| Site of lesion | presentation | Common causes |
| | | |
| Optic nerve | Ipsilateral blindness, absent ipsilateral direct light reflex, absent contralateral consensual light reflex | Optic atrophy, acute optic neuritis and traumatic avulsion of optic nerve |
| Sagittal (central) lesions of optic chiasma | Bitemporal hemianopia | Supra-sellar aneurysms, pituitary tumors,craniopharyngioma, glioma of the third ventricle |
| Lateral chiasmal lesions | Binasal hemianopia | Distension of the third ventricle and atheroma of the posterior communicating arteries |
| Optic tract | Homonymous hemianopia , wernick’s hemianopic papillary response | Syphilitic meningitis, tuberculosis and tumors of the optic thalamus , aneurysms of superior cerebellar or posterior cerebral arteries |
| Lateral geniculate body | Homonymous hemianopia with sparing of papillary reflexes | Syphilitic meningitis, tuberculosis and tumors of the optic thalamus |
| Optic radiation – total fibres involved | Homonymous hemianopia ( sometimes sparing the macula ) | Vascular occlusion , primary and secondary tumors and trauma |
| Optic radiation – lower fibres only involved | Homonymous upper quadrantinopia ( pie in the sky ) | Temporal lobe lesions |
| Optic radiation – upper fibres only involved | Homonymous lower quadrantinopia ( pie on the floor ) | Anterior parietal lesions |
| Visual cortex | Homonymous hemianopia ( usually sparing the macula ) | Vascular occlusion , primary and secondary tumors and trauma |
Monday, December 22, 2008
21 - lesions of visual pathway and their presentations
Monday, December 15, 2008
20 - PGI december 2008 opthalmology mcqs - 1
----------------------------
retinal detachment is normally of three types
1. rhegmatogenous retinal detachment
2. exudative retinal detachment
3. tractional retinal detachment
the causes of the exudative retinal detachment are :
A. systemic causes : toxemia of pregnancy, reno vascular hypertension, polyarteritis nodosa and blood dyscrasias
B. ocular causes are again divided into
B1. inflammations : harada's disease, posterior scleritis, sympathetic opthalmitis, orbital cellulitis
B2. vascular causes : central serous retinopathy , exudative retinopathy of coats
B3. tumors : retinoblastoma ( exophytic type ) and malignant melanoma of choroid
B4. others : perforation of globe and intraocular operation
Saturday, November 15, 2008
19 - AIIMS november 2008 opthalmology mcqs with answers
1q: All of the following are true about horner's syndrome except ?
a. ptosis and miosis in ipsilateral eye
b. heterochromia of the iris
c. anhydrosis of the ipsilateral face
d. apparent exopthalmos
2q: which of the following is true about left abducens nerve palsy ?
a. left side adduction weakness
b. diplopia on left gaze
c. ptosis
d. accomodation paralysis
3q: refractory index is maximum for ?
a. cornea
b. anterior surface of lens
c. posterior surface of lens
d. centroid of lens
4q: inclusion conjunctivitis is caused by ?
a. chlamydia trachomatis
b. chlamydia psittaci
c. gonorrhea
d. herpes
Monday, August 4, 2008
18 - posner-schlossman syndrome
Glaucomatocyclitic crisis is a condition with self-limited recurrent episodes of markedly elevated intraocular pressure (IOP) with mild idiopathic anterior chamber inflammation. It is most often classified as secondary inflammatory glaucoma. In 1948, Posner and Schlossman first recognized glaucomatocyclitic crisis and described the features of this syndrome. For this reason, the entity is often termed Posner-Schlossman syndrome (PSS). They identified the following features:
- Recurrent episodes of mild cyclitis
- Uniocular involvement
- Duration of attack varying from a few hours to several weeks
- Signs of a slight decrease in vision, elevated IOP with open angles, corneal edema with a few keratic precipitates, heterochromia with anisocoria, and a large pupil in the affected eye
- Normal visual fields
- Normal optic disc
- Normal IOP, outflow facility, and all provocative tests between episodes
Since this original description, other cases attributed to glaucomatocyclitic crisis have been found to deviate from these criteria. For instance, some patients with glaucomatocyclitic crisis have abnormal aqueous humor dynamics and may have an underlying primary open-angle glaucoma (POAG). Additional features that are now recognized are as follows:
- Almost exclusively, this condition affects individuals aged 20-50 years.
- Both eyes may be involved at different times but very rarely contemporaneously.
- The rise of IOP is out of proportion to the severity of the uveitis, and this rise in IOP precedes the identifiable inflammatory reaction, often by several days.
Episodic changes in the trabecular meshwork lead to impairment of outflow facility and result in an elevation of IOP. These changes are accompanied by mild intraocular inflammation. In the acute phase of PSS, optic nerve head parameters and retinal flow rates were altered; however, all returned to normal without any permanent damage after resolution of the elevated IOP. Electroretinogram studies in the acute phase demonstrate a selective reduction in the S-cone b-wave.
Causes :
- The etiology of glaucomatocyclitic crisis has remained elusive. Several factors have been postulated as contributors to the development of glaucomatocyclitic crisis, to include the following:
·
- Abnormal vascular process
- Autonomic defect
- Allergic condition
- Variation of developmental glaucoma
- Cytomegalovirus (CMV)
- Herpes simplex virus
- Description of a final common pathway usually includes a reference to changes in the trabecular meshwork leading to a reduction of outflow facility. However, some authors describe an increase in aqueous production.
- Transfer coefficients of fluorescein in aqueous in the anterior chamber, by flow and by diffusion, are elevated during attacks of glaucomatocyclitic crisis. Between attacks, both coefficients return to normal.
- Elevations in IOP are postulated to be secondary to inflammation of the trabecular meshwork, which may be mediated by prostaglandins.
- Prostaglandins, especially prostaglandin E, have been found in higher concentration in the aqueous humor of patients during acute attacks. These levels return to normal between episodes.
·
- In a study using rabbit eyes, prostaglandin E was shown to contribute to a breakdown of the blood-aqueous barrier. This increase in the transfer coefficient of fluorescein is consistent with a similar response in animal eyes to prostaglandin E.
- The vascular effects of prostaglandins may contribute to the tortuosity seen in iris vessels and the leakage demonstrated with fluorescein angiography of the iris.
- To confuse matters, in another animal study, elevated prostaglandins increased outflow facility, which would contribute to a lower IOP and, thus, not be consistent with the reduced outflow facility seen in patients with glaucomatocyclitic crisis during an acute episode.
