20 Paces Cases

Transcript

7th CN Palsy ( LMN TYPE) It is not enough to just diagnose the condition but you have to search for the cause. facial nerve contains three components ( sensory, motor and parasympathetic ) Sensory fibres supply anterior twothird of the tongue, floor of the mouth and palate, and cutaneous sensation from part of the external ear LOOK FOR facial asymmetry - Forehead wrinkles, Nasolabial folds ,Watch spontaneous movements –smiling, blinking. CONFIRM> The side of facial weakness by asking patient to raise eyebrows, shut eyes tight, smile and show teeth and blow up cheeks.. Differential diagnoses : - BELL'S PALSY(DIAGNOSES OF EXCLUSION) -Ramsay Hunt syndrome -Cerebellopontine angle tumor -Parotid tumor -Trauma/surgery -Middle ear disease -Pontine lesion eg stroke, multiple sclerosis -mono neuritis multiplex FROM ETIOLOGICAL POINT OF VIEW LOOK > Ear of the affected side for ( Ramsay Hunt syndrome as the cause ) Scar over the parotid gland and palpate for parotid tumor. Eye movements particularly looking for nystagmus and abducens palsy over the affected side. Check the corneal reflex and facial sensation.(Loss of corneal reflex is an early sign of cerebellopontine lesion) Perform Rinne's and Weber's test (Sensory neural deafness in CP angle tumor). Check Cerebellar signs and pronator drift (pontine lesion). Tell examiner that you would like to do otoscopy (Middle ear disease) & fundoscopy (MS/DM/SLE) .Ask examiner you want to check sensation over ant one third of toungue. Prepare the following questions. 1) What are the common causes of lower motor facial nerv1e palsy? 2) Why there is sapring of upper portion of facial muscles in upper motor lesion of facial nerve? 3) How would manage Bell's palsy? 4) What are three components of facial nerve?. Dr SHUHAIB.MBBS.MD (Internal Medicine).MRCP (UK). Like PACES EXPERIENCE OF A MALAYSIAN TAKING MRCP UK PACES EXAMINATION Singapore Experience (The New Beginning) UK Experience (The Dark Side) Malaysia Experience (The Return of the Jedi) Is PACES a torturing exam ? It was no difficulty for me to get through the Part 1 and Part 2 written exam of MRCP. However, PACES can be a nightmare. Let me share my experience here with those who are planning to sit for the MRCP or the PACES. I took PACES in 3 different regions – Singapore, Edinburgh and Malaysia and finally passed in October 2007. Many people helped me through this exam and I would also like to thank them on the way of my writing. I started preparing for PACES since 2005 and it has been a long way. The people who helped me at that time was my colleague Dr. David, who is also one of the authors of this book. He used to take me for short cases everyday whenever there is an interesting case. His motto was practice, practice and practice. Besides that, Dr. Haniffah who is a consultant Neurologist used to take us for Neuro cases every week. We formed a group of 4 and also started practicing on our own. However, I was rather immature at that time when I sat for the Singapore exam. Singapore Experience (The New Beginning) As cost was an issue for me, I booked a hotel which was average in Singapore but found myself having difficulty in sleeping the whole night, probably due to anxious state. The next morning just 2 hours before the exam, I found out that I have forgotten to bring my tie to Singapore. It caused me more panic as it was not easy to find a tie at 7.30 to 8.00 am as the malls in Singapore were still closed. I had to run all over Orchard Road to find a tie. Fortunately, I arrived at Meritus Mandarin Hotel where there was a souvenir shop who was selling a tie. I bought it and quickly took a taxi to Alexendra Hospital where I took the exam. The exam was slightly delayed and we had to wait in the waiting room with symptoms of thyrotoxcicosis. Just before going in for the exam, I saw a clear cut Neurofibromatosis patient whom I thought was one of the patients for exam. However, I saw him taking the taxi away. I started off with Station 5. I was showed a pair of hands which was classical of arthritis mutilans. There was classical telescoping of the fingers. There was also pitting and onycholysis of the nails. I tried to look for erythematous plaques, however there were only hyperpigmentated patches over the scalp and the legs. So I mentioned that this patient was probably receiving treatment. I was asked the pathophysiology of the telescoping fingers. I was also asked regarding the treatment. The next case was a locomotor station. I was asked to examine the patient’s legs. From a far, I looked at his eyes which were typical of a Graves opthalmopathy. As I saw the leg, it was a clearcut pretibial myxoedema. There was peau d orange appearance and I described the rash. I continued on by looking for signs of hyperthyroidism. I was asked the pathophysiology of pretibial myxoedema. I mentioned that it was due to deposition of the mucopolyscharide. I was also asked which layer of the skin was involved and I mentioned it was the subcutaneous tissue. Next I was brought to a lady with moon face. I was not allowed to touch the lady and was asked to just look and comment on the lady. I said that this lady had features of Cushing’s syndrome. I was asked what the other features of Cushing’s syndrome were. I was then asked on how to investigate a patient with Cushing’s syndrome. I mentioned regarding taking a history from the patient regarding steroid/traditional use then doing a 24 hour urine for cortisol then the dexamethasone suppression test. The examiner then asked if the lady had low dose dexamethosone test which was not suppressed and a high dose dexamethasone test which was not suppressed ? I asked for the ACTH level and the examiner said that it was raised. I said that it is most likely from the pituitary gland, probably a pituitary tumour such as adenoma or craniopharyngioma. The next was the fundus. I was asked to examine the Right fundus. It was totally normal and I panic. I was also told off by the examiner that I was touching the eyelids with the fundoscope and that is why the patient kept on blinking. I apologized and then went on to the left eye. It was a clear cut battlefield fundus. The diagnosis was central retinal vein thrombosis. I was asked regarding the causes of CRVO. Then I was asked regarding the treatment of CRVO. I score 4/4 for this station. Next was Station 1 (Respiratory/Abdomen) I was given a lady who was tachypnoeic and as I examined the lady, I noticed a swelling and peau d orange appeance over the R breast. As I examined the lungs, I noticed an area of bronchial breath sound over the R upper zone and thought the trachea was deviated to the R. There was also signs of R lower zone pleural effusion. I concluded that this patient had R sided pleural effusion with R UZ collapse consolidation most likely secondary to R ca breast with mets. Unfortunately the trachea was actually central and there was no collapse consolidation. I scored 2/2 In the abdomen station, there was a Malay man with clear cut hepatosplenomegaly. Liver was 2 finger breaths and