Candidate 55                                                    Centre: Edinburgh
MRCS Edinburgh (Passed)                                                  Date: December, 2004
MCQs 60 questions with 5 parts= 300 questions. Generally fair with questions on Wilson' disease and corneal dystrophies among others. I think I guessed too many which is not such a good idea as there is negative marking.

Day 2 had vivas 1 and 2 with viva 1 being ophthalmology and medicine and viva 2 being ophthalmic pathology and surgery.

In my first viva I started with medicine.

I was first asked to list the causes of atrial fibrilation-I said ischaemia,thrombosis and ageing.
I was asked the treatment of fibrillation and mentioned warfarin and digoxin. I was asked for side effects of warfarin and said high INR. I was then asked where bleeding occured most commonly and after a lot of thinking said stomach and oesophagus. I could not answer why these areas were most common and was told it was related to acid production.

I was then asked for management of anaphylaxis with FA and gave ABC and was asked about the route for giving adrenaline and said intramuscular but the examiner wanted subcutaneous also.

Next I was asked for the management of a diabetic patient who became unresponsive outside clinic. I said I would suspect hypoglycaemia and would check airway was clear before checking blood sugar and giving glucagon if sugar level was low.

I was then asked for vitamin deficiencies and the eye. I started with vitamin A deficiency and gave night blindness,xeropththalmia and tear problems. The examiner then asked what type of patients in Britain are affected and I gave malabsorption,alcoholics and drug users as the commonest groups as malnutrition is fortunately uncommon.The examiner asked me about vitamin B deficiency which I did not know and then asked about symptoms of  Korsakoff's syndrome.

The second half of viva 1 was ophthalmology.

The second examiner had an apple I book with a number of images.

The first patient showed bilateral proptosis,periorbital oedema and erythema of the eyes and I gave the most likely diagnosis as thyroid eye disease. I was asked for management and about treatment of suspected optic nerve compression including pulsed methylprednisolone and which orbital walls are decompressed.

The next patient had a fecial palsy and I was asked what tests I would want to do. I said I would like to exclude a cerebellopontine angle tumour which could cause facial palsy and was asked which tests I would do-corneal sensation,hearing and ocular motility. I was asked for other causes of facial palsy and said idiopathic. I was asked for any other names for this but did not know and was told it is Bell's palsy.

The next patient's picture was a CT scan of an orbital foreign body. I was asked would I do an MRI scan and said no in case it was metallic which could cause movement of the foreign body.

The next patient showed dystopia and I was asked for possible causes and said space occupying lesions.

My second viva started with pathology.

I was asked if a GP rang up with a contact lens wearing patient who had suspected keratitis whether I would see the patient that evening. I said yes and that I would want to examine the
patient with flourescein to measure the size of any corneal ulcer. I would also take a corneal scrape with gram staining to look for gram positive or negative organisms. I would also take samples for plating as well as for viral infections. I was asked which organisms I would be concerned about and said that pseudomonas would be the most important organism to cover given its virulence and I would start treatment with a broad spectrum antibiotictopically and suggested ciprofloxacin as well as mydriasis and systemic antibiotics. I said I would consider admission also. The examiner asked me if I would change treatment if the ulcer was improving but microbiology showed the present treatment not to be sensitive. I said no given the improvement but that I would consider adding in another antibiotic which was sensitive.

I was next asked what I knew about retinoblastoma. I said that it was a tumour of primitive neural rosettes which can form Flexner-Wintersteiner rosettes on histology. I then mentioned that it was due to deletion of a tumour suppressor gene and had different forms of inheritance. Before I could say more the bell rang for the end of the pathlogy part of the viva.

The second half of the viva was on surgery.

The examiner drew a lesion on the lower lid and asked me for my management. I asked how old the patient was so I could decide on the most likely cause as well as how long the lesion had been there. I was told it was a patient in their seventies and the lesion had been there six months. I said the most likely lesion was a basal cell carcinoma and in such a case I would want to do a pentangle-based incision with a clearance of 3mm to try and ensure all the tumour was removed. The examiner asked why I would do that shape of excision and I said that it was so I could close the lesion by apposing the grey line and allow healing. The examiner asked me if any other lesions were possible and I said in a case of squamous cell carcinoma the same shape of excision would be used but a clearance of 5mm would be needed.

Next I was asked my management of a drunk patient in casualty with a suspected perforating injury. I asked if it was possible to establish visual acuity and said that it was. I said I would then try and examine the patient on the slit-lamp with help from one of the nurses but was told that very limited examination was possible. I next suggested doing a CT scan to see if there was evidence to confirm suspicions of perforation and was told that the patient was cooperative and CT scan confirmed perforation. I was asked whether surgery would be needed that evening and said that examination under anaesthesia would be required and I would discuss the patient with the on-call consultant as well as contacting the
anaesthetist to arrange theatre. Another candidate told me that they had been asked about when SRF drainage would be needed for retinal detachment surgery which I thought quite tough.

Following the vivas we were all asked to attend the college at five o'clock to see if we were successful in getting to the clinical exam with a letter indicating failure and an A4 piece of paper indicating success with the time of the next exam. 

The first clinical exam was surgery and medicine.

I had two examiners who were both pleasant and they took it in turns to ask questions. 

Patient 1 had bilateral lens opacities and a stage 1 macular hole in the right eye and a stage 4 macular hole in the left eye. I was asked for my management and said I would ask the
patient how much the vision in the left eye was troubling them and whether they would be able to posture following macular hole surgery. I was asked if there was any other treatment possible and said there was significant cataract in the right eye and that cataract surgery could be offered.