- Another theory purports an increased aqueous production resulting from elevated levels of aqueous prostaglandins.
- In summary, the exact mechanism by which prostaglandins regulate IOP has not been described, but a direct correlation between elevated levels of prostaglandins in the aqueous humor and the level of IOP has been found during acute attacks of glaucomatocyclitic crisis.
- Evidence exists that glaucomatocyclitic crisis may be associated with POAG. Patients with a 10-year or longer history of PSS are 3 times more likely to develop visual field changes and optic disc changes. These patients may have a higher than normal incidence of corticosteroid responsiveness, leading to an elevated IOP. This must be kept in mind during the treatment of this disorder with corticosteroids.
- Associations with immunogenetic factors also exist; in one study, the presence of human leukocyte antigen Bw54 (HLA-Bw54) was found in 41% of patients.
- Associations with certain allergic conditions and gastrointestinal diseases, most notably peptic ulcer disease, have been described.
Physical examination of the eye :
- On examination, the eye is quiet with either no injection or a mild ciliary flush.
- The pupil often is dilated slightly or sluggishly reactive; the anterior chamber is deep and has an open angle.
- This condition should be differentiated from closed-angle glaucoma with the help of gonioscopy.
- IOP usually is elevated in the range of 40-60 mm Hg.
- IOP is related to the duration of uveitis but not to the degree of uveitis.
- Eyes with active inflammatory disease often have wide swings in IOP, leading to glaucomatous damage.
- The elevated IOP can last for several hours to a few weeks; therefore, it can be missed on initial examination.
- If the elevated IOP is of significant duration and elevation, corneal epithelial edema develops.
- Signs of anterior inflammation are characteristically minimal with faint flare, rare cells, and only a few keratic precipitates that are stellate, flat, nonpigmented, and concentrated over the inferior half of the endothelium.
- Fine keratic precipitates appear after 2-3 days of elevated IOP and resolve rapidly.
- The inflammation never leads to the development of posterior synechiae or peripheral anterior synechiae.
- Fresh precipitates may appear with each episode of increased IOP.
- Heterochromia, described originally, is no longer considered a characteristic of this syndrome.
- Typical of inflammatory conditions, early segmental iris ischemia and associated late iris-vessel congestion have been observed. These vessels leak on iris fluorescein angiography.
Treatment :
Complete medical care for patients presenting with glaucomatocyclitic crisis includes a reasonably thorough history of present illness, a review of drug allergies and sensitivities, a targeted past medical history and review of systems, a complete eye examination, a careful explanation of the disorder in accordance with the patient's level of understanding, and a commitment to long-term follow-up care of the patient.
- Medical therapy should be individualized to meet the patient's needs. Currently, the favored initial treatment is a combined regimen of a topical nonsteroidal anti-inflammatory drug (NSAID) and an antiglaucoma drug.
- Treatment recommendations include the following:
·
- Topical steroids - Prednisolone acetate 1% 1 gtt qid, followed by taper
- Topical antiglaucoma drops - Timolol 0.25-0.5% 1 gtt bid or equivalent, or dorzolamide 2% 1 gtt bid/tid or equivalent (Beta-blockers should be avoided in patients with asthma.)
- Systemic carbonic anhydrase inhibitors - Acetazolamide 250 mg
- Topical NSAIDs - Diclofenac 0.1% 1 gtt tid/qid or equivalent
- Oral NSAIDs - Indomethacin 75-150 mg/d
- Miotics and mydriatic agents seldom are used because they may have further deleterious effects on the blood-aqueous barrier, and long-acting periocular steroids are frowned upon because of lingering IOP effects.
- NSAIDs reduce the inflammatory component by inhibiting the production of prostaglandins, and antiglaucoma medications reduce the influx of new aqueous; both these effects rapidly control the IOP. This combination also avoids potential IOP elevations caused by steroids in steroid-responsive patients.
- Well-informed and educated patients often can sense an impending attack based on ocular symptomatology, and they can institute appropriate self-therapy using an aqueous suppressant and a topical NSAID to blunt IOP elevations associated with treatment delays.
- Carefully observe patients periodically for recurrences of attacks and for development of POAG.
- In the absence of underlying chronic glaucoma, antiglaucoma agents do not prevent recurrences of glaucomatocyclitic crisis; therefore, they are not necessary between episodes.
An occasional patient may require a filtering procedure, which is not effective in preventing recurrences of the episodes of iritis but may be useful in the management of high IOP seen with these episodes. For example, a patient with excessively high pressures threatening vascular perfusion would be a candidate for a filtering procedure. No benefit is gained from laser trabeculoplasty.
Saturday, June 21, 2008
17 - alexander's law of nystagmus
Alexander's law was investigated in normal subjects as well as patients with vestibular lesions.
During sinusoidal rotations of normal subjects, there was no trace of this phenomenon when subjects looked 25 degrees left and right in the dark.
The phenomenon of Alexander's law is therefore created centrally and is not due to any mechanical properties of the orbit.
--During rotation at constant velocity in the dark, normal subjects did weakly demonstrate Alexander's law because of a mild gaze-evoked nystagmus present in normal subjects in the dark.
Gaze-evoked nystagmus from a cerebellar lesion involved a pronounced demonstration of Alexander's law during rotatory nystagmus.
--In patients with a vestibular lesion and a mild spontaneous nystagmus in the dark that obeyed Alexander's law, the nystagmus reversed upon far gaze in the slow-phase direction.
--in patients with a vestibular lesion, the phenomenon of Alexander's law is created by the sum of vestibular nystagmus and an abnormally large gaze-evoked nystagmus that is consequent to the vestibular lesion.
Thursday, June 19, 2008
16 - cherry red spot - macula - causes
answer :
1. Tay sachs disease
2. Sandhoff's disease
3. Gaucher's disease
4. Niemann pick's disease
5. CRAO - central retinal artery occlusion
6. Sialodosis
7. Berlin's edema ( commotio retinae )
8. Gangliosidoses
9. Metachromatic leukodystrophy
10. Multiple sulfatase deficiency
a number of mcqs have been asked from this question in various entrance tests . so be careful . if u know any other causes please post in the comments .
