Image Based MCQ on Ophthalmology

Hello Awesomites!
Yesterday we posted an Image based MCQ on Ophthalmology and here is the answer for it.
#Ophthalmology
#Spot_Dx
Q. What is the most likely diagnosis of the given image? 

A. Ankyloblepharon
B. Symblepharon
C. Pterygium
D. Pseudo pterygium 

The correct answer is B. Symblepharon.
Symblepharon is an adhesion between the eyelid and the eyeball. It can involve just one lid or both. This adhesion of subepithelial scarring can lead to other lid complications such as aberrant lash growth and entropion. Symblepharon can develop as a complication of several diseases and/or etiologies that include:
Severe dry eye syndrome
Stevens-Johnson syndrome
Cicatricial pemphigoid
Chemical injury
Erythema multiforme
Bullous pemphigus
Conjunctival infections associated with conjunctival scarring such as chlamydial, vernal, atopic, and bacterial conjunctivitis
Epidemic keratoconjunctivitis
Burns
Toxic epidermal necrosis

That's all!
Thank you.

MD Mobarak Hussain (Maahii) 

Causes of chemosis mnemonic

Chemosis is known as oedema of conjunctiva.

Reason:due to exudation from the abnormal capillaries.This retained exudate gives a swollen and gelatinous appearance.

Regions: loosely attached areas of the bulbar conjunctiva and fornices.

Causes: ABC

A: Acute inflammations like gonococcal conjunctivitis, panophthalmitis, dacryocystitis, periostitis, orbital cellulitis.

B: Blood conditions (abnormal) like anaemia, urticaria, angioneurotic oedema, lymphocytic infiltration.

C: Circulatory obstruction in conditions like pulsating exophthalmos or due to pressure of an orbital tumour which may interfere with the lymph and blood drainage.

Thanks for reading.

Madhuri

Tay Sachs Disease

Hello Awesomites!
Here's a Blog on Tay Sachs Disease and some common questions related to it.

Tay-Sachs disease

It is a genetic disorder that results in the destruction of nerve cells in the brain and spinal cord. Tay–Sachs disease is caused by a genetic mutation in the HEXA genes on chromosome 15. It is inherited from a person's parents in an autosomal recessive manner. The mutation results in problems with an enzyme called beta-hexosamidase A ,located on lysosomes,which results in the build up of the toxin GM2 ganglioside within cells. The most common type, known as infantile Tay–Sachs disease, becomes apparent around three to six months of age with the baby losing the ability to turn over, sit, or crawl. This is then followed by seizures, hearing loss, and inability to move. An eye abnormality called a cherry-red spot, which can be identified with an eye examination, is characteristic of this disorder. Death usually occurs in early childhood. Less commonly the disease may occur in later childhood or adulthood. These forms are generally milder in nature.Diagnosis is by measuring the blood hexosaminidase A level or genetic testing.

Frequently asked questions -

The substance which accumulates in Tay Sach’s disease is Ganglioside.
Deficiency of enzyme Hexosaminidase-A causes Tay Sach’s disease.
Cherry red spot at macula may be seen in Tay Sach’s disease.

That's all!
Thank you.

MD Mobarak Hussain (Maahii)

Sequence of appearance of papilledema

The optic disc margins start to blur in the following order in papilledema-

1. Superior
2. Inferior
3. Nasal
4. Temporal

Blurring first occurs where the nerve fibre density is the highest.The optic disc being ovoid in shape, with taperings superiorly and inferiorly, the nerve fibre density is higher there. Hence such a sequence.

That's all!

-Sushrut Dongargaonkar

Pills of knowledge in Ophthalmology-Pupil and the third nerve palsy

The parasympathetic fibres passing along with the 3rd cranial nerve which supply the pupil lie towards the periphery of the nerve. Hence, surgical compressive lesions like tumors or aneurysms which compress the 3rd nerve end up involving the pupil as well.

In contrast, medical lesions like diabetis mellitus or hypertension affect the vasa nervosum which supply the nerve starting from its core.These rarely affect the pupil as the outer, peripheral fibres may remain relatively spared.

This however, is not a strict rule.This criterion can just be used for the primary evaluation of the possible lesion.

That's all!

Triad of Retinitis pigmentosa mnemonic

The mnemonic for remembering the Triad of retinitis pigmentosa (RP) is BAD

1. B- jet Black spots which are perivascular.
2. A- Attenuation of arterioles.
3. D- Disc palor.

Thanks for reading.

Madhuri Reddy

Evaluation of Pseudophakia

Clinical evaluation of a case of Pseudophakia.

Pseudophakia is a term used to describe the condition wherein an artificial intraocular lens is implanted after surgery for cataract.

On history - History of cataract surgery present.

On examination -

1) Deep Anterior Chamber (the posterior support for the iris is lost as the IOLs are thinner that the natural lens)
2) Conjunctival flap and subconjunctival hemorrhage ( seen only in recent cases)
3) Scleral/ Corneal incision and scar.
4) Iridodonesis (tremulous iris)
5) Jet black pupil
6) Shimmering light reflex from the IOL.

