamin C buffers O2 as it travels from the retinal vessels towards the lens, which helps to reduce oxidative stress and minimize tissue damage. It also protects the retina from other metabolic and light induced free radicals

186
Q

Water content of vitreous

A

99%

187
Q

RI of vitreous

A

1.3345-1.3348

188
Q

Metabolism of vitreous

A

◦ Minimal metabolic activity occurs here. The vitreous acts as a metabolic buffer and storage area for the retina and the lens
◦ Glucose and glycogen storage occurs here and be used to supplement metabolic activities in the retina during anoxic conditions

189
Q

Age and the viteous

A

gel structure of the vitreous becomes more liquified with age. The following is a summary of the aging changes that result in vitreous liquefaction
◦ With increased age, the liquid portion of the vitreous increases as H2O starts to collect into pockets in a process known as liquefaction
◦ These water pockets cause the vitreous gel to break down, resulting in the aggregation of collagen fibrils into floaters

190
Q

Vitreous syneresis

A

‣ The processes of vitreous liquefaction and condensation are collectively referred to as vitreous syneresis. Oxidative damage is thought to induce structural changes in HA, causing changes in HA-collagen network that promote vitreous syneresis

191
Q

Most common cause of PVD

A

‣ Vitreous syneresis is the most common cause of a PVD; risk factors for PVDs include age, myopia, DM, intraocular surgery, intraocular inflammation, and trauma

192
Q

Where is collagen cxn highst inthe vitreous

A

At the base and lowest at the center of the vitreous

193
Q

Concentration of HA and age in the vitreous

A

concentration of HA remains stable from appx age 20-50. After age 50, HA concentration INCREASES

194
Q

Hemodynamic patterns

A

• blood flow and pressure differences in the eye play a pivotal role in maintaining normal ocular function. Current research is focused on this area because disruptions in normal blood flow have been found to be related to several of the core ocular disease processes, including DM, HTN, and glaucoma. The following equation demonstrates the components that influence blood flow through the vessels:
F=((P[arteries]entering tissue)-(P[veins]leaving tissue))/Resistance

◦ Where F=flow, P=pressure, and R=resistance
195
Q

Mean arterial pressure of arteries entering the eye

A

65mmHg

196
Q

Pressure in the episcleral vein leaving the eye

A

15mmHg

197
Q

Perfusion pressure in the eye

A

indicates how easily blood can pass through a given tissue and is the difference between the pressure of blood flow entering and leaving the eye. Perfusion pressure in the eye is approximately 50mmHg
◦ Arteries (65)-veins(15)=50

198
Q

Ocular perfusion pressure (OPP)

A

diastolic blood pressure -IOP. Glaucoma patients with low OPPs are 1.5x more likely to develop progressive optic neuropathy secondary to ischemia

199
Q

If IOP decreases, OPP

A

Increases

200
Q

If IOP increases, OPP

A

Decreases

201
Q

If diastolic;ic blood pressure decreases, OPP

A

Decreases

202
Q

Autoregulation

A

process by which blood vessels alter their diameter (in the absence of neural control) in order to increase or decrease resistance to blood flow. Pericytes are msot likely responsible for autoregulation within the blood supply of the retina and the optic nerve
◦ Remember that a small blood vessel diameter offers more resistance, resulting in a decrease in blood flow. Retinal arteries are smaller than choroidal arteeis and thus offer more resistance

203
Q

Transmural pressure

A

describes the pressure across the blood vessel wall and is determined by subtracting the pressure outside the vessel from the pressure inside the vessel

204
Q

Critical closing pressure

A

pressure at which the blood vessel collapses and blood flow stops

205
Q

Elevated IOP in acute angle closure does what to blood flow

A

reduction in blood flow through the CRA, leading to decrease in perfusion pressure and increase their vessel diameter through autoregulation to improve perfusion. However, if IOP remains acutely elevated long enough, the CRA will reach its critical closing pressure, resulting in a CRAO. Remember that the immediate threat to vision in acute angle closure is a CRAO!

206
Q

Sympathetic innervation to blood vessels

A

◦ Sympathetic fibers are prevalent throughout the uveal tract but they DO NOT innervate the CRA past the lamina cribrosa and therefore do not influence retinal blood flow
◦ Sympathetic innervation causes vasoconstriction of uveal blood vessels

207
Q

Parasympathetic innervation to blood vessels

A

◦ Parasympathetic fibers from the oculomotor and facial nerves are also prevalent throughout the uveal tract. Most prominent in the anterior uvea and has minimal influence on choroidal and retinal blood flow
◦ Causes vasodilation In response to sudden decrease in pressure

208
Q

IOP and EVP

A

◦ IOP must be greater than EVP so aqueous humor can drain from the AC, through the corneoscleral meshwork, and into the venous system

209
Q

IOP and ICP

A

◦ IOP must be greater than the ICP in order to maintain an axoplasmic (pressure) gradient that flows from the optic nerve towards the brain

210
Q

Papilledema results from

A

reversal in the axoplasmic gradient between the eye and the brain due to an increase in ICP. The reversal causes CSF to spill from the subarachnoid space onto the optic disc margins and the surrounding RNFL.