Sunday, March 2, 2008
15 - acute angle closure glaucoma ( AACG )
Background
Glaucoma is a nonspecific term used for several ocular diseases that ultimately result in increased intraocular pressure (IOP) and decreased visual acuity. Acute angle-closure glaucoma (AACG) is an ocular emergency and receives distinction due to its acute presentation, need for immediate treatment, and well-established anatomic pathology. Rapid diagnosis, immediate intervention, and referral can have profound effects on patient outcome and morbidity.
The acute angle closure literature has been plagued by the lack of a uniform definition and specific diagnostic criteria. Only in recent years has there been a strong push to standardize the definitions of the various forms of angle closure disease. Primary angle closure, primary angle-closure glaucoma, acute angle closure, and acute angle-closure glaucoma were previously used interchangeable. Now, acute angle closure is defined as at least 2 of the following symptoms: ocular pain, nausea/vomiting, and a history of intermittent blurring of vision with halos; and at least 3 of the following signs: IOP >21 mm Hg, conjunctival injection, corneal epithelial edema, mid-dilated nonreactive pupil, and shallower chamber in the presence of occlusion.
Primary angle closure is defined as an occludable drainage angle and features indicating that trabecular obstruction by the peripheral iris has occurred (ie, peripheral anterior synechiae, increased IOP, lens opacities, excessive trabecular pigmentation deposits). The term glaucoma is added if glaucomatous optic neuropathy is present.
Pathophysiology
AACG represents the end stage of processes resulting in the compromised egress of aqueous humor circulation and the subsequent increase in IOP. Aqueous humor is produced by the ciliary body in the posterior chamber of the eye. It diffuses from the posterior chamber, through the pupil, and into the anterior chamber. From the anterior chamber, the fluid is drained into the vascular system via the trabecular meshwork and Schlemm canal contained within the angle.
Several anatomic abnormalities lead to anterior chamber crowding and predispose individuals to AACG. These include shallower anterior chambers, thinner ciliary bodies, a thinner iris, anteriorly situated thicker lens, and a shorter axial eye length. Of the many predisposing anatomical variations, a narrow angle and a thin, floppy iris have the most devastating consequences.
In AACG, the eye's natural response of dilation to environmental or chemical stimuli results in a pathologic iris-lens apposition. The apposition and contact between the lens and the iris is called pupillary block. This term articulates the obstruction and blockage of aqueous flow from the posterior chamber to the anterior chamber. When pupillary block occurs in conjunction with a floppy thin iris, the increasing pressure in the posterior chamber causes the pliable iris, particularly the peripheral region, to bow forward in a process termed iris bombé. Iris bombé further closes the already narrow angle and compromises aqueous drainage thus increasing IOP.
Other proposed mechanisms of AACG include plateau iris, lens swelling, and ciliary block. Plateau iris is less common than pupillary block and is due to anterior insertion of the iris. The superfluous and crowded iris tissue blocks the trabecular meshwork and again leads to increased IOP.
Lens swelling and ciliary block are extremely rare. Lens swelling occurs in cases of cataracts in which hydration forces cause enlargement of the lens and subsequent crowding of the anterior chamber. Forces posterior to the lens can push the lens and iris forward causing ciliary block or vitreous pressure. This can be seen in pan-retinal photocoagulation, scleral buckles, and uveitis.
Frequency
United States
AACG occurs between 1 and 40 times for every 1000 Americans depending on their ethnicity.
Mortality/Morbidity
Outcome after AACG is dependent on duration from onset to treatment, underlying ocular disease, and ethnicity. The degree of IOP elevation has been shown to have less impact on future visual acuity. Studies report that as many as two thirds of individuals with AACG had no visual field loss. However, Asians appear to be more refractory to the initial medical management, and, even after definitive treatment, they experience a progressive increase in IOP and deterioration in visual acuity.
Race
AACG occurs in 1 of 1000 Caucasians, about 1 in 100 Asians, and as many as 2-4 of 100 Eskimos.
Sex
AACG predominately affects females because of their shallower anterior chamber.
Age
Elderly patients in their sixth and seventh decades of life are at greatest risk.
History
Classically, patients are elderly, suffer from hyperopia, and have no history of glaucoma.
- Most commonly, they present with periorbital pain and visual deficits. The pain is boring in nature and associated with an ipsilateral headache.
- Patients note blurry vision and describe the phenomenon of, "seeing halos around objects."
- Careful investigation may elucidate a precipitating factor (ie, dim light, anticholinergic, sympathomimetic medications).
- In a large percentage of patients, extraocular symptoms and systemic manifestations are the chief complaint.
- Patients present with headache and may receive medications for migraines or an evaluation for a subarachnoid hemorrhage.
- Several case reports discuss patients presenting with vomiting and abdominal pain that were misdiagnosed with gastroenteritis.
Physical
- The emergency department evaluation of the eye includes visual acuity, the external eye, visual fields, a funduscopic examination, pupils, ocular motility, and IOP. All of which tend to be affected in AACG.
- Patients complain of blurred vision, and testing reveals the ability only to detect hand movements. They are unable to identify numbers and letters on distance charts or near cards.
- Cornea and scleral injection and ciliary flush are present. The obviously edematous and cloudy cornea obscures the funduscopic examination.
- Increased IOP (normal limit, 10-20 mm Hg) and ischemia result in pain on eye movement, a mid-dilated nonreactive pupil, and a firm globe. Clinicians must take a comprehensive history and perform a thorough physical examination to ensure that this time-sensitive diagnosis is not missed.
Causes
- Shallower anterior chambers; anteriorly situated lens; shorter axial eye length; a thin, floppy iris; and a narrow angle lead to a higher propensity for development of AACG.
DIFFERENTIAL DIAGNOSIS
Acute Orbital Compartment Syndrome
Conjunctivitis
Corneal Abrasion
Corneal Laceration
Corneal Ulceration and Ulcerative Keratitis
Endophthalmitis
Herpes Zoster Ophthalmicus
Iritis and Uveitis
Orbital Infections
Periorbital Infections
Ultraviolet Keratitis
Vitreous Hemorrhage
Other Problems to be Considered
Anterior uveitis
Glaucoma, malignant
Glaucoma, neovascular
Plateau iris syndrome
Lab Studies
- The diagnosis of AACG is predicated upon the clinical presentation of painful vision loss and a physical examination revealing a fixed mid-dilated pupil. No definitive laboratory or imaging studies are available. However, tonometry must be performed and must demonstrate increased IOP.
