BIOSYSTEMS: SEMINARS - milestones, vessels, cil., iprgc, vis. field Flashcards

1
Q

Summarise the development of the eye following closure of neural tube [ocular milestones #1]

A

wk 4: closure of neural tube (start); formation of optic vesicles + lens placode (end)
wk 5: formation of lens vesicle + optic cup (start)
wk 6:development of primary lens fibres + optic nerve (start)
wk 7: establishment of hyaloid artery + completion of closure of choroidal fissure (at start)
wk 7-8: migration of precursor cells to primitive neural retina

*tube - placode - vesicles - cup - fibres - nerve - hyaloid - fissure closure - migration precursor cells

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2
Q

What is coloboma? [ocular milestones #2]

A
  • a congenital defect of the eye that occurs due to incomplete closure of the choroidal fissure
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3
Q

Which structures are affected by coloboma? [ocular milestones #2]

A

Depends on which part of choroidal fissure doesn’t close properly.
If anterior: cornea, iris, ciliary body, lens
if posterior: choroid, retina, optic nerve

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4
Q

What does a coloboma-affected iris look like? [ocular milestones #3]

A

Characteristic keyhole pupil in inferior region

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5
Q

When does fusion of coloboma start? [ocular milestones #2]

A

At around week 5 (fusion starts centrally and proceeds outwardly), complete by week 7

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6
Q

List 3 subtypes of coloboma by the structure they affect. [ocular milestones #2]

A
  1. Iris coloboma
  2. Chorioretinal coloboma
  3. Optic nerve coloboma
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7
Q

What does complete iris coloboma affect? What about partial? [ocular milestones #2]

A

Complete: affects pigmented epithelium (PE) + stroma
Partial: only affects pupillary margin (only oval-pupil, not keyhole)

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8
Q

When does chorioretinal colboma and what does it affect? [ocular milestones #2]

A

When posterior part of choroidal fissure won’t close properly.

Affects: RPE, retina, choroid

(also increases risk of retinal detachment)

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9
Q

How does optic nerve coloboma affect the NRR? (ocular milestones #3]

A

Thinning and absence of NRR in infero-nasal portion

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10
Q

Causes of coloboma? [ocular milestones #2]

A

Inherited: mendelian (AD, AR, or X) or chromosomal abberations (often with co-morbidities)

Environmental:

  • drug use (thalidomide)
  • alcohol (foetal alcohol syndrome)
  • Vitamin A deficiency
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11
Q

What is Microphthalmia and how can coloboma cause it? [ocular milestones #3]

A

Abnormally small eyes with abnormalities such as turned eye

Cause: failure to close fissure causes vitreal fluid drainage (vitreal fluid needed for eye development)

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12
Q

Why would a left eye be turning in intermittently in 2 year old px? [ocular milestones #3]

A

May be due to:

  • coloboma assoc. microphthalmia
  • other unrelated EOM defect
  • CN6 defect
  • high hyperopia/anisometropia
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13
Q

Why might the red-eye effect be stronger in photographs for one eye in 2 yo px [ocular milestones #3]

A

May be due to:

  • left eye atrophy of posterior structures, assoc. with chorioretinal coloboma
  • retinoblastoma (cancer at posterior retina) - can lead to white pupil reflex
  • congenital cataract
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14
Q

What clinical observations could you make/check for in a 2yr old px with turned ey intermittently? [ocular milestones #4]

A
  • ask if during specific task
  • check for anisometropia
  • check for VA (drop in VA with coloboma)
  • check for esophoria/tropia (expect large esotropia for coloboma)
  • check for CN palsy (in ocular motility)
  • check for APD (afferent pupil defect) (for optic nerve coloboma)
  • look at back of eye to check for retinoblastoma
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15
Q

What is the normal average size of the optic nerve head? [ocular milestones #4]

A

About 1.70mm horizontal, 1.90mm vertical

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16
Q

Describe the clinical representation of optic nerve atrophy [ocular milestones #4]

A

Manifest as:

  • change in colour and structure of optic disk
  • with variable degree of visual dysfunction
  • ONH = pallor apearance

note: glaucoma is a common cause of optic nerve atrophy

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17
Q

Clinical features of optic nerve hypoplasia? [ocular milestones #4]

A

Abnormally small ONH, gray-pale disc with double peripapillary ring, vascular tortuosity, thinning of RNFL.

