IRVAN (Idiopathic Retinitis, Vasculitis, Aneurysms, and Neuroretinitis) Syndrome:

 IRVAN (Idiopathic Retinitis, Vasculitis, Aneurysms, and Neuroretinitis) Syndrome:

IRVAN is a subtype of retinal vasculitis. It is a rare clinical entity of unknown etiology. Some authors have speculated an association with positive P-ANCAs (Perinuclear AntiNeutrophil Cytoplasmic Antibodies) systemic vasculitis and antiphospholipid syndrome.

Risk Factors

Slight female preponderance. There is no race predilection. Young or middle-aged people mainly affected.

Stages

* 1 : Macroaneurysms, exudation, neuroretinitis, retinal vasculitis.

* Stage 2 : Capillary nonperfusion (angiographic evidence)

* Stage 3 : Posterior segment neovascularization of disc or elsewhere and/or vitreous hemorrhage.

* Stage 4 : Anterior segment neovascularization (rubeosis iridis)

* Stage 5 : Neovascular glaucoma.

Diagnosis:

Three major criteria (retinal vasculitis, aneurysmal dilations at arterial bifurcations, and neuroretinitis) and 3 minor criteria (peripheral capillary nonperfusion,retinal neovascularization, and macular exudation) are used to diagnose IRVAN.

Signs

Multiple postequatorial arterial aneurysms in the retina and optic disc head.

* Peripapillary lipid exudation associated with macroaneurysms and retinal vasculitis.

* Retinal hemorrhages in posterior pole.

* Peripheral capillary nonperfusion

* Retinal vascular sheathing

* Swelling of the optic nerve

* Retinal neovascularization

* Optic disc neovascularization

Symptoms

Asymptomatic

Sometimes a patient will not complaint about a loss of vision in spite of having a severe disease because it is not affected during initial presentation.

Unspecific symptoms

For instance , multiple visits for a change of glasses due to blurred vision.

Symptoms of Retinal Vasculitis.

Diagnostic procedures

Fundus Fluorescein angiography:

FFA highlights the arteriolar abnormalities. The aneurysms are more evident and the alterations in arteriolar caliber are more obvious. Leakage of fluorescein from the aneurysms is apparent. 

Patients with IRVAN usually have optic nerve head staining. Disc and/or retinal neovascularization show marked fluorescein leakage. 

The areas of peripheral non-perfusion are easier to appreciate with FFA, especially wide-field FFA.

Complications

Anterior segment:

Iris neovascularization, Neovascular Glaucoma, blind eye, painful blind eye.

Posterior segment:

Disc neovascularization, retinal neovascularization, vitreous hemorrhage, tractional retinal detachment, retinal artery occlusion.

Management

Currently, retinal laser photocoagulation and the use of intravitreal injections of anti-vascular endothelial grow factor antibodies ( anti-VEGF ) are considered within the first line of treatment. 

CORNEAL DYSTROPHIES

CORNEAL DYSTROPHIES

we will discuss very briefly about

corneal dystrophies. we will discuss the corneal lactasias particularly the keratoconus the learning objectives of this lecture.

we want to know and have an overview of

different corneal dystrophies

 we want to know about corneal lactasias

particularly symptoms signsdiagnosis and treatment of keratoconus

what are the corneal dystrophies

the corneal dystrophies are a group of

progressive

usually bilateral mostly genetically

determined

non-inflammatory opacifying disorders

age of onset is usually first to four

decades depending upon the type of

dystrophy

but most of the dystrophies presented in

first and second decade

 different layers of the cornea at each layer is having its own dystrophy and outermost layer is the epithelium which is stratified squamous non-keratinized epithelium

multi-layered the basal cells

are conumnular

then comes the bowman layer which is

acellular superficial layer of stroma

and stroma is a regularly arranged layer

of collagen fibers

and spacing is maintained by

proteoglycans

and desmet's membrane is a thin basement

layer of endothelium

and the endothelium is a single layer of

hexagonal cells

which cannot resonate once

they are designated

so the different layers have

corneal dystrophies and the epithelial

dystrophies

are epithelial basement membrane

dystrophy and measurement dystrophy

and different dystrophies of the

government layers

are the most important is the raised

buckler dystrophy

the stromal dystrophies are less

dystrophy which further divided into

type 1 to 3

macular dystrophies and granular

dystrophy

and in the endothelial layer the folks

endothelial dystrophy is most

important

what is the epithelial basement membrane

dystrophy

it is also known as cogn microcystic map

dot fingerprint

dystrophy onset is usually in the second

decade

and few patients develop recreate

coronal erosions

in the third decade which is very very

painful

and patient is uncomfortable and unable

to perform the day-to-day working

here you can appreciate the different

presentation of this

dystrophy dot like

figures epithelium says

fingerprints like

maps and map like editions

in epithelial basement membrane

dystrophy you can also appreciate

block-like capacities

here you can appreciate in this picture

dot glycoprostration and epithelial

microces

and the sub-epithelial map-like patterns

in the lower

figure

and the other type of epithelial

dystrophy is the amazement dystrophy it

is autosomal dominant

inheritance onset usually in the second

year of life

and in this case you can appreciate

intra epithelial cys

maximal in the central region

and the bowmen layer rhys buckler

dystrophy is the autosomal dominant

inheritance

onset is usually in early childhood with

recruited audience

you can also appreciate

polygonal opacities in bowman's layer

and the sensation of the cornea is

reduced

and usually visual impairment is there

due to scarring

at bowman's membrane level

the stromal dystrophy is the most

important is the lattice dystrophy

in this case inheritance is autosomal

dominant

presentation is in first to third decade

here you can appreciate finds padre

branching lattice lines best seen

on retro illumination.

we briefly discussed the macular

dystrophy

this type of dystrophy is least common

dystrophy

but it is visual impairment is

more serious in this case

of dystrophy there is systemic inborn

error of keratin sulfate metabolism

and inheritance is autosomal recessive

usually presentation is first decayed

with gradual

deterioration of vision

in this picture you can appreciate

macular you can see the focal poorly

delineated spots

in the anterior stroma

with irregular cordial surface may be

present

and opacification of the cornea it

increases with the passage of time

and ultimately full thickness normal

involvement.

CORNEAL ULCER

 CORNEAL ULCER

All right so today we are dealing yet

very important topic and that is the

corneal ulcers frequently we get this

problem that how to differentiate

between the different ulcers when it is

bacterial.

when it is viral where it is

fungal what are the most prominent

features and how to decide the treatment

of choice so all right we'll be starting

with first the most common also and that

is the bacterial answer the ulcer is the most common as we

know now what is the most important

cause of this answer as you know the

most important cause of this also is the

epithelial erosion. whenever there is a

patil erosion due to any of the reason

secondary bacterial infection is very

commonly occurring and the most common

bacteria is actually the staph aureus.