Prehospital Care
The patient should be brought to the hospital in an expeditious manner to have IOP reduced. The patient should remain in the supine position as long as possible. The urge to wear eye patches, covers, or blindfolds should be resisted. By maintaining the conditions that cause pupillary dilation, these articles help perpetuate the attack. Their potential negative effects outweigh any cosmetic benefit.
Emergency Department Care
The treatment of AACG consists of IOP reduction, suppression of inflammation, and the reversal of angle closure. Once diagnosed, the initial intervention includes acetazolamide, a topical beta-blocker, and a topical steroid.
Acetazolamide should be given as a stat dose of 500 mg IV followed by 500 mg
Inflammation is an important part of the pathophysiology and presenting symptomology. Topical steroids decrease the inflammatory reaction and reduce optic nerve damage. The current recommendation is for 1-2 doses of topical steroids.
Addressing the extraocular manifestations of the disease is critical. This includes analgesics for pain and antiemetics for nausea and vomiting which can drastically increase IOP beyond its already elevated level. Placing the patient in the supine position may aid in comfort and reduce IOP. It is also believed that while supine, the lens falls away from the iris decreasing pupillary block.
After the initial intervention, the patient should be reassessed. Reassessment includes evaluating IOP, adjunct drops, and considering the need for further intervention such as osmotic agents and immediate iridotomy.
Approximately 1 hour after beginning treatment, pilocarpine, a miotic that leads to opening of the angle, should be administered every 15 minutes for 2 doses. In the initial attack, the elevated pressure in the anterior chamber causes a pressure-induced ischemic paralysis of the iris. At this time, pilocarpine would be ineffective. During the second evaluation, the initial agents have decreased the elevated IOP and hopefully reduced the ischemic paralysis so pilocarpine becomes beneficial in relieving pupillary block.
Pilocarpine must be used with caution. Theoretical concerns exist about its mechanism of action. By constricting the ciliary muscle, it has been shown to increase the axial thickness of the lens and induce anterior lens movement. This could result in reducing the depth of the anterior chamber and worsening the clinical situation in a paradoxical reaction. Despite this, pilocarpine is recommended to be used as an additional agent.
No standard rate of reduction for IOP exists; however, Choong et el identified a satisfactory reduction as IOP less than 35 mm Hg or a reduction greater than 25% of presenting IOP.1 If the IOP is not reduced 30 minutes after the second dose of pilocarpine, an osmotic agent must be considered. An oral agent like glycerol can be administered in nondiabetics. In diabetics, oral isosorbide is used to avoid the risk of hyperglycemia associated with glycerol. Patients who are unable to tolerate oral intake or do not experience a decrease in IOP despite oral therapy are candidates for IV mannitol.
Hyperosmotic agents are useful for several reasons. They reduce vitreous volume, which, in turn, decreases IOP. The decreased IOP reverses iris ischemia and improves its responsiveness to pilocarpine and other drugs. Osmotic agents cause an osmotic diuresis and total body fluid reduction. They should not be administered in cardiovascular and renal patients. Choong et el demonstrated that 44% of patients required the addition of an osmotic agent to decrease IOP.1 Repeat doses may be necessary if no effect is seen and if tolerated by the patient.
Laser peripheral iridotomy (LPI) performed 24-48 hours after IOP is controlled, is considered the definitive treatment for AACG. While LPI is the current definitive treatment, there is evidence to suggest that argon laser peripheral iridoplasty (ALPI) and anterior chamber paracentesis (ACP) may have increasing roles in the management of AACG.
In ALPI, burns are made in the peripheral iris resulting in iris contraction and opening of the angle. Some studies suggest ALPI causes a more immediate decrease in IOP, resulting in better outcomes with fewer side effects than systemic therapy. Systemic therapy must still be used with ACP, but ACP appears to instantaneously relieve symptoms.
The choice of which therapy to use will be made by an ophthalmologist who will evaluate all patients via gonioscopy with complete inspection of the angle. At institutions where an ophthalmologist is immediately available on staff, initial treatment should be performed in conjunction with the specialist.
If there is a delayed interval between the initial presentation and definitive ophthalmologic care, the emergency department physician should begin treatment as described above. After an appropriate reduction in IOP, immediate ophthalmologic evaluation must be ensured. If the IOP is unchanged or increased from the time of treatment, further treatment should be discontinued and the attack most likely will terminate only with LPI. Ocular massage through a closed eyelid may be preformed while waiting for ophthalmology if no other treatment reduces IOP.
Consultations
- Ophthalmologic consultation should be obtained as soon as possible because acute-angle closure glaucoma is an ophthalmologic emergency.
14 - acute angle closure glaucoma - drug therapy
The goal in treatment of AACG is to reduce IOP. Medical management is the first step. A prompt reduction in IOP using topical and systemic medication decreases the duration of elevated IOP and the potential for visual field loss. IOP reduction is accomplished via suppression of aqueous humor production, eliminating pupillary block, and reversing inflammation. As with any medical intervention, intimate knowledge of the drugs, their indications, contraindications, and potential side effects can aid the physician in providing the best treatment and a favorable outcome.
Drug Category: Carbonic anhydrase inhibitors
These are first-line agents that should be used immediately during the initial intervention. They reduce bicarbonate production in the ciliary epithelium and therefore decrease aqueous formation.
| Drug Name | Acetazolamide (Diamox) |
|---|---|
| Description | Reduces rate of aqueous humor formation by direct inhibition of enzyme carbonic anhydrase (CA) on secretory ciliary epithelium, causing, in turn, a reduction in IOP. More than 90% of CA must be inhibited before IOP reduction can occur. May reduce IOP by 40-60%. Effects are seen in about an hour, they peak in 4 h, and trough in about 12 h. Derived chemically from sulfa drugs. If one form is not well tolerated, another form may be better or lower dose of the drug may better tolerated. IV administration of this medication may be used for rapid relief of increased IOP. A beneficial effect occurs when used with miotics or mydriatics. |
| Adult Dose | 500 mg IV stat, followed by 500 mg PO |
| Pediatric Dose | 5-10 mg/kg/dose IV/IM, then 0-15 mg/kg/d PO divided q6-8h |
| Contraindications | Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction |
| Interactions | Can decrease therapeutic levels of lithium and alter excretion of drugs (amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose level in some diabetic patients |
| Drug Name | Methazolamide (Neptazane) |
|---|---|
| Description | Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP. |
| Adult Dose | 50-100 mg PO bid/tid |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; renal impairment |
| Interactions | May increase toxicity of salicylate, digoxin; coadministration with other diuretics may induce hypokalemia; decreases effects of lithium and alter excretion of other drugs by alkalinizing urine |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Caution in respiratory acidosis and diabetes mellitus; impairs mental alertness and/or physical coordination; hematuria, glycosuria, polyuria, hepatic insufficiency, bone marrow suppression, thrombocytopenia/purpura, agranulocytosis, urticaria, pruritus, and rash may occur |
Drug Category: Beta-adrenergic blockers
These agents may lower IOP via their suppression of aqueous humor production and probably not through any affects on the pupil.