211
Q

IOP and pressure in the retinal and uveal arteries

A

◦ IOP must be lower than the pressure in the retina and uveal arteries, allowing nutrients to be delivered from the choroicapillaris to the RPE cells

212
Q

Protein content must be highest in the ____vasculature

A

highest in the cnoroidal vasculature so excess waters is pulled from the retina, across the RPE, and into the choroid, which promotes the adherence between the RPE and the neurosensory retina

213
Q

Choroidal blood flow

A

the majority of blood flow in the ocular vessels occurs in the choroicapillaris
◦ Huge fenestrations within the choroidal vessels allow nutrients to easily diffuse out of the vessels and into the RPE and the outer 5 layers of the retina

214
Q

Primary responsibility of the choroid

A

provide the outer retina with nutrients such as oxygen, glucose, and vitamin A

215
Q

Blood flow of the CB

A

contains the Major Arterial Circle of the Iris that is formed by anastomoses between the ACAs and the LPCAs
◦ Remember the CB and choroidal caps are fenestrated

216
Q

Iris blood flow

A

contains the minor arterial circle of the iris that is formed by anastomaese of the iris and radial vessels. Blood flows from the major circle to the minor circle to the pupillary margin, and then back again

217
Q

Where are there nonfenestrated caps

A

Iris

Retinal vessels

218
Q

Retinal blood flow

A

has dual blood supply. The inner 2/3 is supplied by the CRA, while the outer 1/3 is supplied by the choroid. Remember that the outer plexiform layer is a watershed area that is supplied by both the CRA and the choroid
◦ The CRA forms two networks of caps within the inner retinal layers. The superficial cap network is in the RNFL and the deep cap network is in the INL
◦ The retinal cap networks becomes very dense around the fovea, but remember that the center of the fovea is avascular. The ventral fovea obtains blood supply from the choriocapillaris
◦ The extreme edges of the peripheral retina ar also avascualr

219
Q

DR results from damage to

A

the blood retinal barrier. Increased blood glucose levels damage pericytes and BM of the retina caps, allowing blood and plasma to leak into the retinal tissue. The most important risk factor for development of retinopathy is duration of DM.

220
Q

Composition of the outer disc segment

A

• the outer segment contains stacks of discs that enclose the photopigments (rhodopsin and iodopsins). In rods, rhodopsin is embedded within the disc membranes. In cones, iodopsins are stored in invaginations of the plasma mamba and (NOT within discs

221
Q

Formation of the disc outer segment

A

• photopigments are produced in the PR inner segment and then travel through the cilium to the outer segment. The discs and plasma membranes that enclose the photopigments are produced in the outer segment

222
Q

Composition of photopigments

A

cyanolabe, erythrolabe, and chlorolabe) are used for photopic vision and color vision. Rhodopsin is the photopigment found in rods that is used for scotopic vision. Cone and rod visual pigments contain the same baud structure
◦ Opsin: membrane apoprotein (allows for varied absorption spectrum)
◦ Chromophore: 11-cis-retinal (vitamin A derivative)

223
Q

Vitamin A and PR

A

◦ Vitamin A gains access to the RPE through diffusion through large fenestrations in the choriocapillaris. Vitamin A is an alcohol retinol that is axidized in the RPE to form 11-cis-retinal

224
Q

Formation of visual pigments

A

light absorption in the outer segment damages the photoreceptors and renders them in need of constant replacement
◦ Rod outer segments are shed in the AM via phagocytosis by the RPE
◦ Cone outer segments are shed and renewed in the evening

225
Q

Stages of the visual cycle shorterend verions

A

Retinol—(RPE)—11-cis retinAl—(into PR+light)—all trans retinal—(RPE)—11-cis retinOl—(RPE)—11-cis retinAL

226
Q

Long version of the visual cycle

A

• the transformation of retinoids due to light exposure and their subsequent movement between the retina and RPE is called the visual cycle
◦ Light absorption by a PR results in the transformation of 11-cis-retinal to all-trans retinal
◦ All trans-retinal moves from the disc lumen into the cytoplasm where it is reduced to all trans retinol
◦ All-trans retinol is transported to the RPE cells where it is converted to 11-cis-retinol. 11-cis retinol is then oxidized to 11-cis retinal
◦ 11-cis retinal is shuttled back to the PR for incorporation into the photopigments in the disc outer segments

227
Q

Stargardts is most often due to a mutation in the ______ protein

A

ABCA4 transmembrane protein that is responsible for moving all-trans retinal from the PR disc lumen to the cytoplasm. This results in the accumulation of all-trans retinal within the PR discs, leading to degeneration of the PR and RPE

228
Q

Phototransduction

A

◦ PRs maintain a slight negative electrical charge of about -50mV in the dark. Na+/K+ ATPase pumps on the inner segment plasma membrane use ATP to pump Na+ out of the inner segment while moving K+ inside the inner segment
◦ Na+ then re-enters the inner segment through Na+ channels located in the outer segment
◦ This flow of cations into and out of the cell under dark conditions is referred to as the dark current
◦ The absorption of light by rhodopsin triggers phototransduction, a biochemical cascade that converts absorbed light into an electrical signal. During this process, the dissociated of rhodopsin triggers the activation of the G protein transducin, leading to a cascade that ultimately results in a decrease in the concentration of cGMP
◦ Decreased cGMP levels resutls in the closure of the sodium channels, resulting in an increase in the negative charge of the cell membrane to -65mV. This hyperpolarization of the cell membrane resutls in a decrease in the release of glutamate to bipolar cells

229
Q

Membrane potential of PR in the dark

A

-50mV is more positive than normal cells due to the dark current

Thus PR are depoalrized and constantly release glutamate to bipolar cells. cGMP keeps Na+ channels open to promote depolarization

230
Q

What is the key event in phototransduction

A

Closure of Na Chanel’s

Effectively shits off the PRs bu decreasing their glutamate

231
Q

APs andPRs

A

PRs do not produce APs, they do graded potentials

232
Q

Phototransduction: dark current

A

◦ PRs maintain a slight negative electrical charge of about -50mV in the dark. Na+/K+ ATPase pumps on the inner segment plasma membrane use ATP to pump Na+ out of the inner segment while moving K+ inside the inner segment
◦ Na+ then re-enters the inner segment through Na+ channels located in the outer segment
◦ This flow of cations into and out of the cell under dark conditions is referred to as the dark current

233
Q

Phototransduction: light

A

◦ The absorption of light by rhodopsin triggers phototransduction, a biochemical cascade that converts absorbed light into an electrical signal. During this process, the dissociated of rhodopsin triggers the activation of the G protein transducin, leading to a cascade that ultimately results in a decrease in the concentration of cGMP
◦ Decreased cGMP levels resutls in the closure of the sodium channels, resulting in an increase in the negative charge of the cell membrane to -65mV. This hyperpolarization of the cell membrane resutls in a decrease in the release of glutamate to bipolar cells

234
Q

Cliff notes of what happens in light during phototransduction

A

Decreased cGMP (close Na channels)
Decreased Na+
Hyperpolarized
Decreased glutamate

235
Q

Glutamate in the retina

A

an excitatory NT releases by al lords, cones, bipolar cells, and most ganglion cells in the vertebrate retina

236
Q

GABA and Glycine in the retina

A

inhibitory NT that are relaeased by horizontal cells and most amacrine cells.