Staph aureus is most common in the world

streptococcus pneumoniae so we have most

common in the word as well as we have

most common in pakistan as well as the most

common factor which is actually

responsible for the corneal ulcer is the

epithelial erosion now because most of

the bacteria are not able to invade the

intact epithelium that is why epithelial

erosion is actually the most common

cause of the secondary bacterial

infection but I will say that some

bacteria are much virulence and those

bacteria which are virulent enough which

are aggressive enough which can invade

the intact epithelium they have the risk

of causing corneal ulcers even when

there is conjunctivitis so for example

if I talk about gonococcus guna gokul

conjunctivitis which is most commonly

the purulent conjunctivitis whenever a

patient this systemic type of gonococcal

conjunctivitis which has systemic

features also like we have urethritis. we

have arthritis in all these cases there

is always a risk of the bacterial

infection in the cornea also there is a

risk of corneal involvement also because

it can invade the intact corneal

epithelium now let us see a list which

can invade the intact corneal epithelium

the first important is the Corney

bacterium tip 3 the first important

bacteria is the Corney bacterium def 3

the second one second is the nazaria go

nori nazaria go nori the third important

is the nazaria meningitidis nazaria

meningitidis then the fourth one is the

Listeria food is the Listeria and fifth

is the H influenza and finally we have

the Shigella now this is again I

important mcq all those bacteria which

can invade the internal epithelium are

these and apart from this they will

always cause corneal ulcers whenever

there is epithelial erosion all right

now because there is lot of vascular

ization which is present in the

bacterial corneal ulcer a very important

complaint of this patients these

patients is the pain in fact I can say

that pain is the most dominant feature

as well as most prominent feature of

those patients who are having the

bacterial corneal ulcer and both is due

to the vascularization because it is so

red like why it is so painful both of

them is occurring due to the

vascularization lot of vascularization

reading lot of pain and lot of

congestion

now these bacteria when they are

invading and they are going inside in

the different layers of the cornea as

they reach inside they can also cause

the uveitis uveitis means are ido site

light

when the inflammation is going to the

deeper layers there is active ulceration

from the superficial layers to the

deeper layers this keratitis which could

have started from conjunctivitis also so

this conjunctivitis then keratitis

is going to the deeper layers also it is

involving the iris and ciliary body it

is causing a reduce eye cleitus and that

is why photophobia

photophobia is again a very important

symptom of these patients plus the

inflammatory cells now these

inflammatory cells when they're

collected inside the anterior chamber

because of their happiness the accidents

will always settle at the bottom now

whenever the exudates are settling at

the bottom.

ANATOMY OF THE LENS

ANATOMY OF THE LENS

let's see anatomy of the lens there's no

blood supply or innervation so it

depends on aqueous for nutrient delivery

and waste removal.

we know that what it

does reflects like some interesting

concept. I guess you look at it with

aging terms of changes sometimes there's

a myopic shift sometimes there's a hyper

optic shift. we know it's always

increasing in curvature but the very

changes in index of refraction can alter

the actual refractive effect of that

Size at birth

versus size in adults so those are sort

of important anatomic considerations if

you're cataract surgeon just remembering

that in adult size is really about five

millimeters thick at most so you got

about five millimeters of depth before

you're puncturing a posterior capsule

with whatever instrument you're using

all right the capsule elastic membrane

type for collagen just remember its

thinnest posterior to four microns

pretty impressive how strong it is

despite its  thin nature there. you

can see it's thickest equatorial and

centrally about 14 microns as annuals

microfibrils composed of elastic tissue

they originate for the non pigmented

epithelium of the ciliary body the

insert in a continuous fashion

equatorial region you can see they

insert just a little bit more central

anteriorly versus posteriorly and with

age of course the fibers regress the

equatorial fibers will progressively

they mostly just an tear in poster

fibers  lenz epithelium is a single layer and of course there's active replication and

the anterior equatorial region as we all

know the newly formed cells as we know

they migrate equatorially and posterior

lis forming new lines fibers losing

their organelles that through that

process and of course because they have

no organelles they depend on glycolysis

class let's see

so those highlights here of course no

cells are lost from the lens the oldest

form the nucleus so you'll see that

fetal or embryonic suture pattern and

newest form the outermost aspect at the

you know the cortex we've seen the lens

sutures onyx those who have looked on

slit lamp exam major digitation z--

their the apical and basal cells. we see

optical zones when you look at a lens so

you might notice that there's sort of

this delineation of an endo nucleus a

central lens component versus the EPI

nucleus or cortical material when you

look at cataracts or a similar finding

except it's not a clear lens obviously

it's a cloud at the some degree there's

no morphologic distinction between the

cortex and nucleus though you know we

have these surgical delineations that we

talk about or discuss when you actually

look at it from a pathology assessment

histologically  there's really no

differentiation lens up to the Lens  cells

 those lens cells look the same

let's see crystalline proteins that make

up a lot of what is left over once the

lens has eliminated its organelles you

see some fascinating concepts about it

and

maybe you should read about this

sometime it's not super exciting as

that I know as you age you start to lose

some of the it says here maybe it's the

next slide here membrane structural

proteins and skeletal proteins or

anything highlight that I could take off

of here while you're reading it here it

is  the increase of water with age this is actually you

know important to understand as we get

older protein aggregates into large

particles they become water insoluble

that's going to result in opacity Claire

reduce clarity or cataract so scatter

they scatter lights of course certain

amount of this process appears to be

normal with maturation of lens cells the

seeing clear lenses with the excess of

it results in the cataract formation.

BUMP OF UPPER EYE LID

BUMP  OF UPPER EYE LID

it's the typical history is the bump

developed over a period of days or weeks the eyelid is not red.