| Drug Name | Timolol (Timoptic, Timoptic XE) |
|---|---|
| Description | Reduces elevated and normal IOP by reducing aqueous humor production or possibly the outflow. |
| Adult Dose | 1 gtt of 0.25% or 0.5% solution in affected eye(s) bid; if IOP is maintained at satisfactory levels, reduce dosage to 1 gtt qd in affected eye(s) |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV block; severe chronic obstructive pulmonary disease; overt cardiac failure; cardiogenic shock |
| Interactions | May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects) |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Product may have sulfites, which may cause allergic-type reactions in susceptible patients; may exacerbate or precipitate heart block, asthma, chronic obstructive pulmonary disease, mental changes (especially in the elderly persons) |
| Drug Name | Carteolol (Ocupress) |
|---|---|
| Description | Nonselective beta-adrenergic receptor. Blocks beta1- and beta2-receptors and has mild intrinsic sympathomimetic activity (ISA), with possibly fewer cardiac and lipid profile adverse effects. Precise mechanism by which carteolol decreases IOP is thought to be through reduction of aqueous formation. |
| Adult Dose | 1 gtt in affected eye(s) bid |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; congestive heart failure; asthma; cardiac conduction defects; breastfeeding |
| Interactions | May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects) |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Product may have sulfites, which may cause allergic-type reactions in certain susceptible persons |
| Drug Name | Levobetaxolol (Betaxon) |
|---|---|
| Description | Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces IOP by reducing production of aqueous humor. |
| Adult Dose | 1 gtt in affected eye(s) bid |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; bronchial asthma; severe chronic obstructive pulmonary disease; sinus bradycardia; second- and third-degree AV block; overt cardiac failure; cardiogenic shock |
| Interactions | May have additive systemic effects if patient is already on systemic beta-blockers |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Beta-blockade may potentiate muscle weakness consistent with myasthenic symptoms; product may have sulfites, which may cause hypersensitivity reactions in susceptible persons |
| Drug Name | Levobunolol (AKBeta, Betagan) |
|---|---|
| Description | Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production and may increase outflow of aqueous humor. Dosages of more than 1 gtt of 0.5% levobunolol twice daily have not been shown to be more effective. If IOP not at satisfactory level on this regimen, concomitant therapy can be instituted. However, do not administer 2 or more topical ophthalmic beta-adrenergic blocking agents simultaneously. |
| Adult Dose | 0.5% solution: 1-2 gtt in affected eye(s) qd 0.25% solution: 1-2 gtt in affected eye(s) bid Severe or uncontrolled glaucoma: 0.5% solution bid; closely monitor patient >1 gtt (0.5% levobunolol) bid not shown to be more effective; if IOP not at satisfactory level on this regimen, concomitant therapy can be instituted; do not administer 2 or more topical ophthalmic beta-adrenergic blocking agents simultaneously |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; bronchial asthma; severe chronic obstructive pulmonary disease; sinus bradycardia; second- and third-degree AV block; overt cardiac failure; cardiogenic shock |
| Interactions | May cause bradycardia and asystole when used in combination with systemic beta-blockers (may cause additive effects) |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Beta-blockade may potentiate muscle weakness that is consistent with certain myasthenic symptoms (eg, diplopia, ptosis, generalized weakness); product may have sulfites, which may cause allergic-type reactions in certain susceptible persons |
Drug Category: Alpha-adrenergic agonists
These agents are used as adjunct agents to further decrease IOP secondary to their affect on aqueous humor production.
| Drug Name | Apraclonidine (Iopidine) |
|---|---|
| Description | Potent alpha-adrenergic agent selective for alpha2-receptors with minimal cross-reactivity to alpha1-receptors. Suppresses aqueous production. Reduces elevated, as well as normal, IOP whether or not accompanied by glaucoma. Apraclonidine is relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects. |
| Adult Dose | 1 gtt of 0.5% or 1% in affected eye(s) tid |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; patients on MAO inhibitors or have taken them in the past 14 d |
| Interactions | Monitor pulse and BP frequently when giving cardiovascular drugs; not for use concurrently with MAO inhibitors |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | May exacerbate or precipitate ocular irritation, topical sensitivity, vasovagal attack and optic nerve ischemia in patients with advanced glaucomatous optic neuropathy |
| Drug Name | Brimonidine (Alphagan, Alphagan-P) |
|---|---|
| Description | Selective alpha2 receptor that may reduce aqueous humor formation, may decrease inflow, or may increase uveoscleral outflow. |
| Adult Dose | 1 gtt in affected eye tid |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; patients receiving MAO inhibitor therapy |
| Interactions | Coadministration with topical beta-blockers may further decrease IOP; tricyclic antidepressants may decrease effects of brimonidine; CNS depressants such as barbiturates, opiates, and sedatives may potentiate effects of brimonidine |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals |
| Precautions | May exacerbate or precipitate ocular irritation, topical sensitivity, vasovagal attack and optic nerve ischemia in patients with advanced glaucomatous optic neuropathy |
Drug Category: Corticosteroids
These agents reduce ocular inflammation thereby providing symptomatic relief and augmenting the affects of other medications.