237
Q

1st synapse in the retina

A

OPL (BPH)

238
Q

1st action potential in the retina

A

IPL
(BAG)
Amacrine and ganglion cells use actiona potnetials

239
Q

What cells in the retina use actiona potnetials

A

Ganglion and amacrine cells

240
Q

Bipolar cells receptor fields

A

have a center surround receptive field (spatial antagonism)
◦ Cone cells can hyperpolarize or depolarize the center of a bipolar cells. Thus there are two types of cone bipolar cells that are classified by their respsone to light: ON-center depolarizing or OFF-center hyperpolarizing bipolar cells

241
Q

ON-center bipolar cells

A

inhibited by glutamate and are thus hyperpolarized in the dark. When light is present, less glutamate is released, resulting in depolarization of the ON-center bipolar cells

242
Q

OFF center bipolar cells

A

excited by glutamate and are thus depolarized in the dark. When light is present, less glutamate is released, resulting in hyperpolarization of the OFF-center bipolar cells

243
Q

Rod bipolar cells and light

A

Always depolarize in response to light

244
Q

Horizontal cells

A

receive input from a large number of PRs. They DO NOT have center surround receptive fields
◦ Horizontal cells respond with graded potentials and hyperpolarizae in repsosne to light
◦ Impact the surround responses of bipolar cells by providing inhibitory feedback to PR cells (which then impacts the bipolar cell), or by directly synapsids with the bipolar cell (feed-forward)
◦ Provide lateral inhibition, which helps to fine tune the neural signal sent from neighboring PRs

245
Q

What cells hyperpolarize in light

A

PR
Horizontal cells
OFF center cone bipolar cells

246
Q

Amacrine cells

A

have center/surround receptive fields. They respond with action potentials and always depolarize in repsosne to light
◦ They fine tune the signal between bipolar and ganglion cells (similar to the horizontal cells at the level of the PRs)

247
Q

Ganglion cells

A

have center/surround receptive fields and respond to bipolar cells with action potentials. They are classified into two types based on their repsosne to light: ON-center/OFF-surround or OFF center/ON surround ganglion cells

248
Q

ON-center OFF surround ganglion cells

A

synapse with ON-center bipolar cells and depolarize in repsosne to light

249
Q

OFF center ON surround ganglion cells

A

synapse with OFF center bipolar cells and hyperpolarize in response to light

250
Q

Midget ganglion cells

A

small ganglion cells that have a single dendrite that synapses with one midget bipolar cell, which synapses with a single cone in the fovea, allowing for the resolution of very fine details

251
Q

Aging changes to the retina

A
  • RNFL within the optic nerve decrease, resulting in an increase in the diameter of the vertical cup
  • ILM thickens with age, causing the FLR to become dimmer
  • Rod density decreases with age, although note that scotopic function DOES NOT decline
  • The total number of RPE cells decreases significantly with age. Lipofuscin within RPE cells and drusen increases with age
  • Atrophy increases throughout the retina, including around the optic disc (peripapillary atrophy), throughout the posterior pole (as seen by decrease in pigmentation in the RPE/choroid), and in the periphery (pavingstone degeneration)
252
Q

Pyramidal pathway

A

Crosses at medulla
Voluntary motor
Forms internal capsule in forebrain
Becomes the cortocbulbar tract after decussating
Remaining fibers make up the anterior corticospinal tract and

253
Q

A lesion above the medulla in pyramidal pathway

A

Will lead to problems with motor control on the contralateral side

254
Q

Reticulospinal pathway

A

• involved in the control of complex voluntary movements, as well as the integration of sensory information to direct motor control. These pathways offer an alternative to the pyramidal motor pathway for muscle control
◦ Fibers originate from the reticular formation within the pons and the medulla. They descend ipsilateral and eventually synapse with neurons at the level of the spinal cord

255
Q

Tectospinal pathway

A

• thought to play a role in reflexive head movements in response to visual stimuli
◦ Fibers originate in the superior colliculus. They immediately cross the midline and then descend though the pons and the medulla, traveling anterior to the MLF
◦ Fibers eventually synapse at the cervical level of the spinal cord

256
Q

Vestibulochochlear nerve (CN VIII)

A

cochlear and vestibular Nerves combine to form the vestibulocochlear nerve (CN VIII), which carried info to the primary auditory cortex, the cerebellum, and the spinal cord for hearing and balance

257
Q

Cochlear nerve

A

composed fibers that originate from the spinal ganglion of the cochlea. These fibers travel through the organ of Corti before exiting via the internal meatus and ending at their cell bodies located in the cochlear nuclei of the medulla.
◦ The second order neuron axons ascend on both sides (crossed and uncrossed fibers) of the trapezoid body to the superior olivary complex within the brainstem. This is the first location of bilateral auditory input.
◦ Fibers from the superior olivary complex form the lemniscus pathway and eventually synapse in the inferior colliculus of the midbrain and the medial geniculate body in the thalamus before traveling to the primary auditory cortex

258
Q

Vestibular nerve

A

composed of axons originating from the vestibular ganglion at the distal end of the internal auditory meatus. These fibers join the cochlear nerve of CN VIII and carry sensory information from the semicircular canals and otoliths organs of the ear. Most of the fibers synapse with 4 vestibular nuclei in the medulla and pons. The remaining fibers directly project to the cerebellum via the inferior cerebellar peduncle to control movements necessary for balance