It's not inflamed but there's definite tenderness. Where the bump is located the bump is typically a non-infected occluded oil gland the name of the oil gland is the meibomian gland there are about 50 meibomian glands in each of our upper lids and about 25 meibomian glands in each of our lower eyelids if these glands become obstructed. where the oil that's made in the eyelid. This oil normally produces an oil slick for our tear film to slow down the evaporation rate of our natural tear layer on our eye surface but if these oil glands become obstructed then it's of great concern to the patient the most common treatment that i recommend if the meibomian gland has only been there for a week or less is to apply heat and massage to the eyelid it can take one of two forms if you do it twice a day for about five minutes you can either let hot water from the shower head flow onto the bump and as you massage it you'll liquefy the trapped oil which is semi-solid in the eyelid the heat will liquefy that oil and as you massage it the oil will flow out through the orifices that are just behind the row of eyelashes if you have a shellacean on your lower lid you massage upward if you have a shilazin on your upper lid you massage downward you let the hot water from the hot shower head flow over your eyelid while you're massaging and the eyelid is being heated up if you do that twice a day for a week usually the chalazion  will go away similarly another treatment is to take a hard-boiled egg that's cooked and it's still hot but just not quite hot enough to burn your skin you apply the hard-boiled egg to the upper lid if the chalazin's there or the lower lid if that's where the chalazion is located massage it and again just like hot water it should liquefy the contents of the chalazion and the oil should drain on its own i find there's about a 90%  success rate with this treatment if the has been present for one week or less if you're in the 10 percent that the chalazion does not go away with that treatment that chalazion may kind of just stay with you and so in this particular instance we're going to talk about the patient who contacted us about a month ago she tried the heat but the heat did not make the chalazion go away .  okay so what it is is a blocked oil gland so in your eyelid there are oil glands that run vertically on each lid  glands empty through orifices that are just behind your row of eyelashes so you have a blocked oil gland back there the reason why we wanted you to apply heat was the heat would liquefy the trapped oil that's semi-solid in your eyelid and if you massage it a lot of times it empties through the pores if it's not able to do that we can drain it so we inject the eyelid with an anesthetic you feel that for 10 seconds.

EYE LID DISORDERS

 EYE LID DISORDERS

we'll approach some disorders of the

eyelid here I wanted to do a quick

overview of the anatomy just to orient

ourselves we'll talk about the three

inflammatory disorders - focal

inflammatory disorders known as clays

Ian and horny olam and then a more

diffuse inflammatory disorder called

blepharitis.

which has many causes and

then some other eyelid conditions which

are a little bit less tested  the entropion ectropion and trichiasis certainly though you will

encounter these in clinical practice

especially if we work with a geriatric

population but I would say that these

first three year plays II and cordial

and blepharitis are the most commonly

tested . we're going to talk about and

then tumors these are tumors that occur

elsewhere on the body especially the

skin but I just wanted to briefly talk

about them because they do occur on the

eyelid.So the external I hear some

obvious points the upper lid lower lid

lateral canthus kind of hard to see this

is the right I hear this is the nasal

bridge right here and then the medial

canthus so the lateral medial canthus

are just the ends of the words where the

eyelids come together on the lateral

medial side and this little pink spot

here is probably carbuncle the lacrimal

carbuncle and that's where the tears

come out what you can't see here are

inside is the lacrimal duct which

ultimately empties into the nose and

then the lacrimal gland which is on the

superior and medial aspect of the orbit

orbital septum is just the hole in the

skull where the orbits it's roughly

you'd have to palpate but it's roughly

this area here going a little deeper

you've got the orbital septum as we just

showed the superior and inferior tarsal

flakes the tarsal plates are what give

the eyelid its characteristic structure

and this is just dense connective tissue

then you have the medial and lateral

palpebral ligament and this kind of

holds the eyelid in place then you've

got a laughable sac which ultimately

drains into that carnival

you got three muscles here all the way

are innervated by the facial nerve the

orbicularis oculi muscle muscle which is

traditionally divided up into two parts

and there's the orbital part which is

responsible for forced closure that's

more on the periphery here and then

closer to the eyelids are the palpebral

part and this is responsible for

blinking fin blinking the procerus

muscle sits on the nasal bridge this is

responsible for drawing down your brows

and that helps you make a frown or an

angry face and the frontalis muscle is

on the forehead and this helps you raise

your brows and wrinkle your forehead

looking at the inner lid if you're

looking at a sagittal plane it's pretty

similar this is the upper lid inner lid

is prepared lower lid is pretty similar

so you've got the tarsal plate that we

talked about that connective tissue

within the tarsal plate you have the

 meibomian gland is a sebaceous gland and it just secretes a lipid rich fluid that's responsible for partially responsible for  lubricating  and then the Zeiss gland here which is at the base of the eyelashes this is more external on the eyelid so this is Iceland okay so a

collision is a non-infectious focal

swelling of the eyelid and it's due to

obstruction of a sebaceous gland so that

can be either the Zeiss gland or the

meibomian gland most this is the most

common inflammatory lesion of the eyelid

and it's associated with various

diseases so chronic blepharitis high

blood lipids probably due to the fact

that gives you more cholesterol more

lipids that can be excreted poor hygiene

and then various skin conditions

especially rosacea but also acne and

some other skin conditions so this

typically presents as a painless

swelling or a mass of the eyelid.now

initially when the caladium develops it

can be painful and if it gets large

enough it can be painful but typically

this presents as a painless swelling

painless mass and usually the patient

will seek.

کیلیفورنیا

کیلیفورنیا میں  فلمی ستاروں اور ڈزنی لینڈ کے علاوہ بھی بہت کچھ ہے۔

 یہ ایک ایسی ریاست ہے جہاں حیرت انگیز قدرتی پرکشش مقامات کی ایک بڑی تعداد اس میں شامل ہے۔

 خوبصورت ساحل ، پرسکون صحرا اور شاہی پہاڑ۔

 کیلیفورنیا میں متعدد دلچسپ شراب خانے موجود ہیں۔

 دنیا کی بہترین شراب ان شراب خانوں میں دستیاب ہے۔

 کیلیفورنیا میں دیکھنے کے لئے بہترین مقامات ہیں۔ 

 بگ سور

 کارمیل ہائ لینڈز اور سان سیمون کے درمیان واقع ، بگ سور ایک بڑا ، پتھراؤ والا راستہ ہے۔ کیلیفورنیا کے ساحلی علاقے کی کوئی سرکاری حدود نہیں ہے ، لیکن یہ کیلیفورنیا کے 70 میل دور ہے۔

 مشہور ہائی وے ون۔

 یہ علاقہ روڈ ٹرپ پر جانے والے مسافروں کے لئے مقناطیس کی حیثیت رکھتا ہے ، جو زبردست ریڈ ووڈ کی طرف راغب ہوتے ہیں۔ راستے میں درخت اور دم توڑنے والے ساحل ہیں ۔  ڈرائیونگ کے لئے صرف خوبصورت مناظر سے زیادہ ، یہ علاقہ کافی مقدار میں خشگوار ماحول بھی فراہم کرتا ہے۔ گھومنے پھرنے کے سرفہرست مواقع جو کئی ریاستوں کے پارکوں میں شامل ہیں۔

 کاتالینا جزیرہ۔

 یہ دلکش جزیرہ لاس بحر الکاہل کے قریب 22 میل کے فاصلے پر واقع ہے۔

 یہ ایل اے کے سیاحوں کے لئے ایک پسندیدہ جگہ ہے جہاں دن کا سفر  بہت خشگوار ہوتا ہے۔ 

 سہاگ رات کی جگہ.