| Drug Name | Prednisolone (AK-Pred, Econopred) |
|---|---|
| Description | Used in treatment of acute inflammations following eye surgery or other insults to the eye. In cases of bacterial infections, concomitant use of anti-infective agents is mandatory. If signs and symptoms do not improve after 2 d, reevaluate the patient. Dosing may be reduced, but advise patients not to discontinue therapy prematurely. |
| Adult Dose | Solution: 1-2 gtt of solution into conjunctival sac up to q1h during day and q2h at night prn When a favorable response observed, reduce dosage to 1 gtt q4h; further reduction in dosage to 1 gtt tid/qid may suffice to control symptoms Susp: Shake well before using; 1-2 gtt into conjunctival sac bid/qid; during initial 24-48 h, dosing frequency may be increased prn |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; viral, fungal, or tubercular skin lesions |
| Interactions | Decreases effects of salicylates and toxoids (for immunizations); phenytoin, carbamazepine, barbiturates, and rifampin decrease effects of corticosteroids |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Caution in hyperthyroidism, osteoporosis, cirrhosis, nonspecific ulcerative colitis, peptic ulcer, diabetes, and myasthenia gravis |
Drug Category: Ophthalmic agents, miotic
These agents pull the peripheral iris tissue away from the trabecular meshwork helping to eliminate obstructed aqueous humor flow. They are ineffective during the initial period due to the ischemic paralysis of the iris. Miotics should be used after the immediate management and initial reduction of IOP.
| Drug Name | Pilocarpine (Pilagan, Pilocar, Pilostat) |
|---|---|
| Description | Patients may be maintained on pilocarpine as long as IOP is controlled and no deterioration in visual fields is present. May be used alone or in combination with other miotics, beta-adrenergic blocking agents, epinephrine, carbonic anhydrase inhibitors, or hyperosmotic agents to decrease IOP. Frequency of instillation and concentration are determined by patient's response. Individuals with heavily pigmented irides may require higher strengths. |
| Adult Dose | Solution: 1-2 gtt tid/qid Gel: Apply 0.5-inch ribbon in the lower conjunctival sac of affected eye(s) hs If another glaucoma medication being used hs, use gtt at least 5 min before gel |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; acute inflammatory disease of anterior chamber |
| Interactions | May be ineffective when used concomitantly with nonsteroidal anti-inflammatory agents |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Caution in acute cardiac failure, peptic ulcer, hyperthyroidism, GI spasm, bronchial asthma, Parkinson disease, recent MI, urinary tract obstruction, and hypertension or hypotension |
Drug Category: Hyperosmotics
Hyperosmotic agents increase serum osmolarity and cause a fluid shift from the eye into the vascular space. The subsequent osmotic diuresis reduces IOP.
| Drug Name | Glycerin (Osmoglyn) |
|---|---|
| Description | Used in glaucoma to interrupt acute attacks. Reduces IOP through its diuretic effects. Adds to tonicity of blood until metabolized and eliminated by kidneys. Maximal reduction of IOP occurs 1 h after glycerin administration. The effect lasts approximately 5 h. |
| Adult Dose | 1-2 g/kg PO and repeat q5h prn; alternatively, 1 mL/kg PO as a 50% solution in juice |
| Pediatric Dose | Administer as in adults |
| Contraindications | Documented hypersensitivity; frank or impending acute pulmonary edema, anuria, severe dehydration, and severe cardiac decompensation |
| Interactions | None reported |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Administer orally, never parenterally; for oral use only; avoid in acute urinary retention in preoperative period; continued use may result in weight gain; caution in hypervolemia, diabetes, severely dehydrated individuals, confused mental states, congestive heart disease, and cardiac, renal, or hepatic disease |
| Drug Name | Isosorbide (Ismotic) |
|---|---|
| Description | In the eyes, creates an osmotic gradient between plasma and ocular fluids. Induces diuresis by elevating osmolarity of glomerular filtrate, thereby hindering tubular reabsorption of water. May be used to interrupt an acute attack of glaucoma. Use when less risk of nausea and vomiting, compared with other oral hyperosmotic agents, is needed. |
| Adult Dose | 1.5 g/kg PO initially, followed by 1-3 g/kg PO bid/qid prn |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; anuria, severe dehydration, frank or impending acute pulmonary edema, and severe cardiac decompensation |
| Interactions | None reported |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Use repetitive doses with caution, particularly in patients with diseases associated with salt retention |
| Drug Name | Mannitol (Osmitrol) |
|---|---|
| Description | Reduces elevated IOP when pressure cannot be lowered by other means. Initially assess for adequate renal function in adults by administering a test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow of at least 30-50 mL/h of urine over 2-3 h. In children, assess for adequate renal function by administering a test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow of at least 1 mL/h over 1-3 h. |
| Adult Dose | 1.5-2 g/kg IV as 20% solution (7.5-10 mL/kg) or as 15% solution (10-13 mL/kg) over a period as short as 30 min |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; anuria, severe pulmonary congestion, progressive renal damage, severe dehydration, active intracranial bleeding, and progressive heart failure |
| Interactions | May decrease serum lithium levels |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Carefully evaluate cardiovascular status before rapid administration of mannitol since a sudden increase in extracellular fluid may lead to fulminating CHF; avoid pseudoagglutination, when blood given simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution; do not give electrolyte-free mannitol solutions with blood |
13 - 151 to 200 important mcqs in opthalmology
151- which type of cataract has high visual morbidity ? posterior subcapsular
152- a person suffered blunt trauma to the right eye with immediate loss of vision , on examination the anterior chamber is deep ? diagnosis ? lens dislocation.
153- IOL is mostly implanted in which chamber ? posterior chamber .
154- good vision in dim light and clumsy vision in day light is a feature of which type of cataract ? nuclear .
155- snow blindness is caused by ? ultravoilet rays .
156- diabetic cataract is due to accumulation of ? SORBITOL .
157- cataract is responsible for what percent of blindness in india ? 75 %
158- subluxation of lens is seen in ? MARFAN'S SYNDROME , MARCHESON'S SYNDROME , HOMOCYSTINURIA . there is no dislocation of lens in lowe syndrome
.
159- in cataract following operation , spectacles are advised after how many weeks of operation ? 6 WEEKS .
160- type of cataract produced by steroids ? posterior subcapsular.
161- cataract can be produced in experimental animals by depriving them of which amino acid? TRYPTOPHAN .
162- lens develops from ? surface ectoderm .
163- intraocular lenses are made up of ? PMMA
164- rider's cataract is seen in ? zonular or lamellar cataract.
165- a 55 year old female comes to the eye casualty with history of severe eye pain , redness and dimunition of vision , on examination the visual acuity is 6/60 ,
there is circumcorneal congesiton , corneal oedema and a shallow anterior chamber , which of the following is the best drug of choice?
a- atropine ointment b- i.v mannitol c-ciprofloxacin eye drops d-betamethasone eye drops .