This seemed to satisfy the examiners and the next patient I was shown had bilateral corneal
grafts,bilateral pseudophakia and right trabeculectomy. I was asked for possible reasons for corneal grafts and gave keratoconus,herpes zoster,Fuch's dystrophy and bullous keratopathy as causes. I was asked the most common reason in Britain and said keratoconus. The examiner asked me next what sort of cataract surgery had been done but I was unable to identify the corneal incision and so was not able to be sure on phaco vs extracapsular surgery. The next patient had bilateral corneal dystrophy and I thought at first it was a stromal dystrophy. The examiner asked me to look again and I eventually came up with endothelial dystrophy. The examiner asked me what type of dystrophy this was and I came up with Fuch's dystrophy.

I was then asked to examine a patient with an indirect ophthalmoscope. The patient had been dilated and was sitting in a chair and  I asked if I could examine the patient on the couch and after looking at each other the examiners eventually agreed. The patient was not dilated very well but I was not sure whether to mention this and in the end did not. It was a bit difficult to get a good fundal view and it was a bit disconcerting as one of the examiners was looking in the mirror to check my view. I could see some pigmentary changes superotemporally in the right eye and gave the diagnosis as previous retinal detachment with surgery. I was not asked too many questions about this fortunately as the examiners may have taken the poor view into account. We then went to a second room with more patients and I could see the examiners making notes on a clipboard but fortunately did not see what they had written.

I was asked to take a history from a patient at a slit lamp. The patient was in his forties and had poor vision since childhood. There was also a strong family history and I told the examiners I was considering retinitis pigmentosa. However further questioning revealed that vision was worse during the day so it appeared to be a macular dystrophy. I was then asked to say what treatment was possible and I said that there was no treatments for the condition except for visual aids but I would like to confirm the condition by doing electrophysiology. I was the asked to examine the patient's posterior segment and saw a fairly subtle maculopathy worse right than left. I was then asked what electrophysiology would show and said that there would be an abnorlal EOG . The examiners then asked me what the ERG would show but I did not know. The final patient had bilateral atrophic maculopathy and I gave a possible cause as myopia.

That night there was another wait before knowing if I had got through to the final clinical exam.

The final clinical exam was neurology and ophthalmology.

The two examiners were a bit more stern. I was taken into the first room and asked to comment on a patient with a facial palsy and occlusion to one of his spectacle lenses. I asked the patient to take off his glasses and noted a lateral tarsorrhaphy. The examiner asked me the reason for this and I suggested poor eyelid closure secondary to the facial palsy.
I then did a cover test and found an exotropia indicating sixth nerve involvement and accounting for the occlusion. The examiner asked me what condition I suspected and said cerebellopontine angle tumour. I was asked which other tests I would do and suggested corneal sensation and hearing. The examiner asked which tests I would do for hearing problems and suggested Rinne's and Weber's test using a tuning fork but could not remember which was bone conduction and which was air conduction.

I was next asked to look at a patients hands and saw symmetrical deformity with proximal swelling in keeping with RA. I was asked to say what abnormalities occur in the eye
and gave dry eyes,scleritis and episcleritis. I was asked the types of scleritis possible and gave anterior,psterior and necrotising. I was asked what corneal abnormalities occur and said thinning near the limbus. Next I was asked about treatment and listed NSAIDS,steroids and cyclosporin.

The third patient was examined on the slit-lamp and was a man in his forties. He had a vein occlusion in his right eye with haemorrhages and exudates. I commented that he was young to have had a vein occlusion and said I would like to investigate him for clotting abnormalities as well as routine investigations.

A bell rang and we went to the final room of the examination.

I was taken to a gentleman in his fifties who had been initially referred by his optometrist who had been noted an optic nerve abnormality. On questioning he did not have significant problems apart from slight blurring of vision and headache. At this point the examiner asked me if I noticed any speech problems and said there was a slight dysathria. The examiner said he had some problems with his gait and having realised that he was hinting about a cerebellar problem I asked if the gait was broad-based but the examiner said this had not been noticed. I was asked if there was anything else I could ask and so I asked the patient to say "baby hippopotamus" which was abnormal. I said I suspected cerebellar problems and asked for other tests and I did finger-nose pointing which was abnormal but hand pronation-supination seemed pretty good. Strangely enough I was not to test eye movements which would have been useful. I was asked for possible causes and said space occupying lesions,AV malformations and demyelination. I was asked the chance of optic neuritis being caused by MS and said 50% in males and 70% in females. As the final question the examiner asked if I would tell the patient about possible MS and I said this was a controversial area which seemed to satisfy the examiners.

My next patient was on a slit lamp. He had signs of diabetic retinopathy and I was asked
about HBA1C. I said it was a long term measure of diabetic control but could not remember if it was covalently or non-covalently bonded [answer= covalently] . I was also asked to examine the other eye and the patient  became very photophobic and I had to apologise to the patient to help open his eyes before seeing a 360 degrees indent. The examiner asked me about any other conditions I would worry about in diabetes and said hypertension.The patient was hypertensive.

My last patient had dilatation of his left eye as well as pseudophakia. I commented that the patient was fairly young being in his thirties. The examiner asked if I could see any other abnormalities and looked for heterochromia but could not find any. The examiner asked me to look at the anterior segment again and I eventually saw Lisch nodules and diagnosed NF-1. The examiner said that vision had not improved following surgery and asked why and I suggested optic glioma. I was then asked if given a dilated pupil in one eye it is possible to check for an RAPD and said that the other eye should be looked at and consensual reaction checked.


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