259
Q

Vestibular nerve primary ascending fibers

A

Primary ascending fibers fro the superior and lateral vestibular nuclei carry sensory information to the thalamus which then sends fibers to the primary vestibular cortex

260
Q

Ascending fibers from the superior and medial vestibular nuclei travel through the

A

MLF to the nuclei of CN 3, 4, 6 and help to coordinate head and eye movements

261
Q

Ascending fibers from the inferior and medial vestibular nuclei travel to the cerebellum to help

A

help coordinate balance

262
Q

Descending fibers from the lateral vestibular nuclei form the

A

lateral vestibulospinal pathway that travels along the ipsilateral spinal cord and helps control movements that allow us to walk upright

263
Q

Descending fibers from the medial vestibular nuclei form the

A

vestibulospinal pathway that travels along either side to the thoracic segments of the spinal cord. This pathway helps to integrate head movements with eye movements

264
Q

Spinothalamic pathway

A

• the spinothalamic pathway carries pain and temperature information from the body. Note that thus overall pathway is sometimes called the anterolateral system
◦ Nerve endings in the periphery synapse at the substantia gelatinosa within the dorsal horn of the spinal cord. Fibers that leave the substantial gelatinosa cross the midline and become the lateral spinothalamic pathway
◦ The fibers remain contralteral until they terminate in the ventral posterior thalamus

265
Q

Where does the spinothalamic pathway cross

A

Spine (neck)

266
Q

Trigeminothalamic pathway

A

• carries pain and temperature information from the face. The pathway originates in the trigeminal ganglion cells as well facial pain and temperature receptors that extend into the brainstem at the level of the pons
◦ These axons descend into the medulla (forming a Tracy known as the spinal tract of cranial nerve X), where they synapse onto second order neurons in one of two sub regions of the trigeminal complex of the spinal cord
◦ Axons from the neurons within the trigeminal complex then cross the spinal column in the medulla and ascend contralaterally until they terminate in the thalamus

267
Q

Where does the trigeminothaalmic pathway cross

A

Medulla

268
Q

Medial leminiscus pathway

A

• carries info about touch, pressure, and vibration
◦ Peripheral information from mechanoreceptors in the upper body travels along the cuneate tract, while information from the lower body travels along the gracilis tract (more medially)
◦ These tracts enter at the cervical and lumbar regions of the spinal cord, respectively, and ascend to the cuneatus and gracilis nuclei in the caudal medulla, respectively
◦ Axons from the secondary neurons in this region cross the midline at the level of the medulla and become the internal arcuate fibers. These fibers continue to travel contralaterally until terminating in the VPL

269
Q

Where does the medial leminscus pathway cross

A

Medulla

270
Q

A lesion in the medial lemniscus pathway below the medulla

A

Affects the ipsilateral side, while a lesion above the medulla affects the contralateral side

271
Q

Autonomic pathways

A

• composed of neurons in the CNS and peripheral nervous system that control input to the visceral organs, secretory glands, and smooth muscle of the cardiovascular, digestive, excretory, and thermoregulatory systems of the body. Input from the ANS is NOT voluntary and helps to maintain homeostasis
◦ The ANS is composed of a sequence of two neurons between the CNS and the target tissue. The first (preganglionic) neuron is located within the brainstem or spinal cord. The second (post ganglionic) neuron is located in the autonomic ganglia in the periphery (outside the CNS)

272
Q

Sympathetic nervous system

A

responsible for the fight or flight response. It increases heart rate and BP, dilates the bronchioles, causes vasodilation within skeletal muscles, increases blood glucose levels, and decreases GI motility and blow flow
‣ Pre-ganglionic neurons are located int he thoracic and lumbar sections of the spinal cord in the lateral horn of the grey matter. Their axons ascend the spinal cord to enter the sympathetic chain of ganglia located along the vertebral column
‣ Fibers that carry information to the head and thorax regions synapse within the ganglion of the sympathetic chain. Post-ganglionic fibers within the ganglionic fibers then continue to travel up the spinal cord to their target tissue.
‣ Fibers carrying information to the pelvic and abdominal viscera pass through the sympathetic chain WITHOUT synapsing. They travel to the autonomic plexi that surround the large branches of the abdominal aorta, where they eventually synapse. Post-ganglionic fibers then travel a short distance from the autonomic ganglia to the target tissue
• Autonomic ganglia include the celiac, superior mesenteric, and inferior mesenteric ganglia
‣ Pre-ganglionic sympathetic fibers release Ach. Post-ganglionic sympathetic fibers release NE

273
Q

What is the only gland that innervated directly by pre-ganglionic sympathetic fibers

A

Adrenal gland

274
Q

Parasympathetic nervous system

A

responsible for the rest and digest response. It decreases heart rate, contrasts the bronchioles, increase salivary and lacrimal gland secretions, increases GI motility, and causes pupil constriction and accommodation
‣ Pre-ganglionic neurons are located within the cranial nerve nuclei of the brainstem, or in the 2-4th sacral segments of the spinal cord. The brainstem parasympathetic fibers innervate structures of the head, thorax, and abdomen. The sacral spinal cord parasympathetic fibers innervate pelvic viscera
◦ Post-ganglionic neurons are located within ganglia that are very close or adjacent to their target tissue
◦ Pre and post ganglionic parasympathetic fibers release ACH

275
Q

CT used to scan

A

Bones
Calcification
Urgent

276
Q

What is being compared in a CT

A

Ca2+ density

277
Q

PET scan used for

A

Cancer

Metastasis

278
Q

What does PET compare

A

Glucose uptake

279
Q

MRI used for

A

Soft tissue

280
Q

What does MRI compare

A

Mobile protons

281
Q

Location of the LGN

A

dorsolateral aspect of the thalamus. The following is noteworthy information regarding the LGN

282
Q

Main purpose of the LGN

A

process visual information from the retina before relaying only the most relevant information to the visual cortex. Thus the LGN helps to regulate the strength of the visual signal send to the primary visual cortex