Could be assoc. with hypothalamic/pituitary dysfunction

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18
Q

List and describe the 3 layers of blood vessels (ordered from inner to outer layer) [Blood Vessels #1]

A
  1. Tunica intima: single layer of fenestrated endothelial cells (has valves to stop back-flow)
  2. Tunica media: SMCs allowing for vasoconstriction/dilation
  3. Tunica adventitia: layer of type 1 collagen and fibroblasts for anchoring
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19
Q

Compare the 2 Blood Ocular Barriers: blood aqueous barrier (BAB) and blood retinal barrier (BRB) [Blood Vessels #1]

A

BAB: formed by an epithelial barrier located in the Non-pigmented ciliary epithelium and posterior iris epithelium

BRB: located at 2 levels:
outer barrier in RPE - restricts molecule passage to outer segment of photoreceptors
inner barrier in endothelial membrane of retinal vessels - for preserving vessel homeostasis

Both: these layers have “leaky” tight junctions

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20
Q

What artery provides blood supply to the eye? What are its main subdivisions/branches? [Blood Vessels #1]

A

Ophthalmic artery. Is composed of:

  • central retinal artery: supply inner retina
  • lacrimal artery
  • long posterior ciliary arteries: supply iris + cil. body
  • short posterior ciliary arteries: form arterioles in choroid (also supply cil. body)
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21
Q
How do the following affect IOP?
A: Systolic b.p
B: Systemic b.p
C: Obesity:
D: Glaucoma
E: Normal-tension Glaucoma
[Blood Vessels #2]
A

A: Increased systolic b.p – increase IOP via increased capillary pressure within cil. body
B: Increased systemic b.p – affect episcleral venous pressure
C: Obesity correlated with increased IOP
D: Glaucoma – increased IOP via increased blood volume within cil. body
E: NTG - IOP same

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22
Q

What level of Ocular Perfusion Pressure (OPP) is suggested to increase risk of Glaucoma [Blood Vessels #3]

A

Low OPP

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23
Q

How does our body compensate/counterbalance for low OPP? Can this system be impaired? [Blood Vessels #4]

A

A drop in OPP is counter-balanced by autoregulation:

  • vasodilation (the vessels release NO) + tissue oxygen extraction
  • constant BF + oxygen metabolism maintained
  • neuronal function is preserved
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24
Q

What are the biochemical effects of low OPP (ocular perfusion pressure)? [Blood Vessels #4]