 سانٹا کتالینا ایک چھوٹا جزیرہ ہے جس کی آبادی کے دو اہم مراکز  یہاں دوسرے علاقوں سے آنے والے نۓ شادی شدہ  لوگ سہاگ رات منانے کو ترجیح دیتے ہیں۔

اوولون۔

 جزیرے کے زیادہ تر مسافر بنیادی طور پر اوولون کے علاقے میں رہتے ہیں۔

 حیرت کی بات یہ ہے کہ جزیرے میں امریکی بایسن کی ایک چھوٹی سی آبادی بھی موجود ہے ۔ ایک فلم کی شوٹنگ کے دوران جزیرے کا سارا علاقہ دیکھایا گیا ہے۔ مسافر نجی کشتی ، گھاٹ ، ہیلی کاپٹر یا چھوٹے طیاروں کے ذریعے جزیرے تک پہنچ سکتے ہیں۔

 اس  جزیرے پر ، نقل و حمل صرف سائیکلوں ، ٹیکسیوں اور گولف کارٹس تک محدود ہے۔

 جھیل طاہو۔

 جھیل طاہو نہ صرف امریکہ کی دوسری گہری جھیل ہونے کے لئے متاثر کن ہے ، بلکہ  اس کے ساحل کی لمبائی  جو بہت اچھا قدرتی نظارہ پیش کرتی ہے۔

 میٹھے پانی کی جھیل کیلیفورنیا اور نیواڈا دونوں جگہوں پر پھیلی ہوئی ہے اور یہ سال بھر کا ایک اعلی مقام ہے۔

 1960 کی دہائی کے سرمائی اولمپکس کے انعقاد کے بعد یہ جھیل موسم سرما کے کھیلوں کا مرکز بن گئی۔

 شمالی ساحل پر وادی اسکوا میں۔

 موسم گرما میں پہاڑوں میں پیدل سفر اور جھیل پر کشتی کے سفر کے دوران لوگ گہری اور پر سکون خاموشی سے لطف اندوز ہوتے ہیں۔

 ساحل پر لیزنگ ، تیراکی ، اور بی بی کیو کا بھی وسیع انتظام کیا گیا ہے۔

 سیکوئیا اور کنگز وادی نیشنل پارکس۔

 یہ دونوں قومی پارکس جنوبی صحرا میں ایک دوسرے کے آمنے سامنے  واقع ہیں۔

 نیواڈا پہاڑ  اور  دیو سیکوئیا دونوں اپنے بہت بڑے  درختوں کی وجہ سے مشہور ہیں۔

 یہ درخت 300 فٹ سے زیادہ لمبے ہیں۔ اور ان کے تنوں میں 100 فٹ تک کی لمبائی ہوسکتی ہے۔

 سیکوئا نیشنل پارک ، جو 1890 میں قائم کیا گیا تھا ، پہاڑ ی چوٹیوں کا بھی ایک گھر ہے ، جو متفقہ ریاستہائے متحدہ کا سب سے بلند مقام ہے۔

 دلچسپ بات یہ ہے کہ کنگز وادی امریکہ میں گہری وادی  ہے۔

 پارکس میں وائلڈ لائف چڑیا  گھر ہے ، بشمول بوبکیٹس ، سرمئی لومڑی ، ریچھ

 اور خچر ہرن بھی موجود ہیں۔

 اگر وہ خوش قسمت ہیں ، تو شاید سیاح بھیڑ بکریوں یا پہاڑی شیروں کو تلاش کرسکیں۔

 دونوں پارکس بیک پیکر اور پیدل سفر کے لئےمشہور ہیں۔اور یہاں 14 کیمپ گراؤنڈ  سیاحوں کے لئے دستیاب ہیں۔

 وادی ناپا۔

 ریاستہائے متحدہ میں شراب سے محبت کرنے والوں کے لئے وادی ناپا ایک اولین منزل ہے۔

 اس کی الکحل دنیا کی بہترین الکحل مانا جاتا ہے۔

 بہت ٹریول ایجنٹ سیاحوں  کو ایڈجسٹ کرنے کے لئے بہترین سہولیات مہیا کرتے جو ناپا کا سفر کرتے ہیں ۔اس علاقے میں  بہت سے ایسے مقامات ہیں جہاں دلکش نظارے اور بہترین ہوٹلز ہیں۔جہاں سیاح آرام کیلیے رکتے ہیں۔

 تھوڑی رقم بچانے میں دلچسپی رکھنے والوں کے لئے کیمپنگ گراؤنڈ بھی موجود ہیں

 اس کے علاوہ ، نپا ویلی میں بہت سارے عالمی معیار کے اسپاس بھی موجود ہیں جہاں سیاح  لاڈ پیار کرسکتے ہیں اور لطف اٹھا سکتے ہیں۔

 مختلف طرح کی تفریحی سرگرمیاں ، بشمول گرم ہوا کے غبارے کی سواریوں اور رہنمائی شدہ موٹر سائیکل وغیرہ۔

 سان ڈیاگو.

 حیرت انگیز ساحل ، مثالی آب و ہوا اور پرکشش نظاروں کے ساتھ ، یہ تعجب کی بات نہیں ہے کہ  کیلیفورنیا میں دیکھنے کے لئے سان ڈیاگو ایک مشہور مقام ہے۔

 میکسیکن کی سرحد کے بالکل شمال میں واقع ، سان ڈیاگو ایک چھوٹا سا ساحلی شہر ہے۔ شہر کا ماحول۔

