This is a mechanism by which the eye wards off the secondary effector phase of the immune response arc.
Thus, the cell mediated immunity appears to function less effectively in the uvea compared to the rest of the body.
Possible mechanisms include-
1. Immunomodulatory cytokines produced by the ocular tissues.
2. Immunomodulatory neuropeptides produced by ocular nerves
3. Functionally unique APCs.
4. Compliment inhibitors
..and some other factors.
-Sushrut
The large spaces of choroid act as a sort of trap to organisms, especially fungi. Therefore most fungal lessons of the posterior segment begin as choroiditis.
It's interesting to note that the optic nerve, which is considered to be a purely sensory nerve has some efferent fibres, that is, fibres from the brain to the optic disc. The presumed role of these fibres is in dreams, where the brain sends impulses to the retina, image is generated and it is carried back to the brain via the afferent fibres.
-Sushrut
Some specific antigens when placed in the anterior chamber of the eye result in a suppression of cell mediated immunity, with a normal humoral component.
There is something known as the ' oculo splenic axis' , whereby the antigens travel via the trabecular meshwork and reach the spleen. In the spleen, they secrete MIP 2 which attracts the NK cells. The NK cells in turn secrete IL10 and TGF beta. The T cells in this environment become regulatory cells and suppress the cell mediated immunity. Production of IL2 is suppressed.
The eye is an immuno privileged organ, as it needs to be structurally maintained pristine to preserve it's light carrying capability. ACAID is a mechanism by which Nature attempts to limit unwanted inflammatory responses in the anterior chamber.
It has implications in intraocular tumors, autoimmune, and infectious immune responses.
-Sushrut
PS- The failure of ACAID in the mechanism of lens induced uveitis still remains unexplained!
It can be hard to remember which oblique does what. Remember this. 'Extortion' as we all know is forcing money out of someone. People from the 'inferior' strata of the society extort money. See where am I going?!
So! Inferior oblique causes extorsion( 'extortion' is a bit different- c'mon, be a grammar Nazi!)
What remains? Superior oblique. So..it then is responsible for intorsion.
Similar is the case for superior and inferior recti.
Hope I saved you from ophthalm extorting your precious time.
-Sushrut
Iridodialysis bleeds profusely as the circulus major arteriosus lies near it's root.
Conversely, sphincterotomies or YAG iridotomies hardly bleed. Why? Because the vessels in the iris away from it's root are intertwined within it's musculature. The muscles contract immediately, halting any hemorrhage.
-Sushrut
●Cogan's syndrome (CS) is a chronic inflammatory disorder that most commonly affects young adults. Clinical hallmarks are interstitial keratitis (IK) and vestibuloauditory dysfunction, and associations between CS and systemic vasculitis, as well as aortitis, also exist. There are a range of pathologic findings, most of which reflect immune-mediated injury of the affected tissues; however, despite an association with systemic vasculitis, eye and inner ear specimens of those with CS do not reveal any evidence of vasculitis. The underlying mechanisms responsible for the eye and inner ear disease in CS are unknown.
●The predominant ocular feature of CS is IK, which typically causes eye redness, pain, photophobia, and blurred vision. Slit-lamp examination commonly demonstrates a patchy, deep, granular corneal infiltrate. IK is not essential for the diagnosis; ocular inflammation may involve other parts of the eye and may lead to iridocyclitis, conjunctivitis, episcleritis, anterior or posterior scleritis, or retinal vasculitis.
●The inner ear manifestations of CS are Ménière-like attacks consisting of vertigo, ataxia, nausea, vomiting, tinnitus, and hearing loss. Vestibular dysfunction may also cause oscillopsia, and caloric testing often reveals absent vestibular function. Recurrent episodes of inner ear disease frequently result in profound sensorineural hearing loss. Noninflammatory down-fluctuations in hearing may be difficult to distinguish from those of inflammatory origin. If hearing loss is associated with eye inflammation or other features of active CS or does not resolve within three to five days, an inflammatory origin is more likely.
●When present, the systemic vasculitis associated with CS is a large- or medium- to small-sized vessel vasculitis or an aortitis. The pattern of vessel involvement may be overlapping. Other systemic manifestations of CS include fever, fatigue, weight loss, lymphadenopathy, hepatomegaly, hepatitis, splenomegaly, pulmonary nodules, pericarditis, abdominal pain, arthralgia, arthritis, myalgia, and urticaria. An association with inflammatory bowel disease has also been observed.
●Evaluation of the patient with possible CS requires ophthalmologic examination to establish the presence of IK, scleritis, or episcleritis and to exclude other diseases and ocular pathology; neurologic and otologic examination to establish the presence of vestibuloauditory abnormalities; and rheumatologic examination to seek evidence of systemic vasculitis. We diagnose CS based upon the presence of characteristic inflammatory eye disease and vestibuloauditory dysfunction. The eye and inner ear are nearly equally likely to be the cause of presenting symptoms, while less than 5 percent of patients initially present with systemic manifestations
Bhopalwala. H
●Anterior ischemic optic neuropathy – At least 80 percent of cases of vision loss in patients with GCA are caused by AION . The ischemic insult in arteritic AION is typically the consequence of occlusion of the posterior ciliary artery, a branch of the ophthalmic artery from the internal carotid artery, and the main arterial supply to the optic nerve.
Only about five percent of the total occurrences of AION are due to GCA, the majority being nonarteritic and secondary to atherosclerotic disease . About 40 percent of patients who suffer nonarteritic AION regain some amount of visual acuity, in contrast to visual loss due to GCA, which is more often massive and irreversible .
●Central retinal artery occlusion – CRAO is responsible for approximately 10 percent of the cases of visual loss in GCA . On the other hand, approximately two percent of older patients with CRAO have underlying GCA . Bilateral CRAOs in an older adult should prompt evaluation for GCA.