---------- ans is i.v mannitol ..... as the diagnosis is acute angle closure glaucoma -- the other three drugs are not used in this case . the other drugs used in AACG are
carbonic anhydrase inhibitors ( acetazolamide ), beta blockers( timolol, carteolol, levobetaxolol and levobumolol) , alpha agonists( apvaclonidine brominidine ) ,
opthalmic miotics , steroids and hyperosmotics ( mannitol , glycerine and isosorbide ) .
166- beta blockers are contraindicated in ? hypotension , asthma and depression.
167- the latest technique in cataract surgery is using ? LASER
168- Yttrium laser - after cataract surgery .
169- among the following 4 which is the ideal rehabilitation for aphakia ? a- spectacles b- contact lens c-anterior chamber intraocular lens d- posterior chamber IOL
---------- ans is posterior chamber iol.
170- a child 6 months old , large cornea and photophobia . diagnosis ? CONGENITAL GLAUCOMA . other causes for large cornea like keratoglobus and megalocornea are mostly
asymptomatic except for partial visual impairment seen only in keratoconus . keratoconus is only characterised by hazy cornea due to fragmentation of the bowmans layer .
there is no impairment of vision in megalocornea.
171- drug of choice for acute congestive glaucoma ? 1-2 % PILOCARPINE . ( miotic , muscarinic agonist ,also used in dry mouth and dry throat ( xerostomia )
which can occur as a side effect of radiation therapy to head and neck .as it increases the salivary secretions and sweat secretions . )
172- 100 days glaucoma is seen in ? CENTRAL RETINAL VEIN OCCLUSION.
173- SAFE strategy( WHO VISION 2020 ) is used in the control of ? TRACHOMA .
174- corneal epithelium is ? stratified non keratinised epithelium.
175- cobble stone appearance of the conjuctiva is typically seen with ? SPRING CATARRH
176- tranta's spots alone are seen in vernal kerato conjunctivitis( SPRING CATARRH ) where as the trantas spots and herbert's pits together are seen in TRACHOMA .
177- features of trachoma are - pannus formation , follicles , papillary hypertrophy, herbert's pits and tranta's spots .
178- what is safe strategy ? surgery , antibiotics , facial cleanliness and environment improvement.
179- blindness in a child is most commonly due to ? keratomalacia - vit a deficiency .
180- horner trantas spots - vernal catarrh .
181- the colors best appreciated by the central cones of the fovea - macular region are ? RED AND GREEN .
182- mydriatic used in children for refraction is ? atropine ointment .
183- for refraction in a hypermetropic child , the best drug is ? atropine ointment
184- the term anisometropia indicates refractive error .
185- most sensitive part of the eye ? fovea centralis .
186- what all can be detected by indirect opthalmoscopy ? periphery of the retina , examination of the fovea , examination of the ora serrrata. the base of the vitreous cannot be
viewed by indirect opthalmoscopy .
187- ocular diseases given importance in vision 2020 program ? cataract , trachoma , glaucoma . refractive errors are not given importance .
188- Homonymous hemianopia caused by lesion in ? optic tract , optic radiation and occipital cortex .
189- in paralytic squint - secondary deviation is greater than the primary deviation .
190- nystagmus which is not pathological ? OPTOKINETIC NYSTAGMUS .
191- basal cell carcinoma at inner canthus of eye treatment? WIDE EXCISION AND RECONSTRUCTION .
192- NADPH DEPENDENT ALDOLASE REDUCTASE - enzyme responsible for accumulation of sorbitol in lens in diabetic patients which leads to cataract.
193- causes for pseudo proptosis? bupthalmos , retraction of the upper eyelid and high axial myopia .
194- most common type of lid carcinoma ? basal cell carcinoma .
195- steroid induced cataract is mostly - posterior subcapsular .
196- most common systemic association of scleritis ? RHEUMATOID ARTHRITIS .
197- under the national programme for control of blindness who is supposed to conduct the vision screening of school students ?
--------school teachers .
198- crocodile tears are seen with abnormal facial nerve regeneration.
199- most common allergic manifestation of tuberculosis ? KOEPPE'S NODULES .
200- koeppe's and busaca's nodules are characteristic of - GRANULOMATOUS UVEITIS .
12 - 101 to 150 important mcqs in opthalmology
101- layers of retina from within outwards are : 1- stratum opticum
2- ganglionic layer
3- inner plexi form layer
4- inner nuclear layer ( layer of inner granules )
5- outer plexiform layer
6- outer nuclear layer ( layer of outer granules )
7- layer of rods and cones
102- a patient complains of pain both eyes with congestion , blurrng of vision , photophobia and mucopurulent discharge since one day , many cases
have been reported from the same community , causative agent is a- adeno virus b- entero virus 70 c- herpes simplex d- ECHO virus
----------- answer is entero virus 70 --- because in entero virus there is sudden onset and short duration , where as in adeno virus photophobia and epithelial keratitis
occurs 5 to 14 days after tearing and pain. ( pg- 313- ashish vol 2 )
103- a neonate 30 days old , presented with excessive lacrimatiion and photophobia , he has large and hazy cornea . his both lacrimal duct systems are normal , the diagnosis is ?
a- congenital glaucoma b- keratoconus ( keratoglobus ) c- megalocornea d- hunters syndrome
-----------answer is congenital glaucoma because the symptoms mentioned above are not seen in other three cases . when iop raises in children less than 3 years of age , the size of the globe
increases condition called buphthalmos .( pg 315 - ashish vol 2)
104- HAABS striae - corneal opacities due to rupture in descemets membrane - seen in buphthalmos - congenital glaucoma ( infantile glaucoma ).
105-a 12 year old boy presents with recurrent attacks of conjunctivitis for the last 2 years with intense itching and ropy discharge . the diagnosis is
---------------- VERNAL KERATOCONJUNCTIVITIS ( SPRING CATARRH - cobble stone ) ----- ropy discharge is the clue .
106- 60 year old male patient operated for cataract 6 months back now complains of floaters and sudden loss of vision , the diagnosis is ?
a - vitreous hemorrhage b- retinal detachment c- central retinal artery occlusion d- cystoid mcular edema
---------------answer is retinal detachment , because of all the options only a and b can cause floaters and out of the two vitreous hemorrhage is a acute complication
and the retinal complication is a long term complication .
107- causes of large cornea - keratoconus , megalocornea , bupthalomos ( congenital glaucoma )
108- late post operative complications of cataract surgery? after cataract ( Nd YAG laser ) , retinal detachment , cystoid macular edema , epithelial ingrowth , vitreous touch syndrome .