A
  • mitochondrial dysfunction
  • oxidative stress
  • glial cell upregulation

All 3 of these things cause ganglion cell damage and apoptosis

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25
Which portions of the cil. body epithelium produce and reabsorb aqueous? [cil. body #1]
Anterior portion: produces aqueous | Posterior portion: re-absorbs aqueous
26
What makes up the ciliary stroma? [cil. body #1]
Mainly collagen fibrils and ground substance. Also contains melanocytes and fibroblasts
27
Describe the parasympathetic innervation pathway for ciliary muscle contraction [cil. body #2]
EW nucleus -- CN3 inferior division -- cil. ganglion -- short post. cil. nerves -- cil. muscle
28
Which part of the trabecular meshwork is draining? Which is non-draining? [cil. body #1]
``` Posterior = draining Anterior = non-draining ```
29
Describe the sympathetic innervation pathway for ciliary muscle relaxation [cil. body #2]
Thalamus/Hypothalamus -- Sup. Cerv. Gang. -- long cil. nerve -- cil. muscle
30
List the Near triad [cil. body #2]
- Accommodation - Convergence - Pupil constriction
31
Describe the 3 sequential steps in the Macknight-Civan model of Aqueous secretion [cil. body #3]
1. Na+ and Cl- are transferred from stroma into PE cell using: Na+/H+ antiport, Cl-/HCO3- antiport, Na+/K+/2Cl- symport 2. Solutes pass into NPE cell - through gap junctions 3. NPE cell releases Na+ and Cl- into posterior chamber (via Na+/K+ atpase and Cl- channels)
32
Through which pathway does the majority of aqeuous outflow occur? [cil. body #3]
TM -- Schlemm's Canal -- Collector Channels -- Aqueous Veins -- Episcleral Veins
33
Effect of increased EVP (episcleral venous pressure) on aqueous outflow? [cil. body #3]
Decreases
34
How do adrenergic drugs lower IOP? [cil. body #4]
Alpha agonists and Beta antagonists alpha receptor is coupled to an inhibitory G-protein and the beta receptor is coupled to an excitatory G-protein for the activation of Adenyl Cyclase (AC)
35
How does pilocarpine reduce IOP? [cil. body #4]
Through ciliary muscle constriction, causing the opening of pores in TM (TM relaxation)
36
Can combining alpha agonists with beta antagonists have a greater effect on IOP reduction? [cil. body #5]
Yes
37
What is the effect of the following drugs on IOP? [cil. body #5]: - Apraclonidine - Brimonidine - Timolol - Betaxolol - Acetazolamide - Dorzolamide
All of them decrease IOP. Timolol decreased by the most (33.2%, it is a beta blocker)
38
What is a likely condition for a px who increases IOP by 4mmHg after 2 minutes of near reading? [cil. body case study]
Progressive Myopia
39
What are ipRGCs? (Intrinsically photosensitive retinal ganglion cells) [ipRGC #1]
A.K.A 'melanopsin retinal ganglion cells' Are a type of rGC that responds to light without rod/cone inputs due to the presence of melanopsin, a light sensitive protein
40
What is the role of ipRGCs? (ipRGC #1]
Play a role in non-image forming light responses: - light/dark cycles (sleep-wake cycles) - pupil light reflexes - melatonin production
41
When were ipRGCs discovered? When discovered in humans? [ipRGC #1]
1923 by Clyde Keeler - noticed mice lacking rods/cones still constricted pupils in response to light found in humans in 2005
42
How do ipRGCs cause pupillary light reflex (PLR)? How does the response compare to rods/cones? [ipRGC #2]
ipRGCs project to the pretectum, which is assoc. with PLR Response is slower than rods/cones (and they require more irradiance than rods/cones too)
43
How do ipRGCs modulate the circadian clock? [ipRGC #2]
ipRGCs signal (excitatory) to the suprachiasmatic nuclei (SCN) of the hypothalamus, which serves as the circadian clock.
44
Why is melanopsin required for normal visual processing? [ipRGC #2]
melanopsin increases in baseline firing increase the amplitude and reliability of responses to fast frequency stimuli
45
What is PIPR and how is it caused by ipRGCs? [ipRGC #3]
PIPR = Post Illumination Pupil Response - a sustained constriction of more than 30 seconds in response to high intensity light ipRGCs are maximally sensitive to short-wavelength (blue) light, and they show SUSTAINED FIRING long after light is switched off
46
How can PIPR be used to monitor and diagnose disease? [ipRGC #4]
- used to monitor glaucoma. PIPR often not affected until late-stage glaucoma - diagnose AMD. PIPR is impaired in early AMD
47
List the components of the visual pathway in order [VisField #1]
``` Retina optic nerve optic chiasm optic tract lateral geniculate body optic radiations primary visual cortex ```
48
Which fibres in the retina are crossed? Which are uncrossed? In relation to Visual Pathway [VisField #1]
Nasal fibres = crossed (cross at optic chiasm) | Temporal fibres = uncrossed
49
List the 4 sections of the optic nerve [VisField #1]
1. Intraocular 2. Intraorbital 3. Intracanalicular 4. Intracranial
50
What conditions may be responsible for the following visual field defects? [VisField #2]: 1. Central Scotoma 2. Paracentral Scotoma 3. Arcuate Defects 4. Ceocentral scotoma 5. Complete blindness of ipsilateral eye
Central scotoma: Subretinal oedema Paracentral scotoma: Glaucoma, Oedema Arcuate defects: Glaucoma Ceocentral scotoma: Intrinsic optic nerve disease Complete ipsilateral blindness: Trauma, Compressive tumour, Inflammation
51
What conditions may be responsible for blind spot enlargement? [VisField #2]
- Compression of nerve fibres - Drusen - Myelinated nerve fibres - Optic nerve sheath meningioma
52
Describe the dorsal and ventral nucleus of the LGN [VisField #2]
Dorsal Nucleus: relay station for primary afferent visual pathway Ventral Nucleus: primitive + no visual function in man
53
Describe the nerve fibre distribution in the LGN [VisField #2]
macula fibres: in dorsal wedge peripheral fibres: torwards ventral side superior retinal fibres: in medial horn inferior retinal fibres: in lateral horn
54
How common are lesions in the LGN [VisField #2]
Rare
55
Define Optic Radiation {VisField #2]
axons from the neurons in the LGN. Carries info about the contralateral visual field from the LGN to the primary visual cortex
56
How is the Optic Radiation divided [VisField #2]
Divided into 3 bundles: 1. central bundle - macular nerve fibres 2. superior bundle - inferior contralateral visual field (passes through parietal lobe) 3. inferior bundle (meyer's loop) - superior contralateral visual field (passes through temporal lobe)
57
What visual field defects do the following LGN lesions cause? [VisField #2]: 1. Temporal lobe lesion 2. Pareital lobe lesion
Temporal lobe lesion: cause contralateral homonymous superior quadrantanopia Parietal lobe lesion: cause contra-lateral homonymous inferior quadrantanopia
58
Describe the role of the pituitary gland. Where is it located? [VisField #3]
Regulates thyroid and adrenal glands. Located in the sella turcica just below the mid-optic chiasm
59
How does pituitary adenoma/tumour affect the visual pathway? [VisField #3]
upwards growing of tumour compresses on the inferior/nasal fibres at the anterior knee of willbrand (causing superior/bitemporal visual defect) Then extends towards posterior knee and compresses superior/nasal fibres (thus causing inferior/temporal defect)
60
Non-visual symptoms of pituitary adenoma? {VisField #4]
- loss of body/facial hairs - loss of appetite - weight gain - fatigue - decreased mental function - low blood pressure + electrolyte abnormalities - loss of muscle mass + tone - stunted growth + delayed puberty