283
Q

Drivers for LGN output

A

axons of the retinal ganglion cells terminate in the LGN and are thought to be the “drivers” for LGN output

284
Q

where does LGN receive info (other than retina

A

ulterior colliculus and feedback from the visual cortex regarding the visual signal. These inputs are believed to be “modulators” of LGN output

285
Q

Axons that leave the LGN

A

Optic radiations

286
Q

Magnocellualr layers of the LGN

A

1 and 2 (bottom)(

287
Q

Parvocellular layers of the LGN

A

3-6 (top)

288
Q

Koniocellular layers of the LGN

A

Located between each of the 6 layers throughout the LGN

289
Q

Each layer of the LGN receives input from

A

only one eye; the type of input is dependent on the location of the object in the visual field. This organization allows fibers from each eye that carry information from the same parts of the visual field to lie adjacent to one another in the LGN (retinotopic mapping)
‣ As an example, when an object is located within the right hemifield of each eye, the layers of the LGN on the left side of the brain will respond in the following manner.
• Layers 1, 4, 6 receive fibers from the contralateral (right eye) nasal retina
• Layers 2, 3, 5 receive fibers from the ipsilateral (left eye) temporal retina

290
Q

Layers 1, 4, 6, of LGN

A

Contralateral nasal fibers

291
Q

Layers 2,3,5 of LGN

A

Ipsilateral temporal retinal fibers

292
Q

Traveling medial to lateral in the LGN

A

corresponds to moving from fovea to peripheral visual field

293
Q

Traveling anterior to posterior in the LGN

A

corresponds to moving from inferior to superior VF

294
Q

Traveling dorsal to ventral in the LGN

A

corresponds to the SAME spot in the VF, but the eye providing input differs with each layer

295
Q

Binocular vision processing and LGN

A

does NOT occur at the LGN level- the LGN neurons are still monocular. The visual cortex (V1) is the first location along the visual pathway to combine monocular input for binocular processing

296
Q

Receptive fields of magno and parvo cells

A

center-surround receptive fields, similar to the bipolar and ganglion cells of the retina. Magno and parvo cells differ to their response to illumination, color, contrast, and motion

297
Q

Parvo cells

A

R-G, fine detail, slow motion, and slower speed of transmission of visual signals

298
Q

Magno cells

A

monochromatic, fast movements, large detail, higher speed of transmission due to larger axons

299
Q

Konio cells

A

B-Y contrast

300
Q

Where does primary visual cortex being

A

outer surface of the occipital lobe and extends anteriorly along the medial surface of the lobe to the parieto-occipital sulcus

301
Q

How many layers in primary visual cortex

A

6

each layer containing two maps (one for each eye) of the opposite visual hemifield (unlike LGN)

302
Q

Activity of V1 cells depends on

A

input from the LGN via the optic radiations (the “drivers” of V1 activity); V1 also receives input from several cortical areas

303
Q

First location in the visual pathway that combines monocular input for binocular processing and evaluation of binocular dipsaorty

A

V1

304
Q

First location in the visual pathway that begins evaluating visual input based on the size, orientation, and direction of movements of the somtulus. Also discriminates the shape and texture of objects

A

V1

305
Q

Layer 4 of V1

A

primary visual input from the LGN. Remember that cells are organized into ocular dominance columns that respond to visual input from one eye only. Ocular dominance columns are further organized into hypercolumns, which combine an ocular dominance column from one eye with an irentiation column.

306
Q

What kind of cells are in layer 4 of the primary visual cortex

A

Non-oreitanted cells
Simple cells
Complex cells
End-stopped cells

307
Q

Simple cells of layer 4 of V1

A

have elongated center-surround receptive fields that respond to orientation of the stimulus. This stimulus must be the correct width, orientation ,and located in the correct position within the receptive field in order for a simple cell to respond. They alsos respond to edges, color, and depth. P cells (of the parvocellular system) are simple cells that are organized into blobs within V1. Blobs respond to color. Interblobs respond to size and orientation

308
Q

Non-oriented cells of layer 4 of the primary visual cortex

A

have center surround receptive fields that do not respond to the orientation of the stimulus. They receive input from the LGN

309
Q

Complex cells in layer 4 of primary visual cortex

A

repsond to objects moving in a certain direction with a certain orientation. They do not repsond to the position of the object in space (the complex cell will respond as long as the object is located somewhere in its receptive field. M cells (of the magno system) are complex cells

310
Q

End-stopped cells in layer 4 of primary visual cortex

A

respond to lines with a specific length

311
Q

Layers 2 and 3 of primary visual cortex

A

processing layers and send cons to other cortical layers

312
Q

Layers 5 and 6 of primary visual cortex

A

send axons to subcortical areas (superior colliculus, thalamus, midbrain, pons). Remember that layer 6 provides direct feedback to the LGN, allowing V1 to regulate its own input

313
Q

V1 in a nutshell

A

examines basic stimulus features before relaying information to more complex processing centers known as the extra striate cortex for further processing

314
Q

V2-V5

A

located on the lateral aspect of the occipital cortex. These areas are responsible for complex processing of visual information. Visual input ultimately travels to two locations within the extrastriate cortex

  • inferotemproal cortex
  • middle temporal cortex
315
Q

Inferotemproal cortex

A

allows for identification of the object (“what”). Involves object recognition, visual attention, and object constancy

316
Q

Middle temporal cortex

A

allows for identification of the spatial relationship of the object to its surroundings (“where”). Involves direction, velocity, motion integration, and figure ground segregation

317
Q

Superior colliculus

A

receives information from V1 and from fibers that exit the posterior optic tract prior to reaching the LGN. The SC controls saccades, visual orientation, and foveation. It does NOT analyze visual input for perception

318
Q

FEF

A

receives into only from V1. Located in frontal lobe. Responsible for pupillary repsosne to near objects and voluntary/reflex eye movements