spleen 3 finger breaths. They asked me what I found from the peripheral signs. I only found palmar erythema and said that the most likely diagnosis was chronic liver disease with portal hypertension. Retrospectively I noticed pigmentation in the oral cavity but did not mention it because I could not correlate the findings at that time. They asked me of other differential diagnosis and I gave a list. However coming out from the examination hall, another candidate from Singapore mentioned that he thought it was thalassaemia. It never clicked my mind ‘coz I was so focused with the diseases from Ryder which never mentioned this disease. The case thought me a great deal of lesson. I scored 2/2 Station 2 (History) A 25 year old lady who presented with stiffness and jerky movements, uprolling of the eyeball and drooling of the saliva. Take a history. It was clear from the stem that the lady had fits. However, after detail history, this was the 2nd episode that she had a fit and previously was on antiepileptic but defaulted due to development of rash. She was not pregnant and works in a departmental store selling clothes. She travels by bus. I was asked regarding the social history where I was told that I had not taken a thorough one. They wanted to know her hobbies which I missed and asked me how old her parents were. Of course I did not ask those. I scored 2/3 Station 3 Neurology The stem : Examine this gentlemen’s upper limbs neurologically and locate the site of the lesion This gentleman has wasting of the right upper limb and was unable to move the R upper limb at all. There was also hypotonia with areflexia. Sensory loss pin prick and light touch from C5 to T1. Left upper limb was normal. I finished rather fast and even saw an abrasion wound over the R scapula region. The told me I still had time and I went on examine the lower limbs which were perfectly normal. I mentioned that this gentleman has features of lower motor neuron lesion of the R upper limb with sensory loss from C5 to T1. I mentioned the most likely cause of trauma. I was asked regarding the investigation which I would have performed and I answered Nerve conduction study. They then asked me the other differential diagnosis. I was rather blank but when I wanted to open my mouth, thank god the bell rang. Looking back, I think the answer would be a cervical rib and also Pancoast tumour. I scored 4/4 Cardiovascular I was once told that a scar is a gift ! Well, it could also be the killer…I was rather confident in this station, probably overconfident that I thought to myself after the exam that I certainly had a 4/4 for this station. I was totally wrong and I would have passed this exam at that time if I had a 4/4 The stem : This gentleman had palpitation. Please examine his cardiovascular system. This gentleman had a midline sternotomy scar. The examination was smooth and I could hear a metallic click of the first heart sound. There was also a flow murmur at the left sternal edge. I mentioned that this patient had a mitral valve replacement and in sinus rhythm with no evidence of infective endocarditis and gave my reasons. However I also mentioned that this patient had a raised JVP and a parasternal heave, most likely due to pulmonary hypertension. Later when the feedback came back, I was told that I created the signs for pulmonary hypertension. I was asked the reason for the palpitation and the investigations. Lesson to learn – do not create signs ! I scored 2/2 Station 4 I gave up this station before the exam, hoping other stations would cover this coz I was not good at all in communication previously. Moreover, after the mock exam which was held in Penang GH, I did so badly and thought to myself that it was impossible for me to pass this station. However, it was actually a very straight forward case. This middle aged man who had cough for the past 6 months and CXR and CT scan shows a mass at the left apical region suggestive of a lung malignancy. The task was to break bad news and to advise regarding further investigations. I broke the bad news with empathy and he cried for only e few seconds then later just before it ended, he asked me whether he could go to China. He said that he had booked the flight earlier on and was very eager to go with his wife. I thought that there was a hidden agenda here. So I went on a wrong track and asked regarding the China trip. I asked regarding which part of China and whether it was on a hill and the reason why he was going to China. He cornered me by asking me whether he could or could not go. I said that it should not be a problem though I would want to discuss with his wife. I also mentioned regarding the need for bronchoscopy and staging. The examiner told me that I should not have allowed him to go to China as he would probably not be fit as would need a bronchoscopy, staging and further treatment after that. I guess at that time I was thinking that if China meant so much for him, I didn’t want to see him die without able to fulfill his wishes to go to China. I scored 2/2 So, even though I scored four 4’s in the exam, I still failed because I had too many 2s. The bottom line is that you must get the diagnosis right and not create any signs. I waited for 6 months before I sat for the next exam. Dr. Ma sat after 3 months and passed telling me that passing in London was very easy……yea right, that’s because he passed. UK experience (The Dark Side) I would never forget my experience to UK. The journey was long and the price to pay is enormous. Well I guess for Malaysians to go to UK for an exam is not easy as every pound is almost RM7. This means that you have to multiply by 7 anything that you buy over there. I’m sure a lot of us do lots of locums with sleepless nights or over nights just to get enough money to go for the exam. I guess it is the most expensive bet that I have made. So, for those who are going, my advise is that you should also take it as a holiday(not easy though) ‘coz if you fail, you still gain something. A lot of people helped me through to UK. A group of 5 of us went to UK, 2 taking the MRCP, 2 taking Diploma of Dermatology which happens to be the same time and 1(my wife) just went for shopping. I reached London and spent 4 days there with one day in a Communication lecture course, then traveled to Stoke on Trent whereby I failed to get an attachement there due to some unforeseen circumstances. I stayed in the bed and breakfast for a week. Then I traveled to Edinburgh(Livingston) whereby I was fortunate to have a friend who was in France and allowed me, my wife and 3 other friends to stay in her apartment for 2 weeks. I then traveled to Manchester for a PACES course for 2 days before returning back to Edinburgh. I then went to Glasgow for 4 days to do an attachement plus enjoying the beautiful scenery. People in the hospital were nice and friendly. My exam was in Perth, north to Edinburgh. When I reached Perth by train in the evening, I was already so so tired with traveling. I stayed in the nurses quarters but found it very uncomfortable and could not