Meibomian Glands

 DRY EYE TREATMENT

lipiflow is one of the most advanced dry eye  treatments that someone can get at an eye clinic  

people have had amazing results to help them  with a dry condition but the tricky part  

is that it can be a costly  procedure with no insurance coverage  

so the question is is lipiflow  worth it let's focus in and your vision clear and i make videos all  about the eyes like this one to help you with   those tough decisions you have to make about your  eyes so consider subscribing for my future videos   when they come out now let's focus on lipiflow  lipiflow is one of the most advanced fda approved   dry eye treatments that you can have done at your  eye doctor's office if they have it it targets and   treats the oil glands in your eyelids specifically  if you have meibomian gland dysfunction the oil   glands in your eyelids are called meibomian glands  and they run vertical up and down your eyelids top   and bottom now they're responsible for pumping and  pushing out oil over the top layer of your tears   if you don't have enough oil or the wrong  type of oil then your tears will evaporate   leaving your eyeball exposed to the air causing  them to get dry and inflamed and causing dry ice   symptoms that you might expect now if your  oil glands are clogged or they're shortened   or they're at your feet or you don't have the  right type of oil or their plane not functioning   very well then you have what's called meibomian  gland dysfunction and it's one of the most common   core issues to dry eye problems and that's exactly  what lipiflow treats it treats the core issue it   treats meibomian gland dysfunction now the actual  lipiflow procedure is ran by a computer console   and single use activators now before you actually  do the procedure your eye doctor might do a little   bit of prep work usually they'll put in an  anesthetic eye drop to numb your eyes first   and then they may also debride your eyelids  or clean off any capped hardened oil from your   oil glands and that will make the procedure  more effective then they'll place the actual   activators between your eyeball and your eyelids  top and bottom now what's kind of neat about the   activators especially the white bowl that you see  here is that it serves two functions the inside   will protect your cornea from the actual procedure  the outside is where all the heat is applied and   that's applied to the inner layer of the eyelids  and that's part of what makes this procedure   so effective is that it's applying that the heat  to the inside of the eyelids and not the outside   so once your activators are in place the device  is turned on and the activators are heated up to   exactly 42.5 degrees Celsius the heat that they  found that works the best now each activator has   these little bladders on there that will massage  your oil glands and they massage in a peristaltic   motion pretty much meaning that they start from  the the beginning of the oil glands or the base   of the oil glands and then they'll squeeze  and massage trying to remove and push any   obstruction or hardened oil out of the opening of  the oil gland it's kind of like you're pretty much  just milking your own oil glands now with  this combination where you have the heat   applied to the inside of the eyelids and that  peristaltic massage that combination works really   well at cleaning and clearing out your oil glands  to help them function better in the future now the   procedure lasts exactly 12 minutes you do both  eyes at the same time and then when you're done   they're able to remove the activators  really safely and then you're all finished   now what to expect right after the procedure you  may experience some redness itchiness maybe some  more dryness or inflammation sometimes your eye  doctor may prescribe a steroid eye drop to help.

EYE LID ANATOMY

EYE LID ANATOMY

we will covering the structure of the eye lids. So let's get started about the eyelids. Now the eyelids are basically the folds of the skin along with various structures inside the fact that covers the eye when the eye is closed .

so here you got these are your eyelids and upper eyelid a lower eyelid so these when these eyelids just get closed so as a result what happens that the eye is closed and they meet one another now the upper eyelid as well as the lower eyelid meet each other at the lateral as well as the medial angles and in the center. you have got this fissure. you can see it's an elliptical fissure. So this elliptical fissure that you got in this in-between these two upper and lower eyelid so this is called as your palpebral fissure now moving ahead so just remember you got upper eyelid lower eyelid a little and medial angles as well as a palpable fissure in between now the upper eyelid covers the cornea the upper part of the cornea just a little bit of it where at this blackish portion in the eye this is your cornea and where is the lower eyelid just fall short of covering it so you can see here that it doesn't cover it it just lags behind in order to cover it whereas the upper eyelids covers a small portion of the cornea now moving ahead first of all not at the medial side of the eyeball you can see here so there is a small space that you can see from here to here so this small space and the medial angle is your Leykis like romanís so this small portion is called as the lakers likely - in the latest a criminal's you have got a small elevation so this small elevation is known as the current unlikely merely now this is called as your Karen Carla tremendously whereas just later to the current colectomy you can see a fooled so this fall is called as your this small fold is known as your plica semilunaris so you have got a lake a snake lamellas this pace then you have got the elevation which is called a scaling Conakry - and you have got a full just little to the colonic electric  and this fold is called s de plica semilunaris now moving ahead now if you look at the medial margin of the eyelid you can see here so this is the medial margin of the eyelid you know here that our eyelid is shown so there is a small pep Allah and this small papilla is known as the papal Electra - at the medial margin of the eyelid there is a small pebble ah which is known as the Pepin Electra - and at the tip of the PEC fin Electra military is a small opening that is called as the punctum Lac léman if you can appreciate it here so this small opening is called as the punctum like lamellae now this small Punctum  like lamellae then opens into the canaliculus like lamellae and then the whole form here over here they formed a lacrimal apparatus that drains the tears into the nose so this is your basically we will study it in the further upcoming videos from for now .¹just remember that not the medial margin of tea.i eyelid so there is a small opening a small popula that is called as the popular lacrimal as well as at the tip of the popular like punctum.

TEAR FILM

Tear filam of Eye

 

we have the eye and in the upper outer corner we have a gland called the lacrimal gland it's job is to produce a watery salty solution that is poured onto the eye and then washes the eye and performs some very important functions which we're gonna list here so firstly it will pour through these ducts you can see it has multiple ducts that drain into the eye and when you blink you actually spread this watery salty solution over the eye now what does that do well for one it keeps the eye from drying out so prevents dehydration that's very important because if that is dehydrated you will actually not be able to see clearly another thing it does is it will wash dirt away so your eyes always open it's exposed to dust and whatever else is in the air so it will wash that away and it actually protects the surface of the eye from viruses bacteria well mainly bacteria and any kind of microbes that might be in the air how does it do that well this water solution actually has many anti bacterial proteins in there like lysozymes etc and what these do is they function like they're antibiotic so they will kill any bacteria that land on the surface of the eye thus keeping the eye free of infection and again helping you to see because if you have infection in the eye you're going to have inflammation blood vessels will form you will have a lot of swelling and fluid collection in the eye and you will not be able to see so everything in the eye is directed at allowing you to see really clearly and really well now another amazing thing this watery solution does is you can see this kind of transparent layer we call this the cornea this is what allows light into the eye now the cornea does not have any blood vessels and so the cells in there still need a source of oxygen and they need a kind of fluid to take the waste from the cells away which is this is usually the function of blood since we don't have blood vessels in the cornea the watery solution poured in from the lacrimal gland does this function it dissolves oxygen from the air and it gives it to these cells here and then it washes away their waste as well and then when you blink what you're doing actually apart from spreading the water from this gland across the eye you're actually pushing it into this drainage system now let's look at this which system in a bit more detail so in the inner corner of the eye here we have two holes one hole on top and one hole under we call these the puncta now the Punkt are basically the opening onto these small canals so you have what we call a canaliculi on top and then a canal under as well and this drains the dirty water out so when you blink you push the dirty water through these punks or through the holes into these little canals and then the water is drained into this sack which we call the nasolacrimal sack and this drains into the nose so a great question would be does the water on the surface of the eye from this gland does that evaporate well it would evaporate but we have another layer on top that takes us to our second gland so if we just go back here these this row of glands on the top and we actually should have a row bottom at the bottom as well these are called the meibomian glands you have about 25 to 30 of these glands on top arranged in parallel you can think of them as a row of kind of eye droppers sitting on top of the eye and what they do is they produce an oily liquid or oily secretion. and again this oil is spread over the i/os pushed out over the eye when you blink now what's the purpose of this oily solution well for one it prevents the water you lay under it from evaporating which is amazing spamela and another thing it does is it seals your eyelids.