109- most common late postoperative complication of cataract surgery ? CYSTOID MACULAR EDEMA
110- causes of floaters ? retinal detachment , vitreous hemorrhage , coats disease , eales disease , HTN retinopathy , DM retinopathy , SABE , leukemia , pars planitis, retinal branch vein occlusion, ( LPR )
111- causes of sudden painless loss of vision? CRAO , CRVO , RD , VH , Macular edema due to any cause , anterior ischemic optic neuropathy .
112- a 25 year old lady presents with severe sudden onset of pain , corneal congestion , photophobia and deep anterior chamber in the right eye . the left eye is normal . x ray pelvis shows , sacroiliitis ?
-------------the diagnosis is anterior uveitis . the lady is suffering from ANKYLOSING SPONDYLITIS and the most common ocular manifestation in AS is anterior uveitis . 3 men AS= 1 WOMEN AS.
113- the most common complication of hypermature sclerotic cataract is ? lens dislocation .
114- a male patient with a history of hypermature cataract presents with a 2 day history of ciliary congestion , photophobia , blurring of vision and on examination has a deep
anterior chamber in the right eye , the left eye is normal. the diagnosis is - a - phakomorphic glaucoma b- phakolytic glaucoma c- phakotoxic glaucoma d- phakoanaphylactic uveitis
------------------ ans is phacoanaphylactic uveitis ... no symptoms of glaucoma like severe pain , hazy cornea , fixed dilated pupil. - complications caused by hypermature morgagnian type of
cataract are phacolytic glaucoma( leaked proteins blocking the outflow ) and phacoanaphylactic uveitis ( leaked proteins inducing antigen antibody reaction ) .
115- paralytic patient presents with ? diplopia , deviation, confusion
116-nystagmus which is not pathological ? OPTOKINETIC
117-in a child with retinoblastoma , on x ray we can see ? intra orbital calcification , multiple cranial deposits and widening of the optic foramen. intracerebral calcification is not present .
118- one year old male child with cats eye reflex and increased intraocular tension , diagnosis ? RETINOBLASTOMA
119-what is amblyopia ? partial loss of sight in one or both eyes in the absence of opthalmoscopic or other marked objective signs . congenital or acquired . acquired can be organic ( toxic )
or functional. functional amblyopia results from the psychical suppression of the retinal image . it may be anisometric , strabismic or due to stimulus deprivation.
120- what is amblyopia ex anopsia ? amblyopia due to stimulus deprivation .
121- tests done for visual malingering ( one eye blind ) ? 1-convex lens test 2- prism base down test 3- prism base out test 4- snellens coloured types test ( a good eye can read
only red letters thru a red glass .)
122- what is amourosis ? complete loss of sight in one or both eyes in the absence of opthalmoscopic or other marked objective signs . types a- amaurosis fugax - sudden , temporary
and painless monocular visual loss occuring due to a transient failure of retinal circulation . common causes are carotid transient ischaemic attacks , embolization of retinal
circulation , papilledema , giant cell arteritis , raynaud's disease , migraine , as a prodromal symptom of CRAO or carotid artery occlusion , hypertensive retinopathy and venous
stasis retinopathy . b- uraemic amaurosis - sudden , bilateral ,complete loss of sight occuring probably due to the effect of certain toxic materials upon the cells of the visual centre
in patients suffering from acute nephritis , eclampsia of pregnancy and renal failure .visual loss is associated with dilated pupils which generally react to light , the fundi are usually
normal except for the coincidental findings of the hypertensive retinopathy , when associated . usuallly the vision recovers in 12 to 48 hours .
123- saccade - abrupt involuntary rapid eye movements .
124- field defect seen in pituitary adenomas and craniopharyngiomas - BITEMPORAL HEMIANOPIA ( temporal halfs of both sides lost ) . lesion or compression at the optic chiasma .
125- amblyopia shud be corrected within how many years? 5 years
126- visual defect in optic chiasmal lesion ? bitemporal hemianopia .
127- what is homonymous hemianopia ? visual field defect in which in one eye nasal field is visible and in the other eye temporal field is visible .
128- paralysis of the 3rd , 4th and 6 th nerve with the paralysis of the opthalmic division of the 5 th nerve , localises the lesion to ? CAVERNOUS SINUS .
129- A 25 year old male gives a history of sudden painless loss of vision in one eye for the past 2 weeks .no history of trauma . on examination the anterior segment is normal but there is no
fundal glow . what is the diagnosis ? a- vitreous hemorrhage b- developmental cataract c- optic atrophy d- acute attack of angle closure glaucoma-----
--------- answer is vitreous hemorrhage ... development cataract - there is gradual loss , optic atrophy also gradual loss , angle closure glaucoma acute attack is associated with pain.
130- levator palpebrae superioris is supplied by which nerve ? oculomotor nerve
131- UVEITIS associated with VITILIGO and AUDITORY DEFECTS occurs in ? VOGT - KOYANAGI SYNDROME .
132- sympathetic opthalmia is ? BILATERAL NON SUPPURATIVE UVEITIS .
133- most common cause of anterior uveitis associated with arthritis ? ANKYLOSING SPONDYLITIS.
134- the type of synechiae in iris bombe is ? RING TYPE .
135- SALT AND PEPPER FUNDUS IS SEEN IN ? CONGENITAL SYPHILIS .
136- visible retinal artery pulsations are seen in? increased intraocular tension
137-sudden increase in blood sugar in diabetics causes ? myopia
138- black floaters in a biabetic patient indicate ? vitreous hemorrhage .
139- an young adult male presents with sudden painless loss of vision , he recovered spontaneously within 3 months . diagnosis? central serous retinopathy.
140- berlin's edema is due to ? blunt injury .
141- vitreous hemorrhage in young adults indicates ? EALES DISEASE .
142- degree or development of diabetic retinopathy depends on ? duration of disease.
143- lens contains the oldest cells in ? the nucleus
144- the prominent ocular manifestation seen with the marfans syndrome? ectopia lentis .
145- typical glucocorticoids cause ? cataract and glaucoma .
146- commmonest cause of cataract ? age related .
147- retinal detachment is preceded by ? high myopia , trauma, floaters and flashes
148- laser used in the management of after cataracts ? Nd YAG laser .
149- atopic cataract is that which follows skin diseases like eczema .
150- CHRISTMAS TREE CATARACT IS SEEN IN ? MYOTONIC DYSTROPHY.
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