sleep the whole night. The next morning when I woke up, I was like zombie. Station 3 I started of with the Neurology station. I was asked to examine the patient’s lower limbs. He had stocking distribution of sensory loss with normal motor system examination so I concluded that he had peripheral neuropathy. I was asked the causes and I mentioned DM, drugs and they stopped me asking me which type of drugs. I mentioned anti TB and chemotherapeutic agents. They asked me what was the other big group but I said I was not very sure at the moment. I was also asked the investigations for which I answered FBS and NCS. They asked me why I would want to perform an NCS since it was so clearcut. I mentioned that it could differentiate between axonal and demyelinating and they agreed. During the last one minute, they asked me to assess the patient’s speech. I mentioned that he had dysarthria. They then just said look at the face. At that time the bell rang. My friend in the next session mentioned that the man had resting tremor. This was obviously not there when I examined. Probably he just took his Madopar when I examined him in the first session. I thought I did badly but actually got 3/4 CVS This patient has an ejection systolic murmur at the aortic radiating to the neck with a soft pansystolic murmur at the apex. I concluded in the end that this patient has an aortic stenosis and gave my reasons. I was asked whether there was any other murmur. I said that there was a pansystolic murmur in the apex and thought that it was a Gallavardin phenomenon because the murmur did not radiate to the axilla. I was shot at this point. What did you just mention ? Enlighten us about what you said. Is it pathological ? The examiners obviously have not ever heard about Gallavardin phenomenon and thought I had created something. This time I missed the signs of pulmonary hypertension (In Singapore I created it). I was asked the investigations and as the bell rang, they asked me to look again at the JVP and comment. I said it was raised and they were happier. Station 4 After learning from what I did before the Singapore exam, I was trained by a fantastic communication expert, Dr. Kok Lai Sun who happened to pass the exam in Singapore, the same time I sat for that exam. She used to train me almost everyday during lunch time and this time I felt very confident especially in the part of breaking bad news. This shows that comm. Skill can be learned and practice, so do not give up this station. The stem : A middle aged man with valve replacement on T. Warfarin. Came to casualty with reduced consciousness – CT brain shows a massive intracranial bleed. GSC 3/15 , referred to Neurosurgical – not suitable for surgical intervention. Please break the bad news to the wife who just arrived to the hospital. I broke the news with a warning shot and found out later that the patient actually defaulted the INR appointment. I showed empathy. The examiners asked me what else may I have asked and I said to ask regarding the advance directive. I said I did not ask that because I felt that the patient’s wife was not prepared but I did say I would see her again in the afternoon whereby I planned to ask her that. As I was walking out of the room, the examiners said “Good”.I felt I performed well especially for an Asian in comm.. I scored 3/3 Station 5 This station was so bad that I knew I failed as I came out of the station. The first case was a middle aged lady. The examiner asked me to examine the patient’s eyes. I was not very focus at that time and went to examine the visual field. The examiner said skip that. Then I examined the visual field and he said skip that as well. The as I went to examine the movements of the eyes, I noticed that she had diplopia on certain gaze and also her eyes strted to droop so I went on to check for fatiguability without thinking which station I was in. The examiner got really annoyed and started to show dissatisfaction in my performance. I knew that I had approached the wrong way. He asked me what I was doing and I said but he was really unhappy. So he asked me the causes of diplopia and I mentioned and I also said dysthyroid eye disease but the lady did not have a goiter. He asked me whether goiter was necessary and I said no. So I went on to examine the thyroid function whereby she was euthyroid. Probably this lady only had exopthalmos(slight lower sclera seen but I thought was rather common in the Caucasians) and diplopia. The next was the skin station where it was an obvious necrobiosis lipoidica diabeticorum. I said most likely due to diabetes mellitus. The examiner told me that she was not a diabetic. He then asked me how many percent of necrobiosis lipoidica diabeticorum are diabetics. I made a wild guess of 30%. Later I was asked the differential diagnosis and what I would do. I mentioned skin biopsy but said that normally it is not done if the diagnosis is clear cut. Next was a man sitting on a chair and from a far I noticed that the man had arthropathy of the hands. However I was asked to examine the neck of the patient. This patient had restriction of movement of the neck and I said the possible cause of atlantoaxial dislocation with RA in view of the hands. I was then asked to examine the gait and I knew at once that the patient had features of ankylosing spondylitis. Then I examined the hands and noted some pitting of the nails with symmetrical deforming arthropathy but no rashes. Tying all that together, I said that it is psoriatic arthropathy ankylosing spondylitis type. I was immediately asked to go to the next station. When the answer came back, it was a RA + AS ( I thought seropositive and seronegative never happens together). The fundus station was bad too. I was asked to look at the left fundus. The fundus was not fully dilated and when I looked inside, I noticed a large pigmented scar and nothing else. I was then asked to look at the other eye. I found dot haemorrhage over the left eye. I concluded that the patient had a choroidal scar. The examiner was surprised and asked me about the other eye and I said that there was dot haemorrhages and my differential was a laser scar. It turned out to be a proliferative DM retinopathy. I felt that I may have missed the exudated as the eyes were not fully dilated. I scored 1/1 Station 1 The abdomen was also a nightmare. I was brought to a corner room with a small yellow light by the side. There was a lady with a branulla and I knew that she was definitely an inpatient. She was obese and could not fit in the bed. She was also breathless and was lying at 45 degrees. I was asked to examine the lady’s abdomen. I tried to lower the bed but the examiner stopped me and told me to examine the abdomen as it is. This lady had jaundice(difficult to appreciate as the light was yellow and it was winter) and multiple spider naevi. I was stopped after examining the liver and was asked to present the findings. I thought I felt a liver but it was so difficult as the patient was so obese. I then continued and found ascites. I presented my findings and was