319
Q

Involuntary saccades

A

initiated by input from the FEF and superior colliculus

320
Q

Simple cell receptive field

A

elongated center curround receptive fields that repsond to the orientation of stimuli and can detect complex structures including bars and edges. Their receptive fields are likely a product of the combined input of multiple circular-center-surround RFs of LGN cells

321
Q

Complex cells receptive fields

A

process higher levels of perceptual detail and respond to the motion and orientation of visual stimuli. Their receptive fields do NOT have a center-surround orientation and are a product of combined input from many simple cortical cells

322
Q

End stopped receptive fields

A

hypercomplex) cells process combined input from multiple complex cells. They can respond to line stimuli of a specific length in addition to orientation

323
Q

Hierarchy of visual processing

A

the visual system processes images in a hierarchiacal fashion, with neurons responding to more basic stimuli feeding information to higher order neurons that respond to increasingly complex images

324
Q

Fovea and visual cortex

A

‣ Visual input from the fovea makes up a large percentage of the visual cortex. This phenomenon, known as cortical magnification of the fovea, allows us to identify small central objects and fine detailed more easily

325
Q

EOG measures

A

difference in electrical charge between the front and back of the eye
‣ The EOG analyzes the health of the RPE by examining differences in electrical potentials that are generated as patients perform eye movements under dark adapted and light adapted conditions
‣ Electrodes are attached near the inner and outer canthus of the eye, the patient is instructed to make a series of right and left movements and the electrical potential is recorded over a period of about 30m
‣ The electrical potential is lowest after about 8m of dark adaptation (dark trough) and is highest after about 10m of light adaptation (light rise)

326
Q

Arden ratio

A

EOG
◦ The ratio of light peak/dark trough is the Arden ratio and provides an indication of the health of the RPE:
‣ Arden ratio= light rise/dark trough

327
Q

Bests disease and EOG

A
‣ The best to have...until you are 50
‣ 5 stages 
	• 1: normal fundus, but decreased EOG
	• 2: 2 egg yolks 
	• 5: 50 years old
328
Q

Arden ratio greater than ____ is normal

A
  1. 8

1. 65-1.80 is considered subnormal, and less than 1.65 is considered very abnormal

329
Q

When is EOG helpful

A

diagnosing Best’s disease, stargardts, advanced drusen, and patterned RPE anomalies

330
Q

◦ Records graded potentials produces within the retina in response to light

A

ERG

331
Q

ERG

A

‣ The ERG represents the activity of the outer retinal layers (PR cells and bipolar cells); it does not include the ganglion cell layer
‣ Prior to performing an ERG, the patient is maximally dilated and dark adapted for about 45 minutes. The retina is then flooded with various rates, wavelengths, and intensities of light stimuli
‣ The patient is tested under dark adapted and light adapted conditions, allowing for the isolation of cone and rod function for analysis
• Rod function is isolated by using a blue flash with a slow flicker in a dim background
• Cone function is isolated by using a red flash with a fast flicker in a bright background

332
Q

3 waves of ERG

A

A=negative, PR activity
B=positive, bipolar and muller cells
C=positive, RPE

333
Q

Electronegative ERG

A

Characterized by loss of B wave

334
Q

Proportion of rods to cones

A

13:1

335
Q

Pattern ERG

A

target the ganglion cells by using a complex stimulus rather than a simple flash of light

336
Q

Multifocal ERG

A

record response at multiple locations within the retina, allowing for localization of retinal disease

337
Q

Serial ERGs

A

can be used to track intraocular FBs that cannot be removed

338
Q

RP

A

characterized by vessel attenuation, bone spicule pigmentation, and wavy optic disc pallor. In early cases of RP, only the scotopic (rod) ERG is abnormal. In late stages of RP, the ERG is completely extinguished due to poor function of the rods and cones
◦ Also has central problems
‣ PSC cataracts, CSME, disc drusen (hyaline body)

339
Q

VEP

A

◦ Analyzes electrical response (latency) of brain activity to a visual stimulus
‣ Wires are placed on the area of the scalp overlying the primary visual cortex within the occipital lobe. The patient sits in front of a screen that displays an alternating checkboard pattern
‣ The abrupt pattern differences of the alternating checkerboard produce responses in the visual cortex within 100ms in adults
‣ A normal VEP can detect an anomaly between the fovea and V1, but it cannot localize the defect

340
Q

VEP can be helpful in the diagnosis of

A

optic neuritis, optic nerve tumors, retinal disorders, and demyelinating diseases (MS)

341
Q

Light response

A
  • afferent pupillary fibers travel with the ganglion cell fibers until the posterior 1/3 of the optic tract, when the pupillary fibers exit and travel within the brachium of the superior colliculus to synapse at the pretectal nucleus in the midbrain
  • The fibers then project from the pretectal nucleus to the ipsilateral and contralateral EW nuclei, forming the tectotegmental tract
  • Pre-ganglionic parasympathetic fibers leave each EW nucleus and travel to the CG within the orbit
  • Post ganglionic parasympathetic fibers project from the CG to the iris sphincter and the ciliary muscle
342
Q

Damage to the tectotegmental tract

A

can lead to argyll Robertson pupil, which is characterized by light-near response dissociation. It is associated with neurosyphillis

343
Q

Efferent parasympathetic fibers responsible for miosis and accommodation being in the

A

EW nucleus

344
Q

Anisocoria is always a result of an ____ pathology

A

Efferent

345
Q

Near repsonse

A
  • the near reflex triad of convergence, accommodation, and pupillary constriction occurs when fixation is shifted from a far to a near point
  • In this case, pupillary constriction is mediated by supranuclear input from the FEF instead of the pretectal nucleus
  • The FEF activates the EW nucleus, which projects fibers to the CG, and then on to the sphincter muscle and ciliary muscle, similar to the light repsosne pathway
346
Q

The light and near repsosne both utilize the ______ and the ______ for pupillary constriction

A

EW nuclei

CG ganglion

347
Q

Relationship between pupillary pathway and the CNS

A

• the sympathetic nervous system actively inhibits EW nuclei through supranuclear control
◦ When uninhibited, EW neurons continuously fire action potentials to the sphincter muscle for miosis
◦ Sympathetic stimulation results in supranuclear inhibition, causing a decrease in EW activity and normal pupil size
◦ During sleep or anesthesia, supranuclear input is reduced, causing an increase in EW activity with resulting miotic pupils.

