Medicalnotes384

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

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

CORNEAL DYSTROPHIES

CORNEAL ULCER

ANATOMY OF THE LENS

BUMP OF UPPER EYE LID

EYE LID DISORDERS

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