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The Anatomy and The Function of the Nasolacrimal apparatus

 The Anatomy and The Function of the         Nasolacrimal apparatus

The nasolacrimal apparatus and that's a fancy way of saying we're gonna talk about tiers we're gonna talk about what they're for how they're produced and how they're drained now every human being on the face of the earth at some point has cried we all do it we all have done it even the Prince of all Saiyans has cried at some point in his life the only human being that hasn't cried is of course Chuck Norris he's the only man alive that can make onions cry but assuming that you're not Chuck Norris assuming that you're any other regular human being I don't care how tough of a guy you are you've cried and there's a lot of stimulus for to your production sadness joy overwhelming and motion irritation of the eye and of course onions so first of all what is the purpose of the tears the purpose of tears is to coat the surface of the eyeball and protect it so if for whatever reason you didn't have tears on the surface of your eyeball then your cornea is going to be more susceptible to physical damage and we can't have physical damage of the cornea so you keep the tears on there to lubricate it which help protect it from physical damage but there's another purpose of the tears and it has to do with bacteria so bacteria if you don't kill them and don't control the growth of bacteria you can end up with overgrowth so suppose you had a situation where you didn't have any tears on your eyeball you'd be first of all really itchy that's for sure but you'd have a lot of bacterial growth on your eye and they might even penetrate deeper into the eye socket the reason tears prevent this from happening is because tears contain antimicrobial substances for example they contain a substance called lysozyme this is an enzyme that's present in a lot of léa secretions but in any case what it does is it breaks down bacterial cell walls specifically the peptidoglycan in the bacterial cell walls and then it renders them more susceptible to our immune defenses our innate immune defenses I should say one of the other major antimicrobial properties of tears  is that they are salty I think we all know that that if you've ever tasted your own tears what you think everybody's done at some point they're salty and that salt content actually helps inhibit the growth of a lot of species of bacteria so the major thing about the tears other than providing physical protection is they also provide antimicrobial protection to the eyeball okay now how our tears produced how did they get across the eye and then how do we get rid of them because in any biological system if we've got a way to make something we also have to wait have a way to get rid of it so to produce the tears we have this thing that sits on the lateral superior surface of the eyeball a little bit back it's called the lacrimal gland and of course we can't see this from the surface it's deep a little bit but it is above the eye and on the lateral side so if we didn't have a face here to help us we would know this as a right eyeball because the lacrimal gland has to be on the lateral side of the eye okay and so if it's on the lateral side of the eye this would make this the right eyeball in any case the lacrimal gland is going to make the tears it's going to secrete them onto the surface of the eye by moving them through these excretory lacrimal Dunn's okay and there's going to be several of those that allow the tears to move through the lacrimal gland and onto the surface of the eye Hey and of course these tears are going to help lubricate the eye they're gonna help protect it and so on and so forth and then eventually those tears are gonna make their way over here to something called the lacrimal lake and associated with the lacrimal lake.

UVEAL TRACT

Clinical anatomy of uvl tract

We discussing the anatomy of iris ciliary body and choroid to makethings easier.

we will start with the anatomy of choroid and then everything will make sense so the outermost layer of the choroid is the suprachoroidal lamina this black layer that we are seeing this is the suprachoroidal lamina now there is a space between the suprachoroidal lamina and the sclera that is a suprachoroidal space whereas the posterior ciliary artery and nerves okay we'll discuss about this in another time so the first layer is suprachoroidal layer after this we have stroma the stroma mainly consists of the bulk of vessels and these vessels are arranged according to their size the largest one known as heller layer is the outermost the moderate size one known as settler layer and the innermost the choreo capillaries which are smallest in size and these choreocapillaries are important because they nourish the outer part of the retina means our retinal pigment epithelium and rods and cones means this is the part of retina which is not being supplied by the central retinal artery but by these choreocapillaries this makes it important now we have a basal lamina of our stroma that is the brooks membrane and finally we have retinal pigment epithelium which is separated by a small space between from brooks membrane so the three layers we studied are suprachoroidal layer the stroma and the brooks membrane and finally we have retinal pigment epithelium that is a part of retina okay so now let's make thing easy that this suprachoroidal lamina will continue as supraciliary lamina so the first layer of ciliary body will be supraclearly lamina and then there will be stroma and this stroma will consist of ciliaris muscle the ciliaris muscle is important for accommodation and for uv scleral outflow we have three types of fiber in the cellulose muscle these are longitudinal fiber as you may see there are oblique fibers and there are circular fibers in this room of ciliary body now the longitudinal fiber and the oblique fiber help in the outflow of the aqueous means uv scleral outflow and the circular fiber are the one which help in accommodation the third layer in the ciliary body is the pigment epithelial layer okay now this pigment epithelial layer is the continuation of retinal pigment epithelium um due to paucity of space this is a simatic diagram so just try to understand i have just drawn an arrow that retinal pigment epithelium is the one which contributes to the pigment epithelium of the chloride then we have a non-pigment epithelial layer and this non-pigment epithelial layer is the one which is derived from sensory retina means the layer which will be more inside this will derive the non-pigment epithelium okay so these were the four layers in four important layers of ciliary body the supra ciliary lamina stroma the pigment epithelium derived from retinal pigment epithelium the non-pigment epithelium derived from sensory retina going on with iris will make things more easy the supraciliary lamina continues forward forming interior limiting layer now this interior limiting layer is the one which contains fibroblast and pigment cell and this decides the color of the iris means if this layer is thickened it will result in a dark iris and if this layer is thin there will be a blue iris moreover it also depends on the amount of pigment the second layer as we see is the continuation of is the stroma and this trauma is important because it contains two important muscles sphincter pupillae and dilated papillae also nelson vessels the sphincter papillary being the cause of active meiosis is supplied by um supplied by parasympathetic innervation and are dilated people pupillae being the one which causes active meduses located in the peripheral part of the stroma is one which is responsible for uh which is supplied by a sympathetic innervation the third layer is the interior epitheli

HOW TO PRESCRIBE PRISM GLASSES

 Prescribing Prism

Both phorias and tropias can be accurately measured using prism and cover tests. Initially a cover test is performed to determine the fixing eye and estimate the deviation. This is followed by the prism and alternating cover test, with adjustment of prism strength until refixation movement of the eyes is neutralized.