Oculocardiac Reflex

Oculocardiac Reflex/Aschner phenomenon.

This is one of the trigeminovagal reflexes produced on digital massage of eye. Digital massaging of the eyeball is done to lower intraocular pressure after producing a retrobulbar or a peribulbar block. But rarely....this event is followed by cardiac depression, asystole and even death. The afferent is by the ophthalmic division of trigeminal nerve which relays in the visceral motor nucleus of the vagus nerve. The efferent is carried by the parasympathetic vagus nerve to the heart. It is most commonly seen in pediatric cases during squint surgery.
It is not seen very commonly in adults and in other surgeries as the procedure would involve just one eye and massaging of this eye is not sufficient to produce bradycardia normally.

Treatment: atropine or glycopyrrolate . Cardiopulmonary resuscitation might be needed in severe cases.

Pills of knowledge in Ophthalm- squint and frontal eye field

Mentally challenged people may have a squint as the frontal eye field in the brain cortex is involved in ocular movements as well. It also may explain why somebody's eyes go crazy when they're starting into nothingness.

That's all!

-Sushrut Dongargaonkar

Congenital Corneal Opacities

Congenital Corneal Opacities

Pills of knowledge in Ophthalm- Anterior ciliary artery

The point where the anterior ciliary artery pierces the sclera is often marked by a pigment. This is of particular importance while cauterization as in a bid to make everything look neat and shiny, the pigmented part shouldn't be cauterized as it will cause necrosis of the structures supplied by the artery. 

Pills of knowledge in Ophthalmology- Squint and refractive errors

1.A refractive error should be thoroughly assessed prior to surgical squint correction or the squint may recur.

2. Divergent squint occurs in myopes as the divergent system of muscles is more active during far vision. So, the far vision in myopes being hampered, the eyes try to diverge more.

3. Same goes for hypermetropes. They end up with a convergent squint if left uncorrected.

-That's all!

Sushrut Dongargaonkar

Pills of knowledge in Ophthalm- Posterior staphyloma

A posterior staphyloma is common because the durability of the layers of the eye where the optic nerve enters the eye is lesser in comparison.

-That's all!

Sushrut Dongargaonkar

Pills of knowledge in Ophthalm- Moxifloxacin

Moxifloxacin is the preferred antibiotic in Ophthalmic surgeries and pathologies because it gets concentrated into the anterior chamber and the aqueous.

That's all!


-Sushrut Dongargaonkar

Doyne's macular degeneration

So, the other day the head of my department asked us about Doyne's maculopathy. Couldn't find rest until I searched it up on Google. Here what it is in short-

1. Accumulation of material between
the Bruch's membrane and the retinal pigment epithelium.

2. This results into the formation of a drusen, which is a radially localised
white, large one which spreads over
time.

3. The cause is a mutation in the
EFEMP1 gene,on chromosome
2p16, inherited as an autosomal
dominant trait which results in the
formation of a misfolded protein
which is poorly secreted as well.

4. All this results into a gradual loss of
vision.

5. Photodynamic therapy forms the
mode of treatment for subfoveal nets which may also occur in the disease.

It is also known as 'Honeycomb retinopathy'

That's all!

-Sushrut Dongargaonkar

How is Visual Contrast achieved?

Hello everyone,
Let us discuss Visual contrast today. This question has haunted me for a long time.

Let's start with the basics, the cells in various layers of retina and their function.

Here's a quick review of things you have already read:

1. What is photoreceptor?
It is a rod or cone. It detects light.

2. What is horizontal cell?
It is present between rods and cones. It is inhibitory in function. (It is involved in lateral inhibition which we will discuss later!)

3. What is bipolar cell?
It transmits information from photoreceptor to ganglion cells.



Now, lets come to the details.

4. What are metabotropic receptors?

First of all what you must understand is Metabotropic receptors and Inotropic receptors are receptors present on bipolar cells.

They recieve stimulas from photoreceptors (mostly decreased glutamate is the stimulas).

Metabotropic receptors cause depolarisation that is excitation of centre of receptive field of bipolar cells

5.What are inotropic receptors?
They cause inhibition of centre of receptive field i.e. hyperpolarization. (remember, I for Inhibition)

6. Receptive field - What is it?
It is a region of retina where if the light falls it is going to alter the firing of neurons. (By firing I don’t mean guns :P) It means the action potentials generated and transmitted by the photoreceptors. So each cell has a characteristic receptive field. It can be as small as a dot or as large as this page itself. But don't limit this concept to a photoreceptor only. Almost all sensory cells example in somatosensory system or in auditory system possess a receptive field.

Receptive field of a bipolar cell is arranged into a central disk,
the “center” and a concentric ring, the “surround”, each region responding oppositely to light.

Coming to the crux of the topic i.e. Visual Contrast.

How do the things we have discussed so far help us achieve that?