asked the cause. I said she had features of chronic liver disease and also hepatomegaly and ascites. I was asked the causes of hepatomegaly in chronic liver disease. I was asked the underlying aetiology and I said alcohol, hepatitis. I also mentioned PBC. They asked me whether the liver was big or small in PBC. I said it is small (I was obviously wrong). I scored 1/3 Station 1 (Respiratory) I was shocked when I reach this station and the examiner asked me to do a running commentary on what I find on my way. This patient was tachypnoeic and lung findings suggestive of bilateral lower zone pulmonary fibrosis. I was asked to look at the hands again of which there was very subtle swelling of the MCP joint. I asked the patient whether there was any pain and he mentioned not now but last time. I then said that this patient most likely has rheumatoid lung. They asked me for the causes and I said that I wanted to ask the patient’s occupation and also drug history. I scored 3/3 Station 2 (History) It was a good start in this station but a very bad ending. The interview went on very smoothly. It was a 42 years old lady with central chest pain, gripping and she did mention a few worries. I mentioned that this patient most likely has a cardiac origin chest pain (IHD). They asked me what was against it (It was not on exertion). I was asked the differential diagnosis but did not mention anxiety which was the actual diagnosis. I was asked the investigations and mentioned the investigations for the cardiac. The examiners were not happy because I could not get the diagnosis of anxiety. I scored 1/2 As I went out from the hall, I knew I failed. So, I took the train back to Edinburgh and went on a tour to Edinburgh town. I knew I just wasted about RM20,000 (about 80 nights of locum). But I guess it was an experience I would never forget. Well, at least I saw snow in England(Stoke on trent) when I was there. That was the first time I saw real snow. I was rather depressed when I came back to Malaysia and even applied to change hospital. I am sure that those who have failed twice before would definitely understand my feeling at that time. I even thought of quitting becoming a general practitioner. Well, I do have good friends who tried to console me. I received many sms at that time trying to console me and I do thank all my colleagues in Penang GH who helped me through this period. I then had to decide on whether to take the exam again in Singapore next or to wait for Malaysia. When I reached my house after coming back, I went through the net and applied for the course in Singapore. I did not get a place as I applied rather late. My juniors pass the exam and this gives me even more tension and stress. Well, I guess it is not easy to see your houseman become your specialist. Malaysia experience (The return of the jedi) I promised myself not to make the same mistakes I made again. I prepared myself very hard and more importantly, I prayed very hard too. I had a new sparing partner Dr. Tee CH who helped me much. Dr. Kok LS continued to give me encouragement and lessons on history and communication. I travel to Sungai Petani every Saturday to do short cases, whereby I was taught by Dr. James Smitt who was so nice to take time to train us for short cases every week without fail. I learned so much especially clinical skills from him and it is rare to find people like him. Before the exam I went for courses in IMU, Penang Hospital (which was organized by Dr. Ma) and mock exams (Alor Setar, Penang GH, Sungai Petani). They were indeed helpful not only to gain confidence but to see such beautiful cases. This time I brought everything to KL, especially my tie. I went to KL 2 days before to prevent me getting exhausted the next day from traveling. I booked a 4 star hotel in bukit bintang 2 days before and a 5 star hotel one day before, near the exam centre. I felt so comfortable and for the first time could have a good night sleep the day before the exam. Well, anyway our 5 star hotel is much cheaper than a 3 star hotel in Singapore. This time the first station was the history station which I was not very good in but gave my very best. Station 2 History 55 years old lady with fever for 2 weeks and FBC shows Hb 8.2 g/dL, WBC 2.4 Plt 108. Please take a history from this patient. The lady told me that her GP said she had jaundice and also had a thyroid surgery done 3 years ago for a thyroid ca. The diagnosis was a thyroid ca with bone marrow and liver mets. I was asked the differential diagnosis – SLE, chronic infection eg malaria, BM disease, HIV. I gave my points for and against. I was asked of other infection that could happen if patient was swimming in a pond – I said Leptospirosis. I was also asked the investigations that I would do. Station 3 CNS I was asked to examine the gait of a patient middle aged. On examination of the gait, there was broad based and unable to perform tendem walking, falling to the R side. There was cerebellar signs. I noticed loss of arm swing but there was no tremor and I went on examining the lower limbs which was normal. I was then asked to present and state the cause. I said he had cerebellar signs but could not find out the underlying aetiology. I slowly mentioned the causes. The examiner asked me to examine the tone of the upper limb again and I still felt it was not increase or cogwheel. I said in fact it was reduced, thinking in mind the cerebellar signs I got. Just before the bell rang, he asked me to look at the face and I mentioned masked like most likely Parkinsonism. My other friend in the same exam got the Parkinson features but missed the cerebellar signs. In fact the man had Parkinson Plus syndrome (Olivopontocerebellar degeneration). Station 3 CVS I moved on without thinking of that station which I did not do that well. As I examined the patient, I noticed the patient had collapsing pulse and a Corrigan’s sign. Apex was displaced and normal S2 with a EDM at LSE and ESM at aortic radiating to the carotids. I diagnosed as mixed aortic valve disease with predominant AR. I was asked the causes of the mixed aortic valve and mentioned degenerative, bicuspid valve and collagen vascular disease. I was asked one single blood test I would perform for this patient and I mentioned VDRL. I was asked the other investigations of which I mentioned ECG, CXR and Echo stating what I would like to look for in those investigations. Station 4 Comm The stem was this middle aged man with idiopathic dilated cardiomyopathy and atrial fibrillation on T. warfarin, T. Carvedilol, T. Perindopril, T. Frusemide. Explain the diagnosis to the patient and also the medications that he is taking. After explaining to the patient the diagnosis, he asked me the cause and I mentioned that it is not known even after tests such as Echo, ECG, CXR and so on. I mentioned that this is common and it happens. I explained regarding the medications and he was worried about the T. warfarin as he said that he is working in a construction site and risk of trauma. I told him that the risk is even higher if he does