Phorias

Although most normal individuals have at least some phoria, the vast majority are asymptomatic. If a deviation is uncovered on routine testing in an asymptomatic patient, no treatment is necessary. If a patient is complaining of asthenopia and a deviation is discovered during testing, one must first ensure that there are no coexisting issues prior to attributing the symptoms to a phoria. There are a number of causes for asthenopic symptoms that should be ruled out. Some of these causes are summarized in Table 1. To be sure, some of the refractive causes of asthenopia are via induced phorias.

Once other causes for symptoms are ruled out, phorias should be investigated, and, in certain cases, may benefit from partial prism correction. One indication that the patient will benefit from prisms is minimal prism adaptation during a 15- to 20-minute trial with prisms in the waiting area. Otherwise, if there is a significant adaptation to the prisms, the patient’s symptoms will probably not be improved through the use of prisms, and other therapies, including surgery, should be considered.

Esophoria

As soon as the cover/uncover test identifies an esophoria, the next step is to obtain an accurate cycloplegic refraction because many cases of esophoria are “accommodative,” due to uncorrected or undercorrected hyperopia. It is wise to perform the cover/uncover test for esophoria at both distance and near, for the deviation may be larger at one distance than the other.

After refracting the patient and ensuring that there is no uncorrected hyperopia, one may wish to try a small amount of plus sphere to decrease the accommodative demand, as some cases of esophoria are due to accommodative excess. Such intervention is often enough to treat the condition, but base-out prism may be necessary if refractive methods fail. In situations that require the use of prisms, base-out prism should be prescribed with only the minimum amount of power required to eliminate the symptoms.

Exophoria

Again, careful refraction of the patient can help the management of many cases of exophoria. With refractive correction in place, if any, cover tests should be performed, and accommodation should be evaluated by push-up measurement of accommodative amplitude, or, especially in children, by dynamic retinoscopy. Divergence excess (in contrast to convergence insufficiency) manifests as an increased angle of exophoria in the distance.

In exophoria, correcting both myopia and hyperopia can help improve symptoms, but additional cautions should be taken when correcting hyperopia, as full correction of hyperopia may worsen the symptoms. A several-minute test with hyperopic correction should be attempted to see if exophoric symptoms improve because of clearer imagery or worsen by relaxing accommodation. If they worsen, prescribe the largest correction possible to treat the hyperopia while avoiding exophoric symptoms. A good starting point is one-third of the spherical error. Just as plus lenses can be helpful for esophoria, decreased-power plus lenses or even minus lenses can improve exophoria.

Base-in prisms may also be helpful for the treatment of exophoria. As with esophoria, the least amount of prism that eliminates exophoric symptoms should be used. The cover test should provide an estimate of the power of the prism to be used. Additionally, treating a minor hyperphoria with vertical prisms can allow the patient to compensate for exophoria with no need for horizontal prisms (see below). If divergence excess is found to be the cause of the exophoria, prisms should be avoided. In this situation, base-in prism can cause esophoria at near, which patients do not tolerate well.

Hyperphoria

Both the measurement and treatment for hyperphoria are similar to those for the horizontal heterophorias. One important point regarding hyperphorias is that they often coexist with horizontal heterophorias, and the treatment of one may improve or eliminate the other condition. Therefore if either a horizontal heterophoria or a vertical heterophoria is found, it is important to investigate whether the other is present. Initial attempts at treatment should be focused on the primary phoria with the intention of treating both.

Tropias

various types of tropias can be categorized in a number of ways. Broadly, they can be considered as comitant or incomitant. Surgery is generally the preferred treatment for tropias unless there is a reason not to perform surgery (see above). Therefore prisms for tropias are generally used as a temporizing measure until surgery can be performed.

In general, the measurement and treatment of tropias parallel those of phorias, as discussed above. A 30- to 45-minute patch test can be especially useful in uncovering the full deviation. When measuring incomitant deviations with prisms with each eye “fixing,” it is imperative to switch the prism to always be before the non-fixing eye. Otherwise the “fixing” eye behind the prism will not truly be looking in the intended direction, and major measurement errors can occur. For comitant strabismus, a prism adaptation test can be helpful to help determine treatment. For incomitant strabismus, prisms may be helpful to move an area of single vision to straight ahead.

Anisometropia

Often when patients with anisometropia receive a new pair of glasses, they will complain of double vision, particularly while reading. This double vision is due to the differential prismatic effects of the two lenses when the patient is looking off-center as when reading (as per Prentice’s Rule). In order to improve reading vision, vertical prism can be incorporated into the lower portion of one lens or the other to help compensate for the differential vertical prismatic effect and lessen or eliminate the double vision. These prisms are referred to as slab-off or reverse-slab prisms. The slab-off prism is placed on the more minus or less plus lens, more commonly on glass lenses, and in effect takes away base-down prism (adds base-up prism). The reverse-slab prism is placed on the more plus or less minus lens, most commonly on molded plastic lenses, and adds base-down prism.

Rather than a calculation of the amount of slab-off or reverse-slab prism to prescribe, trial-and-error measurements are preferred because one does not know how much the patient has already compensated to previous anisometropic glasses. Increasing the amount of prism handheld over the lower portion of one lens of the anisometropic correction until the patient can read comfortably is the most reliable way to determine the amount of slab-off or reverse-slab prism to prescribe. Up to 4∆ to 6∆ of slab-off or reverse-slab effect can be obtained when needed.

 Pitfalls in Measuring Deviations

When prisms are used to measure a strabismic deviation in a patient, several easily avoidable mistakes are commonly made.

Positioning

The position in which the prism is held can be critical when measuring a patient’s deviation. There are three intended positions for holding prisms: the Prentice position, the minimum deviation position, and the frontal plane position . Glass prisms are calibrated for the Prentice position and should be held in this manner when making measurements. Plastic prisms, including plastic prism bars, are generally calibrated for the minimum deviation position. As it is difficult to estimate accurately the minimum deviation position, the frontal plane position is a good approximation when using plastic prisms.

