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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

Characteristic keyhole pupil in inferior region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

Thinning and absence of NRR in infero-nasal portion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

About 1.70mm horizontal, 1.90mm vertical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

Low OPP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which portions of the cil. body epithelium produce and reabsorb aqueous? [cil. body #1]

A

Anterior portion: produces aqueous

Posterior portion: re-absorbs aqueous

26
Q

What makes up the ciliary stroma? [cil. body #1]

A

Mainly collagen fibrils and ground substance. Also contains melanocytes and fibroblasts

27
Q

Describe the parasympathetic innervation pathway for ciliary muscle contraction [cil. body #2]

A

EW nucleus – CN3 inferior division – cil. ganglion – short post. cil. nerves – cil. muscle

28
Q

Which part of the trabecular meshwork is draining? Which is non-draining? [cil. body #1]

A
Posterior = draining
Anterior = non-draining
29
Q

Describe the sympathetic innervation pathway for ciliary muscle relaxation [cil. body #2]

A

Thalamus/Hypothalamus – Sup. Cerv. Gang. – long cil. nerve – cil. muscle

30
Q

List the Near triad [cil. body #2]

A
  • Accommodation
  • Convergence
  • Pupil constriction
31
Q

Describe the 3 sequential steps in the Macknight-Civan model of Aqueous secretion [cil. body #3]

A
  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
Q

Through which pathway does the majority of aqeuous outflow occur? [cil. body #3]

A

TM – Schlemm’s Canal – Collector Channels – Aqueous Veins – Episcleral Veins

33
Q

Effect of increased EVP (episcleral venous pressure) on aqueous outflow? [cil. body #3]

A

Decreases

34
Q

How do adrenergic drugs lower IOP? [cil. body #4]

A

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
Q

How does pilocarpine reduce IOP? [cil. body #4]

A

Through ciliary muscle constriction, causing the opening of pores in TM (TM relaxation)

36
Q

Can combining alpha agonists with beta antagonists have a greater effect on IOP reduction? [cil. body #5]

A

Yes

37
Q

What is the effect of the following drugs on IOP? [cil. body #5]:

  • Apraclonidine
  • Brimonidine
  • Timolol
  • Betaxolol
  • Acetazolamide
  • Dorzolamide
A

All of them decrease IOP. Timolol decreased by the most (33.2%, it is a beta blocker)

38
Q

What is a likely condition for a px who increases IOP by 4mmHg after 2 minutes of near reading? [cil. body case study]

A

Progressive Myopia

39
Q

What are ipRGCs? (Intrinsically photosensitive retinal ganglion cells) [ipRGC #1]

A

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
Q

What is the role of ipRGCs? (ipRGC #1]

A

Play a role in non-image forming light responses:

  • light/dark cycles (sleep-wake cycles)
  • pupil light reflexes
  • melatonin production
41
Q

When were ipRGCs discovered? When discovered in humans? [ipRGC #1]

A

1923 by Clyde Keeler
- noticed mice lacking rods/cones still constricted pupils in response to light

found in humans in 2005

42
Q

How do ipRGCs cause pupillary light reflex (PLR)? How does the response compare to rods/cones? [ipRGC #2]

A

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
Q

How do ipRGCs modulate the circadian clock? [ipRGC #2]

A

ipRGCs signal (excitatory) to the suprachiasmatic nuclei (SCN) of the hypothalamus, which serves as the circadian clock.

44
Q

Why is melanopsin required for normal visual processing? [ipRGC #2]

A

melanopsin increases in baseline firing increase the amplitude and reliability of responses to fast frequency stimuli

45
Q

What is PIPR and how is it caused by ipRGCs? [ipRGC #3]

A

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
Q

How can PIPR be used to monitor and diagnose disease? [ipRGC #4]

A
  • used to monitor glaucoma. PIPR often not affected until late-stage glaucoma
  • diagnose AMD. PIPR is impaired in early AMD
47
Q

List the components of the visual pathway in order [VisField #1]

A
Retina
optic nerve
optic chiasm
optic tract
lateral geniculate body
optic radiations
primary visual cortex
48
Q

Which fibres in the retina are crossed? Which are uncrossed? In relation to Visual Pathway [VisField #1]

A

Nasal fibres = crossed (cross at optic chiasm)

Temporal fibres = uncrossed

49
Q

List the 4 sections of the optic nerve [VisField #1]

A
  1. Intraocular
  2. Intraorbital
  3. Intracanalicular
  4. Intracranial
50
Q

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
A

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
Q

What conditions may be responsible for blind spot enlargement? [VisField #2]

A
  • Compression of nerve fibres
  • Drusen
  • Myelinated nerve fibres
  • Optic nerve sheath meningioma
52
Q

Describe the dorsal and ventral nucleus of the LGN [VisField #2]

A

Dorsal Nucleus: relay station for primary afferent visual pathway
Ventral Nucleus: primitive + no visual function in man

53
Q

Describe the nerve fibre distribution in the LGN [VisField #2]

A

macula fibres: in dorsal wedge
peripheral fibres: torwards ventral side
superior retinal fibres: in medial horn
inferior retinal fibres: in lateral horn

54
Q

How common are lesions in the LGN [VisField #2]

A

Rare

55
Q

Define Optic Radiation {VisField #2]

A

axons from the neurons in the LGN. Carries info about the contralateral visual field from the LGN to the primary visual cortex

56
Q

How is the Optic Radiation divided [VisField #2]

A

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
Q

What visual field defects do the following LGN lesions cause? [VisField #2]:

  1. Temporal lobe lesion
  2. Pareital lobe lesion
A

Temporal lobe lesion: cause contralateral homonymous superior quadrantanopia

Parietal lobe lesion: cause contra-lateral homonymous inferior quadrantanopia

58
Q

Describe the role of the pituitary gland. Where is it located? [VisField #3]

A

Regulates thyroid and adrenal glands. Located in the sella turcica just below the mid-optic chiasm

59
Q

How does pituitary adenoma/tumour affect the visual pathway? [VisField #3]

A

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
Q

Non-visual symptoms of pituitary adenoma? {VisField #4]

A
  • 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