not take the T. Warfarin and told him the complications including a stroke.I advise for regular INR check. He was also worried about impotence with the beta blocker. I also mentioned the side effect of chronic cough with the T. Perindopril. It went on quite smoothly and the examiner asked me whether I thought the patient would comply. I said yes and he asked me whether I was sure. I said probably I would need to reinforce this and perhaps my consultant would also help me advise him. I was asked regarding the impotence part but I mentioned that I did try to ask further on why the patient was worried but he just said nothing. Station 5 Fundoscopy I was asked to look at the fundus. There was laser scars in both eyes with lots of hard,soft exudates and also dot blot haemorrhages. There was also flamed shaped haemorrhages in the right eye. Both optic disc looks pale but more on the right. I have never seen such beautiful silver wiring in the left eye before. I told the diagnosis except the optic disc but was later asked regarding that and gave my diagnosis of proliferative diabetic retinopathy with hypertensive retinopathy. I was asked for differential and I said that the left eye could also be a central retinal vein thrombosis as a differential. Hands I was asked to examine the patient’s hands. There was bilateral symmetrical deforming arthropathy over the MCP and PIP joints of both hands. They were rather subtle. There were no nail changes and rashes. There was positive Tinel on the right and a Rh nodule on the R elbow. I went on to examine the movements, function and other systems including the lungs but was stopped. The examiner asked me my diagnosis and I said that it is RA and the disease is inactive and gave my reasons with carpal tunnel syndrome on the R. I was asked regarding what other signs and I looked back and noticed I forgot to mention the wasting and also the swelling over the wrist and mentioned those confidently. I was then asked the signs of activity and as I was answering, the alarm rang for me to go to the next substation. I was asked to examine the pateint’s face. This time I am very focus after my experience from the UK experience(The Dark side). I screen through first without touching the patient from a far and noticed he had large hands and feet. I knew that it was a acromegaly and went on examining the face, tongue, teeth, visual field. Then I went on to the hands and look for proximal myopathy. When I reached the neck, I noticed a small scar at the throat and then I wanted to ask the patient to open the shirt but was asked and the examiner told me it was ok. Then I went on the the feet. I was then asked my findings of which I mentioned it smoothly. I was asked what else in the neck besides the scar and I mentioned a goiter. I was then asked about the feet. I mentioned regarding heel pad of the feet and also a large feet, putting my foot next to the patient’s. The examiner told me that mine was also big and he smiled. Then both the examiners laughed. I was brought to a lady with a rash on the face and was asked to examine the face. I mentioned that she has a malar rash with some areas of hyperpigmentation but no follicular plugging. I was asked other presentation and I mentioned. I was also asked what the commonest mode of presentation neurologically and I said cerebral lupus initially but then later said I was not sure. I was asked regarding activity and mentioned ESR . I was then asked also regarding CRP and said yes I would do that too. Station 1 (Abdomen) This was a young Malay lady who has a moon face at a glance with a scar at the RIF. I thought to myself that this must be a renal transplant ! As I went on to examine her, she did not have any fistula and no evidence of cyclosporine usage. She was pale and there was hepatosplenomegaly with liver 2FB and spleen 4 FB. I was thinking to myself this must be thalassaemia as I missed that in the Singapore experience(The new beginning). But to my surprise as I mentioned hepatosplenomegaly, the examiner stopped me and did not ask me for the underlying cause. He asked me what the mass could be and I said spleen. I was asked how to differentiate between the spleen and the kidney and gave a list. I was then asked how to investigate for it and I said ultrasound abdomen. I was then told that the ultrasound could not pick that up. So I said CT scan abdomen. The examiner then challenged me by saying that the CT scan could also not tell. Then I said MRI. I was then asked which was better of which I said CT scan as I read previously that MRI could cause motion artifacts. He still asked me how I would differentiate and I said I would refer to my consultant and both the examiners laughed. I mentioned CT should be able to tell. I was asked the differentials and I mentioned them including arising form the stomach, colon, pancreas. I mentioned that if I suspect it is from the stomach then perhaps an OGDS may help. I was brought to the next station. Station 1 (Respiratory) This was a young Indian man with clubbing and coarse crepitations over the bases of the lungs. I asked the patient to cough and it was a wet cough and the crepts also changed. I knew at once that it was a bronchiectasis. It is always a fear to differentiate between bronchiectasis and pulmonary fibrosis of lower lobes. I mentioned my diagnosis and said that it is most likely due to pulmonary tuberculosis which was rather endemic here. I was asked how I would investigate and I mentioned CXR and also HRCT to look for reticular nodular appearance which could help me in my management. I was then asked how it would help me in my management of which I mentioned that surgery could be an option if the bronchiectasis is localised. I was asked the other management and mentioned regarding physiotherapy, postural drainage and antibiotics. I also mentioned regarding vaccination and they asked me which type of vaccination I would give. This time I felt much better after the exam and went shopping in Wan Utama as I was staying in One World hotel and also watched Bourne Ultimatum that night. I moved back to a 4 star hotel in Bukit Bintang that night in view of the cost. In conclusion, I think the exam was rather tedious and stressful but did teach me a lot. I had sleepless nights even before obtaining my results from the internet. It took me 2 years just for the PACES and practicing for PACES can be very tiring and I am very glad it is over I am sure that everyone who has gone through this journey have their own experience and I do hope that sharing these experiences will help those who are thinking of taking the MRCP exam ! ACROMEGALY LOOK FOR - Scar (trasfrontal),large hands,protrusion of lower jaw,inter dental separation,Visual field defects,fundosopy (HTN,DM,intracranial tension) ASK ABOUT- Size of hat,shoes,change in appearance,HTN,DM COMMENT ON DISEASE ACTIVITY - Sweating,HTN,glycosuria,Headache,skin tags TESTS - ECG,CXR- Cardiomegaly, Oral GTT- failure of suppression of GH,IGF-1 level,MRI pituitary fossa,thyroid function,prolactin, testosterone, perimetry THE