348
Q

Argyll Robertson pupil

A

ARP=accommodative repsosne pathway

◦ Problem with light response only

349
Q

Aides tonic pupil

A
◦ ADies=Acute Dilated pupil 
◦ Affects light and near response 
	‣ Light response is worse 
	‣ Irregular borders of pupil (vermiform, slow)
◦ Silly Ladies get Adie’s 
	‣ CG affected, young women
◦ Loss of deep tendon reflexes 
◦ Pilocarpine 0.125%
	‣ Would not constrict a normal pupil 
	‣ Increased repcetors in adies 
◦ Complain about near reading
350
Q

Goldman applanation tonometry

A

◦ The probe is designed with a precise size (diameter of 3.06 mm) and weight in order to minimize potential error from the tear film surface tension and corneal elasticity. The probe is used to gently flatten the cornea to obtain a measurement of IOP in mmHg
◦ Goldman tonometry is based on the Imbert-Fick Law, which states that th pressure inside an infinitely thin, dry sphere covered by a thin membrane is equal to the force necessary to just flatten that sphere. It assumes that the force from the surface tension of the tear film cancels the opposing elasticity of the cornea
◦ Goldman’s method assumes that all corneas have the same average thickness of appx 520um. This assumption causes us to over estimate IOP in thicker corneas and to underestimate in thinner corneas

351
Q

What is the avg CCT

A

555

352
Q

Non contact tonometry

A

Based on time interval, most variable

◦ A form of indentation tonometry that utilizes an airstream of known force to flatten a circular area of the cornea. The NCT machine contains a photocell that reaches its optimal output whe n air returns from the corneal surface 
◦ The amount of time between the initiation of the airstream ad the peak response of the photocell is converted to mmHg
◦ IOP measurements are variable and less predictable on compared to Goldmann applanation tonometry
353
Q

Imbert-Fick law

A

◦ Goldman tonometry is based on the Imbert-Fick Law, which states that th pressure inside an infinitely thin, dry sphere covered by a thin membrane is equal to the force necessary to just flatten that sphere. It assumes that the force from the surface tension of the tear film cancels the opposing elasticity of the cornea

354
Q

PASCAL tonometry

A

Good for LASIK, contour, negates CCT

◦ Also known as dynamic contour tonometry. The tonometer tip is contoured and reusable and resembles the shape of the cornea when pressure on both sides of the probe is equal 
◦ The contoured tip helps to minimize the effect of the unique characteristics of the patient’s cornea on the intraocular pressure measurement
355
Q

Average IOP

A

15.5

◦ Two standard deviations=21mmHg (97.5%)
◦ Three standard deviations=22mmHg (99.9%)

356
Q

When is IOP the highest

A

Night (12-6AM), with the peak occurring between 350-530AM

357
Q

24 hours variations of ____ in IOP are common

A

2-5mmHg

358
Q

Glaucoma patients can have a pressure difference of ______ or more throughout the day

A

10mmHg

359
Q

What position has increased IOP

A

Supine

360
Q

Agents that decrease aqueous production

A
◦ BBlockers (AM)
	◦ A2 agonists 
	◦ CAI
	◦ Cardiac glycosides 
	◦ Hyperosmotic agents 
	◦ Significant decline in BP
	◦ Uveitis (the inflamed, sick ciliary body produces less aqueous
361
Q

Aqueous humor balance

A

• in order to maintain the pressure gradient between the posterior and anterior chambers that is necessary for aqueous flow, the amount of aqueous that enters the posterior chamber must be equal to the amount of aqueous that leaves the anterior chamber. This is further complicated by the resistance to outflow inherent in the conventional corneoscleral outflow pathway. Recall that aqueous leaves the anterior chamber through two different routes

362
Q

Corneoscleral outflow

A

Drains 2.25uL/min (80% of aqueous outflow)
‣ Aqueous fowls from the anterior chamber across the TM into schlemm’s canal the episcleral veins drain aqueous from schlemm’s canal
‣ The rate of drainage in this pathway is pressure dependent. In general, as IOP increases, aqueous drainage increases. However, if IOP is acutely elevated, schlemms canal may collapse on itself, preventing entry o aqueous humor into the venous system

363
Q

Uveoscleral outflow

A

Drains only 0.25uL/min (20% of aqueous outflow)
‣ Aqueous drains through the ciliary stroma into the surrounding vessels of the venous system
‣ The rate of aqueous outflow is independent of IOP

364
Q

Summary equation for aqueous outflow

A

F out=corneoscleral (IOP-EVP) + uveoscleral

365
Q

Aqueous produced must be equal to

A

amount of aqueous that is drained from the eye
‣ The total amount of aqueous drainage is a combination of outflow through the corneoscleral meshwork (pressure dependent) and the uveoscleral meshwork (pressure independent)

366
Q

Total amount of aqueous outflow

A

about 2.5 uL/min

367
Q

Total volume of aqueous

A

250uL

368
Q

Total volume of aqueous humor fluid is replaced every ____minutes

A

100

369
Q

Increased EVP and IOP

A

increase in episcleral venous pressure will increase IOP. Wearing a necktie can compress the external jugular vein, which leads to an increase in EVP and a reflex increase in IOP. An acute rise in EVP will result in a 1:1 ratio of increased IOP. Sturge Weber syndrome and AV fistulas are two conditions that can increase EVP

370
Q

Factors influencing IOP

A
  • body position-IOP increased in supine position
  • CCT: thicker CCT cause artificially high IOP readings
  • BP: no consistent effect on IOP
  • Prolonged exercise: decreases IOP
  • Blinking/squeezing eyes/straining: increases IOP
  • Caffeine: occasionally causes a transient rise in IOP
371
Q