●Posterior ischemic optic neuropathy – PION occurs in less than five percent of patients with GCA . It results from the interruption of blood flow to the retrobulbar portion of the optic nerve. Histopathologic examination typically reveals inflammatory occlusion of the short nutrient posterior ciliary arteries .
●Branch retinal artery occlusion – BRAO is distinctly uncommon in GCA, though it has been described.
●Cerebral ischemia — Homonymous hemianopia is a visual field defect involving either the two right or the two left halves of the visual fields of both eyes. The most common cause in GCA is an occipital lobe infarction resulting from a lesion in the vertebrobasilar circulation. In rare cases, bilateral occipital lobe involvement leads to bilateral homonymous field defects and to the development of cortical blindness.
Bhopalwala. H
Causes of vision loss —
Permanent loss of vision in GCA results from arteritic anterior ischemic optic neuropathy (AION), central or branch retinal arterial occlusion (CRAO/BRAO), posterior ischemic optic neuropathy (PION), or, rarely, cerebral ischemia
●Anterior ischemic optic neuropathy – At least 80 percent of cases of vision loss in patients with GCA are caused by AION . The ischemic insult in arteritic AION is typically the consequence of occlusion of the posterior ciliary artery, a branch of the ophthalmic artery from the internal carotid artery, and the main arterial supply to the optic nerve.
Only about five percent of the total occurrences of AION are due to GCA, the majority being nonarteritic and secondary to atherosclerotic disease . About 40 percent of patients who suffer nonarteritic AION regain some amount of visual acuity, in contrast to visual loss due to GCA, which is more often massive and irreversible .
●Central retinal artery occlusion – CRAO is responsible for approximately 10 percent of the cases of visual loss in GCA . On the other hand, approximately two percent of older patients with CRAO have underlying GCA . Bilateral CRAOs in an older adult should prompt evaluation for GCA.
●Posterior ischemic optic neuropathy – PION occurs in less than five percent of patients with GCA . It results from the interruption of blood flow to the retrobulbar portion of the optic nerve. Histopathologic examination typically reveals inflammatory occlusion of the short nutrient posterior ciliary arteries .
●Branch retinal artery occlusion – BRAO is distinctly uncommon in GCA, though it has been described.
●Cerebral ischemia — Homonymous hemianopia is a visual field defect involving either the two right or the two left halves of the visual fields of both eyes. The most common cause in GCA is an occipital lobe infarction resulting from a lesion in the vertebrobasilar circulation. In rare cases, bilateral occipital lobe involvement leads to bilateral homonymous field defects and to the development of cortical blindness.
Bhopalwala. H
In normal eye aqueous humour flow from ciliary body to anterior chamber. In Malignant glaucoma or Aqueous misdirection syndrome, aqueous humour escapes into posterior chamber. Now posterior chamber has two fluids - aqueous and vitreous. This mixture now push our lens forward. This leads to formation of shallow AC.
Now in this case if I give Pilocarpine then ciliary zonules will be slacked which will ultimately causes lens to move more anteriorly, leading to shallow AC.
Remember: Pilocarpine is DOC for acute congestive glaucoma and it is C/I in inverse glaucoma.
So I will need to give drugs which will cause tightening of ciliary zonules. This can happen when I will relax ciliary muscle. Now relaxation of ciliary muscles is done by cycloplegic drugs. Example - Atropine/ Homatropine.
Did you see the contrast?
Atropine is C/I in Acute ACG but it is DOC for inverse glaucoma!
Hope it helps!
That's all
-Demotional bloke
#Medicowesome
#Ophthalmology
Q) In Dengue, all are seen w.r.t eye except:-
1) Cataract
2) Optic neuritis
3) Vitreous hemorrhage
4) Maculopathy
So, you basically cannot solve above problem if you don't know which portion dengue affects in eye.
Dengue affects posterior portion of the eye. So accordingly answer is
Cataract-Option 1
Some basics to cover over here.
Eyeball is divided into two segments or portion.
Anterior segment: Cornea to lens.
Volume - 0.31mL of Aqueous humor.
Posterior segment: Lens to retina.
Volume - 4mL of Vitreous humor.
Anterior segment is divided into two parts:-
Anterior chamber: Cornea to iris.
Volume- 0.25mL of Aqueous humor
Posterior chamber: Iris to lens.
Volume- 0.06mL of Aqueous humor
-Demotional bloke.
Question:
In Diabetic 3rd nerve palsy all are seen except
A) Pupil dilation
B) Outward and downward gaze
C) Ptosis
D) Impaired pupillary reflex
Let us start with the basic.
Mnemonic for extraocular muscles nerve supply
LR6 SO4 Rest3
Lateral rectus is supplied by 6th nerve or abducence nerve and superior oblique by 4th nerve or trochlear nerve and rest all muscles including LPS are supplied by 3rd muscle or occulomotor nerve.
In pupillary reflex,
Afferent nerve: Optic nerve
Efferent nerve: Occulomotor nerve.
So in case of 3rd nerve palsy, we will have less or no actions of all EOM except lateral rectus and superior oblique.
So we will have downward gaze (due to superior oblique) and outward gaze (due to lateral rectus) and Ptosis (because LPS is supplied by 3rd nerve! ).
Pupillary reflex is also disturbed so option 4 is also ruled out.
Here is a trick in this question. In DM and HTN, microangiopathy is seen due to which central fibers are affected.
Central part do not contribute to pupillary reflex.
This leads to no pupil dilation. In case of surgical conditions and trauma, peripheral fibers are affected which causes impaired pupillary reflex or pupil dilation.
-Demotional bloke.