GLUCOSE TOLERANCE TEST IS DIAGNOSTIC - Acromegalics fail to suppress GH below 1mU.IGF-1 is almost always rised in Acromegaly TREATMENT - Most patient are treated with surgery usually trassphenoidal.Radiation if surgery not feasible.Somatostatin analogues (octreotide) or Bromocryptin Can be tried. CAUSE OF DEATH - Cardiac failure,HTN complications,Tumor expansion /hemorrhage Like ADDISON'S DISEASE IN PACES. FINDINGS : There is generalized pigmentation which is more marked in the skin creases (e.g.palmar), in scars, in the buccal mucosa and at pressure points.This suggests Addison’s disease or Nelson’ssyndrome. ( Nelsons syndrome > Look for temporal field defect, abdominal scar of bilateral adrenalectomy). LOOK FOR > loss/sparse axillary hair, presence of Medic Alert bracelet and postural hypo tension/Vitiligo or pernicious anemia to suggest autoimmune in origin,features of mucocutaneous candidiasis to suggest Polyglandular syndromes Type 1/features of thyroid disease ( hyper- or hypothyroidism) to suggest Polyglandular syndrome Type 2/ abdomen for adrenal scar due to previous operation. TELL EXAMINER that you would like to look at patient's CXR to see any evidence of tuberculosis changes in CXR. Associations > vitiligo (15% of patients with idiopathic Addison’s), autoimmune thyroiditis, diabetes mellitus, pernicious anemia and hypoparathyroidism, Premature ovarian failure. Causes :Common causes Autoimmune adrenalitis /Tuberculosis (look for lung signs)/ Bilateral adrenalectomy Other causes > /Amyloidosis /Haemochromatosis/Granulomatous disease (sarcoidosis) / Fungal diseases (histoplasmosis) /Meningococcal and pseudomonal septicaemia/AIDS/Adrenal haemorrhage. OTHER Causes of abnormal generalized pigmentation > ACTH therapy / Cushing’s disease/Thyrotoxicosis/ Ectopic ACTH (especially oat cell carcinoma)/ Mal absorption syndromes/ DRUGS (Amiodarone -grey pigmentation)/Cytotoxics Minocycline/Phenothiazines ( blue- grey pigmentation) /Antimalarials/Haemochromatosis/Argyria/Chronic arsenic poisoning. Confirm diagnosis > Random cortisol Short synacthin test (normal cortisol rise above 600 nmol/l or increase by 300 nmol/l) ACTH level. Like ANKYLOSING SPONDYLITIS - Is a form of the spondyloarthritides, that involves inflammation of the sacroiliac joints, spine, joints, and entheses, as well as extra spinal lesions of the eye, bowel, and heart.. CLINICAL SIGNS TO BE DEMONSTRATED... 1. Reduced range of movements though out spine. 2 .Question mark posture. >> Fixed kypho scoliosis of thoracic spine, extension of cervical spine & absent lumbar lordosis. 3.Increased occiput - wall distance ( >5cm). 4. Schober's test.>>>> 2points marked 15 cm apart on dorsal spine expand by less than 5cm on maximum forward flexion of spine. 5. Reduced chest expansion>> chest expansion (<5cm) on maximum inspiration... Complications you should look for : 5 A's 1.Anterior uveitis ( commonest) 2Apical fibrosis 3.Aortic regurgitation - 4% 4.AV nodal conduction defects. 5.Arthritis.. BRONCHIACTASIS > is a condition in which recurrent or persistent bronchial sepsis leads to irreversibly damaged and dilated bronchi. Clinically features : Chronic productive cough/copious,persistently purulent sputum/Fever/Malaise/Haemoptysis→ can be torrential/Wt loss/Clubbing Causes 1. Post pneumonic (measles, pertussis, tuberculosis) 2. Bronchial obstruction (CA, nodal compression, foreign bodies) 3. Allergic bronchopulmonary aspergillosis 4. Globulin deficiency (congenital/acquired) 5. Kartagener’s syndrome (immotile cilia syndrome). 6. Cystic fibrosis Uncommon 1. Yellow-nail syndrome/2. Riley-Day syndrome/3.Idiopathic Most common organisms INVOLVED > Staphylococcus aureus, Haemophilus influenza, Pseudomonas aeruginosa Complications: • Pneumonia/ Pneumothorax/Sinusitis/Haemoptysis/ Brain abscess/ Amyloidosis Investigations: 1. Sputum C/S 2. CXR 3. CT chest 4. Spirometry 5. Bronchoscopy /bronchography • Assessment of ciliary function • Serum immunoglobulins • Sweat test for CF • Skin prick test for ABPA How would you treat bronchiectasis? The mainstay is good physiotherapy to teach airway clearance techniques/ POSTURAL DRAINAGE . Broncho dilators have a role if there is airway obstruction. Antibiotics should be given in exacerbations, and long-term antibiotics should be considered if there are 3 or more exacerbation a year. Occasionally lung resection may be considered, for example if there is localized disease not adequately managed with medical treatment. Like A candidate's experience:( Past PACES experiences). You may also please feed your experiences . Experience 1 Station 5: HHT>> History was a lady in her 60s admitted with tiredness and SOB. Hb was 6 and Fe deficient. Pt transfused and asking to go home. My task was to take history and focused examination. Pt had no overt symptoms of blood loss on questioning. When I asked pt to move onto couch so I could examine abdomen, examiners stopped me and told me it was normal. I proceeded with the history - pt mentioned in the FH that her dad had similar problems and suffered from nosebleeds - which she had also had over the previous few weeks. I then noticed the teleangiectasia on her lips. I asked her to open her mouth and noted same on buccal mucosa. The questions were focused around management of epistaxis in this case, the mode of inheritance, and whether I thought her anemia was solely due to epistaxis. I thought that she may also be having occult GI blood loss and this should be investigated further. I also tried to examine her chest (AV mals) - examiner asked me what I was listening for. I think some of the other candidates did the same too! Graves Eye Disease and Goiter The second case was a middle aged lady admitted to the hospital with SVT. Asked to take focused history and examination. Immediate observation of exopthalmos and proptosis. Examined neck and thyroid status. Questions were focused on my differentials, which blood tests I would request, and whether I felt see was hyperthyroid, eu, or hypo. Clinically she seemed euthyroid but in light of the history of SVT, hyperthyroidism needed to be excluded. Resp was a pulmonary fibrosis.>> Asked about differentials, CT findings and what honeycombing represented.Abdo was an elderly lady with splenomegaly and a stoma/ascites bag on site of previous paracentesis. (questions were on diff of splenomegaly). Cardio was AR ( I felt there was AS and AR - questions focused on which lesion i felt was the most predominant and the mx of AR) Neuro was a myasthenic patient who only had unilateral ptosis. I thought the instruction in this case was difficult - pt having weakness in arms and legs and blurring of vision. It may be useful to have a system of examining a myasthenic to illustrate the relevant signs or to show examiners that you know what to look for. I didn't have one and I think it showed. History taking was a gent with progressive limb and neck weakness. (? Eaton Lambert, ? MG ?MND). Comm skills >> was a dental nurse recently returned from Africa with new diagnosis of sputum pos TB. ? had exposure to HIV with previous partners whilst in Africa. Mother also died of TB. Lady was a single parent with two young children. CHRONIC KIDNEY DISEASE . Major causes of chronic renal disease in developed countries - (OST clinical medicine) Diabetes melites 34% Glomerulonephritis 21% Hypertension 12% Miscellaneous '10% (including drugs. paraproteinaemia, obstructive uropathy) Polycystic kidney disease 6% Reflux nephropathy 6% Analgesic nephropathy 6% Uncertain 5%.. Hiii FRIENDS THESE ARE THE COMMON CASES CASES FOR PACES YOU MAY COME ACROSS IN YOUR MRCP PACES . YOU MAY PLEASE ADD CASES THAT YOU REMEMBER as Comments please ..... LikeLike · · Share  Ahmad Shaheen and 52 others like this.   