Functions of aqueous

A

◦ Maintains the pressure and shape of the eye and providers a transparent, colorless, refractive index to enhance the overall optics of the globe
◦ Provides nutrition for the avascular cornea, lens, anterior vitreous, and TM
◦ Severe as a collection bin for metabolic waste products of surrounding tissues and clears out inflammatory products and blood from the globe

372
Q

Volume of aqueous

A

250uL that is completely replaced every 2 hours

373
Q

How much aqueous is produced and then drained every minute in the eye

A

2.5uL

374
Q

Osmolarity of aqueous

A

Slightly hyperosmitoc to plasma

375
Q

Viscosity of aqueous

A

1.025-1.040

376
Q

Formation of aqueous

A

• recall that aqueous humor is produced and secreted by the NPCE of the ciliary processes. Aqueous production involves the processes of diffusion, ultrafiltration, and active secretion

377
Q

Diffusion of aqueous

A

◦ Involves the passive movement of ions across a membrane baes on ion size and solubility. Small lipid soluble substances are able to easily diffuse out of the fenestrated capillaries of the ciliary body vasculature into the ciliary stroma. Diffusion plays a minimal role in aqueous production

378
Q

Ultrafiltration of aqueous

A

◦ Involves the passive flow of blood plasma from the caps into the ciliary stroma and is caused by an increase in hydrostatic pressure (pressure from the heart) compared to pressure within the surrounding tissue

379
Q

Main contributor to aqueous production

A

‣ Although substances can leave the blood through diffusion and ultrafiltration, most substances must be actively secreted across the NPCE in order to produce aqueous humor. Active secretion of ions across the ciliary processes into the posterior chamber creates a gradient where the aqueous is hypertonic to the blood by appx 5mOsm.

380
Q

Active secretion

A

◦ Involves the active transport of large, water soluble, charged substances across the NPCE cell membranes against an electrochemical gradient; requires ATP
◦ Active secretion accounts for 80-90% of total aqueous humor formation, providing further evidence that alterations in BP have little effect on aqueous humor formation
◦ The pigmented ciliary epithelium and NPCE have several ion transport mechanisms that’s re essential for aqueous formation. A detailed overview van be found in remingtons text. The following is an over simplified summary of key parts of active secretion
‣ Na+/K+ ATPase pump: located within the NPCE cell. It utilizes ATP to pump Na+ out of the NPCE cell into the posterior chamber (with water following); this pump helps to maintain a gradient that constantly moves Na+ from the ciliary stroma into the PCE
‣ carbonic anhydrase: catalyze the following reaction in the PE cells that yield bicarbonate: CO2 + H20–> H2CO3–>H+ + HCO3
‣ Bicarbonate ions are believed to increase aqueous production by increasing Cl- and Na+ flux into the posterior chamber

381
Q

Active transport of aqueous facilitates the movement of

A

Na, Cl-, and bicarbonate ions to create a gradient for water movement and aqueous humor production. Agents that disrupt this process include oral cardiac glycosides (after the Na+/K+ ATPase pump) and CAIs

382
Q

Things that impede aqueous outflow and may lead to glaucoma

A

Covering the TM
Injury of the TM
Occlusions of the TM

383
Q

Covering of the TM

A

‣ Diabetes: proliferative DR may lead to neo and accompanying fibrous tissue in the angle, causing obstruction of the TM and acute angle closure secondary to PAS formation
• CRVO, OIS, and retinal detachments may also lead to neo of the angle
‣ Uveitis: inflammatory cells may impeded outflow by clogging the TM. Posterior and peripheral anterior synechiae can cause angle closure
‣ Hyphema: blunt truama can lead to bleeding of the iris and/or ciliary body, causing blood to accumulate in the anterior chamber and impede aqueous outflow through the angle

384
Q

Injury to the TM

A

‣ Fuch’s heterochromic iritis: results in chronic inflammation that ca permanently damage the TM
‣ Glaucomatocyclitic crisis: acute inflammation of the TM (trabeculitis) that leads to an acute and dramatic rise in IOP. Pausner-Schlausner syndrome. Rx=steroids
‣ Angle recession glaucoma: trauma to the iris can cause separation of the iris from the iris root, resulting in angle recession and damage to the TM. Angle recession is seen as a very wide ciliary band on gonioscopy. Similar to iridodialysis

385
Q

Occlusions of the TM

A

‣ Pseudoexfoliative glaucoma: aging epithelial cells of the iris BM and lens capsule release pigment and pseudoexfoliative material that accumulates within the angle and damages the TM. Looks like bullseye on the lens
‣ Pigment dispersion glaucoma: pigment is release from the posterior layer of the iris (usually as a result of posterior bowing of the iris against the lens zonules) and accumulates within the angle, causing damage to the TM

386
Q

Composition of the TM

A

◦ The aqueous humor has less protein but more AA than plasma. The concentration of protein in the aqueous is < 1% that of plasma, which limits light scattering
◦ The aqueous humor has high amounts of ascorbate (vitamin C); the concentration of vit C in the aqueous is 20x higher than in plasma
◦ The aqueous humor has more lactate than plasma, primarily a result of anaerobic glycolysis in the lens and cornea
◦ The aqueous humor has less bicarbonate ions than plasma and is slightly more acidic (pH=7.2)

387
Q

Blood aqueous barrier

A

• aqueous formation begins with appx 20% of the substances trickling through the cap walls of the major arteriolar circle of the iris, then through the ciliary stroma, and finally across both ciliary epithelial layers before being transmitted through the tight junctions of the NPCE into the posterior chamber via active secretion
◦ Remember, the ciliary stromal caps are fenestrated and allow substances to diffuse out of the vessels. The tight junctions of the NPCE that line the posterior chamber help tp regulate the substances that ultimately form aqueous humor
◦ The blood aqueous barrier consists of tight junctions located in three places: the iris vessles, the endothelium of schlemms canal, and the NPCE

388
Q

Uveitis is the breakdown of

A

Blood aqueous barrier