Visual Contrast is achieved by two mechanisms:
1. Lateral Inhibition
2. Excitation of Some Bipolar Cells and Inhibition of Others — The Depolarizing and Hyperpolarizing Bipolar Cells.

1. How does lateral inhibition help?
First: It does not allow the signal to spread through the dendritic and axonic trees. Hence point to point transmission occurs.
Second: The direct and indirect pathways accentuate each other. This can be easily understood. Photoreceptor sends excitatory signals to bipolar cell. But the adjacent photoreceptor sends a inhibitory signal through the horizontal cell. Mostly these two neutralize each other so no net stimulus is transmitted to bipolar cell.
      But If the adjacent cell is  unstimulated by light, It will not inhibit the excitatory signals transmitted by the photoreceptor which is stimulated by light. Hence it will allow excitation of bipolar cell.
This allows extra excitation of bipolar cell. We get a better contrast. The area which is dark remains dark. But the area which is bright becomes even brighter. This is what visual contrast is all about.
The fun part of all this is, a lot of visual illusion make use of this principle. Do google "Simultaneous Contrast"  :) .

2. How do different Bipolar cells help?
Because depolarizing and hyperpolarizing bipolar cells lie immediately against each other, this provides a mechanism for separating contrast borders in the visual image, even when the border lies exactly between two adjacent photoreceptors.
We will take a simple example. Suppose light is striking at periphery of two receptive fields. Remember it is shaped like a disk, with a centre and periphery both opposite in nature.Suppose One is On centre bipolar cell and other is Off centre bipolar cell(On centre: Activated when light hits centre but periphery is inactivated and vice versa for Off centre). So only the Off centre bipolar cell will detect it. Hence mixing up of signals is avoided. Again what I get is a sharper border. That is what contrast is all about.

That is how it is all done.

Interesting fact: The cells in the retina don't follow the "all or none" law. Transmission is by Electrotonic conduction. From ganglionic cell onwards cells  follow all or none law.

Thats all,
Thank you,
Chaitanya Inge

Collier's Sign

Hey guys!

Collier’s sign (“posterior fossa stare,” “tucked lid” sign) is elevation and retraction of the upper eyelids, baring the sclera above the cornea, with the eyes in the primary position or looking upward.

This may be seen with upper dorsal midbrain supranuclear lesions (e.g., Parinaud’s syndrome). There may be accompanying paralysis of vertical gaze (especially upgaze) and light-near pupil-
lary dissociation.

The sign is thought to reflect damage to the posterior commissure levator palpebrae superioris inhibitory fibers; causing overactivity of this muscle.

-VM

Cranial nerve III damage (Oculomotor nerve damage mnemonic)

Hello!

The CN III has both motor (central) and parasympathetic (peripheral) components.

Which fibers get affected in diabetes?
Which would lead to loss of pupillary light reflex?
Which fibers are compressed first?
Which would cause the down and out pupil?

Don't know? Check the video out!

Myopic Shift : Explanation

Hi everyone ! So this is a short post on the Second Sight or the Myopic Shift seen in Cataract.

So in people who  have a hypermetropic / presbyopic power , tend to experience a reduction in their refractive errors when Cataract starts to develop. This is called Myopic Shift or Second sight.
This​ occurs most commonly in nuclear cataracts. Now why this occurs is , the lens in early stages of Cataract undergoes sclerosis. That increases the Power of the lens ( this increases the refractive index).
Thus it makes the lens slightly more Powerful , or Convex. Due to this it acts as a correction for Hyperopia/ Presbyopia (Where the error was due to a weaker lens. )
This transient Myopic nature of the eye is called the Myopic Shift.
It does go away when the Cataract progresses as the sclerosis begins to reduce refractive surface in the lens.

Hope this helped! Stay awesome  !
Happy Studying :)

~ A.P.Burkholderia

Terson Syndrome.

Hello everybody!

In this post let's quickly learn about Terson Syndrome.

So what is it?
This Syndrome is a combination of intraocular and subarachnoid haemorrhage secondary to aneurysmal rupture, most commonly arising from the anterior communicating artery.

Terson Syndrome along with other bleeding disorders is included amongst the Systemic causes of vitreous hemorrhage!

Intraocular haemorrhage is also seen to occur with:
1)Subdural haematoma
2)Acute elevation of intracranial pressure

The mechanism of intraocular bleeding:

There is increase in cavernous sinus pressure due to the subarachnoid/subdural hemorrhage leading to stasis in the retinal veins. This stasis in the retinal veins leads to increased intraluminal pressure in the veins making them susceptible to bleed.

The haemorrhage is often Bilateral.
Typically intraretinal and/or preretinal. With this hemorrhage there is a possibility of it leaking in the vitreous.

The vitreous haemorrhage usually resolves in a few months and the long-term, the visual prognosis is good.

I hope you guys found it useful. Do let me know about some neuro-opthalmology syndromes you know about.

Let's learn Together!
-Medha.