View 14 more comments Motaz Özil Hassan Tarig Yesterday at 08:41 · Like  Jiauddin Farhad Thanks a lot ..... following... Yesterday at 09:58 · Like · 1  Alsafi ABolmakarim Eid NEUROFIBROMATOSIS 13 hrs · Like  Motaz Özil Omer Mohammed Alamin 12 hrs · Like  SPOT DIAGNOSIS. LikeLike · · Share  15 people like this.  View 5 more comments  Akhtaruzzaman Shumon CRVO 29 October 2013 at 19:44 · Like · 1  Shuhaib Kunjhibava The diagnosis is central retinal vein occlusion(CRVO). The veins are tortuous and engorged. Hemorrhages are scattered riotously over the whole retina, irregular and superficial, like bundles of straw alongside (papilloedema and soft exudates may also ...See More 1 November 2013 at 01:56 · Edited · Like · 7  Mohammad Jalil CENTRAL RETINAL VEIN THROMBOSIS DIABETIC FOOT/ CHARCOT'S JOINT CASE PRESENTATION There is an ulcer on the sole of the left foot .There is callous formation around ulcer and the normal concavity of foot is lost. There is loss of sensation to light touch, vibration and pinprick in a stocking distribution. The distal pulses are not palpable and there is loss of hair on the lower legs which are shiny.The ankle joint is greatly deformed and swollen. There is PAINLESS restriction of movements at ankle joint & there is crepitus accompanying movement. This patient has peripheral neuropathy, a neuropathic ulceron the sole of his foot ,charcot joint and evidence of peripheral vascular disease. It is likely that he has underlying diabetes mellitus .I want to check fundus & check urine for sugar . NB: Joint should be manipulated very gently. Factors which contribute to the production of diabetic foot lesions are Injury /Neuropathy/Consequent formation of callosities/Small vessel disease/Large vessel disease producing ischaemia and gangrene of the foot/Increased susceptibility to infection/Mal distributed pressure and foot deformity leading to/increased likelihood of friction and trauma Other causes of peripheral neuropathy & charcots joint . Any cause of loss of sensation in a joint may render it susceptible to the development of a neuropathic arthropathy 1 DM 2 Tabes dorsalis 3 Leprosy 4 Syringomyelia 4 Porphyria 5 Amyloidosis 6 Progressive sensory neuropathy (familial). 7.Charcot–Marie–Tooth disease 8.Neurofibromatosis (pressure on sensory nerve roots), *NB: in the predominantly neuropathic foot the pulses may be present or even bounding, and the veins may be prominent (Ward’s sign). Autonomic denervation opens up arteriovenous shunts. Diabetes mellitus (toes – common; mid-foot – more common; ankles – rare).. LikeLik THIS Patient has painful, erythematous discrete, nodular lesions in the anterior aspect of the legs.These lesions are are very typical of erythema nodosum. Proceed by asking for symptoms and looking for signs of diseases that can cause erythema nodosum. ..like the following Have you had a recent sore throat? (post- streptococcal infection). Are you taking any drugs? Do you have a cough or are you short of breath? (sarcoidosis). Do you have chronic diarrhoea? (inflammatory bowel disease). Causes can be memorized - DIPS OUT DRUGS ( Penicillin, sulfa drugs) Infections (streptococcal.) Pregnancy SARCOIDOSIS Oral contraceptive pills) Ulcerative colitis (Inflammatory) TUBERCULOSIS). LikeLike · · Share If you suspect liver disease during PACES examination, check for peripheral stigmata of chronic liver disease which indicate chronic liver disease. TOP 5 causes of chronic liver disease/cirrhosis in MRCP examination are 1.Alcohol (Always the number one cause in western countries) 2. Chronic hepatitis (top in the list in Asian countries) From MRCP, points of view other causes you need to remember- 3. Liver malignancy 4.Cryptogenic (idiopathic), 5.Budd-chiari syndrome and 6.haemochromatosis. Look for ant evidence of decomposition. 3A's > 1. Asterixis, 2.Ascites & 3. Altered consciousness (encephalopathy). Clues that you look for from MRCP point of view > check 1. Parotid swelling/Dupuytren's contracture (Signs of peripheral neuropathy, proximal myopathy, beriberi heart (CCF), cerbellar signs > Alcoholic liver disease 2. Tattoo marks, thrombosed veins > hepatitis B or C (paucity of liver cirrhosis signs in hep C) 3. Skin pigmentation / slate grey skin/2nd & 3rd metacarpal arthropathy > Hemochromatosis 4. Xanthelasma with scratch marks /Middle aged ladies > Primary biliary cirrhosis ( Can keep patient with mild hepatomegaly with sratch marks (cholestasis) & jaundice may not be that evident or with very minimal icterus) 5. Barrel shaped chest with tachypnea – Alpha one antitrypsin deficiency 6. Kayser Fleischer ring, family h/o neuropsychiatric l problem, involuntary movements > Wilsons disease 7. Elevated JVP > heart failure/TR/constrictive pricarditis 8. Palpate Breast for malignancy ( cause liver secondaries). 9. Evidence of Diabetes > fatty liver Causes of enlarged liver in chronic liver disease - Alcoholic liver disease - Primary biliary cirrhosis - Malignant transformation. Like Typical presentation for a patient with hepatic malignancy>> This patient is cochectic.' There is no evidence of anemia, icterus, or stigmata of chronic liver disease. There is no lymphodenapothy.The abdomen is not distended.' and there is no clinical evidence of ascites There is hepatomegaly with a non-tender liver edge palpable 4 inch below the costal margin.' There is also a palpable umbilical nodule.There is no evidence of splenomegaly. There are no audible bruit or a hepatic venous hum.There are no signs· of encephalopathy to suggest hepatic failure' This patient has hepatomegaly. The presence of cachexia and an umbilical nodule suggests malignancy as the most likely cause... LOWER LIMB EXAMINATION IN PACES “Experience is something you don’t get until just after you need it” It is very important that your examination is smooth using acceptable techniques and, always giving the impression that you have done it before many times. Remember the two cardinal rules of neurology: 1.Where is the lesion? 2.What is the lesion? The common lower limbs neurological disorders in PACES includes . (LEARN THE FOLLOWING TOPICS) 1.Spastic paraplegia 2.Hemiplegia 3.Peripheral neuropathy/Flaccid para paresis. 4.Abnormal gait 5.Motor neuron disease 5. subacute combined degeneration of the cord 6.Muscular dystrophy 7.Cauda equina syndrome 8.Friedrich’s ataxia 9.Peroneal muscular dystrophy. 