Adding Prisms

Stacking two prisms in the same direction, especially if one is of high power, can also lead to errors because of the same positioning issues mentioned above. If the two prisms are held in contact with each other, even if the first prism is held in the correct position, the second prism will not be in the correct position in relation to the light leaving the first prism. This will create a stronger prism effect than the sum of the two prisms, leading to a falsely low measurement. If the sum of the two prisms is prescribed, or surgery is based on the prism measurement, the patient will be left undercorrected. It is difficult to estimate accurately the correct position of the second prism in relation to the first, and it is therefore more accurate to simply stack the prisms together and use a conversion table to add their true effects.

Splitting Prisms Between the  Eyes

One might assume that one way to avoid the difficulties of stacking two prisms is to split the prisms between the two eyes and add the powers together. Although this may work for low prism powers, it becomes increasingly inaccurate with increasing prism power. Splitting prisms is preferred over stacking two prisms together in the same direction before one eye, but again using a table of summed prism values is preferred to avoid errors.

Method for Calculating Oblique Prism

There is a simple method to calculate oblique prism from combining a horizontal prism with a vertical prism that does not require trigonometric calculations and requires only a piece of paper, a ruler, a pen or pencil, and the protractor on a phoropter or trial frame.

First, sketch the vector addition of the two prism powers on polar coordinates to determine the approximate angle for the base direction of the oblique prism. Up is base-up, and right is base-in or base-out depending on which eye the prism is intended for.

Then measure off the number of prism diopters of the two component prisms on two adjacent edges of a piece of paper. (One can use any unit for this measurement, but the unit must be consistent. For example, if you have two prisms, one of 3∆ and the second 2∆, measure off 3 cm/inches/etc on one edge and 2 cm/inches/etc on the other edge). Connect the two measurement marks with a line, forming a triangle. Now measure the length of the connecting line you just drew, the hypotenuse of the triangle. This will give you the number of prism diopters for your oblique prism.

Then fold the paper along the hypotenuse, identify the acute angle of the triangle that you estimated using your polar coordinate plot, and measure this angle using the protractor on the phoropter or trial frame, giving you the base direction of the oblique prism.

Uncommon but Important Uses for Prisms Childhood Cranial Nerve Palsies (Third, Fourth, and Sixth Cranial Nerves)

For children with cranial nerve palsies, early treatment is important to prevent amblyopia. Prisms may be used for small, reasonably comitant deviations in order to maintain binocular function. A test with temporary plastic Fresnel prisms is recommended prior to grinding prisms into the child’s lenses. Treatment of a recognized underlying cause is essential, and if prism therapy fails, surgery should be considered.

Prisms for Enhancing Communication

For patients with no useful vision in the deviated eye, prisms can be extremely helpful in improving the appearance of the eyes and facilitating the patients’ communication and interaction with others by alleviating difficulties with eye contact. A prism held opposite the direction of a correcting prism can improve the apparent alignment of the eyes (ie, base-in for esotropia and base-out for exotropia). Expect approximately 1 mm of apparent eye shift for every 8∆ of prism power.

Homonymous hemianopia

Prisms (or mirrors) may be used in patients with homonymous hemianopia to bring images from an area within the visual field defect into the area with retained vision. Although this may be useful on occasion, generally very high prism powers are required, which can create cosmetic problems as well as a confusing visual environment in which objects may appear and disappear from view unexpectedly.

Hemispatial neglect

Patients who experience right hemisphere strokes often experience left hemispatial neglect. Recent studies have shown that yoked prisms which move both visual fields to the opposite side (to the right) improve function in these patients. The mechanism for this improvement is believed to be that in order to compensate for the shifted binocular visual field, the patient must remap his  sensorimotor coordinates leftward, and this has been shown to improve function on the neglected left side.

Nystagmus with head turn

Patients with a head turn to compensate for nystagmus can benefit from yoked prisms, but just as with patients with homonymous hemianopia, they will often require very high prism powers which may lead to decrease in visual acuity (especially with Fresnel prisms), chromatic aberration, heavy lenses, and cosmetic problems, as well as the visual disturbances described above. In spite of these problems, prescription of bilateral yoked prisms, with base in the same direction as the head turn, can keep the patient’s eyes in an eccentric null position while lessening the head turn.

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The visual pathway

 The visual pathway so we're going to take how the light hits the retina and we're going to take it through the optic nerve and all the other different process if you guys have already watched our video on the phototransduction cascade that's going to be very very important that you do that before we get into this visual pathway because we already talked about exactly how those light rates got converted into chemical changes and then electrical changes and how they went down the axon to the ganglion cells which basically made up the optic nerve all right so now we're going to have two eyeballs right

this is the we're going to say this the left eyeball and this is the right eyeball okay now first things first what I want us to try to imagine if we're gonna put a lot of different concepts together when you guys are looking you guys are like looking at anything around you we our eyes are so amazing that they can pick up different types of visual fields so for example this is the right visual field or the right visual field and this is the left eyes visual field okay so what is this one right here this is the right eyes visual field and this one over here is the left eyes visual field okay now with in the visual field you have two different components of this visual field we're going to say this is the nasal so since your you'd have your honker right there pretend this is your nose okay so pretend this structure here is your nose okay since this is the nose these two structures that are near the nasal region this is the nasal component of the visual field alright so this is the nasal component of the visual field and then this one over here would be near the temple so this is the temporal component of the visual field and this over here is going to be the temporal component of the visual field okay now to make it easy though now that we know that this is what it is it's nasal and the temporals these words are going to get interchanged a lot so I do not want to confuse you guys so what I'm going to do is for the sake of it is I'm going to switch nasal and since this is the right visual field this is what gets confusing the right visual field has a left visual field and a right visual field okay so the right eye has a left visual field and a right visual field so we're going to say this is the left visual field and this is the right visual field okay so I just want to make it as simple as I possibly can here this whole right eye is going to have two fields it's going to have the right visual field and last visual field same thing this left eye is going to have two visual fields it's going to have a left visual field and a right visual field okay simple as that now we're going to be able to kind of do this a lot easier now so instead of using the words nasal and tempore but understand those words because it's going to be important lesions okay let's say first off when we're looking out let's say that this part of the retina there's two parts of the retina so this is the right eye this part of the retina is closest to the Temple or the right temple right so we're going to call this part of the retina we're going to call this the temporal Hemi retina okay that's a temporal Hemi retina now here's what gets really funky the temporal Hemi retina is receiving light rays from the left visual field okay so from here this part here this left visual field is hitting this part of the retina okay so if light rays from the left visual field are hitting this part of the hit retina that temporal heavy right now but then the what is this one this one is close to the actual nose so since it's close to the nose this is called the nasal right Hemi retina so it's called the nasal hemorrhage now and it's called the temporal Hemi retina the nasal hemorrhage now is receiving light from the right visual field so the nasal Henry retina is getting hit with light from the right visual field .