10.foot drop Like CARDIOVASCULAR SYSTEM : MITRAL STENOSIS IN PACES - CASE PRESENTATION. Mr X is comfortable at rest. There is a malar flush and a left thoracotomy scar. The pulse is 80/mt,regular small volume ( if patient is in AF - pulse is irregularly irregular & varying volume). JVP not is not raised. Apical impulse is tapping & not displaced There is a left parasternal heave. On auscultation first heart sound is loud, P2 is loud .There is mid-diastolic rumbling murmur better in apical area & in left lateral position. (presystolic accentuation heard ONLY if the patient is in sinus rhythm) . There is opening snap ( if mitral valve is pliable). MY DIAGNOSIS IS MITRAL STENOSIS WITH PULMONARY HYPERTENSION IN SINUS RHYTHM (IN AF if there is ) ,NO SIGNS OF HEART FAILURE (in heart failure if signs of heart failure present) & NO PERIPHERAL STIGMATA OF INFECTIVE ENDOCARDITIS & PATIENT HAD VALVOTOMY IN THE PAST The questions the EXAMINERS ask we will discuss as comments below..... Thanks . Like What do you think the cause of Bilateral ptosis in this patient ? Like YES, Answer is Myesthenia Gravis. Myasthenia gravis is a relatively uncommon disorder. However, it is the most common disorder of neuromuscular transmission.. NEUROFIROMATOSIS IN PACES Neurofibromatosis > AD, involves skin, nervous system and skeleton. There are 2 types: Neurofibromatosis 1 (Von Recklinghausen's disease). Chromosome 17, 1:2500 Cafe au lait spots/ axillary/ inguinal freckling/Lisch nodules in iris (seen in 90%)/peripheral neurofibroma/optic gliomas (2%) ,may have low IQ or renal artery stenosis. Suggest that you would like to order MRI to look for optic glioma /osseous lesions (sphenoid dysplasia or thinning of long bone cortex with or without Pseudoarthroses). Neurofibromatosis 2. (Chromosome 22) Features: bilateral acoustic neuromas sensorineural hearing loss is first sign. cafe au lait spots/juvenile posterior sub capsular lenticular opacity ( a form of cataract). 1)look for fibroma, plexiform neurofibroma, cafe-au-lait spots, axillary freckles, Lisch nodules in the iris . 2). Ask for family history. 3). Check for 1.Hearing (acoustic neuroma) 2.Visual acuity and fundi (optic glioma) 3.Look for kyphoscoliosis 4.Check BP for HPT (phaeochromocytoma IS AN ASSOCIATION) . Common questions examiners would ask you, 1) What is the inheritance pattern of this disease? 2) What are the possible complications of this illness? 3)How do you manage this gentleman? 4) What is your advice if this gentleman is going to get married?. LikeLike · · Share MRCP PACES TIPS ONE CANDIDATE ASKED ME ABOUT DRESS CODE & WHAT A CANDIDATE SHOULD DO , ON THE DAY OF PACES EXAM. I am sharing an official MRCP video & some TIPS I gathered during my PACES preparation . I should thank to the doctor who posted these TIPS on Internet. MRCP PACES TIPS - What to wear for MRCP (UK) PACES? ”Half is skill, half is appeal.” The words of wisdom, Trust me; looking professionally smashing in your best garment will put you in a good stead to impress the examiners. Here are some tips what to wear for a male candidate. 1. Wear a slim-fit dress shirt– you want to aim for snug fit, NOT OVERLY TIGHT which would otherwise encumber your physical examination and compromise your techniques. 2. Wear a slim-fitstraight-cut pants – again, you want the pants to fit just nice and not overly constrictive. 3. Stay away from short-sleeved shirts – they look too casual. 4. Instead, get a long-sleeved dress shirt and fold it to elbow length. This will make you look 100 times more refined. Put on a shining pair of dress shoes. The hue must fit the color of your belt. 5. NO TIES, NO RINGS, NO SUIT,NO WRIST WATCH - In line with the Royal Colleges infection control recommendation. Suits and ties will be completely phased out as exam attire. The weight of jacket and the pretense of a tie is something interfere with your performance when facing 10 tempestuous patient encounters! 6. Meticulous grooming, it goes without saying 7. Wear a reasonable whiff of fragrance, don’t overdo it. 8. Do your shopping early. Get comfortable in the dress attire and wear it a few times before going for the real deal. 9. A candidate who display discerning discretion in his appearance is sure to exude an air of confidence so vital to planting a reassuring impression on the examiners. 10 If you have any more ideas /tips please share.. VIDEO LINK IS BELOW, HAVE A LOOK http://www.youtube.com/watch?v=L9P7PNipoQA Thanks Dr Shuhaib Kunjhibava MBBS,MD (Internal medicine),MRCP (UK). LikeLike · · Share OSTEOGENESIS IMPERFECTA: > This patients sclerae are slaty blue.>> Ask for h/o bone fracture & hearing impairment.Proceed to see any evidence of deformity from poor fracture healing.Patient may be deaf due to otosclerosis). This is a case of Osteogenesis imperfecta. Osteogenesis imperfecta is due to defects in type I collagen.The blueness is due to the thin sclerae allowing choroid pigment to show through.Serum alkaline and acid phosphatase are often elevated and the urine often contains hydroxyproline, pyrophosphate and glycosaminoglycans. There is no specific treatment.Bisphosphonates are tried . Blue sclera may occur in Marfan’s syndrome,Ehlers–Danlos syndrome & Pseudoxanthoma elasticum.... LikeL PRACTICE THIS CASE & WRITE YOUR COMMENTS.> This young lady has joint pain involving both hands of 2 months duration & skin rash. ( Manage this case as STATION - 5 CASE, Your approach should include Introduce yourself to patient, focused history, focused clinical examination (in 6 minutes) & covey your diagnosis & plan of management to the patient & address patient concern in 2 minutes). Practice yourself , that will make you fit for examination. TRY TO COMPLETE THE CASE IN 8 MINUTES). We will discuss the case in the end. LikeLike · · Share  Ahmad Shaheen and 18 others like this.  Mohammed Elagouri history( details of joint pain ....details of rash....then screening of all possible features of sle. like lung heart renal nervous and psychiatric manifestions...history of abortion...drug history for drug induced lupus....history of ttt especially steroids and chloroquine.....and side effects like cushing and retinopathy....childrens born with heart block....social history completely...concerns......examination ...rash alopecia..hands...lower limbs.....lung heart auscultations..abdomen HSM...signs of cushing... 23 October 2013 at 14:38 · Like · 6  Shuhaib Kunjhibava well done Mohammed Elagouri. You covered most of the points in history & focused examination. The remaining part is explain your diagnosis to the patient & plan of management. Address patients concern. And get prepared for questions by examiners (2 minutes session). See specifically for distribution of rash, presence/absence of /any vasculitic rash/Any signs to suggest patient is on long term steroid therapy/ look for other systems involvement. Tell examiner you want to check blood pressure/fundoscopy for cytoid body/ urine for proteinuria and ask for drugs history. Remember in drug-induced SLE patients, their anti-histon antibody is positive.common drugs causing SLE > hydralazine, procainamide and isoniazide.